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S Kabra

Publications and source records attributed to S Kabra.

10 recordsLinked to original sources
PubMed2006

A fatal pulmonary infection by Nocardia brasiliensis.

The reported case is of primary pulmonary nocardiosis, caused by Nocardia brasiliensis, in a immunocompromised patient, which ended fatally despite appropriate treatment. The partially acid fast filamentous bacterium was predominant on direct examination of the sputum. It was cultured on blood agar, MacConkey agar and by paraffin baiting technique. The bacterium was resistant to cotrimoxazole, the drug of choice for nocardiosis.

Adult↗
PubMed2003

Outbreak of Acinetobacter spp septicemia in a neonatal ICU.

An outbreak of Acinetobacter spp infection in the neonatal unit at Lok Nayak Hospital, New Delhi, India, is described. During a 6-month period, 68 strains of Acinetobacter baumannii were isolated from the blood and CSF of 47 neonates admitted to the intensive care unit. Diagnosis of clinically significant bacteremia was made in 36 patients. On environmental/personnel sampling, Acinetobacter spp isolates with similar antibiogram were recovered from intravenous catheter and washbasin. Control of the outbreak was possible only after strict infection control practices in the unit. It was concluded that any clinical multidrug resistant A. baumannii isolate can be a potential nosocomial outbreak strain.

Acinetobacter Infections↗
PubMed1999

Salmonella senftenberg: a new pathogen in the burns ward.

This is the first report of Salmonella senftenberg serovar outbreak in a burns unit. This unit admits about 2000 patients with major burn injuries annually. Routine sampling from wound swabs in December 1995 revealed S. senftenberg in a few samples following which a study was instituted from January to March 1996. Of 446 burn admissions during this period 80 patients were culture positive for S. senftenberg in wound swabs. The protocol for investigation included wound swabs on admission and then at biweekly interval, blood culture studies on clinically toxic patients, anti-microbial sensitivity studies, environmental sampling and hand swabs and stool cultures from about 50 staff members of the burns ward. No wound swab at the time of admission was positive for S. senftenberg. Environmental study and the study of staff members did not reveal any obvious source of the infection. S. senftenberg strains were sensitive to more than seven of the 11 anti-microbials tested at the beginning of the study but later 96.3% of the strains showed multidrug (more than three drugs) resistance. By April 1996 the isolates became negligible and later disappeared completely. The organism resurfaced again in March 1997 and the same study was instituted again on 413 admissions between March and May 1997. Fifty patients were culture positive for S. senftenberg. This time stool sample from one burn dresser tested positive for S. senftenberg. Interestingly, again at the beginning of the second outbreak the Salmonella strains were sensitive to 9 out of 11 anti-microbials tested, but later 96.11% strains became multidrug resistant. S. senftenberg strains showed maximum resistance to amoxycillin (97.5%) and minimum to chloramphenicol, tetracycline and cotrimoxazole (12%). It was noticed that Salmonella strains surfaced in wound swabs after 3-4 weeks of hospital stay. Forty-five out of 130 patients studied, in both the episodes, died due to septicemia. The majority of the patients who died had sustained > 60% TBSA burns. Blood cultures were done in 34/130 patients and eight yielded growth (2 S. senftenberg, 4 Klebsiella spp., and two Pseudomonas spp.)

Adult↗
PubMed1999

Pleuro pulmonary infection with Salmonella group E.

A patient was admitted with a history of cough, shortness of breath and fever. After investigations, he was found to have a left-sided pneumonia with pleural effusion. Culture of the patient's sputum, pleural fluid and blood revealed Salmonella senftenberg. The patient was started on antibiotics according to the sensitivity report and responded to therapy. The past history revealed attempt at suicide by the intake of corrosive acid, which caused an esophageal stricture. The leak of gastric contents into the mediastinum lead to the infection of the pleural cavity and pneumonia.

Adult↗
PubMed1994

BCG revisited.

Explore the source record for details and available documents.

BCG Vaccine↗
PubMed1993

Serum concentrations of rifampicin and isoniazid in tuberculosis.

Ninety-four patients, 1-13 years of age suffering from different types of tuberculosis were investigated for serum rifampicin (RIF) and isoniazid (INH) concentrations using microbiological and fluorimetric methods, respectively. Of these, 64 (68.1%) had pulmonary primary complex (PPC); 20 (21.3%) progressive primary disease (PPD) and 10 (10.6%) tuberculous meningitis (TBM). Patients with PPC, PPD and TBM were given two-drug (6HR), three drug (2HRZ, 4HR) and four drug (2SHRZ, 4HRE, 3HE) regimens, respectively. RIF and INH were administered in a dose of 12 and 10 mg/kg/day, respectively. After 10-12 days of continuous therapy, their serum concentrations were estimated at 0, 2, 4, 6, 8 hours for RIF and 0, 1, 3, 5, 7 hours for INH. For RIF, the time to achieve maximum concentrations (Tmax) was 2 hours, range of mean of maximum concentration (Cmax) 3.38 to 3.88 micrograms/ml, terminal half life elimination (T1/2) 3.03 to 3.81 hours and area under serum concentration curve (AUC) 0-8 hours 24.7 to 28.3 micrograms/ml hours in different forms of tuberculosis. INH had a Tmax of 1 h, Cmax 4.38 to 8.17 micrograms/ml, T1/2 4.0 to 4.98 hours and AUC 0-7 hours 34.1 to 57.5 micrograms/ml hours. The concentrations achieved at 7-8 hours with these dosages were much above those required for therapeutic efficacy (minimum inhibitory concentration), being 50 to 250 times for RIF and 35-60 times for INH. We recommend pharmacokinetic studies with lower doses of RIF and INH for less toxic, equally effective and cheaper antitubercular chemotherapy.

Adolescent↗