Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning
Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning
Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning
INOCULUM SIZE
- Number of microorganisms that must be ingested to
cause disease
Examples:
E. coli, Giardia lamblia, Entamoeba – 10-100 bacteria or
cysts
Vibrio cholerae – 105 – 108 organisms
* Ability of organisms to overcome host defenses has
important implications for transmission
Pathogenic Mechanisms
ADHERENCE
- Adherence to the gastrointestinal mucosa is an initial
step in the pathogenic process
-involve specific cell-surface proteins (virulence
determinants)
Example:
Surface adhesins – V. cholerae
Colonization factor antigen – Enterotoxigenic E.coli
Pathogenic Mechanisms
TOXIN PRODUCTION
1. Enterotoxins
- Act directly on secretory mechanisms in intestinal
mucosa
- Cause watery diarrhea
TOXIN PRODUCTION
1. Enterotoxins
- Heat-labile enterotoxin (LT)
similar to cholera toxin
secretory diarrhea
Enterotoxigenic E.coli
- Heat-stable enterotoxin (ST)
one form causes diarrhea by activation of
guanylate cyclase → inc intracellular cGMP
Pathogenic Mechanisms
TOXIN PRODUCTION
2. Cytotoxins
- Destruction of mucosal cells
- Inflammatory diarrhea
- Produce syndrome of dysentery, with bloody stools
containing inflammatory cells (bacterial cytotoxins)
- Ex. Shigella dysenteriae type 1, Vibrio
parahaemolyticus, Clostridium difficile
Pathogenic Mechanisms
TOXIN PRODUCTION
3. Neurotoxins
- Act directly on central or peripheral nervous system
- Usually produced by bacteria outside the host
- Cause symptoms soon after ingestion
INVASION
- Destruction of intestinal mucosal cells
- Also result in dysentery
Host Defenses
INTESTINAL MICROBIOTA
- Bacteria that normally inhabit the intestine
- An important host defense mechanism
- Composition is as important as the number of
organisms present
- >99% = anaerobic bacteria
- acidic pH
- volatile fatty acids
Host Defenses
GASTRIC ACID
- Important barrier
- Neutralization of gastric acid increases risk of
colonization
- Rotavirus – highly stable to acidity
Host Defenses
INTESTINAL MOTILITY
- Normal peristalsis is the major mechanism for
clearance of bacteria from prox small intestine
Lomotil (diphenoxylate HCl with atropine) for Shigella –
prolong fever and shedding of organisms
Opiates for Salmonella – higher frequency of
bacteremia
Host Defenses
IMMUNITY
- Cellular immune response and antibody production
- Humoral immunity: systemic IgG and IgM, secretory
IgA
- Mucosal immune system – first line of defense
against many GI pathogens
Host Defenses
GENETIC DETERMINANTS
Blood group O
- increased susceptibility to V. cholerae, Shigella,
E.coli 0157, norovirus
Traveler’s Diarrhea
- Noninflammatory etiology
- Evidence of a common-source outbreak
- Ask about: specific food and time of onset of diarrhea
after a meal
Bacterial Food Poisoning
B. cereus
- Emetic form (short incubation period)
mediated by a staphylococcal type of enterotoxin
contaminated fried rice
- Diarrheal form (longer incubation ~8-16 hrs)
caused by enterotoxin resembling E.coli LT
diarrhea and abdominal cramps common
vomiting uncommon
*Not all food poisoning has bacterial cause (ex. Capsaicin
found in hot peppers, toxins in fish and shellfish)
Bacterial Food Poisoning
LABORATORY EVALUATION
Cholera – should be cultured on TCBS (thiosulfate-citrate-bile
salts-sucrose) or TTG agar (tellurite-taurocholate-gelatin)
LABORATORY EVALUATION
Salmonella and Shigella – MacConkey agar(non-lactose
fermenting, colorless colonies)
- Salmonella-Shigella agar
- Selenite enrichment broth
Treatment
* FQ resistant Campylobacter:
- following travel to SE Asia
- Azithromycin
Vaccines:
Rotavirus
S. Typhi and V. cholerae – incomplete and short lived
protection
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