Cerebellar vermian hypoplasia in dogs

Six dogs with cerebellar dysplasia, in which the cerebellar vermis was hypoplastic, are described. Clinical signs in these dogs were noted around 2 weeks of age and included ataxia, dysmetria, and intention tremors. A variable portion of the caudal cerebellar vermis was absent in each dog; portions of the cerebellar hemispheres and flocculus also were absent in some of them. Neurons in certain brain stem nuclei that project to the cerebellum were either chromatolytic or vacuolated. Cerebellar vermian hypoplasia of dogs is analogous to the Dandy-Walker syndrome of human beings.     

Cerebellar vermian hypoplasia in a Cocker Spaniel

An eight-week-old female Cocker Spaniel was presented with ataxia, dysmetria and intention tremor. At 16 weeks, the clinical signs did not progress. Investigation including imaging studies of the skull and cerebrospinal fluid analysis were performed. The computed tomography revealed a cyst-like dilation at the level of the fourth ventricle associated with vermal defect in the cerebellum. After euthanasia, a cerebellar hypoplasia with vermal defect was identified on necropsy. A polymerase chain reaction amplification of cerebellar tissue revealed the absence of an in utero parvoviral infection. Therefore, the cerebellar hypoplasia in this puppy was consistent with diagnosis of primary cerebellar malformation comparable to Dandy-Walker syndrome in humans.     

Congenital bilateral renal hypoplasia in Large White pigs.

Bilateral renal hypoplasia and/or agenesis was detected in 6 of 26 pure-bred Large White piglets in 2 consecutive litters. The affected piglets were all dead at birth. The defect was characterised by a variable nephrogenic zone beneath the renal capsule and by a greatly reduced number of glomeruli which were hypertrophied. The piglets were born to the same sow but they were sired by different boars. Both boars and the sow were related through their pedigree. A genetic basis for the defect, probably involving a recessive gene defect inherited in a simple Mendelian manner, seems likely.     

Nonsuppurative meningoencephalomyelitis of unknown etiology in mink

A central nervous system disease of mink occurred in three unrelated fur farms in Oregon in September, 1981. Only kits four to five months old were affected. Clinical signs consisted of posterior ataxia progressing to complete posterior paralysis with loss of motor control and sensation. Complete or partial recovery occurred in approximately 1.5 months in most mink. Microscopic lesions consisted of severe nonsuppurative meningoencephalitis and meningomyelitis with vacuolation of the white matter of the brain and spinal cord. Canine distemper virus infection and other recognized causes were ruled out on the basis of clinical signs, history, lesions, or laboratory findings. Experimental inoculations of mink with brain and spinal cord specimens from affected mink failed to reproduce the disease.     

Trichlorfon-induced congenital cerebellar hypoplasia in neonatal pigs

The neuroteratogenicity of trichlorfon was evaluated in 3 groups of pregnant sows (8/group). The treatments were: control (no trichlorfon), trichlorfon (60 mg/kg of body weight) in the feed only on day 55 of gestation, or trichlorfon (60 mg/kg of body weight) in the feed on day 55 and day 70 of gestation. One week after farrowing, all newborn pigs were removed from the sows and were euthanatized. Brain and cerebellum weights of the newborn pigs were recorded. Mean cerebellum weights and cerebellum/total brain weight ratios of the neonatal pigs were 3.780 and 0.106 (group 1, n = 26), 3.183 and 0.098 (group 2, n = 42), and 2.986 and 0.088 (group 3, n = 61). Although trichlorfon interfered with cerebellar development and the severity of the trichlorfon-induced cerebellar hypoplasia was dosage-related, ataxia did not develop in the neonatal pigs.     

Cerebellar hypoplasia associated with an avian leukosis virus inducing fowl glioma

Fowl glioma-inducing virus (FGV), which belongs to subgroup A of avian leukosis virus (ALV), shows tumorigenicity and pathogenicity, mainly in the nervous system, and causes astrocytoma and perineurioma. Apart from these neoplasms, cerebellar anomaly was found in chickens infected with FGV in ovo. The study reported here describes the morphologic characteristics of the affected cerebellum. Specific-pathogen-free chickens (C/O) were inoculated with FGV through the yolk sac on the 7th day of incubation. The cerebellar anomaly included diffuse depletion of granular cells of the internal granular layer (IGL), remnants of the external granular layer (EGL), and disorganization of the Purkinje cell layer. These cerebellar changes were observed in all birds except one. In the infected embryos, the EGL was thicker and had an irregular arrangement with a thin molecular layer (ML) and IGL, compared with the control. The granular cells were immunohistochemically positive for ALV common antigen. Immunohistochemical analysis for vimentin revealed disarrangement and decreased number of Bergmann's fibers. Use of the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling method and electron microscopy indicated that apoptotic granular cells were frequently observed in the EGL and ML. These results suggested that the cerebellar anomaly was hypoplasia, principally resulting from the apoptosis of granular cells in the EGL and ML caused by FGV infection and that the cell loss induced obstruction of granular cell migration and disarrangement of Bergmann's fibers in the ML.     

Cerebellar hypoplasia in three sibling cats after intrauterine or early postnatal parvovirus infection

The present report describes the case of an intrauterine or early postnatal parvovirus infection with subsequent cerebellar hypoplasia in three kittens from the same litter. Clinical examination of affected cats revealed neurologic signs indicative of cerebellar ataxia. Due to poor prognosis, animals were euthanised and submitted for necropsy. Post mortem examination demonstrated variable degrees of cerebellar hypoplasia. Histologically, brain lesions were characterised by segmental loss of the external and internal granular layer and decreased numbers of Purkinje cells. Reactive proliferation of astrocytes in the central nervous system was verified by the detection of GFAP-expressing glial cells in affected areas using immunohistochemistry. Furthermore, parvovirus antigen was detected immunohistochemically in neuronal cells of the cerebellum, but not in other parts of the brain and spinal cord or non-neuronal tissues. The present report demonstrates the usefulness of post mortem examination and detection of viral antigen by immunohistochemistry for the discrimination of neurologic disorders in feline species. Neurologic deficiencies due to cerebellar hypoplasia caused by in utero or perinatal feline parvovirus infection should be taken into consideration as differential diagnoses for ataxia in neonatal and juvenile cats.     

多病因呼吸道病

在当今养禽业中，不但旧病复发，且常出现一些新病。其实有些新病早已存在，仅因其发病率低、临诊症状及病变不甚明显或缺乏诊断手段而被忽视。另一方面，微生物本身的基因变化使得其毒力或致病性增强，以及禽类的遗传变异改变了其本身对疾病的易感性和抵抗力也是目前养禽业中旧病复发，新病不断的一大原因。此外，环境条件或饲养管理的改变有利于微生物产生致病性。由于活禽、蛋及禽产品全球性的频繁贸易，难以将某一新病或旧病控制在某一国家或地区。从本期起，本刊对家禽的新病和一些综合征或病因不明的疾病内容加以连载，以飨读者。