Vibrio Cholera and Helicobacter Pylori PDF

Medical Bacteriology Vibrio cholera Helicobacter pylori  VIBRIO Vibrio species are: o motile (a single polar flagella), curved, Gram negative bacilli → comma-shaped rods (vibrions) o facultative anaerobic organisms Their natural environment...

Medical Bacteriology Vibrio cholera Helicobacter pylori  VIBRIO Vibrio species are: o motile (a single polar flagella), curved, Gram negative bacilli → comma-shaped rods (vibrions) o facultative anaerobic organisms Their natural environment is saltwater where they can multiply freely, and they have been find in shellfish and plankton. The major human pathogens are: V. cholera O1 and O139 produce the cholera enterotoxin and are associated with epidemics of cholera  V. cholera pathogenesis Virulence factors: o pili/adhesin factors o flagellum o hemagglutinin-protease (mucinase) for colonization o neuraminidase o siderophores o cholera toxin enterotoxin produce its effect by stimulating adenyl-cyclase activity in mucosal cells V. cholera pathogenesis o abrupt onset of watery diarrhea and vomiting, “rice- water” stools (severly infected patients can lose up to 15 liters of fluid per day) o fluid and electrolyte loss → dehydration, muscle cramps, metabolic acidosis (bicarbonate loss), hypokalemia, hypovolemic shock and renal failure o mortality rate: 70% in untreated patients, < 1% in patients who are treated with replacement of fluids and electrolytes  Diagnosis and therapy of V. cholerae infection Clinical diagnosis Laboratory diagnosis o Microscopic examination (Gram stain) of stool specimens o Culture: bacteria grow in TCBS (thiosulfate-citrate-bile salts-sucrose agar), a selective medium that inhibits gram-positive bacteria and Enterobacteria Therapy o fluid and electrolyte replacement o oral antibiotics: azithromycin or doxycycline or ciprofloxacin  Helicobacter pylori o Curved, Gram-negative bacilli that requires microaerophilic environments to grow o highly motile (corkscrew motility) through 5 to 6 polar flagella o urease-producer → urease allows the bacteria to survive the harsh gastric environment Humans are the primary resevoir for the bacteria, and no animal resevoir has been identified at the present time. Infections are ubiquitous and worldwide, commonly clustered in families or among close contacts as transmission is person-to-person, and by fecal-oral and oral-oral routes. H. pylori has been implicated in the development of multiple gastrointestinal diseases: o type B gastritis o gastric ulcers o gastric cancers: gastric adenocarcinoma of the body and antrum and gastric mucosa- associated lymphoid tissue (MALT) B-cell lymphomas  Pathogenesis of H. pylori infection Lytic enzimes (mucinases) Flagella Pathogenesis of H. pylori infection GASTRITIS PEPTIC ULCERS GASTRIC CANCER  Diagnosis and Therapy of H. pylori infection o urea test on gastric biopsy (invasive) o urea breath test (non-invasive) o detection of H. pylori antigens in stool samples (poor sensitivity) o detection of IgG in serum samples (screening test) TRIPLE THERAPY: Combination of a proton pump inhibitor (e.g., omeprazole), a macrolide (clarithromycin), and a β-lactam (amoxicillin), with administration for 7 to 10 days