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Cutaneous and mucocutaneous plasmacytoma (PCT) is a common neoplasm of dogs. Tumors can be single or multiple and occur predominantly in the oral cavity, lip, ears, digits, and trunk. Although these tumors typically offer no diagnostic challenge for the pathologist, subsets of PCTs with atypical morphologic configurations may make differentiation from other neoplasms difficult. We describe 6 cases of canine cutaneous and mucocutaneous PCT with pseudoglandular arrangement of neoplastic cells. The mean age of affected dogs was 11.3 y, and multiple breeds and sites were affected. Histologically, neoplastic cells were arranged in sheets, packets, and pseudoglandular structures containing central accumulations of blood or eosinophilic material admixed with neoplastic cells and hemosiderin-laden macrophages. Given the presence of pseudoglandular structures resembling neoplastic acini, epithelial neoplasia was occasionally included in the differential diagnosis. Neoplastic cells were strongly immunopositive for multiple myeloma oncogene 1 ( MUM-1) and immunonegative for pancytokeratin AE1/AE3. Canine cutaneous and mucocutaneous PCTs with pseudoglandular morphology may resemble epithelial neoplasia and raise questions about tumor histogenesis.

Aspergillosis is one of the most frequent mycosis affecting avian species. Here is reported an outbreak of aspergillosis affecting 60-day-old white Pekin mallards (Anas platyrhynchos). About 10% of animals in a lot of 200 mallards from a commercial husbandry presented respiratory disorders and skin lesions at slaughter. Three out of 13 animals sent to diagnosis showed, simultaneously, airsacculitis, lung and liver presenting white nodules with variable diameters and elevated, yellowish brown, crusted, multifocal skin lesions located at the base of the feather follicles in the breast. Histopathological examination of lung and liver samples revealed nodules of different sizes with small areas of necrosis surrounded by intense granulomatous inflammation and the presence of fungal hyphae. The skin samples showed dermatitis surrounding a severe necrotizing folliculitis, associated with fungal hyphae. Mycological evaluation of tissues allowed the isolation of Aspergillus fumigatus from the skin samples and Aspergillus flavus from lungs and liver samples. The application of quicklime (CaO) in the litter as part of the disinfection procedures could have contributed to the development of skin lesion in the mallards, predisposing the fungal installation in the damaged site. The occurrence of cutaneous lesions associated with A. fumigatus is a rare manifestation of aspergillosis in birds, and this appears to be the first case reported in white Pekin mallards.

A 6 yr old female Labrador retriever was evaluated for an acute onset of difficulty walking and a head tilt. Initial physical examination revealed bilateral retinal detachment, a left-sided head tilt, positional rotary nystagmus, and lumbar hyperpathia. Pertinent preliminary diagnostic findings included systemic hypertension, bony lysis and adjacent sclerosis of the vertebral endplates of the first and second lumbar vertebrae, and positive urine and blood cultures for a yeast identified as Candida spp. Concerned about disseminated candidiasis after subsequent subretinal aspirates confirmed the presence of a yeast-like organism, therapy with voriconazole was initiated. Because of progressive clinical deterioration and the poor prognosis for recovery, the dog was eventually euthanized. Postmortem histological examination of tissues, including the affected vertebral endplates, revealed numerous intralesional algae compatible with Prototheca spp. To the authors' knowledge, this report is the first to document a case of protothecal diskospondylitis with possible concurrent candidiasis in a dog. Although typically associated with signs referable to the gastrointestinal tract, this report underscores the importance of not excluding protothecosis as a differential diagnosis when such signs are absent. Lastly, the use of voriconazole appears ineffective for reversing the clinical course of late-stage disseminated protothecosis.

Relata-se um surto espontâneo de intoxicação em suínos pela ingestão de sementes de Aeschynomene indica e a reprodução da doença nessa espécie animal. O surto espontâneo ocorreu numa propriedade de criação de suínos localizada na região central do Rio Grande do Sul. Nessa propriedade havia 100 suínos (20 matrizes e 80 suínos jovens de várias categorias). Os suínos eram alimentados com uma ração feita na propriedade pela mistura de 50% farelo de milho, 25% de farelo de soja, 5% de um suplemento vitamínico-mineral de origem comercial e 20% quirera de arroz contaminada por 40% de sementes de A. indica. Embora aparentemente todos os suínos tenham recebido a mesma ração, apenas os suínos de 45 dias de idade foram afetados; as taxas de morbidade, mortalidade e letalidade foram respectivamente 25%-40%, 8,5%-20% e 25%-66%. Os sinais clínicos apareceram cerca de 24 horas após o início da administração da ração contendo sementes de A. indica e incluíam vários graus de incoordenação no andar, quedas, decúbito esternal com membros pélvicos posicionados afastados entre si, decúbito lateral e morte. Não foi possível determinar quantos suínos se recuperaram e quanto tempo levou a recuperação. Um suíno foi submetido à eutanásia e necropsiado na propriedade. A doença foi reproduzida em 5 suínos jovens (A-E) alimentados com uma ração contendo 10% (Suíno A), 15% (Suíno B) e 20% (Suínos C-E) de sementes de A. indica e em um suíno mais velho (Suíno F) que recebeu uma ração com 16,5% de sementes de A. indica. Os sinais clínicos foram semelhantes aos observados nos suínos do surto espontâneo. Os Suínos A, B e F foram submetidos à eutanásia e os Suínos C-E morreram de uma doença aguda respectivamente 16, 21 e 24 horas após o início do experimento. Os achados de necropsia incluíam acentuada hiperemia das leptomeninges em todos os suínos, grandes quantidades de sementes de A. indica no estômago e avermelhamento transmural da parede do intestino e conteúdo intestinal sanguinolento nos Suínos C-E. Um hematoma foi observado no pulmão do Suíno C. Os achados histopatológicos no encéfalo dos suínos alimentados com as maiores concentrações (20%) de sementes de A. indica (C-E) consistiram em áreas focais e simétricas de congestão, edema, hemorragia e tumefação do endotélio vascular em diversos núcleos e no córtex telencefálico. Nos Suínos A e B, que receberam menores concentrações das sementes de A. indica, e no Suíno F, caso espontâneo da doença, as alterações histológicas no encéfalo consistiam de áreas bem definidas de malacia focal simétrica; nessas áreas a neurópila normal era obliterada por numerosos macrófagos espumosos dispostos em estreita aposição, astrocitose e capilares com endotélios tumefeitos. Os focos de malacia focal simétrica em suínos intoxicados com sementes de A. indica afetavam os núcleos cerebelares e vestibulares, a substância negra, o putâmen e os núcleos mesencefálicos, oculomotor e núcleo vermelho. Esses dados indicam que a ingestão de sementes de A. indica é responsável por essa condição neurológica, que a doença pode ser fatal e que parece afetar igualmente suínos jovens e adultos. O desenlace clínico e as alterações patológicas são dependentes da dose e as lesões encefálicas progridem de danos vasculares a edema vasogênico, hemorragia e malacia. A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia.

São descritos a epidemiologia, os sinais clínicos e os achados de necropsia e histopatológicos observados em casos de febre catarral maligna (FCM), que ocorreram de 1973 a 2003 em bovinos de 15 fazendas no Rio Grande do Sul. Em nove ocasiões (60%), a doença ocorreu de forma esporádica, afetando 1-3 bovinos por rebanho, enquanto, em seis fazendas (40%), a FCM ocorreu de forma epizoótica, afetando vários bovinos em cada rebanho. As taxas de morbidade variaram de 2,4% a 20%, e as taxas de letalidade foram de 83,3% a 100%. Bovinos de todas as idades e ambos os sexos foram afetados. Nos casos em que foi possível obter essa informação (9 fazendas), sempre havia ovinos em contato com os bovinos afetados, e o maior número de casos de FCM ocorreu na primavera e verão. A doença clínica era aguda ou subaguda, e os sinais clínicos incluíam febre, corrimento nasal e ocular, conjuntivite, salivação excessiva, hematúria, necrose das papilas bucais que se tornavam rombas, linfadenopatia, diarréia e distúrbios neurológicos. Os achados de necropsia incluíam opacidade da córnea, erosões e ulcerações em várias membranas mucosas do trato alimentar, respiratório, urogenital e conjuntiva; aumento de volume e hemorragia em linfonodos e múltiplos focos brancos nos córtices renais e nas tríades portais hepáticas. Dermatite crostosa foi observada em alguns casos. Os principais achados histopatológicos incluíam vasculite, necrose dos epitélios de revestimento e acúmulos de células inflamatórias em vários órgãos. A vasculite era associada com necrose fibrinóide da túnica média das artérias e acompanhada de infiltrado inflamatório constituído por linfoblastos, linfócitos, plasmócitos e macrófagos. The epidemiology, clinical signs, necropsy and histopathological findings in cases of malignant catarrhal fever (MCF) occurring in cattle from 15 farms in Rio Grande do Sul, Brazil, from 1973 to 2003, are described. In 9 instances (60%) the disease occurred as sporadic cases affecting 1-3 cattle whereas in six farms (40%) MCF occurred as epizootics involving several cattle in each affected herd. Morbidity rates ranged from 2.4% to 20% and lethality rates were 83.3% and 100%. Cattle of all ages and both sexes were affected. Where the information was available (9 farms) sheep were in contact with affected cattle and cases of MCF occurred more frequently in spring and summer. Clinical courses were acute or subacute and clinical signs included fever, nasal and ocular discharges, conjunctivitis, drooling, hematuria, necrosis and blunting of buccal papillae, enlargement of lymph nodes, diarrhea and neurological disturbances. Necropsy findings included opaque corneas, reddening, erosions and ulcerations in several mucous membranes of the alimentary, respiratory and urogenital tracts, and the conjunctiva; enlargement and haemorrhage of lymph nodes and multiple white foci in the renal cortices and in the hepatic portal triads. Crustous dermatitis was observed in some cases. Main histopathological findings included vasculitis, necrosis of the surface epithelia and accumulation of inflammatory cells in several organs. Vasculitis were associated with fibrinoid necrosis of the medial layer of arteries and inflammatory cells included lymphoblasts, lymphocytes, plasma cells and macrophages.

Meningoencefalite granulomatosa foi observada em 7 de 8 vacas leiteiras adultas afetadas por doença granulomatosa sistêmica associada ao consumo de ervilhaca, embora nenhum dos bovinos afetados apresentasse sinais de distúrbios nervosos. Os infiltrados inflamatórios localizavam-se nas leptomeninges e como manguitos perivasculares no interior do encéfalo; consistiam de macrófagos epitelióides, linfócitos, plasmócitos e eosinófilos. Essas alterações inflamatórias variavam de leves a acentuadas de animal para animal e entre diferentes regiões do encéfalo de um mesmo animal. Geralmente, os manguitos perivasculares eram mais acentuados que os infiltrados nas leptomeninges. As regiões do encéfalo afetadas, em ordem decrescente de intensidade, diencéfalo através da massa intermedia; mesencéfalo na altura dos colículos rostrais; ponte e pedúnculos cerebelares, bulbo na altura do óbex, lobo frontal na altura do joelho do corpo caloso e cerebelo. O tipo e a distribuição das alterações inflamatórias são enfatizados em relação ao diagnóstico diferencial de outras doenças e lesões do sistema nervoso central de bovinos no contexto do programa brasileiro de vigilância para a encefalopatia espongiforme bovina. Granulomatous meningoencephalitis was observed in 7 out of 8 adult dairy cows affected by vetch-associated systemic granulomatous disease, although there was no neurological signs associated with the condition. The cellular inflammatory infiltrates were located in the leptomeninges and as perivascular cuffings within the brain and consisted of epithelioid macrophages, lymphocytes, plasm cells and eosinophils. These inflammatory changes varied from mild to severe from animal to animal and among different brain regions of the same animal. Perivascular cuffings were usually more marked than the leptomeningeal infiltrates. Affected brain regions, in decreasing order of intensity, included diencephalon through the level of massa intermedia, mesencephalon at the level of rostral colliculi, pons and cerebellar peduncles, medulla at the level of obex, frontal lobe at the level of the genu of the corpus callosum, and cerebellum. The character and the distribution of the inflammatory changes are emphasized regarding the differential diagnosis with other diseases and lesions of the bovine central nervous system in the context of the Brazilian surveillance program for bovine spongiform encephalopath.

In a survey carried out in tissue specimens from 638 necropsied cats, 13 cases (2.03%) of feline infectious peritonitis were found. Eight of those (61.53%) were of the effusive or wet form and five had the dry non-effusive form of the disease. Ages of affected cats varied from 2-months to 3 yeas. Twelve affected cats (92.30%) were purebreds, five of these cats (38.47%) came from households with more than one cat and three of them came from the same comercial cat raising facility. The duration of clinical courses were 7-45 days and clinical signs included loss of weight, anorexia, diarrhea, jaundice, vomiting, swollen lymph nodes, and neurological disturbances. Necropsy findings, in the wet form included excess of yellowish viscous tanslucent or slightly opaque fluid (50ml-1 liter) in the peritoneal cavity and (in one case) thoracic cavity. Fibrinous exudate covered the serosal surfaces of abdominal organs imparting a whitish, granular, frost-like appearance to them. In the dry form there were multiple granulomatous foci underneath the serosal surface, which extended into the parenchyma of abdominal organs; these findings were particularly prominent in the kidneys. Corneal opacity was observed in one cat. Histologically, there were variable degrees of disseminated piogranulomatous vasculitis and perivasculitis particularly in arterioles. Pyogranulomatous meningitis or meningoencephalitis were observed in three cats with the dry form of feline infectious peritonitis.

São descritos sete surtos e um caso isolado de meningoencefalite por herpesvírus bovino-5 (BoHV-5) em bovinos no Rio Grande do Sul entre 2002 e 2004. Foram afetados bovinos de 1-18 meses, de diversas raças e ambos os sexos. A maior freqüência foi observada em bovinos recém-desmamados e submetidos a outros fatores de estresse. Nesses surtos, de uma população total sob risco de 1.359 bovinos, 54 foram afetados, quatro se recuperaram e 50 morreram espontaneamente ou foram submetidos à eutanásia quando moribundos. Os índices gerais de morbidade, mortalidade e letalidade foram, respectivamente, de 3,97%, 3,67% e 92,59%. A evolução clínica variou de 3-10 dias e os sinais eram caracterizados por depressão, corrimento nasal ou ocular, ranger de dentes, andar em círculos, cegueira, febre, nistagmo, tremores, anorexia, disfagia, sialorréia, incoordenação, pressão da cabeça contra objetos, pêlos arrepiados, taquicardia, taquipnéia, dor abdominal, melena, quedas, decúbito, opistótono, convulsões e movimentos de pedalagem. Dezenove bezerros foram necropsiados. Achados de necropsia foram caracterizados por hiperemia das leptomeninges, tumefação das porções rostrais do telencéfalo, com achatamento das circunvoluções dos lobos frontais; nessas áreas havia focos marrom-amarelados e amolecidos (malacia). Nos casos de evolução clínica mais longa era observada acentuada tumefação, amolecimento e extensas áreas de hemorragia nos lobos frontais telencefálicos. Microscopicamente, todos os bovinos afetados apresentaram meningoencefalite não-supurativa e necrosante, que variou quanto à localização e intensidade nos 19 casos examinados e nas seções de encéfalo de um mesmo caso. A intensidade dessas lesões foi mais acentuada, em ordem decrescente, no córtex telencefálico frontal, nos núcleos da base, tálamo, tronco encefálico, córtex parietal, córtex occipital e cerebelo. O infiltrado inflamatório perivascular era constituído predominantemente por linfócitos e plasmócitos e, menos freqüentemente, neutrófilos. Outros achados incluíam variados graus de gliose, edema, necrose neuronal no córtex telencefálico, caracterizada por encarquilhamento e eosinofilia do citoplasma e picnose nuclear (neurônio vermelho), corpúsculos de inclusão basofílicos intranucleares em astrócitos e neurônios (21,05% dos casos), satelitose e neuronofagia. As áreas de amolecimento do parênquima eram caracterizadas por necrose do componente neuroectodérmico e manutenção das estruturas mesenquimais (vasos e micróglia), com infiltrado de células Gitter e, em casos mais graves, áreas de hemorragia. Nos casos crônicos apenas estruturas vasculares e poucas células Gitter permaneciam, formando uma cavidade entre a substância branca e as leptomeninges (lesão residual). Seven outbreaks and an isolated case of meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) in cattle in Rio Grande do Sul, Brazil, occurring in 2002-2004, are described. From a total population at risk of 1,359 cattle, 54 1-18-month-old calves from both sexes and several breeds were affected and 50 died spontaneously or were euthanatized while moribund. The highest frequency of cases was in recently weaned calves or calves submitted to other stressing factors. General rates of morbidity, mortality and lethality were respectively 3.97, 3.67 and 92.59%. Clinical courses varied from 3-10 days and included depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, nistagmus, trembling, anorexia, dysphagia, drooling, incoordination, head pressing, rough hair coat, tachycardia, tachypnea, abdominal pain, melena, falls, recumbency, opisthotonus, convulsions and paddling. Nineteen calves were necropsied. Necropsy findings were characterized by hyperemia of leptomeninges, swollen rostral portions of the telencephalon, and flattening of frontal lobes gyri; frequently in these frontal areas there were segmental brown-yellow discoloration and softening (malacia) of the cortex. In cases with more protracted clinical courses there were extensive swelling, softening and hemorrhaging of the telencephalic frontal lobes. Microscopically, all affected cattle had a necrotizing non-suppurative meningoencephalitis with variable distribution among the 19 cases and among the various telencephalic regions of the same case. The severity of these changes were more marked, in decreasing order of intensity, in the telencephalic frontal cortex, basal ganglia (nuclei), thalamus, brain stem, parietal telencephalic cortex, occipital telencephalic cortex and cerebellum. Perivascular inflammatory infiltrate consisted predominantly of lymphocytes, plasm cells, and less frequently of neutrophils. Additional microscopic findings included variable degrees of gliosis, edema, neuronal necrosis in the telencephalic cortex characterized by shrinking and eosinophilia of perikaria and nuclear picnosis (red neuron); basophilic intranuclear inclusion bodies in astrocytes and neurons (21.05% of the cases); sattelitosis; and neuronophagia. The areas of softening in the cortical substance consisted of necrosis of the neuroctodermal elements with maintenance of mesenchymal structures (vessels and microglia), infiltrate of Gitter cells, and, in more severe cases, extensive hemorrhages. In chronic cases, only vascular structures and a few Gitter cells remained in the cortical area leaving a cavity between white matter and leptomeninges (residual lesion).