Japanese Encephalitis epidemic in Anantapur district, Andhra Pradesh (October-November, 1999).

Epidemic of Japanese Encephalitis has occurred in Andhra Pradesh during October-November, 1999 affecting 15 out of 23 districts. In total, 873 cases with 178 deaths have been recorded up to the day 29.11.99. The epidemiological investigation has been done in Anantapur district in western Andhra Pradesh, where the outbreak has started in the third week of October. In the district 47 PHC have been affected. On an average 4.5 per cent of 3175 villages have been affected. Average number of cases per affected village have been 1.5. Rural population has been primarily affected. Age groups 1-14 years including infants have been affected but nearly 86.8% of cases have been among 1-9 year age group. The overall case fatality rate has been 18.4 per cent. Clinical features have been high fever, headache, altered sensorium, convulsions and coma. A marked seasonal onset of a few cases per village and 93.75 per cent of human serum samples collected from hospitalised cases showed the evidence of J.E. virus infection indicating that the present outbreak was due to JE virus. High density of Culex vishnui complex mosquitoes has been observed in the area. All the environmental and ecological conditions, temperature, rainfall and relative humidity have been in favour of JE transmission. Analysis of the data for the last 10 years showed that the human JE cases occurred in Anantapur in September-October months, which shifted to October-November, 99. Prolonged draught conditions were observed till October. Possibly the delayed monsoon and congenial atmospheric conditions after monsoon were favourable to the vector species for extra-human cycle of transmission in 1999. Low level transmission leading to small number of cases continued during the succeeding years every September-October till the present epidemic. In all 24 PHCs and urban towns were identified with 212 cases and 39 deaths till 29.11.99.

Aluminium related changes in brain histology: protection by calcium and nifedipine.

Aluminium (Al; 50 mg AlCl3/kg body wt/day) treatment caused a marked change in histological picture of normal brain as indicated by an increased number of vacuolated spaces. These changes returned to normal partially by simultaneous treatment with nifedipine (0.7 mg/kg body wt/day) and completely by similar treatment with 50 ppm calcium (CaCl2; 12.5 mg/kg body wt./day). Neither nifedipine nor calcium treatment alone altered the normal histological condition. The histological changes could not be correlated with the decrease in calcineurin activities in brain as nifedipine decreases calcineurin activity without any histological changes. Hence the histological changes may be considered as specific for Al and not due to a general decrease in calcineurin activity.

Acute nonspecific carditis in adolescents presenting with Stokes-Adams attacks.

Three patients, aged between 12 and 17 years presented with Stokes-Adams attacks as a result of atrioventricular block, atrioventricular silence and ventricular arrhythmias, complicating acute myocarditis. All the patients required temporary pacing for a few days. One patient required hemodialysis for anuria. All the patients made complete recovery.

Characterisaton of human plasma thiol proteinase inhibitors.

Earlier, we had reported purification of three thiol proteinase inhibitors (TPI-1 of 70 kDa, TPI-3 of 195 kDa and TPI-4 of 497 kDa) from human plasma. In the present study we report that TPI-1 binds to papain in the stoichiometry ratio (E/I) of 1:1 while TPI-3 and TPI-4 bind in the ratio of 1.5:1 and 3.2:1 respectively. The K(m) for papain with BAPNA as substrate and Kcat/K(m) values for TPI-1, TPI-3 and TPI-4 were 2.7 x 10(-6) M, 0.84 nM/sec; 3.2 x 10(-6) M, 0.75 nM/sec; and 3.6 x 10(-6) M, 0.72 nM/sec respectively. The Ki values were found to be 1.48 nM for TPI-1, 0.133 nM for TPI-3 and 0.117 nM for TPI-4. The UV absorption and fluorescence emission spectra study suggest involvement of aromatic residues in the binding process. This study suggests that TPI-4 is the most potent inhibitor of thiol proteinases.

Susceptibility status of malaria vectors to insecticides in India.

The use of chemical insecticides for control of malaria vector populations continues to be the mainstay of malaria control strategy in India. Monitoring vector susceptibility to chemical insecticides is an important activity under the National Malaria Eradication Programme to ensure judicious and effective use of chemical Insecticides. 72 entomological zones were established under NMEP in 1977 for undertaking entomological studies in the malaria problematic areas. These zones have been generating insecticide susceptibility data in respect of the various malaria vectors. In this paper the insecticide susceptibility data, in respect of major vectors of malaria as on 1997, is presented.

Purification and physicochemical studies of human plasma thiol proteinase inhibitors.

The physicochemical properties of thiol proteinase inhibitors (TPI) isolated from outdated human blood have been studied. A simple technique which includes ammonium sulphate precipitation, Sephadex G-200 gel filtration and ion-exchange chromatography led to the isolation of 4 isolates namely TPI-1, TPI-2, TPI-3 and TPI-4 having molecular mass of 70, 155, 195 and 497 kDa respectively. The latter two forms are the new isolates unreported previously. They exhibit similar pH stability, inhibition spectra with papain, cathepsin B and trypsin, antigenic properties and glycoprotein nature. The TPI-4, however, was found to be most heat stable showing no decrease in inhibitory activity when heated upto 70 degrees C for 30 min. Our work suggests that TPI-3 and TPI-4 are the oligomers of TPI-1.