Human health effects associated with cyanobacteria are not new. In a recent monogram published by the World Health Organization, they document intoxication occurring in the 10th and 12th century (Chorus and Bartram, 1999). Most often, cyanobacteria toxins have been associated with the poisoning of birds and livestock. However, several high profile cases of human intoxication have occurred in recent years (Kuiper-Goodman et al., 1999). In 1979, the hospitalization of 140 children on Palm Island off Queensland Australian was required due to a massive outbreak of gastroenteritis. Termed the "Palm Island Mystery Disease", its source was traced to the drinking water supplied from a reservoir containing Cylindrospermopsis raciborskii. Construction of the Itaparica Dam and reservoir in 1988 in Bahia, Brazil led to another severe gastroenteritis epidemic traced to unknown cyanobacterial toxin(s) in the drinking water. In this event, more than 2,000 cases, and 88 fatalities were reported over a 42 day period. More recently (1996), a cyanobacterial bloom occurred in the water supply for a hemodialysis center in Caruaru, Brazil. Despite extensive pretreatment (sand, carbon, resin and microfiltration), more than 117 of 136 patients (86%) experienced symptoms and 75 patients (55%) died from the incident. This outbreak was termed the "Caruaru Syndrome". Measurable concentrations of microcystins, produced during the cyanobacterial bloom, were found in the blood serum of all exposed patients and in the liver tissues of the fatalities (Carmichael, 1998). In the United States, adverse human affects have included severe gastroeniteritis reportedly from contaminated drinking water associated with a bloom of Schizothrix calcicola (Lippy and Erb, 1976). Other worries include the widespread distribution of toxic cylindrospermopsin in the Florida surface water supplies and the recent discovery of microcystins in tap water. (Laurie Backer, CDC, personnel communication) Fortunately to date, the toxic effects due to cyanobacteria toxins in the lower Great Lakes ecosystem has been limited primarily to wildlife and animal fatalities. During 1999 and 2000, large die-offs of waterfowl occurred in Lake Erie and Lake Huron. These deaths were associated with type E or C avian botulism. The type E is of special concern in this regard because it typically impacts fish-eating birds such as loons and grebes. Type E toxin has been found in Great Lakes fish (i.e. gobies) and there is potential for these fish to act as vectors for human intoxication (Domaske and Obert, 2001). While the connection with toxic cyanobacteria is tenuous, microcystin-producing cyanobacteria may sensitize the birds to avian botulism (Murphy et al., 2000). The connection between an anatoxin-a producing bloom in Lake Champlain and dog fatalities is more direct. In 1999 and again in 2000, toxic outbreaks of a toxic cyanobacteria resulted in the deaths of several dogs. While human exposure is most likely to occur through toxins contained in drinking water, the most likely mode of ingestion for the dogs was probably not from drinking the water but rather from cleaning their fur after contact with the bloom (Ian Falconer, personal communication). Regardless of the mode of intake, the dogs died within hours with convulsions and symptoms typical of anatoxin-a poising. Water samples were collected from the bloom, along with algal debris on the shore, and zebra mussels growing the site. Chemical analysis using HPLC with fluorescent detection and LCMS confirmed the presence of elevated levels of anatoxin-a (> 1 µg L-1) in these samples and >10 µg g-1 in zebra mussel tissues (Yang et al., 2001; submitted). This occurrence of anatoxin-a in the zebra mussels was especially ominous as it implied a potential for movement of cyanotoxins up the food chain.