Concurrent Gliosarcoma and Choroid Plexus Carcinoma in a Cow.

Brain tumours in cattle are uncommon and the spontaneous development of primary brain tumours of different histological types is rare in both man and animals. In man, multiple concurrent primary tumours of different types are occasionally described. We report the rare simultaneous occurrence of two different primary brain tumours, gliosarcoma and choroid plexus carcinoma, diagnosed by microscopical and immunofluorescence evaluation in an 8-year-old cow with a 2-month history of neurological disease. Gliosarcoma is a rare variant of glioblastoma multiforme, characterized by the presence of malignant glial cells and mesenchymal tissue. This tumour has not been reported previously in animals.

Laboratory-controlled Challenges of Nile Tilapia (Oreochromis niloticus) with Streptococcus agalactiae: Comparisons between Immersion, Oral, Intracoelomic and Intramuscular Routes of Infection.

Streptococcus agalactiae, the aetiological agent of streptococcosis in fish, is an important pathogen of cultured and wild fish worldwide. To gain a better understanding of the pathogenesis of streptococcosis in Nile tilapia (Oreochromis niloticus), and to identify the experimental route of infection that most closely mimics natural disease, fingerlings were challenged with S. agalactiae utilizing different delivery methods. Fingerlings were challenged via intracoelomic injection (ICinj), intramuscular injection (IMinj), orally or by immersion with serial dilutions of S. agalactiae. The dose lethal to 50% of test fish 15 days post challenge was 120 colony forming units (CFU)/fish after ICinj, and 105 CFU/fish after IMinj. Acute mortalities were present in both groups, but were higher in the fish challenged by ICinj. Very low mortalities were observed in the fish challenged via oral or immersion routes. Post-mortem evaluation of survivors revealed classical lesions associated with fish streptococcosis, including granulomatous or lymphohistiocytic epicarditis, splenitis, meningitis, myocarditis, choroiditis and exophthalmia. The information obtained improves our understanding of the pathogenesis of streptococcosis in fish, and provides useful information regarding controlled experimental infections in tilapia challenged with S. agalactiae. Results from this study suggest that IMinj challenge methods are not only suitable to induce streptococcosis in tilapia, but they may be the preferred method to study the pathogenesis of the naturally-occurring disease in this species.

Percutaneous Ultrasound-guided Cholecystocentesis and Bile Analysis for the Detection of Platynosomum spp.-Induced Cholangitis in Cats.

BACKGROUND: Examination of bile could be useful to diagnose Platynosomum spp.-induced cholangitis in cats. Obtaining bile via percutaneous ultrasound-guided cholecystocentesis (PUC) is possible but raises safety concerns in cats with severe cholecystitis. OBJECTIVES: The objectives of this study were to investigate the use of PUC to collect bile samples from cats with known platynosomosis and to determine if bile analysis could be a diagnostic test. ANIMALS: Twenty-seven free-roaming cats positive for Platynosomum spp. eggs via fecal examination. METHODS: In this prospective study, fecal egg counts were performed by double centrifugation with Sheather's solution. Bile was collected using PUC from anesthetized cats. Egg counts in bile were performed with a stereoscope. Euthanasia and postmortem examination were performed immediately after PUC. RESULTS: All cats had ultrasound (US) evidence of cholangitis or cholecystitis. Thirty-nine PUCs were performed with 14 cats having 2 PUCs 12 or 24 days apart. Postmortem examinations showed no overt gallbladder damage or leakage but fresh blood was noted in the gallbladder lumen of 3 cats. Median Platynosomum spp. egg counts were higher in bile (1450 eggs/mL; IQR, 400; 5138 eggs/mL) as compared to feces (46 eggs/mL; IQR, 10; 107 eggs/mL) (P < .001). CONCLUSION AND CLINICAL IMPORTANCE: Bile egg count analysis is an alternative method with higher egg counts as compared to fecal egg count analysis for the diagnosis of platynosomosis. Obtaining bile via US guidance is technically feasible and safe in cats with cholangitis/cholecystitis. Cholecystocentesis and bile analysis are especially relevant for those cats with chronic cholangitis/cholecystitis and negative fecal egg counts for Platynosomum.

Juvenile parameningeal rhabdomyosarcoma in a dog causing unilateral denervation atrophy of masticatory muscles.

A 23-month-old, male, Labrador retriever dog with a history of slowly progressive right-sided atrophy of the masticatory muscles was submitted for necropsy. A highly invasive neoplasm which destroyed adjacent soft tissues including the right trigeminal nerve was found in the right side of the cranial cavity. Metastases to the liver were also present. Microscopical features of the neoplasm were compatible with those of rhabdomyosarcoma, embryonal type. This diagnosis was confirmed by immunohistochemical demonstration of desmin and muscle actin within tumour cells. In human patients, rhabdomyosarcoma is the most common soft tissue sarcoma of childhood and adolescence. Parameningeal rhabdomyosarcomas are well-known topographic variants that are often non-amenable to complete surgical resection and therefore carry a more guarded prognosis. Juvenile parameningeal rhabdomyosarcoma resulting in denervation atrophy of the muscles of mastication has not been reported previously in dogs. Rhabdomyosarcoma should be included in the differential diagnosis of neoplastic conditions in the head and neck region of juvenile dogs presented with cranial nerve palsies or other neurological deficits suggestive of meningeal or central nervous system invasion.

Eccrine adenocarcinoma of the footpads in 2 cats.

Adenocarcinoma of sweat glands of the footpads was diagnosed in 2 cats. Clinical signs included lameness and swelling of multiple digits. Pulmonary metastasis was detected in one case. Diagnosis was based on histopathological and immunohistochemical findings. Eccrine adenocarcinoma should be included in the differential diagnosis of footpads lesions in aged cats.

Liver torsion and associated bacterial peritonitis in a dog.

A Malamute was examined for acute abdominal pain and collapse. Radiographs of the abdomen showed a pneumoabdomen, and a lucent mass in the region of the liver. Abdominocentesis yielded an inflammatory exudate with bacteria compatible with a Bacillus or a Clostridium sp. A quadrate lobe torsion was found at postmortem.

Central nervous system and vertebral malformation resembling the Arnold-Chiari syndrome in a Simmental calf.

Multiple congenital anomalies were identified in a stillborn calf, including severe cerebellar hypoplasia and central nervous system abnormalities resembling the Arnold-Chiari syndrome of malformation of calves. The Arnold-Chiari malformation occurs sporadically and has little economic impact, whereas cerebellar hypoplasia implies the presence of BVD virus in the herd.

Temporal central and peripheral nervous system changes induced by a paralytogenic mutant of Moloney murine leukemia virus TB.

BACKGROUND: The temporal localization of cellular targets for viral replication and the morphopathogenesis of neurodegeneration in the central nervous system (CNS) and peripheral nervous system induced by ts1, a neuropathogenic and lymphocytopathic mutant of Moloney murine leukemia virus-TB, were studied in the highly susceptible FVB/N mouse strain in order to better understand the mechanisms of this neurodegenerative disease. EXPERIMENTAL DESIGN: Newborn FVB/N mice were inoculated intraperitoneally with 0.1 ml of viral suspension containing 10(6) to 10(7) infectious units/ml. The mice were observed daily for clinical signs of disease and killed at specific time points. Their nervous system tissues were collected and processed for light and electron microscopy and for immunohistochemical viral-antigen detection. RESULTS: ts1-Infected FVB/N mice developed a rapidly progressive wasting disease that culminated in hindleg paralysis or paraplegia 30 to 35 days postinoculation (pi). CONCLUSIONS: Clear evidence of CNS lesions involving the cerebellar ventricular system, the grey and white matter of the brain stem and the spinal cord were seen as early as 5 to 10 days pi. These lesions, which began as mild perivascular and paraventricular neuropil spongiform changes and cytoplasmic vacuolation of neuronal and glial cell processes, progressed in severity with time and culminated in almost complete destruction of the white and gray matter in the brain stem and the cervical and lumbar spinal cord. Viruses were detected as early as 5 to 10 days pi in the fourth ventricle choroid plexus and ventricular lumen and budding from endothelial cells within the brain stem and cerebellum. Endothelial, ependymal, microglial, astroglial, and oligodendroglial cells were positive for gp70env. Astroglial and microglial cell proliferation with microglial syncytia formation was detected only within the areas showing spongiform degeneration. Viral replication was consistently high in the capillary endothelial cells of those areas showing spongiform degeneration, whereas in the glial cells, relatively few budding viruses were present. Neurodegeneration was accompanied by demyelinization within the CNS and peripheral nervous system and by hindleg muscle degeneration and necrosis. Multiple cellular targets for ts1 viral infection and replication were detected within the nervous system. The presence of budding virus and the immunodetection of viral antigen in the choroid plexus and ependymal cells of the fourth ventricle and the central canal of the spinal cord demonstrated that cerebrospinal fluid as well as blood can disseminate virus within the CNS. Pathologic and functional changes within the blood-brain barrier and glial system probably account for the neuronal necrosis and spongiform changes that result in paralysis induced by ts1 infection.

Temporal lymphoreticular changes caused by ts1, a paralytogenic mutant of Moloney murine leukemia virus TB.

Inoculation of newborn FVB/N mice with ts1, a mutant of Moloney murine leukemia virus TB, induced severe thymic atrophy, spongiform polioencephalomyelopathy, and fatal posterior paralysis of the affected mice 35-40 days after inoculation. During the early course of infection viral replication was found in the spleen and, more importantly, within the thymus. Of these organs, the thymus was affected most severely by ts1-infection. Thymic weights of infected mice decreased markedly during disease progression, culminating in severe atrophy at the time of paralysis. During the first 10 days after inoculation, the virus replicated within the endothelial lining of splenic and thymic capillaries and was released albuminally into the basement membrane before spreading outwardly into perithelial, epithelial, and reticuloendothelial cells. Within these cells there was productive viral replication and subsequent dissemination of the virus to the thymic T cell population. Early infection (up to 10 days after inoculation) of the thymus induced an increase in thymocytic mitosis, followed by a progressive increase in thymocytic death between 15 and 35 days after inoculation. Thymuses from paralyzed mice killed 30-39 days after inoculation, demonstrated pronounced involution, characterized by loss of lobular architecture, effacement of the cortex and medulla, severe depletion of thymocytes, and partial or complete loss of Hassall's corpuscles. Immunohistochemistry for viral antigens showed positive labeling of splenic megakaryocytes, reticuloendothelial cells, and thymocytes in mitosis, and reticulo-epithelial-endothelial cells of the thymus. The thymic phase of viral replication appeared to be crucial for development of neurological lesions and posterior paralysis.

Light and electron microscopy studies of the ulnar, saphenous, and caudal cutaneous sural nerves of the dog.

Transverse sections of the ulnar, saphenous, and sural nerves taken at specific levels in normal, young-adult beagle dogs were examined qualitatively and quantitatively at both the light and electron microscopic levels. The aim of this investigation was to provide baseline information for future studies of peripheral nerve disease in this species. A systematic sampling technique was used for the determination of nerve components (i.e., unmyelinated axons and Schwann cell and fibroblast nuclei). In all nerves sampled, the average size distribution for unmyelinated axons was unimodal, and most of the axons were 0.4-1.1 micron in diameter. Within this range, there were slight individual and nerve-to-nerve variations in the location of the largest diameter peak. The mean densities of Schwann cell nuclei (numbers/mm2) ranged from 841/mm2 in the palmar branch of the ulnar nerve, to 1,223/mm2 in the caudal cutaneous sural nerve, being nearly four times the average density or fibroblast nuclei. In every animal and in almost every nerve, a few abnormalities were found; and these should be kept in mind when assessing peripheral nerves in the dog.

Alphaherpesvirus saimiri infection in rabbits. 1. Light and electron microscopy study of cutaneous spinal nerves.

A light and electron microscopic study was undertaken to determine pathological changes in cutaneous spinal nerves of rabbits following intradermal inoculation with alphaherpesvirus saimiri (alpha HVS) isolate KM 322. Infected rabbits were killed at 3, 10, 17, 45 days and 2 years after infection. No abnormalities were seen at 3 days postinoculation. In the nerves of the rabbits killed at 10, 17 and 45 days after infection, axonal (Wallerian-type) degeneration was the main pathological feature. Regeneration, manifested by axonal sprouting, was observed in the nerves of the rabbits killed at 45 days post-inoculation. Neural fibrosis and paucity of unmyelinated axons was the final outcome. The severity of the neural damage not only varied according to the progression of the disease but between nerves taken from the same rabbit. This was probably associated with variation in the numbers of virus particles that had reached the dorsal root ganglion of the dermatome served by a particular nerve. Since alpha HVS (isolate KM 322) provides a model system for the study of virus latency in dorsal root ganglia, and consequently for the study of varicellazoster infection in man, these findings give further insight into the pathology of herpetic neuropathy.

Alphaherpesvirus saimiri infection in rabbits. 2. Morphometric studies of cutaneous spinal nerves.

To provide a better insight into the ultrastructural pathology of herpetic neuropathy, quantitative studies were made on cutaneous spinal nerves of normal rabbits and rabbits intradermally infected with alphaherpesvirus saimiri (alpha HVS) isolate KM 322. Marked reductions in the numbers and densities of myelinated and unmyelinated axons were found in the nerves of the rabbits killed 17 and 45 days after the infection. Abnormalities in the size distribution of unmyelinated axons were seen at 45 days post-inoculation where axonal sprouting caused a noticeable shift in the fiber population. Two years after virus inoculation reduction in unmyelinated axons and abnormalities in the fiber size distributions characterized by smaller diameters of both myelinated and unmyelinated axons were detected. In these nerves conspicuous fibrosis caused a significant increase in the endoneurial area. At this stage of the infection regenerative changes involving myelinated fibers were found. Since attempts to detect spontaneous reactivation of alpha HVS infection in rabbits have been unsuccessful, the finding of regeneration 2 years after exposure seems in agreement with the view that regenerated myelinated fibers never attain their original size. In the present study although both types of fibers were damaged, morphometric data suggest that unmyelinated axons were more severely affected. Whether this seemingly selective involvement was due to spreading of the virus between axons sharing the same Schwann cell subunit remains to be proved.