Focal symmetrical encephalomalacia in a goat.

Focal symmetrical encephalomalacia (FSE) is the most prominent lesion seen in the chronic form of enterotoxemia caused by Clostridium perfringens type D in sheep. However, this lesion has not been reported in goats. The current paper reports a case of FSE in a goat from the state of Paraíba in the Brazilian semiarid region. As reported by the farmer, 30, 4-48-month-old animals from a flock of 150 goats died after showing nervous signs, including blindness and recumbence, for periods varying between 1 and 14 days. The flock was grazing native pasture supplemented with wheat and corn bran. Additionally, lactating goats were supplemented with soybeans. A 4-month-old goat with nervous signs was examined clinically and then necropsied 3 days after the onset of clinical signs. Bilateral, focal, and symmetrical areas of brown discoloration were observed in the internal capsule and thalamus. Histologic lesions in these areas consisted of multifocal, bilateral malacia with a few neutrophils; endothelial cell swelling; perivascular edema; and hemorrhages. The etiology of these lesions was not determined. However, FSE is considered pathognomonic for C. perfringens type D enterotoxemia in sheep, and it is speculated that this microorganism was the etiologic agent in the present case. The flock had been vaccinated against type D enterotoxemia only once, approximately 3 months before the beginning of the outbreak. Insufficient immunity due to the incorrect vaccination protocol, low efficacy of the vaccine used, and a diet including large amounts of highly fermentable carbohydrates were suspected to be predisposing factors for this outbreak.

Polioencefalomalacia experimental induzida por amprólio em bovinos / Experimentally amprolium-induced polio-encephalomalacia in cattle

Para estabelecer um modelo experimental para o estudo da etiologia, patologia e patogênese da polioencefalomalacia (PEM) em bovinos, a condição foi induzida em quatro novilhos pela administração oral de amprólio nas doses diárias de 500 e 350mg/kg de peso vivo, respectivamente por 22 e 26-28 dias. Todos os bovinos morreram espontaneamente ou foram eutanasiados in extremis após um curso clínico de 4-7 dias. Três bovinos que receberam 1.000mg/kg de amprólio e dois que receberam 500mg/kg morreram espontaneamente com quadro clínico agudo a subagudo sem desenvolverem sinais e lesões de PEM. Nos novilhos que PEM foi reproduzida, os sinais neurológicos incluíram marcada apatia, incoordenação, posição de cavalete, quedas ocasionais, hiperexcitabilidade, tremores musculares, cegueira, bruxismo, estrabismo, nistagmo, midríase, opistótono, decúbito lateral e movimentos de pedalagem. Os principais achados de necropsia eram restritos ao encéfalo e consistiam de tumefação, achatamento, amolecimento e amarelamento das circunvoluções cerebrais. Histologicamente, havia necrose neuronal segmentar e laminar (neurônios vermelhos) associada a edema, tumefação endotelial, separação das lâminas de neurônios do córtex telencefálico ou entre as substâncias cinzenta e branca e infiltração moderada a acentuada de macrófagos espumosos. Essas alterações eram mais acentuadas nos lobos telencefálicos frontal, parietal e occipital. Adicionalmente, lesões similares e moderadas foram detectadas no mesencéfalo e hipocampo. A necrose neuronal e o edema afetaram uniformemente as camadas de neurônios da substância cinzenta dos lobos telencefálicos frontal, parietal e occipital. Esse modelo experimental de PEM com administração oral de amprólio parece ser útil para o estudo da doença em bovinos, conforme observado anteriormente em ovinos.

In order to establish an experimental model for the study of the etiology, pathology, and pathogenesis of polioencephalomalacia (PEM) in cattle, the condition was induced into four steers by oral administration of amprolium at daily doses of 500 and 350mg per kg of body weight respectively for 22 and 26-28 days. All steers died spontaneously or were euthanized in extremis after being sick for 4-7 days. Three steers that received the drug at 1,000mg/kg and two that received 500mg/kg died spontaneously with acute or subacute clinical signs and without lesions and signs of PEM. In those steers in which PEM was reproduced, the neurological signs included marked apathy, incoordination, sawhorse stance, occasional falls, hyperexcitability, muscle tremors, blindness, grinding of teeth, strabismus, nystagmus, mydriasis, opisthotonus, and lateral recumbency with paddling movements. Main gross lesions were restricted to the brain and included swelling, flattening, softening and yellow discoloration of the cerebral circumvolutions. Histologically, there was segmental laminar neuronal necrosis (red neurons) associated with edema, swelling of endothelial cells, cleavage of laminar neuronal layers or between gray and white matter and moderate to severe infiltration by foamy macrophages (gitter cells). These changes were more marked in the frontal, parietal and occipital telencephalic lobes. Additionally, similar and moderate lesions were detected in the midbrain and hippocampus. Neuronal necrosis and edema affected uniformly the neurons layers of the grey matter of the frontal, parietal and occipital lobes. This experimental model of PEM with oral administration of amprolium may be useful for the study in cattle, as previously observed in sheep.

Nocardial brain abscess.

Nocardial infections, although rare, are challenging for clinicians to treat. The associated mortality rate remains high; such infections usually occur in immunocompromised patients who have predisposing factors such as malignancy, diabetes mellitus, malnutrition and uremia. However, there have been increasing reports of nocardial infections being observed in immunocompetent patients. Nocardial organisms are mostly isolated from plants and soil, and infection occurs most often as a result of inhalation or direct skin inoculation. Nocardial infections disseminate hematogenously from the primary location to distant end organs, including the brain, kidneys, joints and eyes. Sulfonamides are the drug of choice, based on empirical data. Given the high rate of relapse and the characteristic resistance pattern, treatment should be aggressive and continued for months, with antibiotic treatment being adjusted according to the drug sensitivity test. In our institution, there have been three documented patients with a nocardial brain abscess. All patients were treated with surgical evacuation followed by antibiotics. Here, we report on one patient and review the literature.

Encephalomalacia with Enterococcus durans infection in the brain stem and cerebral hemisphere in chicks in Japan.

Fourteen chicks, 7-12 days old, that died or had neurological signs (depression, paralysis, torticollis, incoordination, and rolling) were investigated pathologically and microbiologically. Variably sized foci of malacia were present within the parenchyma of the brain stem (cerebral peduncle, optic lobe, and medulla oblongata) and the cerebral hemisphere. Capillary thrombosis with congestion and hemorrhage was frequently observed within the malacia lesions. Gram-positive cocci were recognized in the blood capillary of malacia lesions. Bacteriologically, Enterococcus durans was isolated from the brain, liver, kidney, lung, and spleen. Detection of gram-positive cocci within the blood vessels in the malacia lesions observed in these cases may more strongly suggest the pathogenic role of E. durans on the malacia lesions in the brain stem and cerebral hemisphere.

Mycoflora of the toxic feeds associated with equine leukoencephalomalacia (ELEM) outbreaks in Brazil.

The mycoflora of 39 feed samples associated with 29 Equine Leukoencephalomalacia (ELEM) outbreaks was studied from 1988 to 1990, in Brazil. Microbiological examination indicated Fusarium spp. as the most frequent mold which occurred in 97.4% of samples followed by Penicillium spp. in 61.5% and Aspergillus spp. in 35.9%. The moisture content of feed implicated in death of horses was above 15% which can favor the development of Fusarium spp. From the genus, F. moniliforme was the predominant species with an occurrence of 82.0%. Two additional species, not commonly associated with animal toxicosis, were isolated in low frequency, F. proliferatum (12.8%) and F. subglutinans (2.6%). It is important to emphasize that the isolation of F. proliferatum and F. subglutinans from feed obtained from the epizootic areas has not been documented previously in Brazil.

Immunohistological study of encephalomalacia in pigs infected with Aujeszky's disease virus.

Seven hysterectomy-derived colostrum-deprived pigs aged 4 weeks were inoculated intranasally with 10(3) plaque-forming units (1 ml) of the Yamagata YS-81 strain of Aujeszky's disease virus. One pig died and five developed encephalomyelitis and trigeminal ganglionitis. Three pigs killed on days 12-16 showed prominent malacic degeneration. Associated with the malacic foci were many lysosome-positive cells. IgG- and IgM-containing cells in the perivascular cuffs and glial nodules were first detected on day 7, after which they increased in number. They were thought to be closely associated with the presence of neutralizing antibody. These findings suggest that inflammatory cells in the brain are of haematogenous origin.

Enterococcus durans infection in young chickens associated with bacteremia and encephalomalacia.

Two unrelated flocks of chicks experienced elevated mortality from 4 to 10 days of age. Clinical signs in affected birds included a full range of neurological disorders. Livers and spleens were grossly enlarged at necropsy. Enterococcus durans was isolated from multiple organs, including brains. Histologically, there were multifocal coagulative necrosis in the liver, areas of malacia in brain stem, and cerebellar white matter. Inoculation of 1-day-old chicks with a suspension of E. durans resulted in bacteremia but did not produce the lesions observed in field cases.

Fumonisin B1 production and vegetative compatibility of strains from Gibberella fujikuroi mating population 'A' (Fusarium moniliforme).

We examined 25 strains of Fusarium moniliforme from eight states known to be associated with equine leukoencephalomalacia, a disease caused by the mycotoxin fumonisin B1. We determined the mating population, mating type, and vegetative compatibility group to which each of these strains belonged. All 25 strains were in the 'A' mating population; 12 were A+ and 13 were A-. Seventeen of the 25 strains were female fertile; these strains also averaged higher levels of fumonisin B1 production than did the strains that were female sterile. Nitrate non-utilizing (nit) mutants were generated in all 25 strains and each strain was assigned to a unique vegetative compatibility group based on the inability of the derived nit mutants to form a prototrophic heterokaryon with complementary nit mutants derived from any of the other strains examined. From these data, we concluded that the production of fumonisin B1 is a general characteristic of strains from the 'A' mating population of Gibberella fujikuroi associated with equine leukoencephalomalacia, since all 25 of the isolates that we examined were genetically distinct individuals.

Cystic encephalomalacia and intrauterine herpes simplex virus infection.

Cystic encephalomalacia occurred in two preterm infants who had proven intrauterine herpes simplex virus type 2 infection. Calcification was evident in the basal ganglia. Follow-up scans indicated that the cysts had resolved over a period of two months in one infant, while in the case of the other, the cysts became progressively larger with significant ventricular dilatation developing. While cystic changes in the brain of preterm infants are usually due to periventricular leukomalacia, intrauterine infection needs to be considered as a possible cause. Antiviral treatment may be of benefit to infants with herpes simplex virus infection.

Chronic lesions of thrombo-embolic meningo-encephalomyelitis in calves.

Six calves showed neurological signs with recumbency for 5 to 30 days. Histologically, they had encephalomyelitis characterized by multiple minute foci of malacia and perivascular microgliosis throughout the central nervous system. Widespread degeneration of the white matter was also detected mainly in the spinal cord. Micro-abscesses and thrombophlebitis, which were occasionally observed in the malacic lesions, suggested that the disease was a feature of infectious thrombo-embolic meningo-encephalomyelitis modified by various factors, including antibiotic therapy.