Abstract

The etiopathogenesis of acute pneumonia, the second most important cause of mortality among neonatal alpacas in Peru, is still poorly understood. The objective of this study was to characterize gross and histopathology lesions, as well as to identify viruses [parainfluenza type 3 (PI-3) and/or bovine respiratory syncytial (BRS)] by direct inmunofluorescence test, and isolate bacteria [ Pasteurella multocida (Pm) and/or Mannheimia haemolytica (Mh)] from 24 fatal acute pneumonia cases of alpaca neonates 7–39 days old. At necropsy the gross lesions corresponded to moderate purulent focal bronchopneumonia or severe necrotic purulent fibrinous ( n = 13), and moderate to severe pulmonary congestion and/or pulmonary edema ( n = 11). Histopathological analysis revealed: acute severe and diffuse necrotizing, fibrinous, suppurative bronchopneumonia ( n = 3), acute mild to moderate and focally diffuse suppurative bronchopneumonia ( n = 10) and acute moderate to severe diffuse congestion and pulmonary edema ( n = 11). Among these 24 fatal cases, 22 yielded virus identification and/or bacterial isolation. Eight of these 22 cases were positive for only one pathogen (5 for viruses and 3 for bacteria), 10/22 were positive for 2 pathogens RSV plus bacteria ( n = 7), PI-3 plus bacteria ( n = 2) and 1 for both bacteria and 4/22 were positive for 3 pathogens [RSV, PI-3 plus bacteria ( n = 3) and PI-3 plus both bacteria ( n = 1)]. Among the affected lung tissues, virus was identified 19 times (13 positive for RSV, 9 for PI-3, and 3/19 for both viruses) whereas bacteria were isolated 14 times [ P. multocida ( n = 8), M. haemolytica ( n = 6), and both bacteria ( n = 2)]. The presence of multiple pathogens was observed in 14/22 positive cases with an observation of virus–bacteria association in 13/14 of the cases. The coexistence of RSV-Pm was the most frequently observed (6/13) followed by the simultaneous presence of RSV-Mh (4/13) and PI-3 Pm or Mh (4/13). These results appear to indicate that acute pneumonia in alpaca neonates may well result from virus and bacterial interactions in a similar way to pneumonic lesions of other ruminants.

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