Human fatalities from cyanobacteria: chemical and biological evidence for cyanotoxins.

An outbreak of acute liver failure occurred at a dialysis center in Caruaru, Brazil (8 degrees 17' S, 35 degrees 58' W), 134 km from Recife, the state capital of Pernambuco. At the clinic, 116 (89%) of 131 patients experienced visual disturbances, nausea, and vomiting after routine hemodialysis treatment on 13-20 February 1996. Subsequently, 100 patients developed acute liver failure, and of these 76 died. As of December 1996, 52 of the deaths could be attributed to a common syndrome now called Caruaru syndrome. Examination of phytoplankton from the dialysis clinic's water source, analyses of the clinic's water treatment system, plus serum and liver tissue of clinic patients led to the identification of two groups of cyanobacterial toxins, the hepatotoxic cyclic peptide microcystins and the hepatotoxic alkaloid cylindrospermopsin. Comparison of victims' symptoms and pathology using animal studies of these two cyanotoxins leads us to conclude that the major contributing factor to death of the dialyses patients was intravenous exposure to microcystins, specifically microcystin-YR, -LR, and -AR. From liver concentrations and exposure volumes, it was estimated that 19.5 microg/L microcystin was in the water used for dialysis treatments. This is 19.5 times the level set as a guideline for safe drinking water supplies by the World Health Organization.

Control of vancomycin-resistant enterococci at a community hospital: efficacy of patient and staff cohorting.

OBJECTIVE: To evaluate the efficacy of patient and staff cohorting to control vancomycin-resistant enterococci (VRE) at an Indianapolis community hospital. DESIGN: To interrupt transmission of VRE, a VRE point-prevalence survey of hospital inpatients was conducted, and VRE-infected or -colonized patients were cohorted on a single ward with dedicated nursing staff and patient-care equipment. To assess the impact of the intervention, staff compliance with contact isolation procedures was observed, and the VRE point-prevalence survey was repeated 2 months after the cohort ward was established. RESULTS: Following the establishment of the cohort ward, VRE prevalence among all hospitalized inpatients decreased from 8.1% to 4.7% (25 positive cultures among 310 patients compared to 13 positive cultures among 276 patients, P=.14); VRE prevalence among patients whose VRE status was unknown before cultures were obtained decreased from 5.9% to 0.8% (18 positive cultures among 303 patients compared to 2 positive cultures among 262 patients, P=.002); and observed staff-patient interactions compliant with published isolation recommendations increased (5 [22%] of 23 interactions compared to 36 [88%] of 41 interactions, P<.0001). CONCLUSIONS: Our data suggest that, in hospitals with endemic VRE or continued VRE transmission despite implementation of contact isolation measures, establishing a VRE cohort ward may be a practical and effective method to improve compliance with infection control measures and thereby to control epidemic or endemic VRE transmission.

A cluster of bloodstream infections and pyrogenic reactions among hemodialysis patients traced to dialysis machine waste-handling option units.

From June 17 through November 15, 1995, ten episodes of Enterobacter cloacae bloodstream infection and three pyrogenic reactions occurred in patients at a hospital-based hemodialysis center. In a case-control study limited to events occurring during October 1-31, 1995, seven dialysis sessions resulting in E. cloacae bacteremia or pyrogenic reaction without bacteremia were compared with 241 randomly selected control sessions. Dialysis machines were examined, dialysis fluid and equipment were cultured, and E. cloacae isolates were genotyped by pulsed-field gel electrophoresis. Each dialysis machine had a waste-handling option (WHO) through which dialyzer-priming fluid was discarded before each dialysis session; in 7 of 11 machines, one-way check valves designed to prevent backflow from the WHO into patient bloodlines were dysfunctional. In the case-control study, case sessions were more frequent when machines with >/=1 dysfunctional check valves were used. E. cloacae with identical pulsed-field gel electrophoresis patterns were isolated from case patients, dialysis fluid, station drains, and WHO units. Our investigation shows that bloodstream infections and pyrogenic reactions were caused by backflow from contaminated dialysis machine WHO units into patient bloodlines. The outbreak was terminated when WHO use was discontinued, check valves were replaced, and dialysis machine disinfection was enhanced.

Liver failure and death after exposure to microcystins at a hemodialysis center in Brazil.

BACKGROUND: Hemodialysis is a common but potentially hazardous procedure. From February 17 to 20, 1996, 116 of 130 patients (89 percent) at a dialysis center (dialysis center A) in Caruaru, Brazil, had visual disturbances, nausea, and vomiting associated with hemodialysis. By March 24, 26 of the patients had died of acute liver failure. METHODS: A case patient was defined as any patient undergoing dialysis at dialysis center A or Caruaru's other dialysis center (dialysis center B) during February 1996 who had acute liver failure. To determine the risk factors for and the source of the outbreak, we conducted a cohort study of the 130 patients at dialysis center A and the 47 patients at dialysis center B, reviewed the centers' water supplies, and collected water, patients' serum, and postmortem liver tissue for microcystin assays. RESULTS: One hundred one patients (all at dialysis center A) met the case definition, and 50 died. Affected patients who died were older than those who survived (median age, 47 vs. 35 years, P<0.001). Furthermore, all 17 patients undergoing dialysis on the Tuesday-, Thursday-, and Saturday-night schedule became ill, and 13 of them (76 percent) died. Both centers received water from a nearby reservoir. However, the water supplied to dialysis center B was treated, filtered, and chlorinated, whereas the water supplied to dialysis center A was not. Microcystins produced by cyanobacteria were detected in water from the reservoir and from dialysis center A and in serum and liver tissue of case patients. CONCLUSIONS: Water used for hemodialysis can contain toxic materials, and its quality should therefore be carefully monitored.

Staphylococcus aureus bloodstream infections among patients undergoing electroconvulsive therapy traced to breaks in infection control and possible extrinsic contamination by propofol.

Infectious complications associated with electroconvulsive therapy (ECT) are extremely unusual. When five of nine patients undergoing ECT at one facility on June 20, 1996 developed Staphylococcus aureus bloodstream infection (BSI), an investigation was initiated. A retrospective cohort study, a procedure review, and observational and microbiologic studies were performed. A case was defined as any patient who had ECT at Facility A from June 1, 1995 through June 20, 1996 and developed S. aureus BSI <30 days after ECT. The post-ECT S. aureus BSI rate was significantly greater on the epidemic day than the pre-epidemic period, (i.e., June 1, 1995 through June 19, 1996) (5 of 9 vs 0 of 54 patients, P < 0.001). All patients during the study period received propofol before ECT. Case patients were more likely than noncase patients to have higher maximum temperature after ECT (median 103.9 degrees F vs 100.0 degrees F, P < 0.03) and a greater time from preparation of intravenous medications to infusion (median 2.1 vs 1.1 h, P = 0.01). All case-patient S. aureus isolates were indistinguishable by pulsed field gel electrophoresis. Our investigation suggests that the ECT-associated S. aureus BSIs were associated with infection control breaks, which possibly led to the extrinsic contamination of propofol. Prevention of propofol-associated infectious complications requires aseptic preparation and use immediately before infusion.

Failures of zidovudine postexposure prophylaxis.

Since 1990, 11 cases of failure of zidovudine (ZDV) postexposure prophylaxis (PEP) for human immunodeficiency virus (HIV) exposure have been reported among healthcare workers (HCWs) around the world. In these cases, ZDV was begun 30 minutes to 8 days (median 1.5 hours) postexposure, at doses of 600-1,200 mg/day (median 1,000 mg/day) for 8-54 days (median 21 days). Five additional failures of ZDV PEP have been reported among non-HCWs exposed to an inoculum of HIV-infected blood larger than what would be expected from a needlestick. These non-HCW cases include one blood transfusion, one suicidal self-inoculation, one assault on a prison guard with a needle-syringe, and two instances of accidental intravenous infusion of HIV-infected blood or blood components during nuclear medicine procedures. One possible reason for these failures of ZDV PEP is that the transmitted strains of HIV may have had reduced sensitivity to ZDV. Collectively, these case reports indicate that if ZDV is protective as PEP, any protection afforded is not absolute.

Pseudo-outbreak of Enterococcus durans infections and colonization associated with introduction of an automated identification system software update.

Enterococci are an important cause of hospital-acquired infections. Since 1989, there has been an increase in the number of nosocomial enterococcal infections caused by strains resistant to vancomycin in the United States. Although many enterococcal species can colonize humans, only Enterococcus faecalis, E. faecium, E. raffinosus, and E. casseliflavus have been implicated in clusters of infection. In January 1996, the Centers for Disease Control and Prevention received a report of an outbreak of vancomycin-resistant enterococci in which 31 of 84 (36.9%) isolates were identified as E. durans. Twenty-nine isolates identified as E. durans were identified to the species level after the introduction of an automated identification system software update (Vitek gram-positive identification card, version R09.1) for the identification of species of gram-positive organisms. When seven isolates initially reported as E. durans were identified to the species level by alternate methods, they were found to be E. faecium. Subsequently, isolates identified as E. durans by the automated system were reidentified by using a rapid streptococcus test, and no further enterococcal isolate has been confirmed as E. durans. Automated microbial analysis is a potential source of error that is not easily recognized. When laboratory findings are discordant with expected clinical or epidemiologic patterns, confirmatory testing by alternate methods should be performed.