Poliomyelitis trends in Pondicherry, south India, 1989-91.

STUDY OBJECTIVES: To assess the poliomyelitis trend, including study of the epidemiological features, and to correlate this with the immunisation coverage of infants. DESIGN: Three annual lameness surveys in children aged 0-60 months employing cluster sampling methods and a series of five cross sectional surveys of immunisation coverage in children aged 12-23 months of age were undertaken. SETTING: Pondicherry, India, 1988-92. SUBJECTS: More than 10,000 children in the age group of 0-60 months took part in the three annual lameness surveys and samples of 210 children aged 12-23 months were covered each year in immunisation coverage surveys. MEASUREMENTS AND MAIN RESULTS: Altogether 50 of 11,461, 24 of 10,093, and 17 of 11,218 children surveyed during 1989, 1990, and 1991 respectively had become lame as a result of poliomyelitis, giving prevalences of 4.4, 2.4, and 1.5 per 1000 children for the three surveys. The corrected prevalences of poliomyelitis were 5.9, 3.2, and 2.0 per 1000 children during 1989, 1990, and 1991 respectively. The proportion of cases aged up to 36 months fell from 48% in 1989 to 12.5% in 1990 and 6% in 1991. The age at onset was less than 1 year in most. The median age at onset was 10.7 months. About 54% of the affected children had received three doses of oral poliomyelitis vaccine (OPV) before the onset of paralysis. In 1988 immunisation coverage for the third dose of OPV was 91% and in 1992 it was 97.6%. The drop out rate for the first versus the third dose of OPV fell from 6.3 in 1988 to 1.9% in 1992. CONCLUSION: Three successive annual lameness surveys showed that poliomyelitis was declining between 1989 and 1991. Five immunisation coverage surveys conducted from 1988 to 1992 showed high initial coverage followed by an improvement in the form of almost universal coverage for OPV.     

A component of Mycobacterium leprae as immunomodulating agent for immune deficient cells of leprosy patients

The delipidified component of the insoluble portion which presumably is the cell wall of Mycobacterium leprae (DCW) was able to induce lymphocyte proliferation in the leucocyte culture from the peripheral blood of lepromatous leprosy patients. Normally these cells show no lymphocyte proliferation in response to M. leprae or their sonicated extract. The delipidified component (DCW) appears to be proteinaceous and able to induce antibodies in rabbit. The DCW has affinity to the sera from lepromatous leprosy patients but not sera from normal healthy individuals or tuberculoid leprosy patients. The ability to induce lymphocyte proliferation is blocked by agglutination of DCW with patient sera, heat treatment of DCW or protease treatment of the component. Along with lymphocyte proliferation, DCW also induces ability in the macrophages to render phagocytosed M. leprae non viable. Thus it is proposed that DCW of M. leprae could be a potent immunomodulator for immunedeficient cells of leprosy patients. The efficacy of DCW as a probable immunoprotector for M. leprae infection in mice has already been demonstrated earlier.     

Redox polymerization, 3. Kinetics of acrylonitrile polymerization initiated by the redox systems cyanoacetic acid/Mn(III) and 2-butanone/Mn(III) in aqueous sulfuric acid

The kinetics of Polymerization of acrylonitrile initiated by the redox systems cyanoacetic acid/Mn(III) and 2-butanone/Mn(III) were investigated in the temperature range of 30 – 50°C in aqueous sulfuric acid. The kinetics are consistent with the formation of a 1 : 1 complex between the reducing agent and Mn(III), its unimolecular decomposition yielding the initiating radical. Extensive oxidation of the primary radical with exclusively mutual termination of growing radicals accounts for the kinetics of the polymerization. Rate and equilibrium constants as well as thermodynamic parameters were evaluated and their significance is discussed.     

A complex component modulating immune-deficient cells in leprosy patients leading to loss of viability of Mycobacterium leprae--a possible vaccine.

Macrophages from peripheral blood of leprosy patients, both multi-bacillary and paucibacillary are unable to kill phagocytosed Mycobacterium leprae due to their inability to produce superoxide (O2-) and hydroxyl radicals (OH.). The macrophages from healthy individuals are able to kill M. leprae along with release of O2- and OH. radicals. The deficiency in the macrophages of both types of leprosy patients is removed by activation of these cells when exposed to a culture supernatant obtained after stimulation of peripheral blood mononuclear cells from the same patients with delipidified cell components of M. leprae which are most likely cell wall proteins. The activation of macrophages also leads to recognition of whole live M. leprae as an antigen by cells from lepromatous patients. This activation of the phagocytes by delipidified cell components is blocked by cyclosporin A, indicating the possible role of several steps involved in immune activation of cells. The observations thus indicate the significant ability of delipidified cell components to eliminate the deficiencies in the macrophages from leprosy patients and restore them to behave like the cells from healthy individuals. Considering all these, it is suggested that delipidified cell components could be potential modulators, and are probably capable of functioning as a vaccine for leprosy.     

Mechanism of immunosuppression in leprosy: presence of suppressor factor(s) from macrophages of lepromatous patients.

Human peripheral blood mononuclear cell proliferation induced by Mycobacterium leprae could be inhibited by the suppressor factor in the lysate of the macrophages of lepromatous leprosy patients. Macrophages from normal subjects and tuberculoid patients did not show production of a suppressor factor. Inhibition occurred only when the factor was present in the initial stages of lymphocyte culture. The factor is heat stable and nondialyzable. Proliferation induced by some mycobacteria and concanavalin A could also be blocked by the factor. Interestingly, blastogenic response by a few other antigens and phytohemagglutinin could not be inhibited by the suppressor factor. Mononuclear cells pretreated with such lysate from lepromatous macrophages for 24 h could induce suppressive activity in the cells in vitro in an autologous system. Treatment of these cells with carbonyl iron after the induction phase, to remove phagocytic cells, did not abolish their suppressive activity. The lepromatous macrophage lysate also generated suppressive activity in a T-lymphocyte-enriched population of normal subjects. These studies are interpreted to indicate that immunosuppression in lepromatous patients is produced by both macrophages and T lymphocytes. The exact phase in which either of these cells acts as a suppressor may be different. Specific suppression by macrophages to M. leprae can be an early event, and nonspecific suppression by T lymphocytes may be a later event in the course of lepromatous leprosy.