Brazilian Deaths Traced to Common Marine Toxins

Environmental Health Perspectives Jul01

Beginning in February 1996, 131 patients who had been treated that month at a dialysis center in the Brazilian city of Caruaru developed symptoms including headache, nausea, vomiting, and blurred vision. One hundred subsequently suffered acute liver failure, and 76 died. Of these 76 victims, 52 deaths are attributed to the cyanotoxin-related disease now called Caruaru syndrome. The waterborne cyanobacterial toxins that killed those 52 patients are likely to claim more lives worldwide as reservoirs become increasingly polluted, warns a team of researchers studying the Brazilian outbreak, the first documented human cases of Caruaru syndrome. "Since many of the world's reservoir- and lake-based water supplies are subject to increasing levels of nutrients, it is highly probable that repeat episodes of cyanotoxin poisoning will occur unless measures are taken to better understand [cyanobacteria's] role in water-based disease," the team writes.

Although they are technically bacteria, cyanobacteria behave like waterborne algae. The toxic cyanobacteria linked to Caruaru syndrome originated in an algal bloom on the Tabocas Reservoir, which supplies Caruaru's water. According to study leader Wayne Carmichael of Wright State University in Dayton, Ohio, toxic blooms are found on many of the world's surface waters. The 40 species of known or suspected toxin-producing cyanobacteria produce six chemical groups of toxins.

Water treatment normally removes toxic cells or deactivates the toxins, but the water used at the dialysis center had not been fully treated. To avoid chlorine residue in the water used for dialysis, the center had trucked water in from the municipal plant after it was treated only with alum flocculation. The dialysis center then further treated the water at its own in-house plant, but the poorly maintained plant failed to remove the cyanotoxins.

Brazilian authorities initially attributed the outbreak to chemical contamination of the water used in dialysis treatment. However, Sandra Azevedo of the University of Brazil in Rio de Janeiro suspected cyanobacterial toxins were the real culprit when the patients died quickly without developing any of the neurologic symptoms associated with chemical poisoning. Carmichael and an international team of researchers traced the syndrome to intravenous exposure to cyanobacterial toxins.

By examining water samples and patients' serum and liver tissue, the researchers identified the major toxin group responsible as hepatotoxic microcystins. They estimated that microcystin concentrations in the water used for dialysis were 19.5 micrograms per liter, nearly 20 times the limit proposed by the World Health Organization as safe for drinking water. The researchers first reported those findings in the 26 March 1998 issue of the New England Journal of Medicine.

Since then, they discovered that the water used in dialysis treatment also was contaminated with the cyanotoxin cylindrospermopsin, which has been linked to an outbreak of liver and kidney disease among 148 people in Australia. Carmichael and his colleagues had suspected that cylindrospermopsin was in the Caruaru water because the organism that produces this cyanotoxin was identified in water samples from the Tabocas Reservoir. To date, however, the researchers have not identified cylindrospermopsin in the Caruaru liver specimens. But that's probably because the specimens were prepared specifically for microcystin analyses, the researches admit.

Carmichael says he and his colleagues recently developed a new method of measuring cylindrospermopsin in liver samples and hope to test it soon. "We want to be able to predict as closely as possible what levels of cylindrospermopsin and microcystins were required to kill these dialysis patients," he says. The researchers call for public officials to help prevent more outbreaks of Caruaru syndrome by protecting surface water supplies.

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