Epidemiology, bacteriology and control of an outbreak of Nocardia asteroides infection on a liver unit.

An outbreak of Nocardia asteroides infection affecting seven patients is described. Over a 5-week period, five patients with liver disease admitted to a ward developed clinical and laboratory evidence of nocardiosis, and two further cases were diagnosed 3 and 5 months later. Three out of the five patients who received specific antimicrobial therapy responded to treatment; in three patients nocardia infection was considered to have contributed to death. In six out of the seven patients, nocardiosis followed immunosuppression. A common-source outbreak was considered to be responsible for infection in the first five patients. In two patients, presentation of infection 5 and 7 months after the first case may have been due to prolonged colonization or subclinical infection with Nocardia. Biotyping of the seven isolates using a fluorogenic biochemical method identified three distinct strains of N. asteroides. The most probable source of Nocardia was contaminated brick and plaster dust arising from building work in an area adjacent to the ward. However, samples of air, dust and water failed to yield N. asteroides. Infection control measures included ward closure followed by thorough cleaning, and formaldehyde fumigation.

Nocardiosis in liver transplantation: variation in presentation, diagnosis and therapy.

Nocardiosis arose in seven of 191 liver transplant patients (3.7%) over a period of 3.5 years. Four patients had only pulmonary lesions while three had disseminated disease. Nocardia asteroides was isolated from three patients following bronchoscopy, percutaneous aspirate of a pulmonary lesion in one patients, and from the skin from the aspirates in three patients. Delay in diagnosis in two cases was due to negative microscopy; in one, the diagnosis was made only after repeated bronchoscopy. Of the seven patients, three (43%) died. In two of these, nocardiosis was considered to have directly contributed to death. Co-existent bacterial and viral infections were present in all patients who died. In vitro susceptibility of the organism to co-trimoxazole was variable and did not necessarily reflect clinical efficacy. In one patient, a good clinical response was achieved with co-trimoxazole despite apparently reduced in vitro susceptibility.

Piperacillin in early neonatal infection.

Seventy infants with suspected bacterial infection in the first 48 hours of life were treated either with piperacillin and flucloxacillin or with penicillin and gentamicin. Infection was confirmed and successfully eradicated in 6 of the 35 infants receiving piperacillin and flucloxacillin. Four infants treated with penicillin and gentamicin had confirmed infection and one deteriorated initially but then recovered when treated with piperacillin. Serum piperacillin concentrations above 100 mg/l and cerebrospinal fluid piperacillin concentrations of 2.6-6 mg/l were noted for up to four hours and 7 hours respectively, even in the absence of inflamed meninges, after administration of piperacillin 100 mg/kg body weight intravenously. Median half life of piperacillin was 6.5 hours and was prolonged in renal impairment. Piperacillin is considered to be a safe and effective first line single agent treatment for early neonatal infection but because some Escherichia coli are resistant to it we recommend that a second agent be used in critically ill infants with neutropenia or meningitis.

Infectious sequelae after endoscopic sclerotherapy of oesophageal varices: role of antibiotic prophylaxis.

In order to determine the incidence of infection following sclerotherapy and the role of antimicrobial prophylaxis, a prospective randomized control study was performed comparing i.v. imipenem/cilastatin, with an infusion of dextrose-saline as a control group. One hundred patients with bleeding esophageal varices were included. All episodes of infection were documented during admission to the unit. Ninety-seven patients were evaluable. Post-sclerotherapy bacteremia developed in six (5.6%) of 107 sclerotherapy sessions in the control group and one (1.1%) of the 88 sclerotherapy sessions in the imipenem/cilastatin group (P < or = 0.1, NS): six of these seven post-sclerotherapy bacteremias occurred after emergency sclerotherapy. Infection within 7 days of the procedure was documented after 43 (22.1%) of the 195 sclerotherapy sessions, 18 (20.5%) in the imipenem/cilastatin group and 25 (23.4%) in the control group (P = NS). These infections were significantly more common after emergency sclerotherapy, 40 (34.8%) of 115 sessions, than after elective sclerotherapy, three (3.8%) of 80 sessions (P < or = 0.0001). A short prophylactic antibiotic regime does not reduce the risk of early bacteremia or the frequency of infection after sclerotherapy. The higher risk of infection after emergency sclerotherapy may be therefore related more to the gastrointestinal hemorrhage and its associated effects than to sclerotherapy.