Blood chemistry was examined in brook trout Salvelinus fontinalis suffering from bacterial gdl disease (BGD) and compared to normal healthy fish under identical conditions. Infected fish showed a marked decrease in serum Na+, Cl-and in osmolality, and a concommitant haemoconcentration as indicated by the increased serum protein and increased packed cell volume. Fish with BGD exhibited an mcreased rate of respiration (tachybranchia) but were not hypoxemic, suggesting that compensatory mechanisms, such as tachybranchia and enhanced recruitment of lamellar reserves, were successful. Nevertheless, the cause of the tachybranchia in BGD-infected fish remains unexplained; it may not be a response to impaired oxygen exchange, although this seems the most likely explanation. The acid-base status did not differ between healthy and diseased fish. These findings suggest that changes in blood components other than acid-base ones constitute the critical, and sometimes fatal changes occurring as a result of BGD infection, rather than hypoxemia. It is suggested that circulatory disturbances resulted from the rapid drop of blood electrolytes, which in turn triggered a fluid shift from the extracellular to the intracellular compartments, leading to haemoconcentration and death. However caused, tachybranchia probably exacerbated the worsening blood chemistry changes resulting from damaged gill epithelium. The implications of these findings for treatment include reducing the rate of ion loss from the gills by raising the salt levels in the water, combined with other chemicals directed specifically at the bacteria.