Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a fattening pig herd comprising 80 animals 13 were affected with clinical manifest toxoplasmosis presumably due to cat feces in the food. Seven pigs died, one was killed in extremis. The clinical signs were anorexia, apathy, fever, cyanosis, dyspnoea and partly hind limb weakness. One pig that died 3 days after onset of clinical signs had widespread necroses in liver and lymphatic organs. Single tachyzoites were detected by immunoperoxidase technique. One pig dying on day 11 and another euthanatized the same day showed severe desquamative and interstitial pneumonia and marked non suppurative meningoencephalomyelitis as well as necrotic foci mostly infiltrated with mononuclear cells in liver, adrenals and lymphatic organs. In all affected organs toxoplasmas were demonstrated histologically and immunohistologically. Every 2 surviving pigs were killed 40 days and 20 weeks, respectively, after recovery. These animals had high antibody titers against toxoplasma gondii and showed severe non suppurative meningoencephalitis and toxoplasma cysts in the brain without preceding clinical signs. In the lymphatic organs a marked hyperplasia was observed.
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PMID:[Toxoplasmosis epizootic in a fattening swine herd]. 822 41

Bovine herpesvirus type 5 (BHV-5) infection in calves causes meningoencephalitis, a fatal disease highly prevalent in South America. To study the pathogenesis of BHV-5 infection in cattle, 12 calves (group 1: acute infection) and 11 calves (group 2: latent infection) were intranasally inoculated with an Argentinean BHV-5 isolate at 10(8) and 10(4.7) tissue culture infective doses, respectively; six calves (control group) were mock infected. At 3 months postinoculation, all of the calves in group 2 and three calves in group 3 were given dexamethasone to reactivate the virus. The animals were euthanatized between days 6 and 17 postinoculation (group 1) and between days 6 and 16 postreactivation (group 2). Seventy-five percent and 91% of animals in groups 1 and 2, respectively, excreted BHV-5 in nasal and ocular discharges. Following dexamethasone administration, 45% of calves shed virus in both types of secretions. Spontaneous virus reactivation and shedding was observed in one calf. Neurologic signs consisting of circling, teeth grinding, ptyalism, jaw chomping, tongue protrusion, and apathy were observed in two animals in group 1 and, during the reactivation period, in four animals in group 2. Macroscopic findings consisted of softening of the cerebral tissue, meningeal hemorrhages and swelling, and edema and hemorrhages of prescapular, retropharyngeal and submandibular lymph nodes. Histologic lesions consisted of meningitis, mononuclear perivascular cuffing, neuronophagia, satellitosis, gliosis, hemorrhage, and necrosis and edema. Lesions in anterior cerebral cortex, medulla, and pons were consistently seen in all the animals of group 1. In the acutely infected animals, lesions in the diencephalon appeared at day 10 postinoculation, whereas in the latently infected calves these lesions were observed as early as at day 6 postreactivation. Latently infected animals developed lesions simultaneously in anterior cortex, medulla, pons, and diencephalon, showing a remarkable difference from the acutely infected group. Trigeminal ganglionitis appeared relatively early in animals of both groups (day 7 postinoculation in group 1 and day 8 postreactivation in group 2).
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PMID:Primary infection, latency, and reactivation of bovine herpesvirus type 5 in the bovine nervous system. 1212 46

A 5-year-old dog was referred with a history of anorexia and apathy for 3 weeks and acute status epilepticus. Ten weeks later the animal was humanely destroyed due to refractory epilepsy despite anti-epileptic medical treatment. Microscopical examination of the brain revealed bilateral malformation of the dentate gyrus with abnormal gyration. Cornu ammonis segments comprised of sparse pyramidal cells accompanied by marked gliosis. Additionally, there was severe generalized disseminated granulomatous meningoencephalitis, mainly localized to the white matter of the cerebral hemispheres. This is the first description of bilateral hippocampal malformation in a dog.
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PMID:Bilateral hippocampal malformation and concurrent granulomatous meningoencephalitis in a dog with refractory epilepsy. 2446 87

A 40-day-old male, blue heeler puppy with hindlimb ataxia, nystagmus, apathy, motor incoordination and hyperaesthesia of the forelimbs died 3 days after the onset of clinical signs. Significant gross findings included cerebellar herniation, cerebral oedema and dilation of the third and right lateral cerebral ventricles due to the accumulation of a purulent exudate. Histopathological examination revealed pyogenic ventriculitis and purulent meningoencephalitis. Pure colonies of a coagulase-positive Staphylococcus were isolated from the purulent cerebral exudate. A polymerase chain reaction assay that targeted the 16S rRNA gene of bacteria amplified the desired product from bacterial colonies. Direct sequencing revealed the organism to be Staphylococcus pseudintermedius. Phylogenetic analyses showed that the organism was antigenically similar to Staphylococcus intermedius and Staphylococcus delphini, being part of the S. intermedius group of bacteria. These findings confirmed the participation of S. pseudintermedius in the development of the pathological manifestations and lesions observed in this puppy.
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PMID:Pyogenic Ventriculitis and Ventricular Empyema associated with Staphylococcus pseudintermedius in a Puppy. 2804 18