CHOLERA

7 pandemics
1. 1817-1823
2. 1826-1837
3. 1846-1862
4. 1864-1875
5. 1883-1896
6. 1900-1926 Caused

by V.cholera
7. 1961-1963 Caused by V.cholera El Tor

in Hamburg, disinfection team

anatomist Filippo Pacini, but his results were not widely known

around the world.

Filippo Pacini

contaminated drinking water in 1854.

He proposed a microbial origin

for epidemic cholera in 1849 and in his major state of the art review of 1855 he proposed a substantially complete and correct model for the aetiology of the disease.

In two pioneering epidemiological field-studies he was able to demonstrate that human sewage contamination was the most probable disease vector in two major epidemics in London in 1854.

V. cholerae, most epidemics are associated with a single serotype,

V. cholerae O1.
In 1992 V.cholerae serogroup O139 (Bengal) was registered as a new causative agent of cholera.

Capsula «-»
They are motile - monotrichous
V. cholerae has two circular chromosomes
Aerobes or

facultative anaerobes
Growth best in alkaline nutrient agar, pH 8.2
at t= 37C
Colonies are small, moist, translucent, round, bluish.
In 1% peptone water, growth occurs in about 6 hours as surface pellicle.

arabinose and lactose.
Indole is formed H2S «-»
Nitrates

are reduced to nitrites
Catalase and oxidase test are positive
Methyl red and urease test are negative
Gelatin is liquefied

genus Vibrio

O-somatic, is type specific
O1 and O139
O1 - A, B, C.
AB – Ogava, AC – Inaba, ABC – Hikojima.

alkaline medium.
Destroyed at 55С in 15 minutes
Killed in few minutes

in gastric juice.
Survive more 4 weeks in river water.
On food stuff survive for 10 days.

toxic effect and causes profuse, watery diarrhea.


V.cholera produced collagenase,

decarboxylase, lipase, mucinase and neuraminidase

and releases an enzymatically active subunit that causes a rise

in cyclic adenosine monophosphate (cAMP) production.
The resulting high intracellular cAMP level causes massive secretion of electrolytes and water into the intestinal lumen.

grows in the infected human gastrointestinal tract.
The enterotoxin, which

consists of two molecular subunits, attaches to the cell membranes of intestinal epithelial cells.
The B subunit binds to molecules on the cell surface and propels the smaller A subunit into the cell, where it stimulates adenylate cyclase, a membrane-associated enzyme that catalyzes the formation of cyclic AMP (cAMP).
The accumulation of cAMP results in massive secretion of salts and water from each affected cell.
The rapid loss of water produces a watery diarrhea that may cause a cholera patient to lose 20 liters of fluid daily.
Such a dramatic loss of water leads to severe dehydration, thickening of the blood, a decrease in blood volume, circulatory collapse (shock), and death if not rapidly treated.

of infection: patients, carriers and contaminated water
Symptom of diseases:
Weakness
Vomiting
Diarrhea

Curved vibrios adhering to epithelial surface.
Vibrio cholerae attachment and

colonization in experimental rabbits. The events are assumed to be similar in human

Put in thermostat (t=37C, 6 hours)
Results:



1% peptone water

1% peptone water 1% peptone water
+ 01 antisera + 0.5% starch

Prepare micropreparation
Gram’s method
Motility exam
Slide Agglutination
with antisera

If <+> & present cholera


clumps

Add Lugol iodine 2-3 drops
Starch + Lugol => blue
V.cholera ferment starch => color not change

of fluids and electrolytes are recommended. The fluid and electrolyte

balance can be maintained by the oral or intravenous administration of electrolytes in the presence of glucose. The glucose is essential because it stimulates uptake of sodium chloride and subsequent osmotic absorption of water.
Two types of vaccines against cholera are available, but they are only about 50 percent effective and confer immunity for only 6 months. In its current state, the vaccine is useless for preventing disease among residents of endemic areas. Several newer vaccines, some composed of toxic fragments, are being tested for use in endemic areas.