Persistence of Corynebacterium diphtheriae in Delhi & National Capital Region (NCR).

Despite the introduction of mass immunization, diphtheria continues to play a major role as a potentially lethal infectious disease in many countries. Delay in the specific therapy of diphtheria may result in death and, therefore, accurate diagnosis of diphtheria is imperative. This study was carried out at National Centre for Disease Control (NCDC), Delhi, India, on samples of suspected diphtheria cases referred from various government hospitals of Delhi and neighbouring areas during 2012-2014. Primary identification of Corynebacterium diphtheriae was done by standard culture, staining and biochemical tests followed by toxigenicity testing by Elek's test on samples positive for C. diphtheriae. The results showed persistence of toxigenic C. diphtheriae in our community indicating the possibility of inadequate immunization coverage.

Effects of cyclosporine on glucose tolerance in the rat.

In a study of prevention of spontaneous diabetes in BB rats by therapeutic doses of cyclosporine (10 mg/kg/day), the male control non-diabetes-prone rats showed glucose intolerance after a 0.25 g/kg glucose load by gavage, at 90 and 130 days of treatment. Non-BB male Wistar rats treated similarly showed glucose intolerance at 1 wk of treatment, with progressive worsening for 5 wk, then sustained up to 12 wk of treatment. Fasting euglycemia was maintained, but both pre- and postchallenge plasma insulin levels were significantly lower with cyclosporine at several time points. Total pancreatic insulin was decreased to one-third that of control after 5 wk. After withdrawal of cyclosporine, glucose tolerance returned to normal in 2 wk. Sprague-Dawley rats responded similarly and in both strains, an increase in the cyclosporine dose to 15 mg/kg/day augmented the glucose intolerance. These results demonstrate that therapeutic doses of this agent induce reversible glucose intolerance due, in part, to inhibition of insulin secretion and also possibly inhibition of synthesis, though a peripheral effect is not excluded. This hyperglycemic effect of cyclosporine has implications for its potential use in type I diabetes mellitus, transplantation, and other autoimmune disease.

Influence of a propionic acid feed additive on performance of turkey poults with experimentally induced poult enteritis and mortality syndrome.

Poult enteritis and mortality syndrome (PEMS) has multiple etiological agents associated with its occurrence, including two viruses and at least three Escherichia coli isolates. Myco Curb (MC) contains organic acids and is used as a feed additive to inhibit growth of many bacteria and toxin-producing molds but not viruses. Studies evaluating the influence of MC on BW, feed conversion, and mortality indicate that turkey poults tolerate MC at 1.25% but not 2.50%, but higher MC content in feed provides greater suppression of growth of bacterial isolates commonly associated with PEMS. In two PEMS experiments, 1.25% MC was blended into poult starter feed and was maintained in the feed for the duration of the 3-wk experiments. In these experiments, 1-d-old commercial poults were placed into battery brooders and were given turkey starter feed and water ad libitum. At 6 d posthatch, PEMS-designated poults were given a 1-mL oral gavage of a 10% suspension of feces from PEMS-infected poults. BW depression due to PEMS was not alleviated by MC, although there was less variation in mean BW of the MC-fed poults, and there was a highly significant reduction in mortality (68% in PEMS-exposed with MC vs. 32.5% in PEMS-exposed without MC). The reduction in mortality in the MC-fed poults was attributed to decreased bacterial content of the gut and to maintenance of packed cell volume and hemoglobin content. It was concluded that MC might be a potential nutritional intervention during PEMS.

Response to cyclosporine administration at onset of diabetes in BB rats.

The metabolic and immunological effects of cyclosporine A given at onset of spontaneous Type I diabetes in BB rats were examined, as an analogy to the current use of this agent in newly-diagnosed human diabetics. Diabetes-prone (BBdp) rats were monitored until appearance of hyperglycemia, at which time treatment with both cyclosporine (10 mg/kg/day) and insulin was immediately started. Cyclosporine induced no remission in any rats and did not affect their daily insulin requirements. After 9 weeks of cyclosporine treatment, islet morphology showed the typical "end-stage" picture in all rats, with essentially total beta cell loss. Pancreatic insulin contents were less than 1% of normal levels. During the 9 weeks of cyclosporine treatment, there was a decrease in numbers of peripheral blood Ia-positive lymphocytes, an increase in OX8+ lymphocytes (suppressor/cytotoxic and natural killer cells) but no change in the other subsets. There was a significant increase in plasma creatinine. We conclude that this dose of cyclosporine started at onset of diabetes in BB rats is unable to arrest and/or reverse the beta cell destructive process.