Family Vibrionaceae

Gram-neg slightly curved rods
Single polar flagellum
Cytochrome oxidase (+)
Most species are halophilic “salt-loving”
Ferment carbohydrates
Facultative anaerobes
Some are bioluminescent

Vibrio cholerae

Classified in serotypes
based on the “O”
Distinguished from other
vibrios biochemically and
by the production of
“choleragen,” a potent
Free living

Classification Species Oantigens Serotypes Biotypes V . c h o le r a e O 1 N on O 1 Ogawa Many strains Inaba Hikijima 02 – 138 139 Bengal El Tor Classical .


108 CFU Infects only humans Main reservoirs – marine shellfish. is generally associated with travelers .S. cholerae: Epidemiology       Infectious dose: 107 .V. cholerae is endemic to certain regions Outbreaks on the Gulf Coast are generally associated with consumption of under-cooked seafood Occurrence in the rest of the U. such as shrimp and oysters V.

Predisposing factors: poor sanitation. cholerae: Epidemiology    Transmission: drinking or bathing in fecallycontaminated water.V. There have been clearly 8 pandemics recorded since 1817. overcrowding. malnutrition. eating contaminated food. .


cholerae: El Tor strain .V.

 Attachment to the brush border of the gut epithelial cells  Motility  Enterotoxin .V. cholerae: Virulence factors   Proteases and mucinases.penetrate mucus layer Adherence factors  Toxin co-regulated pilus (Tcp).

Choleragen      AB type ADP-ribosylating toxin Polypeptide chains. 2 toxic subunits (A1. A2) disulfide bonds and 5 binding subunits B binds to GM1-ganglioside receptor A1 targets Gs alpha protein and catalyzes ADP-ribosylation of the G protein G protein unable to dissociate from adenylate cyclase complex .


cholerae ingested in large numbers •sensitive to stomach acid •large dose needed to cause disease unless patient is achlorhydric or taking antacids colonization of small intestine depends on •motility (polar flagella) •production of mucinase •attachment to specific receptors massive loss of fluid and electrolytes (no damage to enterocytes. no blood or WBC in stool) stool toxin production .The Pathogenesis of Cholera V.

rapid fluid loss. metabolic acidosis. hypokalemia. shock. acid-base imbalance. death Mortality 40-60% if untreated .Clinical Features  Majority of infections mild or asymptomatic  Symptoms entirely due to enterotoxin  Short incubation period (2-3 days)   Massive diarrhea. marked dehydration.

Severe dehydration Washer woman hands .

Cholera Cots Severe Dehydration .

Clinical/Histological features .


cholerae: Diagnosis  Clinical/epidemiological  Dark-field prep of stool    Stool culture on selective agar V.V. cholerae ferments sucrose Reportable disease in USA TCBS Agar .

V. cholerae: Treatment  Replacement of volume • •  oral or IV fluids and electrolytes reduces mortality to <1% Antibiotics not necessary but tetracycline can reduce excretion of vibrios .

cholerae: Prevention     Clean drinking water and adequate sewage disposal Wash fruit and vegetables Microorganism easily killed with usefulness.V. salt water. recommended for travelers . and mineral water Vaccine . but survives in ice cubes.

Vibrio parahemolyticus     Associated with ingestion of contaminated sushi or shellfish Halophilic vibrio Worldwide distribution. more prevalent in Japan It can resemble cholera .

cholerae) Production of a hemolytic cytotoxin (unlike V.V. parahemolyticus: Pathogenesis    Mechanisms of pathogenicity still unclear Invasive organism (unlike V. cholerae) .

vomiting.V. low-grade fever and abdominal cramps  Diagnosis .culture  Treatment . parahemolyticus: Clinical Aspects Short incubation period  Diarrhea.proper cooking of fish and seafood  .not required since disease is self-limiting  Prevention .

V. proteases Prevalent in Texas Gulf Coast Bioluminescent marine bacteria . V.Other Halophilic Vibrios      V. damsela. collagenases. vulnificus. alginolyticus Normal flora of marine life Bioluminescent Potent cytolisins.

erythema and pain.Pathogenesis • Diarrhea or infections of cuts and wounds contaminated with seawater • Rapidly progressive cellulitis • Swelling. bullae and eventually tissue necrosis • Life-threatening bacteremia • Immunocompromised people at high risk .

Clinical presentation .

Vibrio vulnificus infection .

24 hr. .

.48 hr.

receiving immunosuppressants or those with renal problems should not consume raw oysters! .Treatment and Prevention  Quick medical attention  Tetracyclin  Surgical drainage  Patients with cirrhosis.

11 species recognized C. jejuni most commonly associated with human disease . sheep & chicken  Resistant to many antibiotics  Cause zoonotic infections in humans   Family Campylobacteriaceae.Campylobacter  Normal flora of GI and GU tracts of cattle.

Campylobacter jejuni     Most common cause of gastroenteritis in the U. Microaerophilic Thermophilic (grows best at 42° ) Motile curved Gramnegative rods .S.

raw milk. water Poultry often implicated Person-to-person spread common among young children Contact with a sick household pet .infection acquired through contaminated food.C. jejuni: Epidemiology     Similar to Salmonella .

C. jejuni: Age-related incidence .

C. jejuni: Pathogenesis  Infectious dose .400-106 cells (cfu)  Pathogenesis not completely understood    Destruction of ileum. jejunum and colon mucosa Role of enterotoxins and cytotoxins not clear Strains lacking enterotoxin still virulent! .

lower abdominal pain. No chronic carriers .C. later bloody mucopurulent diarrhea. jejuni: Clinical Features      Indistinguishable from diarrhea caused by salmonella Longer incubation period Duration 3 days-3 weeks Usually enterocolitis .initial watery stools.


jejuni O19) Reiter’s Syndrome . tetracyclin . ciprofloxacin.associated with erythromycin. jejuni: Complications   Guillain-Barré syndrome (C.C.

jejuni: Lab Diagnosis   Culture on selective media Takes 2-4 days to grow  Grows best at 42° C  Biochemically inactive  Microaerophilic .C.

proper preparation of poultry. avoid contamination of water No screening for food handlers .Treatment & Prevention      No treatment necessary in mild cases Severe disease treat with erythromycin (children).same as Salmonella . and Ciproflaxin (adults) Treatment effective when given early Prevention .


Gastric ulcers Helicobacter pylori .

basic treatment and prevention. . pylori.Learning Objectives   Understand the bacteriological characteristics. virulence factors and pathogenesis of H. epidemiology. their diagnosis. Identify the clinical syndromes associated with this bacterium.


Barry Marshall from Charlottsville.Helicobacter pylori    First isolated in 1983 by Dr. Australia Association with peptic ulcers Reproduction of Koch’s postulates .

Helicobacter pylori      Gram-negative spiral bacterium Motile with 4-6 flagella Microaerophilic. urease positive Similar to Campylobacter but doesn’t grow at 42°C . grows slowly Oxidase. catalase.

H. pylori : Epidemiology


Humans only host

Other species found in dogs, cats,
ferrets, rats and mice

Acquired during childhood?

Possibly person-to-person transmission

H. pylori : Transmission

50% of adult population in the world
Associated with gastritis, gastric and
duodenal ulcers, and gastric cancer
Clinical findings include nausea, anorexia,
vomiting, epigastric pain
Most people colonized are asymptomatic

H. pylori : Virulence

Adherence factors
Heat-labile cytotoxin
Gastric mucin protease


Only 1% of infected people develop peptic ulcers .H. Lives in mucous layer overlapping gastric epithelium Protected from phagocytes by producing Super oxide dismutase (SOD) and catalase Host’s own inflammatory response damages mucosa. pylori : Pathogenicity     Not-invasive.

Clinical Aspects .


Silver Stain for Biopsies .

pylori : Treatment  Bismuth compounds (Pepto Bismol)  Metronidazole  Ampicillin  Tetracycline  95% cure rates  Some relapses .H.

Gastrointestinal Bacterial Infections – Summary .

• • EPEC EAggEC  Bloody diarrhea • Invasive • • • • • Shigella Salmonella Campylobacter Yersinia EIEC • Cytotoxin • EHEC .Clinical Syndromes (Outcomes)  Watery diarrhea • Toxigenic • • Cholera ETEC • Other mech.

cholerae. . EPEC. No blood or white blood cells present in stool. EAggEC. ETEC. Intestine remains essentially undamaged.Summary     Watery diarrhea is caused by toxigenic bacteria. Major toxigenic bacteria affecting the GI tract are V.

Enterotoxins  Choleragen and LT toxin of ETEC • • •  Bind to a specific receptor GM1 Inhibition of adenylate cyclase Increase cAMP ST toxin of ETEC • Increases guanosin monophosphate .

Smaller stool volumes. Ulceration and inflammation of the mucosa WBC present in stool.Invasive GI Tract Infections     Diarrhea caused by invasion and disruption of the enteric mucosa. . Bacteria affect both small and large intestines.

coli (EHEC) not invasive but causes bloody diarrhea .Invasive Pathogens        Shigella Salmonella Campylobacter Enteroinvasive E. coli (EIEC) Yersinia enterocolitica (minor) Vibrio parahemolyticus (minor) Enterohemorrhagic E.

None in mild cases. 3rd gen.Microorganism Drug of choice ETEC self-limiting. Prophylaxis with Cipro. Erythromycin (children). Te . Ciprofloxacin Shigella Ampicillin (50%) TMP. Ampicillin. Ciprofloxacin. prolong excretion Salmonella endocarditis Bactrim. cephalosporins reduce duration of diarrhea EHEC Supportive Salmonella gastroenteritis none indicated. Amp. EAggEC None indicated EIEC Bactrim. Bactrim. metronidazole. Rifaximin EPEC. Ciprofloxacin. Ampicillin. Ciprofloxacin Typhoid fever Bactrim. Avoid anti-motility drugs Yersinia enterocolitica self-limiting Vibrio cholerae oral or IV rehydration Vibrio parahemolyticus self-limiting Campylobacter jejuni none in mild cases. Ciprofloxacin (adults) Helicobacter pylori Bismuth compounds. Loperamide (Imodium) may shorten duration.