Microbiology Quiz on Cholera and Campylobacter

Bacterial Enterocolitides

• Cholera:

  • Agent: Vibrio cholerae
  • Morphology: Minimal histologic alterations, no invasion, remains in the lumen.
  • Pathogenesis: Flagellar proteins cause motility and attachment, cholera toxin (A and B) causes disease, toxin B binds to GM1 ganglioside, toxin A subunit interacts with cytosolic proteins, activating adenylate cyclase, increasing cAMP, blocking CFTR, and leading to Cl and Na absorption, accumulation of Cl ions, secretion of bicarbonate and Na, and massive diarrhea.
  • Clinical features: Mostly asymptomatic in mild cases, severe cases present with rice water stool with a fishy odor.
  • Location: Endemic in India and Africa, transmission through contaminated water and fecal-oral contact. Shellfish and plankton are reservoirs.

• Campylobacter enterocolitis:

  • Agent: Campylobacter jejuni
  • Pathogenesis: Flagella, cytotoxins, invasion. Organisms attach and proliferate, endocytosis, exit, and invasion of next enterocyte.
  • Clinical features: Acute self-limiting colitis, food poisoning, traveler's diarrhea, possibly dysentery. In severe cases, may show symptoms matching conditions like reactive arthritis, erythema nodosum, and Guillain-Barré syndrome (flaccid paralysis) in some patients with HLA-B27.
  • Location: Reservoir includes chicken, sheep, pigs, cattle; Transmission: ingestion of improperly cooked chicken.

• Shigellosis:

  • Agent: Shigella spp.
  • Morphology: Mucosa hemorrhagic and granular.
  • Pathogenesis: Virulence factors, invasion, and inflammation cascade.
  • Clinical features: Affected site: Left colon and ileum, reservoir: Humans.
  • Location: Reservoir: Humans.

Other Bacterial Infections

• Salmonellosis:

  • Agent: Salmonella enteritidis
  • Pathogenesis: Virulence factors (flagella, bacterial LPS), bacterial growth in endosomes, activation of TLR5 and TLR4, intense inflammation, and mucosal damage.
  • Clinical features: Commonly, self-limiting infection. Severe cases can lead to complications like osteomyelitis in susceptible populations.
  • Location: Reservoir: humans, animals; transmission: food, raw meat, poultry.

• Typhoid fever:

  • Agent: Salmonella enterica (S. typhi, S. paratyphi)
  • Pathogenesis: Organisms taken up by M cells, invasion of M cells, and systemic reactive hyperplasia of phagocytes. S. typhi reside in the gallbladder.
  • Clinical features: Initial dysentery, followed by asymptomatic phase, bacteremia in severe cases, possible complications like abdominal tenderness, rose spots.
  • Location: Reservoir: humans, Transmission: contaminated food or water, person to person.

Viral Gastroenteritis

• Norovirus:

  • Single-stranded RNA.
  • Common cause of nonbacterial gastroenteritis.
  • Self-limiting in immunocompetent individuals.
  • Transmission: Contaminated food, water, airborn droplets

• Rotavirus:

  • Double-stranded RNA.
  • Most common cause of severe childhood diarrhea.
  • Low infective dose, in some regions, maternal antibodies are ineffective in the first six months of a child's life.

• Adenovirus:

  • Most common cause of pediatric diarrhea, often self-limiting.

• Ascaris lumbricoides:

  • Parasitic infection, if disseminated, can result in hepatic abscesses, potentially leading to pneumonia.
  • Transmission: human fecal-oral, contaminated water.

Further Bacterial Infections

• Yersinia:

  • Agent: Y. enterocolitica, Y. pseudotuberculosis, Y.. pestis
  • Pathogenesis:Yersinia binds to B-1 integrins, iron uptake system mediates iron capture and transport.
  • Clinical Feature Mimic acute appendicitis, extraintestinal symptoms, Pharyngitis, arthritis, Erythema nodosum, Chronic anemia, and hemochromatosis.
  • Reservoirs: Cattle, Pigs, and other mammals, transmitted through contaminated food or water.

• Enterotoxigenic E. coli (ETEC):

  • Pathogenesis: Heat-labile toxin (LT), and heat-stable toxin (ST), activates adenylate cyclase, increased cAMP and cGMP, leads to fluid secretion.
  • Clinical Features: Watery diarrhea.
  • Reservoirs: Cows, transmission: contaminated food.

• Enteropathogenic E. coli (EPEC):

  • Pathogenesis: Adherent effacing (A/E) lesions, proteins in the cytoplasm to attach to cells.
  • Clinical Features: Infant's diarrhea.

• Enterohemorrhagic E. coli (EHEC):

  • Pathogenesis: Shiga-like toxins (STx) activate adenylate cyclase.
  • Clinical Features: Bloody diarrhea (possible HUS in some cases), ischemic colitis.
  • Reservoirs: Cows

• Enteroinvasive E. coli (EIEC):

  • Pathogenesis: Invasion of epithelial cells.
  • Clinical Features: Bloody diarrhea.

• Enteroaggregative E. coli (EAEC):

  • Pathogenesis: Attachment to enterocytes, similar to Shigella.
  • Clinical Features: Non-bloody diarrhea.

Protozoal Infections

• Cryptosporidium:

  • Agent: Cryptosporidium spp.
  • Pathogenesis: Oocyst, secretes proteases, releases sporozoites, damages brush-border. Na malabsorption, secretion of Cl leads to diarrhea.
  • Clinical Features: Self-limiting diarrhea in immunocompetent persons; Chronic diarrhea in immunocompromised persons.
  • Transmission: Contaminated drinking water, fecal-oral transmission

• Strongyloides:

  • Agent: Strongyloides spp.
  • Pathogenesis: Filariform larvae is infective stage. Self-sustaining infection, auto-infection
  • Clinical Features: Mucosal damage, iron deficiency anemia, intense irritation, and pruritus, bloody diarrhea.
  • Transmission: Fecal-oral, ingestion

• Schistosoma:

  • Agent: Schistosoma spp.
  • Pathogenesis: Cercariae from snails can penetrate skin, granulomatous reaction.
  • Clinical Features: Granulomatous reaction, bleeding and obstruction.

• Diphyllobothrium latum:

  • Pathogenesis: Larval stage, infection persists, mucosal damage, possible vitamin B12 deficiency.
  • Clinical Features: Megaloblastic anemia in severe cases possible, possible obstruction/bleeding.

• Taenia solium:

  • Pathogenesis: Cysticercus stage.
  • Clinical Feature: Gravid proglottids in feces, presence of cysticerci in muscles of pork, can lead to neurological complications.

• Hymenolepis nana:

  • Pathogenesis: Eggs passed in feces.
  • Clinical Features: Cysticercoid in arthropods (in some cases).

• Entamoeba histolytica:

  • Pathogenesis: Flask shaped ulcer, invasion and destruction of the colonic epithelium.
  • Clinical Features: Amebiasis, potentially life-threatening.

• Giardia lamblia:

  • Pathogenesis: Duodenal trophozoites, cysts.
  • Clinical Features: Diarrhea, usually self-limiting.

Pseudomembranous Colitis

• Agent: Clostridium difficile
• Pathogenesis: Antibiotics disrupt normal colonic flora leading to C. difficile overgrowth, toxin release damaging epithelial cells, inflammation and pseudomembrane formation.
• Clinical Features: Antibiotic-associated colitis/diarrhea, protein loss, hypoalbuminemia, watery diarrhea.

Whipple Disease

• Agent: Tropheryma whipplei
• Pathogenesis: Distended foamy macrophages with PAS-positive granules.
• Clinical Features: Arthritis, fever, lymphadenopathy.