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To determine the cause of an outbreak of Pseudomonas aeruginosa cerebral ventriculitis among eight patients at a community hospital neurosurgical intensive care unit. All had percutaneous external ventricular catheters (EVCs) to monitor cerebrospinal fluid (CSF) pressure.
Cohort study of all patients who had EVCs placed during the epidemic period (August 8-October 22, 1997). A case-patient was any patient with P aeruginosa ventriculitis during the epidemic period. Pulsed-field gel electrophoresis (PFGE) was performed on all isolates.
P aeruginosa was significantly more likely to be isolated from CSF per EVC placed in the epidemic than pre-epidemic (January 1-August 7, 1997) periods (8/61 [13%] vs 2/131 [1.5%], P = 002). During the epidemic period, ventriculitis was significantly more likely after EVC placement in the operating room than in other units (8/24 vs 0/22, P = .004). EVC placement technique differed for EVCs placed in the operating room (little hair was removed, preventing application of an occlusive dressing) versus other hospital units (more hair was removed, and an occlusive dressing was applied). Among patients who had operating room EVC placement, contact with one healthcare worker was statistically significant (7/13 vs 0/8, P = .02). Hand cultures of this worker were negative. All isolates had closely related PFGE patterns.
These data suggest that a single healthcare worker may have contaminated EVC insertion sites, resulting in an outbreak of P aeruginosa ventriculitis. Affected patients were unlikely to have had an occlusive dressing at the EVC insertion site. Application of a sterile occlusive dressing may decrease the risk of ventriculitis in patients with EVCs.
To investigate a cluster of cases of legionnaires' disease among patients at a hospital.
A university hospital that is a regional transplant center.
Retrospective review of microbiology and serology data from the hospital laboratories and prospective surveillance via the radiology department; a case-control study and environmental sampling within the hospital and from nearby cooling towers.
Diagnosis of seven cases of legionnaires' disease in the first 9 months of 1996 led to recognition of a nosocomial outbreak that may have begun as early as 1979. Review of charts from 1987 through September 1996 identified 25 culture-confirmed cases of nosocomial or possibly nosocomial legionnaires' disease, including 18 in bone marrow and heart transplant patients. Twelve patients (48%) died. During the first 9 months of 1996, the attack rate was 6% among cardiac and bone marrow transplant patients. For cases that occurred before 1996, intubation was associated with increased risk for disease. High-dose corticosteroid medication was strongly associated with the risk for disease, but other immunosuppressive therapy or cancer chemotherapy was not. Several species and serogroups of Legionella were isolated from numerous sites in the hospital's potable water system. Six of seven available clinical isolates were identical and were indistinguishable from environmental isolates by pulsed-field gel electrophoresis. Initial infection control measures failed to interrupt nosocomial acquisition of infection. After extensive modifications to the water system, closely monitored repeated hyperchlorinations, and reduction of patient exposures to aerosols, transmission was interrupted. No cases have been identified since September 1996.
Legionella can colonize hospital potable water systems for long periods of time, resulting in an ongoing risk for patients, especially those who are immunocompromised. In this hospital, nosocomial transmission possibly occurred for more than 17 years and was interrupted in 1996, after a sudden increase in incidence led to its recognition. Hospitals specializing in the care of immunocompromised patients (eg, transplant centers) should prioritize surveillance for cases of legionnaires' disease. Aggressive control measures can interrupt transmission of this disease successfully.
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