Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning

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Acute Infectious Diarrheal Diseases

and Bacterial Food Poisoning

Source: Harrison’s Principles of Internal Medicine 19th


Edition

Dr. Christianne Dante – Sajulga


Pathogenic Mechanisms

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

- Ex. Cholera toxin – activates adenylate cyclase → inc


cAMP
Pathogenic Mechanisms

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

- Ex. Staphylococcal and Bacillus cereus toxins


- act on the CNS to produce vomiting
Pathogenic Mechanisms

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

- Most common travel-related infectious illness

- Time of onset: usually 3 days – 2 wks after arrival


(most begin within 3-5 days)
- Generally self-limited (1-5 days)
- Norovirus – most common etiologic agent associated
with outbreaks of acute gastroenteritis
- C. difficile – predominant cause of nosocomial
diarrhea → pseudomembranous colitis
Traveler’s Diarrhea

- Klebsiella oxytoca – cause of antibiotic-associated


hemorrhagic colitis
- Children <5 y/o – most morbidity and mortality
* breastfed - protection
Bacterial Food Poisoning

- 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)

Rotavirus – latex agglutination test (rapid detection)

Norovirus – reverse-transcriptase PCR and specific antigen


enzyme immunoassays

Giardia cysts or Cryptosporidium – immunofluorescence-


based rapid assays
Bacterial Food Poisoning

LABORATORY EVALUATION
Salmonella and Shigella – MacConkey agar(non-lactose
fermenting, colorless colonies)
- Salmonella-Shigella agar
- Selenite enrichment broth
Treatment

Adequate rehydration – mainstay of treatment


ORS – reduced osmolarity/reduced salt
- 2.6 g NaCl, 2.9 g triNa citrate, 1.5 g KCl, 13.5 g
glucose (or 27 g of sucrose) per liter of water

when vomiting – Ringer’s lactate


Treatment

With dysentery (bloody diarrhea and fever)


empiric antibiotic: Fluoroquinolone or macrolide)
* low resistance to FQ (Campylobacter):
1. Fluoroquinolone
- Ciprofloxacin 750mg single dose or
500mg BID x 3 days
- Levofloxacin 500mg single dose or
500mg qd x 3 days
- Norfloxacin 800mg single dose or
400mg BID x 3 days
Treatment

* low resistance to FQ (Campylobacter):


1. Fluoroquinolone
2. Azithromycin
- 1000 mg single dose or 500mg BID x 3 days
3. Rifaximin
- 200mg TID or 400 mg BID x 3 days (not
recommended in dysentery)
Treatment

* FQ resistant Campylobacter:
- following travel to SE Asia
- Azithromycin

• Antimicrobial should NOT be administered to


enterohemorrhagic E. coli
• A number of antibiotics induce replication of Shiga
tocin-producing lambdoid bacteriophages
• May increase risk of HUS and renal failure by 20x (in
enterohemorrhagic E.coli
• Clue: bloody diarrhea with low fever or none at all
Prophylaxis

Bismuth subsalicylate – traveler’s diarrhea


- 2 tabs (525 mg) 4x a day
- effective and safe up to 3 wks
- adverse events: temporary darkening of tongue and
tinnitus

Antimicrobial – not generally recommended


if indicated: Rifaximin

Vaccines:
Rotavirus
S. Typhi and V. cholerae – incomplete and short lived
protection
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