Gastrointestinal pathogens: Vibrio cholerae Prof. Alaa Al-Charrakh Babylon University

Family Vibrionaceae: Include the genera: Gastrointestinal pathogens Family Vibrionaceae: Include the genera: Vibrio V. cholerae: cholera V. parahaemolyticus: gastroenteritis Aeromonas A. hydrophila: gastroenteritis; wound infection Campylobacter C. jejuni: gastroenteritis Helicobacter H. pylori: gastritis; peptic ulcer; gastric cancer, MALToma

Vibrio cholerae -Gram-ve curved rod. Motile by a polar flagellum. -Grow at a high pH (8.5- 9.0) and are rapidly killed by gastric acid. -Oxidase-positive. -Vibrio species inhabit marine environments, and are halophilic.

Antigenic structure & biological classification O antigen: confers serological specificity. Serogroups O1 and O139 cause cholera. V. cholerae O1: Sero-subtypes: Inaba, Ogava & Hikojima Two biotypes of V. cholerae O1: classical and El Tor. Hemolysin V-P test Polymixin B classical - - sensitive El Tor + + resistant

El Tor V. cholerae It was first identified in 1905 at a quarantine camp on the Sinai Peninsula in El-Tor, Egypt. The vibrios were found in the guts of six pilgrims returning from Mecca.

Cholera epidemics - Are associated with V. cholerae O1 - None O1 V. cholerae (O139) reported in Bangladesh in 1992 - In 2007, a lack of clean drinking water in Iraq led to an outbreak of cholera. A total of 181 people were infected, with 10 deaths reported. Basic water sterilization became impossible in some places due to restrictions on the availability of chlorine for water sterilization.

Pathogenesis and Immunity V. cholerae is pathogenic only for humans. Mean infective dose: 108-1010. Gastric acid provides some protection. Mouth intestine attach to the microvilli of the epithelial cells and multiply release cholera toxin. Major virulence factors: Toxin-coregulated pili (TCP): adherence to mucosal cells. Enterotoxin (cholera toxin): produced by O1 and O139 strains. Hemagglutinin-protease: releases bacteria from mucosal cells. other enterotoxins, flagellum, siderophores.

V. cholerae Clinical Diseases Incubation period: 1-4 days. -Sudden onset of nausea and vomiting, and profuse diarrhea with abdominal cramps; "rice water" stool (containing mucus, epithelial cells, and large numbers of vibrios) -rapid loss of fluid and electrolytes profound dehydration that leads to circulatory collapse (hypovolemic shock). Carrier state seldom exceeds 3-4 weeks. The El Tor biotype causes milder disease than the classical biotype.

Cholera Toxin CT is a proteinaceous enterotoxin. It composed of a AB subunit. The B subunit forms a pentameric structure that binds the CT to the receptor on the eukaryotic cells. The A subunit contains the enzyma-tically active portion or the toxin Proteolytic cleavage of the A subunit results in A1 and A2 peptide units which remain linked by a disulfide bond. Cholera Toxin Once the A subunit is internalized by the eukaryotic cell, the disulfide bond is reduced. The A1 subunit contains a ADP-ribosyltransferase which covalently modifies the G protein, which regulates adenylate cyclase. Adenylate cyclase mediates the formation of cAMP The increase in cAMP levels bring about the secretion of chloride and bicarbonate from the mucosal cells into the intestinal lumen

Diagnostic lab tests Specimens: mucus flecks from stool. Smears: Dark-field or phase contrast microscopy may show the rapidly motile vibrios. Culture: peptone agar, blood agar (pH near 9.0), or TCBS (thiosulfate-citrate-bile salts-sucrose) agar. Alkaline peptone broth can be used for enrichment. Biochemical tests Serological tests: slide agglutination tests using anti-O1 or O139 antiserum.

Growth of V. cholerae on TCBS

Treatment Water and electrolyte replacement - most important. Antibiotic treatment: tetracycline or trimethoprim-sulfamethoxazole. Controls: Improvement of sanitation and personal hygiene. Isolation of patients, and their excreta be disinfected. Vaccination: in development.