Pregnancy appears to be a potential risk factor for viral replication and an extreme low immune status of Indian/Asian pregnant women. It is suggested that diminished cellular immunity (indicated by a decrease in CD4, an increase in CD8 cell counts and lowered CD4/CD8 cell ratio) and a high level of steroid hormones that influence viral replication/expression during pregnancy appear to be the plausible reasons for severity of the disease.

No abstract

In this study we have demonstrated that nitric oxide, the product of the arginine dependent pathway of human mononuclear phagocytes effectively kills the M.tuberculosis in-vitro. The release of reactive nitrogen intermediates was triggered by incubation with various proinflammatory cytokines namely IFN gamma,TNF-alpha and IL-1 R. We have earlier shown that human mononuclear phagocytes can be induced to release nitric,oxide (NO) radicals which can kill tumour cells. In the present communication, by using colony forming assays we demonstrated that human mononuclear phagocytes can effectively kill M.tuberculosis by using a NO dependent pathway. Treatment of mononuclear phagocytes with L-arginine resulted in markedly increased killing activity whereas, by using NGMMA, an analogue of L-arginine, the cidal activity could be brought down to the basal level. These results clearly suggest that cytokines, particularly IFN-gamma, induced NO release and its reactive product with oxygen radical, peroxynitrite, could play an important role in the killing of M. tuberculosis by human mononuclear phagocytes. A significant production of interleukin-4 and interleukin-10, by the ex-vivo matured, untreated macrophages from the active tuberculosis patients indicate that regulation of cytokine network to encourage in situ/local production of nitric oxide may be useful in the management of pulmonary tuberculosis.

One-hundred-and-thirty-two children with clinical and radiological evidence of bronchopneumonia/pneumonia were studied over a 1-year period for isolation/detection of bacterial and viral aetiological pathogens. Throat swab, nasopharyngeal aspirate (NPA), and lung aspirate were studied for bacterial and viral cultures. NPA was also subjected to latex agglutination test (LA) for H. influenzae and S. pneumoniae; and immunofluorescent technique (IFAT) and enzyme immunoassay (EIA) for respiratory syncytial virus (RSV). Blood culture for bacterial pathogens, and LA of blood and urine was also undertaken. Haemophilus influenzae was the commonest organism (15 per cent) isolated as the sole pathogen followed by RSV (14 per cent), Klebsiella (13 per cent) and S. pneumoniae (12 per cent). E. coli was the commonest organism (50 per cent) in infants <3 months and was closely followed by RSV (44 per cent), Klebsiella (25 per cent), and S. pneumoniae (18 per cent). Isolation rate of E. coli gradually declined with age. RSV (47 per cent) and H. influenzae (31 per cent) were the commonest organisms between 7 and 24 months. S. pneumoniae and Staph. aureus were common bacterial pathogens identified in all age groups with maximum isolation of 20 and 40 per cent, respectively, in children more than 5 years. Isolation of E. coli, Klebsiella and Staph. aureus was highest from NPA culture, while as S. pneumoniae and H. influenzae were most often detected by LA. Out of 12 cases from whom a lung aspirate was collected, bacterial pathogen could be isolated in six cases (50 per cent). Detection of RSV by EIA was higher than by culture or IFAT. Most of the organisms were resistant to chloramphenicol except for H. influenza. All the isolates of S. pneumoniae were sensitive to all the antibiotics. Bacterial pathogens were isolated/detected in 74 per cent of cases and RSV was the aetiological agent in 49 per cent of cases investigated for viral aetiology. Higher detection rate of RSV is attributed to selection of cases in winter months during a period of suspected epidemic of RSV.

We examined the lymphocyte subsets in peripheral blood, bone marrow and spleen of 11 patients with acute visceral leishmaniasis (VL) and 9 with chronic VL before and after 8 weeks of antileishmanial therapy. On admission, the CD4 cell count was depressed in the peripheral blood of acute and chronic VL cases as compared to the value in 10 normal control subjects. In contrast, CD4 cell counts were higher in the bone marrow in acute and chronic cases, and in splenic aspirates of chronic cases only, compared to normal values. The peripheral blood CD8 cell count, while normal in acute cases, was uniformly low in chronic cases. Counts of CD8 cells were also low in bone marrow of acute and chronic cases, as well as in splenic aspirates of chronic cases only. All these differences were significant (P < 0.05). After treatment, the CD4 cell count in the peripheral blood increased, but decreased in bone marrow and splenic aspirates. The CD8 cell count remained unaltered in the peripheral blood but increased significantly (P < 0.05) in bone marrow and spleen. The results suggest that in VL the peripheral blood picture may not reveal the actual T cell subset profile in the reticuloendothelial system. The changes in CD8 cell counts in the bone marrow and spleen seem to be independent, and are probably influenced by antileishmanial therapy.