Generalized and fatal felid alphaherpesvirus-1 natural infection with liver involvement in a feline leukaemia virus-positive adult cat: a case report.

Generalized and fatal felid alphaherpesvirus-1 (FeHV-1) natural infection with liver involvement is rarely reported in cats, and the occurrence of herpesvirus viraemia with internal organ histologic lesions in adult cats is unknown. A 1.5-year-old cat, female, mixed breed, positive for feline leukaemia virus (FeLV) presented in a veterinary teaching hospital with sneezing, nasal discharge, anorexia, and diarrhoea after two weeks, evolving to inspiratory dyspnoea. Complete blood count and serum biochemistry analysis showed marked leukopenia and thrombocytopenia. After clinical worsening and lack of treatment response, the cat was euthanized. Pathological findings included hepatic necrosis, fibrinonecrotic tracheitis, and bronchointerstitial pneumonia. Marked amounts of coccobacillary bacteria were observed covering the necrotic tracheal and bronchial mucosa, at the cytoplasm of alveolar macrophages, and free in alveoli lumen, mimicking a primary bacterial tracheitis and pneumonia. Both lung and tracheal bacteria exhibited marked immunolabeling in anti-Escherichia coli immunohistochemistry. In addition, rare epithelial cells of bronchi contained round, eosinophilic, intranuclear viral inclusion bodies (4-7 µm) that marginate the chromatin, characteristic of FeHV-1 infection. Strong multifocal anti-FeHV-1 immunolabeling was observed in necrotic epithelial cells of the liver, trachea, and lungs. Generalized herpesvirus infection with the occurrence of acute hepatic necrosis and severe respiratory illness is a potential differential diagnosis in FeLV-positive cats with respiratory signs. The immunodepression in these cats probably favours a FeHV-1 viraemia in addition to the development of opportunistic bacterial infections, such as Escherichia coli, and it is associated with a poor outcome.

Is Methylprednisolone Acetate-Related Insulin Resistance Preventable in Cats?

Methylprednisolone acetate (MPA) is often prescribed to cats despite being recognized eventually as diabetogenic. To assess MPA-related insulin resistance and evaluate the efficacy of metformin or an obesity and diabetes mellitus (O&D) adjuvant diet as protective factors, a randomized clinical trial was conducted with 28 owned cats undergoing glucocorticoid therapy. A single MPA dose of 20 mg intramuscularly was administered to each cat. Controls (n = 10) received only MPA. In the diet group (n = 9), replacement of their habitual diet by ad-libitum feeding of a feline commercial O&D diet (Equilíbrio O&D, Total Alimentos ADM) was made. In the metformin group (n = 9), metformin chlorhydrate 25mg/cat PO/q24h was administered for 30 days. All patients were clinically evaluated at baseline (T0), day 15 (T15), and day 30 (T30) and blood draw for complete blood count, serum biochemistry, and determination of insulin concentrations. Fasting Insulin Sensitivity Index (SI), Amended Insulin to Glucose Ratio (AIGR), Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), and Homeostatic Model Assessment of beta-cell function (HOMA-B) were calculated based on fasting glycemia and insulinemia. All groups showed significantly higher levels (P < .05) of neutrophils, albumin, glucose, cholesterol, triglycerides, and serum insulin at T15. Patients in the metformin group showed also higher SI, AIGR, and HOMA-IR results at T15. Also, at T15, reduced levels (P < .05) of eosinophils, lymphocytes, and creatinine were documented in all groups. An MPA single dose induced changes in insulin sensitivity in cats; however, neither metformin nor O&D feeding used in this study was effective as protective factors against MPA-related insulin resistance.

First molecular characterization of Sarcocystis neurona causing meningoencephalitis in a domestic cat in Brazil.

Sarcocystis neurona is the main agent associated with equine protozoal myeloencephalitis (EPM). Apart from horses, S. neurona has been occasionally described causing neurologic disease in several other terrestrial animals as well as mortality in marine mammals. Herein, we describe the clinical, pathological, and molecular findings of a fatal case of S. neurona-associated meningoencephalitis in a domestic cat. The causing agent was analyzed by multilocus genotyping, confirming the presence of S. neurona DNA in the tissue samples of the affected animal. Significant molecular differences were found in relation to S. neurona isolates detected in other regions of the Americas. In addition, the parasite was identical to Sarcocystis sp. identified in opossum sporocysts in Brazil at molecular level, which suggests that transmission of. S. neurona in Brazil might involve variants of the parasite different from those found elsewhere in the Americas. Studies including more samples of S. neurona would be required to test this hypothesis, as well as to assess the impact of this diversity.

Pulmonary Langerhans cell histiocytosis in cats and a literature review of feline histiocytic diseases.

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.

Phylodynamics of the Brazilian feline immunodeficiency virus.

Feline immunodeficiency virus (FIV), like other retroviruses, displays large genomic divergence when different isolates are compared. In this study, 31 FIV positive samples of domestic cats from Porto Alegre, RS, Brazil were used aiming at a detailed genomic characterization and a better understanding of the molecular epidemiology of the virus in Brazil. The proviral env genes were partially amplified, sequenced and compared with another 237 sequences from different continents. We identified several Brazilian highly supported clades (A, B1, B2, C and D) that suggest independent events of introduction of FIV in Brazil. Forty six reference-sequences from the GenBank were used with our 31 sequences to infer the virus subtypes. Our sequences belong to the subtype B and three of them result from a recombination with the previously described subtype F. The other 28 Brazilian samples belonging to subtype B and another 46 Brazilian sequences from the GenBank were used to estimate the time to the most recent common ancestor of each Brazilian clade, using a Bayesian approach and a relaxed molecular clock model. The analyses of Brazilian sequences suggest several different entries of the virus in the Brazilian cat population between 1981 and 1991.