Multisystemic chromatolytic neuronal degeneration in a Cairn terrier pup

In a four-month-old female Cairn terrier with mild episodic paraparesis, a multisystemic chromatolytic degeneration affected widespread neuronal populations in the brain and spinal cord as well as spinal, autonomic, and enteric ganglia. There was little axon degeneration or cell body loss, and the latter findings may explain the mild clinical signs. Among affected perikarya the extent and distribution of chromatolysis varied. While peripheral lysis of Nissl substance occurred often in spinal motoneurons, central chromatolysis was frequent in brain stem nuclei, and patchy Nissl loss appeared in some neurons including those in the cerebral cortex and spinal dorsal horns. Although prior studies of various chromatolytic neurodegenerations often have demonstrated characteristic massings of neurofilaments, the major, and invariable ultrastructural finding in this study was dispersion and loss of ribosomes. Neurofilamentous accumulations were observed less consistently. The clinical and pathologic findings in this pup were compared and constrasted with those made in prior studies of chromatolytic neurodegenerations.     

Further Studies on the Hypoglossal Nucleus in the Fowl

The delineation of the fowl's hypoglossal nucleus was determined by severing the hypoglossal nerve or its branches and observing retrograde degeneration. Birds were killed 7 or 10 days after surgery, the brains embedded in paraffin and cut at 10 μm. Transection of the hypoglossal nerve stem resulted in chromatolysis near the obex and no chromatolysis was found in the Nuclei cervicales. Severing of the laryngolingual branch led to degeneration phenomena near the obex nearly similar to the degeneration observed after severing of the hypoglossal nervestem. Cutting of the superior laryngeal branch caused a degeneration of cells caudal to the obex, and cutting of the syringeal branch resulted in chromatolysis in about the same area. The origin of the anastomosing branch between the first cervical and hypoglossal nerve was not found because no chromatolytic cells could be detected. Similarly the cutting of several upper cervical nerves did not lead to chromatolysis in the areas we investigated.     

Histological and immunohistochemical studies of changes in myenteric plexuses and in interstitial cells of Cajal associated with equine colic

In this study we investigated the histological changes of the myenteric plexuses and interstitial cells of Cajal (ICC) in gut samples from horses with colic to try to find results useful in the prognostic evaluation of enteric lesions. A morphologic and quantitative study of myenteric ganglia, ganglion cells and neuronal chromatolytic and necrotic changes of 24 horses with colic was performed. For ganglion cells, enteroglial cells and ICC immunolabeling was also performed to identify cell functional disorders. A significant increase of neuronal chromatolysis and necrosis occurred in horses suffering from colic throughout the gut. The neuron-specific enolase (NSE) and synaptophysin immunoreaction quantified with image analysis showed a significant loss of neuronal activity in all intestinal tracts of the animals under study associated with a significant loss of ICC immunoreactivity. The results supports immunohistochemical evaluation of ENS and ICC as a useful tool along with morphometric investigations in the evaluation of gut lesions produced during colic syndrome.     

A progressive neuronopathy in the young cairn terrier

The clinical signs and neuropathological changes of a nervous disease of pedigree cairn terriers are described. Three animals, of both sexes, between five and seven months of age showed hind leg weakness, quadriparesis, ataxia, loss of superficial and deep reflexes and tremor of the head. Pathologically there was chromatolysis of neurons in the spinal cord and brain stem. Although Wallerian-type degeneration was present in the spinal cord and peripheral nerves, its severity did not correlate with the intensity of the neuronal changes. This suggests that the chromatolysis observed may reflect a primary neuronal abnormality rather than represent a secondary change resulting from a primary degeneration of peripheral axons. Although the age of onset and some of the clinical signs are similar to those seen with globoid cell leucodystrophy (an inherited disease which also affects cairn terriers), the presence of lower motor neuron paralysis and the absence of signs of severe brain involvement in progressive neuronopathy should enable the conditions to be distinguished clinically.     

Idiopathic brainstem neuronal chromatolysis and hippocampal sclerosis: a novel encephalopathy in clinically suspect cases of bovine spongiform encephalopathy.

Some of the brains submitted for neurohistopathological examination under the Bovine Spongiform Encephalopathy (BSE) Orders did not show lesions of BSE. They showed neuronal chromatolysis and necrosis of the brainstem, perivascular cuffs and meningeal infiltrates of mononuclear cells and large irregularly shaped vacuoles in the neuropil. About half of them also showed loss of pyramidal neurons in the hippocampus, with astrocytic gliosis. The topography of the brainstem neuronal degeneration and vacuolation was the same in all the cattle, suggesting that neuronal necrosis and chromatolysis, vacuolation and hippocampal sclerosis are part of a spectrum of changes common to a single disease. The cows affected with such changes came from most parts of Scotland with the largest number from the north east. They were of various breeds, mostly suckler cows, and were aged from six to 16 years. Some cows had had no reported access to feed supplements. Clinically, the cows showed a range of neurological signs: tremor, ataxia, apprehension and weight loss were described in more than 80 per cent of the cases. The cause of the disorder was not determined.     

Familial motor neuron disease in Rottweiler dogs: neuropathologic studies

Two 6-week-old female Rottweiler littermates were evaluated for regurgitation, diminished growth, progressive ataxia, and pelvic limb weakness. Clinical examination indicated a progressive, diffuse, lower motor neuron disorder and megaesophagus. The pups were killed at 6 and 8 weeks of age. Lesions included central chromatolysis and swelling of the perikarya in many large motor neurons in the ventral gray matter of the spinal cord. Some involvement of red, oculomotor, trigeminal motor, and ambiguus nuclei of the brainstem was noted. Ultrastructurally, chromatolytic neurons had excess neurofilaments, and an increase in and enlargement of Golgi complexes. Wallerian-like degeneration was prominent in neuropil of spinal cord and in peripheral nerve. Clinical, histological, and ultrastructural findings were consistent with a progressive motor neuron disease.     

Central nervous system pathology in 25 dogs with chronic degenerative radiculomyelopathy

The neuropathology of 20 German shepherd dogs and five German shepherd dog crosses with chronic degenerative radiculomyelopathy were analysed by conventional techniques, immunocytochemistry and electron microscopy. There were previously unrecognised changes in brain nuclei. In the spinal cord, both motor and sensory tracts were involved, principally in their more distal regions. Wallerian degeneration affected the corticorubrospinal pathways in the lateral columns and the ventral funiculi, predominantly in the caudal thoracic and lumbar segments, although more cranial involvement was also observed. The dorsal columns were affected in the caudal lumbar region and the cervical fasciculus gracilis. The regional distribution was variable between cases. Within the brain, abnormalities, including chromatolysis, gliosis and neuronal loss were observed in the red nucleus, lateral vestibular nucleus and, occasionally, in the dentate nucleus. The changes in brain nuclei were compared with those found in dogs at various times after a focal spinal injury. The neuronal changes in the brain may be related to the primary site of damage, and possible aetiological mechanisms are discussed.     

RESULTS OF MYELOGRAPHY IN SEVEN DOGS WITH MYELOMALACIA

Myelomalacia is a hemorrhagic infarction of the spinal cord that can occur as a sequel to acute spinal cord injury. Myelomalacia may be focal or diffuse; the diffuse form is typically associated with cranial migration of neurologic signs ("ascending syndrome") and is often fatal. In a retrospective study of seven affected dogs, diffuse myelomalacia was associated with intervertebral disc extrusion in five dogs, focal myelomalacia was associated with fibrocartilagenous embolus in one dog, and had no apparent cause in one dog. The myelographic signs included a variable degree of contrast medium infiltration into the spinal cord in six dogs (86%) and/or spinal cord swelling in six dogs (86%). In one dog with focal myelomalacia, the only myelographic sign was spinal cord swelling.     

Equine motor neuron disease; a preliminary report

A spontaneous motor neuron disease or neuronopathy was identified in 10 horses from the northeastern United States. Signs of generalized weakness, muscle fasciculations, muscle atrophy and weight loss progressed over 1 to several months in young and old horses of various breeds. Pathologic studies revealed that degeneration and loss of motor neurons in the spinal cord and brain stem resulted in axonal degeneration in the ventral roots and peripheral and cranial nerves and denervation atrophy of skeletal muscle. Many spinal neurons were swollen, chromatolytic and contained neurofilamentous accumulations. Other cell bodies were shrunken and undergoing neuronophagia and some were lost and replaced by glia. This fatal equine motor neuron disease has not been reported previously and its cause has not been determined. The progressive weakness and wasting and the neuronal degenerative changes in these horses were similar to those described in people with sporadic amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease.     

Encephalo-myelopathy in young cats

Nineteen cats, aged three to 16 months, developed neurological signs including hindleg paralysis, head shaking, nystagmus, defective vision and reduced proprioception. Most of the animals were in cat colonies in research centres and were derived from specific pathogen-free stock. One was referred from veterinary practice. Over 40 per cent of litters could be affected constituting a serious commercial loss. Wallerian degeneration affected long tracts in the spinal cord and variously in the brain stem and cerebral white matter. In seven animals there was loss of Purkinje cells in the cerebellum and in eight there was neuronal loss in the spinal cord. Gliosis accompanied all changes. Although no viral agent was isolated the clinical pattern of the disease and evidence from other cases reported in the literature suggest an infectious cause.     

Progressive encephalomyelopathy and cerebellar degeneration in 10 captive-bred cheetahs

Progressive ataxia, with head tremor, developed in 10 captive-born cheetah cubs under six months of age. The condition was usually preceded by coryza and an ocular discharge. Initially the ataxia and weakness affected the hindquarters, then the forelegs, and head tremor developed later. Significant pathological changes were confined to the central nervous system. There was widespread Wallerian degeneration in the funiculi of the spinal cord (except those in the dorsal columns), in the medulla and in the cerebellum. In the cerebellum there was degeneration of Purkinje cells and of the molecular and granular cell layers. There was chromatolysis in the Purkinje cells, the ventral horn cells of the spinal cord and in the neurons of the lateral vestibular nucleus. The olivary nucleus was necrotic. There were foci of inflammatory cells in the molecular layer of the cerebellum and in the medulla. The cause of the disease remains unknown.     

Basset Hound thrombopathia in a 4‐month‐old female Ba‐Shar (Sharp Asset)

A 3‐month‐old female Basset Hound‐Shar Pei mix puppy (Ba‐Shar or Sharp Asset) presented with oral bleeding due to a cracked molar. On physical exam, an aural hematoma was also noted that the owner indicated was chronic. The puppy was hospitalized for over 24 h until the bleeding was brought under control. At 4 months of age, the puppy again presented with oral bleeding due to loss of deciduous teeth and was hospitalized until bleeding was controlled. Coagulation screening tests, platelet numbers, and von Willebrand Factor antigen levels were within reference limits. Based on the presence of platelet‐type bleeding in the face of normal screening test results, samples were submitted for DNA testing for Basset Hound thrombopathia. The puppy tested as affected for the calcium and diacylglycerol regulated guanine nucleotide exchange factor I (CalDAG‐GEFI) mutation causing this disorder. This is the first time thrombopathia has been diagnosed in a “designer” breed.     

Clinical and pathological findings of acute zinc intoxication in a puppy

This report describes the clinical and pathological findings in a case of acute zinc poisoning in a young dog. The puppy suffered four days of progressively more severe vomiting and diarrhoea. Jaundice and pale mucous membranes, severe haematemesis and haemoglobinuria were other findings. Despite intensive therapy, the dog died a few hours after hospitalisation. Postmortem examination revealed a metallic foreign body in the stomach, catarrhal gastritis, hepatomegaly and enlarged, dark kidneys. Histology showed hepatic centrilobular vacuolar degeneration, haemoglobinuric nephrosis with early tubular necrosis, haemosiderosis and extramedullary haematopoiesis, as well as neuronal damage. The foreign body was mainly composed of zinc. Plasma zinc values were markedly raised (34.5 microg/ml; normal range 0.8 to 1.0 microg/ml). Pathophysiological mechanisms of zinc poisoning are discussed.     

California goats with a disease resembling enzootic ataxia or swayback

In a retrospective study typical signs and lesions of enzootic ataxia or swayback were found in 16 young dairy goats from eight widely scattered herds in California. In addition to the constant appearance of chromatolytic neurons in brainstem and spinal cord, and myelin deficiency in certain tracts of the cord, cerebellar hypoplasia was found frequently. Liver copper was subnormal in six of nine kids tested. The disease is viewed as a developmental defect in which failure of neuronal perikaryon metabolism leads to distal axonopathy with secondary demyelination.     

Post-mortem re-cloning of a transgenic red fluorescent protein dog

Recently, the world''s first transgenic dogs were produced by somatic cell nuclear transfer. However, cellular senescence is a major limiting factor for producing more advanced transgenic dogs. To overcome this obstacle, we rejuvenated transgenic cells using a re-cloning technique. Fibroblasts from post-mortem red fluorescent protein (RFP) dog were reconstructed with in vivo matured oocytes and transferred into 10 surrogate dogs. One puppy was produced and confirmed as a re-cloned dog. Although the puppy was lost during birth, we successfully established a rejuvenated fibroblast cell line from this animal. The cell line was found to stably express RFP and is ready for additional genetic modification.     

犬瘟热RT-PCR快速诊断方法的建立

本研究建立了快速诊断犬瘟热感染的RT-PCR方法,并应用该方法对犬瘟热病死犬的脏器及感染犬体表采集样品进行了检测。为确定犬瘟热最佳的隔离检疫周期及采样部位,本研究对一例CDV攻毒犬感染病程收集的口鼻液、粪便、尿液样品进行了对比检测,结果证实粪便、口鼻液等易于获取的样品中CDV病毒滴度较高,并可在发病全程检测到,因此,它们可作为理想的受试样品。     

SINGLE‐SHOT TURBO SPIN ECHO PULSE SEQUENCE FINDINGS IN DOGS WITH AND WITHOUT PROGRESSIVE MYELOMALACIA

Progressive myelomalacia is an uncommon type of ischemic, hemorrhagic spinal cord infarction. Diagnosis can be difficult, but prompt recognition is important. We hypothesized that cerebrospinal fluid signal attenuation on magnetic resonance (MR) images would be more extensive in dogs that developed progressive myelomalacia vs. control dogs. A retrospective analytic cohort study was designed. Dogs were included if they presented for acute paraplegia and loss of deep pain perception and had undergone MR imaging using both sagittal single‐shot turbo spin echo (SSTSE) and standard sagittal T2‐weighted fast spin echo (T2W) pulse sequences. Dogs were divided into progressive myelomalacia and control groups for comparisons. All MR examinations were evaluated by three reviewers blinded to patient outcome. Length of cerebrospinal fluid attenuation was recorded as a ratio to the length of the L2 vertebral body in SSTSE and T2W sequences (CSF:L2_SSTSE and CSF:L2_T2, respectively). Length of intramedullary spinal cord hyperintensity was recorded as a ratio to the length of the L2 vertebral body in T2W sequences. A total of 21 dogs were included (five in the progressive myelomalacia group and 16 in the control group). The mean CSF:L2_SSTSE attenuation value was significantly higher in dogs that developed progressive myelomalacia (CSF:L2_SSTSE = 10.7) compared to controls (CSF:L2_SSTSE = 5.4; P = 0.015). A cut off ratio of attenuation >7.4 provided optimal differentiation between groups in this study. Findings supported the conclusion that dogs with CSF:L2_SSTSE ≤ 7.4 are unlikely to develop progressive myelomalacia while dogs with CSF:L2_SSTSE > 7.4 are indeterminate for progressive myelomalacia.     

Abomasal emptying defect of sheep may be an acquired form of dysautonomia

Abomasal emptying defect (AED) is a disease syndrome that primarily affects Suffolk sheep and is characterized by distension and impaction of the abomasum. No histologic lesion has been consistently associated with this condition. There is no known etiology. In this study, nine cases of AED were identified by necropsy, including three rams and six ewes between 2 and 6 years of age. Four of the cases occurred sporadically, and five ewes were submitted on the same day from a single flock. Histologic examination of celiacomesenteric ganglia from six of the affected sheep revealed scattered chromatolytic or necrotic neurons, without inflammation. Chromatolytic neurons were observed more frequently in AED-affected sheep than in seven healthy Suffolk sheep (P < 0.08, weak statistical support). Neuronal necrosis was not observed in any of the healthy sheep. Lineage records of the flock that suffered an outbreak were incompatible with the possibility of a simple inheritance pattern for this disease; furthermore, the very occurrence of AED in outbreak form is inconsistent with transmission solely by inheritance. Only one of the six tested sheep showed concurrent immunohistochemical evidence of scrapie. The lesion pattern in celiacomesenteric ganglia is suggestive of a neurotoxicosis. Neuronal lesions of AED resemble dysautonomic diseases of humans and other animals.     

Equine myenteric ganglionitis: a case of chronic intestinal pseudo-obstruction

A 4-year-old Standardbred mare was referred to the New York State College of Veterinary Medicine for colic evaluation. Physical examination revealed a small colon impaction which initially responded to conservative medical management. Her signs soon recurred, however, and an exploratory celiotomy was recommended. At surgery the small colon impaction was confirmed. The impaction was evacuated and a surgical biopsy was submitted for histopathologic evaluation. Microscopic examination of H&E and Trichrome sections revealed a massive mononuclear cell infiltration of the myenteric plexus. In addition, there was remarkable fibrosis within the neuropil of the myenteric ganglia and interganglionic fascicles. Postoperatively, the mares's colic signs recurred within two weeks and she was euthanatized. Samples of the proximal and distal small colon as well as the original biopsy site were obtained. Over the intervening two weeks, the inflammatory infiltrate within the myenteric ganglia had subsided, while the previous intraganglionic and fascicular fibrosis had increased substantially. The number of myenteric neurons appeared diminished when compared to age-matched controls. There was evidence of neuronal degeneration among the surviving neurons including central chromatolysis and cytoplasmic vacuolization. Furthermore, many degenerate axons were observed with the electron microscope. This scenario represents an equine example of chronic idiopathic intestinal pseudo-obstruction (CIIP) which has been extensively described in the human literature. In this case, the syndrome arose as a consequence of recurrent inflammatory injury to the mare's enteric nervous system, thereby altering normal gastrointestinal motility. The ensuing neurogenic functional obstruction manifested as frequent bouts of small colon impactions. Equine CIIP should be considered in the differential diagnosis of colic.