During the winters of 2000–01 and 2001–02, 400 trumpeter (Cygnus buccinator; n = 365) and tundra (Cygnus columbianus columbianus; n = 35) swans died in northwest Washington State. The carcasses were collected and frozen for necropsy, completed in May 2001 (n = 172) and May 2002 (n = 228). Although most swans died of lead poisoning, 64 (16%) swans had gross pathologic lesions consistent with aspergillosis (trumpeter swan, n = 62; tundra swan, n = 2). Mild fungal infections consisted of small, nonobstructive lesions in the air sacs, trachea, or lungs, with lesions isolated to 1 area. Severe fungal infections consisted of large, extensive infiltrating lesions in the respiratory tract, with 68% of lesions in more than 1 area (lungs, air sacs, or trachea) and many with complete fibrinous casts within air sacs or trachea. Male swans were twice as likely as females to have fungal lesions, although there was no difference in the ratio of males and females with mild or severe infections. Juvenile swans (<1 year of age) were twice as likely as adults and subadults to have fungal lesions and were also more likely to develop severe versus mild aspergillosis infections (n = 19, n = 1, respectively). Although the number of swans with concurrent lead poisoning and aspergillosis was nearly 30% higher than that of swans with aspergillosis only, when compared with the total number of swans submitted for necropsy, swans with lead poisoning were 75% less likely to have fungal lesions than non-lead–poisoned swans, possibly because of rapid death from lead poisoning.
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Vol. 19 • No. 2