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Functional pheochromocytomas secrete catecholamines and have been associated with cardiovascular lesions in dogs. This study aimed to describe the postmortem pathological findings in the cardiovascular system of dogs with pheochromocytoma and to evaluate the expression of cardiac troponin C in these dogs using immunohistochemical analysis. Twelve cases were identified, with a mean age of 10.6 years. The heart of all dogs was enlarged and with concentric hypertrophy of the left ventricular myocardium. Histological analysis showed cardiomyocyte necrosis and degeneration in the myocardium, with frequent bands of contraction, fibrosis, inflammation, and thickening of the medium-caliber arteries in the myocardium. There was a marked decrease or absence of immunolabeling in necrotic cardiomyocytes. We conclude that IHC for troponin C can be a useful tool for detecting myocardial necrosis in dogs with pheochromocytomas, including early cases of necrosis with only incipient cardiac changes where overt histologic abnormalities are not immediately apparent in the cardiomyocytes., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Pneumonia in cats may cause severe lung injury and consequent death. We describe the post-mortem findings and aetiologies of naturally fatal pneumonia in 78 domestic cats, using gross and histopathological examinations, immunohistochemistry and microbiological techniques. Morphological patterns found were bronchopneumonia (27/78), interstitial (15/78), bronchointerstitial (13/78), granulomatous (8/78), aspiration (8/78) and pyogranulomatous (5/78) pneumonia, and pleuropneumonia (2/78). Bacterial pneumonia was identified as the most common cause (32/78), followed by viral (15/28 feline calicivirus, 10/28 felid alphaherpesvirus 1 and 3/28 both viruses), aspiration (8/78), fungal (5/78) and parasitic pneumonia (5/78). Co-infection with feline immunodeficiency virus and feline leukaemia virus was found in 54 cats. Viral infections involved cats of all ages, indicating the importance of investigating viral causes in cats with respiratory diseases, including in adult and ageing cats., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

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.

We characterized the immunohistochemical expression profiles of dysgerminomas from a 16-y-old maned wolf and 13 domestic dogs using the following biomarkers: Sal-like protein 4 (SALL4), octamer-binding transcription factor 3/4 (OCT3/4), placental alkaline phosphatase (PLAP), c-kit, and vimentin. The maned wolf had nonspecific and long-standing clinical signs of lethargy, anorexia, and weight loss, and was euthanized because of poor prognosis. At autopsy, the left ovary was effaced by a 12 × 8 × 6 cm mass, comprised of anaplastic cells with a mitotic count of 20 mitoses in 10 high power fields. Dysgerminomas from 7 of 13 domestic dogs had nuclear expression of SALL4. Dysgerminomas from the maned wolf and 2 domestic dogs had both nuclear and cytoplasmic expression of SALL4. Cytoplasmic expression of PLAP and OCT3/4 was present in dysgerminomas from the maned wolf and 3 (PLAP) or 4 (OCT3/4) domestic dogs. All dysgerminomas expressed vimentin. Membranous c-kit expression was rare in the dysgerminoma from the maned wolf, and variable in dysgerminomas from 4 domestic dogs. A dysgerminoma from a domestic dog had cytoplasmic expression of c-kit. SALL4 is a useful marker to confirm germ cell origin of dysgerminoma in canids.

There are few pathological and immunohistochemical descriptions of thyroid neoplasms in cats. We investigated neoplasms of the thyroid in 31 cats (average age 15.6 years) in Southern Brazil. Most (96.8%) of these cases were classified as follicular adenomas and were predominantly unilateral and multinodular. Histologically, macrofollicular adenomas were the most common type observed. Carcinomas represented 3.2% of the investigated tumours. By immunohistochemical labelling, thyroglobulin was expressed more commonly than paired box gene 8 or thyroid transcription factor 1 in the follicular adenomas. One carcinoma was immunopositive for thyroglobulin, pancytokeratin, chromogranin A and synaptophysin, suggestive of a calcitonin-negative neuroendocrine carcinoma., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Tuberculosis is a common zooanthroponosis in humans with a high incidence in Brazil, but it may also affect non-human primates (NHPs), of which Old World primates are most commonly involved. Nonetheless, its occurrence in New World primates is unknown, and therefore, this study aimed to describe the infection by Mycobacterium tuberculosis variant tuberculosis in two captive black capuchin monkeys (Sapajus nigritus) in Southern Brazil. The primates were housed in the same enclosure, wherein close contact with humans frequently occurred, and presented apathy, anorexia, and death in a clinical course of 15 days to 2 months. At the necropsy, the tracheobronchial lymph nodes were markedly enlarged and firm to hard and on the cut surface had a caseous aspect. The lungs exhibited two injury patterns: multifocal and disseminated. Microscopically, the lungs exhibited multifocal to coalescing necrotic granulomas and non-necrotic granulomas, with multiple acid-fast bacilli within the cytoplasm of epithelioid macrophages and multinucleated giant cells. Bacilli were also labeled upon immunohistochemistry (IHC) for Mycobacterium tuberculosis. Microbiological culture of lung samples from both cases yielded colonies compatible with M. tuberculosis. The isolates were identified as M. tuberculosis var. tuberculosis through polymerase chain reaction (PCR). Although tuberculosis is poorly described in New World primates, M. tuberculosis var. tuberculosis may cause a highly contagious and progressive disease with high mortality in black capuchin monkeys (S. nigritus).

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., (Copyright © 2020 American Society for Microbiology.)

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.

The objective of this study was to identify species of Angiostrongylus spp. infecting wild carnivores in Southern Brazil, as well as to describe gross and histopathological findings associated with the infection. Necropsy was conducted in 16 wild carnivores parasitized by Angiostrongylus spp. Analysed lungs revealed multifocal dark-red areas of consolidation; in one case, multifocal firm white nodules spread in all pulmonary lobes were observed. In one animal, a focally extensive area of malacia associated with haemorrhage was noted in the encephalon. Histologically, multifocal granulomatous pneumonia or bronchopneumonia, associated with eggs and larvae in blood vessels, lung interstitium, alveoli, and sometimes in bronchi and bronchioles was observed. Adult nematodes were seen within blood vessels. The lesion observed in the brain was characterized as a focally extensive area of malacia associated with gitter cells, haemorrhage, thrombosis and a free intralesional larva. Through molecular techniques, seven positive samples of Angiostrongylus cantonensis were obtained, including the brain sample, and a positive sample of Angiostrongylus vasorum-like, all in Cerdocyon thous. The positive sample for A. vasorum showed 97% similarity with sequences deposited in GenBank, suggesting a new species or subspecies of Angiostrongylus sp. Infection of Lycalopex gymnocercus by Angiostrongylus spp. was confirmed by histological evaluation.

A 9-year-old female American Staffordshire terrier was presented to a veterinary hospital with diarrhoea, severe prostration, hypothermia, dehydration and anaemia. The dog died 6 days after the first consultation. At necropsy examination the serosa of the large intestine showed a granular appearance and the mucosa was thickened, ulcerated and red, with prominent folding. Histological examination revealed marked inflammatory infiltration of macrophages into the mucosa and submucosa of the large intestine. These cells stained positively by the periodic acid-Schiff reaction. Immunohistochemistry showed marked presence of intracytoplasmic Escherichia coli in the macrophages. Bacteriological examination of intestinal sections yielded E. coli growth and the isolate displayed atypical characteristics when compared with strains associated with previously published cases of histiocytic ulcerative colitis (HUC). The molecular characterization showed that the isolate harboured none of the genes associated with enterotoxigenic E. coli strains and harboured only a limited number of genes associated with extra-intestinal pathotypes. Adherent and invasive E. coli are unlikely to have been involved in the pathogenesis of HUC in the present case. HUC is a rare disease with a predisposition for boxer dogs; however, sporadic occurrence in other breeds may occur. This is the first reported case of HUC in an American Staffordshire terrier., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: Trema micrantha is a tree widely distributed throughout the Americas. The tree produces highly palatable leaves that have been associated with natural poisoning in goats, sheep and horses, in which hepatic necrosis and hepatic encephalopathy have been observed., Objectives: This study describes malacia and haemorrhage in the central nervous system (CNS) due to T. micrantha consumption, with minimal to absent hepatic lesions., Study Design: Retrospective case series., Methods: A total of 14 horses with a history of neurological signs and spontaneous consumption of T. micrantha leaves were submitted to necropsy and multiple samples were collected for histopathology. Details of clinical history and signs of the horses were obtained through inquiries to the owners and attending veterinarians., Results: All the 14 horses had neurological signs of ataxia, severe sialorrhoea, involuntary running movements, sternal and lateral recumbency, and death after a clinical course that lasted from 24 h to 9 days. For a few days prior to onset of clinical signs, all horses had spontaneously consumed, potentially toxic doses of T. micrantha leaves. All 14 brains had diffuse yellowish discoloration affecting the rhombencephalon, mesencephalon, diencephalon, telencephalon and corpus striatum. In all cases, the most severe lesions were observed in the pons. Spinal cord lesions were observed affecting the lumbar intumescence, which was swollen with darken and depressed areas at the dorsal and ventral horns, and at the sacral level, which on cut surface displayed a friable and yellowish grey matter. The lesions observed grossly in brain and spinal cord consisted microscopically of severe vasculitis and liquefactive necrosis of white and grey matter of the brainstem, cerebellum and spinal cord., Main Limitations: This is a small retrospective series relying on clinical observations reported by owners and attending veterinarians. The mechanism of action of the plant toxin in the CNS is still unidentified., Conclusion: T. micrantha poisoning in horses causes predominantly a neurological disease, with minimal to absent hepatic lesions., (© 2017 EVJ Ltd.)

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.