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Background: Vascular hamartomas (VH) are rare or simply underdiagnosed injuries in veterinary medicine and represent a non-neoplastic developmental anomaly disorganization and proliferation of endothelial tissue. VH occur in any region of the body, however in the brain present clinical relevance related with the potential for spontaneous bleeding, adjacent tissue compression and convulsive activity. The aim of these report is to describe clinical, pathological and immunohistochemical features of a case of cerebrovascular hamartoma and highlight the diagnosis of these rare brain disorder in dogs. Case: A 10-year-old male dog, a Campeiro Bulldog breed presented convulsions episodes and died before an elective surgical procedure for eyelid nodule removal. Three red nodules were observed in the brain, one between the parietal lobe and the left occipital lobe (in the medium suprasylviam sulcus), the other in the caudal region of the corpus callosum and the third one in the cerebellar cortex. Central nervous system, eyelids and most organs and tissues samples were collected, fixed in 10% formaldehyde and processed for histopathological analysis. Histologically, in the eyelid was detected a sebaceous adenoma. The nervous system samples revealed well-differentiated sizes vascular structures with thin-walled and blood-filled, promoting compression of the brain. Normal neuropile was detected between the vascular structures substantiating cerebral vascular hamartoma diagnosis in the dog. Immunohistochemical assay was conducted with CD31 (monoclonal mouse antibody anti-CD31, Clone JC70A, Dako Corp.) and Von Willebrand factor (monoclonal mouse antibody anti-Von Willebrand factor, Clone F8/86, Dako Corp.) using the biotin-peroxidase-streptavidin method (PolyDetector Plus DAB-HRP, Bio SB) on CNS sections to confirm the vascular origin of the lining cells in the mass. Discussion: Hamartomas are rarely reported in domestic animals and mostly are of vascular origin. VH in nervous tissues can trigger clinical signs related to hemorrhage, brain space occupation, compression and obstructive secondary hydrocephalus. In general, cerebral VH have a slow progression and usually affected animals are asymptomatic. On the other hand, cerebral vascular hamartomas may also cause clinical signs in very young animals about 15 to 16 months old. In humans, clinical presentation of VH may be related with acquired lesions such as trauma, ionizing radiation, and other central nervous system injuries. In the present case, the dog presented convulsion episode only at 10 years old during prechirurgical procedures. The morphological features of the vascular hamartoma we observed in the Campeiro bulldog is classified as capillary teleangiectasia composed by well differentiated capillaries lined with well differentiated endothelial cells interspaced by normal neuronal tissue. Histopathological and immunohistochemical assay are extremely important to differentiate hamartoma from other tumors, since they may be macroscopically similar. The immunolabeling of endotelial cells by anti-CD31 and anti-Von Willebrand factor antibodies in the cerebral VH, highlight the vascular origin of the masses detected. However, it is also important to perform systematic gross examination of the brain in detail to detect even the smallest injuries in asymptomatic animals avoiding underdiagnoses of cerebral VH. [ABSTRACT FROM AUTHOR]

Background: Sodium monensin is a molecule of the group of ionophores antibiotics (IAs) of the polyether carboxylic type produced from the fermentation of Streptomyces cinnamonensis. Cases of IA poisoning in animals usually occur accidentally. Fatal poisoning in horses, a non-target species and with particular sensitivity usually occurs by the consumption of these products from the toxic dose of 2-3 mg/kg. This report aims to describe the epidemiological and clinical-pathological aspects of an outbreak of ionophore antibiotic poisoning in horses due to the consumption of mineral supplementation indicated for ruminants based on sugarcane molasses. Case: Two horses were necropsied. During necropsy, fragments of various organs were collected and fixed in 10% buffered formalin, routinely processed for histology and stained with hematoxylin and eosin. The information obtained from the animal trainer was that 19 horses received approximately 25 kg of low moisture mixture based on sugarcane molasses, enriched with macro and micro minerals, vitamins and additives containing 1000 mg of monensin/kg in the trough. One day after receiving the product, five horses began to develop ataxia, reluctance to move, difficulty of accompanying the herd and arising. Out of the five, three died after three days of evolution, one after six days (equine 1) and another after 15 days (equine 2) [morbidity 26.31%]. At necropsy, diffuse pallor was observed in the gluteus medius, quadriceps femoris, semimembranosus, biceps brachii and deep pectoral muscles. Microscopically the muscle fibers were tumefied with hypereosinophilic sarcoplasm of homogeneous appearance and with loss of striations, pynotic or absent nuclei (necrosis). Multifocal areas of fibers with sarcoplasmic fragmentation were observed, with clusters of irregular eosinophilic debris, flake (floct necrosis) or granule multifocal infiltrate, predominantly of macrophages, plasma cells and eosinophils with occasional multinucleated giant cells. In the heart there was focally a extensive area of necrosis and a discrete eosinophil infiltrate. Discussion: The diagnosis of ionophore antibiotic intoxication in horses was established by epidemiological and clinical-pathological aspects. In the horses affected in this outbreak, the intoxication was due to the ingestion of sugarcane molasses containing proportions of monensin, which is not indicated for equines, becoming an unusual source for this animal species. The clinical signs reported in the intoxication under study are mostly locomotors and are directly linked to poor distribution of sodium, potassium and calcium ions in muscle cells, leading to ionic disorders that modify the muscle neurotransmission by deregulating contraction and altering movement. Usually, death of horses poisoned with IAs is related to heart failure due to degenerative cardiomyopathy. However, due to the subtlety of the histological lesions in the heart, we believe that the cause of death may also be related to a possible respiratory failure owing to a degenerative myopathy of the diaphragmatic muscle. The anatomopathological changes found in the skeletal muscles of equine intoxicated with molasses are similar to those described in this species by other authors. Compounds based on sugarcane molasses formulated for cattle containing monensin should be considered as a potential source of poisoning for horses and as a cause of degenerative myopathy, which may be an alert for caring about the handling and feeding of these animals. [ABSTRACT FROM AUTHOR]

Background: Zooantroponoses that affect pets are rare. Microorganisms involved in human tuberculosis has great importance to public health and has potentiality to produce reverse zoonoses. Infection by Mycobacterium tuberculosis is in top of the most important infectious diseases related to public health. In dogs, the infection occurs through prolonged exposure to aerosols and respiratory secretions from humans. Canine tuberculosis is little reported and known in Brazil, this work aims to describe the anatomopathological findings of the first case of canine tuberculosis in a 5-year-old dog in the Federal District and alert to the presence of this disease in this region. Case: The dog had history of close contact with its owner, who has been treated for pulmonary tuberculosis six months before. At necropsy scattered multifocal, firm, white to yellow-gray nodules, varying in size (3 mm to 10 mm) involving lungs, kidneys, heart, liver and spleen was observed. In frontal and occipital cerebral cortex, pale-gray circular lesions were detected with the same characteristics. The histological findings were, multifocal to coalescent granulomas, well organized with a central core of necrosis with foci of mineralization, surrounded by histiocytes, epithelioid macrophage, rare Langhans giant cells, some intact and degenerate plasma cells and neutrophils, and a rim of reactive fibroblasts producing fibrous connective tissue. Histological staining with ZN revealed free acid-fast bacilli and in the cytoplasm of macrophages and granulomas in all affected organs. The PCR allowed identification of DNA was extracted from formalin fixed paraffin embedded (FFPE) tissues using the ReliaPrep™ FFPE gDNA Miniprep System®, according to the manufacturer's instructions (Promega, EUA). The Speed-Oligo Mycobacteria assay was used to identify the presence of M. tuberculosis complex DNA in tissue samples. Discussion: Zooantroponoses should be considered as differential diagnosis of infectious diseases affecting companion animals. Tuberculosis is a prevalent and highly relevant disease that plagues humans and animals. Canine tuberculosis is neglected what become information on the epidemiological and clinical situation scarce and its diagnosis a challenge. The systemic form of M. tuberculosis infection is rare in dogs, it occurs by contact with secretions of actively infected humans or ingested contaminated food with the bacillus. In the present case the dog contracted the infection by direct contact with owner who had tuberculosis and presented acute clinical alterations resulting from the disseminated form of the disease. Transmission of M. tuberculosis from humans to dogs is considered a determinant in the epidemiological chain of infection in companion animals. Histological lesions in natural cases of tuberculosis in dogs and cats differ from typical tuberculoid granulomas found in cattle and humans. In this case of disseminated tuberculosis in the DF scarce Langhans giant cells in the granulomas was obseved, which is a typical manifestation of the disease in the species. The coloration of Ziehl- Neelsen allows evidence of alcohol-acid-resistant bacilli, as seen in the present report. Health actions aiming prevention and control of tuberculosis should include investigation of the disease in companion animals in households where there are records of human tuberculosis. The anatomopathological and molecular findings confirmed the diagnosis of Mycobacterium tuberculosis infection transmitted by the owner, an uncommon disease in companion animals, a challenge to the clinical diagnosis, and previously unknown in the Federal District. [ABSTRACT FROM AUTHOR]

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