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Baggio, F.

Publications and source records attributed to Baggio, F..

5 recordsLinked to original sources

Histopathological and virus-associated features of Boid Inclusion Body Disease in Boa constrictor

Boid inclusion body disease (BIBD) is a reptarenavirus-induced fatal disease of boid snakes that, while diagnosed with ease due to the pathognomonic intracytoplasmic inclusion bodies (IB), is not yet fully characterized pathomorphologically and with regards to its pathogenesis. The present study retrospectively investigated a random cohort of 50 captive male and female boa constrictors of variable age (neonate to 25 years) for histopathological changes and in situ viral protein (nucleoprotein, NP, and glycoprotein 2, GP2) expression patterns. IB formation and NP expression were scored semiquantitatively. The vast majority of snakes (42/50; 84%) exhibited histopathological changes; these mainly (39/42; 93%) represented inflammatory processes that most frequently affected the gastrointestinal tract. Overall, IB and NP scores were significantly higher in the more recent cases (2020-2025) compared to the older cases (2000-2003). NP scores did not differ between age groups or sex, but were lower in animals with clinical signs and higher in those with histopathological changes. No statistically significant association was found between NP scores and inflammatory processes, neither in general nor in individual organs. GP2 expression, as an indicator of virion assembly, was less consistent than NP expression and generally restricted to individual cells with and without IBs. There was no histological evidence of overt damage in infected cells. Jointly, the results indicate different phases of restrictive and systemic viral replication that are not directly associated with pathological processes and/or clinical signs.

pathology↗

Multifocal cutaneous neoplastic vascular proliferations in a rainbow boa (Epicrates cenchria) collection with boid inclusion body disease

Reports on neoplastic processes in snakes are sparse regardless of their location, origin or behavior. Here, we describe the occurrence of multifocal cutaneous neoplastic processes consistent with hemangioma and hemangioendothelioma, with a differential diagnosis of angiomatosis, in a colony of native Brazilian rainbow boas (Epicrates cenchria) which also included animals affected by boid inclusion body disease (BIBD). Thirteen snakes were affected; seven of these had been introduced from other Brazilian sites years earlier, the others had been bred in house but were not offspring of knowingly affected animals. The breeding regime allowed contact between all female and male animals over the years. The cutaneous lesions were first observed over eight years ago, with additional cases detected during the three following years, but no new cases in the last five years. Two affected animals were subjected to a post mortem examination and were found to suffer from peliosis hepatis as one of the additional pathological changes. BIBD was confirmed in five of the eight examined animals, by histology, immunohistology for reptarenavirus nucleoprotein, and multiplex RT-PCR targeting the reptarenavirus S segment. Reptarenavirus infection was also detected in cells in the cutaneous neoplastic processes. PCRs for Bartonella henselae and B. quintana as well as bacterial DNA in general, performed on a pool of six skin lesions, yielded negative results, ruling out ongoing bacterial infection, like bacillary angiomatosis in humans, of the lesions. The results hint towards an association of reptarenavirus infection and BIBD with neoplastic processes which is worth further investigations.

pathology↗

Haemolymphatic tissues of captive boa constrictor (Boa constrictor): morphological features in healthy individuals and with Boid Inclusion Body Disease

Knowledge on the structure and composition of the haematopoietic tissue (HT) is essential to understand the basic immune functions of the immune system in any species. For reptiles, it is extremely limited, hence we undertook an in-depth in situ investigation of the HT (bone marrow, thymus, spleen, lymphatic tissue of the alimentary tract) in the common boa (Boa constrictor). We also assessed age- and disease-related changes, with a special focus on Boid Inclusion Body Disease, a highly relevant reptarenavirus-associated disease in boid snakes. The HT was subjected to gross, histological and ultrastructural examination, including special stains, immunohistochemistry, in situ hybridization and morphometric analyses. In general, the HT was dominated by T cells and lacked a clear structural organization, such as follicle formation. BIBD was associated with significantly higher cellularity and a granulomatous response in the spleen, and the presence of virus-infected haematopoietic cells in the bone marrow, suggesting the latter as a persistent source of viremia. HighlightsO_LILymphatic tissues of B. constrictor lack organization and are dominated by T cells C_LIO_LIThe thymus of B. constrictor shows slow age-related involution C_LIO_LIBIBD-positive boas show a granulomatous response in the spleen C_LIO_LIReptarenaviruses infect haematopoietic cells in the bone marrow C_LIO_LIReptarenavirus infected bone marrow cells might represent a source of viremia C_LI

pathology↗

Boid Inclusion Body Disease (BIBD) Is Also a Disease of Wild Boa Constrictors

Reptarenaviruses cause Boid Inclusion Body Disease (BIBD), a potentially fatal disease, occurring in captive constrictor snakes boas and pythons worldwide. Classical BIBD, characterized by the formation of pathognomonic cytoplasmic inclusion bodies (IBs), occurs mainly in boas, whereas in pythons, for example, reptarenavirus infection most often manifests as central nervous system signs with limited IB formation. The natural hosts of reptarenaviruses are unknown, although wild constrictor snakes are among the suspects. Here, we report BIBD with reptarenavirus infection in indigenous captive and wild boid snakes in Costa Rica using histology, immunohistology, transmission electron microscopy, next-generation sequencing (NGS), and RT-PCR. The snakes studied represented diagnostic post mortem cases of captive and wild caught snakes since 1989. The results from NGS on archival paraffin blocks confirm that reptarenaviruses have been present in wild boa constrictors in Costa Rica already in the 1980s. Continuous sequences de novo assembled from the low-quality RNA obtained from paraffin embedded tissue allowed the identification of a distinct pair of reptrarenavirus S and L segments in all studied animals; in most cases reference assembly could recover almost complete segments. Sampling of three prospective cases in 2018 allowed examination of fresh blood or tissues, and resulted in identification of additional reptarenavirus segments and hartmanivirus co-infection. Our results show that BIBD is not only a disease of captive snakes, but also occurs in indigenous wild constrictor snakes in Costa Rica, suggesting boa constrictors to play a role in natural reptarenavirus circulation. IMPORTANCEThe literature describes cases of boid inclusion body disease (BIBD) in captive snakes since the 1970s, and in the 2010s, others and we identified reptarenaviruses as the causative agent. BIBD affects captive snakes globally, but the origin and the natural host of reptarenaviruses remains unknown. In this report, we show BIBD and reptarenavirus infections in two native Costa Rican constrictor snake species, and by studying archival samples, we show that both the viruses and the disease have been present in wild snakes in Costa Rica at least since the 1980s. The diagnosis of BIBD in wild boa constrictors suggests that this species plays a role in the circulation of reptarenaviruses. Additional sample collection and analysis would help to clarify this role further and the possibility of e.g. vector transmission from an arthropod host.

microbiology↗

Arenavirus nucleoprotein localizes to mitochondria

Viruses need cells to replicate and, therefore, ways to counteract the hosts immune response. Mitochondria play central roles in mediating innate immunity, hence some viruses have developed mechanisms to alter mitochondrial functions. Herein we show that arenavirus nucleoprotein (NP) enters the mitochondria of infected cells and affects their morphological integrity. We initially demonstrate electron-dense inclusions within mitochondria of reptarenavirus infected cells and hypothesized that these represent viral NP. Software predictions then serve to identify a putative N-terminal mitochondrial targeting signal (MTS) in arenavirus NPs; however, comparisons of wild-type and N-terminus mutated NPs suggest MTS-independent mitochondrial entry. NP does not enter isolated mitochondria, indicating that translocation requires additional cellular factors or conditions. Immune electron microscopy finally confirms the presence of NP within the mitochondria both in vitro and in infected animals. We hypothesize that mitochondria targeting might complement the known interferon antagonist functions of NP or alter the cells metabolic state.

microbiology↗