Cholera

Organism. Vibrio cholerae. Classical cholera is caused by V. cholerae 01, while most of the recent epidemics have been due to the El Tor biotype. V. cholerae 0139, which appeared in 1992, is a more virulent ser-ogroup variant of the El Tor biotype.

Clinical features A profound diarrhoea of rapid onset that leads to dehydration and death should be considered as a case of cholera until proved otherwise. The diarrhoea contains no faecal particles, but is watery and flecked with mucus (not cells), the so-called rice-water stools. The passage of large quantities of fluid leads to rapid and extreme dehydration, which can be fatal. Vomiting can also be present in the early stages.

Diagnosis V. cholerae can be identified from the diarrhoeal discharge, vomitus or by rectal swab. Its characteristic mobility (it vibrates, hence being called a vibrio) can be seen by dark ground or phase-contrast microscopy and is inhibited by specific antiserum. Confirmation of the diagnosis is made by culture on TCBS sucrose agar. A suitable transport medium is Carey Blair, or alternatively 1% alkaline (pH 8.5) peptone water, which can also be used for water samples.

Transmission Classical cholera is a disease of water transmission, whereas El Tor is by both water and food. Generally, epidemic cholera is transmitted by water and endemic cholera by food. It may appear in a seasonal pattern, often in association with other causes of diarrhoea (Fig. 8.2). It is the endemic nature of El Tor and its persistence in the environment that has been responsible for its prodigious spread.

For every clinical case of El Tor cholera, there can be as many as 100 asymptomatic cases, explaining how epidemics spread from one region to another, but not how infection persists in the environment. Vibrios may be able to persist in an aquatic environment, such as in the mucilaginous covering of water plants or fish, in association with copepods or other zooplankton. An alternative method may be due to continuous person-to-person transmission in a sub-clinical asymptomatic cycle. When a susceptible person enters the cycle or there is an environmental or climatic change, a fresh epidemic starts.

V. cholerae in water are easily destroyed by sunlight, chemical action or competing bacteria. However, where these elements are not present, it can survive in fresh water for some time and in saline water for at least a week. The level of salinity needs to be between 0.01% and 0.1% as is found in estuarine or lagoon water. V. cho-lerae in these saline environments can be taken up by shellfish or fish, which then form an alternative method of infection when eaten uncooked.

The isolation of V. cholerae from river water has been perplexing because epidemiological investigations show this source of infection to be important, but bacteriologists have not isolated organisms in sufficient numbers. One possible explanation is the presence of non-agglutinable vibrios (alternatively known as non-cholera vibrios), which are closely related to V. cholerae except that they do not agglutinate antisera. These are known to be mutations so that shifts between typical vibrios and non-agglutinable forms may occur. If this is a regular feature in nature, then it could help to explain where cholera goes to (especially the classical form) during inter-epidemic periods. The appearance of non-01 cholera (vibrio 0139) supports this view.

V. cholerae has been found to remain viable in crude sewage for over a month and in sewage-contaminated soil for up to 10 days, a possible source of infection carried over to rivers or wells. It has been isolated from a number of foodstuffs especially those with a pH between 6 and 8, such as milk produce (e.g. ice cream), sugar solutions, meat extracts or articles of food preserved by salt. Uncooked fish and vegetables, which have been washed or irrigated by sewage effluent, have been responsible for outbreaks.

Direct person-to-person spread or via fomites, such as utensils or drinking straws (in home-brewed alcohol parties), do not appear to be as important as expected. Even for persons attending the death of a cholera victim, it is more likely that infection will result from drinking water or consuming food that has been prepared for the mourning ceremony, rather than from the dead person or their shrouds.

A case of cholera can excrete between 107 and 109 V. cholerae per millilitre of diarrhoeal discharge and since the volume of this discharge may be in excess of 20l/day, the potential for contamination of the environment is enormous. Clearly, though the severe case is unlikely to be anything but a transitory source, it is the asymptomatic case passing from 102 to 105 organisms/g of stool in a spasmodic manner that poses the greatest hazard.

Fig. 8.2. Similar pattern of gastroenteritis and cholera in Calcutta, India (1973-1978). (Reproduced with permission from the Indian Council of Medical Research (1978) National Institute of Cholera and Enteric Diseases, Annual Report, Indian Council of Medical Research, Calcutta.)

A high dose of V. cholerae is required to infect the healthy subject. Some 106-108 organisms are needed, but if the person has a decreased gastric acidity, then 103 organisms may be sufficient. Lowered gastric acidity is found more commonly than expected and may be related to malnutrition or diet. Cannabis smoking is known to de press gastric acidity. Blood group O is associated with an increased severity of cholera.

Carriers are of short duration; 70% of cholera cases are free of vibrios at the end of the first week and 98% by the end of the third. Long-term carriers are rare and of no epidemiological importance.

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