Outbreak of nosocomial Burkholderia cepacia infection and colonization associated with intrinsically contaminated mouthwash.

From August 1996 through June 1998, 69 ventilated, intensive care unit patients at two Arizona hospitals had nosocomial respiratory tract cultures positive for Burkholderia cepacia. Intrinsically contaminated alcohol-free mouthwash was identified by pulsed-field gel electrophoresis as the source of the outbreak.

Outbreak of Pseudomonas aeruginosa ventriculitis among patients in a neurosurgical intensive care unit.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

More than 10 years of unrecognized nosocomial transmission of legionnaires' disease among transplant patients.

OBJECTIVE: To investigate a cluster of cases of legionnaires' disease among patients at a hospital. SETTING: A university hospital that is a regional transplant center. DESIGN: 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. RESULTS: 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. CONCLUSIONS: 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.

Assessment of occupational risk for hantavirus infection in Arizona and New Mexico.

Differentiating occupational exposure from other potential domestic or recreational exposure(s) for Sin Nombre virus (SNV) infection is an epidemiologic challenge. Interviews on work-related activities were conducted, and serum specimens were obtained from 494 workers in Arizona and New Mexico. These workers may have been exposed to rodents and rodent excreta at work, but their primary occupation did not require rodent contact (National Park Service [n = 193]; Navajo Agricultural Product Industry [n = 65], utility companies [n = 169] and plumbing and heating contractors [n = 67]. Within each occupational group (farm workers [n = 57], laborers [n = 20], professionals [n = 70], repairers [n = 211], service industry workers [n = 83], and technicians [n = 53], the majority of workers reported working in areas that had rodent droppings (range, 75 to 95%); 70% of laborers and 64% of service industry workers reported handling rodents. More than 60% of workers in each group, except technicians, reported reopening and cleaning or working in closed spaces. Approximately 90% of laborers, repairers, and farm workers reported hand-plowing. Although the risk for occupationally related SNV infection appears to be low, workers frequently performed risk activities associated with hantavirus pulmonary syndrome (HPS). All workers were seronegative for SNV by enzyme-linked immunoassay or Western blot testing. These findings, the known occupational exposure of some HPS cases, and the high HPS case-fatality rate (52%) support the need for recommendations to reduce human contact with rodents in the workplace. Increased understanding of hantavirus transmission to humans will help focus future recommendations to minimize human exposures effectively.

Epidemiologic linkage of rodent and human hantavirus genomic sequences in case investigations of hantavirus pulmonary syndrome.

Sin Nombre virus (SNV) causes the zoonotic disease hantavirus pulmonary syndrome (HPS). Its mechanisms of transmission from rodent to human are poorly understood. It is possible that specific genetic signature sequences could be used to determine the probable site of each case-patient's exposure. Environmental assessments suggested 12 possible sites of rodent exposure for 6 HPS patients. Rodents were captured at 11 of the 12 sites and screened for SNV infection within 2 weeks of the patient's diagnosis. Viral sequences amplified from tissues of rodents at each site were compared with those from case-patients' tissues. Rodents bearing viruses with genetic sequence identity to case-patients' viruses across 2 genomic segments were identified in 4 investigations but never at >1 site. Indoor exposures to rodents were especially common at implicated sites. By distinguishing among multiple possible sites of exposure, viral genotyping studies can enhance understanding of the conditions associated with infection by SNV.

Hantavirus in the southwestern United States: epidemiology of an emerging pathogen.

In May of this year, an outbreak of sudden, unexplained, and highly fatal respiratory illness of unknown etiology was identified in the four-corners region of the southwestern United States. Within 3 weeks after the collaborative response launched by the state and local health agencies in the affected area, laboratory studies from the federal Centers for Disease Control and Prevention suggested that an acute infection with a previously unrecognized Hantavirus species was responsible for the reported cluster of cases. The hantavirus associated with this outbreak has since been isolated in tissue culture, and diagnostic test systems specific for the newly identified hantavirus have been developed. This article summarizes the history of the outbreak as experienced by investigators from the Arizona Department of Health Services and reviews the epidemiologic and clinical aspects of both the current epidemic and hantaviruses in general. The sudden occurrence of acute illnesses in the Southwest due to a previously unrecognized hantavirus reaffirms that the potential for the emergence of new infectious diseases exists at any place or time in the United States. The response to the outbreak also illustrates how community clinicians and federal, state, and local health agencies work together to promptly identify the emergence of new disease threats, rapidly determine new etiologic agents, and develop and swiftly implement appropriate disease prevention and control strategies.