Comparative morphometric evaluation of hepatic hemosiderosis in wild Magellanic penguins (Spheniscus magellanicus) infected with different Plasmodium spp. subgenera

• Autor(a) principal: Ewbank,Ana Carolina
• Data de Publicação: 2019
• Outros Autores: Strefezzi,Ricardo de Francisco, Sacristán,Carlos, Kolesnikovas,Cristiane Kiyomi Miyaji, Martins,Aryse, Mayorga,Luis Felipe Silva Pereira, Vanstreels,Ralph Eric Thijl, Catão-Dias,José Luiz
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Revista Brasileira de Parasitologia Veterinária (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1984-29612019000100068
• topic: Avian malaria; iron; hemosiderin; liver; morphometry; penguin

Abstract Avian malaria is one of the most important diseases of captive penguins. We employed morphometric techniques to evaluate hepatic hemosiderosis in rehabilitating wild Magellanic penguins (Spheniscus magellanicus) that were negative (n = 9) or naturally infected by different subgenera of Plasmodium spp. (n = 24), according with: Plasmodium subgenera (Haemamoeba, Huffia, Other lineages, and Unidentified lineages), severity of Plasmodium histopathological lesions, and concurrent diseases, age class (juvenile or adult plumage), sex (male, female or not determined), body score (emaciated, thin, good, excellent, not available), molt, presence or absence of oil contamination upon admission, iron supplementation, and rehabilitation center. The percentage of the area occupied by hemosiderin was called ‘Index of Hepatic Hemosiderosis (IHH)’. Plasmodium-positive females presented significantly higher IHH values (17.53 ± 12.95%) than males (7.20 ± 4.25%; p = 0.041). We observed higher levels of congestion (p = 0.0182) and pneumonia (p = 0.0250) severity between Unidentified lineages vs. Huffia. We believe that the hepatic hemosiderosis observed in this study was multifactorial, the result of pathological processes caused by malaria, molting, hemoglobin and myoglobin catabolism during migration, anemia, concomitant diseases, and iron supplementation, all possibly potentiated by decreased liver mass. Further studies are needed to clarify the mechanisms of these hypotheses.