Lesions in bovine progressive degenerative myeloencephalopathy ("Weaver") of Brown Swiss cattle

Gross changes and other necropsy findings in 36 purebred Brown Swiss cattle affected with bovine progressive degenerative myeloencephalopathy were nonspecific. Primary microscopic lesions were confined to the central nervous system, specifically the white matter of the spinal cord, axons in some brainstem nuclei, and Purkinje cells of the cerebellar cortex. Spinal cord lesions involved only the white matter and consisted of axonal degeneration, loss of axons and myelin, and status spongiosus. Axonal degeneration was characterized by swelling and fragmentation of the axoplasm or formation of large, discontinuous swellings referred to as spheroids. Lesions were qualitatively similar at all levels, but quantitatively dissimilar in the same funiculi at different levels. Both ascending and descending fibers were involved but correlation to specific fasciculi was not evident. Lesions always were most severe in thoracic spinal cord segments. Little or no astroglial response, no inflammatory response, and no involvement of gray matter were observed in the spinal cord. Cerebellar lesions were limited to selective degeneration and loss of Purkinje cells and occasional swelling of Purkinje cell axons (torpedos) in the granular layer of the cerebellar cortex. Brainstem lesions were inconsistent and limited to occasional axonal swelling in brainstem nuclei. The pathogenesis of bovine progressive degenerative myeloencephalopathy is unknown and possible mechanisms were discussed. The disease exhibits a familial pattern in Brown Swiss cattle and may be hereditary. Extraneural lesions were considered secondary to central nervous system lesions.     

Evidence for bursal involvement in the pathogenesis of hemorrhagic enteritis of turkeys

The pathogenesis of hemorrhagic enteritis in turkey poults infected with hemorrhagic enteritis virus (HEV) at 3 days or at 2 or 5 weeks of age was compared with pathogenesis in poults that had been chemically bursectomized neonatally and exposed to cell-culture-propagated virus at 2 or 5 weeks of age. Conventional poults exposed to HEV at 2 or 5 weeks developed clinical disease, and mortality ranged from 38% to 100%. In addition to the splenic and intestinal lesions usually seen with HEV infection, the pancreas, bursa of Fabricius, and thymus were also affected. In contrast, although they were free from detectable maternal antibody, poults infected with HEV at 3 days of age failed to develop clinical disease or mortality; however, virus was demonstrated by histological and electron microscopic examinations in spleens of these poults. Neonatal chemical bursectomy completely prevented the clinical signs, gross lesions, and mortality induced by HEV in poults at 2 or 5 weeks of age. These findings strongly suggest that an intact bursa is necessary for HEV to induce disease in turkeys.     

Staphylococcus aureus pneumonia in turkey poults with gross lesions resembling aspergillosis.

The present report describes a case of Staphylococcus (Staph.) aureus pneumonia in turkey poults. Initially, 3-day-old poults with a history of increased mortality were submitted for necropsy. The poults had severe bilateral consolidation of the lungs with miliary caseous nodules. The gross lesions in the lungs were highly suggestive of aspergillosis. The next day, postmortem examinations were performed on 60 dead poults at the farm, and all 60 had similar lung lesions. Histopathologic examination of affected lungs revealed severe subacute multifocal bronchopneumonia with intralesional bacteria. Tissue Gram stain of lung sections demonstrated gram-positive bacterial cocci. Gomori methenamine silver stain of the lungs failed to demonstrate fungal agents. The histologic distribution of the lesions suggested an aerogenous route of infection. Staphylococcus aureus was isolated in pure culture from affected lungs. Hatchery contamination was suspected because of the severity and early onset of the lesions. Bacterial monitoring at the hatchery demonstrated marked Staph. aureus contamination in two setters, a hatcher's air duct, and the poult room. Improved hatchery cleaning and disinfection prevented a reoccurrence of the problem.     

Clinical, pathological and toxicological findings of a iatrogenic selenium toxicosis case in feeder pigs

Histopathological and toxicological analyses confirmed a clinical diagnosis of selenium (Se) intoxication in pigs from a farm in Spain. After an initial episode of diarrhoea, animals presented both dermatological and neurological signs; the most obvious sign was a marked hind limb paresis. Cutaneous lesions consisted on diffuse alopecia, multifocal skin necrosis and coronary band necrosis of the hooves. Central nervous system lesions involved the cervical and lumbar intumescences of the spinal cord and consisted of a severe, bilateral symmetrical poliomyelomalacia of the ventral horns; pons and medulla oblongata also presented lesions of polioencephalomalacia. Analyses of feed and sera from clinically affected pigs revealed a marked increase in Se concentration. Clinical investigations indicated that a failure in Se dosage in feed was the cause of the toxicosis.     

HUMPY BACK OF SHEEP. CLINICAL AND PATHOLOGICAL OBSERVATIONS

Humpy back, a disease of Merino sheep in western Queesland, occurs during mustering for shearing. It is usually seen in summer 6-10 weeks after substantial rainfall and is thought to be caused by the ingestion of a toxic plant. The disease is characterised clinically by a short-stepping, stilted gait of the hind limbs, followed by lowering of the head, arching of the back and inability to continue walking. Histopathological examination of 8 cases from 5 properties revealed a Wallerian degeneration of the white matter throughout the length of the spinal cord with the ventral and lateral columns most severely affected. A similar degenerative change was seen in the posterior cerebellar peduncles of 3 of the sheep. A more severe hind limb incoordination with more extensive degeneration of the white matter of the spinal cord, medulla and cerebellum was seen in a case of humpy back of two years duration. Similar, but much milder, spinal cord lesions were found in apparently unaffected sheep from the same group as the sheep affected with humpy back on 2 properties. Severe myodegeneration of hind limb muscle groups was seen in 3 affected sheep. It was thought to be associated with the long rail journey (1500 km) to the laboratory after the sheep were affected in the field.     

Oxytocin Content of the Cerebrospinal Fluid of Dogs and Its Relationship to Pain Induced by Spinal Cord Compression

Objectives —To determine whether oxytocin exists in the cerebrospinal fluid (CSF) of dogs and whether the amount of oxytocin in the CSF of dogs with neck or back pain caused by spinal cord compression is significantly different than that in the CSF of clinically normal dogs.
Study Design —Prospective controlled study.
Animal Population —A total of 15 purpose-bred beagles and 17 client-owned dogs.
Methods —CSF was collected by needle puncture of the cerebellar medullary cistern after induction of general anesthesia. Oxytocin levels within the samples were determined through radioimmunoassay.
Results —Dogs with spinal cord compression had significantly more oxytocin in their CSF than the clinically normal dogs (13.76 ± 2.0 pg/mL and 3.61 ± 0.63 pg/mL, respectively; P < .0001). Dogs with chronic signs (>7 days) had significantly more oxytocin in their CSF than dogs with acute signs (<7 days) (21.60 ± 0.86 pg/mL and 6.80 ± 0.81 pg/mL, respectively; P < .0001). Both acutely and chronically affected dogs had significantly more oxytocin in their CSF than the controls ( P < .005 and P < .0001 respectively).
Conclusions —Dogs with neck and back pain caused by spinal cord compression have significantly more oxytocin in their CSF than clinically normal dogs. Dogs with chronic clinical signs have significantly more oxytocin in their CSF than dogs with acute clinical signs.
Clinical Relevance —In humans, intrathecal injection of oxytocin is effective in treating low back pain for up to 5 hours. Intrathecal oxytocin may be a logical choice for perioperative analgesia in dogs undergoing myelography because the intrathecal space is accessed for injection of contrast agent.     

Spinal oligodendroglioma with diffuse arachnoidal dissemination in a Japanese Black heifer

A gelatinous focus with cystic spaces, was found in the posterior funiculus of the 2nd to 3rd lumbar levels of the spinal cord of a Japanese Black heifer, 2 years old, with clinical signs of severe dysstasia. Histopathological examination revealed that the spinal lesion consisted of multifocal and diffuse proliferation of round cells with abundant vacuolar cytoplasm and hyperchromatic nuclei. In the lesions there was a number of cystic spaces containing aggregates of small round cells. The neoplastic foci showed a honeycomb structure divided by thin blood vessels, representing typical lesions of oligodendroglioma. Diffuse and multifocal proliferation of these round cells were also recognized in the subarachnoidal space in the sacral spinal cord. Immunohistochemically, the proliferating round cells were negative for glial fibrillary acidic protein. Based on these morphological features, the case was diagnosed as lumbar spinal oligodendroglioma with diffuse arachnoidal dissemination.     

A familial peripheral neuropathy and glomerulopathy in Gelbvieh calves

Nine Gelbvieh calves originating in four herds and clinically presenting with rear limb ataxia/paresis had histopathologically confirmed peripheral neuropathy and a proliferative glomerulopathy. Degenerative lesions were severe in peripheral nerves, dorsal and ventral spinal nerve roots, and less marked in dorsal fasciculi of the spinal cord. Cell bodies of spinal ganglia were minimally diseased; ventral horn neurons occasionally had central chromatolysis and nuclear displacement. Glomerular lesions ranged from mild mesangial hypercellularity to glomerulosclerosis. Pedigree analysis of affected animals from one herd indicated a strong familial relationship and probable hereditary basis for the syndrome.     

Toxicity of excess dicalcium phosphate in the diet of turkey poults

High mortality in 1-week-old commercial turkey poults was attributed to the accidental substitution of dicalcium phosphate in the diet for corn. At necropsy of the affected birds, lesions were observed in the upper gastrointestinal tract, suggesting acute ingestion of a caustic substance. Mortality and gross and microscopic lesions were reproduced experimentally in turkey poults fed diets similar to the diet fed in the field case. The cause of these lesions was attributed to increased pH due to the phosphoric acid content of the diet.     

MAGNETIC RESONANCE IMAGING FINDINGS IN THE SPINE OF SIX DOGS DIAGNOSED WITH LYMPHOMA

Lymphoma is one of the most common neoplasms in the dog. Despite its prevalence and the increasing use of advanced diagnostic imaging in veterinary patients only few reports of magnetic resonance imaging (MRI) findings in spinal lymphoma have been published to date. The purpose of this retrospective case series study was to describe the MRI findings in dogs with confirmed lymphoma affecting the spine and/or paraspinal soft tissues. Medical records were searched for patients that had MRI of the spine and a diagnosis of lymphoma during the period of 2005–2015. Data recorded from retrieved MRI studies were presence of focal or multifocal disease, structures involved, and signal characteristics on T2‐W, short tau inversion recovery (STIR), and T1‐W sequences prior to and following intravenous contrast medium administration. Six dogs met the inclusion criteria. Common findings included multifocal disease (4/6), vertebral involvement (5/6), spinal cord compression (4/6), and involvement of more than one spinal compartment (medullary cavity, vertebral canal, paraspinal soft tissues) (6/6). Vertebral changes were confined to the medullary cavity without evidence of cortical osteolysis. There was questionable involvement of the spinal cord in one case. All spinal and paraspinal lesions identified were T2‐W isointense to hyperintense, STIR hyperintense, T1‐W hypointense to isointense, and showed variable moderate to strong contrast enhancement. Additional lesions identified were enlarged intraabdominal lymph nodes, hepatomegaly, splenomegaly, and a splenic nodule. The STIR and T1‐W postcontrast sequences were subjectively the most useful in identification of the spinal and paraspinal lesions.     

MAGNETIC RESONANCE IMAGING CHARACTERISTICS IN FOUR DOGS WITH CENTRAL NERVOUS SYSTEM NEOSPOROSIS

Neosporosis is a polysystemic disease that can affect dogs of any age and can cause inflammation of the central nervous system. Antemortem diagnosis can be challenging, as clinical and conventional laboratory test findings are often nonspecific. A previous report described cerebellar lesions in brain MRI studies of seven dogs and proposed that these may be characteristic for central nervous system Neosporosis. The purpose of this retrospective study was to describe MRI characteristics in another group of dogs with confirmed central nervous system neosporosis and compare them with the previous report. The hospital's database was searched for dogs with confirmed central nervous system neosporosis and four observers recorded findings from each dog's MRI studies. A total of four dogs met inclusion criteria. Neurologic examination was indicative of a forebrain and cerebellar lesion in dog 2 and multifocal central nervous system disease in dogs 1, 3, and 4. Magnetic resonance imaging showed mild bilateral and symmetrical cerebellar atrophy in three of four dogs (dogs 2, 3, 4), intramedullary spinal cord changes in two dogs (dogs 3, 4) and a mesencephalic and metencephalic lesion in one dog (dog 2). Multifocal brain lesions were recognized in two dogs (dogs 1, 4) and were present in the thalamus, lentiform nucleus, centrum semiovale, internal capsule, brainstem and cortical gray matter of the frontal, parietal or temporal lobe. Findings indicated that central nervous system neosporosis may be characterized by multifocal MRI lesions as well as cerebellar involvement in dogs.     

Poult malabsorption syndrome. I. Malabsorption in poult enteritis.

One-day-old poults were placed on littler on which poults had previously developed diarrhea, increased mortality, and stunting. Small intestines, pancreas, and liver were evaluated histologically. Morphometric evaluations were conducted to determine villous length and crypt depth. Poults were evaluated for malabsorption utilizing D-xylose and lipid absorption tests. Compared with controls, the gastrointestinal tract of affected birds was grossly distended, was fluid-filled, and had thin, flaccid walls on days 5 and 8. Ceca were distended with brown watery fluid and gas on days 5, 8, and 12. No histologic lesions were present in the liver, pancreas, or pancreatic ducts, and only mild inflammatory changes were present in the small intestine. Villous atrophy and crypt hypertrophy were present in the small intestine on days 5, 8, 12, 16, and 21. Morphometry revealed significant decreases in villous lengths and increases in crypt depth throughout the trial. D-Xylose and lipid absorption were significantly decreased on days 8 and 11. Intestinal epithelial damage by infectious agents with subsequent villous atrophy is postulated to have produced malabsorptive diarrhea.     

A multifocal symmetrical necrotising encephalomyelopathy in Angus calves

OBJECTIVE: To define a neurological disorder in Angus calves. PROCEDURE: Clinical and pathological examinations were performed on affected Angus calves from a herd experiencing 1% annual mortality from neurological disease. CLINICAL SIGNS: Angus calves developed ataxia, nystagmus, strabismus, muscular tremors, opisthotonus, bruxism, hyperaesthesia, tetanic spasms and episodic convulsions at 2 to 6 weeks of age. Death occurred 4 to 7 days after the onset of clinical signs. GROSS PATHOLOGY: Bilaterally symmetrical, yellow-grey foci were present in the medulla oblongata. HISTOPATHOLOGY: Symmetrical degenerative lesions affected the dorsal vagal motor, lateral cuneate and olivary nuclei in the medulla oblongata and sometimes the spinal cord, substantia nigra and cerebellar peduncles. Malacia was characterised by spongiosis of the neuropile, vascular hyperplasia, infiltration of gitter cells, spheroid formation and delayed degeneration of neurones. CONCLUSION: Angus calves may develop a multifocal symmetrical necrotising encephalomyelopathy.     

Experimental transmission of turkey viral hepatitis to day-old poults and identification of associated viral particles resembling picornaviruses.

Turkey viral hepatitis (TVH) was experimentally reproduced in two experiments in 1-day-old poults. In the first experiment, an infectious inoculum was prepared from filtered yolk materials harvested from dead embryonating chicken eggs (ECE) previously inoculated with suspensions of liver and pancreas tissues collected from TVH-affected birds in commercial turkey flocks. One-day-old poults given a yolk-sac inoculation or oral gavage with this preparation developed lesions in the liver and pancreas characteristic of TVH at 20 days postinoculation (PI) in 60% and 14% of the experimentally infected birds, respectively. With the identical inoculum, embryo mortality occurred at 8 and 10 days PI in embryonating turkey eggs (ETE) inoculated into the yolk sac. In the second experiment, an infectious inoculum was prepared from filtered yolk materials from dead ETE harvested in the first experiment. One-day-old poults given a yolk-sac inoculation with this filtered yolk material developed lesions in the liver and pancreas within 5 days PI. At 20 days PI, 67% of the experimentally infected birds had similar lesions. With the inoculum given to these poults, embryo mortality occurred at 6, 8, and 10 days PI in ETE inoculated into the yolk sac. Virus particles 26-28 nm in diameter with icosahedral morphology typical of picornaviruses were identified by EM in the yolk sacs of ETE that died in both experiments, and inoculated ETE that died following passage of filtered suspensions of pancreatic tissues collected from affected birds in the first experiment.     

Prevalence of psammoma bodies in meninges and choroid plexuses of raccoons (Procyon lotor) from Parramore Island, Virginia.

Microscopic evidence of multifocal mineralizations (psammoma bodies) were seen in brains of 33/53 (62%) raccoons (Procyon lotor) necropsied on Parramore Island, Virginia. Most mineralized foci had concentric laminations and were present in small capillaries of meninges of the brain (15/33), in choroid plexus (3/33), or at both these sites (13/33). In 2 raccoons, the lesions were confined to the meninges of the proximal cervical spinal cord. In most cases, the affected vessels appeared to have been completely occluded. However, no evidence of ischemic changes in the brain parenchyma was seen, and none of the raccoons had abnormal neurologic signs prior to euthanasia. The condition appears to be a common incidental histopathologic finding in raccoons from the eastern United States. Although the exact cause of this condition is not known, a primary vascular insult with resultant dystrophic mineralization of the affected vessels is suspected.     

Vitamin A deficiency in turkey poults.

Vitamin A deficiency was diagnosed in a commercial flock of 13,000 4-6-week-old turkey poults in the summer of 2004. The birds were initially submitted for examination because of a 3% increase in the reported daily mortality of the flock. Clinically, affected birds had stunted growth and ruffled feathers, showed signs of incoordination, and were depressed. At necropsy, pale white pseudomembranous to mucoid material was observed on the mucosal surface of the tongue, oral cavity, portions of the esophagus, and the crop of some birds. Histologically, there was squamous metaplasia of the mucosal epithelium of the oral mucosa, esophagus, sinuses, nasal glands, bronchi, proventriculus, and the bursa of Fabricius. Vitamin A was not detected in the feed sample at a detection limit of 0.5 mg/kg. Serum vitamin A concentrations in 7 birds were very low and ranged from 0.05 to 0.1 mg/L. Vitamin A concentrations in livers were extremely low (0.1 mg/kg wet weight, 1/7 poults) or undetectable (< 0.1 mg/kg wet weight, 6/7 poults). A diagnosis of vitamin A deficiency was made based on gross and microscopic lesions and vitamin A concentrations in serum, liver, and feed. To the authors' knowledge, this is the first documented case of vitamin A deficiency in poults submitted from a commercial meat turkey producer comparatively depicting the gross and microscopic lesions with those found in other species of birds and mammals.     

Hereditary cerebellar degeneration in three full sibling kittens

Two domestic shorthair littermate kittens had signs of cerebellar dysfunction, first observed between seven and eight weeks of age; a third littermate was unaffected. The signs were progressive and the more severely affected kitten was euthanased after six days. A postmortem examination revealed no gross lesions but the kitten had cerebellar cortical degeneration with extensive loss of Purkinje cells. The second kitten was euthanased at 10 months of age with similar, though more pronounced, changes. One of the two kittens in the next litter of the same parents had similar clinical signs and histopathological findings. The lesions in the cerebellum are interpreted as probably due to genetically determined abiotrophy. In addition, the two older kittens had medullary neuronal changes interpreted as probable neuraxonal dystrophy, and focal vacuolation of the neuropil in the medulla and cervical spinal cord.     

Pathology of natural infections by H5N1 highly pathogenic avian influenza virus in mute (Cygnus olor) and whooper (Cygnus cygnus) swans

Mortality in wild aquatic birds due to infection with highly pathogenic avian influenza viruses (HPAIV) is a rare event. During the recent outbreak of highly pathogenic avian influenza in Germany, mortality due to H5N1 HPAIV was observed among mute and whooper swans as part of a rapid spread of this virus. In contrast to earlier reports, swans appeared to be highly susceptible and represented the mainly affected species. We report gross and histopathology and distribution of influenza virus antigen in mute and whooper swans that died after natural infection with H5N1 HPAIV. At necropsy, the most reliable lesions were multifocal hemorrhagic necrosis in the pancreas, pulmonary congestion and edema, and subepicardial hemorrhages. Major histologic lesions were acute pancreatic necrosis, multifocal necrotizing hepatitis, and lymphoplasmacytic encephalitis with neuronal necrosis. Adrenals displayed consistently scattered cortical and medullary necrosis. In spleen and Peyer's patches, mild lymphocyte necrosis was present. Immunohistochemical demonstration of HPAIV nucleoprotein in pancreas, adrenals, liver, and brain was strongly consistent with histologic lesions. In the brain, a large number of neurons and glial cells, especially Purkinje cells, showed immunostaining. Occasionally, ependymal cells of the spinal cord were also positive. In the lungs, influenza virus antigen was identified in a few endothelial cells but not within pneumocytes. The infection of the central nervous system supports the view that the neurotropism of H5N1 HPAIV leads to nervous disturbances with loss of orientation. More investigations are necessary to clarify the mechanisms of the final circulatory failure, lung edema, and rapid death of the swans.     

A degenerative encephalomyelopathy in 7 Kuvasz puppies

Seven Kuvasz puppies from 2 same-parentage litters developed weakness and ataxia. Six necropsied dogs had lesions in caudate nucleus, cerebellar nuclei and folia, and spinal cord. Lesions seen were felt to be familial or due to the effects of an amprolium-induced thiamine deficiency on the developing brains of these puppies.