Bovine papular stomatitis virus (BPSV) is a parapoxvirus associated with papular and erosive lesions on the muzzle, lips, and oral mucosa of cattle. Teats of milking cows are occasionally affected, and the infection is frequently transmitted to human beings. The present report describes an outbreak of BPSV infection affecting cows in midwestern Brazil, with human involvement. The disease was observed in neighboring small hand-milking farms, affecting 20 milking cows. The signs included painful reddish papules, ulcers, and scabby proliferative lesions on the teats, with a clinical course of 7–12 days. Affected cows presented severe local pain, not allowing the completion of milking. Histologically, acanthosis, spongiosis, and parakeratotic hyperkeratosis with adjacent focally extensive ulcers and multifocal inflammatory infiltrate were observed in the epidermis. Eosinophilic inclusion bodies were noted in the cytoplasm of epithelial cells. Personnel milking the affected cows developed lesions on the hands, painful papules that progressed to ulcerative and scabby lesions in 4–7 days. A polymerase chain reaction using a set of pan-parapoxvirus primers for the B2L gene performed on DNA extracted from scabs amplified a 590-bp product, which when sequenced, revealed similarities of 99%, 85%, and 84% with BPSV, Pseudocowpox virus, and Orf virus, respectively. A phylogenetic tree based on the B2L sequence was constructed, showing that the virus clustered with BPSV isolates. Although clinical cases compatible with BSPV infection have been frequently described in Brazil, the present report identifies the agent associated with cattle and human disease in the country.

The current report describes an outbreak of vesicular disease affecting dairy cows in midwestern Brazil in which a coinfection with 2 poxviruses—Vaccinia virus (VACV) and a parapoxvirus—was demonstrated. Milking cows presented vesicles, painful reddish or whitish papules, and scabby proliferative lesions in the teats and udder, in a clinical course of approximately 10–21 days. Histologically, multifocal areas of moderate to severe acanthosis, spongiosis, hypergranulosis, and parakeratotic or orthokeratotic hyperkeratosis with adjacent focally extensive ulcers were observed in the epidermis. Rounded eosinophilic inclusion bodies were observed in the cytoplasm of epithelial cells of areas with acanthosis or necrosis. Moderate inflammatory infiltrate of lymphocytes, plasma cells, neutrophils, and macrophages were observed in some dermal areas. Two people milking the affected cows developed lesions on the hands, painful papules which progressed to ulcerative and scabby lesions in 4–7 days. Electron microscopy of scabs from 1 cow revealed the concomitant presence of orthopoxvirus and parapoxvirus particles. Scabs from 2 cows were positive by polymerase chain reaction for the parapoxvirus B2L gene; 1 of the scabs was also positive for the VACV vgf gene. Nucleotide sequencing of the B2L amplicon revealed a similarity of 96–99% with Orf virus (ORFV) and lower identity with Pseudocowpox virus (92–95%) and Bovine papular stomatitis virus (85–86%). Nucleotide sequencing of a region of parapoxvirus DNA polymerase gene revealed a high similarity (98–100%) with ORFV sequences. Thus, an unusual coinfection with VACV and a parapoxvirus, likely ORFV, was demonstrated in the outbreak.

A retrospective study was conducted on neurological diseases of cattle in the state of Goiás, Brazil, from March 2010 to August 2017. Samples of three veterinary diagnostic laboratories were analyzed. Diagnosis was established in 170 out of 407 cattle with neurological signs. Epidemiological, clinical, and anatomic pathology features of each case were researched in the files. Main disorders included diseases caused by viruses (rabies 29.41%, meningoencephalitis by bovine herpesvirus 15.88%, and malignant catarrhal fever 1.76%), by bacteria (botulism 5.88%, suppurative meningitis 3.53%, encephalic abscesses 2.94%, listeriosis 1.76%, and thrombotic meningoencephalitis 1.76%), of metabolic origin (polioencephalomalacia 17.06%), of indefinite cause (lymphoplasmacytic meningoencephalitis 11.18%, traumatic hemorrhages 3.53%, and multifocal malacia with gliosis 1.18%), congenital (hydrocephaly 1.18% and multiple malformations 0.59%), toxic (urea poisoning 1.18% and insecticide poisoning 0.59%), and parasitic (meningoencephalitis associated with infection by Trypanosoma sp. 0.59%).

A 12-year-old crossbred female cat was presented for necropsy with a history of anorexia, ataxia, convulsions, and blindness. Grossly, a whitish, firm, and well-circumscribed nodule with an irregular surface of approximately 1.5 cm in diameter was observed in the right dorsal, parietal, and occipital lobes of the brain. Histologically, the tumor was composed of neoplastic astrocytes forming irregular interweaving sheets and bundles. These cells were elongated, spindle-shaped, and bipolar, and some had clear cytoplasm and a dense nuclear chromatin pattern. Extensive areas of cartilaginous and osseous metaplasia were observed. By immunohistochemistry, the neoplastic cells were found to be markedly positive for S-100 protein and glial fibrillary acidic protein. On the basis of morphologic and immunohistochemical features, the diagnosis of pilocytic astrocytoma was made.

The current report describes granulomatous pneumonia due to Spirocerca lupi in 2 free-ranging maned wolves (Chrysocyon brachyurus). Both wolves had multiple, white, 1–1.5 cm in diameter, soft, encapsulated granulomas in the caudal lung lobes, which contained centrally placed parasites on cut sections. Microscopically, there was granulomatous inflammation with numerous intralesional sections of spirurid nematodes. Representative complete adult specimens of nematodes derived from these lesions were submitted for parasitological exam and identified as the spirurid S. lupi. To the authors’ knowledge, there have been no published reports of S. lupi in maned wolves.

Cases of vesicular and exanthematic disease by Vaccinia virus (VACV) have been reported in dairy herds of several Brazilian regions, occasionally also affecting humans. The present article describes eight outbreaks of vesicular disease caused by VACV in dairy herds of six counties of Goiás state, Midwestern Brazil (2010-2012), involving a total of 122 cows, 12 calves and 11 people. Dairy cows (3 to 9 years old) were affected in all cases and calves (2 to 9 months old) were affected in five outbreaks, presenting oral lesions. The morbidity ranged between 8 and 100% in cows, and 1.5 to 31% in calves. In the cows, the clinical signs started with vesicles (2-7mm), painful and coalescent papules (3-8 mm), which resulted in ulcers (5-25mm) and scabs in teats, and, occasionally, in the muzzle. The clinical course lasted from 16 to 26 days. The histopathology of bovine skin samples revealed superficial perivascular inflammatory infiltrate of lymphocytes, plasma cells, neutrophils, macrophages and multifocal areas of acanthosis, spongiosis, hipergranulosis and parakeratotic or orthokeratotic hyperkeratosis with adjacent focally extensive ulcers. Eosinophilic inclusion bodies were noted in the cytoplasm of the keratinocytes. PCR to vgf gene of Orthopoxvirus was positive in samples collected from all outbreaks, and in some cases, genomic VACV sequences were identified by nucleotide sequencing of the PCR amplicons. Infectious virus was isolated in cell culture from scabs from one outbreak. Antibodies to Orthopoxvirus were detected in at least 3 or 4 animals in most outbreaks, by ELISA (outbreaks 1, 2, 3, 4, 5 and 7) or virus-neutralization (outbreak 6). Neutralizing titers ranging from 8 to 64 in outbreak 6. In all outbreaks, VACV infection was suspected based on the clinical and pathological findings and it was confirmed by laboratory tests. Upon the etiological confirmation, other agents associated with vesicular disease were discarded. In all outbreaks, at least one milker who handled the affected cows developed malaise, headache, fever, painful vesico-pustular lesions mainly in the hands, but also in the neck and nose. These results confirm the circulation of VACV in the region and call attention for a correct diagnosis and the adoption of prophylactic and control measures.