Micro 35: GI - Non-inflammatory diarrhea - Bacterial causes
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26 terms
Terms | Definitions |
|---|---|
 Non-inflammatory diarrhea | food associated: foodborne -> ingestion of organisms in food -> toxins produced once colonized the GI (bacteria) -> no bacterial invasion! -> Symptoms: acute watery diarrhea, longer incubation due to colonization with or without fever -> enterotoxins in bacteria |
| E. coli | member of normal (commensal) intestinal flora -> healthy human excretes 10^7 CFU/g of feces -> enterobacteria family, gram negative rods, facultative anaerobes -> produce variety of toxins (virulence factors) -> major opportunistic pathogen |
| Enterotoxigenic E coli (ETEC) | transmission is contaminated food and water (not as common in wealthy countries with good sanitation) -> infective dose (100 million - 10 billion cells -> primary cause of "Traveler's Diarrhea" (not the only cause) -> 20-55,000 cases/year in US |
| Pathogenesis of ETEC | CFA (colonization factor antigen) pili allow for close attachment to brush border of epithelial cells of intestine -> produce and release plasmid encoded enterotoxins -> LT and ST |
| LT | (heat labile) is similar to cholera - A subunit with 5 B subunits -> binds to cell and A subunit enters cell and phosphorylates adenylate cyclase -> increase in cAMP - water and electrolytes out of cell -> causing diarrhea |
| ST | (heat stable) - activates guanylate cyclase - increase in cGMP - water and electrolytes out of cell -> causes diarrhea |
| Treatment of ETEC | oral rehydration therapy, not normally antibiotics (typically self limiting) |
| Enteropathogenic E. coli (EPEC) | infantile diarrhea, childhood diarrhea (most commonly in developing countries - 50% mortality rate) -> pathogenesis not fully understood -> no CFA and no enterotoxins -> has plasmid borne (EAF) bundle forming pilus (BFP) which causes effacement of microvilli (alters absorptive properties of small intestine), minor cause of traveler's diarrhea |
| Treatment of EPEC | rehydration therapy (first line), trimethoprim/flouroquinolones |
| Vibrio Cholerae | single curved gram negative rods -> motile (single polar flagellum) -> non spore forming, oxidase + -> O and H antigens (classic strains are O1 and O139 serotype) -> ferment sucrose and mannose NOT arabinose -> acid sensitive, halotolerant (likes high salt concentrations for growth) -> infective dose is 10^8 (with solid food -> protects organisms from acidity within stomach)-10^10 (with fluid) -> colonize small intestine (within hours) -> secrete AB toxin |
| Cholera toxin | AB toxin, bacteriophage encoded -> binds ganglioside GM1 receptor and A subunit enters cell and activates adenylate cyclase-> increases cAMP -> water and electrolytes out of cell -> causes severe diarrhea (20-30L/day) -> "rice water stool" |
| Cholera | diarrhea that contains flakes, hypovolemic shock, acidosis, vomiting, muscle cramps -> stool contains 10^8 organisms/mL |
| Treat cholera | Oral and/or IV administrated glucose (if given early enough should be sufficient), tetracycline can reduce duration of diarrhea -> prevent with vaccine (10^9 killed cells -> lasts 3-6 months -> only effective against O1 serotype -> NOT RECOMMENDED) -> primary prevention is sanitation and personal hygiene (humans are only natural hosts) |
| Diagnosis, isolation and identification of vibrio-cholera | look for clinical presentation -> screening of stool sample (look for oxidase activity), make sure you tell them to screen for this specific organism (not routine) -> use Thiosulfate-citrate-bile salts-sucrose (TCBS) agar -> (sucrose is differentiating agent between other species -> sucrose +) |
| Clostridium perfringens | cause necrotic enteritis (darmbrand and pig-bell -> rare: papa new guinea -> type C) OR type A food-borne infection (major cause of food-borne infection in US -> strain type A) |
| Type-A C. perfringens | found in dust -> 50% of raw/frozen meat contain it -> human feces have 10^3-10^6 cells/g |
| Pathogenesis of C. perfringens | ingest vegetative cells and spores -> germinate within intestine -> colonize small intestine -> release CPE (C.P. enterotoxin) |
| Clinical features of C. perfringens | no fever, nausea or vomiting -> watery diarrhea with severe abdominal pain -> mortality rate is 0 |
| Diagnose C. perfringens | case history and symptoms -> large spores in feces, vegetative cells in food sample -> presence of enterotoxin in feces |
| Bacillus cereus | diarrhea and abdominal pain -> incubation is 8-16 hours, duration is 12-24 hours -> meats, vegetables, sauces, pasta, desserts and dairy products -> LT enterotoxin (production of vegetative growth - late exponential phase in small intestine -> adenylyl cyclase -> increased cAMP) |
| Food poisoning | short incubation within 4 hours -> emetic toxin -> vomiting (ST neurotoxin) |
| Food borne infection | longer incubation (8-16 hours) -> enterotoxin, watery diarrhea -> LT protein |
| Colonization of the small intestine and production of an enterotoxin (C. perfringens) | Watery diarrhea the morning after a turkey dinner -> no fever, vomiting, nausea or bloody stools |
| S. Aureus | Ingestion of a preformed enterotoxin in the food |
| EPEC | colonization of the SI, effacement of the microvilli |
| C. Botulinum and bacillus cereus | ingestion of a preformed neurotoxin |
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