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
antigens
Distinguished from other
vibrios biochemically and
by the production of
choleragen, a potent
enterotoxin
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

V. cholerae: Epidemiology

Infectious dose: 107 - 108 CFU

Infects only humans
Main reservoirs marine shellfish, such as shrimp
and oysters
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.S. is generally
associated with travelers

V. cholerae: Epidemiology

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

V. cholerae: El Tor strain

V. cholerae: Virulence factors

Proteases and mucinases- penetrate mucus

layer
Adherence factors
Toxin co-regulated pilus (Tcp).
Attachment to the brush border of the gut
epithelial cells

Motility

Enterotoxin

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

The Pathogenesis of Cholera

V. 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

Clinical Features

Majority of infections mild or asymptomatic

Symptoms entirely due to enterotoxin

Short incubation period (2-3 days)

Massive diarrhea, rapid fluid loss, acid-base

imbalance, marked dehydration, hypokalemia,
metabolic acidosis, shock, death
Mortality 40-60% if untreated

Severe dehydration

Washer woman hands

Cholera Cots

Severe Dehydration

Clinical/Histological features

V. cholerae: Diagnosis

Clinical/epidemiological

Dark-field prep of stool

Stool culture on
selective agar

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

V. cholerae: Prevention

Clean drinking water and adequate sewage

disposal
Wash fruit and vegetables
Microorganism easily killed with
chlorination, but survives in ice cubes, salt
water, and mineral water
Vaccine - limited usefulness,
recommended for travelers

Vibrio parahemolyticus

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

V. parahemolyticus: Pathogenesis

Mechanisms of pathogenicity still unclear

Invasive organism (unlike V. cholerae)
Production of a hemolytic cytotoxin
(unlike V. cholerae)

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

Other Halophilic Vibrios

V. vulnificus, V. damsela,
V. alginolyticus
Normal flora of marine
life
Bioluminescent
Potent cytolisins,
collagenases, proteases
Prevalent in Texas Gulf
Coast

Bioluminescent
marine bacteria

Pathogenesis

Diarrhea or infections of cuts and wounds

contaminated with seawater

Rapidly progressive cellulitis

Swelling, erythema and pain, bullae and

eventually tissue necrosis

Life-threatening bacteremia

Immunocompromised people at high risk

Clinical presentation

Vibrio vulnificus infection

24 hr.

48 hr.

Treatment and Prevention

Quick medical attention

Tetracyclin

Surgical drainage

Patients with cirrhosis,

receiving
immunosuppressants or
those with renal
problems should not
consume raw oysters!

Campylobacter

Normal flora of GI and GU tracts of cattle,

sheep & chicken

Resistant to many antibiotics

Cause zoonotic infections in humans

Family Campylobacteriaceae; 11 species

recognized

C. jejuni most commonly associated with

human disease

Campylobacter jejuni

Most common cause

of gastroenteritis in
the U.S.
Microaerophilic
Thermophilic (grows
best at 42 )
Motile curved Gramnegative rods

C. jejuni: Epidemiology

Similar to Salmonella - infection acquired

through contaminated food, raw milk,
water
Poultry often implicated
Person-to-person spread common among
young children
Contact with a sick household pet

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!

C. jejuni: Clinical Features

Indistinguishable from diarrhea caused

by salmonella
Longer incubation period
Duration 3 days-3 weeks
Usually enterocolitis - initial watery
stools, lower abdominal pain, later bloody
mucopurulent diarrhea.
No chronic carriers

C. jejuni: Complications

Guillain-Barr syndrome (C. jejuni O19)

Reiters Syndrome - associated with
erythromycin, ciprofloxacin, tetracyclin

C. jejuni: Lab Diagnosis

Culture on selective
media
Takes 2-4 days to
grow

Grows best at 42 C

Biochemically inactive

Microaerophilic

Treatment & Prevention

No treatment necessary in mild cases

Severe disease treat with erythromycin
(children), and Ciproflaxin (adults)
Treatment effective when given early
Prevention - same as Salmonella - proper
preparation of poultry, avoid
contamination of water
No screening for food handlers

Gastric ulcers

Helicobacter pylori

Learning Objectives

Understand the bacteriological

characteristics, epidemiology, virulence
factors and pathogenesis of H. pylori.
Identify the clinical syndromes
associated with this bacterium, their
diagnosis, basic treatment and prevention.

Helicobacter pylori

First isolated in 1983

by Dr. Barry Marshall
from Charlottsville,
Australia
Association with peptic
ulcers
Reproduction of Kochs
postulates

Helicobacter pylori

Gram-negative spiral
bacterium
Motile with 4-6 flagella
Microaerophilic, grows
slowly
Oxidase, catalase,
urease positive
Similar to
Campylobacter but
doesnt grow at 42C

H. pylori : Epidemiology

Unknown

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

infected
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

Urease
Motility
Adherence factors
Heat-labile cytotoxin
Gastric mucin protease
Hemolysin
Lipopolysaccaharide

H. pylori : Pathogenicity

Not-invasive. Lives in mucous layer

overlapping gastric epithelium
Protected from phagocytes by producing
Super oxide dismutase (SOD) and catalase
Hosts own inflammatory response damages
mucosa.
Only 1% of infected people develop peptic
ulcers

Clinical Aspects

Silver Stain for Biopsies

H. pylori : Treatment

Bismuth compounds (Pepto Bismol)

Metronidazole

Ampicillin

Tetracycline

95% cure rates

Some relapses

Gastrointestinal Bacterial
Infections Summary

Clinical Syndromes (Outcomes)

Watery diarrhea
Toxigenic

Cholera
ETEC

Other mech.

EPEC
EAggEC

Bloody diarrhea
Invasive

Shigella
Salmonella
Campylobacter
Yersinia
EIEC

Cytotoxin

EHEC

Summary

Watery diarrhea is caused by toxigenic

bacteria.
Intestine remains essentially undamaged.
No blood or white blood cells present in
stool.
Major toxigenic bacteria affecting the GI
tract are V.cholerae, ETEC, EPEC,
EAggEC.

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

Invasive GI Tract Infections

Diarrhea caused by invasion and

disruption of the enteric mucosa.
Bacteria affect both small and large
intestines.
Smaller stool volumes.
Ulceration and inflammation of the
mucosa WBC present in stool.

Invasive Pathogens

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

Microorganism

Drug of choice

ETEC

self-limiting. Loperamide (Imodium) may shorten

duration. Prophylaxis with Cipro, Bactrim, Rifaximin

EPEC, EAggEC

None indicated

EIEC

Bactrim, Ciprofloxacin, 3rd gen. cephalosporins reduce

duration of diarrhea

EHEC

Supportive

Salmonella gastroenteritis

none indicated; prolong excretion

Salmonella endocarditis

Bactrim, Ampicillin, Ciprofloxacin

Typhoid fever

Bactrim, Ampicillin, Ciprofloxacin

Shigella

Ampicillin (50%) TMP, Ciprofloxacin.

None in mild cases. Avoid anti-motility drugs

Yersinia enterocolitica

self-limiting

Vibrio cholerae

oral or IV rehydration

Vibrio parahemolyticus

self-limiting

Campylobacter jejuni

none in mild cases. Erythromycin (children),

Ciprofloxacin (adults)

Helicobacter pylori

Bismuth compounds, metronidazole, Amp, Te