Harvey's Garden

Infectious gastroenteritis

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aliasesCholera, Shigellosis, Shigella

3 min read

Shigellosis

  • Etiology: Shigella spp. Gram-negative, non-motile, non-lactose fermenting, H2S-negative bacilli.
    • S. sonnei: Most common in US/developed countries.
    • S. flexneri: Most common in developing countries.
    • S. dysenteriae: Causes severe disease/outbreaks (produces Shiga toxin).
  • Transmission: Fecal-oral route, contaminated food/water, person-to-person contact.
  • High infectivity: Very low infectious dose (10–100 organisms); highly resistant to gastric acid.
  • Risk factors: Daycare centers, crowded living conditions, international travel, MSM, poor sanitation.
  • Mechanism: Highly virulent with a very low infectious dose (as few as 10-100 organisms) because it is acid-stable. It invades the gastrointestinal mucosa, primarily in the large intestine, through M cells of Peyer’s patches. It then escapes the phagosome and spreads laterally from cell to cell using the host’s actin filaments (no hematogenous spread), causing mucosal ulceration and inflammation.
    • Toxin: Some strains, particularly S. dysenteriae, produce Shiga toxin, which inactivates the 60S ribosomal subunit, inhibiting protein synthesis. However, the primary cause of pathology is direct mucosal invasion.
  • Clinical features
    • Incubation: 1–4 days.
    • Initial phase: High fever, crampy abdominal pain, watery diarrhea. c
    • Classic presentation: Progression to frequent, small-volume bloody/mucoid diarrhea (dysentery) with severe tenesmus (painful urge to defecate).
    • PE: Lower abdominal tenderness, hyperactive bowel sounds, dehydration signs.
    • Pediatric feature: High risk of febrile seizures due to rapid temperature spikes (often before GI symptoms start).

Cholera

  • Pathogen: Vibrio cholerae
  • Infectivity
    • Acid-labile (grows well in an alkaline medium)
    • High infective dose required (over 108 pathogens)
    • Gastric acid provides a natural barrier against V. cholerae infection
      • Patients on long PPI are more easily to get infected t

Noncholera Vibrio infection

  • Transmission / Exposure:
    • Ingestion of raw or undercooked seafood (especially raw oysters).
    • Direct exposure of open wounds/cuts to contaminated saltwater or brackish water or marine life.
  • High-Risk Populations (V. vulnificus bacteremia/severe wound infection):
    • Chronic Liver Disease (CLD) / Cirrhosis (highest mortality risk).
    • Hemochromatosis / Iron overload states (excess free iron enhances bacterial growth and virulence). c
    • Immunocompromised states (DM, ESRD, HIV, active malignancy).
  • Clinical Presentation:
    • V. vulnificus: Rapid (within hours) necrotizing soft-tissue infection w/ hemorrhagic bullae; fulminant septic shock. c
    • V. parahaemolyticus: Watery or bloody gastroenteritis after eating raw oysters.
  • Diagnosis: Blood/wound culture on TCBS agar (Gram-negative curved rods).
  • Key Differential: 
    • Aeromonas hydrophila: Diff by exposure to freshwater or leeches (vs saltwater/marine environments for Vibrio).
    • Streptococcus pyogenes (GAS Necrotizing Fasciitis): Diff by lack of saltwater/seafood exposure; Gram stain shows Gram-positive cocci in chains.
    • Clostridium perfringens (Gas Gangrene): Diff by dirty deep-wound trauma/soil contamination, prominent crepitus, and Gram-positive rods on stain.
  • Management:
    • V. vulnificus / Sepsis: Emergent surgical debridement + IV Doxycycline + Ceftriaxone.
    • Gastroenteritis: Supportive (oral rehydration).
  • Complications: Septic shock, DIC, necrotizing fasciitis (>50% mortality in cirrhotic pts).

Campylobacter enteritis (campylobacteriosis)

  • Epidemiology & Risk Factors
    • Pathogen: Campylobacter jejuni (curved/seagull-shaped GNR, thermophilic [42°C], oxidase [+]).
    • #1 cause of bacterial gastroenteritis in US.
    • Source: Undercooked poultry (most common), unpasteurized milk, contaminated water, infected pets (puppies).
  • Clinical Features
    • Prodrome: High fever, chills, headache 24–48 hr prior to GI onset.
    • GI: Severe crampy abdominal pain (mimics acute appendicitis or IBD), profuse bloody diarrhea, tenesmus.
  • Diagnosis
    • Initial/Diagnostic: Stool PCR panel (rapid).
    • Confirmatory/Gold Standard: Stool culture at 42°C on selective media (Campy-BAP).
    • Microscopy: Stool with darting motility and gull-wing GNRs.
  • Differential Diagnostics
    • Salmonella: Eggs/poultry/reptiles; less pseudoappendicitis.
    • Shigella: Daycare/low infectious dose, high fever/seizures, HUS risk.
    • EHEC: No high fever, undercooked beef, high HUS risk (Abx contraindicated).
    • Yersinia: Pork, prominent pseudoappendicitis (mesenteric adenitis).
  • Management
    • Mild/Moderate: Supportive (ORT/IVF). Avoid antimotility agents (e.g., loperamide). c
    • Severe/High-risk (fever, >7 days, immunocompromised, pregnancy): Azithromycin (1st-line); fluoroquinolones (2nd-line due to resistance).
  • Complications
    • Guillain-Barré Syndrome (GBS): Molecular mimicry (LOS vs GM1 gangliosides) ascending paralysis 1–3 wks post-infection.
    • Reactive Arthritis: HLA-B27 asymmetric oligoarthritis, urethritis, conjunctivitis.
    • Erythema nodosum, Toxic megacolon.

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