Mediastinal ganglioneuroma in a puppy.
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Animals↗
Biomedical subjects
B A Summers
Publications and source records attributed to B A Summers.
Pathogenesis of rotavirus infection in various age groups of chickens and turkeys: pathology.
Various age groups of turkeys, White Leghorn chickens, and broiler chickens were inoculated with turkey rotavirus strain Tu-2 or with chicken rotavirus Ch-2, and the development of rotavirus-induced lesions were evaluated macroscopically and microscopically (light microscopy and scanning electron microscopy). Morphometric evaluations were conducted to determine morphologic changes in the villi of infected turkeys. Macroscopic lesions that were found in turkeys, but not in chickens, consisted of pallor of the intestinal tract and distension of the cecum with frothy or nonfrothy fluid contents. Histologic lesions in turkeys consisted of basal vacuolation of enterocytes, separation of enterocytes from the lamina propria (with subsequent desquamation), villus atrophy accompanied by widening of the lamina propria, scalloping of the villus surface, fusion of the villi, and leukocytic infiltration of the lamina propria. Scanning electron microscopy indicated roughened villus surfaces, distortion of the normal morphologic features of the villi, and loss of microvilli in cells located on the tips of the villi. Most of the lesions disappeared by 8 days after inoculation. Results of the morphometric evaluations indicated that the crypt length had increased and the villus-to-crypt ratio had significantly decreased, compared with that of noninoculated control turkeys. Broilers greater than or equal to 21 days old and White Leghorn chickens greater than or equal to 35 days old had minimal leukocytic infiltration of the lamina propria and minimal loss of microvilli in cells located on the tips of the villi. The loss of microvilli was more extensive in chickens greater than or equal to 119 days old than in younger birds. Generally, turkeys 1 to 112 days old developed more severe lesions than did chickens, and lesions were more pronounced in turkeys at 112 days of age.
Age Factors↗
Brain-stem auditory evoked responses in diagnosis of central pontine myelinolysis.
Central pontine myelinolysis (CPM) developed in association with acute adrenocortical insufficiency during correction of severe hyponatraemia in a 58-year-old woman. Repeated CT scanning and NMR imaging were normal from the onset of the illness. Electroencephalography and brain-stem auditory evoked responses showed abnormalities consistent with a brain-stem lesion, which resolved as the patient made a gradual but incomplete recovery. Our observations illustrate the value of electrophysiological monitoring in CPM and support the proposed association between this condition and the rapid correction of an electrolyte imbalance.
Adrenal Insufficiency↗
Tremors in Samoyed pups with oligodendrocyte deficiencies and hypomyelination.
Over a 3-year period a breeder of Samoyed dogs observed six litters in which one or more pups at 3 weeks of age showed generalized tremors and an inability to stand. One affected pup, a 5-week-old male, was referred for clinical and pathological evaluation. Gross and microscopic studies including immunocytochemical demonstration of myelin basic protein, revealed a lack of myelin throughout the central nervous system. Ultrastructural studies revealed that a total absence of normal myelin was associated with oligodendroglial deficiencies. Oligodendrocytes were immature in appearance, greatly reduced in number, and incapable of forming compact myelin. Astrocytosis and an increase in the third type of neuroglial cells were observed. The changes differed from those reported in other canine forms of hypomyelinogenesis and were compared with hypomyelinating diseases in other species. The findings suggested that this hypomyelination was the result of retarded gliogenesis.
Animals↗
Canine hip dysplasia: concepts and diagnosis.
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Animals↗
Cerebral angioendotheliomatosis in a dog.
A 6-year-old dog which presented with weakness of the hind limbs progressed to a cerebral disorder with altered sensorium. The cerebrospinal fluid (CSF) protein was elevated, but no cells were found. Autopsy revealed severe hemorrhages in the basal nuclei and diencephalon. Histology of the lesions showed many meningeal and parenchymal blood vessels filled with neoplastic mononuclear cells. Electron microscopy of the tumor cells demonstrated ribosomes, granular endoplasmic reticulum, mitochondria, and a few lysosomes. Immunocytochemical procedures to demonstrate Factor VIII-related antigen were negative. This appears to be the first recorded case of cerebral angioendotheliomatosis in domestic animals and closely resembles the syndrome in man.
Animals↗
Persistence of virulent canine distemper virus in lymphoblastoid cell lines.
Persistent infection with virulent canine distemper virus (CDV-SH) was established in 2 human lymphoblastoid B cell lines (Wi-L2 and Raji), and one human (HSB), one simian (1670) and one canine (CT-45-S) lymphoblastoid T cell line. Cell free virus from persistently infected T cell lines was avirulent for dogs but virulence was maintained during 31 cell passages in persistently infected B cell lines.
Animals↗
Syncytia formation: an aid in the diagnosis of canine distemper encephalomyelitis.
Syncytia formation has been observed in response to experimental Canine Distemper Virus (CDV) infection in specific-pathogen-free Beagle dogs. Multinucleated giant cells are most frequently found in white matter lesions of the brain and in the anterior uvea of the eye. Lymph nodes and the lung are occasionally positive, while the leptomeninges will also rarely harbour syncytia. The mechanism of syncytia formation and their possible importance in the pathogenesis of the disease are briefly discussed. Widespread tissue syncytia formation is a feature of CDV infection which should assist in identifying cases of non-suppurative encephalitis in the dog caused by this agent.
Animals↗
Renal encephalopathy in a cow.
A 14-month-old Holstein heifer collapsed suddenly and died. Significant gross post mortem findings were limited to the kidneys. Histopathological examination revealed a severe, chronic, diffuse, interstitial nephritis. Microscopic examination of the brain revealed a multifocal spongiform encephalopathy, closely resembling that seen in cattle with hepatic encephalopathy. As is well recognized in man, this is a case of encephalopathy resulting from renal failure.
Acute Kidney Injury↗
Canine distemper encephalomyelitis: variation with virus strain.
Disease induced by 3 virulent strains of Canine Distemper Virus (CDV) was compared in specific pathogen-free Beagle dogs. All strains produced an encephalomyelitis but variation was observed in the severity, clinical course and resulting neuropathology. Infection with Snyder Hill strain of CDV was consistently acute; dogs either succumbed 14 to 19 days post-inoculation (PI) or recovered. Lesions in the neuraxis were those of a polioencephalomyelitis. In contrast, CDV strain A75-17 produced subacute to chronic disease in which demyelination was the predominant finding. Some dogs succumbed, generally around 28 to 42 days PI. Total recovery was again recorded for some members of the group. Others developed persistent central nervous system (CNS) infection but remained clinically stable until electively killed with barbiturate, up to 62 days PI. CDV strain R252 also induced delayed, predominantly white matter disease with a mixed pattern of mortalities, persistent infections and recoveries, similar to A75-17. Neutralizing antibody responses correlated with the disease course. Dogs which died had low serum titres or lacked serum antibody. Recovering dogs had the earliest and highest titres. A few dogs with persistent CNS infection had antibody in the cerebrospinal fluid also. Current concepts of the pathogenesis of canine distemper encephalomyelitis (CDE) are discussed and a basis for the strain-dependent clinical and pathological expression of CDE is proposed. Viral strain appears to be an important factor in this common disease of the canine CNS.
Animals↗
Canine distemper and experimental allergic encephalomyelitis in the dog: comparative patterns of demyelination.
The pattern of virus-induced and allergic demyelinating encephalomyelitis in the dog were compared. The predominant pattern of myelin loss in canine distemper (CD) infection was focal, periventricular and was initially noninflammatory. In contrast, sensitization to myelin produced a uniform pattern of central nervous system (CNS) myelinolysis which was disseminated, inflammatory and perivascular. Ultrastructurally, virus-infected neuroglia participated in the demyelination in CD, whereas infiltrating haematogenous mononuclear cells predominated in the lesions of experimental allergic encephalomyelitis (EAE). Areas of predilection within the CNS differed, being influenced by viral spread in CD and by vascular factors in EAE. In CD, the paramyxovirus appears to play a central role in the process of demyelination. In contrast to EAE, however, these studies do not support the view that autoreactivity to myelin contributes to the pathogenesis of CD demyelinating encephalomyelitis.
Animals↗
Does virus persist in the uvea in multiple sclerosis, as in canine distemper encephalomyelitis?
Epidemiological studies suggest that multiple sclerosis (MS) might be triggered by an infectious agent. Uveitis has been observed in a small percentage of MS patients. Dogs with canine distemper encephalomyelitis, another demyelinating disease of the central nervous system, have an anterior uveitis which is usually mild and asymptomatic, and dogs with persistent CNS infection and chronic distemper encephalomyelitis harbour virus persistently in the uvea. These observations in dogs suggest that pathological and virological studies of the uveitis associated with MS would be worth while.
Animals↗
Virus-induced hydrocephalus in the dog.
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Animals↗
Intoxication by Solanum fastigiatum var. fastigiatum as a cause of cerebellar degeneration in cattle.
A bovine cerebellar disorder of recurrent seizures characterized by loss of equilibrium, extension of the head and thoracic limbs, opisthotonus, nystagmus and falling to the side or backwards is described from 16 farms in the Brazilian state of Rio Grande do Sul. The main pathologic features were vacuolation, degeneration and loss of Purkinje cells with axonal spheroids in the cerebellar granular layer and white matter. Electron microscopic study of Purkinje cells showed cytoplasmic membranous bodies, similar to those observed in human and animal gangliosidoses. Feeding trials in calves demonstrated that the disease is an intoxication caused by ingestion of Solanum fastigiatum var. fastigiatum. A hypothesis is proposed that the intoxication is an induced lysosomal storage disease, probably a gangliosidosis.
Animals↗
Experimental Toxocara canis infection in cynomolgus macaques (Macaca fascicularis).
Visceral larva migrans was produced in 16 cynomolgus macaques (Macaca fascicularis) experimentally inoculated with 45,000 embryonated eggs of Toxocara canis as a single bolus or in 3 divided doses. The hematologic and serologic changes were similar to those observed in children with visceral Toxocara infection. Neurologic signs developed in 3 animals and were characterized by ataxia and nystagmus. Growth rates were diminished in inoculated animals when compared with the rates in noninoculated controls. Diagnostic antibody titers as measured by enzyme-linked immunosorbent assay were noted in all inoculated macaques by the 4th week, and these titers persisted during the 7-month period of observation. Antibody to Toxocara was not detected in the aqueous or vitreous humors. Lesions comprised severe granulomatous hepatitis and encephalomyelitis. Intraocular lesions associated with larval migration were not observed.
Animals↗
Degenerative joint disease: multiple joint involvement in young and mature dogs.
Radiologic, pathologic, and ancillary methods were used to determine the occurrence of degenerative joint disease involving multiple joints of immature and adult dogs. Animals were selected for the development of hip joint dysplasia and chronic degenerative joint disease. Of disease-prone dogs, 82% (45 of 55 dogs) had radiologic changes, indicative of hip dysplasia, by 1 year of age. At necropsy, more abnormal joints were identified than by radiographic examination. Among 92 dogs between 3 to 11 months of age that had joint abnormalities, 71% had hip joint involvement; 38%, shoulder joint involvement; 22%, stifle joint involvement; and 40% had multiple joint involvement. Polyarthritis was asymptomatic and unexpected. Radiographic examination of older dogs also revealed evidence of degenerative joint disease in many joints. Multiple joint involvement was substantiated at necropsy of young and mature dogs. A similar pattern of polyarticular osteoarthritis was revealed in a survey (computer search) of necropsy reports from medical case records of 100 adult and elderly dogs. Usually, the joint disease was an incidental observation, unrelated to the clinical disease or to the cause of death. The frequent occurrence of degenerative changes in several joints of dogs aged 6 months to 17 years indicated that osteoarthritis may be progressive in these joints and raises the possibility that systemic factors are involved in the disease process.
Age Factors↗
Pansteatitis mimicking infectious peritonitis in a cat.
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Adipose Tissue↗
Interferon in cerebrospinal fluid. A marker for viral persistence of canine distemper encephalomyelitis.
Interferon (IFN) was measured in serum and cerebrospinal fluid (CSF) of dogs after experimental (intranasal) infection with different strains of virulent canine distemper virus (CDV). Viral strains employed produced neurological changes in dogs that range from acute inflammatory to subacute, delayed demyelinating encephalomyelitis. With few exceptions, first appearance of serum-IFN correlated with the first elevated body temperature 4 days post-infection (p.i.). By 16 days p.i. IFN had disappeared from the serum of all infected dogs. In contrast, IFN was constantly detectable in CSF in dogs with CDV infection of the central nervous system (CNS). It was first detected 5 days p.i., was continuously detectable during the variable preclinical phase and into the period when signs of acute or delayed encephalomyelitis were evident. Dogs from which CDV would be retrieved from CNS tissue at necropsy always had CSF-IFN (up to 56 days p.i.). In contrast, dogs that recovered from infection, substantiated at necropsy by minimal, resolving CNS lesions and non-detectable virus, had IFN in CSF demonstrable for only a brief post-inoculation period. CSF-IFN appears to be a valid marker for CDV persistence in the canine CNS and may have broader applications.
Animals↗