Vibrio Cholerae: Morphology, Culture, Pathogenicity, Treatment

Vibrios are actively motile by means of a polar flagellum, they are Gram negative, rigid, curved rods. The name ‘vibrio’ is derived from the characteristic vibratory motility. They are as poor genius and non capsulated. Vibrios are present in marine environments and surface waters worldwide. The most important member of the genus is Vibrio choleraewhich is the causative agent of cholera.

Morphology

Cholera vibrio is a short, curved, cylindrical rod, about 1.5 x 0.2 – 0.4 micrometer in size, with rounded or slightly pointed ends. The cell is typically comma shaped but the curvature is often lost on subculture. Its S – shaped or spiral forms may be seen due to two or more cells lying end to end. Pleomorphic is frequent in old cultures.

In stained films of mucous flakes from acute cholera cases, the vibrios are seen arranged in parallel rows, it was described by Koch as the ‘fish in stream’ appearance.

Cultural Characteristics

The cholera vibrio is strongly aerobic, growth being scanty and slow anaerobically. They grow in temperature range of 16 – 40 C (optimum 37 C). growth is better in an alkaline medium the range of pH being 6. 4 – 9.6 (optimum 8.2). NaCl is required for optimal growth though high concentrations (6% and above) are inhibitory.

It grow well on ordinary media. On nutrient agar, after overnight growth, colonies are moist, translucent, round discs, about 1 – 2 mm in diameter, with a bluish tinge in transmitted light. The growth has a distinctive odour. 

On MacConkeys agar, the colonies are colorless at first but become red reddish on prolonged incubation due to the late fermentation of lactose. 

On blood agar, colonies are initially surrounded by a zone of greening which later becomes clear due to hemodigestion. 

Biochemical Reactions

Carbohydrate metabolism is fermentation, producing acid, but no gas. Cholera vibrios ferment glucose, mannitol, maltose, mannose and sucrose but not inositol, arabinose, or lactose. Though, lactose may be split very slowly.

Indole is formed and nitrates are reduced to nitrites.

Resistance

Cholera vibrios are susceptible to heat, drying and acids, but resist high alkalinity. They are destroyed at 55 C in 15 minutes.

Dried on linen or thread, they survive for 1 – 3 days but die in about three hours on cover slips.

Survival in water is influenced by its pH, temperature, salinity, presence of organic pollution and other factors.

In laboratory, vibrios survive for months in sterile sea water, and this has been suggested as a method for the survival of vibrios in nature.

The vibrios do not survive for any length of time, in Ganges water of India, due to the apparently large amounts of vibriophages present.

They survive in clean tap water for thirty days. In untreated night soil, they may survive for several days. Vibrios are susceptible to the common disinfectants.

Pathogenesis

Natural infection with cholera occurs only in humans and not in animals. 

A number of animal models have been developed which have helped in understanding the pathogenic mechanisms in cholera. the first of these was the rabbit ileal loop model of De and Chatterjee (1953).

In human infections, the vibrios enter orally through contaminated water or food. Vibrios are highly susceptible to acids, and gastric acidity provides an effective barrier against that.  High does of vibrios given along food or sodium bicarbonate caused clinical cholera in 80 – 100% of them.

In the small intestine, vibrios are enabled to cross the protective layer of mucus and reach the epithelial cells by chemotaxis, motility, mucinase and other proteolytic enzymes.

Vibrios multiplying on the intestinal epithelium produce a toxin (choleragen, cholera enterotoxin, cholera toxin, CT or CTX) which is very similar to the heat labile toxin (LT) of E. coli in structural, chemical, biological and antigenic properties.

CT production is determined by a filamentous phage integrated with the bacterial chromosome. It can also replicate as a plasmid which can be transmitted to nontoxigenic strains, rendering them toxigenic.

CT, TCP and other virulence factors are regulated by the ToxR gene product, ToxR protein.

Laboratory Diagnosis

Stool, collected in the acute stage of the disease, before the administration of antibiotics, is the most useful specimen for laboratory diagnosis. Isolation of cholera vibrios from such stools is a simple matter as they are present in very large numbers.

Treatment

The treatment of cholera consists essentially of the prompt and adequate replacement of lost fluid and electrolytes. Oral administration of fluid containing glucose and electrolytes, either alone or supplemented by intravenous fluids is highly successful and freely available method of treating cholera.

Cereal based preparations are equally effective and usually more acceptable. Antibacterial therapy is of secondary importance. Oral tetracycline was recommended for reducing the period of vibrio excretion and the need for parenterally fluids.

Initially cholera vibrios were uniformly susceptible to all antibiotics active against Gram negative bacilli, but since 1979, multiple drug resistant strains have become increasingly common.

Reference: The Text Book Of Microbiology