Vibrio Cholera Overview

Vibrio Cholera

• Vibrio species are motile, curved, Gram-negative bacilli (comma-shaped rods).
• Vibrio species are facultative anaerobic organisms.
• Their natural habitat is saltwater, where they multiply in shellfish and plankton.
• Major human pathogens include V. cholerae, V. parahaemolyticus, and V. vulnificus.
• V. cholera 01 and 0139 produce cholera enterotoxin, linked to cholera epidemics.
• V. cholera virulence factors include pili/adhesins, flagellum, hemagglutinin-protease, neuraminidase, siderophores, and cholera toxin.
• Cholera toxin induces massive diarrhea by increasing adenyl cyclase activity in mucosal cells.
• Severe V. cholera infection can result in severe fluid loss and electrolyte imbalances, leading to dehydration, muscle cramps, metabolic acidosis, and potentially hypovolemic shock and renal failure.
• Mortality rates are high in untreated cases, but are low in cases with fluid and electrolyte replacement therapies.
• Diagnosis involves microscopic examination (Gram stain) of stool samples and culturing the bacteria using TCBS agar (thiosulfate-citrate-bile salts-sucrose agar).
• Treatment involves fluid and electrolyte replacement, with antibiotic options such as azithromycin or doxycycline or ciprofloxacin.

Helicobacter Pylori

• H. pylori is a curved, Gram-negative bacillus requiring microaerophilic environments.
• H. pylori are highly motile (corkscrew motility) due to 5-6 polar flagella.
• H. pylori produce urease, which allows them to survive in harsh gastric environments.
• Humans are the primary reservoir for H. pylori.
• H. pylori infection can be transmitted from person to person, and through fecal-oral and oral-oral routes.
• Infections are ubiquitous and commonly cluster in families..
• H. pylori is linked to several gastrointestinal diseases, including:
  • Type B gastritis
  • Gastric ulcers
  • Gastric cancers (gastric adenocarcinoma of the body and antrum and gastric mucosa-associated lymphoid tissue [MALT] B-cell lymphomas)
• H. pylori virulence factors include:
  • Lytic enzymes (mucinases)
  • CagA protein
  • VacA protein
  • Attachment factors
  • Flagella
• H. pylori can cause inflammation and damage to the stomach lining, leading to gastritis and ulcers.
• H. pylori infections often cause alteration of signaling pathways, cytoskeletal rearrangement, and disruption of tight junctions.
• Diagnosis methods include urea breath tests (non-invasive), gastric biopsy (invasive), and detection of H. pylori antigens in stool samples or IgG in serum samples.
• Treatment often involves triple therapy, consisting of a proton pump inhibitor, a macrolide, and a beta-lactam antibiotic, for 7-10 days.