Monensin poisoning outbreak in free-ranging and captive birds.

Monensin poisoning is uncommon and has been rarely reported in birds. This work aimed to described clinical-pathological aspects of an outbreak of monensin poisoning in captive and free-ranging birds. Thirty-seven of 600 captive birds fed a diet containing 893.19 mg/kg of monensin died within 10 days (mortality 6.17%). There was no ionophore antibiotics on the feed label supplied to captive birds, which established an error in feed production. Necropsies were performed on twelve animals: Muscovy duck (Cairina moschata) (2/12), greater rhea (Rhea americana) (2/12), black-necked swan (Cygnus melancoryphus) (2/12), garganey (Anas querquedula) (1/12), ostrich (Struthio camelus) (1/12), and common pigeon (Columbus livia) (4/12). These four common pigeons were free-ranging birds and died after eating the same contaminated feed. Birds were mainly found dead, however in animals which clinical signs were observed (Columba livia, Rhea americana, Cairina moschata, Anas querquedula, and Struthio camelus), they included incoordination, inability to stand, and intense prostration, that ranged from 24 to 72 h until death. Grossly, five birds had focally extensive pale firm areas in the myocardium and two had in the skeletal muscles, one being concomitant lesions. Histologically, muscle necrosis and degeneration were observed in striated musculature (skeletal and/or heart) in all birds analyzed. Monensin poisoning outbreaks can affect free-ranging birds that are fed on external feeders, as well as captive birds, due to an error in the feed formulation.

Pulmonary acinar adenocarcinoma in a captive lioness (Panthera leo).

Neoplasms in wild felids are more frequently observed in captive animals, of which clinicopathological features of pulmonary tumors are not commonly described. This study aimed to describe the clinical and pathological aspects of a case of diffuse pulmonary acinar adenocarcinoma in a 23-year-old, captive lioness with clinical history of dyspnea, progressive weight loss and inappetence. At necropsy, the lungs were mildly pale, moderately firm, and the pleural surface was diffusely irregular with multifocal to coalescent, grey to white areas. No masses or superficial nodules were detected, but, on the cut surface, there were numerous, spherical, firm, white to yellow areas up to 0.5 cm in diameter affecting all pulmonary lobes. Histologically, in the lungs, there were extensive, non-delineated areas of neoplastic proliferation of columnar, ciliated epithelial cells arranged in irregular tubuloacinar structures. Immunohistochemical analysis revealed immunolabeling of neoplastic cells for pan-cytokeratin and thyroid transcription factor-1. Napsin-A exhibited only scarce and scattered immunolabeling in the neoplastic cells. The gross, histologic and immunohistochemical findings confirmed the final diagnosis of primary diffuse pulmonary adenocarcinoma.