Slightly Curved Bacilli

Vibrio Members of this genus share many characteristics with enteric bacteria such as Escherichia and Salmonella Found in water environments worldwide (among the most common bacteria in surface waters). Vibrio cholerae is the most common species to infect humans Vibrio cholerae serogroup O1 (Ogawa & Inaba serotypes) It has 2 biotypes: classical and ElTor Causes cholera Humans become infected with V. cholerae by ingesting contaminated food and water Found most often in communities with poor sewage and water treatment There are 100 O serogroups. Many vibrios share a single heat labile flagellar H Ag

Vibrio They are curved aerobic rods motile by a polar flagellum A large inoculum (108) is required to cause disease because the bacteria are susceptible to the acidic stomach environment Cholera toxin (enterotoxin) is the most important virulence factor of V. cholerae Lemon drops during epidemics

GM1

Cholera Pathology Some infections are asymptomatic or cause mild diarrhea Incubation period is 1-4 days Can cause severe disease resulting in abrupt watery diarrhea and vomiting (20-30L/day) “Rice-water stool” is characteristic Results in severe fluid and electrolyte loss, dehydration, shock, acidosis, anuria Can progress to coma and death Mortality rate in untreated cases is 60%

Diagnosis, Treatment, and Prevention Usually based on the characteristic diarrhea Selective medium : TCBS (thiosulphate, citrate, bile salt, sucrose agar) pH 8.5-9.5 Vibrio cholerae is a sucrose fermenter Vibrio parahemolyticus is a non-sucrose fermenter

Treatment Treatment Prevention Fluid and electrolyte replacement Antimicrobial drugs are not as important because they are lost in the watery stool Tetracyclines reduce stool output and shorten the period of excretion of vibrios Resistance via plasmids is developing An attack is followed by immunity of unknown duration Prevention Adequate sewage and water treatment can limit the spread of V. cholerae

Epidemiology Epidemics caused by classical biotype through the early 1960s El Tor biotype prevailed in the late 1960s It is endemic in Southeast Asia Ships have carried it to ports all around the world in ballast water It is spread by person to person contact, water, food, and flies There are seldom carriers

Other Diseases of Vibrio Vibrio parahaemolyticus It is halophilic and does not ferment sucrose Results from ingestion of shellfish or raw fish Incubation period is 12-24 hours Causes cholera-like gastroenteritis Vibrio vulnificus Causes septicemia following consumption of contaminated shellfish Infections can result from washing wounds with contaminated seawater (skin lesions)

Campylobacter Gram negative rods with comma, S or “gull wings” shapes Motile with a single polar flagellum, non-sporing. One of the most common causes of gastroenteritis in the developed world Many animals serve as reservoirs for the bacteria where they cause sepsis, abortion or enteritis Humans become infected by consuming contaminated food, milk, or water Infections produce bloody and frequent diarrhea that is self-limiting Spread of the bacteria can be reduced by proper food handling and preparation

Campylobacter jejuni A common human pathogen causing enteritis Poultry is the most common source of infection The source of infection may be food, drink, contact with infected animals or humans and their excreta Organisms multiply in the small intestine, invade the epithelium and produce inflammation causing appearance of RBCs and WBCs in stools resembling shigellosis.

Culture Selective medium is Skirrow’s medium (VPT). Colonies are colourless or grey (tear drop) or watery or round Incubation atmosphere: microaerophilic with reduced O2 (5%) and added CO2 (10%) Incubation temperature 42-43ºC Oxidase and catalase positive

Treatment Self limited Erythromycin: shortens the duration of fecal shedding of bacteria

Other Campylobacters Other species include Campylobacter fetus (cattle & sheep), Campylobacter coli (pigs) and Campylobacter lari (animals and birds). Campylobacter fetus can cause systemic infections in immunocompromised patients.

Helicobacter pylori Was originally placed with campylobacters but it has sheathed flagella and is urease positive Slightly helical, Gram-negative highly motile bacterium that colonizes the stomach of its hosts It is present on the gastric mucosa of 20% of persons under 20 years and increases up to 80% in adults in developing countries The natural history of infection is not well known but it is likely that person to person transmission and common source infections occur Once acquired, infection persists for years or for life.

Virulence factors H.pylori produces numerous virulence factors that enable it to colonize the stomach It is a strong producer of urease Flagella that enable the pathogen to burrow through the mucous lining the stomach Adhesins facilitate binding to gastric cells H. pylori also produces a protease that modifies the gastric mucous and further reduces the ability of acid to diffuse through the mucous. Toxins and lipopolysaccharide A toxin that inhibits acid production by stomach cells

Pathogenesis Associated with antral gastritis Important in Peptic ulcer (duodenal) Warren-MarshalL & Koch’s postulates Optimum pH 6-7, killed at low pH Gastric mucous is relatively impermeable to acid and has a strong buffering capacity. On the lumen side of the mucous, pH is low 1-2 While on the epithelial side the pH is about 7.4 H. pylori is found deep in the mucous layer near the epithelial surface

Pathogenesis (cont.) H. pylori also produces a potent urease which yields ammonia and further buffers the acid. H. pylori is quite motile even in mucous and is able to find its way to the epithelial surface H. pylori invades the epithelial cell surface to a limited degree Toxins and lipopolysaccharide may damage the cells also IgM, IgG & IgA are produced and persist in chronic infections

Phagocytosed bacteria survive in leukocytes by catalase and superoxide dismutase

Diagnosis, Treatment, and Prevention Mainly histologically (biopsy) Presence of H. pylori can be demonstrated by a positive urease test Biochemical tests provide a definitive identification Treatment Antimicrobial drugs are used in combination with drugs that inhibit acid production (triple therapy) Prevention Prevention is difficult because the exact mode of transmission is unknown

                           A gastric MALT-lymphoma