Some observations on the detection of cholera carriers.
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Biomedical subjects
Publications and source records attributed to D Barua.
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Cholera carrier studies in the Philippines in 1964-66 showed a prevalence rate of 21.7% among household contacts of cholera patients, and 8.4% in occupants of houses next door to one where a cholera patient lived, as opposed to 0.34% in the general population. The duration of the carrier state among 19 household carriers isolated for examination varied from 5 to 19 days. The vibrio concentration in the stool of contact carriers was 10(2)-15(5) per gram, as compared with 10(6)-19(9) per ml of rice-water stool in cholera cases.The agglutinin titre increased with time for carriers, as it does for patients. It declined to a very low level 8-12 weeks after recovery, with the exception of one proved long-term carrier.The strains isolated from carriers were identical in all respects, including virulence in infant rabbits, with strains isolated from patients-except that 3 carrier strains were rough.
The first known long-term carrier of cholera, found in the Philippines, is described. The carrier, Dolores M., who had suffered from El Tor cholera in August 1962, continued intermittently to excrete vibrios of the same characteristics as the original isolates until the date of reporting (1966). Duodenal intubation proved that the vibrios are lodged in her biliary tract. Her serum antibody titre continued to remain high in the absence of vaccination against cholera.
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During March through June 1964, an epidemic of acute non-vibrio diarrhoeal disease, closely simulating cholera, occurred in Calcutta. To clarify the etiology and pathophysiology and improve the therapy of this illness, bacteriological and metabolic studies were performed on 145 consecutive hypotensive adult male patients admitted with acute diarrhoeal disease to the Calcutta Infectious Disease Hospital. Bacteriological and serological studies clearly demonstrated that the majority of patients with acute diarrhoeal disease admitted during this period of time were not suffering from V. cholerae infection; no known pathogen could be recovered from 86% of such patients. Biochemical studies indicated that, in contrast to the findings in cholera, factors other than saline depletion contributed to hypotension in many of the patients with non-vibrio diarrhoeal disease. Although the majority of the acute diarrhoeal patients responded well to the 2: 1 saline: lactate regimen which is consistently successful in treating adult cholera patients, six of the non-cholera patients required prolonged administration of vasopressor drugs as an adjunct to fluid and electrolyte repletion therapy.
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In the course of studies of immunity to experimental cholera in man, 10(5) or 10(6) Vibrio cholerae were given to 66 college students and other community volunteers under quarantine in an isolation ward. HLA antigen and blood group determinations were carried out to test the hypothesis that severity of clinical cholera is dependent in part upon genetically-determined host susceptibility. Fifty-five volunteers developed diarrhoea; 38 had mild illness and 17 had severe cholera (stool volume greater than or equal to 5.0 litres). HLA antigens were found in similar frequency in volunteers with severe, mild or no diarrhoea; antigen A1, A2, A3 and B7 were most common. Blood group O, however, was found in 64% of persons with severe cholera versus 36-38% of volunteers with mild or absent illness. Thus, while no correlation was found between HLA type and severity of cholera, these results do support the claims of other investigators that blood group O is found more frequently in patients with severe cholera than in the normal population.
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