T Bhattacharya — Page 2

In an earlier study Ascaris-specific IgG4 antibody was found to be elevated in cases of ascariasis. However, the usefulness of the elevated levels of this antibody in Ascaris infection as a diagnostic marker has not been well established. In India, in early 1999, blood samples of 83 cases of Ascaris infection, 35 cases of other nematode infection and 53 control subjects (without any helminth infection) were tested for anti-Ascaris IgG4 by ELISA. Further anti-Ascaris IgG4 levels in the blood of Ascaris-infected patients were determined, after eradication of the worms with drugs, at regular intervals to ascertain the duration of elevation of titre of the serological marker following initial infection. This information would indicate the sensitivity of the test as a diagnostic marker for recent infection. Blood samples of 422 rural people were also tested for anti-Ascaris IgG4 titre to ascertain the prevalence of ascariasis in the community. High levels of anti-Ascaris IgG4 antibody (OD 1.246 +/- 0.212) were found in all the 83 Ascaris-infected subjects compared to controls (OD 0.158 +/- 0.047). Anti-Ascaris IgG4 antibody levels of other nematode-infected subjects were comparable to the controls. Anthelmintic treatment of 8 Ascaris-infected subjects caused sequential fall of IgG4 level in their blood, and its titre reached control level within 6 months of deworming. Of 422 individuals from the rural community 229 (54.3%) had significantly high levels of specific IgG4 antibody against Ascaris excretory-secretory antigen, suggesting that they were infested with Ascaris. Thus, this study demonstrated that anti-Ascaris IgG4 antibody is a very sensitive and specific marker for the diagnosis of Ascaris infection. Utilizing this test, a significant number of a rural population could be diagnosed with Ascaris infection in West Bengal, India.

Adolescent↗

PubMedDate not supplied

Vibrio cholerae O139 in Calcutta, 1992-1998: incidence, antibiograms, and genotypes.

We report results of surveillance for cholera caused by Vibrio cholerae O139 from September 1992, when it was first identified, to December 1998. V. cholerae O139 dominated as the causative agent of cholera in Calcutta during 1992-93 and 1996- 97, while the O1 strains dominated during the rest of the period. Dramatic shifts in patterns of resistance to cotrimoxazole, neomycin, and streptomycin were observed. Molecular epidemiologic studies showed clonal diversity among the O139 strains and continuous emergence of new epidemic clones, reflected by changes in the structure, organization, and location of the CTX prophages in the V. cholerae O139

Base Sequence↗