Cholera. Lesson № 6 презентация

Cholera dates back to the most ancient times. There were 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

1892 cholera outbreak in Hamburg, Germany, hospital ward
1892 cholera outbreak in Hamburg, disinfection team

The bacterium had been originally isolated in 1854 by Italian anatomist Filippo Pacini, but his results were not widely known around the world.
Filippo Pacini

John Snow
John Snow (1813-1858) found a link between cholera and 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.

Robert Koch identified
V. cholerae in 1885.
Robert Koch

Robert Koch
Isolator of V.cholera
Nobel of Medicine,1905

Taxonomy
FAMILY VIBRIONACEAE
Genus: Vibrio
Species: V.cholerae
Biovars: Cholerae (1883) and El Tor (1906)

Although there are more than 130 different serogroups of 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.

FAMILY VIBRIONACEAE
VIBRIO CHOLERAE
Gram «-» curved rods
Spores «-» 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.

TSBC agar

Biochemical properties
Ferment glucose, mannitol, maltose, mannose, sucrose (acid), but not 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

Heiberg, group 1
Mannose «+» acid
Saccharose «+» acid
Arabinose «-»

VIBRIO CHOLERAE
Antigens: H - flagellar , is common for genus Vibrio O-somatic, is type specific
O1 and O139
O1 - A, B, C.
AB – Ogava, AC – Inaba, ABC – Hikojima.

Resistance
Susceptible to heat, drying, acid and common disinfectants but resist 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.

Toxin Production
V.cholera produced enterotoxin called cholerogen which has a powerful toxic effect and causes profuse, watery diarrhea.
V.cholera produced collagenase, decarboxylase, lipase, mucinase and neuraminidase

Cholerogen
Toxin binds to the plasma membrane of intestinal epithelial cells 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.

Cholera enterotoxin (cholerogen-exotoxin) is produced by the pathogen as it 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.

Disease in Men
Cholera is transmitted by the fecal-oral route
Source of infection: patients, carriers and contaminated water
Symptom of diseases:
Weakness
Vomiting
Diarrhea

Scanning electron microscopy during early infection. Curved vibrios adhering to epithelial surface.
Vibrio cholerae attachment and colonization in experimental rabbits. The events are assumed to be similar in human

Development of diseases

Symptom of disease
rice water stool

Rapid Diagnosis
Material: feces, vomit, drinking water
Inoculate into 3 test tubes
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

Bacteriological Examination

DifferIdeIens of Biovars of Cholera Vi

Treatment and Immunoprophylaxis
In treating cholera, antibiotics, and continual replacement 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.

Treatment
Cholera bacteriophages
Antibiotic of Tetracycline group
Pathogenic therapy
Control of dehydration