Round 2 Flashcards
(245 cards)
1
Q
Initial upper GI bleed management
A
Remember ABC’s
Airway?
CPR?
IV access
At least 2 large bore IVs
Infusion
Crystalloid
Blood products
2
Q
Varices
A
Presentation: Dramatic bleeding, usually hematemesis
Causes: Portal hypertension
Associated with: Liver disease/cirrhosis
Treatment: Octreotide or Vasopressin Proton Pump inhibitor Non-selective Beta-blocker Variceal band ligation
3
Q
Responsible for tolerance
A
Treg cells
4
Q
NSAIDs and Peptic Ulcer Disease
A
Direct injury effects
Systemic effects
COX inhibition and prostaglandin production
Prostaglandins in the gut regulate mucus secretion and basal bicarbonate secretion
Prostaglandins are trophic for gastric epithelia and play role in feedback inhibition of gastric acid secretion
COX-2 selective inhibitors still pose risk for PUD
5
Q
Intraepithelial Barrier
A
Intraepithelial Lymphocytes (IEL) promote barrier repair and are rapidly recruited Majority of IELs express CD8 (recognize MHC class I Ag) Two types of TCR αβ, thymus derived γδ, non-thymic derived 15% of small intestine IEL 40% of colonic IEL Produce keratinocyte growth factor
6
Q
Lamina Propria
A
Reservoir to 70-80% total lymphocytes Predominate T cells are CD4, recognize MHC class II Ag
7
Q
M Cells
A
Some bacteria and viruses cross the epithelial barrier via M Cells
8
Q
α-Defensin
A
Neutrophils, NK cells, Paneth cells
9
Q
β-Defensin
A
Leukocytes and Epithelial cells
10
Q
Paneth Cells
A
Small intestine is lined with villi interspersed with Crypts.
Paneth cells harbor pro-defensin 5
Degranulation occurs following bacteria penetration
11
Q
Type 1 Interferons
A
(IFN-α/β)
Induces MHC Class I expression
Kill Infected Host Cell
12
Q
Natural resistance-associated macrophage proteins
A
remove mn to starve bacteria
13
Q
Calprotectin
A
Broad spectrum scavenger of divalent cations is Calprotectin, S100 protein that sequesters Ca, Fe, Zn and Mn
14
Q
Lipocalin
A
remove lipids to starve bacteria
15
Q
indoleamine 2,3-dioxygenase
A
Tryptophan removal to starve bacteria
16
Q
anti-inflammatory mediators
A
IL-10, IL-1ra
17
Q
pro-inflammatory mediators
A
IFN-gamma, TNF-alpha, IL-12
18
Q
TH1 Lymphocytes
A
Acute Inflammation
19
Q
IFN-γ
A
Acute Inflammation
20
Q
M-1 Macrophage
A
Acute Inflammation
21
Q
IgG
A
Acute Inflammation
22
Q
sIgA
A
Acute Inflammation
23
Q
CTL cells
A
Acute Inflammation
24
Q
NK cells
A
Acute Inflammation
25
TH2
Chronic Inflammation
26
TH17 Lymphocytes
Chronic Inflammation
27
IL-4
Chronic Inflammation
28
IL-17
Chronic Inflammation
29
M-2 Macrophage
Chronic Inflammation
30
IgE
Chronic Inflammation
31
Eosinophils
Chronic Inflammation
32
Basophils
Chronic Inflammation
33
secretory diarrhea
characterized as an infection of the proximal small bowel marked by watery diarrhea that does NOT contain fecal leukocytes. Viruses that cause gastroenteritis do not infect the colon
34
Rotavirus Clinical presentation:
gastroenteritis
35
Norwalk Virus (Norovirus) Clinical presentation:
gastroenteritis
36
Adenovirus Clinical presentation:
gastroenteritis (do not confuse with other serotypes of adenoviruses that cause respiratory tract infections)
37
Rotavirus Pathology:
transmitted via the fecal to oral route. After ingestion of the virus it travels in the GI tract (the virus particle is stable within the low pH of the gastrointestinal system) to eventually infect the villus cells of the proximal small intestine. Here the virus replicates within these cells eventually lysing these cells which leads to the impaired adsorption of carbohydrates and other nutrients. This can lead to vomiting followed by watery diarrhea.
38
Norwalk Virus (Norovirus) Pathology:
fecal to oral transmission usually through direct contact or through contaminated food and water. Causes a local infection and inflammation in the proximal small intestine.
39
Adenovirus Pathology:
fecal to oral transmission. Causes a local infection and inflammation in the proximal small intestine. If inhaled into the lungs some respiratory symptoms can be present.
40
Rotavirus Diagnosis:
stool specimen, serology for the virus. Electron microscopy and RT-PCR also possible.
41
Norwalk Virus (Norovirus) Diagnosis:
not typically done. When done it is through visualization of the virus in stool specimens or PCR/serology of stool and/or vomit specimens.
42
Adenovirus Diagnosis:
PCR detection of the viral genome within a stool sample
43
Rotavirus Treatment:
rehydration (supportive). There is a rotavirus vaccine (live oral attenuated).
44
Norwalk Virus (Norovirus) Treatment:
usually not required because it is self-limited. When done, treatment consists of rehydration (supportive) if there is severe fluid loss. Outbreaks can be minimized through proper food handling, clean water supplies, and hand washing.
45
Adenovirus Treatment:
self-limiting infection in immunocompetent individuals. Supportive care only.
46
Rotavirus
because rotaviruses cause no inflammation, diarrhea has no blood. Infection before 6 months of age is uncommon due to passive IgA immunity from the mother’s colostrum. However, by age 3, almost every individual worldwide (~95%) has been infected and develops lifelong immunity. Virus particle contains a double-layered capsid.
47
Norwalk Virus (Norovirus)
this virus is a major cause of group-related or institutional diarrhea.
48
Adenovirus
major cause of acute infantile gastroenteritis. These serotypes of adenoviruses rarely cause fever or respiratory tract symptoms.
49
bifidobacteria
are among the first colonizers in breast-fed infants
50
Staphylococcus aureus
Gram +CocciCatalase +Coagulase +Also a common infectious agent of surgical wounds and cause of scalded skin syndromein food that sits around for a whileno need for antibiotics for a food borne infection
51
Bacillus cereus
Gram +Large Bacilliendospore-formingFacultative anaerobeMostly motileβ hemolytic Box-car shaped Also frequently found on skin and is a threat in hospitals as it produces biofilms that adhere easily to invasive devices. This produces chronic persistent infection, as the biofilm can periodically release B. cereus into the bloodstreamB. Cereus spores are commonly found in the soil and sometimes in plant foods that are grown close to the ground – such legumes, cereals, spices etc..Spores can survive rice cooking processDuration for both only about 24 hrsBecause of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen. B. cereus in food and vomitus or feces of same serotype Large numbers of B. cereus of serotype known to produce endotoxinOnly necessary when tracking outbreaks
52
Clostridium botulinum
Gram +BacilliSpore-formingObligate anaerobeMotileSpores or toxin are the important issues for transmission of botulism
53
Staphylococcus aureus Symptoms:
Symptoms:nausea, vomiting, stomach cramps, and diarrhea for 1-3 daysAppear 1-7 hrs following ingestion of foodSelf-limiting, once toxin is gone, illness is gone
54
Staphylococcus aureus diagnosis
Positive diagnosis:Toxin-producing S. aureus can be identified in stool or vomitMost 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).Only necessary when tracking outbreaks
55
Bacillus cereus infection
Infection takes two forms:Emetic (vomiting):Diarrheal:Duration for both only about 24 hrs
56
Bacillus cereus Emetic infection
Emetic (vomiting):1 to 6 hours incubationNausea and vomitingresembles the vomiting illness caused by Staphylococcus aureus enterotoxinsCaused by preformed enterotoxin that forms holes in membranesSelf limiting
57
Bacillus cereus Diarrheal infection
Diarrheal:6-15 hours incubationclinically similar to the symptoms of Clostridium perfringens infectionWatery diarrhea and abdominal crampsMechanism: Caused by large molecular weight enterotoxin that causes intestinal fluid secretion, probably by several mechanismsThis toxin is not likely pre-formed!Ingestion of large amounts of bacteria cause it to generate the toxin in the small intestineVulnerable populations might get sicker and require antibioticsPoor outcomes for systemic infection
58
Bacillus cereus diagnosis
Because of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen. B. cereus in food and vomitus or feces of same serotype Large numbers of B. cereus of serotype known to produce endotoxinOnly necessary when tracking outbreaks
59
Botulism
Food borne botulism: ingesting toxinWound botulism: producing toxin Infant botulism: ingested sporesNot really a GI illness, diarrhea not prominent
60
Botulism Diagnosis
Symptoms and history, results of physical exam indicate botulismTests to exclude other causes of the illnessOrganism or toxin in stool sample only indirect evidence
61
Treatment for foodborne botulism
Ventilator if respiratory failure and paralysisAntitoxin if paralysis is not yet completeRemove contaminated food if still likely in gut
62
Botulism toxin
neurotoxinirreversibly blocks the release of acetylcholine from the motoric end plate which results in muscle weakness and paralysisToxin is absorbed from GI tract to bloodstream
63
Symptoms, botulism
Toxin already produced, symptoms can begin when toxin hits GI tractdouble vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness
64
Symptoms, infant botulism
Incubation period, spores have to produce toxin-forming bacterialethargic, feed poorly, are constipated, and have a weak cry and poor muscle toneCan lead to paralysis of respiratory system and other muscles
65
Clostridium perfringens
Gram +BacilliSpore-formingObligate anaerobeNon-motileEnterotoxin binds to receptors in endothelial cell junctions, then generates pores in host mucosa cells.“C. perfringens infection often occurs when foods are prepared in large quantities and kept warm for a long time before serving”
66
Clostridium perfringens Symptoms
Symptoms:Diarrhea and abdominal crampsIncubation 6 to 24 hours (typically 8-12)Symptoms last for less than 24 hoursUsually NO fever or vomitingThe illness is not passed from one person to another
67
Clostridium perfringens Positive diagnosis
Positive diagnosis:Detection of toxin or high amounts of bacteria in fecesC. perfringens normally present in the GI tract, the problem is when you ingest a C. perfringens load high enough to produce enough toxin to generate symptoms
68
Clostridium perfringens Treatment
Treatment:Usually self-limiting, but more serious, longer-lasting cases in immunocompromised individuals should be treated to avoid complications
69
Campylobacter jejuni
Gram -Bacilli (Spirilli)microaerophilicMotileCold sensitive (often leads to false negatives)get it from poultryOne unique feature is that campylobacter cannot usually multiply in food.Symptoms:diarrhea, cramping, abdominal pain, and fever2-5 day incubationSymptoms can last a weekCan have vomiting, diarrhea can be bloodyMechanism: Symptoms are an inflammatory response to cell invasionPositive Diagnosis: stool culturePossible complication: Guillain-Barré syndrome
70
Salmonella enterica
Gram -BacilliNon spore formingH2S positive & lactose negativeMotile, flagellated
71
Salmonellosis
Symptoms:diarrhea, fever, and abdominal cramps 12 hr to 3 day incubationSymptoms typically last 4 to 7 daysMost persons recover without treatmentRemember: reactive arthritis as a possible complicationDiagnosis: we know for sure with a stool cultureTreatment: Hydration. Antibiotics only necessary if infection spreads beyond gut
72
Vibrio parahaemolyticus
Gram (-)Vibrio (curved rod)facultative anaerobesFlagellated, motileOxidase +water lovingDiagnosis: Vibrio may be isolated from cultures of stool, wound, or blood. Form pores in red blood cells but also in epithelial cells, disrupting gut homeostasissushi and shellfish
73
Vibrio parahaemolyticus Symptoms
Fairly mild bloody diarrhea, stomach cramps, fever, nausea, and/or vomiting, Symptoms last less than a week. In the immunocompromised, it can spread to the blood and cause serious or deadly infections in other parts of the body
74
Listeria monocytogenes
Gram positive rod-shaped bacteriaAlthough a rare illness, a leading cause of death by foodborne illnessGram (+)BacillusNon-fastidious!!!Flagellated, motileNon spore formingOxidase -Diagnosis: Stool sample ID inappropriatePositive ID is the bacterium found in a normally sterile siteImmune cells spread Listeria to other organsTrojan horseLiver is a major targetmilk, cheese, seafood, deli
75
Listeriosis
Mild GI infection for mostMore vulnerable are older adults, pregnant women, newborns, and adults with weakened immune systems OPPORTUNISTICFever and muscle aches or stiff neck, or if you develop while pregnant: fever and chillsMeningitis and sepsis in vulnerable populations
76
Shigella
Gram (-)BacillusFacultative anaerobenonmotile (distinguishes from e. coli)Non spore formingMainly lactose negative, H2S (-) (distinguishes from e. coli)Shigella sonnei: most Shigella-caused GI illnessesShigella flexnori: causes bacillary dysenteryShigella dysenteriae: rarest but most severe dysenteryinvade through m cellsSince Shigella is invasive, if not treated it can spread beyond the GI tract and cause complicationsAntibiotics for more severe cases, most usually resolve without antibioticsPossible complication: hemolytic uremic syndrome (HUS)
77
What is dysentery
Frequent, small bowel movements with blood and mucus, accompanied by rectal pain and spasms (tenesmus)
78
Shigella Transmission
Transmission: Mostly bacterium passing from stools or soiled fingers of one person to the mouth of another person.
79
Shigella Symptoms:
Symptoms: diarrhea (often bloody)feverstomach crampsSymptoms start 1-2 days following exposureUsually resolves in 5 to 7 days.
80
E. coli
Gram (-)BacillusFacultative anaerobemotileNon spore formingMainly lactose positiveDiarrheaUrinary tract infectionNeonatal sepsisGram-negative sepsisETECSTECTreatment: antibiotics generally not recommended (decaying bacteria release toxins)Tracking outbreaks: commercial PCR and antibody-based kits.
81
ETEC
Traveler’s Diarrhea, diarrhea in childrenactivates adenylate cyclase, end result water into lumen, NO bacterial penetration.
82
STEC
penetrates like Shigilla toxin. hemorrhagic colitis (HC) and/or HUS can result as a complication; children more vulnerable
83
E. coli Symptoms:
profuse watery diarrhea and abdominal crampingCan progress to bloody diarrhea for STECFever, chillsNausea with or without vomiting, loss of appetiteLess common: headache, muscle aches and bloatingIncubation:1-3 days ETEC, 3-8 for STEC Illness typically lasts 3-4 days, less than 10.
84
cholera toxin
Activates adenylate cyclase cAMP → Na+ absorption, Cl- excretionWater moves into lumen
85
typhoid fever
Only fecal-oral contaminant, no other host, so water is a big source of contaminatonDrinking water, unwashed fruits/veggiesTravelers are vulnerableVaccine availableLife-threatening illnessIn GI tract and then to bloodstreamHigh fevers (103-104 °F)Weakness and headacheStomach pains, loss of appetite, diarrhea or constipation Sometimes, a rash of flat, rose-colored spotsAfter symptoms clear, person could become a carrierAntibiotic treatment is recommended
86
High inoculum organisms
Tens of thousands or more neededExamples: Vibrio cholerae, C. perfringens
87
Clostridium difficile
Gram +BacilliSpore-formingObligate anaerobeMotileMakes exotoxinsantibiotic diarrhea
88
Giardia lamblia
Also most common intestinal parasite in USGiardiasis (aka Beaver Fever) is the foe of backpackers/hikersSymptoms for 1-2 weeks or more, may seem to resolve and then come backMechanism: presence of parasite causes loss of epithelial absorptive surface area. Trophozoites: Attachment but not penetrationFoul-smelling diarrheaFilter water in areas where Giardia cysts are likely to exist. Water does not need to be contaminated with human sewage. Wildlife can deposit cysts.
89
Cryptosporidium parvum
Often seen when a sanitation system failsPool/waterpark chlorination/UV treatmentStorms or issues with drinking waterDiarrhea symptoms for 1-2 weeks to ~30 days, may seem to resolve and then come backMechanism: Absorption impaired and secretion enhanced when intestinal epithelial cells are infected by Cryptosporidium“Crypto” is opportunisticHIV/Immunocompromised individualsChronic Diarrhea/fluid lossCan be fatalWatery, frequent, non-bloody stoolDisrupts epithelial microvilli, slides into host cells, enveloping itself in the host cell membraneOocysts to sporozoites and backCoccidia subclass
90
Entamoeba histolytica
AmebiasisMore prevalent in tropical/subtropical climatesOnly 10-20% of infected individuals will become ill (CDC)Of US population, male homosexuals most vulnerableBloody, mucus-ey loose stoolRelatively mild symptoms butCan invade the liver and form an abcessX-ray/ultrasound to detect abscess or tissue damageCysts in stool sample. Must differentiate from non-pathogenic entamoeba, takes a specialist.cytotoxic
91
Metronidazole, Tinidazole
Tissue antiparasitic- low concentration in intestine, oral dose almost completely absorbed with high bioavailabilityDespite this, it is the drug of choice to treat symptomatic Giardia infection, even though organism that does not penetrate the epithelium!!Reminder: all about metronidazole/Tinidazole in lectures relating to treatment of H. pyloriDisulfiram reaction, avoid alcoholDisturb normal GI florabreaks down into toxic metabolites, damages DNA
92
Nitazoxanide
Mechanism: Interferes with pyruvate::ferredoxin oxidoreductase enzyme dependent electron transfer, essential to anaerobic energy metabolism protein Selectivity: Species difference in electron transferDistribution: Rapidly metabolized to tizoxanide. Parent compound is not detected in plasma. Moderately absorbed (33%), primarily luminal. For Crypto, used in combination with retroviral therapy for AIDS patients if at all, because of ineffectiveness
93
Iodoquinol
Mechanism: UnknownToxicity: loss of visual acuityUse with caution in patients with thyroid disease – its use interferes with certain thyroid testsDistribution: only 10% of the drug is absorbed so it works locally on the protozoa including cysts in the GI tract, luminal antiparasitic (amebicide)
94
Paromomycin
Mechanism: Aminoglycoside- targets 30S subunit ribosomeToxicity: Diarrhea, other GI effects including issues with intestinal flora because it has activity against some bacteria.Distribution: Luminal antiparasitic- Minimal absorption after oral administrationOtotoxicity, nephrotoxicity
95
TMP-SMX
Spectrum: Broad spectrum, many bacteria, but also effective against apicomplexans including Toxoplasma and Cystoisospora (formerly Isospora), and Cyclosporahits folic acid system
96
Enterobius vermicularis
Staple-sized wormspinwormsWorldwide distribution, most common helminth infection in USPrevalence can reach 50% in children, caregivers of infected children, and institutionalized individuals.Symptom: perianal pruritisAcquired by ingestion of pinworm eggsEggs can remain viable on surfaces for 2-3 weeks
97
Necator americanus/Ancylostoma duodenale
Pruritic Papular Erythematous RashHookworms are bloodsuckers…Major symptom is iron-deficiency anemia¼ ml/day/worm
98
Strongolides stercoralis
Autoinfection possible, especially with Immunosuppressed individualsStomach and GI complaintsRespiratorydry coughthroat irritationSkinan itchy, red rash that occurs where the worm entered the skinrecurrent raised red rash typically along the thighs and buttocks.
99
Trichuris trichiura
Diagnosis:Eggs in feces have a characteristic barrel-shaped appearanceFinger clubbing best indicator ofseverity of infestationBloody diarrhea = iron deficiency anemiaHeavy cases:Frequent, painful stools with mucus, water and blood, tenesmusRectal prolapse
100
Ascaris lumbricoides
Disease: ascariasisDisease: IF symptoms are experienced, abdominal discomfortIf a severe case, intestinal blockagesUltrasonography and radiology to determineHas a lung stage of life cycle, may cause coughDiagnosis: eggs w/thick shells
101
Albendazole and Mebendazole
Broad-spectrum benzimidazole drugsRoundworms and tapewormsDistribution: Limited oral absorption, albendazole is better absorbed if targeting tissue-migrating larvae is importantBroad-spectrum benzimidazole drugsMechanism: Binds to parasite β-tubulin and inhibits the formation of microtubulesDeath can take several days, for some helminths more than one dose may be necessarySpecificity: differences in tubulinToxicity: Systemic toxic affects on liver/bone marrow rareAbdominal pain, nausea, dizziness, headacheEmbryotoxic and teratogenic in pregnant ratsEvidence suggests safe for use in children when warranted
102
Pyrantel pamoate and Levamisole
Mechanism:Levamisole selectively opens a restricted subgroup of nematode acetylcholine receptor (AChR) ion channels in nematode nerve and muscle. depolarization entry of calcium through the opened channels, and an increase in sarcoplasmic calcium, producing spastic muscle contraction the parasite is then unable to maintain its location (often in the intestine) and is then swept away, effecting the cure. Toxicity: Causes nausea, vomiting, diarrheaDistribution: Poorly absorbed
103
Ivermectin
Mechanism: Binds to glutamate-gated chloride channels in invertebrate nerve and muscle cells, causing deactivation of channel: worm paralysis and death by starvationResistance: efflux transportersToxicity:Generally well-tolerated Itching, swollen lymph glands and rarely dizzinessInflammatory reaction due to death of adult wormsSpecificity: This type of channel restricted to phyla Nematoda and Arthropoda. in humans are only in the CNS , Doesn’t cross blood-brain barrierSpectrum: Nematodes- Ascaris, Strongyloides and Onchocerca
104
secretory diarrhea
characterized as an infection of the proximal small bowel marked by watery diarrhea that does NOT contain fecal leukocytes. Viruses that cause gastroenteritis do not infect the colon
105
Rotavirus Clinical presentation:
gastroenteritis
106
Norwalk Virus (Norovirus) Clinical presentation:
gastroenteritis
107
Adenovirus Clinical presentation:
gastroenteritis (do not confuse with other serotypes of adenoviruses that cause respiratory tract infections)
108
Rotavirus Pathology:
transmitted via the fecal to oral route. After ingestion of the virus it travels in the GI tract (the virus particle is stable within the low pH of the gastrointestinal system) to eventually infect the villus cells of the proximal small intestine. Here the virus replicates within these cells eventually lysing these cells which leads to the impaired adsorption of carbohydrates and other nutrients. This can lead to vomiting followed by watery diarrhea.
109
Norwalk Virus (Norovirus) Pathology:
fecal to oral transmission usually through direct contact or through contaminated food and water. Causes a local infection and inflammation in the proximal small intestine.
110
Adenovirus Pathology:
fecal to oral transmission. Causes a local infection and inflammation in the proximal small intestine. If inhaled into the lungs some respiratory symptoms can be present.
111
Rotavirus Diagnosis:
stool specimen, serology for the virus. Electron microscopy and RT-PCR also possible.
112
Norwalk Virus (Norovirus) Diagnosis:
not typically done. When done it is through visualization of the virus in stool specimens or PCR/serology of stool and/or vomit specimens.
113
Adenovirus Diagnosis:
PCR detection of the viral genome within a stool sample
114
Rotavirus Treatment:
rehydration (supportive). There is a rotavirus vaccine (live oral attenuated).
115
Norwalk Virus (Norovirus) Treatment:
usually not required because it is self-limited. When done, treatment consists of rehydration (supportive) if there is severe fluid loss. Outbreaks can be minimized through proper food handling, clean water supplies, and hand washing.
116
Adenovirus Treatment:
self-limiting infection in immunocompetent individuals. Supportive care only.
117
Rotavirus
because rotaviruses cause no inflammation, diarrhea has no blood. Infection before 6 months of age is uncommon due to passive IgA immunity from the mother’s colostrum. However, by age 3, almost every individual worldwide (~95%) has been infected and develops lifelong immunity. Virus particle contains a double-layered capsid.
118
Norwalk Virus (Norovirus)
this virus is a major cause of group-related or institutional diarrhea.
119
Adenovirus
major cause of acute infantile gastroenteritis. These serotypes of adenoviruses rarely cause fever or respiratory tract symptoms.
120
bifidobacteria
are among the first colonizers in breast-fed infants
121
Staphylococcus aureus
Gram +CocciCatalase +Coagulase +Also a common infectious agent of surgical wounds and cause of scalded skin syndromein food that sits around for a whileno need for antibiotics for a food borne infection
122
Bacillus cereus
Gram +Large Bacilliendospore-formingFacultative anaerobeMostly motileβ hemolytic Box-car shaped Also frequently found on skin and is a threat in hospitals as it produces biofilms that adhere easily to invasive devices. This produces chronic persistent infection, as the biofilm can periodically release B. cereus into the bloodstreamB. Cereus spores are commonly found in the soil and sometimes in plant foods that are grown close to the ground – such legumes, cereals, spices etc..Spores can survive rice cooking processDuration for both only about 24 hrsBecause of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen. B. cereus in food and vomitus or feces of same serotype Large numbers of B. cereus of serotype known to produce endotoxinOnly necessary when tracking outbreaks
123
Clostridium botulinum
Gram +BacilliSpore-formingObligate anaerobeMotileSpores or toxin are the important issues for transmission of botulism
124
Staphylococcus aureus Symptoms:
Symptoms:nausea, vomiting, stomach cramps, and diarrhea for 1-3 daysAppear 1-7 hrs following ingestion of foodSelf-limiting, once toxin is gone, illness is gone
125
Staphylococcus aureus diagnosis
Positive diagnosis:Toxin-producing S. aureus can be identified in stool or vomitMost 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).Only necessary when tracking outbreaks
126
Bacillus cereus infection
Infection takes two forms:Emetic (vomiting):Diarrheal:Duration for both only about 24 hrs
127
Bacillus cereus Emetic infection
Emetic (vomiting):1 to 6 hours incubationNausea and vomitingresembles the vomiting illness caused by Staphylococcus aureus enterotoxinsCaused by preformed enterotoxin that forms holes in membranesSelf limiting
128
Bacillus cereus Diarrheal infection
Diarrheal:6-15 hours incubationclinically similar to the symptoms of Clostridium perfringens infectionWatery diarrhea and abdominal crampsMechanism: Caused by large molecular weight enterotoxin that causes intestinal fluid secretion, probably by several mechanismsThis toxin is not likely pre-formed!Ingestion of large amounts of bacteria cause it to generate the toxin in the small intestineVulnerable populations might get sicker and require antibioticsPoor outcomes for systemic infection
129
Bacillus cereus diagnosis
Because of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen. B. cereus in food and vomitus or feces of same serotype Large numbers of B. cereus of serotype known to produce endotoxinOnly necessary when tracking outbreaks
130
Botulism
Food borne botulism: ingesting toxinWound botulism: producing toxin Infant botulism: ingested sporesNot really a GI illness, diarrhea not prominent
131
Botulism Diagnosis
Symptoms and history, results of physical exam indicate botulismTests to exclude other causes of the illnessOrganism or toxin in stool sample only indirect evidence
132
Treatment for foodborne botulism
Ventilator if respiratory failure and paralysisAntitoxin if paralysis is not yet completeRemove contaminated food if still likely in gut
133
Botulism toxin
neurotoxinirreversibly blocks the release of acetylcholine from the motoric end plate which results in muscle weakness and paralysisToxin is absorbed from GI tract to bloodstream
134
Symptoms, botulism
Toxin already produced, symptoms can begin when toxin hits GI tractdouble vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness
135
Symptoms, infant botulism
Incubation period, spores have to produce toxin-forming bacterialethargic, feed poorly, are constipated, and have a weak cry and poor muscle toneCan lead to paralysis of respiratory system and other muscles
136
Clostridium perfringens
Gram +BacilliSpore-formingObligate anaerobeNon-motileEnterotoxin binds to receptors in endothelial cell junctions, then generates pores in host mucosa cells.“C. perfringens infection often occurs when foods are prepared in large quantities and kept warm for a long time before serving”
137
Clostridium perfringens Symptoms
Symptoms:Diarrhea and abdominal crampsIncubation 6 to 24 hours (typically 8-12)Symptoms last for less than 24 hoursUsually NO fever or vomitingThe illness is not passed from one person to another
138
Clostridium perfringens Positive diagnosis
Positive diagnosis:Detection of toxin or high amounts of bacteria in fecesC. perfringens normally present in the GI tract, the problem is when you ingest a C. perfringens load high enough to produce enough toxin to generate symptoms
139
Clostridium perfringens Treatment
Treatment:Usually self-limiting, but more serious, longer-lasting cases in immunocompromised individuals should be treated to avoid complications
140
Campylobacter jejuni
Gram -Bacilli (Spirilli)microaerophilicMotileCold sensitive (often leads to false negatives)get it from poultryOne unique feature is that campylobacter cannot usually multiply in food.Symptoms:diarrhea, cramping, abdominal pain, and fever2-5 day incubationSymptoms can last a weekCan have vomiting, diarrhea can be bloodyMechanism: Symptoms are an inflammatory response to cell invasionPositive Diagnosis: stool culturePossible complication: Guillain-Barré syndrome
141
Salmonella enterica
Gram -BacilliNon spore formingH2S positive & lactose negativeMotile, flagellated
142
Salmonellosis
Symptoms:diarrhea, fever, and abdominal cramps 12 hr to 3 day incubationSymptoms typically last 4 to 7 daysMost persons recover without treatmentRemember: reactive arthritis as a possible complicationDiagnosis: we know for sure with a stool cultureTreatment: Hydration. Antibiotics only necessary if infection spreads beyond gut
143
Vibrio parahaemolyticus
Gram (-)Vibrio (curved rod)facultative anaerobesFlagellated, motileOxidase +water lovingDiagnosis: Vibrio may be isolated from cultures of stool, wound, or blood. Form pores in red blood cells but also in epithelial cells, disrupting gut homeostasissushi and shellfish
144
Vibrio parahaemolyticus Symptoms
Fairly mild bloody diarrhea, stomach cramps, fever, nausea, and/or vomiting, Symptoms last less than a week. In the immunocompromised, it can spread to the blood and cause serious or deadly infections in other parts of the body
145
Listeria monocytogenes
Gram positive rod-shaped bacteriaAlthough a rare illness, a leading cause of death by foodborne illnessGram (+)BacillusNon-fastidious!!!Flagellated, motileNon spore formingOxidase -Diagnosis: Stool sample ID inappropriatePositive ID is the bacterium found in a normally sterile siteImmune cells spread Listeria to other organsTrojan horseLiver is a major targetmilk, cheese, seafood, deli
146
Listeriosis
Mild GI infection for mostMore vulnerable are older adults, pregnant women, newborns, and adults with weakened immune systems OPPORTUNISTICFever and muscle aches or stiff neck, or if you develop while pregnant: fever and chillsMeningitis and sepsis in vulnerable populations
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Shigella
Gram (-)BacillusFacultative anaerobenonmotile (distinguishes from e. coli)Non spore formingMainly lactose negative, H2S (-) (distinguishes from e. coli)Shigella sonnei: most Shigella-caused GI illnessesShigella flexnori: causes bacillary dysenteryShigella dysenteriae: rarest but most severe dysenteryinvade through m cellsSince Shigella is invasive, if not treated it can spread beyond the GI tract and cause complicationsAntibiotics for more severe cases, most usually resolve without antibioticsPossible complication: hemolytic uremic syndrome (HUS)
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What is dysentery
Frequent, small bowel movements with blood and mucus, accompanied by rectal pain and spasms (tenesmus)
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Shigella Transmission
Transmission: Mostly bacterium passing from stools or soiled fingers of one person to the mouth of another person.
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Shigella Symptoms:
Symptoms: diarrhea (often bloody)feverstomach crampsSymptoms start 1-2 days following exposureUsually resolves in 5 to 7 days.
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E. coli
Gram (-)BacillusFacultative anaerobemotileNon spore formingMainly lactose positiveDiarrheaUrinary tract infectionNeonatal sepsisGram-negative sepsisETECSTECTreatment: antibiotics generally not recommended (decaying bacteria release toxins)Tracking outbreaks: commercial PCR and antibody-based kits.
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ETEC
Traveler’s Diarrhea, diarrhea in childrenactivates adenylate cyclase, end result water into lumen, NO bacterial penetration.
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STEC
penetrates like Shigilla toxin. hemorrhagic colitis (HC) and/or HUS can result as a complication; children more vulnerable
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E. coli Symptoms:
profuse watery diarrhea and abdominal crampingCan progress to bloody diarrhea for STECFever, chillsNausea with or without vomiting, loss of appetiteLess common: headache, muscle aches and bloatingIncubation:1-3 days ETEC, 3-8 for STEC Illness typically lasts 3-4 days, less than 10.
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cholera toxin
Activates adenylate cyclase cAMP → Na+ absorption, Cl- excretionWater moves into lumen
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typhoid fever
Only fecal-oral contaminant, no other host, so water is a big source of contaminatonDrinking water, unwashed fruits/veggiesTravelers are vulnerableVaccine availableLife-threatening illnessIn GI tract and then to bloodstreamHigh fevers (103-104 °F)Weakness and headacheStomach pains, loss of appetite, diarrhea or constipation Sometimes, a rash of flat, rose-colored spotsAfter symptoms clear, person could become a carrierAntibiotic treatment is recommended
157
High inoculum organisms
Tens of thousands or more neededExamples: Vibrio cholerae, C. perfringens
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Clostridium difficile
Gram +BacilliSpore-formingObligate anaerobeMotileMakes exotoxinsantibiotic diarrhea
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Giardia lamblia
Also most common intestinal parasite in USGiardiasis (aka Beaver Fever) is the foe of backpackers/hikersSymptoms for 1-2 weeks or more, may seem to resolve and then come backMechanism: presence of parasite causes loss of epithelial absorptive surface area. Trophozoites: Attachment but not penetrationFoul-smelling diarrheaFilter water in areas where Giardia cysts are likely to exist. Water does not need to be contaminated with human sewage. Wildlife can deposit cysts.
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Cryptosporidium parvum
Often seen when a sanitation system failsPool/waterpark chlorination/UV treatmentStorms or issues with drinking waterDiarrhea symptoms for 1-2 weeks to ~30 days, may seem to resolve and then come backMechanism: Absorption impaired and secretion enhanced when intestinal epithelial cells are infected by Cryptosporidium“Crypto” is opportunisticHIV/Immunocompromised individualsChronic Diarrhea/fluid lossCan be fatalWatery, frequent, non-bloody stoolDisrupts epithelial microvilli, slides into host cells, enveloping itself in the host cell membraneOocysts to sporozoites and backCoccidia subclass
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Entamoeba histolytica
AmebiasisMore prevalent in tropical/subtropical climatesOnly 10-20% of infected individuals will become ill (CDC)Of US population, male homosexuals most vulnerableBloody, mucus-ey loose stoolRelatively mild symptoms butCan invade the liver and form an abcessX-ray/ultrasound to detect abscess or tissue damageCysts in stool sample. Must differentiate from non-pathogenic entamoeba, takes a specialist.cytotoxic
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Metronidazole, Tinidazole
Tissue antiparasitic- low concentration in intestine, oral dose almost completely absorbed with high bioavailabilityDespite this, it is the drug of choice to treat symptomatic Giardia infection, even though organism that does not penetrate the epithelium!!Reminder: all about metronidazole/Tinidazole in lectures relating to treatment of H. pyloriDisulfiram reaction, avoid alcoholDisturb normal GI florabreaks down into toxic metabolites, damages DNA
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Nitazoxanide
Mechanism: Interferes with pyruvate::ferredoxin oxidoreductase enzyme dependent electron transfer, essential to anaerobic energy metabolism protein Selectivity: Species difference in electron transferDistribution: Rapidly metabolized to tizoxanide. Parent compound is not detected in plasma. Moderately absorbed (33%), primarily luminal. For Crypto, used in combination with retroviral therapy for AIDS patients if at all, because of ineffectiveness
164
Iodoquinol
Mechanism: UnknownToxicity: loss of visual acuityUse with caution in patients with thyroid disease – its use interferes with certain thyroid testsDistribution: only 10% of the drug is absorbed so it works locally on the protozoa including cysts in the GI tract, luminal antiparasitic (amebicide)
165
Paromomycin
Mechanism: Aminoglycoside- targets 30S subunit ribosomeToxicity: Diarrhea, other GI effects including issues with intestinal flora because it has activity against some bacteria.Distribution: Luminal antiparasitic- Minimal absorption after oral administrationOtotoxicity, nephrotoxicity
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TMP-SMX
Spectrum: Broad spectrum, many bacteria, but also effective against apicomplexans including Toxoplasma and Cystoisospora (formerly Isospora), and Cyclosporahits folic acid system
167
Enterobius vermicularis
Staple-sized wormspinwormsWorldwide distribution, most common helminth infection in USPrevalence can reach 50% in children, caregivers of infected children, and institutionalized individuals.Symptom: perianal pruritisAcquired by ingestion of pinworm eggsEggs can remain viable on surfaces for 2-3 weeks
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Necator americanus/Ancylostoma duodenale
Pruritic Papular Erythematous RashHookworms are bloodsuckers…Major symptom is iron-deficiency anemia¼ ml/day/worm
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Strongolides stercoralis
Autoinfection possible, especially with Immunosuppressed individualsStomach and GI complaintsRespiratorydry coughthroat irritationSkinan itchy, red rash that occurs where the worm entered the skinrecurrent raised red rash typically along the thighs and buttocks.
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Trichuris trichiura
Diagnosis:Eggs in feces have a characteristic barrel-shaped appearanceFinger clubbing best indicator ofseverity of infestationBloody diarrhea = iron deficiency anemiaHeavy cases:Frequent, painful stools with mucus, water and blood, tenesmusRectal prolapse
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Ascaris lumbricoides
Disease: ascariasisDisease: IF symptoms are experienced, abdominal discomfortIf a severe case, intestinal blockagesUltrasonography and radiology to determineHas a lung stage of life cycle, may cause coughDiagnosis: eggs w/thick shells
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Albendazole and Mebendazole
Broad-spectrum benzimidazole drugsRoundworms and tapewormsDistribution: Limited oral absorption, albendazole is better absorbed if targeting tissue-migrating larvae is importantBroad-spectrum benzimidazole drugsMechanism: Binds to parasite β-tubulin and inhibits the formation of microtubulesDeath can take several days, for some helminths more than one dose may be necessarySpecificity: differences in tubulinToxicity: Systemic toxic affects on liver/bone marrow rareAbdominal pain, nausea, dizziness, headacheEmbryotoxic and teratogenic in pregnant ratsEvidence suggests safe for use in children when warranted
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Pyrantel pamoate and Levamisole
Mechanism:Levamisole selectively opens a restricted subgroup of nematode acetylcholine receptor (AChR) ion channels in nematode nerve and muscle. depolarization entry of calcium through the opened channels, and an increase in sarcoplasmic calcium, producing spastic muscle contraction the parasite is then unable to maintain its location (often in the intestine) and is then swept away, effecting the cure. Toxicity: Causes nausea, vomiting, diarrheaDistribution: Poorly absorbed
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Ivermectin
Mechanism: Binds to glutamate-gated chloride channels in invertebrate nerve and muscle cells, causing deactivation of channel: worm paralysis and death by starvationResistance: efflux transportersToxicity:Generally well-tolerated Itching, swollen lymph glands and rarely dizzinessInflammatory reaction due to death of adult wormsSpecificity: This type of channel restricted to phyla Nematoda and Arthropoda. in humans are only in the CNS , Doesn’t cross blood-brain barrierSpectrum: Nematodes- Ascaris, Strongyloides and Onchocerca
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secretory diarrhea
characterized as an infection of the proximal small bowel marked by watery diarrhea that does NOT contain fecal leukocytes. Viruses that cause gastroenteritis do not infect the colon
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Rotavirus Clinical presentation:
gastroenteritis
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Norwalk Virus (Norovirus) Clinical presentation:
gastroenteritis
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Adenovirus Clinical presentation:
gastroenteritis (do not confuse with other serotypes of adenoviruses that cause respiratory tract infections)
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Rotavirus Pathology:
transmitted via the fecal to oral route. After ingestion of the virus it travels in the GI tract (the virus particle is stable within the low pH of the gastrointestinal system) to eventually infect the villus cells of the proximal small intestine. Here the virus replicates within these cells eventually lysing these cells which leads to the impaired adsorption of carbohydrates and other nutrients. This can lead to vomiting followed by watery diarrhea.
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Norwalk Virus (Norovirus) Pathology:
fecal to oral transmission usually through direct contact or through contaminated food and water. Causes a local infection and inflammation in the proximal small intestine.
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Adenovirus Pathology:
fecal to oral transmission. Causes a local infection and inflammation in the proximal small intestine. If inhaled into the lungs some respiratory symptoms can be present.
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Rotavirus Diagnosis:
stool specimen, serology for the virus. Electron microscopy and RT-PCR also possible.
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Norwalk Virus (Norovirus) Diagnosis:
not typically done. When done it is through visualization of the virus in stool specimens or PCR/serology of stool and/or vomit specimens.
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Adenovirus Diagnosis:
PCR detection of the viral genome within a stool sample
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Rotavirus Treatment:
rehydration (supportive). There is a rotavirus vaccine (live oral attenuated).
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Norwalk Virus (Norovirus) Treatment:
usually not required because it is self-limited. When done, treatment consists of rehydration (supportive) if there is severe fluid loss. Outbreaks can be minimized through proper food handling, clean water supplies, and hand washing.
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Adenovirus Treatment:
self-limiting infection in immunocompetent individuals. Supportive care only.
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Rotavirus
because rotaviruses cause no inflammation, diarrhea has no blood. Infection before 6 months of age is uncommon due to passive IgA immunity from the mother’s colostrum. However, by age 3, almost every individual worldwide (~95%) has been infected and develops lifelong immunity. Virus particle contains a double-layered capsid.
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Norwalk Virus (Norovirus)
this virus is a major cause of group-related or institutional diarrhea.
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Adenovirus
major cause of acute infantile gastroenteritis. These serotypes of adenoviruses rarely cause fever or respiratory tract symptoms.
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bifidobacteria
are among the first colonizers in breast-fed infants
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Staphylococcus aureus
Gram +CocciCatalase +Coagulase +Also a common infectious agent of surgical wounds and cause of scalded skin syndromein food that sits around for a whileno need for antibiotics for a food borne infection
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Bacillus cereus
Gram +Large Bacilliendospore-formingFacultative anaerobeMostly motileβ hemolytic Box-car shaped Also frequently found on skin and is a threat in hospitals as it produces biofilms that adhere easily to invasive devices. This produces chronic persistent infection, as the biofilm can periodically release B. cereus into the bloodstreamB. Cereus spores are commonly found in the soil and sometimes in plant foods that are grown close to the ground – such legumes, cereals, spices etc..Spores can survive rice cooking processDuration for both only about 24 hrsBecause of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen. B. cereus in food and vomitus or feces of same serotype Large numbers of B. cereus of serotype known to produce endotoxinOnly necessary when tracking outbreaks
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Clostridium botulinum
Gram +BacilliSpore-formingObligate anaerobeMotileSpores or toxin are the important issues for transmission of botulism
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Staphylococcus aureus Symptoms:
Symptoms:nausea, vomiting, stomach cramps, and diarrhea for 1-3 daysAppear 1-7 hrs following ingestion of foodSelf-limiting, once toxin is gone, illness is gone
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Staphylococcus aureus diagnosis
Positive diagnosis:Toxin-producing S. aureus can be identified in stool or vomitMost 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).Only necessary when tracking outbreaks
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Bacillus cereus infection
Infection takes two forms:Emetic (vomiting):Diarrheal:Duration for both only about 24 hrs
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Bacillus cereus Emetic infection
Emetic (vomiting):1 to 6 hours incubationNausea and vomitingresembles the vomiting illness caused by Staphylococcus aureus enterotoxinsCaused by preformed enterotoxin that forms holes in membranesSelf limiting
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Bacillus cereus Diarrheal infection
Diarrheal:6-15 hours incubationclinically similar to the symptoms of Clostridium perfringens infectionWatery diarrhea and abdominal crampsMechanism: Caused by large molecular weight enterotoxin that causes intestinal fluid secretion, probably by several mechanismsThis toxin is not likely pre-formed!Ingestion of large amounts of bacteria cause it to generate the toxin in the small intestineVulnerable populations might get sicker and require antibioticsPoor outcomes for systemic infection
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Bacillus cereus diagnosis
Because of its ubiquity, B. cereus often is ignored or dismissed as a contaminant when found in a culture specimen. B. cereus in food and vomitus or feces of same serotype Large numbers of B. cereus of serotype known to produce endotoxinOnly necessary when tracking outbreaks
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Botulism
Food borne botulism: ingesting toxinWound botulism: producing toxin Infant botulism: ingested sporesNot really a GI illness, diarrhea not prominent
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Botulism Diagnosis
Symptoms and history, results of physical exam indicate botulismTests to exclude other causes of the illnessOrganism or toxin in stool sample only indirect evidence
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Treatment for foodborne botulism
Ventilator if respiratory failure and paralysisAntitoxin if paralysis is not yet completeRemove contaminated food if still likely in gut
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Botulism toxin
neurotoxinirreversibly blocks the release of acetylcholine from the motoric end plate which results in muscle weakness and paralysisToxin is absorbed from GI tract to bloodstream
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Symptoms, botulism
Toxin already produced, symptoms can begin when toxin hits GI tractdouble vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness
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Symptoms, infant botulism
Incubation period, spores have to produce toxin-forming bacterialethargic, feed poorly, are constipated, and have a weak cry and poor muscle toneCan lead to paralysis of respiratory system and other muscles
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Clostridium perfringens
Gram +BacilliSpore-formingObligate anaerobeNon-motileEnterotoxin binds to receptors in endothelial cell junctions, then generates pores in host mucosa cells.“C. perfringens infection often occurs when foods are prepared in large quantities and kept warm for a long time before serving”
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Clostridium perfringens Symptoms
Symptoms:Diarrhea and abdominal crampsIncubation 6 to 24 hours (typically 8-12)Symptoms last for less than 24 hoursUsually NO fever or vomitingThe illness is not passed from one person to another
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Clostridium perfringens Positive diagnosis
Positive diagnosis:Detection of toxin or high amounts of bacteria in fecesC. perfringens normally present in the GI tract, the problem is when you ingest a C. perfringens load high enough to produce enough toxin to generate symptoms
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Clostridium perfringens Treatment
Treatment:Usually self-limiting, but more serious, longer-lasting cases in immunocompromised individuals should be treated to avoid complications
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Campylobacter jejuni
Gram -Bacilli (Spirilli)microaerophilicMotileCold sensitive (often leads to false negatives)get it from poultryOne unique feature is that campylobacter cannot usually multiply in food.Symptoms:diarrhea, cramping, abdominal pain, and fever2-5 day incubationSymptoms can last a weekCan have vomiting, diarrhea can be bloodyMechanism: Symptoms are an inflammatory response to cell invasionPositive Diagnosis: stool culturePossible complication: Guillain-Barré syndrome
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Salmonella enterica
Gram -BacilliNon spore formingH2S positive & lactose negativeMotile, flagellated
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Salmonellosis
Symptoms:diarrhea, fever, and abdominal cramps 12 hr to 3 day incubationSymptoms typically last 4 to 7 daysMost persons recover without treatmentRemember: reactive arthritis as a possible complicationDiagnosis: we know for sure with a stool cultureTreatment: Hydration. Antibiotics only necessary if infection spreads beyond gut
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Vibrio parahaemolyticus
Gram (-)Vibrio (curved rod)facultative anaerobesFlagellated, motileOxidase +water lovingDiagnosis: Vibrio may be isolated from cultures of stool, wound, or blood. Form pores in red blood cells but also in epithelial cells, disrupting gut homeostasissushi and shellfish
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Vibrio parahaemolyticus Symptoms
Fairly mild bloody diarrhea, stomach cramps, fever, nausea, and/or vomiting, Symptoms last less than a week. In the immunocompromised, it can spread to the blood and cause serious or deadly infections in other parts of the body
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Listeria monocytogenes
Gram positive rod-shaped bacteriaAlthough a rare illness, a leading cause of death by foodborne illnessGram (+)BacillusNon-fastidious!!!Flagellated, motileNon spore formingOxidase -Diagnosis: Stool sample ID inappropriatePositive ID is the bacterium found in a normally sterile siteImmune cells spread Listeria to other organsTrojan horseLiver is a major targetmilk, cheese, seafood, deli
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Listeriosis
Mild GI infection for mostMore vulnerable are older adults, pregnant women, newborns, and adults with weakened immune systems OPPORTUNISTICFever and muscle aches or stiff neck, or if you develop while pregnant: fever and chillsMeningitis and sepsis in vulnerable populations
218
Shigella
Gram (-)BacillusFacultative anaerobenonmotile (distinguishes from e. coli)Non spore formingMainly lactose negative, H2S (-) (distinguishes from e. coli)Shigella sonnei: most Shigella-caused GI illnessesShigella flexnori: causes bacillary dysenteryShigella dysenteriae: rarest but most severe dysenteryinvade through m cellsSince Shigella is invasive, if not treated it can spread beyond the GI tract and cause complicationsAntibiotics for more severe cases, most usually resolve without antibioticsPossible complication: hemolytic uremic syndrome (HUS)
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What is dysentery
Frequent, small bowel movements with blood and mucus, accompanied by rectal pain and spasms (tenesmus)
220
Shigella Transmission
Transmission: Mostly bacterium passing from stools or soiled fingers of one person to the mouth of another person.
221
Shigella Symptoms:
Symptoms: diarrhea (often bloody)feverstomach crampsSymptoms start 1-2 days following exposureUsually resolves in 5 to 7 days.
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E. coli
Gram (-)BacillusFacultative anaerobemotileNon spore formingMainly lactose positiveDiarrheaUrinary tract infectionNeonatal sepsisGram-negative sepsisETECSTECTreatment: antibiotics generally not recommended (decaying bacteria release toxins)Tracking outbreaks: commercial PCR and antibody-based kits.
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ETEC
Traveler’s Diarrhea, diarrhea in childrenactivates adenylate cyclase, end result water into lumen, NO bacterial penetration.
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STEC
penetrates like Shigilla toxin. hemorrhagic colitis (HC) and/or HUS can result as a complication; children more vulnerable
225
E. coli Symptoms:
profuse watery diarrhea and abdominal crampingCan progress to bloody diarrhea for STECFever, chillsNausea with or without vomiting, loss of appetiteLess common: headache, muscle aches and bloatingIncubation:1-3 days ETEC, 3-8 for STEC Illness typically lasts 3-4 days, less than 10.
226
cholera toxin
Activates adenylate cyclase cAMP → Na+ absorption, Cl- excretionWater moves into lumen
227
typhoid fever
Only fecal-oral contaminant, no other host, so water is a big source of contaminatonDrinking water, unwashed fruits/veggiesTravelers are vulnerableVaccine availableLife-threatening illnessIn GI tract and then to bloodstreamHigh fevers (103-104 °F)Weakness and headacheStomach pains, loss of appetite, diarrhea or constipation Sometimes, a rash of flat, rose-colored spotsAfter symptoms clear, person could become a carrierAntibiotic treatment is recommended
228
High inoculum organisms
Tens of thousands or more neededExamples: Vibrio cholerae, C. perfringens
229
Clostridium difficile
Gram +BacilliSpore-formingObligate anaerobeMotileMakes exotoxinsantibiotic diarrhea
230
Giardia lamblia
Also most common intestinal parasite in USGiardiasis (aka Beaver Fever) is the foe of backpackers/hikersSymptoms for 1-2 weeks or more, may seem to resolve and then come backMechanism: presence of parasite causes loss of epithelial absorptive surface area. Trophozoites: Attachment but not penetrationFoul-smelling diarrheaFilter water in areas where Giardia cysts are likely to exist. Water does not need to be contaminated with human sewage. Wildlife can deposit cysts.
231
Cryptosporidium parvum
Often seen when a sanitation system failsPool/waterpark chlorination/UV treatmentStorms or issues with drinking waterDiarrhea symptoms for 1-2 weeks to ~30 days, may seem to resolve and then come backMechanism: Absorption impaired and secretion enhanced when intestinal epithelial cells are infected by Cryptosporidium“Crypto” is opportunisticHIV/Immunocompromised individualsChronic Diarrhea/fluid lossCan be fatalWatery, frequent, non-bloody stoolDisrupts epithelial microvilli, slides into host cells, enveloping itself in the host cell membraneOocysts to sporozoites and backCoccidia subclass
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Entamoeba histolytica
AmebiasisMore prevalent in tropical/subtropical climatesOnly 10-20% of infected individuals will become ill (CDC)Of US population, male homosexuals most vulnerableBloody, mucus-ey loose stoolRelatively mild symptoms butCan invade the liver and form an abcessX-ray/ultrasound to detect abscess or tissue damageCysts in stool sample. Must differentiate from non-pathogenic entamoeba, takes a specialist.cytotoxic
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Metronidazole, Tinidazole
Tissue antiparasitic- low concentration in intestine, oral dose almost completely absorbed with high bioavailabilityDespite this, it is the drug of choice to treat symptomatic Giardia infection, even though organism that does not penetrate the epithelium!!Reminder: all about metronidazole/Tinidazole in lectures relating to treatment of H. pyloriDisulfiram reaction, avoid alcoholDisturb normal GI florabreaks down into toxic metabolites, damages DNA
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Nitazoxanide
Mechanism: Interferes with pyruvate::ferredoxin oxidoreductase enzyme dependent electron transfer, essential to anaerobic energy metabolism protein Selectivity: Species difference in electron transferDistribution: Rapidly metabolized to tizoxanide. Parent compound is not detected in plasma. Moderately absorbed (33%), primarily luminal. For Crypto, used in combination with retroviral therapy for AIDS patients if at all, because of ineffectiveness
235
Iodoquinol
Mechanism: UnknownToxicity: loss of visual acuityUse with caution in patients with thyroid disease – its use interferes with certain thyroid testsDistribution: only 10% of the drug is absorbed so it works locally on the protozoa including cysts in the GI tract, luminal antiparasitic (amebicide)
236
Paromomycin
Mechanism: Aminoglycoside- targets 30S subunit ribosomeToxicity: Diarrhea, other GI effects including issues with intestinal flora because it has activity against some bacteria.Distribution: Luminal antiparasitic- Minimal absorption after oral administrationOtotoxicity, nephrotoxicity
237
TMP-SMX
Spectrum: Broad spectrum, many bacteria, but also effective against apicomplexans including Toxoplasma and Cystoisospora (formerly Isospora), and Cyclosporahits folic acid system
238
Enterobius vermicularis
Staple-sized wormspinwormsWorldwide distribution, most common helminth infection in USPrevalence can reach 50% in children, caregivers of infected children, and institutionalized individuals.Symptom: perianal pruritisAcquired by ingestion of pinworm eggsEggs can remain viable on surfaces for 2-3 weeks
239
Necator americanus/Ancylostoma duodenale
Pruritic Papular Erythematous RashHookworms are bloodsuckers…Major symptom is iron-deficiency anemia¼ ml/day/worm
240
Strongolides stercoralis
Autoinfection possible, especially with Immunosuppressed individualsStomach and GI complaintsRespiratorydry coughthroat irritationSkinan itchy, red rash that occurs where the worm entered the skinrecurrent raised red rash typically along the thighs and buttocks.
241
Trichuris trichiura
Diagnosis:Eggs in feces have a characteristic barrel-shaped appearanceFinger clubbing best indicator ofseverity of infestationBloody diarrhea = iron deficiency anemiaHeavy cases:Frequent, painful stools with mucus, water and blood, tenesmusRectal prolapse
242
Ascaris lumbricoides
Disease: ascariasisDisease: IF symptoms are experienced, abdominal discomfortIf a severe case, intestinal blockagesUltrasonography and radiology to determineHas a lung stage of life cycle, may cause coughDiagnosis: eggs w/thick shells
243
Albendazole and Mebendazole
Broad-spectrum benzimidazole drugsRoundworms and tapewormsDistribution: Limited oral absorption, albendazole is better absorbed if targeting tissue-migrating larvae is importantBroad-spectrum benzimidazole drugsMechanism: Binds to parasite β-tubulin and inhibits the formation of microtubulesDeath can take several days, for some helminths more than one dose may be necessarySpecificity: differences in tubulinToxicity: Systemic toxic affects on liver/bone marrow rareAbdominal pain, nausea, dizziness, headacheEmbryotoxic and teratogenic in pregnant ratsEvidence suggests safe for use in children when warranted
244
Pyrantel pamoate and Levamisole
Mechanism:Levamisole selectively opens a restricted subgroup of nematode acetylcholine receptor (AChR) ion channels in nematode nerve and muscle. depolarization entry of calcium through the opened channels, and an increase in sarcoplasmic calcium, producing spastic muscle contraction the parasite is then unable to maintain its location (often in the intestine) and is then swept away, effecting the cure. Toxicity: Causes nausea, vomiting, diarrheaDistribution: Poorly absorbed
245
Ivermectin
Mechanism: Binds to glutamate-gated chloride channels in invertebrate nerve and muscle cells, causing deactivation of channel: worm paralysis and death by starvationResistance: efflux transportersToxicity:Generally well-tolerated Itching, swollen lymph glands and rarely dizzinessInflammatory reaction due to death of adult wormsSpecificity: This type of channel restricted to phyla Nematoda and Arthropoda. in humans are only in the CNS , Doesn’t cross blood-brain barrierSpectrum: Nematodes- Ascaris, Strongyloides and Onchocerca
