Necrotizing meningoencephalitis associated with cortical hippocampal hamartia in a Pekingese dog

A 4-year-old male Pekingese dog was referred to the clinic with a history of recurrent seizures and progressive abnormal gait and behavior, which did not respond to treatment. At necropsy, a large cortical defect in the right temporo-parietal cortex, malacia of subcortical white matter, right basal nuclei, and capsula interna, as well as abnormalities of the right hippocampus were observed. Histological examination of the brain revealed moderate to severe nonsuppurative meningoencephalitis in the left cerebral hemisphere and extensive infarction-like lesions with milder inflammation in the right hemisphere. In the right hippocampus, the pyramidal cells were arranged in a gyrus-like pattern and intermingled with gemistocytic and fibrillary astrocytes. The histopathological features of the inflammatory lesions were consistent with necrotizing meningoencephalitis and resembled those described in so-called Pug dog encephalitis. The hippocampal changes were interpreted as dysplasia (monolateral hippocampal cortical hamartia), unrelated to clinical signs and necrotizing inflammatory lesions.     

Adherent gram-positive cocci on the intestinal villi of two dogs with gastrointestinal disease

Two dogs were examined for clinical signs of chronic gastrointestinal disease. Duodenal mucosal biopsy specimens, obtained endoscopically, revealed histologic lesions of adherent gram-positive cocci on the villus epithelium of both dogs. The positive gram stain and morphologic features of the adherent cocci were suggestive of Streptococcus organisms. Indirect tests for intestinal bacterial overgrowth were not diagnostic, suggesting that the adherent cocci were a primary lesion. Rapid clinical response following dietary manipulation and the initiation of medical management was observed in both dogs. The dogs of this report draw similarities to Streptococcus durans infection previously reported in pigs, foals, and a single pup. The pathogenesis of enteric disease associated with adherent gram-positive cocci in dogs remains ill-defined.     

Spongy transformation of the brain in sheep with lupinosis.

Spongy transformation in the brain of sheep affected with chronic lupinosis in the field is described. Identical lesions were reproduced in sheep with experimental acute and chronic lupinosis. The primary brain lesion was vacuolation of the white matter of the brain stem with no malacia, neuronal damage or gliosis being present. The extent and severity of the vacuolation was related to the severity of the liver lesion.     

Neurotropism of highly pathogenic avian influenza virus A/chicken/Indonesia/2003 (H5N1) in experimentally infected pigeons (Columbia livia f. domestica)

This investigation assessed the susceptibility of experimentally infected pigeons to the highly pathogenic avian influenza virus (HPAIV) H5N1 that caused recent outbreaks of avian influenza in birds and humans in several countries of Asia. For this purpose 14 pigeons were infected ocularly and nasally with 10(8) EID50 and clinical signs were recorded and compared with five chickens infected simultaneously as positive controls. The chickens demonstrated anorexia, depression, and 100% mortality within 2 days postinoculation. Three of the pigeons died after a history of depression and severe neurological signs consisting of paresis to paralysis, mild enteric hemorrhage, resulting in a mortality of 21%. Gross lesions in these pigeons were mild and inconsistent. Occasionally subcutaneous hyperemia and hemorrhage and cerebral malacia were observed. Microscopic lesions and detection of viral antigen were confined to the central nervous system of these pigeons. In the cerebrum and to a minor extent in the brain stem a lymphohistiocytic meningoencephalitis with disseminated neuronal and glial cell necrosis, perivascular cuffing, glial nodules, and in one bird focally extensive liquefactive necrosis could be observed. The remaining nine pigeons showed neither clinical signs nor gross or histological lesions associated with avian influenza, although seroconversion against H5 indicated that they had been infected. These results confirm that pigeons are susceptible to HPAIV A/chicken/Indonesia/2003 (H5N1) and that the disease is associated with the neurotropism of this virus. Although sentinel chickens and most pigeons did not develop disease, further experiments have to elucidate whether or not Columbiformes are involved in transmission and spread of highly pathogenic avian influenza.     

Immunohistochemical distribution of viral antigens in pigs naturally infected with porcine teschovirus

A distribution of porcine teschovirus (PTV) antigens in pigs naturally infected with PTV is presented using the method of immunohistochemical examination. In the nervous system, PTV antigens were found in the cytoplasm of neuronal cells and glial cells distributed in the spinal ventral horn and brain stem, and also in the cytoplasm of ganglion cells in the spinal ganglion. No antigens were seen in the cerebral hemisphere. In the nervous system, the distribution of PTV antigens was consistent with lesions characteristic of nonsuppurative encephalomyelitis. In the other examined organ, PTV antigens were observed in bronchiolar epithelial cells in the lung, hepatocytes in the liver, epithelial cells in the tonsils and the myenteric nerve plexus in the small and large intestine.     

Polioencephalomalacia in captive harbour seals (Phoca vitulina)

In a colony of 11 harbour seals (Phoca vitulina Linné 1758) two episodes of central nervous disorders occurred within 2 years causing fatalities in seven adult animals. Clinical signs comprised dyspnoea, anorexia, apathy, incoordination and lateral recumbency. Vitamin B complex therapy was successful once. Pathomorphological examination of seven carcasses revealed acute and subacute malacia of the cerebellar grey matter. Additional acute malacic lesions located in the cerebral cortices and basal ganglia were observed. Mesencephalic nuclei were less severely affected and displayed acute changes. Despite intense search for environmental toxins and infectious agents, the cause of the fatalities remained undetermined. However, the type and pattern of the lesions are most suggestive of a thiamine deficiency.     

Morphologic and immunoperoxidase study of neurologic lesions in naturally acquired rabies of raccoons.

Histopathologic (hematoxylin and eosin [HE]) and immunoperoxidase (streptavidin-biotin complex) methods were used for examination of formalin-fixed tissues of rabid raccoons from an enzootic area of Pennsylvania. Extensive morphologic lesions of rabies encephalitis were present in the cerebrum and the brain stem regions. Negri bodies were detected by both methods and were present in the brain (cerebral cortex, hippocampus, brain stem, cerebellum, and cervical spinal cord) and in the ganglia of the trigeminal nerves. The viral inclusions were also seen in ganglion cells in the tongue, parotid salivary glands, pancreas, intestines, and adrenal glands. These sites were not associated with any inflammatory cellular infiltrate. The immunoperoxidase method was superior to HE for the detection of Negri bodies. Because lesions of rabies encephalitis were consistently observed in the cerebrum, brain stem, and cervical spinal cord regions, these areas of the brain should be included when raccoons are examined by the fluorescent antibody test for rabies.     

Brain abscess in a Japanese black calf: utility of computed tomography (CT)

Computed tomography (CT) was used for diagnosis of brain abscess in a 6-month-old, Japanese black calf presented with neurological dysfunction, compulsive circling and vision disturbance. CT images showed asymmetric lateral ventricles, and presence of intra-cranial multiple low absorption lesions surrounded by capsule suggestive of abscess in the right cerebral hemisphere. Postmortem examination revealed marked swelling of right cerebral hemisphere and olfactory bulb. Multilocular large abscess containing creamy pus was found to occupy most area of periventricular and lateral ventricle. Fusobacterium necrophrum was isolated from the abscess contents as the causative agent. These results demonstrate that CT is useful tool for tentative diagnosis of bovine brain abscess.     

Cerebral metabolism in brains of rats infected with neuropathogenic murine leukemia viruses

Friend murine leukemia virus A8 and PVC211 cause spongiform neurodegeneration in rat brains. Glutamate is an important neurotransmitter synthesized from alpha-ketoglutaric acid, an intermediate product of the citric acid cycle, and glutamine is synthesized from glutamate. To examine the brain metabolism of rats infected with neuropathogenic viruses, the amount of glutamate and glutamine in the brains of rats infected with A8, PVC211, and non-neuropathogenic 57 was measured using high performance liquid chromatography, and the (13)C-label incorporation into the C4 position of glutamate and glutamine from [1-(13)C] glucose was measured with (13)C nuclear magnetic resonance. In the cerebral hemisphere and region containing the brain stem and basal ganglia of rats infected with A8 and PVC211 at 8-9 weeks post-infection (wpi), the amount of glutamine was decreased compared with the 57-infected rats. The amount of glutamate was decreased in the cerebral hemisphere of the A8-infected rats and the region containing the brain stem and basal ganglia of PVC211-infected rats at 8-9 wpi. The amount of [4-(13)C] glutamine and [4-(13)C] glutamate in the cerebral hemisphere and region containing the brain stem and basal ganglia of rats infected with A8 and PVC211 at 8-9 wpi was equivalent to that of the 57-infected rats. These results suggest that in the brains of rats infected with neuropathogenic viruses, de novo synthesis of glutamate and glutamine is not decreased, but the ability to maintain quantitative levels of glutamate and glutamine is decreased compared with the brains of rats infected with non-neuropathogenic virus.     

Cerebral phaeohyphomycosis in a Birman kitten

Extract

A 6-month-old female Birman kitten was presented for long-lasting and repeated seizures. It initially had some response to treatment but deteriorated and was euthanised. At necropsy, the brain was swollen and some of the caudal cerebellum was compressed into the foramen magnum. The right cerebral hemisphere was enlarged and had a round, dark, 5 mm-diameter focus on the dorsal surface of the rostral sigmoid gyrus of the frontal cerebrum. There were smaller dark areas extending caudally into the endomarginal gyrus. When the fixed brain was sliced transversely, the lesions were grey-coloured or translucent and involved most of the rostral half of the right cerebral hemisphere. Histologically, there was severe, extensive pyogranulomatous inflammation with some interspersed areas of spongiosus and oedema. Within the granulomas were variable numbers of branching, pigmented, thin-walled, septate fungal hyphae. Cladosporium bantianum (trichoides) was isolated from the brain. This is the most frequent agent reported from cases of cerebral phaeohyphomycosis.     

Spontaneous listeric encephalitis and neuritis in sheep. Light microscopic studies

Sixteen of 17 sheep with spontaneous listeric encephalitis had neuritis characterized by diffuse and focal intrafascicular and perineural accumulations of lymphocytes, plasma cells, macrophages and neutrophils in one or more cranial nerves. Nine sheep had extensive trigeminal neuritis which was usually unilateral. Brain lesions were mainly in the stem and were foci of macrophages or neutrophils or both, malacia, neutrophilic neuronophagia, vascular cuffing, and meningitis. Lesions in the brain and trigeminal ganglia were most severe on the same side as the affected trigeminal nerve. Gram-positive bacilli were in proximal parts of cranial nerves in foci of inflammatory cells and occasionally in morphologically intact nerve fibers. Organisms in the brain were in phagocytes in areas of inflammation and in scattered neurons and axons. The results were consistent with centripetal migration of the infectious agent along one or more branches of the trigeminal nerve to the brain and dissemination in the brain stem occurring, at least partly, along fiber tracts. Intraaxonal movement of bacteria probably is a mechanism involved in the pathogenesis of this disease.     

Bluetongue virus-induced hydranencephaly in cattle

Direct inoculation of bluetongue virus into 125-day bovine fetuses resulted in development of hydranencephaly. The earliest lesions after virus inoculation were a severe necrotizing encephalitis, which was most prominent in the cerebrum, and an associated nonsuppurative meningitis. At birth, the brains of infected fetuses had thin-walled cerebral hemispheres, dilated lateral ventricles, and cerebral cysts. No gross lesions were observed in the brain stem or cerebellum. Two morphologically different lesions were present in the brain of a fetus sacrificed 20 days after virus inoculation. There were discrete foci of hemorrhagic cerebral necrosis that resembled infarcts and widespread microcavitations of the intermediate and subventricular zones. Changes consistent with vascular damage were present in the brains of fetuses sacrificed 12 and 20 days after virus inoculation. Calves with bluetongue virus-induced hydranencephaly would have poor viability, but they would not be expected to have any significance as virus reservoirs.     

Pathology of listerial encephalitis in chickens in Japan

Neural signs (torticollis, drowsiness) and mortality were observed in five chickens of a native chicken flock (reared for meat) that included 450 male birds on a farm that had 2300 native chickens and 1120 layers. Histologic lesions were observed in the medulla oblongata, optic lobe, cerebellum, and spinal cord of the affected birds. The lesions, which were most severe in the medulla oblongata, were massive abscesses with rarefaction (demyelination and malacia) of the parenchyma with gram-positive bacteria. The degenerative and necrotic areas were characterized by fibrin thrombosis, hemorrhages, and congestion in the blood vessels. Immunohistochemically, the bacteria positive for L. monocytogenes antigen were observed in the medulla oblongata, cerebellum, and spinal cord. Ultrastructurally, the small rod-shaped and thin-cell-walled bacteria were observed in the parenchyma of the medulla oblongata. Listeria monocytogenes (serotype 4b) was isolated from the medulla oblongata and spinal cord. The pathogenesis of listerial encephalitis in chickens was discussed.     

Intracerebral migration of Cuterebra larva in a kitten

Verminous encephalitis in a 4-week-old kitten was manifested by depression, hysteria, and terminal convulsions. Necropsy revealed a second instar of Cutebra sp in the right cerebral hemisphere. The main lesions in the brain were those of acute focal hemorrhagic encephalomalacia.     

Lethal cerebrospinal elaphostrongylosis in a reindeer calf.

Lethal elaphostrongylosis in a reindeer calf is described. The calf showed signs of abnormal behaviour, mental confusion and reduced vision due to lesions in the brain parenchyma caused by migrating mature Elaphostrongylus rangiferi. Traumatically caused malacia and secondary axon degeneration were observed in all brain areas. Nematodes were found in the skeletal muscles, epidural space of the spinal cord, and in the subdural spaces and leptomeninges of the cord and brain. Developing nematode ova were sectioned along migratory tracks in the brain, in the subdural space of the cord, epidural adipose tissue, perineurium of the spinal nerve roots and in the lungs.     

Pathogenicity of a Hong Kong-origin H5N1 highly pathogenic avian influenza virus for emus, geese, ducks, and pigeons

The H5N1 type A influenza viruses that emerged in Hong Kong in 1997 are a unique lineage of type A influenza viruses with the capacity to transmit directly from chickens to humans and produce significant disease and mortality in both of these hosts. The objective of this study was to ascertain the susceptibility of emus (Dramaius novaehollandiae), domestic geese (Anser anser domesticus), domestic ducks (Anas platyrhynchos), and pigeons (Columba livia) to intranasal (i.n.) inoculation with the A/chicken/Hong Kong/220/97 (H5N1) highly pathogenic avian influenza virus. No mortality occurred within 10 days postinoculation (DPI) in the four species investigated, and clinical disease, evident as neurologic dysfunction, was observed exclusively in emus and geese. Grossly, pancreatic mottling and splenomegaly were identified in these two species. In addition, the geese had cerebral malacia and thymic and bursal atrophy. Histologically, both the emus and geese developed pancreatitis, meningoencephalitis, and mild myocarditis. Influenza viral antigen was demonstrated in areas with histologic lesions up to 10 DPI in the geese. Virus was reisolated from oropharyngeal and cloacal swabs and from the lung, brain, and kidney of the emus and geese. Moderate splenomegaly was observed grossly in the ducks. Viral infection of the ducks was pneumotropic, as evidenced by mild inflammatory lesions in the respiratory tract and virus reisolation from oropharyngeal swabs and from a lung. Pigeons were resistant to HK/220 infection, lacking gross and histologic lesions, viral antigen, and reisolation of virus. These results imply that emus and geese are susceptible to i.n. inoculation with the HK/220 virus, whereas ducks and pigeons are more resistant. These latter two species probably played a minimal epidemiologic role in the perpetuation of the H5N1 Hong Kong-origin influenza viruses.     

Postanaesthetic cerebral necrosis in five horses

After being anaesthetised for between one hour 40 minutes and seven hours, five adult horses developed acute neurological signs and extensive cerebrocortical necrosis. Four of them had had abdominal surgery for colic and one had had repeated orthopaedic interventions. Between five hours and seven days after the surgery, all five horses suddenly developed severe signs of a predominantly prosencephalic disturbance: bilateral blindness with normal pupillary light responses, abnormal behaviour varying from propulsive pacing to head pressing profound lethargy and generalised seizures. They were euthanased between 24 hours and three weeks after the onset of these signs. In three of the cases a gross examination of the brain revealed patchy malacia of the cerebral grey matter and some discolouration of the adjacent white matter. Microscopical examination revealed lesions that varied from laminar neuronal necrosis in the grey matter of the cerebral cortex to more diffuse necrosis of the cortex and underlying white matter. Four of the five cases had had a period of hypercapnea while anaesthetised, and two of them (and possibly a third) had also had hypoxaemia.     

自发性急性犬瘟热的原发性脱髓性脑病

为了进一步观察犬瘟热病毒引起的原发性脑损伤和包涵体形成的特点，调查脑组织的损伤与神经症状的关系，对10只急性犬瘟热病犬的脑组织进行了详细的病理学研究。为了仔细地观察病变，本试验按照解剖学关系将脑组织分成3个大部分和11个切面，即大脑(4个切面)，脑干(5个切面)和小脑(2个切面)。组织切片经HE、LFB和免疫组织化学染色后进行检查，结果表明：在大脑，脱髓呈弥漫性发生，程度较轻；脑干的周围或靠近第三脑室的白质脱髓较重；小脑在轻度或中度脱髓的基础上常出现严重的多发性脱髓灶。脱髓部呈空泡或海绵状，有少量胶质细胞存在，但无炎性反应。脱髓性病损是非时称性发生，对神经束没有特殊的亲和力。在脑室的室管膜细胞内发现有较多的嗜酸性胞浆或核内包涵体。用抗犬瘟热病毒抗体染色，带有包涵体的室管膜细胞呈现强阳性反应。部分锥体细胞，神经核细胞和漓氏细胞变性、溶解或胞浆深染。胞核浓缩。这种变化以小锥体神经细胞表现得最为明显。根据此研究结果，作者认为由犬瘟热病毒引起的原发性脑组织损伤是一种脱髓性脑病，而不是脑炎变化；位于室管膜细胞内的包涵体对于脑组织犬瘟热的确诊具有重要的作用；由于犬瘟热病毒引起神经细胞的损伤是非特异性的，对脑组织的侵害是非对称性的。对神经束的作用无特殊的亲和力，所以患犬瘟热的犬在临床上可出现不同的神经症状。     

Hypertensive encephalopathy in cats with reduced renal function

The clinical, hemodynamic, and pathologic features of hypertensive encephalopathy in two cats with reduced renal mass are described. The cats developed a progressive syndrome of lethargy, ataxia, blindness, stupor, and seizures following an abrupt increase in blood pressure associated with a surgical reduction in renal mass. The cats had severe gross brain edema, evidenced by cerebellar changes of caudal coning and cranial displacement over the corpora quadrigemina and cerebral changes of widening and flattening of the gyri. Histologically, interstitial edema was most pronounced in the cerebral white matter. Hypertensive vascular lesions were present as hyaline arteriolosclerosis in one cat and hyperplastic arteriolosclerosis in the other. Rare foci of parenchymal microhemorrhages and necrosis were also observed. Systemic hypertension (especially severe or rapidly developing) accompanied by neurologic signs and the pathologic findings of diffuse brain edema with cerebral arteriolosclerosis are consistent with an etiologic diagnosis of hypertensive encephalopathy.