Microbiology Lecture 45 Bacterial Gastrointestinal Diseases

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Cholera Epidemiology

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Epidemic cholera caused by the O-1 (the classic and El Tor biotype forms) and O-139 types
--Others cause diarrheal disease
spread through contaminated drinking waterand food, no p2p
High Infectious Dose
Worldwide distribution: massive human morbidity and mortality.
US: Gulf Coast/Travel Associated--> not harbingers of epidemics
Periodic epidemics and pandemics
frequent attendant of disasters (natural and human-made)
Reservoir: 20% of human aSx cariers in endemic regions, zooplankton
(1854 John Snow)

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Cholera Clinical Manifestations

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1-5 days incubation: Colonization of small intestine mucosa WITHOUT change in physical integrity

Cardinal feature : abrupt onset massive watery diarrhea (1 liter /hour)
"Rice water” stools
Rapid Death from dehydration. electrolyte loss

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Vibrio cholerae morphology, biochemistry

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nonspore-forming Gram negative facultatively anaerobic vibrio
Oxidase positive
Motile, polar flagellum
Classified by O antigens: O-1 & O-139 infect humans

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O-1 Vibrio cholerae

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Classic epidemic cholera
Epidemic-associated biotypes “classic” and “El Tor”
El Tor hardier, dominant cause of O-1 serogroup-caused cholera epidemics

Both biotypes may be divided into additional epidemic–associated serotypes; [Inaba, Ogawa, Hikojima]

No cross-reaction with O-139 Vibrio cholerae

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O-139 Vibrio cholerae

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Newly recongized cholera agent

O-1 LPS synthesis genes replaced

no corss rxn with O-1 V cholera = reinfection

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Cholera toxin

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AB enterotoxin of Cholera from phage 9kb ctx genes
ctx = filamentous m13 related virus
ctx virus receptor endoced by tcp (toxin coregulated pilus) pathogenicity island, VPI, the genome of the filamentous VPI phage

B: Binds Surface G1
A: ADP-ribosylates a cAMP regulatory GTP binding protein
cAMP levels increase-->hypersecretion-->severe diarrhea

ToxR gene/protein senses environment, controls txp and ctx expression
best in small intestine with [iron]low. quorum sensing deactivates pilus.


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VPI phage

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filamentous phage
lysogenic conversion with vibrio cholera-->Vibrio cholerae pathogenicity island
tcp gene (toxin coregulated pilus) encodes for both an attachment pilus
and for receptors for the CTX Phage
CTX Phage (Cholera Toxin) encodes AB endotoxin which produces diarrhea

ToxR gene/protein senses environment, controls txp and ctx expression
best in small intestine with [iron]low. quorum sensing deactivates pilus.

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V cholerae Dx

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Direct microscopic examination of stool
Large numbers of vibrio-shaped bacteria present
Not easy to observe (despite numbers) -- typically look for motility

Culture--grows on most media use for stool cultures
Dies in acidic dry environments
Best: base, high salt: Thiosulfate citrate bile salts sucrose (TCBS): opaque yellow colonies

Rapid agllutination tests, specific antiseras

Non-lysogenic V cholerae may cause diarrhea, but not cholera

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Cholera Treatment

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Mild disease- Oral rehydration solution (ORS) administration, glucose enhances Na uptake

Severe cases- IV Lactated Ringer’s solution until pulse restoration, then oral glucose rehydration solution
Antibiotics: Tetracycline. Ciprofloxacin, TMP-SMX

Fluid Secretion continues after bacteria gone because Toxin still around

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Index Case for an Outbreak

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(Index case = first pt.)

Often member of carrier's household (20% of humans in endemic regions are carriers)

El Tor O-1 V cholerae survives better than classic O-1 as carrier.

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Cholera Susceptibility factors

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More severe in blood group O

Acid sensitive: achlorohydria, reduced gastric acidity, reduced gastric retention.
Neutralized pH= 10kx reduxn in inoculum

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Cholera Vaccine

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killed organism/toxoidvaccine

Short lived-immunity, with side effects, not fnx vs all endemic strains

Travelers should take prophylactic tetracycline
Not needed mostly because high infectious dose if hygiene good

Live attenuated strains not good since toxicity from lysogenic conversion

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Preventing Cholera

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Travelers should take prophylactic tetracycline
Not needed mostly because high infectious dose if hygiene good

Proper Control of Sewage

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Most common cause of bacterial food-borne illness in Japan

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V. parahaemolyticus:

Gastroenteritis to a mild cholera-like illness

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V. parahaemolyticus

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self-limiting disease gastroenteritis to a mild cholera-like illness
normal inhabitant of coastal ocean and estuary waters

Consumption of raw or undercooked shellfish has been a recurrent source of human infection.

Summer disease, World-wide distribution, endemic in Japan, US Gulf Coast

Oxidase positive, will form green colonies on TCBS agar

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V. vulnificus

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coastal marine and estuary waters
associated with oysters, seawater with oyesters
more common when warm (Summer Disease)

particularly virulent: wound infections, acute-self-limiting diarrhea, and fatal septicemia (raw oyesters + liver dysfunx/underlying debilitation--> bullous skin lesions, vomiting, shock, tx with tetracycline)

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37Recognizing VibrioInfections

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1% sodium chloride is required for the growth of this microbe


Sucrose non-fermenters: Usually forms green colonies on TCBS agar (though V Cholera = yellow)

If a vibrio suspected, request TCBS agar or vibrio isolation favorable agar.

Probably significantly under-diagnosed

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V Cholera

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related to El Nino