Word number in abstract and importance: 221 and 143 Word number in text: 4687 ABSTRACT 3 Boid Inclusion Body Disease (BIBD) is a transmissible viral disease of captive snakes that 4 causes severe losses in snake collections worldwide. It is caused by reptarenavirus infection, 5 which can persist over several years without overt signs, but is generally associated with the 6 eventual death of the affected snakes. Thus far, reports have confirmed existence of 7 reptarenaviruses in captive snakes in North America, Europe, and Australia, but there is no 8 evidence that it also occurs in wild snakes. BIBD affects both boas and pythons, the habitats 9 of which do not naturally overlap. Herein, we studied Brazilian captive snakes with BIBD 10 using a metatranscriptomic approach, and report the identification of novel reptarenaviruses, 11 hartmaniviruses, and a new species in the family Chuviridae. The reptarenavirus L segments 12 identified represent six novel species, while we only found a single novel reptarenavirus S 13 segment. Until now, hartmaniviruses had been identified only in European captive boas with 14 BIBD, and the present results increase the number of known hartmanivirus species from four 15 to six. The newly identified chuvirus showed 38.4%, 40.9%, and 48.1% amino acid identity to 16 the nucleoprotein, glycoprotein, and RNA-dependent RNA polymerase of its closest relative, 17Guangdong red-banded snake chuvirus-like virus. Although we cannot rule out the possibility 18 that the found viruses originated from imported snakes, the results suggest that the viruses 19 would circulate in indigenous snake populations. 20Reptarenavirus NP expression was mainly restricted to the IBs (Figs. 2B and 3B, C), whereas 129 hartmanivirus NP was also detected throughout the cytoplasm (Fig. 2C). 130 Analysis of the identified reptarenavirus sequences. 131We used the PAirwise Sequence Comparison (PASC) web tool (available at 132 https://www.ncbi.nlm.nih.gov/sutils/pasc/viridty.cgi?textpage=overview), recommended by 133 the Arenaviridae study group of the International Committee on Taxonomy of Viruses 134 (ICTV) for arenavirus classification (16), to analyze the identified reptarenavirus segments. 135The PASC results showed that we had recovered CDSs for seven novel L and two novel S 136 segments ( Table 2). The PASC analysis identified one of the L segments in snake #1 as UHV-137

Objectives The aim of this study was to report the clinical, radiographic and pathological features of pulmonary Langerhans cell histiocytosis in four cats, and carry out a literature review of feline histiocytic diseases. Methods Necropsy reports archived at the Department of Veterinary Pathology of the Federal University of Rio Grande do Sul were reviewed. The clinical information was then obtained from the clinical records at the Veterinary Hospital. Routine samples had been collected during necropsy, fixed in 10% formalin, routinely processed for histology, and stained with hematoxylin and eosin. Samples of lung were submitted for bacterial and fungal culture. Tissue sections of lung underwent immunohistochemical testing for vimentin, pancytokeratin, CD18, CD3, CD79αcy, E-cadherin and Iba1. Results This disease affected mixed breed cats aged 7–14 years. Clinical signs consisted of severe mixed inspiratory and expiratory restrictive dyspnea, lethargy and anorexia. Thoracic radiographs revealed different lesion profiles, predominantly of an interstitial and alveolar pattern. Grossly, the lungs were diffusely firm and did not collapse. The pleural surface was bright and irregular due to multifocal-to-coalescent, well-demarcated, white, firm nodules that also extended into and obliterated the pulmonary parenchyma. Histological changes were characterized by poorly demarcated infiltration with histiocytic cells arranged in cohesive groups within the alveolar, bronchiolar and bronchial spaces. Histiocytic cells had intense cytoplasmic immunolabeling for vimentin and Iba1, and robust membrane immunolabeling with CD18 and E-cadherin; these cells were negative for CD3, CD79αcy and pancytokeratin in all cases. Conclusions and relevance This article confirms that pulmonary Langerhans cell histiocytosis is a rare disease that occurs in middle-aged to older cats and causes widespread involvement of the pulmonary parenchyma, inducing acute or chronic, progressive respiratory disease characterized by mixed restrictive dyspnea that eventually leads to death. While a definitive clinical diagnosis is challenging, the nodular appearance of the pulmonary changes, together with the histological and immunohistochemistry findings, suffice for diagnostic confirmation of pulmonary Langerhans cell histiocytosis.

Boid inclusion body disease (BIBD) is a transmissible viral disease of captive snakes that causes severe losses in snake collections worldwide. It is caused by reptarenavirus infection, which can persist over several years without overt signs but is generally associated with the eventual death of the affected snakes. Thus far, reports have confirmed the existence of reptarenaviruses in captive snakes in North America, Europe, Asia, and Australia, but there is no evidence that it also occurs in wild snakes. BIBD affects boa species within the subfamily Boinae and pythons in the family Pythonidae, the habitats of which do not naturally overlap. Here, we studied Brazilian captive snakes with BIBD using a metatranscriptomic approach, and we report the identification of novel reptarenaviruses, hartmaniviruses, and a new species in the family Chuviridae. The reptarenavirus L segments identified are divergent enough to represent six novel species, while we found only a single novel reptarenavirus S segment. Until now, hartmaniviruses had been identified only in European captive boas with BIBD, and the present results increase the number of known hartmaniviruses from four to six. The newly identified chuvirus showed 38.4%, 40.9%, and 48.1% amino acid identity to the nucleoprotein, glycoprotein, and RNA-dependent RNA polymerase, respectively, of its closest relative, Guangdong red-banded snake chuvirus-like virus. Although we cannot rule out the possibility that the found viruses originated from imported snakes, the results suggest that the viruses could circulate in indigenous snake populations. IMPORTANCE Boid inclusion body disease (BIBD), caused by reptarenavirus infection, affects captive snake populations worldwide, but the reservoir hosts of reptarenaviruses remain unknown. Here, we report the identification of novel reptarenaviruses, hartmaniviruses, and a chuvirus in captive Brazilian boas with BIBD. Three of the four snakes studied showed coinfection with all three viruses, and one of the snakes harbored three novel reptarenavirus L segments and one novel S segment. The samples originated from collections with Brazilian indigenous snakes only, which could indicate that these viruses circulate in wild snakes. The findings could further indicate that boid snakes are the natural reservoir of reptarena- and hartmaniviruses commonly found in captive snakes. The snakes infected with the novel chuvirus all suffered from BIBD; it is therefore not possible to comment on its potential pathogenicity and contribution to the observed changes in the present case material.

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Toxoplasmosis is a widely distributed disease that infects birds and mammals, including humans. Acute clinical course of toxoplasmosis is considered to be rare among domestic rabbits (Oryctolagus cuniculus). The aim of this study was to present the first report of fatal acute disease caused by Toxoplasma gondii type BrIII genotype, a typical Brazilian clonal lineage, in a domestic rabbit. T. gondii was identified in histological sections of spleen and liver tissue, and these tissues were also immunohistochemically positive for T. gondii. After the histopathological and immunohistochemical confirmation of T. gondii, the genotype of this pathogen was determined via PCR-RFLP with 11 markers (SAG1, SAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1, Apico, and CS3) and via microsatellite (MS) analysis with 15 markers (TUB2, W35, TgMA, B18, B17, M33, IV.1, X1.1, M48, M102, N60, N82, AA, N61, and N83). This study shows that type BrIII genotype, circulating in Brazil in different hosts, can cause acute disease in a naturally infected animal host. The described case also involves the first reported occurrence of the 291 allele for the typing marker TUB2 in a type BrIII strain, emphasizing the genetic diversity of T. gondii in Brazil.

Primary hepatic neoplasms are mostly detected in cattle as incidental findings in slaughterhouses or diagnosed at the necropsy, wherein it may be related to the cause of death. A proper characterization of primary hepatic neoplasms is essential to provide an accurate diagnosis, especially at the slaughter lines, in order to reduce erroneous condemnations. This work aimed to characterize the gross, histological, and immunohistochemical features of primary liver neoplasms detected in slaughtered cattle in Southern Brazil. Nineteen primary hepatic neoplasms were identified. Grossly, these lesions were classified according to their distribution, as focal, multifocal, or diffuse. Histologically, the shape and arrangement of the cells, as well as possible malignant features were evaluated. Immunohistochemistry (IHC) was also performed for biliary epithelium (anti-CK7) and hepatocytes (anti-Hep Par-1) markers. Hepatocellular carcinoma (84.2%) was the most frequently detected hepatic neoplasm, followed by cholangiocarcinoma (15.8%), and these were only identified in adult cows. Hepatocellular carcinomas occurred as solitary masses or multifocal nodules, which on the cut surface were often green. Cholangiocarcinomas occurred as multifocal nodules, occasionally showing an umbilicated appearance. Histologically, hepatocellular carcinomas had mostly trabecular and solid patterns, while cholangiocarcinomas presented mostly a solid arrangement. Upon IHC, all hepatocellular carcinomas were immunolabeled for anti-Hep Par-1, ranging from mild (25%), moderate (31.2%) to marked (43.7%), while immunolabeling for anti-CK7 was detected only in one case of cholangiocarcinoma.

Objectives This study aimed to characterize the cytologic, pathologic and immunohistochemical (IHC) aspects of feline giant-cell sarcoma. Methods Biopsy and necropsy reports from the Department of Veterinary Pathology were retrieved, and 13 cases of pleomorphic sarcoma (PS) were selected according to the established epidemiologic, pathologic and IHC criteria. All samples were fixed in 10% formalin, routinely processed for histology, and stained with hematoxylin and eosin. Samples also underwent IHC testing for vimentin, ionized calcium-binding adaptor molecule 1 (Iba-1), desmin, actin and S-100. Results The mean age of the affected cats was 9.5 years, and females were over-represented. Most neoplasms were observed in the flank, lateral thorax, limbs and interscapular region, and were >2 cm in diameter. Cytology analysis revealed highly cellular preparations with three distinct populations (spindle cells, small round cells and multinucleated giant cells) in a dense eosinophilic stroma. Histologically, PS was composed of a combination of these three populations. IHC labeling for vimentin and Iba-1 was strongly positive for spindle cells and multinucleated giant cells, respectively. Desmin/actin showed variable labeling among the samples. S-100 was negative in all samples. Conclusions and relevance PS is a neoplasm of mesenchymal origin, also known as malignant fibrous histiocytoma. The predominant subtype in this study that affected the cats was the giant-cell type, characterized by the presence of multinucleated giant cells among spindle-shaped cells. These findings are similar to those described in human patients; thus, a comparison between the neoplasms seen in these species might be useful, and the knowledge of biologic behavior and overall treatment approach for humans could be extrapolated to cats.

RESUMO.-As enfermidades fúngicas são diagnósticos diferenciais de diversas morbidades de caráter infeccioso, degenerativo ou proliferativo neoplásico, principalmente em gatos, que é a espécie mais suscetível a estas. Este trabalho descreve os achados anatomopatológicos de doenças fúngi-cas em gatos no período de janeiro de 2005 a dezembro de 2015 pelo SPV-UFRGS. Foram revisados 1.274 protocolos de necropsia e encontrou-se 17 casos de micoses, correspondendo a 1,33% dos diagnósticos. Quanto às amostras provenientes de biopsias, foram verificados 2.615 protocolos e detectou-se 59 casos de doenças fúngicas, totalizando 2,25% dos diagnósticos, sendo revisados seus achados macroscópi-cos, microscópicos, colorações especiais e cultivo micológico. O principal diagnóstico encontrado foi esporotricose com 34 casos de biópsia e cinco de necropsia. Criptococose obteve seis diagnósticos na necropsia e 13 na biópsia. O pseudomicetoma dermatofítico possui cinco casos de biópsia e dois de necropsia. Histoplasmose obteve um diagnóstico na necropsia e dois na biópsia. Aspergilose teve dois casos diagnosticados na necropsia. Candidíase e feo-hifomicose obtiveram um caso cada. Em quatro ocasiões, não se pode identificar o agente envolvido na lesão e foram classificados conforme a alteração morfológica em: dermatite fúngica, enterite fúngi-ca, rinite micótica e dermatite e osteomielite fúngica. Através deste trabalho, pode-se identificar que a esporotricose foi o diagnóstico de doença fúngica mais frequente em felinos, seguido da criptococose e pseudomicetoma dermatofítico.