Bad Bug Book Flashcards

Question

Paralytic Shellfish Poisoning Food Sources:

Answer 1

Food Sources: PSP generally is associated with **bivalves**, such as _mussels, clams, cockles, oysters, and scallops_ (excluding the scallop adductor muscle)

Answer 2

Mortality: This disease generally is not life-threatening

Answer 3

Onset: Onset of the disease, depending on the dose of toxin ingested, may be as little as **30 minutes to 3 hours**.

Answer 4

Symptoms and course of illness: DSP is primarily observed as a generally **mild gastrointestinal disorder**; i.e., nausea, vomiting, diarrhea, and abdominal pain, accompanied by chills, headache, and fever. Symptoms may last as long as **2 to 3 days**, with **no chronic** effects.

Answer 5

Food Sources: DSP generally is associated with **mussels**, **oysters**, and **scallops**

Answer 6

Mortality: No fatalities have been reported

Answer 7

Onset: Onset of this disease occurs within a few **minutes** to a few hours

Answer 8

Symptoms and course of illness: Both **gastrointestinal** and **neurologic** symptoms characterize NSP, including tingling and numbness of lips, tongue, and throat; muscular aches; dizziness; diarrhea; and vomiting. Duration is fairly short, from a few hours to several days. Recovery is complete, with few after-effects.

Answer 9

Food Sources: NSP generally is associated with **oysters** and **clams** harvested along the Florida coast and the Gulf of Mexico. In 1992 / 1993, NSP was linked to shellfish harvested from New Zealand.

Answer 10

Mortality: All fatalities, to date, have involved **elderly** patients

Answer 11

Onset: The toxicosis is characterized by onset of **gastrointestinal** symptoms within **24 hours**; **neurologic** symptoms occur within **48 hours**.

Answer 12

Symptoms and course of illness: Human clinical signs of domoic acid toxicity are reported as mild **gastrointestinal** symptoms (vomiting, diarrhea, abdominal pain), from an oral dose of _0.9-2.0 mg_ domoic acid (DA)/kg body weight. **Neurologic** effects (confusion, short-term memory loss, disorientation, seizure, coma) are reported from an oral dose of _1.9-4.2 mg_ DA/kg body weight. The toxicosis is particularly serious in **elderly** patients, and includes symptoms reminiscent of Alzheimer’s disease.

Answer 13

Food Sources: ASP generally is associated with **mussels**. Other taxa of interest include _scallops_, _razor clams_, _market squid_, and _anchovy_

Answer 14

Mortality: No known fatalities to date.

Answer 15

Onset: Symptoms appear in humans within **hours** of eating AZA-contaminated shellfish.

Answer 16

Symptoms and course of illness: Symptoms are predominantly gastrointestinal disturbances resembling those of diarrhetic shellfish poisoning and include nausea, vomiting, stomach cramps, and diarrhea. Illness is self-limiting, with symptoms lasting 2 or 3 days

Answer 17

Food Sources: AZAs have been detected in **mussels**, **oysters**, **scallops**, **clams**, **cockles**, and **crabs**

Answer 18

Diagnosis of shellfish poisoning is based entirely on observed symptomatology and recent dietary history

Answer 19

Good statistical data on the occurrence and severity of shellfish poisoning are largely unavailable, which undoubtedly reflects the inability to measure the true incidence of the disease. Cases are frequently misdiagnosed and, in general, infrequently reported. The proliferation (sometimes referred to as “blooms”) of the toxin-producing algae and subsequent toxin events or outbreaks of illness appear to be increasing around the world.

Answer 20

All humans are susceptible to shellfish poisoning. A disproportionate number of shellfishpoisoning cases occur among (1) tourists or others who are not native to the location where the toxic shellfish are harvested and (2) fishermen and recreational harvesters. This may be due to disregard for either official quarantines or traditions of safe consumption

Answer 21

PSP – 0.8 ppm (80 μg/100 g) saxitoxin equivalents  NSP – 0.8 ppm (20 mouse units/100 g) brevetoxin-2 equivalents  DSP – 0.16 ppm total okadaic acid equivalents (i.e., combined free okadaic acid, dinophysistoxins, acyl-esters of okadaic acid and dinophysistoxins)  ASP – 20 ppm domoic acid (except in the viscera of Dungeness crab, for which the action level is 30 ppm)  AZP – 0.16 ppm azaspiracid 1 equivalent

Answer 22

PSP – Despite widespread PSP closures, poisoning events still occur and are generally associated with recreational harvest. For example, in July 2007, a lobster fisherman harvested mussels from a floating barrel off Jonesport, ME (an area that was currently open to shellfish harvesting), and he and his family ate them for dinner. All four consumers became ill with PSP symptoms, and three of them were admitted to the hospital. It was apparent that the barrel of mussels had originated further up the coast in an area that had been banned to commercial harvest. DSP – Although there have been numerous outbreaks of diarrhetic shellfish poisoning around the world, until recently there were no confirmed cases of DSP in the U.S. that were due to domestically harvested shellfish. However, in 2008, a large portion of the Texas Gulf Coast was closed to the harvesting of oysters due to the presence of okadaic acid in excess of the FDA guidance level. Although no illnesses were reported, these were the first closures in the U.S. due to confirmed toxins. In 2011, approximately 60 illnesses occurred in British Columbia, Canada, and 3 illnesses occurred in Washington State due to consumption of DSP-contaminated mussels. Subsequent harvesting closures and product recalls were issued. NSP – Until NSP toxins were implicated in more than 180 human illnesses in New Zealand, in 1992/1993, NSP was considered to be an issue only in the U.S. Outbreaks of NSP are rare where programs for monitoring K. brevis blooms and shellfish toxicity are implemented. An NSP outbreak involving 48 individuals occurred in North Carolina, in 1987. A series of NSP cases occurred along the southwest coast of Florida, in 2006, after people consumed recreationallyharvested clams from waters unapproved for shellfish harvesting. ASP - The first human domoic acid poisoning events were reported in 1987, in Canada. While domoic acid exposure still exists, there have been no documented ASP cases since 1987, following implementation of effective seafood toxin-monitoring programs. AZP – There have been no confirmed cases of AZP in the U.S. from domestically harvested product. Examples from around the world include: (1) Several AZP intoxications (20 to 24) were reported in Ireland, in 1997, following consumption of mussels harvested from Arranmore Island. (2) An AZP outbreak involving 10 people was reported in Italy, after they consumed contaminated mussels produced in Clew Bay, Ireland. (3) In 1998, in France, 20 to 30 AZP illnesses were attributed to scallops that originated in Ireland. (4) In 2008, the first recognized outbreak of AZP in the U.S. was reported, but was associated with a mussel product imported from Ireland.

Answer 23

Scombrotoxin is a combination of substances, histamine prominent among them. Histamine is produced during decomposition of fish, when decarboxylase enzymes made by bacteria that inhabit (but do not sicken) the fish interact with the fish’s naturally occurring histidine, resulting in histamine formation. Other vasoactive biogenic amines resulting from decomposition of the fish, such as putrescine and cadaverine, also are thought to be components of scombrotoxin. Time / temperature abuse of scombrotoxin-forming fish (e.g., tuna and mahi-mahi) create conditions that promote formation of the toxin. Scombrotoxin poisoning is closely linked to the accumulation of histamine in these fish.

Answer 24

FDA has established regulatory guidelines that consider fish containing histamine at 50 ppm or greater to be in a state of decomposition and fish containing histamine at 500 ppm or greater to be a public health hazard

Answer 25

No deaths have been confirmed to have resulted from scombrotoxin poisoning.

Answer 26

Dose: In most cases, histamine levels in illness-causing (scombrotoxic) fish have exceeded 200 ppm, often above 500 ppm. However, there is some evidence that other biogenic amines also may play a role in the illness.

Answer 27

Onset: The onset of intoxication symptoms is rapid, ranging from minutes to a few hours after consumption.

Answer 28

Disease / complications: Severe reactions (e.g., cardiac and respiratory complications) occur rarely, but people with pre-existing conditions may be susceptible. People on certain medications, including the anti-tuberculosis drug isoniazid, are at increased risk for severe reactions

Answer 29

Symptoms: Symptoms of scombrotoxin poisoning include tingling or burning in or around the mouth or throat, rash or hives, drop in blood pressure, headache, dizziness, itching of the skin, nausea, vomiting, diarrhea, asthmatic-like constriction of air passage, heart palpitation, and respiratory distress

Answer 30

Duration: The duration of the illness is relatively short, with symptoms commonly lasting several hours, but, in some cases, adverse effects may persist for several days.

Answer 31

Route of entry: Oral.

Answer 32

Pathway: In humans, histamine exerts its effects on the cardiovascular system by causing blood-vessel dilation, which results in flushing, headache, and hypotension. It increases heart rate and contraction strength, leading to heart palpitations, and induces intestinal smooth-muscle contraction, causing abdominal cramps, vomiting, and diarrhea. Histamine also stimulates motor and sensory neurons, which may account for burning sensations and itching associated with scombrotoxin poisoning. Other biogenic amines, such as putrescine and cadaverine, may potentiate scombrotoxin poisoning by interfering with the enzymes necessary to metabolize histamine in the human body

Answer 33

Scombrotoxin poisoning is one of the most common forms of fish poisoning in the United States. From 1990 to 2007, outbreaks of scombrotoxin poisoning numbered 379 and involved 1,726 people, per reports to the Centers for Disease Control and Prevention (CDC). However, the actual number of outbreaks is believed to be far greater than that reported

Answer 34

Fishery products that have been implicated in scombrotoxin poisoning include tuna, mahi-mahi, bluefish, sardines, mackerel, amberjack, anchovies, and others. Scombrotoxin-forming fish are commonly distributed as fresh, frozen, or processed products and may be consumed in a myriad of product forms. Distribution of the toxin within an individual fish or between cans in a case lot can be uneven, with some sections of a product capable of causing illnesses and others not. Cooking, canning, and freezing do not reduce the toxic effects. Common sensory examination by the consumer cannot ensure the absence or presence of the toxin. Chemical analysis is a reliable test for evaluating a suspect fishery product. Histamine also may be produced in other foods, such as cheese and sauerkraut, which also has resulted in toxic effects in humans

Answer 35

Diagnosis of the illness is usually based on the patient’s symptoms, time of onset, and the effect of treatment with antihistamine medication. The suspected food should be collected; rapidly chilled or, preferably, frozen; and transported to the appropriate laboratory for histamine analyses. Elevated levels of histamine in food suspected of causing scombrotoxin poisoning aid in confirming a diagnosis.

Answer 36

All humans are susceptible to scombrotoxin poisoning; however, as noted, the commonly mild symptoms can be more severe for individuals taking some medications, such as the antituberculosis drug isoniazid. Because of the worldwide network for harvesting, processing, and distributing fishery products, the impact of the problem is not limited to specific geographic areas or consumption patterns

Answer 37

The official method (AOAC 977.13) for histamine analysis in seafood employs a simple alcoholic extraction and quantitation by fluorescence spectroscopy. Putrescine and cadaverine can be analyzed by AOAC Official Method 996.07. Several other analytical procedures to quantify biogenic amines have been published in the literature

Answer 38

to be completed

Answer 39

Mortality: Death is from respiratory-muscle paralysis and usually occurs within 4 to 6 hours, with a known range of about 20 minutes to 8 hours

Answer 40

Lethal dose: The minimum lethal dose in humans is estimated to be 2 to 3 mg (1/500 of a gram).

Answer 41

Onset: The first symptom of intoxication is a slight numbness of the lips and tongue, typically appearing between 20 minutes to 3 hours after ingestion, depending on the ingested dose. With higher doses, symptoms can start within minutes.

Answer 42

Illness / complications: Tetrodotoxin acts on both the central and peripheral nervous systems. After the initial slight oral numbness, the next symptom is increasing paraesthesia in the face and extremities, which may be followed by sensations of lightness or floating. Headache, epigastric pain, nausea, diarrhea, and/or vomiting may occur. Occasionally, some reeling or difficulty in walking may occur. The second stage of the intoxication includes progressive paralysis. Many victims are unable to move; even sitting may be difficult. There is increasing respiratory distress. Speech is affected, and the victim usually exhibits dyspnea, cyanosis, and hypotension. Paralysis increases, and convulsions, mental impairment, and cardiac arrhythmia may occur. The victim, although completely paralyzed, may be conscious and, in some cases, completely lucid until shortly before death. There is no antidote for TTX poisoning, and treatment is symptomatic and supportive. Patients who receive ventilatory support recover fully, in most cases.

Answer 43

Duration: It is generally considered that if victims survive the initial 24 hours, they are expected to recover fully. It is known that TTX is cleared from the human body relatively quickly (in days) through the urine. Other symptoms, such as muscle weakness, can persist longer. No chronic effects have been reported

Answer 44

Route of entry: Oral.

Answer 45

Pathway: Tetrodotoxin acts directly on voltage-activated sodium channels in nerve tissue. Toxin binding to the channel blocks the diffusion of sodium ions, preventing depolarization and propagation of action potentials. All of the observed toxicity is secondary to action-potential blockage.

Answer 46

Only a few cases of intoxication from TTX have been reported in the U.S., and only from consumption of pufferfish. In Japan, however, 1,032 cases of pufferfish poisoning (PFP) were reported from 1965 through 2007, with 211 fatalities. In 1983, the Japanese Ministry of Health, Labour, and Welfare enacted guidance for pufferfish harvest and consumption, thereby greatly reducing the number of illnesses and mortalities from commercial product. Between 2002 and 2006, however, 116 incidents of PFP, with 223 individuals intoxicated and 13 mortalities, were reported, suggesting that problems still occur. Most of these illnesses were from home-prepared meals made from recreationally harvested fish.

Answer 47

As many as 19 species of pufferfish occur in U.S. waters, many of which contain TTX

Answer 48

Only muscle, skin, and testicles from a single species (Takifugu rubripes, a.k.a. tiger puffer or torafugu) are allowed entry into the U.S. from Japan. These products must be processed in a certified facility by trained personnel and certified as safe for consumption by the Japanese government. Any pufferfish products imported outside the guidelines of this agreement are subject to detention without physical examination, under FDA Import Alert #16-20. Due to the fact that imported pufferfish are limited to a single species (T. rubripes) processed and certified as safe prior to importation, the domestic puffer (sea squab) fishery targets a nontoxic species, and the U.S. does not import other species known to contain TTX (i.e. trumpet shells, xanthid crabs, etc.) for food. The FDA makes no recommendations for control of TTX in seafood in its Fish and Fisheries Products Hazards and Controls Guidance. However, due to recent issues with the illegal importation of misbranded Asian pufferfish and the recent appearance of saxitoxin in east-coast Florida southern pufferfish (Sphoeroides nephelus) – described in the sidebar below – FDA advises consumers who choose to consume pufferfish to consume only those from known safe sources.

Answer 49

The diagnosis of PFP is based on the observed symptomatology and recent dietary history. A case definition is available from the Centers for Disease Control and Prevention.

Answer 50

All humans are susceptible to TTX poisoning. This toxicosis may be avoided by not consuming pufferfish or other animal species containing TTX. In the U.S., most other animal species known to contain TTX are not usually consumed by humans. Poisoning from TTX is of major public health concern primarily in Japan and other Indo-Pacific countries, where "fugu" is a traditional delicacy. In Japan, it is prepared and sold in special restaurants, where trained and licensed individuals carefully remove the viscera to reduce the danger of poisoning. Due to its import restrictions and high value, there is potential for intentional mislabeling and illegal importation, particularly of prepared, frozen fish products. Several firms have been placed on the FDA Import Alert list for species misbranding and illegal importation of pufferfish.

Answer 51

The mouse bioassay for paralytic shellfish poisoning (PSP) can be used to monitor TTX in seafood products. An HPLC method with post-column reaction with alkali and fluorescence has been developed to determine TTX and its associated toxins. The alkali degradation products can also be confirmed as their trimethylsilyl derivatives, by gas chromatography. Mass spectrometry methods have been developed and show good sensitivity and selectivity. Antibody- and receptorbased methods are also available. To date, none of these chemical methods have been validated for regulatory compliance.

Answer 52

On April 29, 1996, three cases of TTX poisoning occurred among chefs in California who shared contaminated fugu (pufferfish) brought from Japan by a co-worker as a prepackaged, ready-toeat product. The quantity eaten by each person was minimal, ranging from approximately ¼ to 1½ oz. Onset of symptoms began approximately 3 to 20 minutes after ingestion, and all three chefs were transported by ambulance to a local emergency department. Three deaths were reported in Italy, in 1977, following consumption of frozen pufferfish imported from Taiwan and mislabeled as angler fish. In 2007, it was reported that fish sellers in Thailand were selling meat from a highly poisonous species of pufferfish labeled as salmon. This practice led to the death of 15 people over a 3-year period. In 2007, four separate incidents of TTX poisoning occurred in California, Illinois, and New Jersey, all linked to the pufferfish species L. lunaris imported from China, illegally invoiced as monkfish to avoid import restrictions. For several of the poisonings, the product in question was being sold as “bok,” a Korean term for pufferfish. The sidebar below describes 28 cases of PFP, from consumption of southern pufferfish, (Sphoeroides nephelus) that occurred on the U.S. east coast between 2002 to 2004, believed to be due not to TTX, but from accumulation of saxitoxins

Answer 53

The aflatoxins (AFs) are mycotoxins produced by certain fungi and can cause serious illness in animals and humans. The four major aflatoxins are AFB1, AFB2, AFG1, and AFG2. In adverse weather or under poor storage conditions, these toxins are produced mainly by certain strains of Aspergillus flavus and A. parasiticus in a broad range of agricultural commodities, such as corn and nuts

Answer 54

aflatoxin M1 (AFM1), is produced by mammals after consumption of feed (or food) contaminated by AFB1. Cows are able to convert AFB1 into AFM1 and transmit it through their milk. Although AFM1 in milk is, by far, not as hazardous as the parent compound, a limit of 0.5 parts per billion is applied, largely because milk tends to constitute a large part of the diet of infants and children

Answer 55

Documented epidemics of AF poisoning in the following countries illustrate mortality rates from outbreaks: - In northwest India, in 1974, there were 108 fatalities from 397 illnesses. AF levels of 0.25 to 15 mg/kg were found in corn. - In 1982, in Kenya, there were 20 hospital admissions, with a 60% mortality rate, with AF intake at 38 µg/kg of body weight. - In 1988, in Malaysia, 13 Chinese children died of acute hepatic encephalopathy after eating Chinese noodles. Aflatoxins were confirmed in postmortem samples from the patients. - In 2004 and 2005, one of the largest aflatoxicosis outbreaks on record occurred in rural Kenya, resulting in illness in 317 people, 125 of whom died. AFcontaminated homegrown maize with an average concentration of 354 ng/g was the source of the outbreak

Answer 56

The toxic level of AF in humans is largely unknown. In one example, a laboratory worker who intentionally ingested AFB1 at 12 µg/kg body weight for 2 days developed a rash, nausea, and headache, but recovered without ill effect. In a 14-year follow-up of the worker, a physical examination and blood chemistry, including tests for liver function, were normal. In animals, the effects of AFs on health depend on the species of the animal, level and duration of exposure, and nutritional status. Among various animals, median lethal dose (i.e., LD50) values obtained with single doses showed wide variation, ranging from 0.3 mg/kg body weight in rabbits to 18 mg/kg body weight in rats.

Answer 57

AFs have been found to be moderately to highly toxic and carcinogenic in almost every animal species tested, including monkeys, although AFs do not affect all animals equally. The main factor in tolerance relates to the nature of the digestive system. Ruminants are more tolerant, and swine, chickens, ducks, and ducklings (and pet and wild birds) are more sensitive. Other factors contributing to differences in animal susceptibility to AFs include breed variety, nutrition, sex, age, environmental stress, and presence of other disease agents

Answer 58

Onset: Not applicable.

Answer 59

From acute exposure: Acute exposure to high doses of AFs can result in aflatoxicosis, with the target organ being the liver, leading to serious liver damage. AFs inhibit the normal functions of the liver, including carbohydrate and lipid metabolism and protein synthesis

Answer 60

From chronic exposure at sublethal doses: cancer, impaired protein formation, impaired blood coagulation, toxic hepatitis, and probable immunosuppression. In animals, AFs may cause, in addition, reduced weight gain and reduced feed-conversion efficiency AFB1 is the most potent known natural carcinogen and is the most abundant of the AFs.

Answer 61

Symptoms: The disruption and inhibition of carbohydrate and lipid metabolism and protein synthesis associated with aflatoxicosis can lead to hemorrhaging, jaundice, premature cell death, and tissue necrosis in liver and, possibly, other organs. Other general symptoms include edema of the lower extremities, abdominal pain, and vomiting.

Answer 62

Route of entry: Oral.

Answer 63

Pathway: There is sufficient evidence that AFB1 can interact with DNA, producing damage. If the DNA is not repaired, a mutation can occur that may initiate the cascade of events required to produce cancer. After activation by cytochrome P450 monooxygenases, AFB1 is metabolized to form a highly reactive metabolite, AFB1-exo-8,9-epoxide. The exo-epoxide binds to the guanine moiety of DNA at the N7 position, forming trans-8,9-dihydro-8-(N7-guanyl)-9 hydoxyAFB1 adducts, which can rearrange and form a stable adduct. This can be measured in tumor tissues. AFB1-DNA adducts can result in GC-to-AT transversions. This specific mutation at codon 249 of the p53 tumor suppressor gene may be important in the development of HCC. Studies of liver-cancer patients in Southeast Asia and subSaharan Africa, where AF contamination in foods was high, have shown that a mutation in the p53 at codon 249 is associated with a G-to-T transversion. Biomarkers continue to serve as important tools in the epidemiology of HCC

Answer 64

In 2004, according to the Worldwide Regulations for Mycotoxins 2003, a Compendium published by the Food and Agriculture Organization, more than 76 countries have legislated limits on aflatoxins, ranging from 0 to 35 ng/g. Subsequently, in developed countries, AF contamination has rarely occurred in foods at levels that cause acute aflatoxicosis in humans. AF acute and chronic exposures are more likely to occur in developing countries where no regulatory limits, poor agricultural practices in food handling and storage, malnutrition, and disease are problems. Aflatoxicosis in humans has been reported in many countries, including India, China, Thailand, Ghana, Kenya, Nigeria, Sierra Leone, and Sudan. Human epidemiologic studies were initiated, in 1966, in Africa. To date, in the U.S., no human aflatoxicosis outbreak has been reported; however, dogs died in an outbreak, in 1998. In 2005, a number of dogs and cats died from eating aflatoxincontaminated pet food.

Answer 65

In the U.S., AFs are commonly found in corn (maize), sorghum, rice, cottonseed, peanuts, tree nuts, copra, cocoa beans, figs, ginger, and nutmeg. AFM1 may be found in milk and dairy products. Aflatoxin M1 also may be found in human breast milk, as has been the case in Ghana, Kenya, Nigeria, Sudan, Thailand, and other countries, from a mother’s chronic exposure to dietary AFs.

Answer 66

People who have aflatoxicosis might exhibit the following characteristics.  Liver damage may be evidenced by jaundice and its characteristic yellowing of tissues.  Gall bladder may become swollen.  Immunosuppression may provide an opportunity for secondary infections.  Vitamin K functions may decrease.  High levels of AFB1-albumin adducts may be present in plasma. AF exposure can be monitored through the use of biomarkers that detect the presence of AF metabolites in blood, milk, and urine, and excreted DNA adducts and blood-protein adducts. AFB1-albumin adducts can be measured in blood; AFM1 and AFB1-DNA adduct (AFB1-guanine adduct) can be detected in the urine of people consuming sufficient amounts of AFB1

Answer 67

Human susceptibility to AFs can vary with sex, age, health, nutrition, environmental stress, and level and duration of exposure. In many cases, exposure is due to consumption of a single, affected dietary staple. Also see “Frequency” section, above.

Answer 68

A bulk sample must be taken following a sampling plan, so that it is accurately representative of the toxin levels present throughout the lot. A subsample is removed from the bulk sample and subjected to sample preparation. The subsample is comminuted with proper grinding and mixing mills. The sample preparation variability decreases with decreasing particle size. A test sample is removed from the properly comminuted sample for analysis.

Answer 69

Two important aspects that can affect sampling variability include the sample-selection procedure and the distribution among contaminated particles within a lot. Using proper sampling equipment and procedures can reduce the effects of sample selection. Increasing sample size can reduce the effects of the distribution of contaminated particles within a lot.

Answer 70

Analytical methods can be divided into quantitative or semiquantitative assays and rapid screening tests. Sample cleanup is a time-consuming step and usually consists of extraction with solvent, liquid-liquid partition, and/or chromatographic separation and determination. Thin-layer chromatography (TLC) is among the most widely-used analytical methods. This simple and inexpensive technique is especially useful for AF analysis in developing countries, screening purposes, and multi-mycotoxin analysis. Since the late 1970s, AF-specific antibodies have been developed. The antibody development has led to the development of enzyme-linked immunosorbent assays (ELISAs) for AFs. The ELISAs are mainly used in screening methods. With advances in instrumentation, chromatographic methods for AFs have expanded from TLC to high-performance liquid chromatography (LC) with fluorescence detection. Hyphenated methods, such as LC/mass spectrometry (MS) or LC/MS-MS, have also been developed for AF quantitation and confirmation of identities.

Answer 71

Gempylotoxin is an indigestible wax, composed of C32, C34, C36, and C38 fatty acid esters, with the main component C34H66O2 (Ukishima, et al.), generally found in the fish escolar (Lepidocybium flavobrunneum) and its relative oilfish (Ruvettus pretiosus), sometimes called cocco. escolar's muscle contained about 20% lipid, and 88.8% consisted of wax. The wax was composed of C32, C34, C36 and C38 compounds, and the main component was C34H66O2. The alcohol components were mainly C16:0 and C18:1, as well as those of sperm whale (Physeter catodon) wax. The fatty acid components were mainly C18:1 and smaller amounts of highly unsaturated fatty acids.

Answer 72

Humans can’t digest this wax, which, in some people, acts as a purgative if consumed. The resulting illness is called gempylid fish poisoning or gempylotoxism

Answer 73

Mortality: None known.

Answer 74

Onset: Symptoms have been reported to start between 1 and 90 hours after the fish is consumed, with a median onset of 2.5 hours

Answer 75

Symptoms: Diarrhea, often consisting of an oily orange or brownish-green discharge (keriorrhoea), without major fluid loss; abdominal cramps; nausea; headache; and vomiting

Answer 76

Duration: Symptoms usually abate within 1 to 2 days.

Answer 77

Route of entry: Oral.

Answer 78

Cases may occur sporadically (i.e., in isolation from one another) or in clusters, usually when the fish is eaten in group settings

Answer 79

Symptoms usually are associated with ingestion of escolar (Lepidocybium flavobrunneum) or oilfish (Ruvettus pretiosus). Other products have been implicated in illness (including butterfish, rudderfish, walu, white tuna, and Taiwanese seabass). In most cases, these products were actually escolar or oilfish, but were marketed under inappropriate local or vernacular names, such as those used where the species was harvested (e.g. walu, butterfish). Species substitution or misbranding occurs when a deceptive and misleading name is used (e.g., white tuna or Taiwanese seabass). The FDA maintains a guide to acceptable market names for food fish sold in interstate commerce (The Seafood List), to avoid this confusion among consumers and resulting inadvertent illness. Additional deep-sea fish species, such as orange roughy (Hoplostethus atlanticus) and oreo dory (Allocyttus spp., Pseudocyttus spp., Oreosoma spp., and Neocyttus spp.), are known to contain lesser amounts of the same indigestible wax esters.

Answer 80

Diagnosis is per symptoms, particularly of oily, orange or greenish-brown diarrhea, and history of having consumed this type of fish

Answer 81

Not everyone who eats the fish becomes ill to the same extent. Level of illness may be related to the quantity eaten.

Answer 82

An outbreak that occurred in New South Wales, in October 2001, provides an example. Of 44 people who attended a conference at which lunch was served, 22 became ill, with a median postlunch incubation period of 2.5 hours. Among those, all of the 17 who met the case definition had eaten fish for lunch; none of the attendees who did not become ill had eaten fish. Eighty percent of the people who became ill had diarrhea, often oily; half had abdominal cramps and almost half had nausea; more than one-third had a headache; and one-quarter had vomiting. Analysis of the oil in the fish that had been served for lunch was consistent with escolar.

Answer 83

After a fish is turned into fillets or steaks, it can be very hard to determine exactly what species it is. FDA scientists are now using DNA barcoding to find out. DNA barcoding uses genetic material in fish to identify them. This method of definitive identification helps the FDA enforce policies on proper labeling of escolar and other fish (Gempylotoxin ) Pufferfish can be poisonous, depending on the type of pufferfish and the parts that are eaten (tetrodotoxin)

Answer 84

to be completed from page 254

Answer 85

Pyrrolizidine alkaloids are a large class of naturally occurring alkaloids containing pyrrolizidine rings. More than 600 pyrrolizidine alkaloids are known. They are widely distributed in the plant kingdom, particularly in the Boraginaceae, Compositae, and Leguminosae families. Some of these alkaloids cause illness in humans and other animals.

Answer 86

Pyrrolizidine alkaloids are a large class of naturally occurring alkaloids containing pyrrolizidine rings. More than 600 pyrrolizidine alkaloids are known. They are widely distributed in the plant kingdom, particularly in the Boraginaceae, Compositae, and Leguminosae families. Some of these alkaloids cause illness in humans and other animals.

Answer 87

Mortality: Possible, when liver or lung damage is extensive.

Answer 88

Toxicity dose: Variable among different pyrrolizidine alkaloids.

Answer 89

Illness / complications: Most cases of pyrrolizidine alkaloid toxicity result in moderate to severe liver damage. In some cases, the lungs are affected; pulmonary edema and pleural effusions have been observed. Lung damage may be prominent and has been fatal. Chronic illness from ingestion of small amounts of the alkaloids over a long period proceeds through fibrosis of the liver to cirrhosis. The carcinogenic potential of some pyrrolizidine alkaloids has been proven in rodents, and the National Toxicology Program recently has accepted riddelliine as a human carcinogen.

Answer 90

Symptoms: Gastrointestinal symptoms usually are the first sign of intoxication. They consist predominantly of abdominal pain, with vomiting, and development of ascites. Other early clinical signs include nausea and acute upper gastric pain, acute abdominal distension with prominent dilated veins on the abdominal wall, fever, and biochemical evidence of liver dysfunction. Jaundice may be present.

Answer 91

Duration: Death may ensue from 2 weeks to more than 2 years after poisoning, but patients may recover almost completely if the alkaloid intake is discontinued and the liver damage has not been too severe.

Answer 92

Route of entry: Oral.

Answer 93

Pathway: Mediated by cytochrome P450

Answer 94

Worldwide, reports of pyrrolizidine alkaloid intoxication are associated mainly with consumption of dietary supplements containing pyrrolizidine alkaloids and grains contaminated with weeds that contain pyrrolizidine alkaloids. Although the occurrence has been rare, there have been periodic reports of pyrrolizidine alkaloid intoxication in the United States, mainly due to consumption of herbal teas and dietary supplements that contained pyrrolizidine alkaloids; mainly the herb comfrey (Symphytum spp.).

Answer 95

Worldwide, reports of pyrrolizidine alkaloid intoxication are associated mainly with consumption of dietary supplements containing pyrrolizidine alkaloids and grains contaminated with weeds that contain pyrrolizidine alkaloids. Although the occurrence has been rare, there have been periodic reports of pyrrolizidine alkaloid intoxication in the United States, mainly due to consumption of herbal teas and dietary supplements that contained pyrrolizidine alkaloids; mainly the herb comfrey (Symphytum spp.).

Answer 96

Diagnosis of poisoning from pyrrolizidine alkaloids often is difficult, since they usually are excreted within 24 hours, while symptoms of the poisoning might not appear until days or weeks after the toxins were ingested. Key clinical features of the veno-occlusive disease that typically is indicative of pyrrolizidine alkaloids may include hyperbilirubinemia, painful hepatomegaly, and fluid retention. Diagnosis usually is made on the basis of symptoms and on patients’ reports of having ingested substances associated with pyrrolizidine alkaloids.

Answer 97

All humans are believed to be susceptible to the hepatotoxic pyrrolizidine alkaloids. Males are more susceptible than females, and fetuses and children show the highest sensitivity. Home remedies and consumption of herbal teas in large quantities can be a risk factor and are the most likely causes of alkaloid poisonings in the U.S. In 2001, FDA advised all dietary supplement manufacturers to remove from the market products that contained comfrey and were intended for internal use.

Answer 98

The pyrrolizidine alkaloids can be isolated from the suspect commodity by any of several standard alkaloid extraction procedures. The toxins are identified by thin-layer chromatography. The pyrrolizidine ring is first oxidized to a pyrrole, followed by spraying with Ehrlich reagent, which gives a characteristic purple spot. A colorimetric test employing Ehrich reagent also can be used to detect most common pyrrolizidine alkaloids, except the otonecine-type. Liquid and gas-liquid chromatography, in conjunction with mass spectrometric methods, also are available for identifying the alkaloids in trace amounts.

Answer 99

Intoxication reported from Afghanistan’s Gulran province in 2008. List of Morbidity and Mortality Weekly Reports, from the Centers for Disease Control and Prevention, relating to this toxin.

Answer 100

from primitive cartilaginous fish, such as stingrays, to more advanced, bony fish such as scorpionfish, stonefish, weeverfish, blennies, and, as noted, lionfish. Venom injections from certain stonefish species (Synanceja horrida, S. trachynis, and S. verrucosa) are the most notorious among venomous fish, and have been responsible for numerous deaths from incidents in coastal Indo-Pacific waters.

Answer 101

Venomous fish are found in diverse habitats, from freshwater streams to coral reefs to the open ocean. The greatest variety is found in the waters surrounding Indo-Pacific island countries, eastern and southern Africa, Australia, Polynesia, the Philippines, Indonesia, and southern Japan. Most venomous fish inhabit shallow, inshore waters among coral reefs and rocks. They generally swim slowly and are non-migratory, and tend either to be brightly colored or to blend in with their environments. Stonefish, as their name suggests, are well camouflaged in their native habitat, and most lethal envenomations have occurred through accidental contact (i.e., being stepped on) by recreational divers and fishermen

Answer 102

Fish venoms are complex mixtures of proteins and enzymes, each with its own biological activity, most of which have yet to be isolated and characterized. Studies have shown that many fish venoms are chemically and pharmacologically similar. Fish venoms are known to have cardiovascular, neuromuscular, inflammatory, and cytolytic properties. No fish venom mixtures have been fully characterized, and only a few components (e.g. stonustoxin, a lethal compound from the stonefish Synanceja horrida, which causes severe hypotension) have been purified and studied in detail. Although fish venoms are believed to be unstable and heat labile, no thorough studies have been performed on the potency of venom components after fish harvest or death.

Answer 103

Fish venom is produced in specialized glands associated with distinct venom-delivery structures. Most of these structures are spines located on the dorsal (back), pectoral, pelvic, anal, caudal (tail) or opercular (cheek) surfaces. The venom-producing glands are usually located in a groove on the surface or at the base of the spine. The size and complexity of this glandular tissue varies by species. Unlike other venomous creatures, such as spiders, wasps, and snakes, in which venom can be actively injected through a bite or sting, fish venom is delivered involuntarily when a spine pierces the tissue of the victim, leading to rupture of the spine’s sheath, and venom passes into the puncture wound.

Answer 104

In terms of envenomation by puncture, the severity of symptoms depends on the fish species, amount of venom delivered, and age and health status of the victim. The most common symptom associated with envenomation by puncture is acute, localized pain disproportionate to the size or severity of the wound. This symptom reaches its greatest intensity within 60 to 90 minutes and, if untreated, can last 8 to 12 hours. In addition to the localized symptoms and complications associated with the puncture wound itself, systemic symptoms occur in a limited number of victims. They include dizziness, nausea or vomiting, difficulty breathing, chest pain, abdominal pain, hypotension, and generalized weakness. Stonefish envenomations appear to be the most potent and may result in death from hypotension, arrhythmia, and/or pulmonary edema. A secondary consequence of handling fish with venomous spines is bacterial infection of the wound, particularly from species with barbed spines (e.g. catfish, stingrays) that can break off and become embedded in the victim. Medical attention should be sought in cases in which the spines cannot be removed or systemic symptoms persist.

Answer 105

The most common and effective treatment for acute pain from fish envenomation is immersion of the affected area in hot (45 C, not boiling) water for as long as is tolerable by the patient. Tetanus or antibiotic treatment may be administered by a health professional, if secondary infection of the wound is suspected. For severe cases of stonefish envenomation, commercial antivenom is available. In laboratory studies, this product has been shown to be effective in reducing the potency of several scorpionfish venoms, including those from the devil stinger (Inimicus japonicus), lionfish (Pterois volitans, P. lunulata, and P. antennata), and zebra turkeyfish (Dendrochirus zebra).

Answer 106

Lectins are widely occurring, sugar-binding proteins that perform a variety of biological functions in plants and animals, including humans, but some of them may become toxic at high levels. Besides inducing mitosis, lectins are known for their ability to agglutinate many mammalian red blood cell types, alter cell-membrane transport systems, alter cell permeability to proteins, and generally interfere with cellular metabolism. Among the lectins known to have toxic effects is phytohaemagglutinin, which occurs at relatively high levels in the seeds of legumes (e.g., beans). The role of this compound in defense against plant pests and pathogens has been established. This hemagglutinin also is used in research; for example, to trigger DNA and RNA synthesis in T lymphocytes, in vitro. PHAs are used to test competence of cell-mediated immunity; for example, in patients with chronic viral infections.

Answer 107

Not reported

Answer 108

Toxic dose: As few as four or five raw beans can trigger symptoms.

Answer 109

Onset: Usually begins with extreme nausea and vomiting within 1 to 3 hours of ingestion of the product, with diarrhea developing later within that timeframe.

Answer 110

Illness / complications: Upper and lower gastrointestinal illness. Vomiting may become severe.

Answer 111

Symptoms: In addition to vomiting and diarrhea, abdominal pain has been reported by some people.

Answer 112

Duration: Recovery usually is rapid, within 3 to 4 hours after onset of symptoms, and spontaneous, although some cases have required hospitalization

Answer 113

Route of entry: Oral (consumption of uncooked or undercooked kidney beans).

Answer 114

Pathway: The mechanism and pathway of toxicity is not known, but oral ingestion of lectins is known to reduce intestinal absorption and cause weight loss, growth retardation, and diarrhea in several animal species.

Answer 115

This syndrome has occurred in the United Kingdom with some regularity. Seven outbreaks occurred in the U.K. between 1976 and 1979. Two more incidents were reported by the Public Health Laboratory Services (PHLS), of Colindale, U.K., in the summer of 1988. Reports of this syndrome in the United States are anecdotal and have not been formally published

Answer 116

Phytohaemagglutinin, the presumed toxic agent, is found in many species of beans, but is in highest concentration in red kidney beans (Phaseolus vulgaris). The unit of toxin measure is the hemagglutinating unit (hau). Raw kidney beans contain from 20,000 to 70,000 hau, while fully cooked beans contain from 200 to 400 hau. White kidney beans, another variety of Phaseolus vulgaris, contain about one-third the amount of toxin as the red variety; broad beans (Vicia faba) contain 5% to 10% the amount that red kidney beans contain. The syndrome usually is caused by ingestion of raw, soaked kidney beans, either alone or in salads or casseroles. Several outbreaks have been associated with beans cooked in slow cookers (i.e., countertop appliances that cook foods at low temperatures for several hours) or in casseroles that had not reached an internal temperature high enough to destroy the glycoprotein lectin.

Answer 117

PHA is destroyed by adequate cooking. Some variation in toxin stability has been found at different temperatures. However, Bender and Readi found that boiling the beans for 10 minutes (100 C) completely destroyed the toxin. Consumers should boil the beans for at least 30 minutes to ensure that the product reaches sufficient temperature, for a sufficient amount of time, to completely destroy the toxin. Slow cookers should not be used to cook these beans or dishes that contain them. Studies of casseroles cooked in slow cookers revealed that the food often reached internal temperatures of only 75 C or less, which is inadequate for destruction of the toxin.

Answer 118

Diagnosis is made on the basis of symptoms, food history, and exclusion of other rapid-onset food-poisoning agents (e.g., Bacillus cereus, Staphylococcus aureus, arsenic, mercury, lead, and cyanide).

Answer 119

All people, regardless of age or gender, appear to be equally susceptible; the severity is related to the dose ingested. In the seven outbreaks mentioned below, the attack rate was 100%.

Answer 120

The difficulty in food analysis is that this syndrome is not well known in the medical community. Other possible causes, such as Bacillus cereus, staphylococcal food poisoning, and chemical toxicity, must first be eliminated. If beans were a component of the suspect meal, analysis is quite simple, based on hemagglutination of red blood cells (hau).

Answer 121

The genus Salmonella is divided into two species that can cause illness in humans:  S. enterica  S. bongori Salmonella enterica, which is of the greatest public health concern, is comprised of six subspecies:  S. enterica subsp. enterica (I)  S. enterica subsp. salamae (II)  S. enterica subsp. arizonae (IIIa)  S. enterica subsp. diarizonae (IIIb)  S. enterica subsp. houtenae (IV)  S. enterica subsp. indica (VI) Salmonella is further subdivided into serotypes, based on the Kaufmann-White typing scheme first published in 1934, which differentiates Salmonella strains by their surface and flagellar antigenic properties

Answer 122

Salmonella is a motile, non-sporeforming, Gramnegative, rod-shaped bacterium in the family Enterobacteriaceae and the tribe Salmonellae. Non-motile variants include S. Gallinarum and S. Pullorum

Answer 123

Salmonella can cause two types of illness, depending on the serotype: (1) nontyphoidal salmonellosis and (2) typhoid fever, both of which are described below. The symptoms of nontyphoidal salmonellosis can be quite unpleasant, but this illness is generally self-limiting among healthy people with intact immune systems (although it can cause lifethreatening illness even in healthy people). Typhoid fever is more serious and has a higher mortality rate than does nontyphoidal salmonellosis.

Answer 124

Caused by serotypes other than S. Typhi and S. Paratyphi A ((Note that species names are italicized, but serotype names are not.)

Answer 125

Mortality: Generally less than 1%; however, S. Enteritidis has a 3.6% mortality rate in outbreaks in nursing homes and hospitals, with the elderly being particularly affected.

Answer 126

Onset: 6 to 72 hours after exposure.

Answer 127

Infective dose: As low as one cell, depending on age and health of host and strain differences among members of the genus.

Answer 128

Symptoms: Nausea, vomiting, abdominal cramps, diarrhea, fever, headache

Answer 129

Duration: Symptoms generally last 4 to 7 days, with acute symptoms usually lasting 1 to 2 days or longer, depending on host factors, the dose ingested, and strain characteristics

Answer 130

Complications: (1) Dehydration and electrolyte imbalance may occur as a result of diarrhea and vomiting. This can lead to death in the very young, the elderly, and the immunocompromised, if not treated promptly. (2) In 2% of culture-proven cases, reactive arthritis (i.e., arthritis from an immune reaction to the infection – an autoimmune response – rather than directly from the infection itself) may follow 3 to 4 weeks after the onset of acute symptoms. Indications of reactive arthritis may include, for example, joint inflammation, urethritis, uveitis, and/or conjunctivitis. (3) Nontyphoidal Salmonella can sometimes escape from the gastrointestinal tract into the body and cause blood poisoning (septicemia) or infect the blood, internal organs, and/or joints (bacteremia). S. Dublin is sometimes associated with this complication.

Answer 131

Route of entry: oral (e.g., ingestion of contaminated food, fecal particles, or contaminated water).

Answer 132

Pathway: Penetration and passage of Salmonella organisms from gut lumen into epithelium of small intestine, where inflammation occurs. There is evidence that enterotoxin may be produced, perhaps within enterocytes.

Answer 133

Caused by serotypes S. Typhi and S. Paratyphi A, both of which are found only in humans

Answer 134

Mortality: Untreated, as high as 10%.

Answer 135

Onset: Generally 1 to 3 weeks, but may be as long as 2 months after exposure.

Answer 136

Infective dose: Fewer than 1,000 cells

Answer 137

Symptoms: High fever, from 103° to 104°F; lethargy; gastrointestinal symptoms, including abdominal pains and diarrhea or constipation; headache; achiness; loss of appetite. A rash of flat, rose-colored spots sometimes occurs.

Answer 138

Duration: Generally 2 to 4 weeks.

Answer 139

Illness / Complications: Septicemia, with colonization of other tissues and organs; e.g., may lead to endocarditis. Septic arthritis may occur, in which the infection directly affects the joints and may be difficult to treat. Chronic infection of the gallbladder may occur, which may cause the infected person to become a carrier

Answer 140

Route of entry: Oral (e.g., ingestion of contaminated food, fecal particles, or contaminated water).

Answer 141

Pathway: Penetration and passage of typhoid Salmonella organisms from gut lumen into epithelium of small intestine and into the bloodstream (i.e., septicemia), which may carry the organisms to other sites in the body, where inflammation occurs. There is evidence that enterotoxin may be produced, perhaps within enterocytes.

Answer 142

Annually in the United States:  Nontyphoidal salmonellosis – A recent report from the Centers for Disease Control and Prevention (CDC) estimates that 1,027,561 cases of domestically acquired nontyphoidal salmonellosis occur annually in the U.S., when under-reporting and under-diagnosis are taken into account.  Typhoid fever – In terms of domestically acquired S. enterica serotype Typhi, the same CDC report estimated that a mean of 1,821 cases occur annually in the U.S. Additional cases in the U.S. are associated with foreign travel. The report estimates that 433 cases of typhoid fever in the U.S., overall (i.e., whether or not they are domestically acquired), are culture-confirmed. The last case of a foodborne, noncarrier-based typhoid outbreak in the U.S. was in 1999 and was associated with the tropical fruit mamey.

Answer 143

Salmonella is widely dispersed in nature. It can colonize the intestinal tracts of vertebrates, including livestock, wildlife, domestic pets, and humans, and may also live in environments such as pond-water sediment. It is spread through the fecal-oral route and through contact with contaminated water. It may, for example, contaminate meat, farm-irrigation water (thus contaminating produce in the field), soil and insects, factory equipment, hands, and kitchen surfaces and utensils. Since S. Typhi and S. Paratyphi A are found only in human hosts, the usual sources of these organisms in the environment are drinking and/or irrigation water contaminated by untreated sewage. It is highly recommended that only potable water and cooked vegetables be consumed in areas where these organisms are endemic.

Answer 144

Various Salmonella species have long been isolated from the outside of egg shells, but S. Enteritidis can be present inside the egg. This and other information strongly suggest vertical transmission; i.e., deposition of the organism on the albumen (egg white) side of the yolk-sack membrane (vitelline membrane) by an infected hen, prior to shell formation.

Answer 145

Serological identification of cultural isolates from stool. Genetic identification of approximately 100 Salmonella serotypes from pure culture is now possible, but the remaining 2,400-plus serotypes can be identified only through traditional serotyping.

Answer 146

Anyone, of any age, may become infected with Salmonella. Particularly vulnerable are people with weak immune systems, such as the very young and the elderly, people with HIV or chronic illnesses, and people on some medications; for example, chemotherapy for cancer or the immunosuppressive drugs used to treat some types of arthritis. People with HIV are estimated to have salmonellosis at least 20 times more than does the general population and tend to have recurrent episodes.

Answer 147

Isolation and detection methods have been developed for many foods having prior history of Salmonella contamination. Conventional culture and identification methods may require 4 to 6 days for presumptive results. To screen foods, several rapid methods are available, which require 1 to 2 days. These rapid methods include antibody and molecular (DNA or RNA) based assays, but in most cases, require a cultural means to confirm the presence of Salmonella, for regulatory purposes.

Answer 148

Campylobacter jejuni is a nonsporeforming, Gram-negative rod with a curved- to S-shaped morphology. Many strains display motility, which is associated with the presence of a flagellum at one or both of the polar ends of this bacterium. Members of the Campylobacter genus are microaerophilic; i.e., they grow at lower-thanatmospheric oxygen concentrations. Most grow optimally at oxygen concentrations from 3% to 5%. Thus, these bacteria generally are fairly fragile in the ambient environment and somewhat difficult to culture in the laboratory. Additional conditions to which C. jejuni are susceptible include drying, heating, freezing, disinfectants, and acidic conditions.

Answer 149

Campylobacter jejuni (80% of Campylobacter infections), C. coli and C. fetus. C. coli and C. jejuni cause similar disease symptoms. C. fetus infections often are associated with animal contact or consumption of contaminated foods and beverages and are especially problematic for fetuses and neonates, in whom the mortality rate may be up to 70%

Answer 150

The CDC attributes an estimated 76 deaths in the United States, per year, to campylobacteriosis.

Answer 151

Infective dose: In general, the minimum number of ingested Campylobacter cells that can cause infection is thought to be about 10,000. However, in trials, as few as 500 ingested Campylobacter cells led to disease in volunteers. Differences in infectious dose likely can be attributed to several factors, such as the type of contaminated food consumed and the general health of the exposed person.

Answer 152

Onset: The incubation period, from time of exposure to onset of symptoms, generally is 2 to 5 days.

Answer 153

Disease / complications: The disease caused by C. jejuni infections is called campylobacteriosis. The most common manifestation of campylobacteriosis is selflimiting gastroenteritis, termed “Campylobacter enteritis,” without need for antimicrobial therapy. When antimicrobial therapy is indicated, erythromycin or ciprofloxacin are most commonly prescribed. A small percentage of patients develop complications that may be severe. These include bacteremia and infection of various organ systems, such as meningitis, hepatitis, cholecystitis, and pancreatitis. An estimated 1.5 cases of bacteremia occur for every 1,000 case of gastroenteritis. Infections also may lead, although rarely, to miscarriage or neonatal sepsis. Autoimmune disorders are another potential long-term complication associated with campylobacteriosis; for example, Guillain-Barré syndrome (GBS). One case of GBS is estimated to develop per 2,000 C. jejuni infections, typically 2 to 3 weeks post infection. Not all cases of GBS appear to be associated with campylobacteriosis, but it is the factor most commonly identified prior to development of GBS. Various studies have shown that up to 40% of GBS patients first had Campylobacter infection. It is believed that antigens present on C. jejuni are similar to those in certain nervous tissues in humans, leading to the autoimmune reaction. Reactive arthritis is another potential long-term autoimmune complication. It can be triggered by various kinds of infections and occurs in about 2% of C. jejuni gastroenteritis cases. Hemolytic uremic syndrome and recurrent colitis following C. jejuni infection also have been documented.

Answer 154

Symptoms: Fever, diarrhea, abdominal cramps, and vomiting are the major symptoms. The stool may be watery or sticky and may contain blood (sometimes occult – not discernible to the naked eye) and fecal leukocytes (white cells). Other symptoms often present include abdominal pain, nausea, headache, and muscle pain.

Answer 155

Duration: Most cases of campylobacteriosis are self-limiting. The disease typically lasts from 2 to 10 days.

Answer 156

Route of entry: Oral.

Answer 157

Pathway: The mechanisms of pathogenesis by C. jejuni are not well understood and usually vary based on the virulence genes present in a particular strain. In general, C. jejuni cause infections by invading and colonizing the human gastrointestinal tract. Motility appears to be an important factor in C. jejuni pathogenesis, enabling the bacterium to invade the human intestinal mucosa. The mechanisms by which cellular invasion by C. jejuni cause the observed symptoms remain a mystery. In genomesequencing studies, researchers were not able to identify the presence of toxin genes that likely contribute to diarrhea and other common symptoms.

Answer 158

Campylobacter species are believed to be the third leading cause of domestically acquired bacterial foodborne illness in the United States, with an estimated 845,024 cases occurring annually, according to a 2011 Centers for Disease Control and Prevention (CDC) report. According to data from FoodNet, the incidence of cases of campylobacteriosis reported to the CDC in 2008 was 12.68 per 100,000 individuals, which is a decrease of 32% over the last decade. For each reported case of campylobacteriosis, it is estimated that 30 cases are unreported.

Answer 159

Major food sources linked to C. jejuni infections include improperly handled or undercooked poultry products, unpasteurized (“raw”) milk and cheeses made from unpasteurized milk, and contaminated water. Campylobacter infection in humans has been linked to handling and eating raw or undercooked meat and poultry, whether fresh or frozen. Avoiding cross contamination of uncooked items from raw meat and poultry products, thorough cooking, pasteurization of milk and dairy products, and water disinfection are effective ways to limit food- and water-borne exposure to Campylobacter. Reduction of risk from contaminated poultry products can be achieved through good hygienic practices by manufacturers and consumers.

Answer 160

Special incubation conditions are required for isolation and growth of C. jejuni cells, since the organism is microaerophilic. Samples from stool or rectal swabs are inoculated directly onto selective media, or they can be enriched to increase recovery. To limit growth of competing organisms, media used for cultivation usually are supplemented with blood and antimicrobial agents. The cultures are incubated at 42ºC, under microaerophilic conditions (5% oxygen and 5% to 10% carbon dioxide), for optimal recovery

Answer 161

Children younger than 5 years old and young adults 15 to 29 years old are the populations in whom C. jejuni gastroenteritis most commonly is detected. The highest incidence of infection is among infants 6 to 12 months old. C. jejuni bacteremia may also affect pregnant women, leading to infection of the fetus, which can lead to miscarriage or stillbirth. The incidence of infection is estimated to be 40-fold greater in people with HIV/AIDS, compared with others in the same age group.

Answer 162

Isolation of C. jejuni from food is difficult, because the bacteria are usually present in very low numbers. For isolation from most food products, samples are rinsed and the rinsate is collected and subjected to pre-enrichment and enrichment steps, followed by isolation of C. jejuni from the agar medium

Answer 163

The Yersinia genus has 11 species; 4 are pathogenic, but only Y. enterocolitica and Y. pseudotuberculosis cause gastroenteritis. Y. enterocolitica and Y. pseudotuberculosis are small, rod-shaped, Gram-negative bacteria. The former is often isolated from clinical specimens, such as wounds, feces, sputum, and mesenteric lymph nodes. However, it is not part of the normal human flora. Y. pseudotuberculosis has been isolated from diseased human appendix. Both pathogens are transmitted through the fecal-oral route. Y. enterocolitica is psychrotrophic (i.e., a microorganism that grows well at low temperature) and has the ability to grow at temperatures below 4°C. The doubling time, at 30°C, is 34 min; at 22°C, is 1 hr; and at 7°C, is 5 hrs. It can withstand freezing and can survive in frozen foods for extended periods. In fact, Y. enterocolitica has survived better in artificially contaminated food stored at room and refrigeration temperatures than at an intermediate temperature. It persists longer in cooked foods than in raw foods, due to increased nutrient availability Y. enterocolitica has between 10% and 30% DNA homology with the Enterobacteriaceae family and is 50% related to Y. pseudotuberculosis and Y. pestis. Genetic analysis of Y. pestis revealed it to be a clone of Y. pseudotuberculosis, which evolved sometime between 1,500 to 20,000 years ago

Answer 164

Mortality: Fatalities are extremely rare.

Answer 165

Infective dose: The medium infective dose for humans is not known, but is estimated to be between 104 to 106 organisms. The infective dose and clinical presentation of symptoms may depend on pathogen (strain-dependent) and host factors. For example, in some cases, in people with gastric hypoacidity, the infective dose may be lower.

Answer 166

Onset: Incubation times from 1 to 11 days have been observed, but occasionally last for several months.

Answer 167

Illness / complications: In some patients, complications arise due to the strain type causing the initial infection and specific human immunologic leukocyte antigen, HLA-B27. These sequelae include reactive arthritis; glomerulonephritis; endocarditis; erythema nodosum (which occurs predominantly in women); uveitis; thyroid disorders, such as Graves’ disease; hyperthyroidism; nontoxic goiter; and Hashimoto’s thyroiditis. Y. enterocolitica has been associated with reactive arthritis, which may occur even in the absence of obvious symptoms. The frequency of such postenteritis arthritic conditions is about 2% to 3%. In Japan, Y. pseudotuberculosis was implicated in the etiology of Kawasaki’s disease. Another complication is bacteremia, which raises the possibility of disease dissemination. However, this is rare. Performance of unnecessary appendectomies also may be considered a major complication of yersiniosis, as one of the main symptoms of the disease is abdominal pain in the lower right quadrant. Treatment includes supportive care, since the gastroenteritis is self-limiting. If septicemia or other invasive diseases occur, antibiotic therapy with gentamicin or cefotaxime (doxycycline and ciprofloxacin) typically are administered.

Answer 168

Symptoms: Infection with Y. enterocolitica manifests as nonspecific, self-limiting diarrhea, but may cause a variety of autoimmune complications, as noted above. Most symptomatic infections occur in children younger than 5 years old. Yersiniosis in these children is frequently characterized as gastroenteritis, with diarrhea and/or vomiting; however, fever and abdominal pain are the hallmark symptoms. A small proportion of children (less than 10%) produce bloody stools. Children usually complain of abdominal pain and headache and sore throat at the onset of the illness. Yersinia infections mimic appendicitis and mesenteric lymphadenitis, but the bacteria may also cause infection in other sites, such as wounds, joints, and the urinary tract.

Answer 169

Duration: The illness might last from a few days to 3 weeks, unless it becomes chronic enterocolitis, in which case it might continue for several months

Answer 170

Pathway: As zoonotic pathogens, Y. enterocolitica and Y. pseudotuberculosis enter the gastrointestinal tract after ingestion of contaminated food or water. Gastric acid is a significant barrier to infection. The infective dose might be lower among people with gastric hypoacidity. Both pathogens harbor plasmid (pYV)-encoded virulence genes that affect pathogenesis. These include an outer-membrane protein, YadA (Yersinia adhesion A), and the genetic suite comprising the type III secretory system. This process usually is facilitated by Yops proteins, which contribute to the ability of Y. enterocolitica cells to resist phagocytosis by causing disruption (cytotoxic changes) of mammalian (human) cells.

Answer 171

Yersiniosis is far more common in Northern Europe, Scandinavia, and Japan than in the United States. It does not occur frequently and tends to be associated with improper food-processing techniques. Y. enterocolitica is a more frequent cause of yersiniosis than is Y. pseudotuberculosis, and cases have been reported on all continents. Different biotypes of Y. enterocolitica have been associated with infections around the world, with the most common biotype being 4/O:3. Information on Y. pseudotuberculosis is not as well defined and, as such, is reported less frequently than is Y. enterocolitica.

Answer 172

Strains of Y. enterocolitica can be found in meats (pork, beef, lamb, etc.), oysters, fish, crabs, and raw milk. However, the prevalence of this organism in soil, water, and animals, such as beavers, pigs, and squirrels, offers many opportunities for Yersinia to enter the food supply. For example, poor sanitation and improper sterilization techniques by food handlers, including improper storage, may be a source of contamination. Raw or undercooked pork products have drawn much attention as a source of Y. enterocolitica, and Y. pseudotuberculosis, particularly since Y. enterocolitica has been associated with pigs.

Answer 173

Yersiniosis may be misdiagnosed as Crohn’s disease (regional enteritis) or appendicitis. Diagnosis of yersiniosis begins with isolation of the organism from the human host’s feces, blood, or vomit, and sometimes at the time of appendectomy. Confirmation occurs with the isolation, as well as biochemical and serological identification, of Y. enterocolitica from both the human host and the ingested food. Diarrhea occurs in about 80% of cases; abdominal pain and fever are the most reliable symptoms. Y. enterocolitica or Y. pseudotuberculosis in patients with acute gastroenteritis can be readily isolated via conventional bacteriological media designed to isolate Yersinia. It is much more challenging to isolate these pathogens in asymptomatic carriers or from foods. Since many Y. enterocolitica isolated from non-human sources are not considered pathogenic, it is imperative to distinguish these isolates from pathogenic Yersinia species. Molecular-based assays, particularly PCR methods, have been developed to target Y. enterocolitica and can be used to rapidly confirm the pathogenicity of the isolate. Several PCR primer sets are directed to either plasmid-borne genes, e.g., virF or yadA, or chromosomally located loci, such as ail. Serology is used to identify the biotype (based on biochemical analysis) and serogroup (O-antigen). Sera from acute or convalescent patients are titered against the suspect serotype of Yersinia spp.

Answer 174

The most susceptible populations for the main disease and potential complications are the very young (\< 10 years), the debilitated, the very old, and people undergoing immunosuppressive therapy. Those most susceptible to post-enteritis arthritis are people with the antigen HLA-B27 (or related antigens, such as B7).

Answer 175

The isolation method is relatively easy to perform, but in some instances, cold enrichment (25 g sample of the food mixed with 225 ml of Peptone Sorbitol bile broth for 10 days at 10°C) may be required. Y. enterocolitica can be presumptively identified in 36 to 48 hours using biochemical testing or API 20E or Vitek GNI. The genes encoding for invasion of mammalian cells are located on the chromosome, while a 70 kb plasmid, present in almost all pathogenic Yersinia species, encodes most of the other virulence-associated phenotypes. PCR-based assays have been developed to target virulence genes on both the chromosome and plasmid.

Answer 176

To date (book: 2012), no foodborne outbreaks caused by Y. pseudotuberculosis have been reported in the U.S., but human infections transmitted via contaminated water and foods have been reported in Japan (Fukushima et al. 1988) and Finland (Jalava et al. 2004). Y. pseudotuberculosis has been implicated in a number of food-related outbreaks, but the number of foodborne outbreaks from Y. enterocolitica is higher.

Answer 177

Shigella sonnei, S. boydii, S. flexneri, and S. dysenteriae

Answer 178

Shigellae are Gram-negative, non-motile, non-sporeforming, rod-shaped bacteria. Shigella species, which include Shigella sonnei, S. boydii, S. flexneri, and S. dysenteriae, are highly infectious agents. Some strains produce enterotoxins and Shiga toxin. The latter is very similar to the toxins produced by E. coli O157:H7. Humans are the only host of Shigella, but it has also been isolated from higher primates. The organism is frequently found in water polluted with human feces. In terms of survival, shigellae are very sensitive to environmental conditions and die rapidly. They are heat sensitive and do not survive pasteurization and cooking temperatures. In terms of growth, shigellae are not particularly fastidious in their requirements and, in most cases, the organisms are routinely cultivated in the laboratory, on artificial media. However, as noted in subsequent sections, the relative difficulty of cultivating this organism is dependent, in part, on the amount of time within which stool or food samples are collected and processed. Shigella species are tolerant to low pH and are able to transit the harsh environment of the stomach. These pathogens are able to survive and, in some cases, grow in foods with low pH, such as some fruits and vegetables. They are able to survive on produce commodities packaged under vacuum or modified atmosphere and can also survive in water, with a slight decrease in numbers.

Answer 179

The illness caused by Shigella is shigellosis (also called bacillary dysentery), in which diarrhea may range from watery stool to severe, life-threatening dysentery. All Shigella spp. can cause acute, bloody diarrhea. Shigella spp. can spread rapidly through a population, particularly in crowded and unsanitary conditions.

Answer 180

S. dysenteriae type 1 causes the most severe disease and is the only serotype that produces the Shiga toxin, which may be partially responsible for cases in which hemolytic uremic syndrome (HUS) develops. S. sonnei produces the mildest form of shigellosis; usually watery diarrhea. S. flexneri and S. boydii infections can be either mild or severe.

Answer 181

Mortality: In otherwise healthy people, the disease usually is self-limiting, although some strains are associated with fatality rates as high as 10-15%. (See Illness / complications section, below.)

Answer 182

Infective dose: As few as 10 to 200 cells can cause disease, depending on the age and condition of the host

Answer 183

Onset: Eight to 50 hours.

Answer 184

Illness / complications: In otherwise healthy people, the disease usually consists of selflimiting diarrhea (often bloody), fever, and stomach cramps. Severe cases, which tend to occur primarily in immunocompromised or elderly people and young children, are associated with mucosal ulceration, rectal bleeding, and potentially drastic dehydration. Potential sequelae of shigellosis include reactive arthritis and hemolytic uremic syndrome.

Answer 185

Symptoms: May include abdominal pain; cramps; diarrhea; fever; vomiting; blood, pus, or mucus in stools; tenesmus (straining during bowel movements).

Answer 186

Duration: Uncomplicated cases usually resolve in 5 to 7 days. Most of the time, the illness is self-limiting. In some circumstances, antibiotics are given; usually trimethoprim-sulfamethoxazole, ceftriaxone, or ciprofloxacin.

Answer 187

Route of entry: The fecal-oral route is the primary means of human-to-human transmission of Shigella. With regard to foods, contamination is often due to an infected food handler with poor personal hygiene.

Answer 188

Pathway: The disease is caused when Shigella cells attach to, and penetrate, colonic epithelial cells of the intestinal mucosa. After invasion, they multiply intracellularly and spread to contiguous epithelial cells, resulting in tissue destruction. As noted, some strains produce enterotoxin and Shiga toxin similar to those produced by E. coli O157:H7

Answer 189

A recent Centers for Disease Control and Prevention (CDC) report on domestically acquired foodborne illnesses in the United States revealed that about 15,000 laboratory-confirmed isolates are reported each year, with estimates of actual occurrence ranging from 24,511 to 374,789 cases (average of 131,243). About 31% of these are estimated to be foodborne. Estimates of foodborne illness episodes (mean) caused by 31 pathogens placed Shigella as the sixth most frequent cause (after norovirus, Salmonella species, Clostridium perfringens, Campylobacter, and Staphylococcus aureus, in that order).

Answer 190

Episodes of shigellosis appear to follow seasonal variations. In developed countries, the highest incidences generally occur during the warmer months of the year.

Answer 191

Most cases of shigellosis are caused by ingestion of fecally contaminated food or water. In the case of food, the major factor for contamination often is poor personal hygiene among food handlers. From infected carriers, this pathogen can spread by several routes, including food, fingers, feces, flies, and fomites. Shigella is commonly transmitted by foods consumed raw; for example, lettuce, or as nonprocessed ingredients, such as those in a five-layer bean dip. Salads (potato, tuna, shrimp, macaroni, and chicken), milk and dairy products, and poultry also are among the foods that have been associated with shigellosis.

Answer 192

Diagnosis is by serological or molecular identification of cultures isolated from stool. Shigella may be more difficult to cultivate if stool samples are not processed within a few hours.

Answer 193

All people are susceptible to shigellosis, to some degree, but children 1 to 4 years old, the elderly, and the immunocompromised are most at risk. Shigellosis is very common among people with AIDS and AIDS-related complex

Answer 194

Shigellae remain a challenge to isolate from foods. A molecular-based method (PCR) that targets a multi-copy virulence gene has been developed and implemented by FDA. Improvements in the bacterial isolation method continue and should be available in the near future. The window for collecting and processing Shigella from foods, for cultivation, may be days (rather than hours, as is the case with stool), depending on the food matrix and storage conditions; e.g., temperature. Shigella species can be outgrown by the resident bacterial populations found in foods, which may reflect the usual low numbers of the organism present in foods and, in some foods, a very large number of non-Shigella bacteria. Another factor that reduces the chance of isolating Shigella from foods may be the physiological state of the pathogen at the time of analysis. Environmental conditions could affect its ability to either grow or survive in any food matrix.

Answer 195

Vibrio parahaemolyticus m is a Gram-negative, curve-shaped rod frequently isolated from the estuarine and marine environments of the United States and other tropical-to-temperate coastal areas, worldwide. Optimal temperatures for V. parahaemolyticus are 20°C to 35°C; it can grow at temperatures up to 41°C. It is slowly inactivated at temperatures \<10°C (minimum growth temperature), and cultures should never be stored in refrigerators. V. parahaemolyticus is halophilic; the highest abundance in oysters is at 23 ppt salt. It is lysed almost immediately in freshwater; thus, it is not usually transmitted via the fecal-oral route. At least 0.5% NaCl is required in all media, and 2% NaCl is optimal. Like other vibrios, V. parahaemolyticus is highly susceptible to low pH, freezing, and cooking. Most strains of V. parahaemolyticus produce a capsule, but all strains can be killed by common disinfectants, such as bleach and alcohol.

Answer 196

Mortality: Death occurs in approximately 2% of gastroenteritis and 20% to 30% of septicemia cases.

Answer 197

Infective dose: The FDA V. parahaemolyticus Risk Assessment states that the ID50 (median infective dose) is 100 million organisms. However, evidence from an outbreak in 2004 suggests an infectious dose \>1,000-fold less than in the FDA risk assessment.

Answer 198

Onset: The incubation period is 4 to 90 hours after ingestion of the organism, with a mean of 17 hours

Answer 199

Illness / complications: V. parahaemolyticus-associated gastroenteritis is the name of the infection caused by consumption of this organism. It is usually mild or moderate. Diarrhea caused by this organism is usually self-limiting, with less than 40% of reported cases requiring hospitalization and/or antibiotic treatment. Although the illness is generally mild or moderate, V. parahaemolyticus can also cause septicemia in susceptible people. Those at risk include people with diabetes, liver disease, kidney disease, cancer, AIDS, or other illnesses that result in an immunocompromised state, and those on immunosuppressive medications. In addition to the foodborne gastrointestinal illness, this organism also can cause wound infections. This occurs either through exposure of a pre-existing wound to contaminated marine or estuarine water or through wounds incurred while handling fish, shellfish, or crustaceans.

Answer 200

Symptoms: Diarrhea, abdominal cramps, nausea, vomiting, fever, and bloody diarrhea may be associated with gastroenteritis infections caused by this organism.

Answer 201

Duration: The median duration of the illness is 2 to 6 days.

Answer 202

Route of entry: Oral (in the case of foodborne, gastroenteritis infections. As noted, wound infections also can occur through direct exposure).

Answer 203

Pathway: The complete pathway by which V. parahaemolyticus causes disease remains unclear. However, it is known that TDH is a pore-forming toxin that lyses red blood cells and can attack intestinal cells, disrupting the electrolyte balance. The mechanism of TRH toxin is similar to TDH, disrupting electrolyte flux in intestinal cells

Answer 204

The Centers for Disease Control and Prevention (CDC) estimates that about 45,000 illnesses from V. parahaemolyticus occur each year, in the United States, and that about 86% of them are foodborne. A correlation exists between probability of infection and warmer months, when water temperatures are greater than 15°C (59°F). CDC estimates that only 1 in 20 cases of V. parahaemolyticus are reported, and it is likely that hospitalization and death are rare among unreported cases.

Answer 205

In the U.S., infections with this organism generally are associated with consumption of raw or improperly cooked oysters. Other seafood products, including finfish, squid, octopus, lobster, shrimp, crab, and clams, have been linked to V. parahaemolyticus illnesses, more frequently in Asian countries. . Improper refrigeration of seafood products contaminated with this organism will allow its proliferation, which increases the possibility of infection.

Answer 206

Diagnosis is made by culturing the organism from a person’s stool, wound, or blood (in septicemia cases).

Answer 207

Anyone who eats raw or improperly cooked seafood products is susceptible to infection by this organism. People with compromised immune systems are at greater risk of septicemia and death

Answer 208

Many food isolates are non-pathogenic; therefore, testing food isolates for the virulence determinants is recommended. The BAM recommends a DNA probe and/or a PCR procedure for identification of genes responsible for TDH and TRH production. Additionally, there are more recent molecular methods available for virulence characterization, many of which can be applied directly to seafood products, to screen for the presence of pathogenic organisms prior to isolation.

Answer 209

Shellfish were linked to 177 cases in New York, Oregon, and Washington, in 2006. In 2004, in Alaska, 62 cases were linked to consumption of raw oysters

Answer 210

Coxiella burnetii, a Gram-negative, obligate intracellular bacterium, is the causative agent of Q fever. Coxiella are noted for their resistance to extremely harsh physical conditions, such as heat, low and high pH, and desiccation, due to a tough, spore-like stage. These cells may survive for long periods in the environment and in contaminated foods, such as unpasteurized milk. Due to C. burnetii’s ability to be disseminated via aerosols and its low infective dose, the Centers for Disease Control and Prevention (CDC) have declared it a Category B potential bioterrorism agent. Coxiella burnetii has long been considered the most heat-resistant non-spore-forming pathogen found in milk, making it the benchmark organism for determining proper pasteurization conditions

Answer 211

Mortality: \< 1%

Answer 212

Infective dose: Presumed to be fewer than 10 bacteria.

Answer 213

Onset: May occur as soon as 2 weeks after exposure; average time to symptoms is 20 days.

Answer 214

Illness / complications: The infection sometimes is asymptomatic. Symptomatic individuals with acute Q fever experience a flu-like disease. Infections generally are easy to resolve with antibiotic treatment. Complications that may occur in more serious cases include pneumonia, hepatitis, and myocarditis.

Answer 215

Symptoms: Symptoms may vary considerably among individuals, but commonly include very high fever (105°F); severe headaches; muscle aches; chills; profuse sweating; nausea, vomiting, and/or diarrhea; a dry cough; and abdominal and/or chest pain.

Answer 216

Duration: The fever usually lasts 1 to 2 weeks and generally is self-limiting.

Answer 217

Route of entry: Transmission of C. burnetti is primarily through inhalation of aerosolized bacteria, although transmission via ingestion of contaminated unpasteurized (“raw”) milk or dairy products or via tick bite also is possible.

Answer 218

Pathway: Once the bacteria enter host cells, the bacteria multiply in protective vacuoles before lysing the host cells and spreading to other, non-infected cells.

Answer 219

Mortality: If untreated, may be \> 60%

Answer 220

Onset: Chronic Q fever may develop 6 weeks to years after the acute illness.

Answer 221

Illness / complications: Less than 5% of infected patients will exhibit chronic Q fever. This more severe disease typically occurs in patients who are already compromised due to pregnancy, heart-valve disease, or other illness. A majority of cases involve endocarditis, but may also include hepatitis, encephalitis, pericarditis, meningitis, or pneumonia

Answer 222

Symptoms: Symptoms depend on the tissue affected; e.g., symptoms of endocarditis, hepatitis, encephalitis, pericarditis, meningitis, or pneumonia

Answer 223

Duration: Although often curable with extended (\> 18 months) antibiotic treatment, 50% of patients are prone to relapses.

Answer 224

Since first becoming a reportable disease, the number of Q fever cases has steadily increased, from 17 cases with onset in 2000 to more than 160 cases with onset in 2007. In 2008, after CDC began recording cases based on type of Q fever, 132 cases, total, were reported, consisting of 117 acute and 15 chronic cases. Since that time, 90 to 110 acute and 20 to 25 chronic cases of Q fever have been reported each year.

Answer 225

C. burnetii is found nearly worldwide and is excreted in the urine, milk, feces, and birth products of its various hosts, which include humans, cattle, sheep, goats, reptiles, and birds. Ticks also are a reservoir and may transmit the bacteria directly, via bite, or indirectly, via infected feces. Inhalation of aerosolized bacteria is the most common route of transmission, although transfer also may occur through ingestion of contaminated unpasteurized milk or dairy products and, as noted, via ticks.

Answer 226

Q fever clinical diagnosis is difficult, due to the many different diseases it mimics. However, polymerase chain reaction (PCR) can be used for early detection of the disease when more conventional antibody tests are not useful. After full development of the disease, less-sensitive serological tests, such as an indirect immunofluorescence assay (IFA) against C. burnetiispecific antibodies, are capable of confirming the diagnosis.

Answer 227

Q fever is associated most with occupations in the livestock industry, especially where aerosolization of livestock birth products may be common. Q fever is more common in males than in females and in adults more than in children, probably due to the occupational characteristics of livestock workers. The average age of affected individuals is 45 to 50 years old. Women are at risk of miscarriage if infected

Answer 228

The FDA-mandated level of pasteurization for milk sold in interstate commerce is lethal to C. burnetii, essentially obviating the need to detect the organism in this product. Were analysis for C. burnetii necessary, a live animal host or tissue culture would be required for propagation of the organism.

Answer 229

In July, 2011, three women, in Michigan (ages 30 to 40), were diagnosed with acute Q fever after drinking unpasteurized raw milk obtained as part of a herd-share arrangement. In April 2011, in Washington state, an outbreak involving six illnesses occurred, presumed to have been caused by inhalation of barnyard dust particles contaminated by infected goats. Some of these goats were sold and were suspected of being the source of a Montana outbreak that included six cases. An extremely large outbreak in the Netherlands caused nearly 4,000 illnesses over a 4-year span, starting in 2007. In this case, dairy goats and sheep appeared to be the sources of the outbreak, with 30 farms experiencing extremely high livestock abortion rates

Answer 230

Brucella spp. are small, Gram-negative, short, non-sporeforming coccobacilli. Members of the genus Brucella, of which there are six recognized species, belong to a class of Proteobacteria known as Alphaproteobacteria. Diverse groups of organisms comprise this class, including symbionts and plant pathogens, intracellular animal pathogens, and environmentally ubiquitous bacteria. Strictly defined, Brucella spp. are facultative, intracellular parasites able to invade, and replicate in, phagocytes of the host and to multiply in bacteriologic media. CO2dependent B. abortus strains exist, and B. ovis grows only in atmospheres containing 5-10% CO2. While evidence suggests that Brucella spp. can survive in the environment, it is less clear whether or not the bacteria can proliferate extensively outside the host. Unlike other pathogenic bacteria, Brucella spp. do not possess plasmids or lysogenic bacteriophages, which accounts for the organism’s relatively (but not entirely) static genome. Were Brucella to possess these factors, they would likely result in changes to the organism’s pathogenicity, by enabling the organism to undergo more rapid exchange of genetic material or by introduction of the attacking bacteriophage’s DNA into Brucella’s DNA, respectively.

Answer 231

B. melitensis (sheep, goat), B. abortus (cattle), B. suis (pigs, hares, reindeer, wild rodents), B. neotomae (desert wood rats), B. canis (dogs), and B. ovis (sheep). All except B. ovis and B. neotomae are known to be infectious to humans

Answer 232

slide agglutination is very useful for distinguishing “smooth” strains (i.e., those with an O-polysaccharide-containing outer-membrane lipopolysaccharide: B. melitensis, B. abortus, B. suis, and B. neotomae) from “rough” strains (i.e., those without an O-polysaccharide-containing outer-membrane lipopolysaccharide: B. ovis and B. canis).

Answer 233

Mortality: Less than 2%.

Answer 234

Infective dose: Undefined for humans; however, it is estimated that fewer than 500 cells are enough to establish infection. Humans appear to be more susceptible to B. melitensis than to the other species that infect humans.

Answer 235

Onset: Following exposure, signs of illness usually appear within 3 weeks, but longer incubation periods are not unusual.

Answer 236

Disease / complications: In the beginning stage of illness, septicemia results after multiplication of the organism in regional lymph nodes. Patients have the intermittent fevers and sweating that are the hallmarks of brucellosis, along with other potential symptoms (described in Symptoms section, below). If the diagnosis of brucellosis is delayed or the disease is left untreated, the disease may become chronic, and focalizations of brucellosis in bones (i.e., brucellar spondylitis) and joints may occur. Other potential complications include bacterial endocarditis, meningioencephalitis, and myocarditis. Allergic hypersensitivity (dermal) is not uncommon and should be a consideration for laboratory workers or others with repeated exposures to the organism or antigens.

Answer 237

The antibiotics most commonly used to treat human brucellosis include tetracycline, rifampicin, and the aminoglycosides. However, due to a high likelihood of relapse, health officials recommend the administration of more than one antibiotic for up to 6 weeks. Common combinations include doxycycline plus rifampicin or doxycycline plus streptomycin. For approximately 90% of patients, such aggressive therapy is enough to treat the infection and prevent relapse.

Answer 238

Symptoms: Potential initial signs of illness include intermittent (i.e., “undulant”) fever, chills, sweating, weakness, malaise, headache, and joint and muscle pain. Patients who develop complications may show symptoms of endocarditis or myocarditis, such as shortness of breath, arrhythmia, edema, or chest pain; meningoencephalitis, such as severe headache, stiff neck, confusion, or seizures; or spondylitis, such as back pain.

Answer 239

Duration: With appropriate antibacterial therapy, it is possible to see resolution of disease in only a few weeks; however, even with treatment, symptoms may reappear and last for months or even years.

Answer 240

Route of entry: Oral; e.g., through ingestion of contaminated raw milk or milk products. Inhalation; e.g., by laboratory personnel in the clinical setting. Via skin wounds; e.g., in slaughterhouse workers and veterinarians. In rare instances, human-to-human transmission may occur through, e.g., reproduction or breast-feeding.

Answer 241

Pathway: Humans most commonly come into contact with Brucella through cutaneous, respiratory, or gastrointestinal routes of exposure, allowing the bacteria access to both the blood and reticuloendothelial system. How Brucella, an intracellular parasite, survives intracellularly and its pathogenesis pathway in humans are not well understood. It is clear that the organism’s ability to live and replicate within the phagocytic cells of the reticuloendothelial system (e.g., macrophages) is a critical component of its ability to evade host defenses and establish disease chronicity. Once inside the macrophage, some bacteria are killed; however, a subpopulation can be transported into the intracellular spaces (i.e., the replicative phagosome) of the macrophage and multiply unnoticed and without inducing cell death. When moved to the lymph nodes, macrophages die and can release large amounts of bacteria. In humans, the infection is primarily focused within the reticuloendothelial system, but, in other animal hosts, the organism targets the placental trophoblast cells of pregnant animals, causing fetuses to be aborted. Human cases of spontaneous abortion have been noted following infections with Brucella, similar to occurrences associated with another intracellular pathogen, Listeria monocytogenes, that likewise affects dairy products.

Answer 242

Study of human neutrophils found in the bloodstream demonstrated different responses for different species of Brucella. For example, the bacteria were killed more readily in neutrophils infected with B. abortus than in those infected with B. melitensis. However, strains of B. abortus andB. melitensis in which the virulence was attenuated showed no difference.

Answer 243

Effects of Brucella on animal hosts: Brucella species generally do not cause illness in their primary (animal) hosts. In many cases, the only evidence of infection appears when a pregnant host suffers an abortion. Male animals can asymptomatically harbor the organism in their reproductive organs. Although Brucella strains have a strong preference for their host animals, interspecies transmission does occur through close physical contact with the bacterium. B. ovis and B. canis appear to have a substantially reduced virulence for animals other than their hosts.

Answer 244

According to a recent estimate by the Centers for Disease Control and Prevention (CDC), 839 cases of foodborne brucellosis occur each year in the United States, if under-reporting and under-diagnosis are taken into account. Vaccination of domestic livestock has largely controlled the disease in the U.S. and Canada.

Answer 245

Brucellosis in humans is usually associated with consumption of unpasteurized milk and soft cheeses made from the milk of infected animals.

Answer 246

Most often, the diagnosis of brucellosis relies on the isolation of the organism from blood or bone marrow. In addition, a number of immunologic techniques exist for detection of anti-Brucella antibodies. The organism may also be isolated from the liver, spleen, bone marrow, or cerebrospinal fluid. The growth of Brucella from blood culture is notoriously slow, contributing to difficulties in diagnosis. In the case of disease progression to focalizations or chronic infections, histologic changes and radiologic evidence of erosion of lumbar vertebrae are useful for diagnosis. Localization of infection in the spinal column, brucellar spondylitis, is not uncommon with chronic infection. Appearance of Pedro Pons’ sign (erosion at the anterior superior angle of lumbar vertebra) and bone spurs (osteophytosis) are classic indications of brucellar spondylitis

Answer 247

Veterinarians and farm workers are at particular risk of infection, due to occupational exposure to tissues of aborted animal fetuses, which may contain millions of organisms. Brucellosis in humans tracks the distribution of animal illness. Human cases of brucellosis are found primarily in developing countries with animal cases and a high level of consumption of unpasteurized milk products. In the U.S., human cases linked to domestically produced milk or milk products are largely nonexistent; cases are almost exclusively linked to unpasteurized milk products imported from certain areas of Latin America. This is in contrast to countries such as Mexico, where both human and animal infection of B. melitensis have been reported in every state. Other focal points for both animal and human infection caused by B. melitensis include countries with large goat populations, including Mediterranean Europe, Africa, the Middle East, India, and parts of Asia.

Answer 248

Risk of transmission arises during laboratory procedures that cause the organism to become airborne (e.g., pouring of broths, sample centrifugation). For this reason, all manipulations generating bioaerosols should be done in a class II biological safety cabinet, using Biosafety 3 containment practices and facilities.

Answer 249

Currently no method is available for routine analysis of foods for Brucella spp.

Answer 250

Vibrio cholerae serogroups O1 and O139

Answer 251

Virulence of V. cholerae serogroups O1 and O139 is predicted by the production of an enterotoxin called cholerae toxin (CT) and the toxin co-regulated pilus (TCP).

Answer 252

These organisms are Gram-negative, slightly curved, rod-shaped bacteria that occur naturally in aquatic environments. V. cholerae O1 and O139 are the most hardy of the pathogenic Vibrio spp. and have the ability to survive in freshwater and in water composed of up to ~3% salt. However, these organisms are very susceptible to disinfectants, cold temperatures (especially freezing), and acidic environments. They are readily inactivated at temperatures \>45 C, and cooking food is lethal to V. cholerae O1 and O139. V. cholerae O139 is unique among V. cholerae strains, in that it is encapsulated. However, this does not appear to provide greater pathogenicity or resistance to common disinfectants, such as ethanol and bleach

Answer 253

Mortality: Without rehydration therapy, this disease has a 30% to 50% mortality rate; however, with timely treatment, the fatality rate is less than 1%.

Answer 254

Infective dose: It is estimated that ingestion of 1 million organisms is required to cause illness.

Answer 255

Onset: Symptoms usually appear within a few hours to 3 days of ingestion.

Answer 256

Illness / complications: Infection with V. cholerae serogroups O1 or O139 causes mild to severe diarrhea. Approximately 20% of those infected have watery diarrhea, and 10% to 20% of those develop severe watery diarrhea (characteristic rice-water stools) and vomiting. Cholera gravis, the most severe form of cholera infection, is characterized by severe fluid and electrolyte loss from vomiting and profuse, watery diarrhea. Complications include tachycardia, hypotension, and dehydration.

Answer 257

V. cholerae O1 and O139 infections can be treated with antibiotics, though rehydration therapy is generally sufficient. Doxycycline and/or tetracycline are the antibiotics of choice; however, some resistance to tetracycline has been reported

Answer 258

Symptoms: The illness generally presents with abdominal discomfort and diarrhea that may vary from mild and watery to acute, with rice-water stools. Vomiting also occurs in some cases.

Answer 259

Duration: Mild gastroenteritis cases usually resolve within a few days of symptom onset. Cases requiring medical intervention via rehydration therapy or antibiotic treatment can persist longer, depending on severity of illness when treatment is initiated.

Answer 260

Route of entry: Oral.

Answer 261

Pathway: CT is an enterotoxin that enters epithelial cells of the intestine and causes secretion of electrolytes and water into the lumen of the intestine. This water loss results in severe diarrhea and dehydration. It is known that CT is a multi-subunit toxin encoded by the ctxAB operon. Additionally, genes responsible for formation of the TCP (toxin coregulated pilus) are essential for infection.

Answer 262

No major outbreaks of cholera have occurred in the United States since 1911. However, sporadic cases and small outbreaks have been reported since 1973, suggesting an environmental reservoir in the U.S. The Centers for Disease Control and Prevention (CDC) estimates that 84 cases of foodborne cholera occur in the U.S. annually. This organism causes an estimated 11 million cases per year worldwide, excluding outbreaks. Nearly 90% of cases and 70% of outbreaks from 1995 to 2005 occurred in Africa.

Answer 263

Sources In the U.S., infections with these organisms have been associated with a variety of seafoods, including molluscan shellfish (oysters, mussels, and clams), crab, lobster, shrimp, squid, and finfish. Illness generally results from consumption of these seafoods raw, improperly cooked, or cross contaminated by a raw product. Although cooking kills these bacteria, serogroups O1 and O139 can grow in shellfish that have been contaminated after cooking, and prompt refrigeration of food remnants is important for prevention of this illness. In areas where V. cholerae serogroup O1 and/or O139 is endemic, infections can occur from ingestion of water; ice; unwashed, contaminated food; and seafood.

Answer 264

Diagnosis Cholera can be confirmed only by isolation of the causative organism from the diarrheic stools of infected people.

Answer 265

Target Populations All people are believed to be susceptible to infection. However, infection is more likely to occur among people in impoverished areas, poorly developed areas, and areas with a high population density. Cholera is most severe in children suffering from malnutrition. People who have not previously been exposed to the organism are more likely to become infected, as immunity is usually conferred by infection. Improved sanitation and hygiene can help prevent the disease

Answer 266

Food Analysis FDA’s Bacteriological Analytical Manual (BAM) describes the methods most commonly used to isolate this organism from foods. Pathogenic and non-pathogenic forms of the organisms do exist; therefore, testing food isolates for the virulence determinants is recommended. The BAM recommends a PCR method for detection of the gene responsible for cholera toxin (CT) production.

Answer 267

Examples of Outbreaks In the U.S., two cases of cholera were reported following Hurricanes Katrina and Rita, in 2005. Internationally, the reported outbreak of cholera that occurred in Haiti, in October 2010, included an estimated 530,000 illnesses and at least 7,000 deaths. As is the case with the other Vibrio spp., there is a seasonal trend associated with outbreaks; illnesses are more likely to occur in the warmer months.

Answer 268

V. cholerae non-O1 non-O139 are more hardy than most of the other pathogenic Vibrio spp. and have the ability to survive in freshwater and in water composed of up to ~3% salt. However, these organisms are very susceptible to cold temperatures, including freezing, and acid environments. Additionally, cooking food thoroughly kills V. cholerae non-O1 non-O139. V. cholerae nonO1 non-O139 are not encapsulated, and are susceptible to common disinfectants, such as ethanol and bleach.

Answer 269

Mortality: The fatality rate is about 5%, generally among people with the predisposing conditions listed above.

Answer 270

Infective dose: It is suspected that large numbers (more than 1 million) of the organism must be ingested to cause illness.

Answer 271

Onset: Symptoms usually appear within 1 to 3 days of ingestion

Answer 272

Illness / complications: Diarrhea resulting from ingestion of this organism is generally self-limiting. However, septicemia infections can result, and there is approximately a 5% fatality rate associated with non-O1 non-O139 V. cholerae, generally in people having predisposing conditions similar to those for V. vulnificus infection.

Answer 273

Symptoms: Diarrhea, abdominal cramps, and fever are the predominant symptoms associated with this illness, with vomiting and nausea occurring in approximately 25% of infected people. Approximately 25% of infected people have blood and mucus in their stool.

Answer 274

Duration: Symptoms usually resolve within 7 days.

Answer 275

Route of entry: Oral. (Occasionally, infections with this organism that are not foodborne occur in wounds and ears.)

Answer 276

Pathway: Very little is known about how non-CT producing strains of V. cholerae cause disease. These strains generally produce other types of enterotoxins, such as RTX (repeats in toxin); however, none have been shown to be absolutely necessary for infection.

Answer 277

The Centers for Disease Control and Prevention (CDC) estimates that 17,564 cases of foodborne illness from these Vibrio species occur annually in the U.S. In the spring of 2011, the first oyster-associated V. cholerae O75 outbreak in the U.S. occurred. There were 10 illnesses associated with consumption of raw oysters from Florida.

Answer 278

Sporadic cases generally occur along the coasts of the U.S. and are associated with consumption of raw, improperly cooked, or cross-contaminated seafood during the warmer months.

Answer 279

Diagnosis Diagnosis of a V. cholerae infection is made by culturing the organism from patients’ diarrheic stool or from the blood of patients with septicemia.

Answer 280

Target Populations Anyone who eats raw shellfish is susceptible to diarrhea caused by this organism. As noted above, cirrhotic or immunocompromised people may develop severe complications, such as septicemia.

Answer 281

Food Analysis FDA’s Bacteriological Analytical Manual (BAM) describes the methods most commonly used to isolate this organism from foods. Pathogenic and non-pathogenic forms of the organisms do exist; therefore, testing food isolates for the virulence determinants is recommended. The BAM recommends a PCR method for the detection of the gene responsible for CT production

Answer 282

This organism generally is associated with sporadic illnesses and rarely causes outbreaks. In the spring of 2011, the first oyster-associated V. cholerae O75 outbreak in the U.S. occurred. There were 10 illnesses associated with consumption of raw oysters from Florida

Answer 283

s Gram-negative, curve-shaped bacterium is found in estuarine environments and is associated with various marine species, such as plankton, shellfish, crustaceans, and finfish. It is found throughout coastal waters of the continental United States. Optimal temperatures for V. vulnificus are between 20°C to 35°C; it can grow at temperatures up to 41°C. It is slowly inactivated at temperatures \<10°C (minimum growth temperature), and cultures should never be stored in refrigerators. V. vulnificus is halophilic; the highest abundance in oysters is at 23ppt. It is lysed almost immediately in freshwater; thus, it is not usually transmitted via the fecal-oral route. At least 0.5% NaCl is required in all media, and 2% NaCl is optimal. Like other vibrios, V. vulnificus is highly susceptible to low pH, freezing, and cooking. Most strains of V. vulnificus produce a capsule, but all strains can be killed by common disinfectants, such as bleach and alcohol

Answer 284

Mortality: Death occurs in an average of 35% of septicemia cases (and 20% of woundinfection cases).

Answer 285

Infective dose: The infective dose from ingestion of V. vulnificus is largely unknown, since human feeding studies involving this organism would be unethical. The FAO/WHO V. vulnificus Risk Assessment (VVRA) provides a dose response based on U.S. epidemiologic data and estimates that (1) a dose of 1,000 organisms can cause illness and (2) at a total dose of 1 million organisms, the risk of disease for susceptible people is 1:50,000

Answer 286

Onset: The range of time to onset of gastroenteritis symptoms may be approximately 12 hours to 21 days. (Onset of symptoms in cases of wound infection may be in as few as 4 hours.) The mean time to septicemia is 4 days.

Answer 287

Illness / complications: In healthy people, ingestion of this organism can cause gastroenteritis that generally remains localized and is self-limiting. Among susceptible people, the organism may cause primary septicemia (septic shock). Susceptible people include those with a predisposing condition; for example, those who are immunocompromised or have high serum iron levels (usually due to liver disease). More than 60% of those with septicemia develop secondary lesions on the extremities, similar to those found in wound infections. V. vulnificus also can cause wound infections directly, either through wounds incurred while handling fish, crustaceans, or shellfish, or when a pre-existing wound is exposed to marine or estuarine waters harboring the organism. Wound infections caused by V. vulnificus are characterized by inflammation at the wound site, which can progress to cellulitis, bullous lesions, and necrosis. The infection can become systemic, with affected people developing fever, chills, altered mental status, and hypotension. Secondary lesions from septicemia, as well as primary wound infections caused by direct contact, frequently require surgical debridement or amputation

Answer 288

Symptoms: Gastroenteritis caused by V. vulnificus is characterized by fever, diarrhea, abdominal cramps, nausea, and vomiting. Onset of septicemia is characterized by fever and chills, occasionally accompanied by vomiting, diarrhea, abdominal pain, and/or pain in the extremities.

Answer 289

Duration: In uncomplicated cases, gastroenteritis is self-limiting. The mean duration of septic illness is 1.6 days (i.e., the brief duration is reflective, in part, of the high mortality associated with septicemia).

Answer 290

Route of entry: The gastroenteritis form of illness caused by V. vulnificus results from ingestion of the organism.

Answer 291

Pathway: V. vulnificus harbors many putative virulence factors, including capsule, pili, hemolysins, metalloproteases, and enterotoxins. However, none of these factors has been shown unequivocally to be essential in causing disease; much remains unknown

Answer 292

Sporadic illnesses have been attributed to this organism, but no foodborne outbreaks have been reported. The Centers for Disease Control and Prevention (CDC) estimates that 96 cases of foodborne illness from V. vulnificus occur annually in the U.S. Sporadic cases are more prevalent during the warmer months, when water temperatures are higher than 20°C (68°F).

Answer 293

More than 90% of V. vulnificus illnesses in the U.S. are associated with consumption of raw Gulf Coast oysters. Ingestion of clams and shrimp also has been associated with disease. Thorough cooking or freezing kills the organism, so illnesses usually occur from consumption of raw seafood or cooked seafood that has been contaminated with raw product.

Answer 294

The culturing of the organism from wounds, diarrheic stools, or blood is diagnostic of this illness.

Answer 295

Anyone who eats raw seafood products harboring V. vulnificus, or cooked seafood products cross contaminated with the organism, may develop gastroenteritis. People with predisposing conditions are the most susceptible to septicemia and should eat seafood products only if they have been properly cooked. Predisposing conditions include chronic liver disease (cirrhosis, hepatitis, liver transplantation, or cancer of the liver), elevated serum iron levels (hemachromatosis), compromised immune system (chemotherapy, steroid or other immunosuppressive medication use, AIDS), other chronic illnesses (diabetes, renal disease, intestinal disease), and insufficient gastric acid. Anyone may develop wound infections from contact with estuarine waters

Answer 296

FDA’s Bacteriological Analytical Manual (BAM) describes the methods most commonly used to isolate this organism from foods. More recent molecular methods are available that can be applied directly to seafood products to screen for the presence of V. vulnificus prior to isolation.

Answer 297

No outbreaks of V. vulnificus have been reported. Sporadic cases occur throughout the year, increasing in frequency during the warmer months.

Answer 298

Cronobacter, formerly Enterobacter sakazakii, is a Gram-negative, motile, rod-shaped, non-sporulating pathogenic bacterium that can cause foodborne illness, primarily among infants and immunocompromised adults. It is a rare cause of invasive diseases, including bacteremia, meningitis, and necrotizing enterocolitis. The organism is able to survive in lowmoisture foods, such as powdered infant formula, for long periods.

Answer 299

Mortality: The infection usually has a very high case-fatality rate, which ranges from 10% to 80%. Newborn infants are particularly at risk; infants older than 6 months rarely are affected. Higher case-fatality rates are often associated with premature or lowbirthweight infants. In recent years, the highest mortality has been in healthy term infants who developed septicemia.

Answer 300

Infective dose: The infective dose has not been determined, but scientists have speculated that a reasonable estimate might be similar to that of Escherichia coli O157:H7 (that is, low; e.g., 10 to 100 organisms)

Answer 301

Onset: Symptoms occur in infants within a few days. The onset in adults is unknown, as cases in adults have been rare and the food sources usually have not been determined. : Symptoms occur in infants within a few days. The onset in adults is unknown, as cases in adults have been rare and the food sources usually have not been determined.

Answer 302

Illness / complications: Cronobacter can cause bloodstream and central nervous system infections. The organism also has been associated with sepsis, meningitis, and necrotizing enterocolitis, although it has not been firmly established as a causative agent. Meningitis survivors may develop severe neurologic complications.

Answer 303

Symptoms: Symptoms are often severe and may include poor feeding response, irritability, jaundice, grunting respirations, instability of body temperature, seizures, brain abscess, hydrocephalus, and developmental delay.

Answer 304

Duration of symptoms: Among survivors, colonization varies from 2 to 8 weeks. Among fatalities, death may occur within a few hours to several days after the first signs of sepsis appear.

Answer 305

Route of entry: Most infections are caused by oral entry, although rare cases of wound infection also have been reported.

Answer 306

Pathway: The pathogenesis of Cronobacter-induced neonatal meningitis and enterocolitis is not fully understood. The organism appears to adhere to host cell surfaces instantaneously, then reproduce to an optimal concentration. The adhesion of Cronobacter to epithelial cells is mainly non-fimbriae-based, and other, unidentified virulence factors also might contribute to the binding.

Answer 307

Relatively few cases of Cronobacter infection have been documented, and the organism has rarely been isolated from food products and clinical samples. Since 1958, there have been 120 reported cases of Cronobacter infection in infants, with an average of fewer than 5 reported cases, per year, worldwide. Some epidemiologic studies suggest a Cronobacter infection rate of less than 1% among patients with suspected symptoms. However, this does not take into account potential false-negative identifications

Answer 308

Cronobacter infections in infants often have been associated with contaminated powdered infant formula products. Cronobacter has been isolated from powdered infant formula, rehydrated infant formula, and utensils used to prepare infant formula. Powdered infant formula is not sterile, and its nutrients provide good conditions for the growth of Cronobacter after reconstitution. It has an aw of ca. 0.2. Cronobacter is able to survive such dry conditions. Survival of Cronobacter in powdered infant formula for up to 2 years has been reported. The capsule formation of Cronobacter may contribute to its strong desiccation resistance. Because Cronobacter does not survive pasteurization used in powdered milk production, it has been suggested that Cronobacter contamination happens mainly following the spraying dry step. This could be due to either a contaminated post-drying environment or addition of ingredients that are heat-sensitive, but are added after pasteurization treatment. Some early surveys reported a 10% to 15% contamination rate of Cronobacter in infant formula products, with less than 1 CFU/ 25 g in all samples. Some recent surveys isolated Cronobacter from 2% to 10% infant formulas, dried infant foods, milk powders, cheese products, and other dried foods. Foods other than infant formula rarely have been associated with Cronobacter. However, it has been isolated from bread, cereal, rice, fruit, vegetables, legume products, herbs, spices, milk, cheese, meat, and fish. It has also been isolated from the environment of these foods’ processing facilities.

Answer 309

Identification of culture isolated from tissue, blood, cerebrospinal fluid, or urine aspirated through the bladder wall is necessary for diagnosis of Cronobacter-associated diseases.

Answer 310

Cronobacter infections often are associated with newborns and infants. Neonatal infections may result from contact with Cronobacter in the birth canal or through post-birth environmental sources. Immunosuppression, premature birth, and low birth weight may increase the risk of infection. Approximately 50% of the children infected with Cronobacter are younger than 1 week old, and 75% of the children infected are younger than 1 month old. Adults are considered a low-risk group; however, a few cases of Cronobacter infections in immunocompromised and elderly adults also have been reported.

Answer 311

In 2002, FDA devised a method for the detection of Cronobacter in powdered infant formula, which involved enrichment in water and Enterobacteriaceae enrichment broth, and plating on violet red bile glucose agar and Trypticase Soy Agar. However, this method is time-consuming, and evidence showed that it offered poor selectivity for Cronobacter in the presence of competing background flora. Recently, FDA completed the validation of a new method for the detection of Cronobacter in powdered infant formula, which uses real-time PCR technology to significantly improve the performance of the detection.

Answer 312

Memphis, Tennessee, 1988 – An outbreak of Cronobacter-induced septicemia and meningitis was associated with powdered infant formula contaminated with Cronobacter. Four neonates were involved in the outbreak, and a blender was suggested as the possible contamination source. All isolates from the infant formula and the infants had the same plasmid profile and multilocus enzyme profile. Knoxville, Tennessee, 2001 – An outbreak of Cronobacter infections was linked to a powdered infant formula specific for individuals with special nutritional needs and malabsorption problems. Ten infants tested positive for Cronobacter, and one died following antibiotic treatment. New Mexico, 2009 – An outbreak of Cronobacter infections involved two unrelated infants. No other common exposures other than infant formula were identified for the two infants, who were fed the same brand. However, Cronobacter culture isolated from clinical samples demonstrated different pulsed-field gel electrophoresis (PFGE) patterns. A sample from an opened can of powdered infant formula tested positive for Cronobacter, with a PFGE pattern that was indistinguishable from the clinical isolate from one infant

Answer 313

Aeromonas hydrophila, Aeromonas caviae, Aeromonas sobria, Aeromonas veronii

Answer 314

Aeromonas hydrophila is a Gram-negative, facultative anaerobic, rod-shaped bacterium that belongs to the genus Aeromonas and is ubiquitous in all freshwater environments and in brackish water. Some strains of A. hydrophila are capable of causing gastroenteritis and other infections in humans. Aeromonads also can cause illness in fish, amphibians, and domestic animals, and are listed on the Contaminant Candidate List by the Environmental Protection Agency (EPA). Some Aeromonas species can cause human infections, particularly in immunocompromised people.

Answer 315

Mortality: For gastroenteritis, the mortality rate is not known. The mortality rate for septicemia caused by Aeromonas may be 33% or higher. (Infections that were not foodborne – skin or soft tissue infections caused by Aeromonas, particularly in immunocompromised people with conditions such as liver disease or malignancy – can result in mortality rates of 60% to 75%.)

Answer 316

Infective dose: The infective dose of this organism is unknown, but SCUBA divers who have ingested small amounts of water have become ill, and A. hydrophila has been isolated from their stools. Although the organism possesses several virulence factors that could cause human illness, volunteer feeding studies using healthy adults and high concentrations of organism (104 to 1010 cells) have failed to elicit human illness. However, an outbreak associated with shrimp salad contaminated with A. hydrophila, at approximately 107 cfu/gm of food, has been reported.

Answer 317

Onset: The incubation period associated with gastroenteritis is unknown (as strong challenge studies of volunteers and an animal model are lacking), although the onset of diarrhea appears to be greater than 24 hours.

Answer 318

Illness / complications: The link between A. hydrophila and human gastroenteritis has not yet been firmly established. The link between the pathogen and disease in humans is based mostly on epidemiologic data. Clinically, different types of gastroenteritis are associated with A. hydrophila, including mild diarrhea to a Shigella-like dysenteric illness characterized by loose stools containing blood and mucus, and colitis. In people with weak or impaired immune systems, diarrhea can be chronic and severe. Rarely, the dysentery-like syndrome is severe.  In people with impaired immune systems, A. hydrophila may spread throughout the body and cause systemic infections. Examples of those at risk include people with cirrhosis or various kinds of cancer and those treated with immunosuppressive drugs or who are undergoing cancer chemotherapy. A. caviae and A. veronii biovar sobria also may cause enteritis and, in immunocompromised people or those with malignancies, septicemia. Along with hydrophila, these bacteria account for the majority of human clinical isolates of Aeromonas.  Aside from foodborne infections, Aeromonas spp. are well documented as causative agents of wound infection, usually linked to water-related injuries or aquatic recreational activities.

Answer 319

Symptoms: Range from mild diarrhea to dysentery-like symptoms, including blood and mucus in the stool, to symptoms of septicemia.

Answer 320

Duration: The gastroenteritis associated with the milder form of the disease is usually self-limiting, with watery diarrhea present for a few days to a few weeks. However, people with the severe dysentery-like syndrome may have symptoms for several weeks.

Answer 321

Route of entry: The foodborne form of the illness results from ingestion of a sufficient number of the organisms in foods (from animal origin, seafood, or produce) or water. (As noted, infection resulting not from ingestion, but from open wounds, may lead to tissue infections and septicemia.)

Answer 322

Pathway: Illness is thought to be caused by toxins (aerolysin) and other virulence factors produced by aeromonads.

Answer 323

The relative frequency of A. hydrophila disease in the United States is unknown, since efforts to ascertain its true incidence have only recently been attempted. Most cases have been sporadic, rather than associated with large outbreaks

Answer 324

A. hydrophila frequently has been found in fish and shellfish. It has also been found in market samples of meats (beef, pork, lamb, and poultry) and produce

Answer 325

A. hydrophila can be cultured from stools or from blood by plating the organisms on an agar medium containing sheep blood and the antibiotic ampicillin. Ampicillin prevents the growth of most competing microorganisms. The species identification is confirmed by a series of biochemical tests. The ability of the organism to produce the enterotoxins believed to cause the gastrointestinal symptoms can be confirmed by tissue-culture assays.

Answer 326

All people are believed to be susceptible to gastroenteritis from Aeromonas, although it is most frequently observed in very young children. People with impaired immune systems or underlying malignancy are susceptible to the more severe or systemic infections.

Answer 327

A. hydrophila can be recovered from most foods by direct plating onto a solid medium containing starch as the sole carbohydrate source and supplemented with antibiotics, such as ampicillin, to reduce the growth of most competing microorganisms. PCR-based assays have been developed to detect pathogenic A. hydrophila and differentiate non-pathogenic strains from pathogenic isolates

Answer 328

Plesiomonas shigelloides is a Gram-negative, motile, non-sporulating, oxidase-positive, rodshaped bacterium that has been found in many aquatic ecosystems. This bacterium has been isolated from freshwater (ponds, streams, rivers), estuarine water, and marine environments. The pathogen has been isolated from warm-blooded and cold-blooded animals, including freshwater fish and shellfish, and from many types of animals, including cattle, goats, swine, cats, dogs, monkeys, vultures, snakes, and toads. P. shigelloides is not considered a commensal organism found in humans. The ingested P. shigelloides organism does not always cause illness in the host animal, but may reside temporarily as a transient, noninfectious member of the intestinal flora. It has been isolated from the stools of patients with diarrhea, but is also sometimes isolated from healthy individuals (0.2% to 3.2% of the population). Under laboratory conditions, P. shigelloides is able to grow at temperatures between 8o C and 45o C, with an optimal range from 25o C to 35o C. Growth is reduced in low temperatures (less than 10o C), pH less than 4.5, and in salt (NaCl) above 5%. P. shigelloides cells are killed by pasteurization.

Answer 329

 Mortality: Not very common, although one fatality of a newborn has been reported.

Answer 330

Infective dose: The infective dose is presumed to be quite high; at least greater than 1 million organisms

Answer 331

Onset: Symptoms may begin 20 to 50 hours after consumption of contaminated food or water.

Answer 332

Illness / complications: P. shigelloides gastroenteritis usually is a mild, self-limiting infection, although a more severe, dysenteric form of gastroenteritis may occur. Infected people may also exhibit other symptoms, such as severe abdominal pain, cramping, nausea, vomiting, low-grade fever, chills, headache, and some dehydration. There is a paucity of reports on extra-intestinal diseases caused by P. shigelloides, but the organism has been shown to be responsible for septicemia, bacteremia, meningitis, septic arthritis, osteomyelitis, peritonitis, cellulitis, and pneumonia. Extraintestinal complications, regardless of the organism’s portal of entry (e.g., open wounds), may occur more frequently in people who are immunocompromised or seriously ill with cancer, blood disorders, or hepatobiliary disease. Neonates with meningitis most likely were infected by vertical transmission; mortality rate approaches 80%. Septicemia is more commonly found in adults

Answer 333

Symptoms: Symptoms may include fever, chills, abdominal pain, nausea, diarrhea, and/or vomiting. Diarrhea is watery, non-mucoid, and non-bloody. In severe cases, it may be greenish-yellow, foamy, and blood-tinged, and may contain mucus and polymorphonuclear leukocytes, and some patients experience severe abdominal cramps, vomiting, and some level of dehydration

Answer 334

Duration: Generally about 1 to 7 days, but diarrhea can last as long as 21 days.

Answer 335

Route of entry: Oral; ingestion of contaminated water or foods causes the foodborne illness (vs. infection of open wounds).

Answer 336

Pathway: The pathogen has several putative virulence factors, but the exact role of these proteins has not been elucidated. P. shigelloides synthesize toxins, including heat-stable toxins, heat-stable and heat-labile enterotoxin, cholerae-like toxins, hemolysin, cytotoxins, and iron sequestration in host cells. Other reported factors that indicate pathogenicity potential include cell adhesion, cell invasiveness, and apoptotic Caco-2 cell death. A direct link between these virulence factors, combined with the paucity of epidemiologic data, reflect the current debate about the true pathogenic potential of P. shigelloides.

Answer 337

The rate of P. shigelloides infection in the United States is unknown. Gastrointestinal P. shigelloides illness in healthy people may be so mild that they do not seek medical treatment. Most P. shigelloides strains associated with human gastrointestinal disease have been from stools of diarrheic patients living in tropical and subtropical areas. Such infections are rarely reported in the U.S. or Europe because of the self-limiting nature of the disease. Most cases reported in the U.S. involve the elderly and very young and people who have pre-existing health problems, such as cancer or sickle-cell anemia, or are immunocompromised.

Answer 338

Most human P. shigelloides infections are suspected to be waterborne, occur in the summer months, and correlate with environmental contamination of freshwater (e.g., rivers, streams, ponds). The organism may be present in unsanitary water that has been used as drinking water or recreational water, or water used to rinse foods that are consumed without cooking or heating. The usual route of transmission of the organism in sporadic or epidemic cases is by ingestion of contaminated water, raw shellfish, or improperly cooked or raw foods. Additional aquatic sources include crabs, fish, and oysters.

Answer 339

The pathogenesis of P. shigelloides infection is not known. The organism is suspected of being toxigenic and invasive. Its significance as an enteric (intestinal) pathogen is presumed because of its predominant isolation from stools of patients with diarrhea. It is identified by common bacteriological analysis, serotyping, and antibiotic sensitivity testing.

Answer 340

Anyone is susceptible to infection. Infants, children, and chronically ill people are more likely to experience protracted illness and complications. The pathogen also is associated with traveler’s diarrhea.

Answer 341

P. shigelloides may be recovered from food and water by methods similar to those used for stool analysis. The keys to recovery, in all cases, are selective agars that enhance the survival and growth of these bacteria over the growth of the background microflora. Suitable media to isolate P. shigelloides from foods include xylose-sodium deoxycholate-citrate, inositol-brilliant green, and Plesiomonas agars. Identification following recovery may be completed in 12 to 24 hours. PCR-based assays that have been reported in the literature can specifically detect P. shigelloides; genetic targets include the 23S rRNA gene and the hugA gene.

Answer 342

Enterotoxigenic Escherichia coli (ETEC) are highly motile, Gram-negative, rodshaped bacteria. They are characterized by production of several virulence factors, including both heat-labile (LT) toxin and heat-stable (ST) toxins, as well as several colonization-factor antigens.

Answer 343

 Mortality: The World Health Organization attributes 380,000 deaths (worldwide) to ETEC, mostly among children, each year.

Answer 344

Infective dose: Volunteer feeding studies showed that a high dose, ranging from 10 million to 10 billion ETEC cells, may be needed to cause an infection in adults. Children may be affected by a smaller dose.

Answer 345

Onset: Usually 26 hours after ingestion of contaminant, but can range from 8 to 44 hours

Answer 346

Disease / complications: Illness from ETEC is usually self-limiting, mild, and brief. However, some severe forms last longer and resemble cholera, with up to five or more daily passages of rice-water-like stools that result in severe dehydration. Antibiotic treatment usually is not required in ETEC infections, but seems to be effective in reducing the duration and severity of illness. In infants and elderly and debilitated patients, particularly, appropriate electrolyte replacement therapy may be necessary

Answer 347

Symptoms: Infection is characterized by sudden onset of diarrhea that is watery and without blood or mucus, rarely accompanied by high fever or vomiting. Other symptoms include abdominal cramps, low-grade fever, nausea, and malaise.

Answer 348

Duration of symptoms: Most cases last a few days; however, severe forms can last up to 19 days.

Answer 349

Pathway: After ingestion, ETEC colonizes the small intestine, where the toxins that induce fluid secretion are produced

Answer 350

ETEC outbreaks are infrequent in the United States, but infections are a more common occurrence among travelers to foreign countries. ETEC infections are endemic in many developing tropical countries and areas with poor hygiene standards. Infections are more prevalent in the warmer, wet months.

Answer 351

Most ETEC outbreaks are linked to consumption of contaminated food or water. ETEC is often found in feces of asymptomatic carriers, and humans appear to be the most likely source of ETEC. In 1975, a large outbreak affecting 2,000 people was traced to sewage-contaminated water at a national park. Contaminated well water in Japan and water supplies aboard cruise ships also have been implicated in ETEC outbreaks. Foodborne outbreaks of ETEC have occurred in restaurants and at various catered functions. Examples of implicated foods include Brie cheese, curried turkey, mayonnaise, crabmeat, deli food, and salads. In most of these cases, foods became contaminated with ETEC via infected food handlers or through the use of contaminated water during preparation. ETEC infection does not appear to be transmitted by person-to-person contact, but some hospital infections have occurred and probably were caused by unsanitary conditions

Answer 352

During the acute phase of infection, large numbers of ETEC cells are excreted in feces. Since generic E. coli are also abundantly present in the bowels, ETEC strains can be differentiated from other E. coli by in vitro immunochemical assays, tissue culture, or gene probes and PCR assays specific for LT and ST toxin genes. Commercial kits that use antibodies to detect these toxins are also available

Answer 353

Presence of ETEC in foods can be determined by plating culture enrichment of food samples onto media that are selective and differential for E. coli and testing the isolates for presence of LT and ST toxins, using PCR or commercial kits that use antibodies specific to the toxins. Because of its high infectious dosage, ETEC analyses usually are not performed unless generic E. coli levels are very high.

Answer 354

EPEC are Gram-negative, rod-shaped bacteria. They are characterized by the presence of the locus for enterocyte effacement (LEE) pathogenicity island, which carries multiple virulence factors, including the eae gene that encodes for intimin and, together with the tir gene (intimin receptor), allows intimate adherence of EPEC to intestinal epithelial cells. In the 1940s and 1950s, EPEC was a frequent cause of infantile diarrhea in the United States. Currently, EPEC infections are less important in developed countries, but continue to be a common cause of diarrhea in developing countries, especially in children less than 2 years old.

Answer 355

Mortality rates from 25% to 50% have been reported in the past. In developed countries, better treatment and medical facilities have greatly reduced mortality, but some deaths still occur.

Answer 356

Infective dose: EPEC is highly infective in infants, and the dose is presumably very low. Adults, however, are not as susceptible. Volunteer feeding studies showed that 10 million to 10 billion cells are needed to cause diarrhea in adults, provided that gastric acid first has been neutralized by bicarbonate.

Answer 357

Onset: Onset of diarrhea is often rapid, occurring as soon as 4 hours post ingestion of EPEC.

Answer 358

Illness / complications: The diarrhea can be mild; however, the infection sometimes can be severe. Fluid and electrolyte imbalance may need to be corrected, to prevent dehydration.

Answer 359

Symptoms: Profuse, watery diarrhea; vomiting; and low-grade fever.

Answer 360

Duration: Diarrhea occasionally is protracted, lasting from 21 to 120 days

Answer 361

Pathway: After ingestion, EPEC adheres to intestinal mucosa and causes extensive disarrangement of the digestive-absorptive enzyme system, resulting in nutrient malabsorption

Answer 362

Foodborne outbreaks of EPEC are sporadic. Incidence varies on a worldwide basis, but countries with poor sanitation practices have the most frequent outbreaks. Many of these occur in day-care centers and pediatric wards.

Answer 363

Source(s) and prevalence of EPEC are controversial, because foodborne outbreaks are sporadic. Foods implicated in past EPEC outbreaks have included raw beef and chicken, but any food exposed to fecal contamination is strongly suspect.

Answer 364

Diagnosis consists of culturing for E. coli from stools of infected people and testing the isolates for the ability to cause attachment and effacing (A/E) lesions on tissue culture cells. PCR assays can also be used to test the isolates for LEE genes, but since Enterohemorrhagic E. coli (EHEC) also carry LEE, the isolates also have to be tested for Shiga toxins (Stx). EPEC are distinguished from EHEC by the presence of LEE and absence of Stx.

Answer 365

EPEC infections most often occur in infants, especially those who are being bottle fed. Poorquality water used to rehydrate infant formulae in underdeveloped countries may be the source of EPEC in bottle-fed infants.

Answer 366

Presence of EPEC in foods can be determined by plating culture enrichment of food samples onto media that are selective and differential for E. coli and testing the isolates for EPEC traits by tissue culture or PCR. Shiga toxins (Stx) assays are also essential to distinguish EHEC from EPEC. EPEC are characterized by the presence of LEE and absence of Stx.

Answer 367

In the mid 1990s, an EPEC outbreak in Minnesota was traced to a buffet, but no specific food item was identified. In 1995, two outbreaks in France affected 59 people and were traced to mayonnaise, lettuce, and pickles.

Answer 368

Like generic E. coli, toxin-producing Shiga-toxigenic Escherichia coli (STEC) are Gram-negative, rodshaped bacteria, but are characterized by the production of Shiga toxins (Stx). Depending on the reference cited, there are 200 to 400 STEC serotypes, many of which have not been implicated in human illness; however, a subset of STEC called enterohemorrhagic Escherichia coli (EHEC), the topic of this chapter, includes only those that cause serious illness. Serotype O157:H7 is the prototypic EHEC strain.

Answer 369

Although O157:H7 is currently the predominant strain and accounts for ~75% of the EHEC infections worldwide, other non-O157 EHEC serotypes are emerging as a cause of foodborne illnesses. In the United States a group often referred to as the “big 6” (O111, O26, O121, O103, O145, and O45) accounts for the majority of the non-O157:H7 serotypes isolated from clinical infections and, therefore, is currently a focus of concern. However, other EHEC serotypes, such as O113, O91, and others, also can cause severe illness. As a result, the non-O157 EHEC serotypes of public health concern can change quickly, depending on outbreak incidents, and can vary with countries and geographic regions.

Answer 370

EHEC are characterized by:  production of Stx, including Stx1 and/or Stx2. Stx1 is nearly identical to the toxin produced by Shigella dysenteriae Type I. There are many subtypes of both toxins, and some subtypes of Stx2 appear to be implicated in human illness. Stx2 is most often associated with severe sequelae, such as hemolytic uremic syndrome (HUS), which is characterized by acute renal failure.  presence of LEE (“locus for enterocyte effacement”; pathogenicity island that encodes for intimin, a protein that enables bacterial attachment to epithelial cells).

Answer 371

Mortality: Patients whose illness progresses to HUS have a mortality rate of 3% to 5%.

Answer 372

Infective dose: The infective dose of EHEC O157:H7 is estimated to be very low, in the range of 10 to 100 cells. The infective dose of other EHEC serotypes is suspected to be slightly higher.

Answer 373

Onset: Symptoms usually begin 3 to 4 days after exposure, but the time may range from 1 to 9 days

Answer 374

Disease / complications: Infections from EHEC may range from asymptomatic-to-mild diarrhea to severe complications. The acute symptoms are called hemorrhagic colitis (HC), characterized by severe abdominal cramps and bloody diarrhea, which may progress to such life-threatening complications as HUS or thrombotic thrombocytopenia purpura (TTP) – conditions that are most often associated with O157:H7, but that also can occur with other EHEC serotypes. About 3% to 7% of HC cases progress to HUS or TTP

Answer 375

Some evidence suggests that Stx2 and intimin are associated with progression to severe disease, such as HUS. Kidney cells have a high concentration of Stx receptors; hence, the kidney is a common site of damage. Some survivors may have permanent disabilities, such as renal insufficiency and neurological deficits.

Answer 376

Antibiotic therapy for EHEC infection has had mixed results and, in some instances, seems to increase the patient’s risk of HUS. One speculation is that antibiotics lyse EHEC cells, releasing more Stx into the host.

Answer 377

Symptoms: Hemorrhagic colitis is characterized by severe cramping (abdominal pain), nausea or vomiting, and diarrhea that initially is watery, but becomes grossly bloody. In some cases, the diarrhea may be extreme, appearing to consist entirely of blood and occurring every 15 to 30 minutes. Fever typically is low-grade or absent

Answer 378

Duration: In uncomplicated cases, duration of symptoms is 2 to 9 days, with an average of 8 days

Answer 379

Route of entry: Oral (e.g., ingestion of contaminated food, water, or fecal particles).

Answer 380

Pathway: After ingestion, EHEC attaches to intestinal epithelial cells via LEE-encoded factors and produces Stx that are internalized, activated, and can pass into the bloodstream to become systemic.

Answer 381

There are about 63,000 cases of EHEC infections in the U.S. yearly, according to a report by the Centers for Disease Control and Prevention (CDC) . Ground beef and beef products continue to be implicated in most infections; however, contaminated produce increasingly has been implicated as a vehicle. As for STEC non-O157, the CDC estimates that 112,752 cases, per year, are attributed to foodborne illness in the U.S.

Answer 382

EHEC O157:H7 was first identified in an outbreak, in 1982, in which hamburgers from a fastfood restaurant were the vehicle. In 1991, hamburgers from fast-food restaurants were implicated in another outbreak, which affected about 700 people in four states. In the mid 1990s, a large outbreak was traced to unpasteurized juices. The largest O157:H7 outbreak on record took place in Japan; radish sprouts were implicated and about 10,000 people were affected. Since then, O157:H7 has been implicated in numerous outbreaks that involved lettuce, salads, various types of sprouts, and, in 2006, bagged spinach. In 2009, an O157:H7 outbreak in the U.S. was traced to frozen, raw cookie dough.

Answer 383

Raw or undercooked ground beef and beef products are the vehicles most often implicated in O157:H7 outbreaks. Earlier outbreaks also implicated consumption of raw milk. O157:H7 can develop acid tolerance, as evidenced by infections in which acid foods (

Answer 384

Unlike generic E. coli, EHEC O157:H7 do not ferment the sugar sorbitol, so an effective method is to plate patient’s bloody diarrhea samples onto sorbitol MacConkey medium to screen for sorbitol non-fermenting isolates. These are then typed serologically using antibodies to the O157 and the H7 antigens. However, as other EHEC serotypes are increasingly causing illness, clinical samples are now simultaneously tested for the presence of Stx using commercially-available antibody kits. Any STEC strains found are then serotyped and identified. There are also many PCR assays specific for Stx genes that may be used for screening clinical samples.

Answer 385

All people are believed to be susceptible to hemorrhagic colitis, but young children and the elderly are more susceptible and at higher risk for the illness to progress to more severe complications. Others with weak immune systems also are at risk, such as people with some chronic diseases or AIDS, and people on immunosuppressive medications; for example, some drugs used for arthritis and cancer chemotherapy.

Answer 386

Presence of EHEC O157:H7 in foods can be determined by plating culture enrichment of food samples onto selective and differential media. Unlike typical E. coli, O157:H7 do not ferment sorbitol and are negative with the MUG assay, so these tests are commonly used to distinguish O157:H7 strains from other E. coli prior to serological testing for the O157 and H7 antigens and also for the presence of Stx genes by PCR. Molecular assays also exist that can specifically detect O157:H7 strains using unique mutational markers. Detection of non-O157:H7 EHEC, however, is more complex, due to the lack of unique traits. For non-O157 EHEC, food enrichment is first screened for Shiga toxin using an antibody assay or for Stx genes by PCR. Enrichment cultures that are positive for Stx are plated on agar media, and multiple isolates are then tested for Stx genes, in order to obtain a pure culture isolate. These putative STEC isolates are then retested for virulence genes and their serotype determined. This process is both time-consuming and labor-intensive and may require screening hundreds of isolates. There are numerous commercially-available kits to test for Stx, O157, and a few other EHEC serotypes. However, there are several Stx subtypes and many EHEC serotypes, and not all of these can be detected by commercial test kits. The Escherichia coli link to the FDA Bacteriological Analytical Manual, Chapter 4, provides a description of methods to test for common E. coli. Methods for EHEC and O157:H7 are described in Chapter 4a.

Answer 387

EIEC is a Gram-negative, rod-shaped, enterotoxin-producing bacterium that closely resembles Shigella. Both are characterized by their ability to invade colonic epithelial cells. The genetic information required for the invasion phenotype is encoded within a 37 kilobase region on a virulence plasmid, which can vary in size from 180 kb in S. sonnei to 220 kb in S. flexneri and EIEC. There is a high degree of homology among these plasmids, and they are functionally interchangeable. The illness caused by EIEC is a mild form of bacillary dysentery, similar to that caused by Shigella spp.

Answer 388

Mortality: A recent estimate of domestically acquired foodborne illness in the United States, by the Centers for Disease Control and Prevention (CDC), lists a death rate of zero for diarrheagenic E. coli other than Shiga-toxigenic and enterotoxigenic E. coli.

Answer 389

Infective dose: The infective dose of EIEC is thought to be in the range of 200 to 5,000 cells, somewhat higher than that of Shigella. The difference in the dose may depend on which virulence plasmid these pathogens harbor.

Answer 390

Onset: The symptoms usually occur within 12 to 72 hrs after ingestion of contaminated foo

Answer 391

Illness / complications: The illness generally is self-limiting, with no known complications.

Answer 392

Symptoms: Mild dysentery; abdominal cramps, diarrhea, vomiting, fever, chills, and generalized malaise. Stools often contain blood and mucus.

Answer 393

Duration: Usually resolves in 5 to 7 days.

Answer 394

Route of entry: Oral. Person-to-person transmission can also occur

Answer 395

Pathway: The pathogenesis of EIEC is similar to that of Shigella species. The process begins with cellular invasion via endocytic vacuoles. Once internalized, the vacuoles are lysed, the bacteria multiply intracellularly, and spread laterally to other cells. EIEC also produce an enterotoxin, which may be involved in causing the watery diarrhea that precedes the dysentery symptoms associated with EIEC

Answer 396

EIEC outbreaks are not frequent in the U.S. However, it may be misidentified or confused with shigellosis; therefore, its actual prevalence may be underestimated.

Answer 397

No specific foods are frequently associated with EIEC infections. Infected humans are the only known reservoirs of EIEC; hence, any food contaminated with human feces from an ill individual, either directly or via contaminated water, can be infectious.

Answer 398

Imported Camembert cheese was implicated in an epidemic of gastroenteritis caused by EIEC that affected 226 people in 96 outbreaks, in 1971. A tofu product contaminated with EIEC affected 670 people in Japan, in 1988. In 1994, a restaurant-associated EIEC outbreak in Texas, which affected 370 people, was traced to contaminated guacamole.

Answer 399

Diagnosis consists of culturing for E. coli from stools of infected individuals and testing the isolates for invasiveness using tissue cultures or animal models. EIEC isolates may also be identified using PCR assays to test for the presence of inv genes. These assays, however, will detect both EIEC and Shigella spp., so additional assays are needed for differentiation

Answer 400

All populations are susceptible to EIEC infections.

Answer 401

Presence of EIEC in foods can be determined by plating culture enrichment of food samples onto media that are selective and differential for E. coli and testing the isolates for the presence of inv genes. EIEC in foods can also be detected using inv gene-specific PCR assays, testing either directly or on food-sample enrichments.

Answer 402

Clostridium perfringens is an anaerobic (but aerotolerant) Grampositive, spore-forming rod that produces enterotoxin. The bacterium is relatively cold-tolerant, and its spores are heat-resistant. Nonpathogenic C. perfringens is widely distributed in the environment and is frequently found in the intestines of humans and many domestic and feral animals. Spores of the organism persist in soil, sediments, and areas subject to human or animal fecal pollution

Answer 403

Among the many isotypes of C. perfringens, type A almost always contains the cpe gene (the enterotoxin gene, which causes food poisoning), and types B, C, D, and E sometimes contain this gene

Answer 404

Foodborne illness caused by C. perfringens can take two forms. 1) The gastroenteritis form is very common and often is mild and self-limiting. Depending on the strain, it may also develop as more severe gastroenteritis that leads to damage of the small intestine and, potentially, but rarely, fatality. 2) The other form, enteritis necroticans or “pig-bel disease” (a name reportedly derived from pidgin English, referring to the characteristic swollen bellies and other severe symptoms that resulted from feasts on contaminated pork in New Guinea), is rare in the United States, more severe than the other form of the illness, and often fatal. For Consumers: A Snapshot Once this bacterium (estimated to be the second leading bacterial cause of foodborne illness in the U.S.) is eaten in contaminated food, it makes a toxin in the intestines. The toxin causes two major kinds of foodborne illness (and can cause other diseases transmitted in ways other than food). (1) One of the illnesses is very common, and the usually mild cramps and watery diarrhea start within 8 to 16 hours. For most people, symptoms go away by themselves in 24 hours, although they can be worse and last up to a week or two in very young or old people, or longer in people with weak immune systems (for example, people with HIV/AIDS or people on cancer chemotherapy or drugs that treat rheumatoid arthritis by lowering the actions of the immune system). The more serious, longer‐lasting cases, especially, should be treated to prevent complications, like fluid imbalance that can cause heart‐rhythm problems and other problems. (2) The other illness, called “pig‐bel” (enteritis necroticans), is much more severe and often fatal, but is very rare in the U.S. Symptoms include pain and gassy bloating in the abdomen, diarrhea (maybe bloody), and vomiting. Knowing more about the bacterium, Clostridium perfringens, can help you understand how to protect yourself. The bacteria make tiny spores – a survival mode in which they make an inactive form that can exist without nutrition and that develops very tough protection against the outside world – which can survive cooking. After food is cooked, the spores can turn into full‐fledged bacteria as the food cools – and here’s the most important part: these bacteria multiply much faster than do most other kinds of bacteria. That means that if you cook meats (one of the higher‐risk foods for this “bug”) or other foods, then leave them at room temperature, this bacterium can multiply to levels that can make you sick a lot faster than other bacteria can. Refrigerating food within a couple of hours of cooking, or sooner, slows down the bacteria and greatly lowers your chance of illness. And remember that this bacterium also can contaminate raw foods, like vegetables. Washing your fresh produce in clean, running water helps protect you. Both forms of the disease result from ingestion of large numbers of C. perfringens, which replicates much more quickly than do most other bacteria. This raises the likelihood that, compared with other bacteria, C. perfringens will more quickly reach pathogenic levels in contaminated food left unrefrigerated and that consumers who eat the food may ingest large doses of the bacterium.

Answer 405

Mortality: In 1999, the Centers for Disease Control and Prevention (CDC) estimated that, overall, C. perfringens annually accounts for 26 deaths in the U.S. Common gastroenteritis form: A few deaths resulting from diarrhea-induced dehydration and other complications have been reported, and usually were among debilitated or elderly people.  Pig-bel form (enteritis necroticans): This disease is often fatal. As noted, it is extremely rare in the U.S.

Answer 406

Infective dose: Symptoms are caused by ingestion of large numbers ( \> 106 ) vegetative cells or \>106 spores/g of food. Toxin production in the digestive tract (or in vitro) is associated with sporulation. This disease is characterized as a food infection; only one episode has ever implied the possibility of intoxication (i.e., disease from preformed toxin)

Answer 407

Onset: Symptoms occur about 16 hours after consumption of foods containing large numbers (\>106 live vegetative cells or \>106 spores) of C. perfringens capable of producing the enterotoxin

Answer 408

Illness / complications: Complications are rare in the typical, mild gastroenteritis form of the disease, particularly among people under 30 years old. Elderly people are more likely to have prolonged or severe symptoms, as are immunocompromised people. The more severe form of the disease may cause necrosis of the small intestine, peritonitis, and septicemia.

Answer 409

Symptoms: Gastroenteritis form: Common characteristics include watery diarrhea and mild abdominal cramps. Pig-bel form (enteritis necroticans): Abdominal pain and distention, diarrhea (sometimes bloody), vomiting, and patchy necrosis of the small intestine.

Answer 410

Duration: The milder form of the disease generally lasts 12 to 24 hours. In the elderly or infants, symptoms may last 1 to 2 weeks

Answer 411

Pathway: CPE protein usually is released into the intestines when the vegetative cells lyse on completion of sporulation. This enterotoxin is responsible for the clinical presentation in humans. The enterotoxin induces fluid and electrolyte losses from the GI tract. The principal target organ for CPE is believed to be the small intestine. Pig-bel disease involves production of beta toxin, which is highly trypsin-sensitive. Of note: consumption of large amounts of sweet potatoes, which generally contain trypsin inhibitor, could contribute to progression of the disease. The effects of low gastrointestinal levels of trypsin appear to have been demonstrated in Germany around the end of World War II and post-war, when starvation and high levels of potato consumption contributed to low levels of this enzyme in the population. These were thought to have been major cofactors in the occurrence of pig-bel disease in Germany during that period.

Answer 412

Perfringens poisoning is one of the most commonly reported foodborne illnesses in the U.S. The CDC estimates that 965,958 domestically acquired cases occur annually in the U.S., second only to Salmonella when considering bacterial causes of foodborne illness. Thirty-four outbreaks in 2006 (i.e., not including isolated cases) included 1,880 cases. At least 51 outbreaks were reported annually in the U.S. from 2001 to 2005. Typically, 50 to 100 people are affected in one outbreak. It is probable that many outbreaks go unreported, because the implicated foods and patients’ feces are not tested routinely for C. perfringens or its toxin

Answer 413

In most instances, the actual cause of poisoning by this organism is temperature abuse of cooked foods. Small numbers of the organism often are present after the food is cooked, due to germination of its spores, which can survive high heat and can multiply rapidly as a result of a fast doubling time (\<10 minutes for vegetative cells), depending on temperature and food matrix. Therefore, during cool-down (109-113°F) and storage of prepared foods, this organism can reach levels that cause food poisoning much more quickly than can other bacteria. Meats (especially beef and poultry), meat-containing products (e.g., gravies and stews), and Mexican foods are important vehicles for C. perfringens foodborne illness, although it is also found on vegetable products, including spices and herbs, and in raw and processed foods. Spores of some C. perfringens strains can survive boiling water for an hour or longer in a relatively protective medium (e.g., a cooked-meat medium).

Answer 414

Perfringens poisoning is diagnosed by its symptoms and the typical delayed onset of illness. Diagnosis is confirmed by detection of the toxin in patients’ feces. Bacteriologic confirmation can also be done by finding exceptionally large numbers of the bacteria in implicated foods or in patients’ fecal samples

Answer 415

Institutional settings (such as school cafeterias, hospitals, nursing homes, prisons, etc.), where large quantities of food are prepared several hours before serving, are the most common circumstance in which C. perfringens poisoning occurs. The young and elderly are the most frequent victims of C. perfringens poisoning. As with other infections, immunocompromised people are at higher risk of severe illness than are others; e.g., those with HIV/AIDS or undergoing cancer chemotherapy or immunosuppressive drugs for rheumatoid arthritis or other inflammatory conditions.

Answer 416

Standard bacteriological culturing procedures are used to detect the organism in implicated foods and in feces of patients. Serological assays are used for detecting enterotoxin in the feces of patients and for testing the ability of strains to produce toxin. With the introduction of PCRbased methods, toxin typing using antiserum neutralization tests in mice is no longer practical.

Answer 417

Staphylococcal species are Gram-positive, nonmotile, catalase-positive, small, spherical bacteria (cocci), which, on microscopic examination, appear in pairs, short chains, or bunched in grape-like clusters. Staphylococci are ubiquitous and impossible to eradicate from the environment. Many of the 32 species and subspecies in the genus Staphylococcus are potentially found in foods due to environmental, human, and animal contamination. Several staphylococcal species, including both coagulase-negative and coagulase-positive strains, have the ability to produce highly heatstable enterotoxins that cause gastroenteritis in humans. S. aureus is the etiologic agent predominantly associated with staphylococcal food poisoning. S. aureus is a versatile human pathogen capable of causing staphylococcal food poisoning, toxic shock syndrome, pneumonia, postoperative wound infection, and nosocomial bacteremia. S. aureus produces a variety of extracellular products, many of which act as virulence factors. Staphylococcal enterotoxins can act as superantigens capable of stimulating an elevated percentage of T-cells.

Answer 418

S. aureus is one of the most resistant non-sporeforming human pathogens and can survive for extended periods in a dry state. Staphylococci are mesophilic. S. aureus growth, in general, ranges from 7°C to 47.8°C, with 35°C being the optimum temperature for growth. The growth pH range is between 4.5 and 9.3, with an optimum between 7.0 and 7.5. Staphylococci are atypical, in that they are able to grow at low levels of water activity, with growth demonstrated at aw as low as 0.83, under ideal conditions. Optimum growth of S. aureus occurs at aw of \>0.99. For the most part, strains of S. aureus are highly tolerant to salts and sugars.

Answer 419

Staphylococcal enterotoxins are single-chain proteins with molecular weights of 26,000 to 29,000. They are resistant to proteolytic enzymes, such as trypsin and pepsin, which allows them to transit intact through the digestive tract. There are five classical enterotoxin serotypes: SEA, SEB, SEC1,2,3, SED, and SEE and the more recently described SEG, SEH, and SEI; all exhibit emetic activity. There are also SE-like enterotoxin serotypes, SElJ-SElU; these SE-like designations have not been confirmed to exhibit emetic activity. The different SE serotypes are similar in composition and biological activity, but are different in antigenicity and are identified serologically as separate proteins

Answer 420

Mortality: Death from staphylococcal food poisoning is uncommon, although it has occurred among the elderly, infants, and severely debilitated people.

Answer 421

Infective dose: The intoxication dose of SE is less than 1.0 microgram. This toxin level is reached when S. aureus populations exceed 100,000 organisms/g in food. This level is indicative of unsanitary conditions in which the product can be rendered injurious to health. In highly sensitive people, ingestion of 100 to 200 ng of enterotoxin can cause symptoms. The population of S. aureus at the time of analysis may be significantly different, and not representative of, the highest population that occurred in the product. This should be taken into consideration when examining foods.

Answer 422

Onset: The onset of symptoms usually is rapid (1 to 7 hours) and in many cases acute, depending on individual susceptibility to the toxin, amount of toxin ingested, and general health

Answer 423

Illness / complications: Staphylococcal food poisoning generally causes self-limiting, acutely intense illness in most people. Not all people demonstrate all symptoms associated with the illness. The most common complication is dehydration caused by diarrhea and vomiting.

Answer 424

Symptoms: When ingested, the enterotoxin may rapidly produce symptoms, which commonly include nausea, abdominal cramping, vomiting, and diarrhea. In more severe cases, dehydration, headache, muscle cramping, and transient changes in blood pressure and pulse rate may occur

Answer 425

Duration: The illness is relatively mild and usually lasts from only a few hours to one day; however, in some instances, the illness is severe enough to require hospitalization.

Answer 426

Route of entry: Consumption of food contaminated with enterotoxigenic S. aureus or ingestion of the preformed enterotoxin.

Answer 427

Pathway: Staphylococcal enterotoxins are stable in the gastrointestinal tract and indirectly stimulate the emetic reflex center by way of undetermined molecular events. It is thought that the vagus nerve is involved in the sequence of events that produce the emetic response

Answer 428

S. aureus is the cause of sporadic food poisoning episodes around the world. The Centers for Disease Control and Prevention (CDC) estimates that, in the United States, staphylococcal food poisoning causes approximately 241,188 illnesses, 1,064 hospitalizations, and 6 deaths each year. The true incidence is unknown for a number of reasons, including poor responses from victims during interviews with health officials; misdiagnosis of the illness, which may be symptomatically similar to other types of food poisoning (such as vomiting caused by Bacillus cereus emetic toxin); inadequate collection of samples for laboratory analyses; improper laboratory examination; and, most important, many victims do not seek medical attention because of the short duration of the illness. Although it is under-reported, staphylococcal food poisoning remains a common cause of foodborne illness as indicated by the recent Centers for Disease Control and Prevention (CDC) report (see Resources section, Scallan et al.).

Answer 429

Staphylococci are widely distributed in the environment. They can be found in the air, dust, sewage, water, milk, and food, or on food equipment, environmental surfaces, humans, and animals. Foods frequently implicated in staphylococcal food poisoning include meat and meat products; poultry and egg products; salads, such as egg, tuna, chicken, potato, and macaroni; bakery products, such as cream-filled pastries, cream pies, and chocolate éclairs; sandwich fillings; and milk and dairy products. Foods that require considerable handling during preparation and are kept slightly above proper refrigeration temperatures for an extended period after preparation are frequently involved in staphylococcal food poisoning. Unless heat processes are applied, staphylococci are expected to exist in any and all foods that are handled directly by humans or are of animal origin. Destruction of viable cells by heat does not destroy the biological activity of preformed staphylococcal enterotoxins. These toxins are highly heat stable and can remain biologically active.

Answer 430

Staphylococcal food poisoning is diagnosed based on isolation of the pre-formed enterotoxin or the isolation of enterotoxigenic staphylococci from the suspect food consumed and/or the vomitus or feces of the patient. The food history and rapid onset of symptoms often are sufficient to diagnose this type of food poisoning. Suspect foods are collected and examined for presence of viable staphylococci and preformed enterotoxin. The most conclusive test is the linking of an illness with a specific food, or in cases in which multiple vehicles exist, detection of pre-formed enterotoxin in food sample(s)

Answer 431

All people are believed to be susceptible to this type of bacterial intoxication; however, intensity of symptoms may vary.

Answer 432

A number of serological methods have been developed for detection of pre-formed enterotoxin in foods. These same methods are also utilized for determining the enterotoxigenicity of S. aureus isolate from a food product. Enrichment isolation and direct plating are the methods frequently used for detecting and enumerating S. aureus in foods. Non-selective enrichment is useful for demonstrating presence of injured cells, whose growth is inhibited by selective enrichment media. Enumeration by enrichment isolation, or selective enrichment isolation, may be achieved by determining either the direct plate count or the most probable number (MPN) of S. aureus present. The MPN procedure is recommended for surveillance of products expected to have a small population of S. aureus and a large population of competing organisms. Direct plating method is suitable for analysis of foods in which a population of S. aureus is expected to be greater than 100 CFU/g. During outbreak investigations, it is recommended that foods be tested for pre-formed enterotoxin and to determine enterotoxigenicity of isolates. Currently ELISA-based methods are those most widely used to identify staphylococcal enterotoxins. Several commercially available enzyme-linked immunosorbent assays use both monoclonal and polyclonal antibodies. The intensity of the color reaction or florescence is proportional to the amount of toxin present in the sample. These extraction and detection methods are described in detail in the BAM online chapter 13A. Steps during food processing and preservation, including treatment with heat, acidulation, or chemicals, and other treatments stress the staphylococcal enterotoxin protein. A processed product may have serologically inactive and undetectable toxin, while the toxin protein remains biologically active and can cause illness. Procedures have been developed to chemically treat suspect samples that may contain denatured enterotoxins, to restore serological activity, so that the toxin can be detected using classical serological methods. When food has been treated to eliminate viable microorganisms, as in pasteurization or heating, DNA-based techniques, such as PCR, or direct microscopic observation of the food (if the cells were not lysed), can assist in identification and diagnosis. Pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) are the most common molecular subtyping techniques used for staphylococcal species; these are powerful tools that can be used when viable staphylococci are isolated from the implicated food, victims, and suspected carriers, such as food handlers.

Answer 433

Among 5,824 children who had eaten lunch served in 16 elementary schools in Texas, 1,364 became ill. The lunches were prepared in a central kitchen and transported to the schools by truck. Epidemiologic studies revealed that 95% of the ill children had eaten chicken salad. The day before, frozen chickens had been boiled for 3 hours, then deboned, cooled to room temperature with a fan, ground into small pieces, placed into l2-inch-deep aluminum pans, and stored overnight in a walk-in refrigerator, at 42°F to 45°F. The next morning, the remaining ingredients were added and blended in with an electric mixer. The food was placed in thermal containers and transported to the various schools, from 9:30 a.m. to 10:30 a.m., where it was kept at room temperature until served, from 11:30 a.m. to noon. Bacteriologic examination of the chicken salad revealed large numbers of S. aureus.

Answer 434

In 1989, multiple staphylococcal foodborne diseases were associated with canned mushrooms. Enterotoxin type A (SEA) was identified in several samples of unopened cans from the same lot. (CDC Morbidity and Mortality Weekly Report, June 23, 1989, Vol. 38, #24.) S. intermedius, typically considered a veterinary pathogen, was isolated from butter blend and margarine implicated in a 1991 food poisoning outbreak. SEA was detected in both clinical and food isolates implicated in this food-related outbreak involving more than 265 cases in the western US. (Khambaty et al., 1994)

Answer 435

Bacillus cereus is a Gram-positive, facultatively anaerobic, endosporeforming, large rod. These and other characteristics, including biochemical tests, are used to differentiate and confirm the presence of B. cereus, although these characteristics are shared with B. mycoides, B. pseudomycoides, B. thuringiensis and B. anthracis

Answer 436

 determination of motility (most B. cereus strains are motile)  presence of toxin crystals (B. thuringiensis)  hemolytic activity (B. cereus and others are beta hemolytic, whereas B. anthracis usually is non-hemolytic)  rhizoid growth, which is characteristic of B. cereus var. mycoides.

Answer 437

B. cereus is widespread in the environment and often is isolated from soil and vegetation. The optimal growth temperature is 28°C to 35°C, with a minimum growth temperature of 4°C and a maximum of 48°C. Growth can occur in pH ranges from 4.9 to 9.3, and the organism tolerates 7.5% salt concentration.

Answer 438

The diarrheal type of illness is caused by a large-molecular-weight protein. The vomiting (emetic) type of illness is associated with cereulide, an ionophoric lowmolecular-weight dodecadepsipeptide that is pH-stable and heat- and protease- resistant. The non-antigenic peptide is stable after heating at 121°C for 30 minutes, cooling at 4°C for 60 days, and at a pH range of 2 to 11.

Answer 439

Mortality: Albeit rare, the emetic enterotoxin of B. cereus foodborne illness has been implicated in liver failure and death in otherwise healthy individuals. Similarly, a newly identified cytotoxin has been isolated from a B. cereus strain that caused a severe outbreak and three deaths.

Answer 440

Infective dose: The presence of large numbers of B. cereus (greater than 106 organisms/g) in a food is indicative of active growth and proliferation of the organism and is consistent with a potential human health hazard. The number of organisms most often associated with human illness is 105 to 108 ; however, the pathogenicity arises from preformed toxin.

Answer 441

Onset: Diarrheal type: 6 to 15 hours after consumption of contaminated food. Emetic type: 0.5 to 6 hours after consumption of contaminated foods

Answer 442

Disease / complications: Although both forms of foodborne illness associated with the diarrheal and vomiting toxins produced by B. cereus are generally mild and self-limiting, more severe and fatal forms of the illness have been reported. Other clinical manifestations of B. cereus invasion and infection that have been observed include severe systemic and pyogenic infections, gangrene, septic meningitis, cellulitis, panophthalmitis, lung abscesses, infant death, and endocarditis, and, in cows, bovine mastitis.

Answer 443

Symptoms: Diarrheal type: The symptoms of B. cereus diarrheal-type food poisoning include watery diarrhea, abdominal cramps, and pain, mimicking those of Clostridium perfringens food poisoning. Nausea may accompany diarrhea, but vomiting (emesis) rarely occurs. Emetic type: The symptoms of the emetic type of food poisoning include nausea and vomiting, paralleling those caused by Staphylococcus aureus foodborne intoxication

Answer 444

Duration of symptoms: The symptoms usually subside after 24 hours of onset

Answer 445

Route of entry: Consumption of food contaminated with enterotoxigenic B. cereus or with the emetic toxin.

Answer 446

Pathway: Cereulide has been shown to be toxic to mitochondria by acting as a potassium ionophore. Using a house musk shrew animal model, researchers have found that a serotonin5-HT3 receptor-mediated mechanism is associated with the emetic syndrome. Two of the diarrheal enterotoxins are composed of multicomponent proteins that have dermonecrotic and vascular permeability activities and cause fluid accumulation in ligated rabbit ileal loops. The third type of enterotoxin is a member of the β-barrel toxin family and is similar to the β-toxin of Clostridium perfringens.

Answer 447

In a recent Centers for Disease Control and Prevention (CDC) report on domestically acquired foodborne illness in the United States, the estimated number of episodes of B. cereus illness annually was given as 63,400. The numbers of confirmed outbreaks reported to the CDC in 2005, 2006, and 2007 were 4, 3, and 6 and affected 69, 35, and 100 people, respectively. However, an average of 37.6 suspected outbreaks occurred during this same period, affecting more than 1,000 people. Foods that were associated with outbreaks included beef, turkey, rice, beans, and vegetables. Other outbreaks may go unreported or are misdiagnosed because of symptomatic similarities to Staphylococcus aureus intoxication (B. cereus vomiting type) or Clostridium perfringens food poisoning (B. cereus diarrheal type).

Answer 448

A wide variety of foods, including meats, milk, vegetables, and fish, have been associated with the diarrheal-type food poisoning. The vomiting-type outbreaks generally have been associated with rice products; however, other starchy foods, such as potato, pasta, and cheese products, also have been implicated. Food mixtures, such as sauces, puddings, soups, casseroles, pastries, and salads, frequently have been linked with food-poisoning outbreaks.

Answer 449

Confirmation of B. cereus as the etiologic agent in a foodborne outbreak requires either (1) isolation of strains of the same serotype from the suspect food and feces or vomitus of the patient, (2) isolation of large numbers of a B. cereus serotype known to cause foodborne illness from the suspect food or from the feces or vomitus of the patient, or (3) isolation of B. cereus from suspect foods and determination of their enterotoxigenicity by serological (diarrheal toxin) or biological (diarrheal and emetic) tests. The rapid-onset time to symptoms in the emetic form of the disease, coupled with some food evidence, is often sufficient to diagnose this type of food poisoning.

Answer 450

A variety of methods have been recommended for the recovery, enumeration, and confirmation of B. cereus in foods. More recently, a serological method has been developed for detecting the putative enterotoxin of B. cereus (diarrheal type) isolates from suspect food sources. Recent investigations suggest that the vomiting-type toxin can be detected through animal models (cats, monkeys) or, possibly, by cell culture.

Answer 451

Listeria monocytogenes is a Gram-positive, rod-shaped, facultative bacterium, motile by means of flagella, that is among the leading causes of death from foodborne illness. It has 13 serotypes, including 1/2a, 1/2b, 1/2c, 3a, 3b, 3c, 4a, 4ab, 4b, 4c, 4d, 4e, and 7. Among them, serotypes 1/2a, 1/2b, and 4b have been associated with the vast majority of foodborne infections. L. monocytogenes is hardy; it is salt-tolerant and not only can survive in temperatures below 1°C, but also grow in these conditions, unlike many other pathogens. It is also notable for its persistence in food-manufacturing environments. The bacterium is ubiquitous in the environment and can be found in moist environments, soil, and decaying vegetation.

Answer 452

Listeria monocytogenes, L. ivanovii (Of the five other species in the genus Listeria – L. grayi, L. innocua. L. ivanovii, L. seeligeri and L. welshimeri – only L. ivanovii is considered pathogenic, and mainly in ruminants, rather than in humans. )

Answer 453

Although not a leading cause of foodborne illness, L. monocytogenes is among the leading causes of death from foodborne illness. A recent report by the Centers for Disease Control and Prevention (CDC) estimated that domestically acquired foodborne L. monocytogenes causes 255 deaths in the U.S. annually. The severe form of the infection has a case-fatality rate of 15% to 30%, overall. When listerial meningitis occurs, the case-fatality rate may be as high as 70%; from septicemia, 50%, overall; and in perinatal/neonatal infections, more than 80%.

Answer 454

Infective dose: The infective dose of L. monocytogenes is undetermined, but is believed to vary with the strain and susceptibility of the host, and the food matrix involved also may affect the dose-response relationship. In cases associated with raw or inadequately pasteurized milk, for example, it is likely that fewer than 1,000 cells may cause disease in susceptible individuals. As noted, however, the infective dose may vary widely and depends on a variety of factors.

Answer 455

Onset: Gastroenteritis caused by L. monocytogenes has a relatively short incubation period, from a few hours to 2 or 3 days. The severe, invasive form of the illness can have a very long incubation period, estimated to vary from 3 days to 3 months.

Answer 456

Illness / complications: L. monocytogenes infection causes two forms of disease in humans: 1) non-invasive gastrointestinal illness, which generally resolves in otherwise healthy people. 2) the much more serious, invasive form of the illness, which may cause septicemia and meningitis. Manifestations of L. monocytogenes infection tend to be host-dependent. In people with intact immune systems, it may cause acute febrile gastroenteritis, the less severe form of the disease. In vulnerable populations, however, the more severe form of the disease may result in sepsis and spread to the nervous system, potentially causing meningitis. In elderly and immunocompromised people who develop the severe form, it usually manifests in this manner. Pregnant women, who are disproportionately infected with L. monocytogenes, may experience mild, flu-like symptoms; however, their offspring do not fare as well – they may abort or be stillborn, and those born alive may have bacteremia and meningitis. Onethird of confirmed cases of maternal-fetal L. monocytogenes infections lead to abortion or stillbirth.

Answer 457

Symptoms: Otherwise healthy people might have mild symptoms or no symptoms if infected with L. monocytogenes, while others may develop fever, muscle aches, nausea and vomiting, and, sometimes, diarrhea. When the more severe form of the infection develops and spreads to the nervous system, symptoms may include headache, stiff neck, confusion, loss of balance, and convulsions.

Answer 458

Duration: The duration of symptoms generally depends on the health status of the infected person. The symptoms can last from days to several weeks.

Answer 459

Pathway: The pathogenesis of L. monocytogenes is unique, because the organism is able to spread directly from cell to cell in the host, rather than having to “travel” interstitially to reach other cells. Once the bacterium enters the host’s monocytes, macrophages, or polymorphonuclear leukocytes, it can reproduce, and it is bloodborne. Groups of proteins on the L. monocytogenes cell surface enable it to survive in phagocytic cells and enhance its cell-to-cell spread.

Answer 460

Based on a survey collected through 1997 by the Centers for Disease Control and Prevention (CDC), listeriosis was responsible for approximately 2,500 illnesses and 500 deaths in the United States annually. By 2008, the number of L. monocytogenes infections had declined 36 percent, compared to the period from 1996 to 1998. There was a moderate increase in the incidence of L. monocytogenes from 2008 to 2009; however, it was still lower than the incidence measured 10 years before that. More recently, the 2011 CDC report cited above estimated that L. monocytogenes causes 1,591 cases annually.

Answer 461

Many foods have been associated with L. monocytogenes. Examples include raw milk, inadequately pasteurized milk, chocolate milk, cheeses (particularly soft cheeses), ice cream, raw vegetables, raw poultry and meats (all types), fermented raw-meat sausages, hot dogs and deli meats, and raw and smoked fish and other seafood. L. monocytogenes can grow in refrigerated temperatures, which makes this organism a particular problem for the food industry. Potential contamination sources include food workers, incoming air, raw materials, and foodprocessing environments. Among those, post-processing contamination at food-contact surfaces poses the greatest threat to product contamination.

Answer 462

The main target populations for listeriosis are:  pregnant women/fetuses/neonates - perinatal and neonatal infections;  persons immunocompromised by, for example, corticosteroids, anticancer drugs, graft suppression therapy, AIDS;  cancer patients, particularly leukemic;  (less frequently reported) diabetic, cirrhotic, asthmatic, and ulcerative colitis patients;  the elderly;  healthy people – some reports suggest that healthy people are at risk, and that antacids or cimetidine may predispose them to the infection. Some studies suggested that healthy, uncompromised people could develop the disease, particularly if the food eaten was heavily contaminated with L. monocytogenes.

Answer 463

Identification of culture isolated from tissue, blood, cerebrospinal fluid, or another normally sterile site (e.g., placenta or fetus) is needed for diagnosis of L. monocytogenes infection. Stool cultures are not informative, since some healthy humans may be intestinal carriers of L. monocytogenes.

Answer 464

Methods of analyzing foods for purposes of identifying L. monocytogenes are complex and timeconsuming. The present FDA method, revised in January 2003, uses a single enrichment broth, buffered Listeria enrichment broth, and requires 24 to 48 hours of enrichment, followed by a variety of agars and, finally, biochemical confirmation. Total time to identification is from 5 to 7 days. Many other enrichment broths, such as UVM broth and Fraser broth, are also included in various protocols. Agars that have been extensively evaluated include Oxford agar, PALCAM, LPM plus esculin and ferric iron and MOX. New molecular biology techniques have been used to develop various rapid-screening kits for L. monocytogenes. These kits generally rely on ELISA, PCR, and probe-based identification

Answer 465

L. monocytogenes has caused significant outbreaks worldwide over the past decades. Some examples are listed below. Los Angeles, 1985. A large-scale listeriosis outbreak occurred in Los Angeles County, California, due to the consumption of contaminated Mexican-style soft cheese. Human listeriosis cases reported numbered 142. Among them, 93 cases occurred in pregnant women or their offspring, and the remaining cases occurred in non-pregnant adults. The outbreak led to 48 deaths, including 20 fetuses, 10 neonates, and 18 non-pregnant adults. An investigation of the cheese plant suggested that the cheese was commonly contaminated by unpasteurized milk. The outbreak strain was serotype 4b. U.S., 1989, 2000. A serotype 1/2a strain was isolated from a single case of human listeriosis in 1989, which was caused by the consumption of processed meat. Eleven years later, the same strain isolated from sliced turkey produced by the same processing plant was implicated in a listeriosis outbreak. This provides a powerful illustration of L. monocytogenes’s tenacity and prolonged survival in food-processing environments. U.S., 1998 to 1999. A large scale multistate outbreak of listeriosis caused at least 50 cases in 11 states. Six adults died, and two pregnant women had spontaneous abortions. Contaminated hot dogs were linked to this outbreak. All L. monocytogenes isolates from these cases were serotype 4b. U.S., 2002. A multistate outbreak of listeriosis in the Northeastern U.S. resulted in 46 cases, including 7 deaths and 3 stillbirths or miscarriages in eight states. The outbreak was linked to eating sliceable turkey deli meat. L. monocytogenes was isolated from 1 food product and 25 environmental samples from a poultry-processing plant. The isolate from the food product had a PFGE pattern different from the outbreak strain; however, two environmental isolates from floor drains had an identical PFGE pattern to that of outbreak patient isolates, suggesting that the plant might have been the source of the outbreak. The outbreak strain was serotype 4b. Canada, 2008. A widespread outbreak of listeriosis occurred in Canada and was linked to deli meat produced by a Maple Leaf Foods plant in Toronto, Ontario. The outbreak caused 57 confirmed cases in seven provinces, and 22 people died. The outbreak strain was serotype 1/2a.

Answer 466

Gram-positive, aerobic, nonmotile, straight or slightly curved, rod-shaped bacterium that lacks an outer cell membrane. It does not have spores or capsules and is classified as an acid-fast bacterium, because in staining procedures its lipid-rich cell wall resists decolorization by acids. Some other species of the genus Mycobacterium include M. tuberculosis, M. leprae, M. africanum, M. avium, and M. microti. Members of the Mycobacterium tuberculosis complex, which includes M. tuberculosis and M. bovis, are the causative agents of human and animal tuberculosis. Mycobacterium bovis is a causative agent of foodborne human tuberculosis (although it may also be transmitted via the airborne route, if it subsequently infects the lungs and results in active disease). Mycobacterium species are considered hardy because of their unique cell walls, which enable them to survive long exposures to chemical disinfectants, including acids, alkalis, and detergents, and because they are able to resist lysis by antibiotics. M. bovis can survive in the environment for several months in cold, dark, moist conditions and for up to 332 days at a temperature range of 12°C to 24°C. Some species of Mycobacterium are very difficult to grow (i.e., fastidious), unlike most bacterial pathogens, and could take up to 20 days to 2 years to culture. Optimum growth temperatures range from 25°C to more than 50°C. Mycobacterium species are referred to as rapid growers if they show visible growth colonies within 7 days, while those that require more than 7 days are referred to as slow growers. M. bovis is slow-growing in culture media. Mycobacteria are widespread in nature, but the primary sources are water, soil, mastitic cows, and gastrointestinal tracts of animals. Mycobacterium bovis is pathogenic for cattle and some other animals, but also has been shown to be infectious to humans and, therefore, is a pathogen of concern to humans.

Answer 467

Mortality: Death can result if the infection is left untreated. The Centers for Disease Control and Prevention (CDC) recently reported that an estimated three deaths (mean) are associated with M. bovis annually in the U.S.

Answer 468

Infective dose: The infective dose of Mycobacterium bovis in cattle could be as low as 1 CFU (6-10 organisms), while the precise infective dose for humans is still unknown; it is suggested to be on the order of tens to millions of organisms.

Answer 469

Onset: Symptoms generally appear months to years after initial infection. Some infected persons do not show any signs of the disease.

Answer 470

Illness/complications: Ingestion of food contaminated with M. bovis can result in infection of the gastrointestinal tract or other parts of the body; for example, the lungs or the lymph nodes. (See Pathway section, below.) The disease may result in death, if untreated

Answer 471

Symptoms: Typical symptoms include fever, night sweats, fatigue, loss of appetite, and weight loss. Other symptoms depend on the part of the body affected; for example, chronic cough, blood stained-sputum, or chest pain, if the lungs are affected; or diarrhea, abdominal pain, and swelling, if the gastrointestinal tract is affected. Infections in humans also may be asymptomatic

Answer 472

Duration: Duration of illness depends on the immune status of the infected person. Symptoms could last for months or years, which necessitates a longer treatment period. Individuals with symptoms of lung involvement should avoid public settings until told by their health-care providers that they are no longer a risk to others.

Answer 473

Route of entry: Mostly through ingestion (oral). Inhalation or direct contact with mucous membranes or broken skin, although not common, also are potential routes of exposure.

Answer 474

Pathway: M. bovis can be taken up by alveolar macrophages in the lung, especially if transmission is by the aerosol route (pulmonary tuberculosis). From there it is carried to the lymph nodes, where the organism can migrate to other organs. M. bovis can multiply in these cells and in interstitial spaces, leading to formation of tubercle lesions. Gastrointestinal tuberculosis also causes the associated lymph nodes to form tubercles, although the organism may not spread to other organs.

Answer 475

The CDC recently reported that an estimated 60 cases of human foodborne M. bovis tuberculosis (mean) are acquired in the U.S. each year.

Answer 476

Cattle and raw cow’s milk are the typical sources of M. bovis; hence, food vehicles of particular concern include unpasteurized cow’s milk and its products. The organism can be transmitted to humans through consumption of raw (unpasteurized) contaminated milk or other dairy products and raw or undercooked meat, such as venison, of infected animals. It can also be contracted through aerosol droplets; however this mode of transmission is less common, as is transmission via contact with the flesh of an infected animal (for example, via a wound or during slaughtering)

Answer 477

All people are susceptible to M. bovis infection. Those who consume unpasteurized milk or products made with unpasteurized milk, especially young children, the elderly, and individuals with weak immune systems (for example, people with AIDS) are at higher risk of the disease than are others.

Answer 478

Mycobacterium bovis is identified by isolating the bacteria from lymph nodes in the neck or abdomen, or from sputum produced by coughing. It is important to culture the organism in the laboratory and identify isolates according to cultural, biochemical, and molecular (DNA) techniques. Culturing and identification of Mycobacterium bovis are complicated and pose a risk of infection to laboratory personnel if safety procedures are not strictly followed.

Answer 479

Analysis of food for presence of M. bovis is challenging and complex. A variety of scientifically validated cultural, biochemical, and molecular techniques are utilized to identify M. bovis and distinguish it from other members of the M. tuberculosis complex. (See citation for Harris BN et al. in Resources section, below, for examples.)

Answer 480

Michigan, 1994-2007. Two cases of tuberculosis due to M. bovis occurred. One case, in 2002, probably resulted due to consumption of unpasteurized milk by the patient or to the fact that the patient lived in a tuberculosis-endemic farm area. A second case occurred in 2004, due to exposure of the patient to infected deer. Investigations revealed that the outbreak strains related to the two human cases were genotypically the same as the deer/cattle outbreak strain. New York City, New York, 2001-2004. This outbreak involved a multi-agency investigation in which there were 35 cases of human M. bovis illness in New York City. The investigation showed that fresh cheese from Mexico was implicated in the infection. One fatality was recorded (a 15-month-old boy).

Answer 481

Clostridium botulinum is an anaerobic, Gram-positive, spore-forming rod that produces a potent neurotoxin. The spores are heat-resistant and can survive in foods that are incorrectly or minimally processed. Seven types of botulinum are recognized (A, B, C, D, E, F and G), based on the antigenic specificity of the toxin produced by each strain. Most strains produce only one type of toxin, but strains producing dual toxin types have been reported. The organism and its spores are widely distributed in nature. They are found in both cultivated and forest soils; bottom sediments of streams, lakes, and coastal waters; in the intestinal tracts of fish and mammals; and in the gills and viscera of crabs and other shellfish.

Answer 482

(Types C and D cause botulism in animals

Answer 483

Types C and E also cause botulism in birds

Answer 484

Types A, B, E and F cause human botulism.

Answer 485

No outbreaks of type G have been reported.)

Answer 486

neurotoxin. Botulinum toxin causes flaccid paralysis by blocking motor nerve terminals at the neuromuscular junction. The flaccid paralysis progresses symmetrically downward, usually starting with the eyes and face, to the throat, chest, and extremities. When the diaphragm and chest muscles become fully involved, respiration is inhibited and, without intervention, death from asphyxia results.

Answer 487

The infection results in flaccid paralysis of muscles, including those of the respiratory tract

Answer 488

Three major types of botulism are known: foodborne botulism and infant botulism, which also is foodborne. The third type, wound botulism, is not foodborne

Answer 489

Recommended treatment for foodborne botulism includes early administration of botulinum antitoxin, available from the Centers for Disease Control and Prevention (CDC), and intensive supportive care, including mechanical breathing assistance. An antitoxin for infant botulism (Botulism Immune Globulin Intravenous, abbreviated BIG-IV) also is available and should be administered as early in the illness as possible. Antimicrobial therapy is not recommended, due to concerns about increased toxin release as a result of cell lysis.

Answer 490

Mortality: The mortality rate is high if treatment is not immediately administered. The disease is generally fatal in 5% to 10% of cases

Answer 491

Infective dose: An extremely small amount – a few nanograms – of the toxin can cause illness.

Answer 492

Onset: Adult: Usually 18 to 36 hours after ingesting food containing the toxin, although times have varied from 4 hours to 8 days. Infant: Generally follows a period of normal development.

Answer 493

Adult: Initial symptoms may include double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. If the disease is not treated, symptoms may progress to paralysis of the arms, legs, trunk, and respiratory muscles. Early signs of intoxication consist of marked lassitude, weakness and vertigo, usually followed by double vision and progressive difficulty in speaking and swallowing. Difficulty in breathing, weakness of other muscles, abdominal distention, and constipation may also be common symptoms Infant: Constipation after a period of normal development is often the first sign of infant botulism. This is followed by flat facial expression; poor feeding (weak sucking); weak cry; decreased movement; trouble swallowing, with excessive drooling; muscle weakness; and breathing problems.

Answer 494

Duration: Patients with severe cases that involve paralysis of the respiratory muscles may need mechanical ventilation and intensive care for weeks or months.

Answer 495

Route of entry: Oral, for foodborne infection. (Infection of wounds also occurs).

Answer 496

Pathway: Clinical presentation develops after a person ingests the pre-formed toxin, or if the organisms grow in the intestines or in wounds, followed by toxin release. The ingested botulinum toxin (an endopeptidase enzyme) blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system. The toxin acts by binding presynaptically to high-affinity recognition sites on the cholinergic nerve terminals and decreasing the release of acetylcholine, causing a neuromuscular blocking effect. (This mechanism laid the foundation for development of the toxin as a therapeutic tool; e.g., when temporary inactivation of specific muscles is needed for therapeutic or cosmetic purposes.) C. botulinum produces the toxin as a complex of proteins, among which is the neurotoxic moiety. The toxin is synthesized as a relatively inactive single-chain polypeptide with a molecular weight of ~150 kDa. It becomes an active toxin by selective proteolytic cleavage to yield the heavy and light chains that are linked by a single disulphide bond and non-covalent interactions. The toxin’s light chain is a Zn++-containing endopeptidase that blocks acetylcholine-containing vesicles from fusing with the terminal membrane of the motor neuron, resulting in flaccid muscle paralysis.

Answer 497

(page 111)

Answer 498

General info: The types of foods involved in botulism vary according to food preservation and cooking practices. Any food conducive to outgrowth and toxin production can be associated with botulism. This can occur when food processing allows spore survival and the food is not subsequently heated before consumption, to eliminate any live cells. Almost any type of food that is not very acidic (pH above 4.6) can support growth and toxin production by C. botulinum. Salt concentration from 4% to 5% is needed for inhibition of its spores (especially regarding type E), with a 5% concentration completely inhibiting their growth. Salt concentrations slightly lower than those providing inhibition tend to extend spore outgrowth time at low temperatures. A variety of foods, such as canned corn, peppers, green beans, soups, beets, asparagus, mushrooms, ripe olives, spinach, tuna fish, chicken and chicken livers, liver pate, luncheon meats, ham, sausage, stuffed eggplant, lobster, and smoked and salted fish have been associated with botulinum toxin. Infant botulism: Of the various potential environmental sources, such as soil, cistern water, dust, and foods, honey is the one dietary reservoir of C. botulinum spores linked to infant botulism by both laboratory and epidemiologic studies. Honey should not be fed to infants under 12 months of age.

Answer 499

All people are believed to be susceptible to botulism

Answer 500

Although botulism can be diagnosed by clinical symptoms alone, differentiation from other diseases may be difficult. The most direct and effective way to confirm the clinical diagnosis of botulism in the laboratory is to demonstrate the presence of toxin in the serum or feces of the patient or in the food the patient consumed. Currently, the most sensitive and widely used method for detecting toxin is the mouse neutralization test. This test takes 48 hours. Culturing of specimens takes 5 to 7 days.

Answer 501

Since botulism is foodborne and results from ingestion of preformed C. botulinum toxin, determination of the source of an outbreak is based on detection and identification of toxin in the food involved. The most widely accepted method is the injection of extracts of the food into passively immunized mice (mouse neutralization test). The test takes 48 hours. This analysis is followed by culturing all suspect food in an enrichment medium, for detection and isolation of the causative organism

Answer 502

Enterococci are Gram-positive, catalasenegative, facultative anaerobes that normally are spherical and ovoid, are less than 2 µm in diameter, and occur in chains or pairs or singly. They are opportunistic pathogens and, in general, are able to survive harsh conditions. Virulence factors in enterococci include cytolysin/hemolysin, gelatinase, serine protease, adhesins, and enterococcal surface protein. Optimal growth temperature for enterococci is 35o C. They may grow at temperatures up to 45o C, and reports of minimum growth temperature have varied from 10o C to 20o C. They can grow in 6.5% NaCl broth and in broth with a relatively high pH of up to 9.6. Enterococci hydrolyze esculin in a medium containing 40% bile salts. These characteristics may be used for isolation and identification of the bacterium. At the same time, they present a challenge for control of pathogenic isolates.

Answer 503

Enterococci are also divided into five physiological groups, by most laboratories, based on acid formation in mannitol and sorbose broths and hydrolysis of arginine. The grouping information is very useful for medical personnel. Identification of enterococci to species level by For Consumers: A Snapshot Anyone can become infected with the Enterococcus bacterium, but the people most likely to suffer serious problems are those who already have other serious illnesses. In otherwise healthy people, it may cause diarrhea, cramps, nausea, vomiting, fever, and chills, starting 2 to 36 hours after they eat contaminated food. Enterococcus can be passed to people in different ways, and not much is yet known about how often it’s transmitted by food. But it is known that meat and milk that aren’t processed or cooked properly or that are handled in unsanitary ways are among the foods that can transmit it. A major concern about Enterococcus is that it has become resistant to some antibiotics that were used to treat it – that is, those antibiotics no longer kill it. You can help protect yourself from getting foodborne illness from this and other bacteria or viruses by following basic food‐safety tips; for example, by not using unpasteurized (“raw”) milk or certain cheeses and other food made from it, by thoroughly cooking meat or food that contains meat, and by washing your hands, kitchen equipment, and other surfaces before and after you handle food. conventional methods can take up to 10 days. However, identification of enterococci to group level can be done in 2 days, in most cases.

Answer 504

The toxin cytolysin is produced by some E. faecalis strains. It displays both hemolytic and bactericidal activities.

Answer 505

Enterococcus infection is notable largely as a hospital- or community-acquired illness; not much information is available regarding the foodborne illness. The organism is not on the list of Centers for Disease Control and Prevention (CDC) notifiable diseases or on the outbreak summary report. In general, Enterococcus poses a serious threat mainly to people who are debilitated by other, grave underlying conditions. The emergence and global spread of vancomycin-resistant and multi-drug resistant enterococci pose a major threat to human heath and have serious implications for health care. Research suggests that clinically relevant gentamicin-, glycopeptide-, and streptogramin-resistant enterococci can be transmitted to humans via consumption of food animals. Overall, however, the dearth of data on Enterococcus transmitted by food requires that the information in this Disease section of the Bad Bug Book be approached with the understanding that it is unknown how much of it applies to foodborne Enterococcus.

Answer 506

Mortality: Enterococcal infections are not a leading cause of death in the United States. However, the mortality rate for bacteremia associated with Enterococcus faecium may be as high as 50%. The mortality rate for endocarditis – a potential consequence of Enterococcus infection – is 15% to 20%.

Answer 507

Infective dose: An infective dose of at least 107 cells has been reported for Streptococcus D, the organism under which Enterococcus originally was classified.

Answer 508

Onset: Two to 36 hours after contaminated food is ingested.

Answer 509

Disease / complications: Enterococci, in general, can cause many different infections, such as endocarditis, bacteremia, urinary tract infections, intra-abdominal and pelvic infections, and nosocomial infections, and neonatal infections. Ampicillin, penicillin or vancomycin, ureidopenicillin, streptomycin, and gentamicin are used singly or in combination for treatment of various enterococcal infections.

Answer 510

Symptoms: Symptoms may include diarrhea, abdominal cramps, nausea, vomiting, fever, chills, dizziness. The infection may produce a clinical syndrome similar to staphylococcal intoxication (see chapter on Staphylococcus aureus).

Answer 511

Reports regarding frequency of enterococcal infections associated with foods in the U.S. alone or elsewhere are limited. However, it is reported that, in human clinical specimens, about 80% to 90% of enterococcal infections were caused by E. faecalis and 5% to 20% by E. faecium. Several enterococcal species less frequently isolated from humans include, for example, E. avium, E. casseliflavus, E. cecorum, E. dispar, E. durans, E. gallinarum, E. gilvus, E. hirae, E. mundtii, E. pallens, and E. raffinosus, which have been detected in clinical samples

Answer 512

Because enterococci can grow and survive in harsh environments, they are almost ubiquitous in nature. They can be found in animals, birds, insects, plants, soil, and water. They are commensal bacteria in human and animal gastrointestinal tracts, and less common in other parts, such as the genitourinary tracts, oral cavities, dental plaque, and skin. Some enterococci have been used as starters in cheese-making and in other fermented milk products. Examples of food sources have included sausage, evaporated milk, cheese, meat croquettes, meat pie, pudding, raw milk, and pasteurized milk. Entrance into the food chain is often due to underprocessing of food or unsanitary food preparation.

Answer 513

Culturing of stool samples, blood, and suspect food is recommended. Enterococcus spp. generally grow well on blood-based media. Usually, 5% sheep, horse, or other animal blood are added to the media. Molecular methods, such as polymerase chain reaction (PCR), also are available.

Answer 514

All people are susceptible. However, people with serious underlying conditions, children, and people 65 years and older, in nursing homes, are more vulnerable.

Answer 515

Suspect food is examined microbiologically by nonselective and selective medium techniques, which can take up to 7 days. Group specificities are determined by Lancefield group-specific antisera. Both biochemical and DNA techniques are used for identification.

Answer 516

Toxoplasma gondii are obligate intracellular parasites that belong to the family Sarcocystidae. T. gondii is ubiquitous and is found around the world. In some locations, up to 95% of the local human population is or has been infected with T. gondii. These locales are often in hot, humid climates and lower altitudes. T. gondii has a complex life cycle that includes a separate asexual and sexual cycle and involves a definitive and an intermediate host. The asexual cycle occurs in a wide range of intermediate hosts that include warmblooded vertebrates, such as birds, carnivores, rodents, pigs, primates, and humans. The sexual cycle occurs exclusively in the definitive host, the wild and domestic feline. Domesticated cats are the principal definitive hosts and shed infectious oocysts in their feces. Oocysts are resistant to the effects of many environmental factors and can persist for several years, under certain conditions. Other important stages of the life cycle of T. gondii include bradyzoites and tachyzoites. Oocysts must undergo sporulation, forming bradyzoites that are released by proteolytic enzymes in the host. This form then invades intestinal epithelial cells and is transformed into tachyzoites, which are capable of dissemination through blood or lymph. It is this form that can also transit the placenta. The disease this pathogen produces is toxoplasmosis.

Answer 517

This parasite can withstand environmental stresses. Oocysts can remain infective for approximately 150 to 400 days in water at temperatures ranging from 4 to 37ºC. Similar observations have been made of oocysts in soil. Desiccation (drying) can also be a factor; oocyst infectivity persists longer in a moist environment than in a dry region. Tissue cysts containing T. gondii are likewise affected by temperature. Exposure to temperatures at or below -13o C, for at least 24 h, will usually kill cysts. Meats should be cooked at selected temperatures to ensure that any T. gondii cysts are killed. The USDA recommends that meats be cooked at 68.2ºC (155ºF) or higher, with a 3-minute rest. Ground meat and wild game meats should be heated at 71.1ºC (160ºF) or higher, whereas poultry should be cooked at 73.9ºC (165ºF) or higher. It appears that microwave heating of any of the above meats is not reliable for killing all of the T. gondii cysts. For further information about preventing T. gondii infections from foods, see the Jones and Dubey reference below.

Answer 518

Mortality: T. gondii is a ubiquitous parasite that can have significant morbidity and mortality in congenitally infected fetuses and in immunocompromised individuals. The disease is usually self-limiting, but can be fatal to a fetus via a mother who ingested the parasite, usually after becoming pregnant, leading to miscarriage or stillbirth. If left untreated, toxoplasmosis can impose a high mortality rate.

Answer 519

Infective dose: Not known

Answer 520

Onset: Five to 23 days after ingestion from contaminated food, water, and fingers.

Answer 521

Illness / complications: Women who become infected during pregnancy typically are asymptomatic, although the parasite (tachyzoites) can cross the placenta. In infected pregnant women, the fate of the fetus falls into three possibilities: miscarriage or stillbirth; head deformities; or brain or eye damage. Some of the clinical manifestations of T. gondii infections in the unborn include hydrocephalus or microcephaly, intracranial calcification, and chorioretinitis. A newborn may become infected at birth with T. gondii, but not show any apparent symptoms of infection. However, latent infections in these individuals may cause loss of vision, when they are adults (ocular toxoplasmosis); seizures; or mental disabilities. In addition, immunocompromised individuals may develop pneumonitis, retinochoroiditis, brain lesions, and central nervous system diseases. Sulfa compounds, specifically sulphadiazine and pyrimethamine, are the chemotherapeutics of choice for treating toxoplasmosis. These drugs are usually well tolerated by infected individuals and are most effective when administered during the acute stage of infection (active multiplication of the parasite). Although treatment with sulfonamides will limit tissue cyst growth, they appear to have little effect on subclinical infections and usually will not eradicate infection.

Answer 522

In acute toxoplasmosis, sore lymph nodes and muscle pains develop in 10-20 % of patients and can last for several weeks, after which symptoms no longer are exhibited. Symptoms of ocular toxoplasmosis are blurred or reduced vision, tearing of, or redness in, the eye; pain; and sensitivity to light. In healthy individuals, toxoplasmosis usually is asymptomatic. In some cases, flu-like symptoms may appear, such as swollen lymph glands, fever, headache, and muscle aches. Death is rare in acute cases. In immunocompromised individuals, such as patients with organ transplants, AIDS, or cancer, or who are taking immunosuppressive medications, toxoplasmic encephalitis is a common clinical manifestation that can be fatal. Additional symptoms include confusion, nausea, poor coordination, and seizures. Several published reports (see Torrey et al., below) suggest a link between prenatal infection with toxoplasmosis and the potential for schizophrenia later in life. Individuals who progress to chronic infections may develop cysts in various muscle tissues, including brain, heart, and skeletal tissues.

Answer 523

Duration: Infected, but otherwise healthy, individuals often display no symptoms; the host’s immune system usually keeps the parasite in check and prevents it from causing illness. If illness does occur, mild flu-like symptoms (acute phase) usually last for several weeks, but can fade in a few days to months, then disappear. However, the T. gondii parasite can remain in the host as tissue cysts (bradyzoites), but in this latent state are inactive. Reactivation of bradyzoites can occur under certain circumstances, such as when an infected person becomes immunosuppressed by other diseases or medication; under these conditions, toxoplasmosis (chronic) can develop.

Answer 524

Route of entry: The primary routes of entry are (1) consumption of undercooked or raw, parasite-encysted (with bradyzoites) meats (e.g. lamb; goat; pork; poultry; game meats, such as venison; horse), (2) ingestion of contaminated water or soil with cat feces or through the fecal-oral route, via fomites (e.g., knives, utensils, cutting boards), fingers, or other foods that had contact with raw, contaminated meat, (3) congenital transmission, in which a pregnant mother passes the parasite to the fetus via transplacental transmission, and (4) possibly through raw oysters, clams, and mussels

Answer 525

Pathway: Toxoplasma gondii has a very complex life cycle, in which cats (or Felids) are the primary or “definitive” host; the animal in which parasitic sexual reproduction occurs to produce infective parasitic life forms. Cats become infected with T. gondii by eating sporulated (mature) oocysts from contaminated environmental sources or T. gondiiencysted tissue sources (such as rodents). Large numbers of immature oocysts shed by infected cats require several days in the environment to sporulate and become infective. Oocysts are very resistant to most environmental conditions and can survive for more than a year outside of the definitive host. Intermediate hosts, i.e. humans, birds, pigs, sheep, goats, and cattle, become infected after eating food or drinking from contaminated water sources. In the cat, the mature oocyst is degraded to release infectious organisms into the intestine. Some will invade and replicate within intestinal epithelial cells; others will penetrate through the intestinal wall and replicate throughout the body. These fast-replicated forms are called tachyzoites. Tachyzoites that develop within the intestinal epithelium will differentiate into sexual forms, fertilize, and develop into immature oocyts that are then shed into the environment. Infected cats will begin shedding within 3 to 10 days, and this will last for 10 to 14 days. Tachyzoites that eventually localize in tissue other than the intestinal epithelium will transform (because of an immune response by the cat) into bradyzoites contained within tissue cysts. Infection of the intestinal epithelium does not occur in the intermediate host. As in the cat, parasites will penetrate the intestinal epithelium and migrate throughout the host as tachyzoites. Tissue infection and the host immune response will cause the formation of bradyzoite-filled tissue cysts. These will remain viable throughout the life of the host, and these encysted bradyzoites are infectious to cats and other intermediate hosts. In acute infections in humans, intestinal epithelial cells are the primary site of invasion, with potential subsequent spread to other sites, such as the brain, heart, and skeletal muscle

Answer 526

T. gondii is considered a formidable foodborne pathogen in the United States. In a 2011 report (Scallan et al., 2011) by the Centers for Disease Control and Prevention (CDC), T. gondii is listed as a prominent etiological agent that causes an estimated 86,686 foodborne- related illnesses in the U.S. annually. Of note: this pathogen causes approximately 4,428 hospitalizations per year and is responsible for nearly 327 deaths per year, ranked second, behind Salmonella. T. gondii infections can also lead to acute ocular disease; nearly 4,800 cases per yearWorldwide, the number of people infected is estimated to be more than 30%. However, variations occur from country to country. In France and Germany, most of the population may be infected by this parasite, whereas in some countries, such as South Korea, it is quite rare for anyone to be infected. In the U.S., more than 60 million people may be infected; approximately 22.5% of the population. T. gondii infections are found in 500 to 5,000 newborns in the U.S.; not a surprising number, given that approximately 89% of women of childbearing age may have been exposed to this parasite and can pass it to their newborn children, particularly if the woman has a primary infection during pregnancy.

Answer 527

More than 60 million men, women, and children in the U.S. are estimated to carry T. gondii; most are asymptomatic. However, T. gondii infections in pregnant women pose a serious health concern to the fetus. When a woman becomes infected with T. gondii, either at conception or during pregnancy, the parasite can cross the placenta and infect the fetus. These neonates can either be asymptomatic, or the infection can lead to a range of disabilities; e.g., hydrocephalus, developmental delay, or death. Pregnant women and immunosuppressed people should avoid consuming raw or undercooked meat, unpasteurized goat’s milk, and untreated water. Toxoplasmosis is not transmitted via person-to-person. The notable exception is the transplacental transfer of the parasite of pregnant women to their fetuses, via congenital transmission; blood transfusion; or organ transplantation.

Answer 528

The primary source of the T. gondii parasite is feces from domestic and wild cats (Felidae). Cats are the only animal that sheds oocysts in its feces and contaminates the environment with them. Transmission occurs from environmental contact, through intermediate hosts, such as birds, rodents, pigs, sheep, and cattle; e.g., feeding on oocyst-contaminated feed, water, or soil. The primary mode of foodborne transmission is ingestion of undercooked or raw meats (e.g., pork, lamb, or wild game) containing tissue cysts from a chronically infected host or by the consumption of food (fruits and vegetables) contaminated with cat feces or drinking of water containing sporulated oocysts. In addition, placing hands to mouth after handling cats, their litter box or feces, or anything that may have come in contact with their feces is a source of transmission. Any material that comes in contact with parasite-laced feces is at risk of being contaminated.

Answer 529

Diagnosis of T. gondii typically is performed by serological testing that targets the immunoglobulin IgG and IgM, available in different formats: enzyme-linked immunosorbent assays (ELISA), immunoblots, dye test, and indirect fluorescent antibody test. These tests typically detect the host’s antibodies generated within several weeks of infection and, in some cases, estimate the length of infection, as this is an important factor regarding pregnant women. In the latter, the target immunoglobulin is IgM. In some cases, direct observation of the parasite in stained tissue samples, cerebrospinal fluid (CSF), or other biopsy material can be performed, although it is very time-consuming and, in some cases, difficult to extract a specimen. Molecular techniques are used for detecting T. gondii DNA in the amniotic fluid in cases of congenital transmission (mother-to-child transmission). Ocular toxoplasmosis diagnosis usually is based on symptoms, appearance of lesions in the eye, serologic testing, and observation of the infection’s course.

Answer 530

Infection is usually asymptomatic, with no obvious symptoms in immunocompetent and otherwise healthy individuals. When symptoms do occur, such as fatigue, flu-like symptoms, muscle aches and pains, and swollen glands, they are usually mild and short-lived. Those most affected are individuals with an impaired immune system and pregnant women. In such cases, illness may be life-threatening, particularly to a developing fetus.

Answer 531

Analysis of foods usually is achieved by serology, although tissue cysts may be observed in stained biopsy specimens from infected meats

Answer 532

Parasites like T. gondii usually will enter the food chain via three scenarios. These include direct contamination of food ingredients or farm-fresh produce; through contaminated water sources used in irrigation, washing, or processing of foods; and through direct human transfer by food handlers or processors or in the home. Epidemiologic evidence suggests that most outbreaks of illness in humans occur through consumption of uncooked or undercooked meat containing viable tissue cysts. Documented outbreaks have been described in which the ingestion of infected meat, such as uncooked pork, was the major source of infection. However, large-scale outbreaks linked to municipal water sources and consumption of unfiltered water have altered such thinking. This includes outbreaks in Canada, in 1994, attributed to a contaminated municipal water supply, and in several regions of Brazil.

Answer 533

Giardia lamblia (also referred to as Giardia intestinalis or Giardia duodenalis) is a single-celled, enteric protozoan parasite that moves with the aid of five flagella, which also assist with attachment to intestinal epithelium. Giardia is infective in the cyst stage, when it is also extremely resistant to environmental stressors, including cold temperatures and chemicals. As noted in the Sources section, below, chlorine concentrations typically used for post-harvest rinsing do not kill the cysts, which are hard to wash off of types of produce that don’t have smooth surfaces. The Sources section also notes that infected food handlers often are implicated in outbreaks

Answer 534

Reservoirs for Giardia include the intestine of infected humans or other animals (e.g., cats, dogs, cattle, deer, and beavers). Organisms that appear identical to those that cause human illness have been isolated from domestic animals (dogs and cats) and wild animals (beavers, muskrats, bears). A related, but morphologically distinct, organism infects rodents, although rodents may be infected with human isolates in the laboratory

Answer 535

Routes of transmission include contaminated water, food, and person-to-person contact with someone who is ill with giardiasis, especially when adequate fecal-oral hygiene is lacking.

Answer 536

Mortality: Giardiasis generally is not associated with mortality in otherwise healthy people

Answer 537

Infective dose: Ingestion of one or more cysts may cause disease

Answer 538

Onset: Usually 1 to 2 weeks after ingestion of a cyst(s)

Answer 539

Illness / complications: Giardiasis is self-limiting in most people. However, some (less than 4%) remain symptomatic for more than 2 weeks, possibly leading to a malabsorption syndrome and severe weight loss. Severe dehydration due to loss of fluids is a major concern, especially in young children. Malabsorption of vitamins, protein, and iron all are possible with chronic infections, and it has been suggested that, in children, this can result in stunted growth and development. Chronicity of infection is correlated with an absence of secretory IgA in the intestinal lumen. About 40% of those who are diagnosed with giardiasis develop disaccharide intolerance during infection and up to six months after resolution of infection. Lactose (i.e., milk sugar) intolerance is most frequently observed due to intestinal epithelial cell brush border damage by the Giardia trophozoites. Several strains of G. lamblia have been isolated and described through analysis of their proteins and DNA; type of strain, however, is not consistently associated with disease severity. Different people infected with the same strain have various degrees of symptoms, and the symptoms of an individual may vary during the course of the disease. Flagyl (metronidazole) is normally quite effective in terminating infections and is the first-line choice. However, treatment lasts for up to 7 days, and substantial side effects are not uncommon. Tinidazole (brand names: Tindamax and Fasigyn) is another effective drug against giardiasis, as it inhibits DNA synthesis. In some patients, it is better tolerated than is flagyl, due to fewer side effects and because treatment is given in a single dose. Chronic cases of giardiasis are frequently refractory to drug treatment. In some immune-deficient individuals, giardiasis may contribute to a shortening of the life span. Prophylactic treatment usually is not considered.

Answer 540

Symptoms: Infections sometimes are asymptomatic. When symptoms are present, they generally consist of especially malodorous diarrhea, malaise, abdominal cramps, flatulence, and weight loss.

Answer 541

Duration: Generally 2 to 6 weeks, unless the illness becomes chronic, in which case it may last for months or years and may become difficult to treat.

Answer 542

Pathway: The mechanism by which Giardia causes disease is largely unknown. Investigators have been unable to confirm reports that the organism produces a toxin. Infrequently, it has been found in the duodenal cells of its hosts, but this probably is not responsible for the symptoms of the disease. The organism has been found inside host duodenum cells, but this is an infrequent occurrence that is, more than likely, not responsible for disease symptoms. Mechanical obstruction of the absorptive surface of the intestine has been proposed as a possible pathogenic mechanism.

Answer 543

In 2002, giardiasis became a nationally notifiable disease. The overall incidence of infection in the United States is estimated to be 2% of the population. Asymptomatic infections are largely undocumented, yet are known to occur. Giardiasis surveillance in the U.S. from 1998-2005 showed a range of 19,708 to 24,226 reported cases annually, which were distributed throughout nearly all U.S. jurisdictions. According to a more recent estimate by the Centers for Disease Control and Prevention (CDC), 76,840 cases of giardiasis (most of them from contaminated water, but some from contaminated food) occur each year in the U.S., if under-reporting and under-diagnosis are taken into account. Giardiasis is more prevalent among children than among adults, possibly because many individuals seem to have a lasting immunity after infection. However, chronic, symptomatic giardiasis is more common in adults than in children. Some seasonality of infections is noted, with more cases observed in the U.S. during summer months, and might reflect increased outdoor recreation and exposure to contaminated water (e.g. lakes, swimming pools).

Answer 544

Infection typically results after ingestion of soil, water, or food contaminated with feces of infected humans or animals. Giardiasis is most frequently associated with consumption of contaminated water. However, foodborne outbreaks that were associated with vegetables and lettuce-based salads were reported in 2005 and 2007 and included 65 cases. Infected food handlers are very often implicated in giardiasis outbreaks, suggesting the ease of foodborne transmission. For example, an infected food handler preparing raw vegetables that were later served in an office cafeteria was the probable cause of nearly 30 cases. Giardia cysts are not killed by chlorine levels typically used to rinse produce post-harvest, and are especially difficult to wash off of complex food surfaces like leafy greens and berries.

Answer 545

Giardia lamblia is frequently diagnosed by visualizing the organism, either the trophozoite (active reproducing form), or the cyst (the resting stage that is resistant to adverse environmental conditions) in stained preparations or unstained wet mounts of liquid stool, with the aid of a microscope. Giardia cysts are 10 to 20 µm in length and are easily distinguished from much smaller Cryptosporidium oocysts. Commercial direct fluorescence antibody kits are available to stain the organism, with reported sensitivities and specificities reaching 100%. Organisms may be concentrated by sedimentation or flotation; however, these procedures reduce the number of recognizable organisms in the sample. Therefore, a single stool specimen is usually insufficient for diagnosis. Enzyme linked immunosorbant assays (ELISAs) that detect excretory secretory products of the organism, as well as cyst wall proteins, are also available. In addition, nonenzymatic immunoassays exist. When compared with microscopy, such tests have sensitivities and specificities ranging from 85% to 100%.

Answer 546

Giardiasis occurs throughout the population, although the prevalence is higher in children than in adults; especially in children 2 to 5 years old, in daycare, where a child-to-child passage rate as high as 50% has been noted. Studies have estimated a 15% prevalence rate in U.S. children and prevalence rate up to 30% in children from younger than 10 years old in developing countries. Adults who recreate outdoors (e.g. hunters, backpackers) and may ingest contaminated water are also particularly vulnerable, due to increased exposure to Giardia in the environment. Other high-risk groups include individuals with certain antibody deficiencies and those with decreased gastric acidity.

Answer 547

Food is analyzed by thorough surface cleaning of the suspected food and sedimentation of the organisms by centrifugation of wash material. A fluorescent antibody staining technique is then used to identify Giardia cysts.

Answer 548

Entamoeba are single-celled protozoan parasites capable of infecting a wide variety of hosts. All species are characterized by a life cycle that alternates between two distinct stages. The cyst stage is the infectious, but nonreplicative, form of the parasite that will develop in the intestine of the host into active trophozoites capable of replicating. Trophozoites multiply by binary fission and can also produce cysts. A rigid wall protects the cysts, which may remain viable in a moist environment for weeks to months. The cysts can survive freezing and are not always killed by chlorination; however, they do not survive desiccation or temperatures above 50°C.

Answer 549

Entamoeba histolytica causes amebiasis (or amoebiasis).

Answer 550

Mortality: According to the World Health Organization (WHO), amebiasis is the third leading cause of death due to parasitic disease globally. The WHO estimates that approximately 50 million people worldwide suffer from invasive amebic infection each year, resulting in 40,000 to 100,000 deaths annually. The global case fatality rate is reported to be 2% in adults and 26% in children. In the United States, cases of Entamoeba histolytica infection are not common, and mortality is likely to be rare.

Answer 551

Infective dose: The infective dose in humans is reported to be fewer than 10 cysts

Answer 552

Onset: Invasive intestinal disease may occur days to years after initial infection; however, the condition generally will be manifested within 2 to 4 weeks after first exposure to this parasite

Answer 553

Illness / complications: About 10% of E. histolytica infections result in clinical symptoms. Intestinal amebiasis manifests mostly as asymptomatic colonization, in which the parasite lives within the digestive system, but does not penetrate intestinal cells. Most infected people eliminate the parasite from the gut within 12 months. In some people, the disease will progress into amoebic colitis after invasion of the intestinal mucosa. On rare occasions (2% to 20% of symptomatic infections), the disease will spread extraintestinally, mostly to the liver, causing amebic liver abscess, or to the brain, spleen, lungs, or genitourinary tract. The disseminated forms of the disease are associated with higher mortality rates. Given the small, but substantial, risk of invasive disease and the potential to transmit infection to others, the WHO recommends treating all cases of proven E. histolytica, regardless of symptoms. Different regimens are available, depending on the disease’s stage of progression

Answer 554

Symptoms: When symptoms do occur, they usually begin within months after amoebas first enter the body. The severity of the symptoms associated with intestinal amebiasis ranges from mild diarrhea to a severe, dysentery-like illness with mucus and blood in the diarrhea and abdominal distention. A chronic infection often leads to weight loss and fatigue. Amoebic liver abscess is characterized by fever, pain in the upper right abdomen, nausea, unintentional weight loss, and liver tenderness.

Answer 555

Duration: E. histolytica may reside in the intestine for years without causing symptoms. Invasion of the intestine will cause symptoms that can last from a few days to several weeks, in the absence of treatment. Treatment may be necessary to prevent recurrent attacks.

Answer 556

Route of entry: The primary mode of infection is the fecal-oral route. Both cysts and trophozoites are passed in the feces, but trophozoites do not survive gastric acid.

Answer 557

Pathway: Epidemiologic observations suggest that genetic differences within the host or the parasite itself may determine the outcome of clinical infection; however, what triggers the invasive phenotype in E. histolytica has not been elucidated. To become invasive, trophozoites secrete toxins that break down the intestinal protective mucus layer, destroy the colonic intestinal barrier, and counter the defense mechanisms of the host.

Answer 558

The global prevalence of infection was estimated, in 1986, to be 10% of the world’s population. However, this estimate was made prior to the separation of E. histolytica and non-virulent E. dispar, which seems to be more prevalent worldwide. Most infections, morbidity, and mortality occur in South and Central America, Africa, and Asia (Far East and Indian subcontinent). In the U.S., the combined prevalence of E. histolytica / E. dispar is estimated to be 4%.

Answer 559

As noted in the Organism section, above, cysts have several characteristics conducive to survival in the environment. Once they are excreted into the environment, fecal contamination can result in E. histolytica cysts in drinking water, foods, hands, surfaces, and other objects. Water is the most common source of contamination. Raw foods also may be a source of infection, after contamination by a food handler or by irrigation / rinse water, especially if the food is maintained in a moist environment. Humans are the only hosts for E. histolytica. People who have chronic amebiasis or are asymptomatic can excrete several million cysts per day. During the acute phase of the illness, people tend to shed more trophozoites than cysts.

Answer 560

Clinically, it is desirable to distinguish pathogenic E. histolytica from non-pathogenic E. dispar and E. moshkovskii. Light microscopic examination of fecal specimens for cysts and trophozoites does not allow for such differentiation, unless red blood cells are identified inside trophozoites, a strong indication of invasive amebiasis. Biopsy, serology, antigen detection and molecular assays can be used for the specific diagnosis of E. histolytica; however, some of these technologies are less accessible to areas of the world where amebiasis is endemic.

Answer 561

Infection with E. histolytica is endemic in many parts of the world where sanitation is poor. Children are among the most affected. In industrialized countries, this infection is most common among immigrants from endemic areas, travelers to developing nations, and in institutionalized populations. Males are more prone to develop amebic liver abscess than are females.

Answer 562

The FDA Bacteriological Analytical Manual describes use of successive rinses and sedimentation steps in detergent solutions to recover protozoa from vegetables (Chapter 19; Section V; see Resources section). However, the procedure is not very sensitive, as less than 1% of the initial parasitic population may be recovered. In addition, the cysts may be too damaged for efficient microscopic diagnosis.

Answer 563

In developed countries, amebic infections tend to cluster in households, in institutions housing people with developmental delayed, or among sexual partners. Large outbreaks remain rare. The largest outbreak in the U.S. occurred during the 1933 World’s Fair, in Chicago, and involved sewage contamination of drinking water, leading to about 1,400 cases and 98 deaths. More recently, an outbreak of amebiasis was reported in the Republic of Georgia, with 177 cases recorded between May 26 and September 3, 1998, including 71 cases of intestinal amebiasis and 106 probable cases of liver abscess. Water contamination was suspected, but not confirmed.

Answer 564

Cryptosporidium parvum is an obligate, intracellular protozoan parasite first recognized as a human pathogen in 1976. The organism is transmitted via oocysts (i.e., the infectious stage in the organism’s life cycle) and shed in feces. Among C. parvum’s notable characteristics is the oocyst’s pronounced resistance to most chemical disinfectants, including chlorine, although it is susceptible to drying and the ultraviolet portion of sunlight. Even after a 90-minute contact time with standard concentrations of chlorinecontaining compounds, the reduction in levels of viable organisms is barely appreciable. Other notable characteristics are C. parvum’s particular risk to, and often poor or fatal outcome among, immunocompromised people, including those with HIV/AIDS, and the amount of fluid loss the infection can cause through diarrhea.

Answer 565

Outside of humans, C. parvum has also been isolated from cattle, sheep, and goats.

Answer 566

A number of other Cryptosporidium species (C. canis, C. felis, C. meleagridis, and C. muris) can infect humans; however, such infections are rare and usually are detected and/or isolated from immunocompromised persons or children. C. hominis resembles C. parvum in appearance and life cycle characteristics, but infects only humans.

Answer 567

Mortality: Death from cryptosporidiosis is very rare. However, immunocompromised people have increased morbidity and mortality associated with cryptosporidiosis.

Answer 568

Infective dose: As few as 10 to 100 oocysts. Oocysts are excreted in a fully infective form

Answer 569

Onset: Onset of illness follows an incubation period of 7 to 10 days.

Answer 570

Illness / complications: Intestinal cryptosporidiosis is self-limiting in most otherwise healthy people. Some infected people are asymptomatic; in others, symptoms may range from mild to profuse diarrhea, with passage of 3 to 6 liters of watery stool per day. In some outbreaks involving day-care centers, diarrhea has lasted from a week to a month. Dehydration is a major concern, particularly for pregnant women and young children and immunocompromised people in whom the infection becomes chronic. Immune status has a strong influence on the severity and duration of symptoms and illness. In people with AIDS and in other immunocompromised people, C. parvum infections are notorious for their severe symptoms and outcomes, including chronic and/or copious diarrhea and dehydration, and may lead to death. This population may have the disease for life, and the major fluid loss they experience may contribute to their death. Among people with concurrent HIV infection, the CD4+ count can help predict the severity of cryptosporidiosis, according to the Centers for Disease Control and Prevention (CDC). A level less than 180 cells/mm3 appears to be a trigger point; above that level, cryptosporidiosis usually self-resolves. Extraintestinal forms of cryptosporidiosis exist, with biliary cryptosporidiosis being the most common type. Other forms involve the lungs and middle ear. People with AIDS are more susceptible than are others to extraintestinal cryptosporidiosis

Answer 571

Preventing dehydration is critical, given the large amount of fluid loss typical of this illness. To date, there is no known drug that is effective as a treatment for cryptosporidiosis. Some relief from diarrhea has been noted with administration of spiramycin given near the onset of infection. The FDA has approved nitazoxanide for the treatment of diarrhea in immunocompetent people. A limited number of studies also have reported value in administering azithromycin, nitazoxanide, and paromomycin to Cryptosporidium-infected people with AIDS.

Answer 572

Symptoms: The most common symptom is profuse, watery diarrhea, along with nausea, vomiting, and cramping. Fever can also accompany these symptoms. As noted, the severity and duration of diarrhea usually is increased in immunodeficient people, in whom the diarrhea may become chronic and who are more susceptible to extraintestinal symptoms

Answer 573

Duration: Two to 14 days in immunocompetent people; often prolonged or chronic in immunocompromised people. It is important to note that excretion of oocysts can last for up to several months after diarrhea has resolved. In addition, high percentages of people without overt symptoms have been found to shed oocysts. This is of major concern, since people who appear healthy may be transmitting the illness through inadequate hygiene or even through use of recreational-water facilities – especially since one bowel movement may result in the release of up to 109 oocysts.

Answer 574

Pathway: Cryptosporidiosis is acquired through ingestion of the oocyst, the organism’s infective stage. The oocyst is 4 to 6 µm in diameter, about half the size of a red blood cell. After being ingested, C. parvum oocysts attach themselves to gastrointestinal epithelial cells, where reproduction takes place. The zygotes become one of two types of sporulated oocysts: one with a thin wall, which excysts in the gastrointestinal tract and can cause continued infection of the host, and the other with a thick wall, which is shed in the feces and infects other hosts. The mechanism by which the organism causes illness – e.g., whether or not a toxin is present – is not fully understood. The mechanisms underlying extraintestinal cryptosporidiosis also are unclear; however, it is believed that the intestines are the originating site.

Answer 575

Direct human surveys indicate a prevalence of about 2% of the population in North America. Serological surveys indicate that 80% of the United States population has had cryptosporidiosis at some point in life. Data from the Centers for Disease Control and Prevention (CDC), collected from 2004 to 2007, indicate an increase in cryptosporidiosis across the U.S. Estimates by the CDC, updated in 2011, place the number of annual illnesses due to cryptosporidiosis to be in the tens of thousands, much higher than the 7,500 that are laboratory-confirmed. The extent of illness associated with reactive sera is not known.

Answer 576

Food Cryptosporidium spp. contamination could occur, theoretically, with any food touched by an infected food handler or from contact with an environmental source of oocysts (e.g. animal manure). In addition to various foods, such as fresh produce, juices and milk may be contaminated. Water Large outbreaks also have been associated with contaminated water supplies. Irrigation water might be a potential source of food contamination, even if the water is chlorine-treated. Recreational water, such as swimming-pool water, continues to be a major vehicle for transmission of Cryptosporidium oocysts. The oocysts are notoriously hard to inactivate with disinfectants, like chlorine, and can remain infectious for up to a year in both freshwater and seawater. Treated human wastewater can contain oocysts and could contaminate recreational waters, as can direct contamination by a person with poor hygienic practices.

Answer 577

Because Cryptosporidium oocysts are shed in the infected person’s feces, stool samples are collected and analyzed with a combination of light microscopy and acid-fast staining. Care needs to be taken, as oocysts can be confused with yeast cells or mistaken for Cyclospora cysts or even completely overlooked due to their small size. Commercially available kits use highly specific fluorescent antibodies to stain and positively identify the organisms isolated from feces as Cryptosporidium spp. Diagnosis also has been made by staining the trophozoites in intestinal and biopsy specimens. Pulmonary and tracheal cryptosporidiosis is diagnosed by biopsy and staining. Molecular-based tests (i.e., PCR) have also been developed and successfully implemented in some laboratories.

Answer 578

Cryptosporidiosis can affect anyone; however, as noted, the most severe symptoms occur in immunocompromised people. Those with AIDS seem to be highly susceptible, with the possibility of developing a chronic state of illness and an extraintestinal manifestation of disease. People at increased risk of cryptosporidiosis include those who share a household with an infected person, health-care workers, day-care personnel, users of recreational waters, and those traveling to endemic areas. Child day-care centers serve a large, susceptible population and frequently report outbreaks. Incidence of disease is higher in child day-care centers that serve food, compared with those that do not.

Answer 579

FDA’s Bacteriological Analytical Manual includes a method for examination of fresh produce and liquids (milk, juice, water, cider) for Cryptosporidium spp.

Answer 580

See CDC’s cryptosporidiosis surveillance, U.S., 2006-2008. A number of recognized foodborne outbreaks of cryptosporidiosis occurred in the U.S. in the 1990s. Some of the most notable include:  Minnesota (chicken salad)  Maine and New York (apple cider)  Washington (unknown food)  In October 2003, locally produced (Northeast Ohio) ozonated apple cider was linked to an outbreak of cryptosporidiosis.

Answer 581

Cyclospora are single-celled protozoan parasites and are classified as obligate intracellular coccidian parasites in the phylum Apicomplexa. Species of Cyclospora develop in the gastrointestinal tract of vertebrates throughout their entire live cycle. Immature (unsporulated) oocysts are then shed in feces. Though there are many species of Cyclospora, only Cyclospora cayetanensis has been observed to cause illness in humans

Answer 582

Infective dose: The minimum infective dose of oocysts, the oocyst sporulation rate, and their survival under different environmental conditions are unknown.

Answer 583

Onset: The onset of illness from infection with Cyclospora cayetanensis is usually 7 to 10 days from the time of ingestion.

Answer 584

Disease / complications: This parasite can cause protracted diarrheal illness in both immunocompetent and immunocompromised humans. Infection with Cyclospora oocysts and its accompanying illness is associated with eating fresh foods contaminated with feces. Immature Cyclospora oocysts that are shed in feces require a period of time, usually 1 to 2 weeks, outside the body (exposed to the environment) to mature and become infective. Cyclosporiasis, the illness caused by infection with Cyclospora cayetanensis, is characterized by prolonged, watery diarrhea, and intestinal distress

Answer 585

Symptoms: Symptoms typically include watery diarrhea, with frequent, sometimes explosive bowel movements. Other common symptoms include loss of appetite, weight loss, abdominal cramping and bloating, nausea, and fatigue. In some instances, more severe, flu-like symptoms (headache, vomiting, fever, and body aches) may be observed, while in others no overt symptoms are observed.

Answer 586

Duration: If left untreated, symptoms may persist for days to months. Relapses are possible

Answer 587

Pathway: Cyclospora cayetanensis infects cells that line the small intestine.

Answer 588

Cases of cyclosporiasis are exceedingly rare. Though several large outbreaks of food-associated illness have been documented in the late 1990s and early 2000s, sporadic individual cases and small clusters of illness rarely exceed 100 to 200 cases, per year. Strong evidence suggests that Cyclospora infection is seasonal. For example, epidemiologic studies indicated that, in Peru, the season was from December to July; in the U.S., May to July; and in Nepal, May to August.

Answer 589

Foods implicated in outbreaks of cyclosporiasis include imported fresh produce, such as raspberries, basil, and several varieties of lettuce.

Answer 590

Identification of this parasite is made through symptoms and through microscopic examination of stool specimens. Shape and size characteristics of immature (unsporulated) oocysts present in the stool help to confirm a Cyclospora infection. Cyclospora cayetanensis oocysts are perfectly round and 8 to 12 micrometers in diameter. In addition, when viewed by ultraviolet fluorescence microscopy, Cyclospora oocysts have the appearance of a pale-blue halo.

Answer 591

People of all ages are susceptible to infection with Cyclospora cayetanensis. Those who live in tropical and sub-tropical regions of the world are at greater risk. Though not fully understood, disease transmission and illness appear to be seasonal and have frequently been associated with the rainy season in those affected areas. People who travel to these areas are at risk.

Answer 592

Because of its size and the inability to culture Cyclospora cayetanensis in the laboratory, it is extremely difficult to isolate and detect this pathogen from foods, since the levels of contamination are usually low. Currently food rinses are analyzed by microscopic examination and by molecular biological methods, such as PCR. Key points for laboratory analysis are included in:  FDA method (eBAM 19a): Cyclospora and Cryptosporidium (2004) Detection of Cyclospora and Cryptosporidium from Fresh Produce: Isolation and Identification by Polymerase Chain Reaction (PCR) and Microscopic Analysis.  FDA Laboratory Information Bulletin 4044 (1996).

Answer 593

Trichinella spp. are parasitic roundworms (nematodes). The larvae of these worms, which reside in animal skeletal muscle, infect other animals or humans that consume them. Among several Trichinella species and genotypes, Trichinella spiralis found in domestic and wild pigs causes the most human illness worldwide. Other Trichinella species generally found in animals other than domestic pigs, particularly in wild game, also cause human illness. These include T. murrelli, T. nativa, T. pseudospiralis, and Trichella genotype T6 in North America

Answer 594

First-stage worm larvae, about 1 mm long, may lie dormant for years in the host’s skeletal muscle, waiting to be consumed by a new animal or human host. Upon ingestion by a new host, the larvae activate and invade the epithelium of the small intestine. After four molts over 1 to 2 days, male and female worms become sexually mature and find each other in the small intestine to mate. About 5 days after they were consumed as firststage larvae, fertilized adult females begin shedding newborn first-stage larvae in the host’s intestine. Each female releases thousands of newborn larvae that leave the intestine and migrate throughout the host’s body via the lymph and blood circulatory systems. The migrating larvae can invade most host tissues, including heart, brain, eye, lung, and liver; however, they survive only in skeletal muscle, where they settle and become infective to the next host

Answer 595

Trichinellosis, or trichinosis, is the name of the disease caused by Trichinella larvae consumed in undercooked meat.

Answer 596

Mortality: Mortality is rare; roughly 0.2 percent of clinical cases worldwide result in death

Answer 597

Infective dose: The ingestion of two viable larvae (male and female) that successfully mature and mate can result in infection with thousands of newborn larvae; however, ingestion of several larvae are normally needed to enable successful reproduction and noticeable symptoms. A statistical analysis of disease outbreak data estimated that ingestion of 5 larvae resulted in a mean 1% chance of observable disease symptoms; ingestion of 10 larvae resulted in a 7.5% chance; and ingestion of 100 larvae resulted in a 45% chance.

Answer 598

Onset: The acute symptoms of trichinellosis, which correspond with the migration of newborn larvae, typically begin 1 to 4 weeks following the consumption of contaminated meat, depending on the severity of the case. The initial intestinal infection may cause earlier mild gastrointestinal symptoms, particularly if many larvae are consumed.

Answer 599

Symptoms: o The duration and severity of symptoms are variable, depending on such factors as how the meat was prepared, the number of larvae ingested, the Trichinella species, and the immune status of the patient. o Symptoms associated with the initial invasion of the intestinal epithelium by ingested larvae are usually mild or not apparent, but may include diarrhea, abdominal discomfort, and, possibly, nausea and vomiting. o The acute and sometimes severe symptoms of trichinellosis, which are associated with newborn larval invasion of body tissues, commonly include muscle pain, fever, and weakness. Facial swelling, particularly around the eyes, is often present.

Answer 600

Complications: While larvae survive only in skeletal muscle, complications can develop, because larvae migrate through, and may perish in, various other organs. Invasion of heart, brain, or lung tissue, and subsequent inflammation, sometimes leads to death. Complications usually develop within the first 2 weeks of infection and are more common with heavy infections.

Answer 601

Duration: Within a few weeks, larvae-producing females are inactivated and eliminated from the intestine by the patient’s immune system. The acute symptoms associated with newborn larval migration gradually decline over the course of a few weeks, as newborn larvae become dormant in skeletal muscle. Patients remain asymptomatic while Trichinella larvae live in their muscles for years; however muscle pain, fever, and other symptoms can sometimes linger

Answer 602

Route of entry: Oral ingestion of live larvae in undercooked meat. The disease is not transferred from person to person.

Answer 603

Early symptoms, if present, resemble common gastrointestinal illness, and the patient usually does not seek treatment. Diagnosis of the later, acute-phase symptoms is difficult, because their onset is often weeks after the undercooked meat was eaten, and the symptoms are varied and may be similar to other diseases, such as the flu. Confirmation of trichinellosis is based on the presence of typical symptoms, combined with laboratory test results, and, sometimes, evidence of consumption of parasitized meat. Infected patients usually have an elevated eosinophil blood cell count. Immunological tests (ELISA, Western blot) are used to detect the presence of Trichinella-specific antibodies in the patient’s blood serum; however, these antibodies take 2 or more weeks to develop. Sometimes a muscle biopsy for the presence of larvae is performed. If larvae are recovered from a food source or patient, the exact species can be determined using molecular methods

Answer 604

Timely treatment usually includes anthelmintic drugs to remove any remaining fertile adult worms from the intestine. Normal anthelmintic doses generally do not kill the newborn larvae migrating in tissues, nor is this desirable, because of the possibility of a hazardous inflammatory response to dead larvae in sensitive organs. Therefore, early diagnosis and treatment is needed in order for anthelmintics to effectively reduce the severity of disease by shortening the period of newborn larval production. Glucocorticosteroid drugs may be used to reduce inflammatory and allergic immune responses that may cause complications and to reduce pain. Anthelmintic drugs are always used with early glucocorticosteroid administration, because the steroid may disrupt the immune system’s normal ability to remove fertile worms from the intestine. Severely infected or pregnant persons should be hospitalized during acute symptoms, to ensure prompt treatment of any complications.

Answer 605

Infective Trichinella larvae occur in undercooked meats from carnivorous and omnivorous mammals, reptiles, and birds. The most important source worldwide is the domestic pig; however, in the U.S. and other developed countries, the risk of infection from domestic pigs has been dramatically reduced. Pork now causes less than half of U.S. Trichinella infections, while meats other than pork, particularly from game animals, cause the most illness. More than 150 mammalian species are known to harbor Trichinella larvae, including horses, boars, bears, cattle, walruses, seals, cougars, deer, badgers, beavers, raccoons, foxes, dogs, skunks, squirrels, cats, and rats. Undercooked bear meat has caused several illnesses in North America

Answer 606

Target populations include hunters and other consumers of undercooked game, people who eat undercooked pork attained from a questionable source, and people who eat traditional uncooked meat dishes, such as walrus and horse meat.

Answer 607

Between 2000 and 2007, an average of 13 laboratory-confirmed illnesses were reported, per year, through the U.S. National Notifiable Disease Surveillance System. However, adjusting for under-diagnosis and under-reporting, the frequency of domestically acquired trichinellosis is estimated to be between 40 and 340 illnesses per year. Much higher infection rates per capita occur in less-developed pork-consuming nations and in countries that have disruptions in modernized pork production due to political upheavals.

Answer 608

Trichinellosis is prevented by thoroughly cooking meat. See Section 3-401 of the FDA Food Code for details on safe cooking times and temperatures for meats. Ready-to-eat pork products distributed in the U.S. must be processed in a manner that inactivates Trichinella spiralis, or the source carcass must be inspected for the presence of Trichinella larvae. Pork sold in grocery stores is intended to be cooked by the consumer and is not inspected for Trichinella. However, preventive controls implemented at commercial pig farms have reduced Trichinella-contaminated pork in the U.S. to negligible levels. These controls include cooking meat byproducts fed to pigs and preventing rodents from entering pig enclosures. A small chance still exists to attain commercial pork from a domestic or foreign farm using poor pig-husbandry practices; therefore, the careful consumer should continue to thoroughly cook pork to inactivate Trichinella and other potential pathogens. Commercial deep-freezing processes are sometimes used to deactivate Trichinella larvae in ready-to-eat pork products, in which the principle species of concern is T. spiralis. Freezing is not an appropriate preventive control to use at home or to use with non-pork animals; freezingresistant species of Trichinella are found in non-pork and game meats. Trichinella larvae have been shown to survive in frozen bear meat for 5 years

Answer 609

Carcasses may be directly inspected for Trichinella larvae using an artificial digestion method. A pepsin and acid mixture is used to dissolve the meat and leave the digestion-resistant larvae, which are then concentrated and enumerated under a microscope. A sample usually consists of 1 gram of meat from a location in the carcass that is ordinarily most infected with larvae. This method does not ensure that the carcass is free from infection, but with proper usage it will consistently detect at least one larva when there are more than three larvae per gram of meat. Carcasses used for ready-to-eat pork products that do not undergo any other USDA-approved Trichinella deactivating process must be inspected using a more sensitive 5-gram sample. Consistently negative inspection results provide powerful statistical evidence that the source area or herd is Trichinella-free. Tests to detect Trichinella antibodies in animal blood serum are sometimes used to survey pig herds, wild animal populations surrounding pig production facilities, and wild-game populations. The sensitivity of serology testing is lower for light infections, and serology does not detect recently parasitized animals that have not yet developed sufficient antibodies, a process that takes 2 to 9 weeks

Answer 610

In May 1988, an Alaskan woman and her sister-in-law became ill with trichinellosis. They had consumed dried walrus meat, whale blubber, beaver, and ducks. A walrus had been killed and divided among residents of two villages. Of the 51 persons who ate the walrus meat, 27 became ill with case-defined trichinellosis. In January 1995, a hunter shot a cougar in Idaho and made cougar jerky by salting and smoking the meat. A couple of weeks later, he became ill with trichinellosis symptoms. The jerky and cougar were found to contain Trichinella nativa and Trichinella genotype T6 larvae. The hunter had distributed the jerky to 14 other persons, 9 of whom were also found to have case-defined trichinellosis. In August 2000, four hunters from Wisconsin killed a black bear in Alaska and fried and ate the meat the same day. Two to four weeks later, they all came down with typical acute trichinellosis symptoms. The bear meat was analyzed and found to contain 24 Trichinella larvae per gram

Answer 611

The pork tapeworm (Taenia solium), the beef tapeworm (Taenia saginata), and the Asian tapeworm (Taenia asiatica) are flatworm parasites in the class Cestoda that mature in the human small intestine.

Answer 612

These tapeworms require a mammalian intermediate host and a human final host to complete their life cycles. Worm segments (proglottids) filled with mature eggs separate from adult tapeworms and pass with human feces, or, in the case of T. saginata, the proglottids can crawl out on their own. The eggs can survive for months on the ground or in water. Pigs and cattle will consume human feces and may ingest Taenia eggs with feces or with food and water. After pigs ingest T. solium or T. asiaticia eggs, or cows ingest T. saginata eggs, the oncosphere larvae hatch, penetrate the gut, and disseminate to various tissues via the bloodstream. After encysting in tissue, the larvae develop into bladder-like cysticerci, about 1 cm in size, that live for many months. In humans, T. solium larvae encyst in tissue, just as in the pig intermediate host; however, the cysticerci in human tissue cannot complete the worm’s life cycle. To complete the worm’s life cycle, humans must ingest live cysticerci in undercooked pork or beef. Ingested cysticerci activate and attach to the intestinal wall, where they grow 2 to 7 meters long and produce eggs for many years.

Answer 613

The disease caused by intestinal infection with adult Taenia tapeworms is taeniasis. The disease is similar among the three species. However, infection with T. solium is more serious than the others, because of the risk of cysticercosis, the disease caused by tissue infection with T. solium larval cysts (cysticerci). Neurocysticercosis, in which cysticerci lodge in brain tissue, is the severe form of cysticercosis.

Answer 614

Mortality: o Taeniasis: None known. o Cysticercosis: Death occurs in a small percentage of neurocysticercosis cases.

Answer 615

Infective dose: o Taeniasis: Ingestion of one live cysticercus larva in meat or viscera of pork or beef can result in infection with an intestinal tapeworm. o Cysticercosis: Ingestion of one T. solium egg may result in a tissue infection with one cysticercus larva. Ingestion of multiple eggs increases the likelihood of serious illness.

Answer 616

Onset: o Taeniasis: Tapeworms mature in the intestine and begin to release eggs about 2 to 4 months after live cysticerci are ingested. o Cysticercosis: Cysticerci larvae reach full size in tissues about 2 months after T. solium eggs are ingested. Neurocysticercosis symptoms may be delayed for several years.

Answer 617

Symptoms: o Taeniasis: Usually asymptomatic, but may cause abdominal pain, nausea, diarrhea, change in appetite, and general malaise. o Cysticercosis: Cysts located in the brain may be asymptomatic or can present multiple symptoms depending on the number, location, size, and condition of cysts, and on the immune response of the patient. Common neurocysticercosis symptoms include seizures, increased intracranial pressure, headache, and altered mental status. Cysts in the eye usually affect vision. Muscular and subcutaneous cysts may be felt, but do not cause much pain.

Answer 618

Taeniasis: Complications are unlikely. T. solium proglottids rarely may rupture while in the small intestine, releasing eggs that may auto-infect the individual with cysticercosis. o Rarely, motile T. saginata proglottids block the biliary duct, pancreatic duct, or appendix.

Answer 619

Cysticercosis: Live cysticerci can mask themselves from the immune system, resulting in few symptoms. However, when cysticerci degenerate, either naturally or from drug treatment, the immune system reacts, and severe inflammation can result. Cysts in brain tissue (parenchyma) are associated with seizures and are the most common cause of epilepsy in countries in which Taenia is endemic. Cysts that lodge in brain-fluid spaces (ventricles, subarachnoid space) may cause blockage of cerebrospinal fluid leading to hydrocephalus (water on the brain), inflammation of the meninges, or other complications. Cysts in the brain’s fluid spaces can grow very large (10 to 20 cm). Cysts in the eye can cause permanent vision damage.

Answer 620

Taeniasis: Adult worms can live for years in the intestine, but can be effectively eliminated with anti-Taenia drugs. o Cysticercosis: Cysticerci live for months, but remain in tissue for years. Neurological symptoms may appear several years after infection, and gradually decline with degradation and elimination of the cysticerci. Calcareous remnants in brain parenchyma are associated with recurring seizures years later.

Answer 621

Pathway: o Taeniasis: Ingested cysticerci in insufficiently cooked pork and beef activate and attach directly to the wall of the small intestine using suckers and/or hooks on the head (scolex). o Cysticercosis: Eggs released in feces of pork tapeworm carriers (humans) contaminate the environment. Persons become infected when contaminated food, fingers, or soil enter the mouth. Oncosphere larvae hatch, penetrate the intestine, disseminate in the bloodstream, and encyst to become cysticerci in the central nervous system, musculature, or visceral organs.

Answer 622

Taeniasis occurs in populations that consume raw or undercooked beef and pork, particularly in regions with poor sanitary facilities and where, out of economic necessity, livestock are allowed to roam freely. In the United States, the disease occurs primarily in individuals who have traveled or immigrated from endemic regions in Latin America, India, Asia, Eastern Europe, and Africa. Cysticercosis occurs where there is a high incidence of taeniasis caused by the pork tapeworm (T. solium). Persons infected with an adult T. solium, or living with an infected person, are particularly likely to accidentally ingest eggs and get cysticercosis.

Answer 623

Taeniasis: The primary source is infected beef and pork. Governments and farmers can reduce the occurrence of contaminated meats by implementing sanitary toilet facilities, controlled animal roaming, and meat inspection. Individuals can prevent taeniasis and other diseases by thoroughly cooking beef and pork product. In roasts and steaks, the center of the thickest part should measure at least 145° F for at least 3 minutes. Ground meat should reach 160° F because of the increased bacterial pathogen hazard.

Answer 624

Cysticercosis: An adult T. solium pork tapeworm in the human intestine can produce hundreds of thousand of eggs, per day, that can survive for months under harsh environmental conditions. Eggs contaminate surfaces and food when toilet or handwashing facilities are inadequate or improperly used; for example, when food handlers have poor personal hygiene practices. Risk of cysticercosis is reduced by frequent handwashing, by keeping fingers and other objects away from the mouth, and by avoiding questionable food-service establishments in endemic areas, such as where humans and pigs live in close proximity under poor sanitary conditions. A healthy individual should be tested for Taenia infection if a family member or other close contact is found to have cysticercosis or taeniasis.

Answer 625

These worms infect tens of millions of people worldwide. Taeniasis and cysticercosis are not nationally reportable diseases in the U.S. T. saginata appears to cause the most cases of taeniasis, but is less hazardous than T. solium, because it does not cause cysticercosis. In recent years, T. solium cysticerci have not been found in commercial pork in the United States. T. saginata cysticerci are still occasionally found in cattle. Between 1985 and 1994, T. saginata cysticerci were found in 1 to 2 beef carcasses per 10,000 inspected. Most cases of taeniasis occurring in the U.S. are attributed to travel or immigration from endemic areas, mostly in Latin America. T. solium eggs, introduced by tapeworm carriers traveling from endemic regions, continue to cause cysticercosis in the U.S. Nine percent of a cross-section of the El Paso, Texas, population tested positive for taeniasis in 2004, and several cases of neurocysticercosis have been reported in that city. Between 1991 and 2008, about 7,000 Los Angeles County residents were discharged from hospitals after treatment for cysticercosis (including repeated hospitalizations for the same infection). About 4,000 of these hopitalizations were for neurocysticercosis. According to a survey of death certificates, about 221 cysticercosis-related deaths occurred in the United States from 1990 to 2002.

Answer 626

Taeniasis: Diagnosis is difficult because the disease is usually asymptomatic. Detection often occurs when the patient sees proglottids in stool or undergarments. Traditionally a stool specimen is examined microscopically for characteristic Taenia eggs; however, this test is not reliable. A more sensitive fecal ELISA test has good diagnostic results in research settings. Anthelmintic drugs effectively eliminate adult tapeworms. The tapeworm species can sometimes be determined by examination of expelled proglottids and/or the scolex. Molecular sequencing, where available, should be used to determine the exact species.

Answer 627

Cysticercosis: Symptoms usually occur a long time after infection, leading to difficulty relating symptoms to the cause; because the disease is uncommon in the U.S., misdiagnosis can occur. Computed tomography and magnetic resonance imaging are needed to identify the number, location, size, and other important characteristics of cysticerci in the brain. Less expensive serological techniques are constantly improving and may be used to confirm diagnosis and track the course of disease. Cysts in the eye are viewed with an ophthalmoscope. Cysts under the skin can be felt and may be biopsied. Treatment of neurocysticercosis varies with specific circumstances. Seizures, inflammation, and hydrocephalus must first be stabilized before considering treatment for the parasite. Treating cysticerci in the brain with anthelmintic drugs may activate a severe immune response, causing excessive inflammation; therefore, antiinflammatory and anthelmintic drugs are used judicially to facilitate removal of cysts. Shunts may be inserted to relieve intracranial pressure, and open or endoscopic surgery may be used to remove cysticerci in accessible locations. Recovered larvae should be identified for epidemiological reasons, because other tapeworm species also may cause cysticercosis.

Answer 628

Regulatory authorities inspect pork and beef carcasses for “measled” meat by feeling and visually examining susceptible muscles for cysticerci. Animals may also be tested by more sensitive serological methods.

Answer 629

Taeniasis and cysticercosis are endemic in much of the world. Outbreaks may go unrecognized until complications manifest. In 1978, there was a large cysticercosis outbreak in West New Guinea after infected pigs were introduced into that country. The disease was recognized when there was an epidemic of burn victims who sustained their injuries during neurocysticercosisinduced seizures that occurred as they slept near fireplaces. In 1990, a neurocysticercosis outbreak occurred in an Orthodox Jewish community, in New York City, that did not eat pork. The source of infection was thought to be recently immigrated housekeepers infected with pork tapeworms.

Answer 630

Anisakis simplex complex (herring worm)  Pseudoterranova (Phocanema, Terranova) decipiens complex (cod or seal worm)  Anisakis physeteris  Contracaecum species A. simplex has been responsible for the majority of human infections, with most of the rest due to P. decipiens. These two species are now known to be complexes of multiple species that are distinguishable only by genetic analysis. These worms average 2 to 3 cm in length.

Answer 631

Mortality: None known.

Answer 632

Infective dose: One worm.

Answer 633

Onset: Symptoms usually occur within 24 hours after consumption of affected raw or undercooked fish, but may be delayed by as long as 2 weeks

Answer 634

Symptoms / complications: Non-invasive anisakiasis is often asymptomatic or sometimes is diagnosed when the affected person feels a tingling sensation in the throat and coughs up or manually extracts a nematode. Invasive anisakiasis occurs when a worm burrows into, and attaches to, the wall of the stomach or intestine. The ulceration results in an inflammatory response in which eosinophils (white blood cells) respond and a granuloma (nodule) forms at the point of worm attachment. The symptoms may include severe stomach or abdominal pain, nausea, vomiting, and diarrhea. Symptoms may be mild, or may be characterized by a mild to strong allergic response. Occasionally, inflammation disrupts normal intestinal flow, leading to constipation. Rarely, worms penetrate through the digestive tract and are found in the body cavity. Some people have allergic reactions when consuming dead Anisakis remnants in cooked or previously frozen fish, and some fish handlers have reportedly become hypersensitive to touching infected fish

Answer 635

Duration of symptoms: Unless complications develop, anisakiasis is a self-limiting disease in humans. Marine mammals are the worms’ natural final host. Humans are an accidental host, and, in humans, the worm dies and is eliminated spontaneously from the lumen of the digestive tract within about 3 weeks. However, pain associated with inflamed lesions may occasionally persist for weeks to months after the worm has died. Symptoms usually clear immediately if the worm is removed early.

Answer 636

Pathway: Burrowing in gastrointestinal mucosa.

Answer 637

In cases in which the patient vomits or coughs up a worm, the disease may be diagnosed by morphological examination of the nematode. The symptoms of invasive anisakiasis may be misdiagnosed as appendicitis, Crohn’s disease, gastric ulcer, gastrointestinal cancer, and other gastrointestinal diseases. Thus, a history of having eaten raw or undercooked fish is potentially an important diagnostic clue. An endoscopic fiber-optic device, preferably, is used to visually diagnose and remove worms attached in the stomach and small intestine. In severe cases that cannot be diagnosed and treated endoscopically, abdominal surgery may be performed. Microscopic examination is used to identify a recovered nematode to the genus or “species complex” level, while molecular methods can be used to determine the exact species. Elevated eosinophil counts (eosinophilia) may be detected during the early inflammatory response. Radiology also has been used as a diagnostic aid. Diagnostic tests for antibodies in human blood serum have been developed; however, antibodies may not yet be present or may be present from a previous infection, and some tests may cross-react with other parasites, such as Ascaris lumbricoides.

Answer 638

Treatment may include steroids, antibiotics, and isotonic glucose solution. Anthelmintic drugs are not generally considered appropriate, but have been used with some success. The worm will die and pass naturally, but endoscopic removal is considered the best treatment for severe pain.

Answer 639

The frequency in the United States is unknown, because the disease is not reportable and can go undetected or be mistaken for other illnesses. Anisakiasis was first recognized in the 1960s. During the 1970s, about 10 cases per year were reported in the literature. The frequency is probably much higher, due to home preparation of raw or undercooked fish dishes. In Japan, more than 1,000 cases are reported annually.

Answer 640

These larval worms may be found in the viscera and/or flesh of almost all ocean fish and cephalopods, and occur frequently in cod, haddock, fluke, Pacific salmon, herring, flounder, monkfish, and squid. Fish and cephalopods consumed raw or undercooked, whether marinated, pickled, cold-smoked, or braised, pose a risk of infection

Answer 641

The FDA Food Code guidelines for cooking fish should suffice to inactivate these worms in fish and cephalopods. The guidelines for fish are as follows: cook the fish to an internal temperature of 145ºF for 15 seconds; to 155ºF for comminuted fish, such as fish cakes, and 165ºF for stuffed fish. Commercial processors and retailers may use a specific deep-freeze process to kill parasites in fish products that are served without thorough cooking. The food and fishery industries may obtain detailed information about freezing methods for killing seafood parasites in the current edition of the FDA Fish and Fishery Hazards and Controls Guidance.

Answer 642

Candling (examination of fish on a light table) is used by commercial processors to reduce the number of visible nematodes in certain white-fleshed fish known to be infected frequently. This method is not totally effective, nor is it very adequate to remove even the majority of nematodes from fish with pigmented flesh. Pepsin digestion is used in scientific studies to dissolve fish tissue while leaving pathogenic parasites intact. Because this method is time-consuming, it is generally not used for routine food analysis.

Answer 643

Diphyllobothrium latum and about 13 other flatworms of the genus Diphyllobothrium are intestinal parasites of humans and other fisheating mammals and birds. They are also called “broad tapeworms” and “fish tapeworms.”

Answer 644

The disease caused by this organism, diphyllobothriasis, results from consumption of Diphyllobothrium spp. larvae, which are found in the meat and viscera of raw or undercooked fresh fish. After consumption, the larvae attach in the small intestine and grow rapidly. Eggs begin to be produced and expelled in the patient’s stool as early as 15 days after consumption of the larvae. Adult tapeworms grow up to 32 feet (about 10 meters) long and can produce about a million eggs per day

Answer 645

Infective dose: One or more larval worms.

Answer 646

Onset: The tapeworm produces eggs as early as 15 days after consumption; however, the infection usually is not noticed

Answer 647

Symptoms / complications: Infection with Diphyllobothrium usually presents no noticeable symptoms, or the symptoms are mild, including abdominal discomfort, diarrhea, and altered appetite. The tapeworm absorbs a great amount of vitamin B12, which, in prolonged or heavy cases, may cause a vitamin B12 deficiency that rarely leads to anemia. Intestinal obstruction has been known to occur in rare massive infections.

Answer 648

Patients often become initially aware of an infection by observing pieces of the tapeworm in their stools. Diagnosis is made by demonstration of the characteristic eggs during microscopic examination of a stool sample. The eggs are easily confused with similarly shaped parasitic trematode eggs. Molecular methods may be used to identify Diphyllobothrium to the species level

Answer 649

Worms can survive in the small intestine for more than 25 years, but are easily expelled with drugs (praziquantel and niclosamide) when the worms are discovered

Answer 650

Diphyllobothriasis is considered a minor public health problem, and records are no longer maintained on the frequency of the disease. From 1977 to 1981, in the United States, 100 to 200 cases were reported, per year. The actual number of cases was probably much higher, considering asymptomatic and mild cases that went unreported. An estimated 20 million people currently are infected, worldwide

Answer 651

Human infection with Diphyllobothrium is caused by eating raw or undercooked fish dishes (including those that have been marinated, salted, or cold-smoked); e.g., sushi, sashimi, ceviche, and tartare. Tasting ingredients of fish dishes before they are cooked (e.g., gefilte fish) also can cause infection. Infective larvae are found in the meat and viscera (i.e., eggs, liver) of freshwater and marine finfish from temperate latitudes. In North America, these fish include Pacific salmon and freshwater fish, such as pike, perch, walleye, burbot, char, Alaska blackfish, dolly varden, whitefish, and trout. Imported, fresh fish from temperate climates also may contain infective larvae.

Answer 652

The FDA Food Code guidelines for cooking fish should suffice to inactivate these worms. The guidelines for fish are as follows: cook the fish to an internal temperature of 145ºF for 15 seconds; to 155ºF for comminuted fish, such as fish cakes, and 165ºF for stuffed fish. Commercial processors and retailers may use a specific deep-freeze process to kill parasites in fish products that are served without thorough cooking. The food and fishery industries may obtain detailed information about freezing methods for killing seafood parasites in the current edition of the FDA Fish and Fishery Hazards and Controls Guidance.

Answer 653

Any consumer of raw or undercooked fish.

Answer 654

Foods are not routinely analyzed. Microscopic inspection of thin slices of fish flesh, or artificial digestion of the flesh, can be used to detect the “plerocercoid” larvae.

Answer 655

An outbreak involving four Los Angeles physicians occurred in 1980. These physicians all consumed sushi (a raw fish dish) made of tuna, red snapper, and salmon. Others who did not consume the sushi made with salmon did not contract diphyllobothriasis. In 1980, the CDC determined that 19 of 25 diphyllobothriasis cases in the Los Angeles area likely resulted from consuming salmon. A few individual cases in foreign countries have been attributed to the consumption of Pacific salmon originating in North America

Answer 656

Nanophyetus salmincola is a small parasitic trematode (fluke) in the flatworm phylum.

Answer 657

Nanophyetiasis is the name of the human disease caused by these intestinal flukes when they are consumed live in raw or undercooked fish. At least one newspaper report has referred to the disease as "fish flu." These worms also are known to carry a bacterium that causes a serious, sometimes fatal disease in dogs (salmon poisoning disease); however, this bacterium is not known to infect humans

Answer 658

Mortality: None known, in humans

Answer 659

Infective dose: Approximately 500 worms are required to elicit symptoms

Answer 660

Route of entry: Oral. Ingestion of worm larvae (metacercariae) encysted in fish flesh or viscera; also by handto-mouth contact while handling infected fish

Answer 661

Onset: Eggs can be detected in stool about 1 week after a contaminated fish is ingested

Answer 662

Symptoms: Patient complaints include abdominal pain, diarrhea, gas / bloating, and nausea / vomiting. Seven of 20 reported cases in the United States were asymptomatic. Increased numbers of circulating eosinophils (\>500/µl) were found in 50% of the cases

Answer 663

Duration: Without treatment, symptoms may last several months

Answer 664

N. salmincola eggs released by adult worms hatch as miracidium larvae in rivers and streams. Miracidium larvae penetrate a pleurocerid stream snail (first intermediate host) and undergo asexual replication. Cercariae larvae are shed by the snail and penetrate the skin of a fish (secondary intermediate host), where they encyst as metacercariae larvae in the fish flesh and viscera. The final hosts are fish-eating mammals and birds. When a mammal (including humans) consumes an infected fish, the larvae attach and mature in the small intestine.

Answer 665

Target populations include consumers of raw or undercooked (including home-smoked) fish from the sources discussed below.

Answer 666

Fresh fish originating in, or passing through, coastal streams of Oregon, Washington, northern California, southeast Alaska, and British Columbia, where the intermediate snail host lives, are sources of infection with this worm. Salmonids (e.g., salmon, trout, steelhead) are more heavily infected with larval worms. Fish from areas of eastern Siberia and Brazil that have appropriate pleurocerid snail intermediate hosts may also contain the worm. In anadromous fish (fish that migrate from freshwater streams / lakes to the ocean and return), the infective cysts survive the period spent at sea. Aquacultured salmonids fed only pelleted feed could be infected if the fry / smolts originated from hatcheries with water sources that contain N. salmincola cercariae.

Answer 667

The FDA Food Code guidelines for cooking fish should suffice to inactivate these worms. The guidelines for fish are as follows: cook the fish to an internal temperature of 145ºF for 15 seconds; to 155ºF for comminuted fish, such as fish cakes, and 165ºF for stuffed fish. Commercial processors and retailers may use a specific deep-freeze process to kill parasites in fish products that are served without thorough cooking. The food and fishery industries may obtain detailed information about freezing methods for killing seafood parasites in the current edition of the FDA’s Fish and Fishery Hazards and Controls Guidance.

Answer 668

In the U.S., 20 of the 23 known cases were in patients of a single Oregon clinic. Because symptoms are mild or absent, many cases probably are not identified. Two cases occurred in New Orleans, well outside the endemic area, reflecting the likelihood of interstate commerce of commercial fish containing the parasite. In some villages in eastern Siberia, more than 90% of the human population is infected with this worm.

Answer 669

Differential diagnosis is indicated by gastrointestinal symptoms and a history of eating fresh raw or undercooked salmonids from endemic areas. Definitive diagnosis is made by detecting the worm’s characteristic eggs in the patient’s stool. The eggs are difficult to distinguish from those of Diphyllobothrium latum; however, the treatment for both infections is the same.

Answer 670

Nanophyetiasis is a mild illness, and the worms will pass naturally, if the practice of eating undercooked fish is stopped. Treatment with anthelmintic drugs (e.g., praziquantel) clears the symptoms and stops egg production.

Answer 671

There are no established methods for detection of Nanophyetus salmincola cysts in fish flesh. The cysts are small (0.5 mm long by 0.25 mm wide). Candling with the aid of a dissecting microscope, or pepsin HCl digestion, should detect heavily infected fish. A homogenationsedimentation technique has been used, with reported success

Answer 672

Larval Eustrongylides spp. are large red roundworms (nematodes) that are ½ to 4½ inches (15 to 115 millimeters) long. The larvae are found in fish.

Answer 673

The disease (eustrongylidiasis) is caused by Larval Eustrongylides spp when contaminated live or raw fish are consumed and the larval nematode penetrates the wall of the human intestine

Answer 674

Infective dose: One live larval worm can cause an infection.

Answer 675

Route of entry: Oral.

Answer 676

Onset: Symptoms develop within 24 hours after a contaminated live or raw fish is eaten.

Answer 677

Symptoms: In the five cases reported, penetration of the worm into the gut wall was accompanied by severe abdominal pain

Answer 678

Complications: The abdominal pain is similar to appendicitis, and four of the five reported cases required investigative surgery. During surgery, worms were found in the peritoneal cavity or in the process of penetrating the gut wall. Intestinal damage and inflammation can occur during gut penetration, and other tissues could be damaged during any subsequent larval migration. The disease has the potential to cause bacterial infection of the peritoneal cavity from intestinal contents or the worm itself.

Answer 679

Duration of symptoms: Unknown. The symptoms were resolved by surgery. In one suspected case in which surgery was not performed, the symptoms resolved in 4 days.

Answer 680

Adult Eustrongylides spp. live in the gastrointestinal tract of fish-eating birds, such as herons, egrets, and mergansers (the definitive hosts). The parasite’s eggs pass with bird feces into the water. The eggs may be eaten by, and the larvae develop in, an oligochaete worm that lives in fresh or brackish water (an intermediate host). Fish become infected with parasite larvae by eating contaminated oligochaete worms, contaminated smaller fish, or directly from consumption of the parasite’s eggs. Parasite larvae encyst in the fish’s viscera and/or muscle. Birds become infected by eating contaminated fish, worms, or other intermediate hosts (amphibians and reptiles also have been reported as intermediate hosts). Humans may ingest live larvae with raw or undercooked fish. While the parasite cannot complete its life cycle in humans, it may attach to, and penetrate, the wall of the human digestive tract.

Answer 681

The target populations are consumers of raw or undercooked fish that have not been previously frozen to kill parasites. Four of the five cases reported resulted from fishermen swallowing live, whole minnows used for bait.

Answer 682

Eustrongylides larvae are found in the flesh and viscera of a wide variety of fish from fresh, brackish, or salt waters. Whole minnows (i.e., that still contain the viscera) from estuaries may be a significant source, because their viscera frequently contain the larvae. Fish-eating bird populations near fresh or brackish water have the highest prevalence of the adult parasites; therefore, nearby fish, or fish that feed on fish that pass through such areas, are more likely to be contaminated. For example, fish raised in freshwater ponds with numerous fish-eating birds present may contain greater numbers of these worms.

Answer 683

Extremely rare; only five cases reported.

Answer 684

The illness is not fully diagnosed until the worm is identified after surgery. The abdominal pain that occurs is similar to the symptoms of appendicitis; however, parasitic worm infection may be suspected if the patient has recently eaten raw or incompletely cooked fish. Endoscopic, nonsurgical discovery and removal of the worm also may be possible

Answer 685

These large red worms may be seen without magnification in fish flesh and are normally very active after death of the fish. The larva is similar in appearance to that of the kidney worm (Dioctophyma renale). (The giant kidney worm – Dioctophyma renale – is a close relative of Eustrongylides that normally matures in the right kidney of fish-eating mink and other fish-eating mammals. The kidney worm is a potential human health hazard in raw or undercooked freshwater fish from endemic areas. To date, no human cases have been reported in the U.S.)

Answer 686

Balamuthia mandrillaris, Naegleria fowleri, and Acanthamoeba species

Answer 687

■ Granulomatous amebic encephalitis (GAE) - caused by Acanthamoeba spp. and Balamuthia mandrillaris.

Answer 688

Primary amebic meningoencephalitis (PAM) - caused by Naegleria fowleri.

Answer 689

Acanthamoeba keratitis, or amebic keratitis, (AK) - caused by Acanthamoeba spp.

Answer 690

Ascariasis and trichuriasis are the names of the infections caused by Ascaris lumbricoides and Trichuris trichiura, respectively. Ascariasis also is known as the common roundworm infection or large roundworm infection, and trichuriasis as whipworm infection. Eggs of these “soil-transmitted” nematodes are deposited in the feces from infected individuals and develop in warm, moist soil, becoming infective after a few weeks. The eggs stick to surfaces and may be carried to the mouth by soil-contaminated hands, other body parts, fomites (inanimate objects), or foods.

Answer 691

Ingested Ascaris eggs hatch in the small intestine, and the larval worms penetrate the intestinal wall and make their way to the lungs by way of the circulatory system. In the lungs, they break out of the pulmonary capillaries into the air sacs, ascend into the throat, and, finally, descend to the small intestine again, where they grow to a length of 6 to16 inches (15 to 40 cm). Infection with one or a few Ascaris spp. may be asymptomatic, unless a worm is noticed when passed in the feces, or, on occasion, when a worm is crawling up into the throat and trying to exit through the mouth or nose. Heavy infections are associated with abdominal distension and pain, nausea, loss of appetite, and vomiting. The worm’s lung migration may cause a self-limiting pneumonia

Answer 692

Trichuris sp. eggs hatch in the intestine, and the larvae mature directly in the intestinal epithelium, without migrating to the lungs. When mature, the tail of the worm breaks through the epithelium and protrudes into the intestinal lumen. Adult worms stay attached in one place in the intestinal caecum or colon and are 1 to 2 inches (3 to 5 cm) long, with slender heads and thickened tails. Most trichuriasis infections are light and asymptomatic. Moderate to heavy infections result in symptoms that may include abdominal pain, diarrhea, passage of mucus and blood in the stool, nausea, vomiting, anemia, and rectal prolapse.

Answer 693

Complications: Complications are correlated with the number of worms infecting the individual. Heavy aggregates of worms may cause intestinal blockage and other intestinal complications, particularly in small children. Not all larval or adult worms stay on the path that is optimal for their development; those that wander may locate in the bile or pancreatic ducts, appendix, and other sites, causing inflammation or obstruction. Worm-wandering may be stimulated by fever, some drugs, or spicy meals.

Answer 694

Chronic infection with either of these worms is thought to contribute to growth retardation and slowed mental development in malnourished children.

Answer 695

Humans worldwide are infected with A. lumbricoides and T. trichiura. The occurrence of eggs in domestic municipal sewage indicates that infection rates are high. A survey of U.S. state laboratory results from 1987 showed T. trichiura in 1.2% and A. lumbricoides in 0.8% of stool samples tested, although infection severity in the U.S. is usually light and asymptomatic. Infection rates are much higher worldwide and, combined, these worms infect more than a quarter of the world’s population.

Answer 696

These worms release thousands of eggs, per day, that can remain infectious in soil for years. The eggs are found in contaminated soils and in insufficiently treated fertilizers made from human sewage. Although the eggs are transmitted to humans primarily through hand-to-mouth contact, they may be transmitted via raw consumption of food crops that were contaminated with insufficiently treated sewage fertilizer.

Answer 697

Ascariasis and trichuriasis are a particular problem in areas of poor sanitation where human feces are deposited on the soil. Children up to age 10 have the highest frequency of infection. Consumers of uncooked vegetables and fruits that are fertilized with untreated sewage are at risk. Persons in close association with pigs or who consume raw crops fertilized with pig manure may also be at risk. These diseases are also associated with the practice of consuming earth (geophagy)

Answer 698

strains known to cause disease in humans, which exist primarily in genetic clusters within genogroups I, II, and IV, whereas the viruses belonging to the other genogroups have been shown to infect other animals (primarily cattle, swine, and mice).

Answer 699

Common names of the illness, which is the leading cause of foodborne illness in the United States, are viral gastroenteritis, acute nonbacterial gastroenteritis, food poisoning, and winter vomiting disease.

Answer 700

Mortality: Overall, these illnesses account for 26% of hospitalizations and 11% of deaths associated with food consumption

Answer 701

Infective dose: The infective dose is very low; it is estimated to be as low as 1 to 10 viral particles, and the particles are excreted at high levels by both symptomatic and asymptomatic people (as high as 1 x 1012 million viral particles/g feces).

Answer 702

Onset: A mild, brief illness usually develops between 24 and 48 hours after contaminated food or water is consumed (median in outbreaks: 33 to 36 hours), but onset times within 12 hours of exposure have been reported

Answer 703

Illness / complications: Norovirus illness is self-limiting, but can be very debilitating as a result of the high rate of vomiting. Recovery is usually complete and without evidence of long-term effects. Dehydration is the most common complication, especially among the very young, the elderly, and patients with underlying medical conditions.

Answer 704

No specific therapy exists for viral gastroenteritis, in general, or NoV infection, in particular. For most people, treatment of NoV infection is supportive; besides rest, it consists primarily of oral rehydration and, if needed, intravenous replacement of electrolytes. Currently no antiviral medication is available, and antibiotics are not effective for treating NoV infection. Presently no vaccines are available to prevent NoV infection, although this is an active area of research.

Answer 705

Symptoms: Symptoms usually present as acute-onset vomiting (often explosive); watery, non-bloody diarrhea with abdominal cramps; and nausea. Explosive, projectile vomiting usually is the first sign of illness and is often used to characterize the illness. Headache, low-grade fever, chills, and muscle aches may also occur. The severity of symptoms appears to be higher in hospitalized patients, immunocompromised people, and elderly people, compared with younger adults and other groups. Studies suggest that 30% of people infected with NoV display no gastrointestinal illness or associated symptoms, but still excrete high levels of virus in their stool. These distinct groups of people are considered to be silent shedders of NoV.

Answer 706

Duration: Symptoms generally persist for 12 to 60 hours, with a mean period of 24 to 48 hours. Most people report feeling better within 1 to 2 days. However, for hospitalized patients, immunocompromised people, and the elderly, vomiting and diarrhea generally resolve within 72 to 96 hours, while the non-specific symptoms, such as headache, thirst, and vertigo, could persist up to 19 days.

Answer 707

Route of entry: Foodborne norovirus illnesses have been epidemiologically linked into three distinct classes: with cases associated with consumption of ready-to-eat (RTE) foods contaminated by food workers; with environmental contamination of produce; or with consumption of molluscan shellfish harvested from contaminated water. In each of these classes, transmission occurs through the fecal-oral route (or vomit, on occasion), and is often associated with improper sanitation controls or their application. Secondary transmission following foodborne illness is common, due to the high levels of virus that are excreted.

Answer 708

Pathway: Norovirus infection causes gastroenteritis, an inflammation of the stomach and the small and large intestines. However, the precise pathogenic pathway of infection is unknown, which has hampered progress in propagating the virus in the laboratory.

Answer 709

The Centers for Disease Control and Prevention (CDC) estimates that noroviruses cause 5.5 million illness annually in the U.S. (estimated range: 3.2 million to 8.3 million cases of foodborne illness), which accounts for 58% of all foodborne illnesses. Of these illnesses, approximately 0.03% (mean, 14,663; range, 8,097 to 23,323) require hospitalization, and less than 0.1% of these illnesses results in death (mean,149; range, 84 to 237).

Answer 710

NoV outbreaks have been associated with consumption of contaminated water, including municipal water, well water, stream water, commercial ice, lake water, and swimming pool or recreational surface-water exposure, as well as floodwater. Salad ingredients, fruit, and oysters are the foods most often implicated in norovirus outbreaks. However, any ready-to-eat food that is that is handled by ill food workers may be contaminated. Nearly 29% of all NoV foodborne outbreaks from 1997-2004 could be attributed to food purchased or served at a restaurant or delicatessen. Molluscan shellfish, particularly oysters, have been commonly identified in NoV-related gastroenteritis outbreaks, worldwide. However, this represents a different etiology that does not necessarily involve a contaminated food worker.

Answer 711

Clinical diagnosis, without the results of diagnostic tests used to identify NoV-associated illness, includes the following four criteria (Kaplan et al., 1982):  vomiting in more than 50% of affected persons in an outbreak;  a mean (or median) incubation period of 24 to 48 hours;  a mean (or median) duration of illness of 12 to 60 hours;  lack of identification of a bacterial pathogen in stool culture. Confirmation of a clinical diagnosis of NoV infection can be achieved by performing analytical tests on serum, stool, and, in some instances, vomitus. Diagnosis also can be achieved by examining blood serum samples for a rise in virus-specific serum antibody titers, measured by enzyme immunoassay (i.e., ELISA or EIA). This analysis is premised on an increased serum titer (generally a four-fold increase) of immunoglobulins – IgA, IgG, and IgM – against the presumed viral antigen in acute or convalescent sera; however, this approach requires the collection of multiple sera samples from patients, to allow identification of an increase in sera antibodies. These have been commercially marketed to detect NoV in fecal material; however, this approach has had only a 55% level of accuracy, when compared with a reverse transcription polymerase chain reaction (RT-PCR) approach. The applicability of these assays is also limited by the requirement to collect stool specimens from acute or convalescent patients for accurate determination. Examination of stool specimens for norovirus can be performed by microscopy (direct electron microscopy or immunoelectron microscopy), to visualize viral capsids, but requires the virus to be found at high densities (generally \>106 /g). Molecular techniques, such as RT-PCR, have been successfully used to detect the presence of viral nucleic acids in stool and vomitus. RT-PCR is the preferred method of diagnosis, since it is significantly more sensitive than microscopy; does not require a large, expensive electron microscope with highly skilled personnel; and has the ability to rapidly differentiate genogroups, which could be instrumental in follow-up epidemiologic investigations, to determine the route and distribution of NoV in the community.

Answer 712

Illness due to NoV may impact people of any age, but has been reported, through populationbased studies, to be more prevalent among the elderly and children under 5 years old. Evidence suggests that there is a genetic predisposition to acquiring infection that is dependent on the patient’s blood type (ABO phenotype). Prior infection by NoV does not provide long-term immunity, and reinfection by the same strain can occur several months after the initial infection. The rapid spread of secondary infections is particularly evident in areas where a large population is enclosed within a static environment, such as in institutions, college campuses, schools, military operations, hotels, restaurants, recreational camps, hospitals, nursing homes, day-care facilities, and cruise ships, or after natural disasters, such as hurricanes and earthquakes.

Answer 713

NoV has been successfully isolated from, and detected in, oysters, irrigation and ground water, and deli meats associated with illnesses. Quantitative RT-PCR (qRT-PCR) is the most sensitive method for NoV detection in food extracts and is an improvement over conventional RT-PCR, due to its increased specificity and sensitivity. Assays using this RT-PCR technology for NoV detection and quantitation are commercially available.

Answer 714

See Book page 172

Answer 715

HAV is classified with the enterovirus group of the Picornaviridae family, genus Hepatovirus, and is comprised of single positive-stranded RNA genome of approximately 7.5 kilobases. This RNA molecule is protected from the environment by a protein capsid (“shell”) comprised of multiple copies of three or four proteins. HAV is a non-enveloped (i.e., no lipid-containing envelope), hydrophobic virus 22 to 30 nm in size, with icosahedral symmetry with 20 sides. There are six HAV genotypes (I-VI), as determined by RNA sequence analysis at the VP1-2A junction of the virus genome. Genotypes I, II, and III contain strains associated with human infections, with the majority of human strains grouped within genotypes I and III. Genotypes I-III have been further divided into sub-genotypes A and B for each genotype. Most nonhuman primate strains are grouped within genotypes IV, V, and VI. Despite the identification of multiple genotypes/strains, this is the only known serotype for HAV. Humans and several species of non-human primates are the only known natural hosts for HAV.

Answer 716

Mortality: The overall death rate among people with hepatitis A (that is, liver involvement; the term “hepatitis A” is used to refer to the disease, not to the virus) is approximately 2.4%. Increased age (over 50 years old) slightly increases the death rate. Overall, hepatitis A accounts for \< 0.001% of all foodborne-associated deaths. Although fulminant (severe, rapidly progressing) disease is rare, the mortality rate is much higher, at 70% to 80%, as noted in the Illness / complications section, below.

Answer 717

Infective Dose: The infective dose of HAV is presumed to be low (10 to 100 viral particles), although the exact dose is unknown. The viral particles are excreted in the feces of ill people (symptomatic and asymptomatic) at high densities (106 to 108 /gm) and have been demonstrated to be excreted at these levels for up to 36 days post-infection.

Answer 718

Onset: In symptomatic patients, mean incubation phase is 30 days (range 15 to 50 days).

Answer 719

Illness / complications: HAV infections can be asymptomatic or symptomatic. Infections usually are asymptomatic in children younger than age 6 and symptomatic in older children and adults. When disease does occur, it is usually mild and recovery is complete within 1 to 2 weeks, although it may last up to several months, in which case it is also generally self-limiting. HAV infection is not considered to be chronic; however, a prolonged or relapsing disease lasting up to 6 months in 10-15% of patients has been reported. Patients feel chronically tired during convalescence, and their inability to work can cause financial loss. An atypical, and rare, clinical outcome of acute HAV infection is fulminant hepatitis or fulminant hepatic disease, which occurs in less than 1% to 1.5% of cases. This more severe outcome of acute HAV infection and illness involves massive hepatic necrosis, with acute liver failure, and has a high case-fatality rate (70% to 80%). The reasons for progression to acute, severe, or fulminant hepatitis remain unclear; however, it is known that patients with an underlying chronic liver disease are at particularly high risk for fulminant disease or liver failure. Factors that may play a role in severe hepatic disease progression include the nature of the host response (e.g., genetic, immunologic, or physiologic), the viral pathogen (e.g., strain virulence), and/or viral dosage (e.g., viral inoculums, patient viral load, or levels of viral replication). A hepatitis A vaccine is available

Answer 720

Symptoms: Symptoms associated with HAV infection include fever, anorexia, nausea, vomiting, diarrhea, myalgia, hepatitis, and, often, jaundice. Jaundice generally occurs 5 to 7 days after onset of gastrointestinal symptoms; however, in 15% of reported jaundice cases, the jaundice was not preceded by gastrointestinal symptoms.

Answer 721

Duration: Typically 1 to 2 weeks, although prolonged or relapsing cases may continue for up to 6 months in a minority of patients.

Answer 722

Route of entry: HAV may cause infection through various routes. The route of entry for the foodborne infection is oral.

Answer 723

Pathway: The exact mechanism of HAV pathogenesis is not fully understood. The route of entry for foodborne HAV typically is the gastrointestinal tract. From the intestinal tract, the virus is transported to the liver via the blood, where hepatocytes generally are thought to be the site of viral replication. The virus is thought to be excreted by the hepatocytes and transported to the intestinal tract via bile. However, some studies suggest that initial replication may occur in crypt cells of the small intestine.

Answer 724

An estimated 1,566 cases of hepatitis A from consumption of contaminated food occur annually in the United States. This constitutes a small portion (1% to 1.5%) of the total number of patients infected with HAV. Overall, hepatitis A accounts for \< 0.001% of all foodborne-associated hospitalizations in the U.S. Hepatitis A from any cause (i.e., not just the foodborne illness) has a worldwide distribution occurring in both epidemic and sporadic fashion. In the U.S., from 1980 through 2001, an average of 25,000 cases of hepatitis A was reported to the Centers for Disease Control and Prevention (CDC) annually. However, correcting for under-reporting and asymptomatic infections, CDC estimates that an average of 263,000 HAV infections, from all causes, occurred annually in the U.S. during this period. Until 1995, the overall incidence of HAV infection in the U.S. was cyclic, with nationwide increases occurring every 10 to 15 years (Figure 1). Since 1995, the estimated overall number of reported HAV infections in the U.S. has been declining. This significant decrease (with the most significant decrease occurring in children) appears to coincide with the vaccination program, for children and adolescents 2 to 12 years old, that began in the U.S. in 1996.

Answer 725

HAV is excreted in feces of infected people and can produce clinical disease when susceptible people consume contaminated water or foods. Cold cuts and sandwiches, fruits and fruit juices, milk and milk products, vegetables, salads, shellfish, and iced drinks are commonly implicated in outbreaks. Water, shellfish, and salads are the most frequent sources. Contamination of foods by infected workers in food-processing plants and restaurants also is common. In the U.S., the estimated transmission rate of this virus by person-to person contact was 22%. Of that, 8% was associated with day-care settings, 5% with international travel, 5% with illegal injectable drug use, and 4% with consumption of common-source contaminated food or water. The transmission routes for 65% of cases are unknown. Low income, low education level, crowding, and lack of access to safe drinking water and sanitation facilities are associated with increased rates of HAV infection

Answer 726

Clinical diagnosis of an HAV infection can be achieved by performing the appropriate analytical tests on serum or stool specimens. HAV diagnosis is generally performed by immunoglobulin (Ig) anti-hepatitis A antibody tests, IgM or IgG, in which an increase in virus-specific serum antibody titers is indicative of a recent HAV infection. One notable limitation for these antibodybased tests is that they cannot readily distinguish a recent HAV infection from increased antibody titer due to immunization, which can lead to elevated IgG and/or IgM being elicited against HAV. In addition to antibody testing, which also includes the use of immunoelectron microscopy, the use of molecular tests premised on reverse transcription polymerase chain reaction (RT-PCR) can also be utilized. Commercial kits are available to assist in HAV diagnosis.

Answer 727

All people are considered susceptible to HAV infection. Immunity can be developed by exposure and/or immunization that elicit an immune response that confers long-term immunity. In the U.S., the percentage of adults with immunity increases with age (10% for those 18 to 19 years of age to 65% for those over 50 years old). The increased number of susceptible people allows common-source epidemics to evolve rapidly.

Answer 728

Methods have been developed to detect HAV in the food commodities most often implicated in HAV-associated illnesses; most notably, produce and shellfish. The manner in which the food is analyzed is dependent on the presumed location of contamination. For example, produce methods generally use a method to wash the viruses from the surface, whereas shellfish methods extract the virus from the digestive tract. Following extraction, the viruses are concentrated to suitable levels, so that detection via RT-PCR can be performed. These methods currently used by specialized regulatory laboratories to analyze suspected food for HAV are undergoing rigorous validation to verify that they are suitable for routine analysis.

Answer 729

Hepatitis A is endemic throughout much of the world. Major national epidemics occurred in 1954, 1961, and 1971. Foods continue to be implicated in HAV outbreaks, which continue to occur in the U.S. following consumption of contaminated produce and shellfish. The most notable recent HAV outbreaks, in the U.S., that were associated with foods include:  1987 - Louisville, Kentucky- lettuce (imported)  1998 - Ohio- green onions (Mexico/California)  2000 - Kentucky and Florida- green onions (from Mexico) or tomatoes (California)  2003 - Tennessee, North Carolina, Georgia, Pennsylvania – green onions (Mexico)  2005 - Tennessee, Alabama – oysters (Louisiana) Case Example: In August 2005, at least 10 clusters of hepatitis A illness, totaling 39 people, occurred in four states among restaurant patrons who ate oysters. Epidemiologic data indicated that oysters were the source of the outbreak. Trace-back information showed that the implicated oysters were harvested from a specific Gulf Coast shellfish-growing area. A voluntary recall of oysters was initiated in September. HAV was detected in multiple 25-gm portions in one of two recalled samples, indicating that as many as 1 of every 15 oysters from this source was contaminated (Shieh, 2007).

Answer 730

While hepatitis E Virus (HEV) is considered to be labile when not in the acidic conditions found in the gastrointestinal tract or in fecal material, studies have demonstrated that it can withstand thermal inactivation at temperatures near those expected to be found within a rare-cooked steak (approximately 57°C). HEV is more labile than is the hepatitis A virus (HAV), and the levels of viable virus decrease rapidly at higher temperatures. Repeated freezing and thawing can gradually decrease the levels of any infectious virus, and HEV is no different, but also, perhaps, not worse, when compared with other enteric viruses. Moreover, like other enteric viruses, HEV does not have a lipid envelope, which contributes to its ability to somewhat withstand exposure to alcohols and detergents. HEV does seem especially susceptible to high salt concentration

Answer 731

HEV has a much more extensive host range, including primates, pigs, rats, cattle, chicken, and sheep. Existing microbiological and epidemiologic data suggest a potential role of swine in the human transmission of HEV: global existence of antiHEV seropositive swine, genetic relatedness of swine and human isolates, interspecies transmission of swine and human strains, recovery of HEV from pork products implicated in disease outbreaks, and high seroprevalence levels among swine caretakers.

Answer 732

At least five genotypes exist [human, swine (1-4) and avian (5)], with only a single serotype recognized. Genotype 3 can be found in swine worldwide and is the strain involved in autochthonous transmission resulting in mild, if any, symptoms and disease in humans.

Answer 733

HEV is a known cause of epidemic and intermittent (sporadic) cases of enterically-transmitted acute hepatitis. The disease caused by HEV is called hepatitis E, or enterically transmitted non-A non-B hepatitis (ET-NANBH). Other names include fecal-oral non-A non-B hepatitis, and A-like non-A non-B hepatitis. Hepatitis E was acknowledged as a distinct disease only as recently as 1980. Since there is no specific treatment for hepatitis E, other than treatment of symptoms, prevention is the best course of action. Note: This disease should not be confused with hepatitis C, also called parenterally transmitted non-A non-B hepatitis (PT-NANBH), or B-like non-A non-B hepatitis, which is a common cause of hepatitis in the United States.

Answer 734

Mortality: The fatality rate is 0.5 to 4%, except in pregnant women, in whom casefatality rates can reach 27%. Death usually occurs in those with previous liver disease.

Answer 735

Infective dose: The infective dose is not known

Answer 736

Onset: Incubation period following exposure can range from 3 to 8 weeks, with a mean of 5.7 weeks.

Answer 737

Illness / complications: Hepatitis caused by HEV is clinically indistinguishable from hepatitis A disease. The disease usually is mild and self-resolves in 2 weeks, with no sequelae. However, chronic hepatitis has been reported in organ transplant recipients and in patients with active HIV infections. Epidemiologic studies have established an association between HEV-infected pregnant women and incidences of fatal fulminant hepatic failure.

Answer 738

Symptoms: Symptoms are most often seen in patients between the ages of 15 to 40, but, in younger children, the absence of symptoms, including jaundice, is common and results in infections not being recognized and documented. Symptoms include jaundice, malaise, anorexia, abdominal pain, arthralgia, hepatomegaly, vomiting, and fever.

Answer 739

Duration: Extended viremia and fecal shedding are not typical. The disease usually is mild and self-resolves in 2 weeks, with no sequelae. Virus excretion has been noted as long as 2 weeks after jaundice appears, but peaks during the incubation period, as does viremia. Notably, HEV is shed in lower titers than is HAV.

Answer 740

Route of entry: HEV is transmitted by the fecal-oral route. Person-to-person spread is not common. Pig-organ and human liver transplantations and blood transfusions may also be involved in HEV transmission.

Answer 741

Pathway: The pathogenic pathway for HEV is not completely understood. After the consumption of contaminated food or water, the virus reaches the liver from the intestinal tract, but the exact route and mechanism are not clear. From studies conducted in infected non-human primates and swine, we know that HEV primarily replicates in gall-bladder and liver cells. Replication also has been established in extrahepatic sites, such as the small intestine, lymph nodes, colon, and salivary glands. However, evidence of viral replication has not been documented in the spleen, tonsil, or kidney. Some of the highest virus load has been noted in bile samples. The injury to the liver sometimes noted following infection could be related to triggered immunological responses and (possibly), additionally, to morphological changes (cytopathic effects) caused by the virus invading liver cells.

Answer 742

Epidemic hepatitis E is primarily a disease of concern in developing countries, due to inadequate public sanitation infrastructure (inadequate treatment of drinking water and sewage). Notably, within developing countries, the majority of sporadic cases of viral hepatitis can be attributed to HEV, rather than to the other major hepatotropic viruses (hepatitis A, B, or C). Major waterborne epidemics have occurred in Asia and North and East Africa. Locally acquired (autochthonous) cases of hepatitis E in industrialized countries, including the U.S. and Europe, are increasing. Seroprevalence studies in the U.S. and Europe report a 1% to 25% prevalence of HEV antibodies in healthy individuals. Reports suggest that cases of HEV disease in industrialized countries are autochthonous, largely overlooked, segregate into genotype III, and lack a precise source of infection.

Answer 743

Waterborne and foodborne transmission have been documented. For example, zoonotic spread involving group consumption of undercooked wild boar meat has been recognized in Japan, and viable HEV has been recovered from commercially sold pork livers in the U.S. Infectious HEV also has been isolated from swine feces and stored waste material. Food safety concerns arise when human and swine agricultural waste is used for irrigation of produce, such as tomatoes and strawberries, likely to be eaten raw and potentially without washing, or when such waste contaminates waters where shellfish are harvested. Evidence exists that implicates shellfish as a foodborne source of infection for two of the eight cases of HE identified in the UK, in 2005. In Europe and the U.S., HEV has been recovered from municipal sewage. Figatellu, a pig liver sausage commonly eaten raw in France, also has been recently implicated in hepatitis-E-related disease. Because of the increasing trend in the U.S. to both hunt and eat wild boar meat and evidence suggesting that these animals can harbor HEV, the proper handling of the carcass and thorough cooking of any meat should be considered.

Answer 744

Diagnosis of HEV disease is based on the epidemiologic characteristics of an outbreak and by exclusion of hepatitis A and B viruses by serological tests. Confirmation requires identification of the 27-34 nm virus-like particles, by immune electron microscopy, in feces of acutely ill patients or by molecular detection of genomic RNA in serum or feces. Because of the dangers of rapidly progressing, severe disease in pregnant women, hospitalization should be considered. Since HEV infection can often cause mild, if any, symptoms in immunocompetent individuals, this disease is largely under-diagnosed in developed countries

Answer 745

The disease is most often seen in young to middle-age adults (15 to 40 years old). Pregnant women appear to be exceptionally susceptible to severe disease, and excessive mortality has been reported in this group. Immunocompromised people are at risk of chronic HEV disease. High anti-HEV seroprevalence rates have been seen in those occupationally in close contact with swine

Answer 746

Human rotaviruses (HRV) are quite stable in the environment and have been found in estuary samples at levels as high as 1 to 5 infectious particles/gallon. Sanitary measures adequate for bacteria and parasites seem to be ineffective for endemic control of rotavirus, as similar incidence of rotavirus infection is observed in countries with both high and low health standards. Rotaviruses are stable in a wide pH range, with the infectivity being unaltered at pH of 3 to 11, but rapidly inactivated at pH of 2.5 and below or at 11.5 and above. They are stable at low temperatures of -20°C and 4°C, with minimal loss of titer after 32 days, and are stable during 6 freeze / thaw cycles. Rotaviruses are stable for up to 4 days at 37°C and rapidly inactivated at 56°C. Rotaviruses are inactivated by UV light and by disinfectants, including chlorine, H202, and ethanol. These viruses belong to a genus of doublestranded RNA viruses in the Reoviridae family. They have a genome consisting of 11 double-stranded RNA segments surrounded by three protein layers. The outer protein layer is composed of VP4 and VP7; the middle layer is composed of VP6; and an inner layer is composed of VP2. Six serological groups have been identified, three of which (groups A, B, and C) infect humans.

Answer 747

Mortality: Childhood mortality caused by rotavirus is relatively low in the U.S., with an estimated 20 to 60 deaths per year, but reaches approximately 0.5 million deaths per year, worldwide. A recent CDC report estimates that, in the U.S., there are zero deaths annually from domestically acquired rotavirus.

Answer 748

Infective dose: The infective dose is presumed to be 10 to 100 infectious viral particles.

Answer 749

 Onset: The incubation period for rotavirus is estimated to be less than 48 hours.

Answer 750

Illness / complications: Rotaviruses cause acute gastroenteritis, usually with complete recovery. Infantile diarrhea, winter diarrhea, acute nonbacterial infectious gastroenteritis, and acute viral gastroenteritis are names applied to the infection caused by the most common and widespread group A rotavirus. Temporary lactose intolerance may occur. Rotavirus is shed in large numbers (1012 infectious particles/ml of feces) before, and for several days after, symptoms resolve. Infectious doses can be readily acquired through contaminated hands, objects, or utensils. Asymptomatic rotavirus excretion has been well documented and may play a role in perpetuating endemic disease.

Answer 751

Symptoms: Rotavirus gastroenteritis has symptoms ranging from self-limiting, mild, watery diarrhea, with complete recovery, to severe disease characterized by vomiting, watery diarrhea, and fever, which can lead to dehydration, hypovolemic shock, and, in severe cases, death. Symptoms often start with a fever (greater than 101ºF) and vomiting, followed by diarrhea. Severe diarrhea without fluid and electrolyte replacement may result in severe dehydration and death. Association with other enteric pathogens may also play a role in the severity of the disease.

Answer 752

Duration: Diarrhea generally lasts 3 to 7 days

Answer 753

Route of entry: Rotaviruses are transmitted via the fecal-oral route. Infected food handlers may contaminate foods that require handling without further cooking. However, person-to-person spread through contaminated hands is probably the most important means by which rotaviruses are transmitted in close communities, such as pediatric and geriatric wards, day-care centers, and family homes.

Answer 754

Pathway: Rotavirus infects the mature absorptive enterocytes in the ileum and causes diarrhea by virus-associated cell death and release of a non-structural protein, which may trigger an intracellular calcium-dependent signaling pathway. Rotavirus may activate secretomotor neurons of the enteric nervous system that stimulate secretion of fluids and solutes.

Answer 755

Group A rotavirus is endemic worldwide and is the leading cause of severe diarrhea among infants and young children, accounting for about half of the cases requiring hospitalization. More than 3 million cases of rotavirus gastroenteritis occur annually in the U.S.; of these, 15,433 cases are foodborne, according to a recent estimate by the Centers for Disease Control and Prevention (CDC). In temperate areas, it occurs primarily in the winter, but in the tropics, it occurs throughout the year. The number of cases attributable to food contamination is unknown, but this route of transmission is thought to be rare. After the introduction of a vaccine for rotavirus in 2006, the CDC found that rotavirus activity during 2007 and 2008 was substantially lower than that reported during 2000-2006. Group B rotavirus, also called adult diarrhea rotavirus or ADRV, has caused major epidemics of severe diarrhea affecting thousands of persons, of all ages, in China. Group C rotavirus has been associated with rare and sporadic cases of diarrhea in children in many countries. However, the first outbreaks were reported from Japan and England.

Answer 756

person-to-person fecal-oral spread is the most important means of transmission, but foods such as salads, fruits, and hors d’oevres that do not require further cooking and are handled by an infected food worker also may transmit rotaviruses.

Answer 757

Rotavirus cannot be diagnosed by clinical symptoms alone. Laboratory testing of stool samples is required for a diagnosis of rotavirus, although it is generally not done. The most common laboratory tests that are available are enzyme immunoassays (EIA) and latex agglutinations (LA). EIA is the test most widely used to screen clinical specimens, and several commercial kits are available for group A rotavirus. Other assays include electron microscopy (EM) and culture and molecular techniques, including reverse transcriptase polymerase chain reaction (RT-PCR)

Answer 758

Humans of all ages are susceptible to rotavirus infection. Children 3 months to 2 years old, premature infants, the elderly, and the immunocompromised are particularly prone to more severe symptoms caused by infection with group A rotavirus.

Answer 759

To date, the virus has not been isolated from any food associated with an outbreak, and no satisfactory method is available for routine analysis of food. However, it should be possible to apply procedures that have been used to detect the virus in water and in clinical specimens, such as RT-PCR, to food analysis.

Answer 760

Astroviruses are classified in the family Astroviridae. Human astroviruses (HAstVs);  Sapoviruses (SaV) are classified in the family Caliciviridae ('Star of David'). Enteric adenoviruses (HuAd) are classified in the family Adenoviridae Parvoviruses, including Human Bocavirus (HBoV), are members of the Bocavirus genus of the Parvoviridae, belong to the family Parvoviridae. Aichi virus (AiV) is classified in the family Picornaviridae family as a member of the Kobuvirus genus

Answer 761

Onset: Usually 10 to 70 hours after contaminated food or water is consumed.

Answer 762

Viral gastroenteritis is usually a mild, self-limiting illness. The clinical features are milder, but otherwise indistinguishable from, rotavirus gastroenteritis. Co-infections with other enteric agents may result in more severe illness that lasts longer.

Answer 763

Symptoms: May include nausea, vomiting, diarrhea, malaise, abdominal pain, headache, and fever.  Duration: Generally 2 to 9 days.

Answer 764

Astroviruses cause sporadic gastroenteritis in children under 4 years of age and account for about 4% of the cases hospitalized for diarrhea. Most American and British children over 10 years of age have been found to have antibodies to the virus. Sapoviruses cause a sporadic gastroenteritis similar to norovirus in populations ranging from children to the elderly. The infections are more frequent in children under age 5 than in adults. Enteric adenoviruses cause 5% to 20% of the gastroenteritis in young children and are the second most common cause of gastroenteritis in this age group. By 4 years of age, 85% of all children have developed immunity to the disease. Bocaviruses have been implicated in sporadic cases of gastroenteritis in children and adults, with 0.8 to 9.1% of stools screening positive for bocaviruses. Aichi virus has been associated with sporadic outbreaks in children and adults in Asian countries and Brazil.

Answer 765

Viral gastroenteritis is transmitted by the fecal-oral route via person-to-person contact or ingestion of contaminated foods and water. Food handlers may contaminate foods that are not further cooked before consumption. Enteric adenovirus may also be transmitted by the respiratory route. Shellfish have been implicated in illness caused by many of these viruses.

Answer 766

The target populations for these viruses are young children and the elderly, with sporadic outbreaks occurring among all populations. Infection with these viruses is widespread and seems to result in development of immunity.