Evaluation of Cytology for Diagnosing Avian Pox in Wild Turkeys ( Meleagris gallopavo).

Avian pox virus is a common cause of proliferative skin disease in wild turkeys ( Meleagris gallopavo); however, other etiologies may produce grossly indistinguishable lesions. Common methods for diagnosing avian pox include histopathology, virus isolation, and PCR. While these methods are sufficient in most cases, each has their limitations. Cytology is a cost-effective and rapid approach that may be useful when traditional diagnostics are not feasible. The objective of this study was to evaluate the performance of cytology relative to histopathology and PCR for avian pox diagnosis in wild turkeys. Fifty wild turkeys were submitted for necropsy due to nodular skin lesions on unfeathered skin of the head. Of these, five had similar skin lesions on the unfeathered legs and 26 had plaques on the mucosa of the oropharynx or esophagus. Representative skin, oropharyngeal, and esophageal lesions from all birds were examined with cytology and histopathology. Skin lesions on the head of each bird were also tested for avian pox virus via PCR. Histopathology and PCR were equally sensitive in diagnosing avian pox from skin lesions on the head. There were no significant differences between cytologic and histopathologic diagnosis of avian pox from skin lesions on the head (sensitivity = 97.4%, specificity = 100.0%), legs (sensitivity = 75.0%, specificity = 100.0%), or from lesions in the oropharynx and esophagus (sensitivity of 62.5%). Similarly, there were no significant differences between PCR and cytology for diagnosis of pox viral skin lesions of the head. Relative to PCR detection of avian pox virus, cytology had a sensitivity of 90.0% and a specificity of 90.0%. These results suggest that cytology is a useful tool for diagnosis of avian pox in wild turkeys.

Second-generation Anticoagulant Rodenticide Poisoning in a Captive Andean Condor (Vultur gryphus).

A 28-year-old female Andean condor (Vultur gryphus) housed in an outside exhibit at the National Aviary in Pittsburgh, PA, began showing signs of weakness. Toxicosis with an anticoagulant rodenticide was suspected because its mate had died 1 day earlier from possible brodifacoum poisoning. A rapid decline in the packed cell volume, despite vitamin K1 treatment, necessitated a blood transfusion with blood from bald eagles (Haliaeetus leucocephalus) and Steller's sea eagles (Haliaeetus pelagicus). Supportive therapy after transfusion included vitamin K1 (5 mg/kg IM q12h) as well as enrofloxacin, vitamin B complex, selenium and vitamin E, and subcutaneous fluids as needed. After a 39-day treatment period, a tapering dosage of vitamin K1 was initiated, and treatment ended after 17 weeks. However, 2 weeks later, the bird suffered from a potential relapse. It was successfully treated with a repeat tapering vitamin K1 regimen lasting a total of 4 months.