Unit 1: Bacterial GI Infections Flashcards
(115 cards)
1
Q
Acute disease due to Vibrio cholerae infection of the GI tract
A
Cholera
Disease is distributed worldwide, cause of massive human morbidity and mortality
2
Q
Clinical manifestation of cholera
A
Bacteria colonize the small intestine mucosa with the colonized mucosa showing NO change in physical integrity
ACUTE AND MASSIVE WATERY DIARRHEA (1L/hour) is the main feature.
3
Q
Rice water stools
A
Cholera
4
Q
Why do you end up dying with cholera?
A
Rapid depletion of fluids and electrolytes leading to hypovolemic shock, metabolic acidosis, and death.
5
Q
Incubation period for cholera
A
1-5 days —> abrupt onset of symptoms
6
Q
SSx of cholera
A
Muscle cramps, poor skin turbot, wrinkled skin over fingers (‘washerwoman hands’), sunken eyes, missing pulse in extremities
Extreme water stools the cause of most of these (b/c dehydration)
7
Q
So what does Vibrio cholerae look like?
A
Gram negative Bent rod shape (vibrio, duh) Nonspore-former Facultative anaerobe Motile, polar flagellum
8
Q
Diagnosing cholera
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Culture!
Final ID is with group specific antisera
9
Q
Treatment of cholera
A
For the majority of patients, successful therapy usually only requires replacement of fluids/electrolytes
Provide by IV route if patient can’t take oral fluids
10
Q
Epidemic cholera is now recognized to be caused by the _____ and ______ types.
A
O-1 and O-139
Other types cause diarrheal disease
11
Q
Cholera is spread through _____________________.
A
Contaminated drinking water (and food)
Not easily spread person-to-person
12
Q
Causative microbes for cholera are found naturally in ____________________
A
Marine coastal areas and estuaries, including the United States Gulf Coast Region.
Asymptomatic human carriers are important as reservoirs
13
Q
Massive cholera epidemics have emerged recently in …
A
Haiti and Yemen
14
Q
Is prophylactic treatment necessary for travelers to cholera endemic regions?
A
Prophylactic tetracycline has been used but NOT typically needed in most people practicing normal hygiene since the infectious dose is high
Primary prevention means is proper control of sewage.
15
Q
Tell me about these awesome new cholera vaccines…
A
Dukoral - oral, O-1 killed whole cells PLUS choleragen toxioid (may also help prevent traveler’s diarrhea due to ETEC)
Shanchol - oral, I valentines O-1 and O-139 killed whole cells
Vaxchora - oral, attenuated (live) O-1 vaccine FOR TRAVELERS
Euvichol - oral, kill whole O-1 and O-139 cells
16
Q
The three vibrio species we discussed
A
V. cholerae
V. parahaemolyticus
V. vulnificus
17
Q
Vibrio species causing a gastroenteritis to a mild cholera-like illness
A
V. parahaemolyticus
18
Q
The most common cause of food-borne illness in Japan
A
V. parahaemolyticus
19
Q
Vibrio species with seasonal infection pattern, organism receding in winter
A
V. parahaemolyticus
20
Q
Where can you find V. parahaemolyticus?
A
Normal inhabitants of coastal ocean and estuary waters
Endemic in US Gulf coast waters, most US cases are frequently associated with mishandling infected seafood (improper refrigeration)
21
Q
Vibrio species associated with oysters
A
V. vulnificus - also a normal inhabitant of coast marine and estuary waters
22
Q
Seasonality of V. vulnificus
A
More common when warm
23
Q
How do V.vulnificus infections normally begin?
A
Wound infections through direct contact of open wound with seawater or oysters
24
Q
How does one get sepsis from V.vulnificus?
A
Consumption of raw oysters —> eruption of bullous skin lesions, shock
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What condition is usually associated with V.vulnificus infection?
History of oyster consumption with suspicion of liver dysfunction (commonly, alcoholism)
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Treatment for V.vulnificus sepsis
Tetracycline
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Apparent from wound infections and sepsis, how else might V.vulnificus present itself?
Acute self-limiting diarrhea associated with raw oyster consumption
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Antigenic classification scheme used to identify pathogenic forms of Escherichia coli
```
O antigen (LPS) = serogroup
At least 160 serogroups exist
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H antigen (flagella) = serotype
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_________ resembles V.cholerae in disease process but usually milder.
ETEC (Enterotoxigenic E.coli)
Adheres to mucosa of small intestine and produces symptoms by elaboration of toxins that induce watery diarrhea
Usually only fatal in infants
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The most typical disease caused by ETEC in the US
Traveler’s diarrhea - partial immunity in adults in endemic/epidemic areas
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_________ vaccine MAY offer some protection against traveler’s diarrhea because ETEC toxin is almost identical to __________.
Dukoral (cholera) vaccine - choleragen toxin
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Diarrhea that becomes bloody after 1-3 days with cramps, vomiting; fever not always present
Enterohemorrhagic E.coli (EHEC)
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Emerging pathogen, only recently recognized as a cause of disease
Enterohemorrhagic E.coli (EHEC)
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Eschericia species which releases Shiga-like toxin (SLT)
Enterohemorrhagic E.coli (EHEC)
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EHEC can be fatal due to ...
hemolytic uremic syndrom (HUS) development
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Predominate form of EHEC
O157:H7
But other strains are now designated as STEC (Shiga toxin producing E.coli) that may also induce HUS
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Complications of O157:H7 EHEC infection
Hemolytic Uremic Syndrom (HUS) - acute renal failure with poor prognosis a few days after bloody diarrhea
HUS only occurs with bacteria that express Shiga toxin (8-10% of O157:H7 infections, higher for O104:H4
More common to see this in elderly and very young patients
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Why are O157:H7 infections not typically treated with antibiotics?
Risk of HUS induction
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What media is used to differentiate O157:H7 for EHEC diagnosis?
MacConkey’s sorbitol agar can differentiate it from normal flora E.coli because the pathogenic strain cannot ferment sorbitol and appears white on the plate while other E.coli strains appear bright red/pink
Use of this agar is NOT necessarily automatic - inform the lab that you suspect a case of O157:H7
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Treatment for O157:H7
Oral rehydration, vigilance for renal function decline
Extreme caution with antibiotics to avoid inducing HUS
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Reservoir for O157:H7
Cattle
Infections are typically associated with beef and raw milk
Undercooked hamburger is classic infection source
Also being discovered in other food (Veggies) - may reflect low level contamination of food processing plants with cow manure
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Person to person transmission of O157”H7 is possible because...
It is an extreme low-dose pathogen
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E.coli O104:H4
New form of Enterogaggregative E.coli that has emerged in Europe, traced to alfalfa sprouts.
HUS production, high case fatality rate
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Campylobacter jejuni microbe description
```
Gram negative
Curved rod (sea gull shaped)
Motile
Microaerophilic
Grows well at 42˚C
```
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Clinical manifestations of campylobacter jejuni infection
Incubation period is 1-7 days
Very commonly patient has prodrome with fever, headache, malaise, myalgia 12-24 hours before diarrhea onset
Enteritis with diarrhea - loose stools to frank dysentery, fever, abdominal pain (cramping)
Self-limiting (improvement after several days)
Convalescent carriage and excretion for 2-3 weeks after disease.
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Microbe associated with prodrom 12-24 hours before the diarrhea
Campylobacter
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Severe acute abdominal pain in lower right quadrant that mimics appendicitis
Campylobacter
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Primarily reservoir for campylobacter
Intestinal tract of animals, BIRDS especially and transmission by food source primarily
Poultry products are frequently contaminated
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Eating undercooked chicken is the classic way to get this disease
Campylobacter
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This GI pathogen is unusual in that the highest infection rate is in young adults
Campylobacter
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Campylobacter infections peak when?
Summer months
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Complications of Campylobacter infection
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Reiters syndrome (urethritis, polyarthritis, conjunctivitis)
In HLA-B27 individuals, mostly males
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Guillain-Barré syndrome
Paralytic syndrome due to immune attack on myelinated peripheral nervous system tissues
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Chief known precipitation of Gillian-Barre paralytic syndrome
Campylobacter jejuni
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Important clues to diagnosing Campylobacter
Fever and prodrome
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Treatment for Campylobacter
Erythromycin
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Overview of H. Pylori
Chronic active gastritis and peptic ulceration
Gram negative, curved rods
Highly motile
Copious production of urease
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Clinical manifestations of H.pylori infections
Epithelial cells of pylori are primary targets
Gastritis, cramps, halitosis, nausea, and vomiting
Eradication of bacteria is not necessarily correlated with relief of symptoms
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H.pylori virulence factors
Urease - produces CO2 and NH4+ that raises pH and protects H.pylori - allows infection to be detected
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Source/reservoir of H.pylori
Probably humans
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Risks/associations for H.pylori
Smoking is a risk factor
Association with stomach adenocarcinoma
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Diagnosis of H.pylori
Histology also detection in biopsy samples plus culture
CLO test - detection of urease activity in biopsy tissue by pH change
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H.pylori treatment
Optimal abx therapy not yet evolved
Combo of antibiotics (tetracycline) pluse bismuth-containing drugs
Patient may be re-infected after antibiotic eradication (by family/contacts)
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Clinical manifestations of shigella infections
Facultative intracellular enteric bacilli causing an inflammatory disease of the large bowel
Invades and multiplies in colon epithelial cells
Incubation period is 72 hours
Disease ranges from moderate diarrhea to severe dysentery
Initial symptoms - fever, cramps, vomiting, watery diarrhea which progresses to dysentery in severe forms - blood, mucous and PMN’s in stools, fever, cramps
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Description of shigella
```
Gram negative rods
Nonspore-former
Facultative anaerobe
Nonmotile (usually)
Lactose nonfermenting
```
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How to diagnose shigellosis
Suspect in any patient with fever and diarrheal disease
Blood and mucous in feces plus acute onset suggest invasive disease
PMNs and RBCs on microscopic exam of feces suggest invasive disease but not seen in diarrhea caused by enterotoxins
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What is special about culturing shigella?
Must plate samples QUICKLY
Choice of precise sample influences probability of success
Blood-tinged flecks of mucus are ideal samples for the micro lab
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Treatment of shigella
Usually self-limiting in otherwise healthy patients
Fluid replacement
Effective antibiotic therapy may shorten course and eliminate carrers but is problematic b/c many shigella are multiple antibiotic resistant
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Complications of shigella
Shedding during convalescence is typical and long-term carrier state is possible
Reiter’s syndrome in HLA B27 individuals (nonspecific acute inflammatory arthritis)
Hemolytic uremic syndrome (HUS)
S.dysenteriae (type 1 infection) is a Shiga toxin producer
Acute renal failure with poor prognosis
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Types of bacteria that have Reiter’s syndrome as complications
Shigella (esp S.dysenteriae)
| Campylobacter
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_______ are the soles reservoir for the shigella species
Humans
Person-to-person is the primary mode of transmission
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The four species of Shigella
Group A - S.dysenteriae
Group B - S.flexneri
Group C - S.boydii
Group D - S.sonnei
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In the US, cases are primarily due to which two species of shigella
S.flexneri and S.sonnei
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Age group most susceptible to shigella
Children age 1-4
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Shigella prevention
Hand washing in the single most important control measure
Education
Supervised hand washing for kids
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Salmonella microbes are the normal gut flora of _____
Birds and other animals
Human infection is primarily through food contamination
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Clinical manifestations of salmonella infections
Incubation of 12-48 hours
Sudden onset of disease - fever, chills, cramps, diarrhea, vomiting
2-3 days duration in normal host
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Patients at greater risk for Salmonella infection
```
Infants
The elderly
Cancer patients
AIDS patients
Diabetics
Persons on abx therapy
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Description of salmonella microbes
```
Gram negative rods
Nonspore-former
Facultative anaerobe
Motile
Lactose nonfermenting
```
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What’s special about salmonella nomenclature
Serological variants (“serovars”) are named as if they are true species
Salmonella typhi —> Typhoid fever
Salmonella typhimurium —> food poisoning
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Diagnosis of salmonella
Sample any food remaining to culture
Fecal matter
Blood if fever is evident (but might not be present in blood if in peak of fever)
Fluorescent Antibody (FA) tests allow for rapid and accurate serological confirmation - each isolate is typed by state lab personnel
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Treatment of salmonellosis
Supportive therapy for patients of otherwise normal good health
Maintain fluid and electrolytes
Abx not required if disease is not systemic - AIDS patients require special care
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Primary reservoirs for salmonella
```
Animals/foods of animal origins:
• Eggs
• Beef products and cattle
• Pigs and pork products
• Also companion animals and pets
```
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Usual route for infection with salmonella
Contaminated food or water
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Peaks of incidence for salmonella
Infants more susceptible - highest incidence in infants and children 6 months to 5 years
Infection has a strong seasonal trend - sharp increases are evident in summer and fall
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Convalescent salmonella patients
A convalescent carrier state is recognized, 1-2 months duration, infants may shed for up to a year
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Reasons why salmonella infections are increasing
Food processing changes - shift to large scale facilities increases risk of massive common source outbreaks
“Modified atmosphere packaging” intended to keep produce fresh-looking promotes growth of pathogens
Changing consumer preferences for fresh food items (ie salads) has led to more cases by cross-contamination
Changes in animal husbandry promote pathogen colonization/transfer
• Feeding of slaughterhouse remains and fish meal to chickens
• Chicken infections lead to egg contamination in utero, so even an untracked egg is unsafe
87
Why are most eggs pasteurized in the US now?
Chicken infections with salmonella can lead to egg contamination in utero - even an uncracked, clean egg can be unsafe
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What is pseudomembranous colitis?
An antibiotic-induced disease caused by Clostridium difficile
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Description of C.diff microbe
Gram positive bacillus
Anaerobic
Spore former (subterminal)
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Clinical manifestations of C.difficile
Difficult to distinguish from ulcerative colitis, crohn’s disease, chronic IBD on clinical findings alone
Three types of disease resulting from C.difficile are at issue:
A. Diarrhea with lower abdominal cramping - no systemic symptoms
B. Severe colitis w/o pseudomembrane - profuse diarrhea, pain, and systemic symptoms (fever, nausea, malaise, dehydration)
C. CLASSIC PSEUDOMEMBRANOUS COLITIS (PMC) - same suite of symptoms for severe colitis, with elevated yellowish plaques 2-10mm over inflamed regions of mucosa
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PMC diagnosis
Detection of toxin in feces
Gram stain of stool will reveal gram positive rods with subterminal spores
Culture
Many hospitals screen all abx-associated diarrhea patients for toxin
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PMC treatment
Fluid and electrolyte replacement
Discontinue abx therapy
Administer new abx (oral vanco or metro)
Experimental treatment based on reconstitution of bowl flora undergoing trial
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PMC complications
A significant fraction of patients (10-20%) will relapse and some will suffer multiple relapses
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Main predisposing factor for C.difficile
Disruption of normal gut flora (secondary to abx treatment) —> subsequent colonization by C.diff and release of toxins
10% of pop carries C.diff bacteria as normal flora w/o problem
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Clostridium perfringens type A is a common cause of ...
Acute food borne diarrheal disease in the US
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What does C.perfringens typeA look like?
```
Gram positive
Rod shaped
Nonmotile
Anaerobe (aerotolerant)
Spore-former
```
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Clinical manifestations of C.perfringens type A infections
Short incubation period
Moderate severe diarrhea, abdominal cramping (no vomiting)
Complete recovery in a day
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Epidemiology of clostridium perfringens
Common member of gut flora of humans and animals
Consumption of grossly contained meat/poultry. Contaminated meat with cooking that is inadequate to destroy spores; food is allowed to stand w/o refrigeration, enabling spores to germinate; When vegetative cells are eaten, stomach acid induces sporulation and producation of enterotoxin
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Diagnosing clostridium perfringens
Onset and course of disease is FAST
HIGH dose organism
Detection of large numbers of this microbe in food and feces
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Treatment for Clostridium perfringens
Fluid replacement if necessary
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Description of Bacillus cereus
Gram positive
Rod shaped
Aerobic
Spore former
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Two disease forms observed involving B.cereus...
1) Emetic form - preformed toxin is ingested, causing GI symptoms 1-5 hours after ingestion of contaminated food (vomiting, cramps, diarrhea)
2) Diarrheal form - Ingestion of large numbers of vegetative cells that produce enterotoxin after exposure to stomach acid; Abdominal pain, profuse watery diarrhea 1-17 hours after ingestion of contaminated food.
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Treatment of B.cereus infection
Relief of symptoms
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Diagnosis of B.cereus
Afebrile disease with a fast onset and course
High index of suspicion if upper GI illness is evident 1-5 hours after eating or lower illness 5-17 hours after eating
B.cereus disease is often confused with clostridial or staph food poisoning
To Dx, isolate more than 10^5 B.cereus per gram of food or feces
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Spores of Bacillus cereus are commonly found on ...
grains and vegetables, esp rice
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Prevention of B.cereus infection
Prevent poisoning sequence by proper food handling. Prompt refrigeration of all grain foods after cooking.
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__________ is second only to Salmonella as a cause of food borne disease
Staphylococcal food borne diseases
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Staphylococcal GI disease is caused by...
Consumption of heat stable preformed toxin in foods
Under the proper set of conditions, it is possible to have disease without colonization or infection of the host with this agent
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Clinical manifestations of staphylococcal infections
Acute emetic and diarrheal disease caused by the ingestion of preformed heat stable toxin
Short incubation period of 1-6 hours after food consumption
Nausea, vomiting, diarrhea, cramps, acute salivation
Self-limiting - complete recovery in 1-4 days
110
Primary virulence factor for staphylococcal infections
Enterotoxin A - water soluble, heat stable (tolerates boiling for 30 min)
Emetic response is elicited by this toxin - absorbed in gut, stimulus reaches CNS and sends impulse to the vomiting center
Diarrheal effects - enhanced fluid transmucosal movement into lumen coupled with decreased water absorption
111
The source of staphylococcal GI infections
Humans are the source of the organisms and accidentally inoculate food during preparation.
Toxin is undetectable in food, the food quality appears fine, there is no smell or bad taste.
Toxin produced quickly in warm conditions in a few hours
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Diagnosis of staphylococcal intoxication
Afebrile disease, not directly communicable
High index of suspicion with short time between eating and symptoms eruption
Custard filled baked goods, canned foods, processed meats, potato salad
Enterotoxin tests are available and reliable
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Treatment of staphylococcal intoxication
Symptomatic relief
Abx are of no benefit b/c it’s an intoxication, not infection
Toxemia like this are short duration since no additional growth of organism/production of toxin will occur after food ingestion
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Prevention of staphylococcal intoxication
Examination of food handlers
| Proper refrigeration
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Common characteristics of food borne diseases
Staphylococcus, B.cereus, C.perfringens
Abx not useful, because they’re all intoxications
Not directly transmissible between patients
Afebrile
Toxemia - fast onset and course
Common factors - inadequate cooking, re-heating, or refridgeration of foods
