Seroimmunity to rubella virus infection in young adult females in Delhi.
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Biomedical subjects
Publications and source records attributed to S Khare.
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Between 1986 and early 1989, 47 patients of subacute sclerosing panencephalitis (SSPE) were referred to the National Institute of Communicable Diseases, Delhi from different hospitals of Delhi. They were 40 (87%) males and 7 (13%) females. The age at onset of illness ranged from 4 to 18 yr. Thirty (63.9%) patients gave history of measles attack in the first two years of life. All but one patient gave a past history of measles attack. Only one patient gave history of measles immunization. The titres of haemagglutination inhibiting antibodies to measles virus in serum in SSPE patients ranged from 1:8 to 1:2048 and in CSF from 1:4 to 1:256, while in control group, it ranged from 1:2 to 1:128 in serum and nil to 1:2 in CSF. The geometric means of haemagglutination inhibiting antibodies in serum and CSF of SSPE patients were 10 and 15 times higher than in the control group.
Between June and September, 1986, an outbreak of measles occurred in Pilkhi Primary Health Centre area (population 56,000) in Tehri Garhwal district, Uttar Pradesh, India. Overall, 1092 cases were identified and 62 died; case-fatality ratio was 5.7%. Illness was restricted primarily to children below 15 years of age; 38% cases were in children under 5 and 58% between 5-14 years of age. To better characterize the outbreak, a survey was conducted in 13 affected villages. The age of the cases ranged from 5 months to 19 years (median = 7.0 years). The age-specific attack rates were 22.4%, 54.5%, 46.2% and 35.3% for children under 1, 1-4, 5-9, 10-14 years of age respectively. In as many as four villages, the attack rate in children below ten was 80% or more. Secondary attack rate among family members was 70%. Overall, 82% of children with measles developed complications which consisted mainly of pneumonia, diarrhoea and dysentery. The age-specific case-fatality ratios in infants and children 1-4 years of age were 23.1% and 11.5% respectively; thereafter the rates tended to decline with increasing age and was higher in females than in males (less than 0.05). Pneumonia which was a complication in 39% of measles cases contributed to 56% of deaths. Traditional beliefs and customs in the area were strong and did not encourage treatment of measles cases. Although a measles vaccination programme has been launched in India since 1985, only 30 districts could be covered during the first year and another 90 during 1986.(ABSTRACT TRUNCATED AT 250 WORDS)
Immunoglobulins profile was carried out in 60 cases of measles (30 each with and without complications) and 30 age and sex matched controls. Antibody titres and immunoglobulins levels (IgG, IgM and IgA) were determined by hemagglutination inhibition and single radial immunodiffusion techniques, respectively. Though higher IgG and IgM levels were found in complicated cases compared to controls, more importantly lower IgA levels were seen in these cases. As most of the measles complications are secondary bacterial infections of mucosal surfaces, it is postulated that these patients might have been selected for a relatively severe form of the disease due to either a pre-existing or induced IgA deficiency.
Fifty-two children who had received at least 3 properly spaced doses of oral polio-vaccine and had developed acute poliomyelitis inspite of vaccination were studied clinically and serologically. This group (A) was compared with 28 children with poliomyelitis who had not received any vaccination (Group B). A much higher incidence of provocative injection and a better muscle power on presentation was seen in Group A as compared to Group B. Polio-virus type 2 was the commonest etiological agent in Group A (42.3%) whereas type I virus was most commonly seen in Group B (78.6%). A total 53.8% of cases of Group A had protective antibody titres to at least one poliovirus type in the acute phase sera, compared to only 4% from Group B. Six per cent from Group A had protective antibodies to all three virus types, disease in these cases was caused by non-polio agents. Two cases in Group A were possibly vaccine induced paralysis. Recovery, after 60 days, was much better in Group A as compared to Group B. Mortality in the two groups was comparable.
In this prospective study, immune status of children vaccinated in infancy was determined at age 12-18 months. In 200 children, preimmunization protective measles hemagglutination (HI) antibody titres (greater than or equal to 1:8) were present in 38.5% of children of 6-8 months, the frequency decreased to 17.6 and 14.3% in age groups 9-11 and 12-18 months, respectively followed by an increasing incidence of 52.5% in those more than 18 months of age. Paired measles HI titre was estimated in 56 children, the post vaccination sample was taken at age 12-18 months, 3-9 months after measles vaccination. Most of the children (98.0%), with no detectable antibody titre, had a protective titre. Again a significant number (p less than 0.001) of children aged 12-18 months had protective HI titres compared to non-vaccinated. These findings suggest that when vaccinated at 9-11 months in our country, there is no need for revaccination later.
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A prospective study of group B streptococcal (GBS) carriage and disease was conducted over 6 years. Carriage rates at delivery for mothers and infants were 20% and 12%, respectively. Forty-five cases of GBS disease occurred in infants, 24 "early-onset" disease and 21 "late-onset" disease. The combined attack rate for early and late disease was 3.3 per 1000 live births over the 6 years. The rate of early-onset disease was highest in infants found to be heavily colonized at birth: 50 per 1000 live births. Twenty-three of 24 had evidence of intrauterine-acquired infection. All GBS serotypes were represented. Preterm delivery, prolonged labor, premature rupture of membranes, and maternal infection enhanced the risk of early disease. Septicemia was the predominant form of late-onset disease (15 of 21 cases); GBS type III accounted for 19 of 21 cases. Ten of 21 infants with late infections were colonized at birth with the GBS type that subsequently caused disease. Thus a maternal source of infection was identified in 34 of the 45 infants. These data reveal consistent year-to-year carriage and disease rates in the study population.
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Changes in liver acid hydrolase activities during the infection of albino rats, Mastomys or mice with Plasmodium berghei are described. B-Glucosidase, B-galactosidase and N-acetyl-B-D-glucosaminidase exhibited widely different responses with acid phosphatase and cathepsin-B the least responsive and are likely to be causally related to immunity of animals.
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The pattern of activity of certain membrane-associated enzymes was followed in the erythrocytes of Plasmodium berghei-infected Mastomys natalensis. Parasitized erythrocytes were separated from non-parasitized populations by percoll-density gradient centrifugation. The activity of adenylate cyclase was markedly increased while those of ATPase, acid phosphatase, beta-glucuronidase and N-acetyl-beta-D-glucosaminidase were considerably decreased in the membrane preparations of parasitized erythrocytes as compared to normal erythrocytes. There was a decrease in the activity of ATPase and an increase of adenylate cyclase in the membrane preparations of non-parasitized erythrocytes. However, other enzymes did not alter to a significant extent in non-parasitized erythrocytes. Chloroquine (in vitro) stimulated adenylate cyclase, Na+, K+-ATPase and Ca++Mg++-ATPase while acetylcholinesterase was significantly inhibited.
Activities of certain acid hydrolases of the spleen were followed in three different rodents during the course of Plasmodium berghei infection. In albino rats where sterile immunity against the infection develops, the specific activities of a few acid hydrolases first declined then increased from day 7 and showed a several-fold increase over control values when there were no detectable parasites in peripheral circulation. In contrast, in Mastomys natalensis and albino mice which succumb to infection the levels of these enzymes were reduced throughout the course of infection. These results indicate a close correlation between host resistance to infection and the level of lysosomal enzymes in spleen.
The phospholipid composition of yeast plasma membrane was manipulated by two different methods: (i) by using two auxotrophic strains KA101 (cho1) and MC13 (Cho+) which required phospholipid bases for growth and (ii) by supplementing Saccharomyces cerevisiae (3059) cells with high concentration of choline or ethanolamine. It was possible to enrich the plasma membrane with phosphatidylcholine (PC) or phosphatidylethanolamine (PE) by both methods. The uptake of amino acids, e.g., glycine, glutamic acid, leucine, lysine methionine, phenylalanine, proline and serine, was significantly reduced in PC- or PE-enriched cells. However, the extent of reduction in transport was variable among different strains. A fluorescent probe, 1-anilino-8-naphthalene sulfonate (ANS), was used to monitor the structural changes induced by altered phospholipid composition. It was observed that the relative fluorescence intensity of bound ANS was decreased as a consequence of PC or PE enrichment. The decrease in fluorescence was probably associated with reduced number of available binding sites (n) and increased apparent dissociation constant (Kd). Furthermore, our results also suggest that a critical level of PE or PC is required for proper functioning of yeast membrane.
A decrease in the influx of several amino acids was observed following gamma-irradiation. At low dose (2.5 Gy), which does not affect cell survival, a stimulation in the uptake was visible; moreover, sulphydryl loss and lipid peroxidation were also evident. With further increase in the dose of radiation, a parallel increment in the loss of sulphydryl groups and production of malonaldehyde was observed. Radioprotectors like L-cysteine and dithiothreitol were shown to shield the radiation-induced loss of sulphydryl and damage to transport and survival. Reduced glutathione, on the other hand, exhibited protection at the level of sulphydryl damage only. N-ethylmaleimide, a well known hypoxic cell radiosensitizer, enhanced the radiosensitivity with respect to survival; it, however, had no effect on amino acid transport. Oxygen enhancement of radiation damage to transport and cell survival and the radioprotection by sodium formate under these circumstances, and more so by anoxia, were demonstrated. The results indicate that the manifestation of damage to membrane structure and function precedes any observable loss of survival.
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