Vibrios, Campylobacters and Associated Bacteria General Characteristics: Gram-negative rods Widely distributed in nature

Vibrio cholerae General Characteristics Curved rods/ Comma-shaped Aerobic Grow at very high pH Motile with polar flagellum No spores

Vibrio cholerae

Vibrio cholerae Clinical Findings Cholera Incubation period: 1-4 days S/S; nausea, vomiting, abdominal cramps, "rice water" stool (contains mucus, epithelial cells and large volume of vibrios), rapid fluid and electrolyte loss

Vibrio cholerae Pathology Enterotoxin- causes hypersecretion of water and electrolytes Attach to the microvilli Pathogenic only to humans Non-invasive

Vibrio cholerae Basis of classification: O antigen V. cholerae strain O group 1 - causes classical cholera Serotypes: Ogawa, Inaba, El Tor V. cholerae non-O1 - causes cholera-like disease *El Tor biotype cause milder diarrhea than the classic types

Vibrio cholerae Diagnostic Laboratory Tests Treatment Dark-field or phase-contrast microscopy Peptone or TCBS (Thiosulfate Citrate Bile salts Sucrose) agar Treatment Fluid and electrolyte replacement Tetracycline

Vibrio cholerae Epidemiology, Prevention and Control Mortality rate with treatment is 25-50% Worldwide epidemics: 1960 - classical biotype 1905 - El Tor biotype was discovered 1960 - pandemic in Asia, Middle East, and Africa

Vibrio cholerae Endemic in India and Southeast Asia Transmission: person-to-person contact (water, food, flies) Carrier state: 3-4 weeks

Vibrio parahaemolyticus Halophilic Causes acute gastroenteritis Transmission: ingestion of contaminated seafood Incubation period: 12-24 hrs S/S: nausea, vomiting, abdominal cramps, fever, watery to bloody diarrhea The disease subsides after 1-4 days with no treatment other than restoration of water and electrolytes Occurs worldwide

Vibrio parahaemolyticus TCBS Agar

Vibrio vulnificus Halophilic Can cause skin lesions, enteritis, bacteremia

Camylobacter jejuni General Characteristics Gram-negative rods with comma, S or "gull-wing" shapes Motile with single polar flagellum Do not form spores

Camylobacter jejuni

Camylobacter jejuni Campylobacter enteritis Clinical Findings S/S: crampy abdominal pain, profuse diarrhea with blood, headache, malaise, and fever Illness is self-limited to 5-8 days

Camylobacter jejuni Pathogenesis Virulence factor: lipopolysaccharide with endotoxic activity Invade the epithelium and produce inflammation that results in the appearance of RBC and WBC in stools

Helicobacter pylori Previously known as Campylobacter pylori Spiral-shaped, gram-negative rod Motile Strong producer of urease Grow at pH 6.0-7.0

Helicobacter pylori It is present in the gastric mucosa of less than 20% of persons under age of 30 but increase in prevalence in elderly Mode of transmission: person-to-person Causes gastritis and appears to be important in the pathogenesis of duodenal (peptic) ulcer H. pylori modifies the gastric mucus and further reduces the ability of acid to diffuse through the mucus

Camylobacter jejuni Diagnostic Laboratory Test Microscopy: dark-field or phase-contrast Culture: Skirrow's and Campy BAP medium Epidemiology and Control Mode of transmission: oral route from food (milk), drink, contact with infected animals, sexual activities