ArticleBMC veterinary research2026
Retrospective analysis of possible associations between Pneumocystis spp. and five immunosuppressive viral pathogens in three wild carnivore species.
Article in BMC veterinary research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Pneumocystis spp. proliferate under immunosuppressive conditions in mammalian lungs, and several pathogens have been discussed as potential contributors to fungal proliferation. This study aimed to investigate the possible associations between Pneumocystis spp. and immunosuppressive viruses in Serbian wild mammals. A total of 108 wild carnivores - including golden jackals (Canis aureus), Eurasian badgers (Meles meles), and red foxes (Vulpes vulpes) - were collected from Veliko Gradište, Stara Pazova, and Ugrinovci during the 2022/2023 hunting season. The presence of Pneumocystis spp., canine parvovirus 2 (CPV-2), pseudorabies virus (PRV), canine distemper virus, canine coronavirus, and canine herpesvirus was assessed using conventional PCR and real-time PCR. Pneumocystis spp. were detected in 40.7% of all sampled animals (20/60 golden jackals, 4/9 Eurasian badgers, and 20/39 red foxes). CPV-2 was detected in three golden jackals (5.0% of tested golden jackals, 2.8% of all sampled animals), while PRV was found in two golden jackals (3.3% of tested golden jackals) and three red foxes (7.7% of tested red foxes; overall 4.6%). Co-infections of Pneumocystis spp. and PRV were identified in one golden jackal and two red foxes, while Pneumocystis spp. were absent in CPV-2-positive animals. All samples tested negative for other viral pathogens. No significant differences in the pathogens' presence were observed between age groups, sexes, or sampling locations. The mean threshold cycle (Ct) values were 33.6 for Pneumocystis spp., 24.0 for CPV-2, and 31.3 for PRV. While the CPV-2 and PRV viral loads were high in co-infected samples, Pneumocystis spp. loads were associated only with subclinical infections. These findings suggest that the examined viral pathogens were unlikely to play a significant role in the development of clinically apparent Pneumocystis pneumonia, despite their potential to modulate or impair immune function. However, given the low viral prevalence and the lack of histopathological evaluation, a potential contribution of viral immunomodulation cannot be completely excluded.
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