Observations on diseases of the central nervous system of sheep in New Zealand

Extract

The purpose of this paper is to describe the salient features of the neurological conditions seen in sheep in New Zealand which are associated with changes in the central nervous system. Several of the conditions associated with perinatal mortality will be mentioned only briefly in this paper as the details will be included in a subsequent paper on ovine perinatal mortality. Some of the entities to be described have been reported before and are reviewed. Others are described here for the first time.     

Rapid test for the preclinical postmortem diagnosis of BSE in central nervous system tissue.

The efficacy of a rapid test for detecting PrP(Sc) in central nervous system tissue was evaluated for the postmortem diagnosis of BSE at different times during the course of the disease. One hundred and six samples of brain, at the level of the medulla oblongata, and spinal cord, derived from the experimental study of the pathogenesis of BSE carried out in Great Britain between 1991 and 1995, were examined. PrP(Sc) was detected in the samples from most of the exposed animals killed 32 months or more after they had been exposed to the agent, and before the onset of clinical signs which were first recorded at 35 months. Comparisons with the results of histology, fibril detection, PrP immunohistochemistry and mouse bioassay indicated that the rapid test is at least as sensitive as these conventional confirmatory diagnostic methods and its result can be obtained more quickly.     

Spina bifida with associated malformations of the central nervous system in Dorper-cross sheep

Abstract

CASE HISTORY: In 2008, six lambs within a flock of Dorpercross sheep were born with musculoskeletal and neurological disease. Clinical signs included hindlimb weakness, and urinary incontinence.

CLINICAL FINDINGS: All lambs had focal, inverted areas of alopecic skin over the caudal sacrum, and short, often kinked tails. Four affected lambs were subject to euthanasia, and necropsied. On gross examination, the arches of sacral vertebrae were absent, and spinal nerves and meninges were adherent to the overlying subcutis. Other gross lesions included narrow, elongated skulls, herniation of the occipital lobes into the caudal fossas, hydrocephalus, and syringomyelia. One lamb had coning of the cerebellar vermis, but cerebellar herniation through the foramen magnum was not identified.

DIAGNOSIS: Spina bifida, with associated malformations of the central nervous system.

CLINICAL RELEVANCE: Examination of breeding records suggested either an autosomal recessive or partially penetrant autosomal dominant pattern of inheritance. Because of the associated tail lesions it is proposed that the pathogenesis of this syndrome involves a defect in development of the tail bud (secondary neurulation), that tethering of the spinal cord resulted in the clinical signs, and abnormal pressure of the cerebral spinal fluid resulted in the defects in the skull and brain.     

Distribution of the rabies virus in the central nervous system of naturally infected foxes]

Quantitative distribution of rabies virus and the character of immunofluorescence in various parts of the central nervous system [CNS] and salivary glands were investigated in 21 naturally infected foxes. A mean death period was recorded in mice infected with the virus obtained from various parts of the CNS and salivary glands of the investigated foxes. The highest average titer of the virus was found out in the salivary glands - 4.46 log MLD50 per 0.03 ml i. c. The average titer was 2.30 log in the cornu ammonis, 1.99 log in the lobus olifactorius, 1.80 log in the spinal cord of the sacro-lumbar region, 1.73 log in the cortex, 1.71 log in the medulla oblongata, and 1.64 log in the cerebellum. The highest intensity of specific fluorscence was recorded in the thalamus, lobus piriformis, and cornu ammonis. In these regions, numerous round fluorescent inclusion bodies similar to Babes-Negri bodies occurred. Babes-Negri bodies in the cornu ammonis of foxes were proved in 81% of cases. Mice infected with the virus obtained from the salivary glands showed the shortest mean death period - 12.2 days and from the cornu ammonis it was 14.6 days. In virus infection from the other parts of the CNS the mean death period ranged from 16.0 to 17.4 days.     

Natural scrapie: detection of fibrils in extracts from the central nervous system of sheep

Extracts from the cervical spinal cord and from the medulla, thalamus, cerebellum and cerebral cortex of the brains of 10 sheep, histopathologically confirmed as cases of scrapie, were examined by electron microscopy for the presence of scrapie-associated fibrils. Characteristic fibrils were observed in all the extracts except for that from the thalamus of one sheep. No fibrils were found in any extracts from three control sheep. A comparison of these results with a similar study of 22 cases of bovine spongiform encephalopathy (BSE) suggests that in cases of scrapie the area of the brain chosen for the detection of fibrils is less critical than in cases of BSE, in which fibrils are more readily extracted from areas of the brain stem.     

Total protein, albumin quota, and electrophoretic patterns in cerebrospinal fluid of dogs with central nervous system disorders

Cerebrospinal fluid was analyzed for total protein, albumin quota, and electrophoretic patterns of albumin and alpha-, beta-, and gamma-globulins in 10 healthy dogs and 35 dogs with CNS disorders. Values obtained in healthy dogs were used to establish control data. Samples also were collected from dogs with neurologic diseases that were classified according to clinical and pathologic diagnosis as inflammation, neoplasm, and spinal cord compression. The albumin quota and total CSF albumin values were used as indicators of blood-brain barrier disturbance. Four patterns were observed on agarose electrophoresis that included intrathecal immunoglobulin production, intrathecal immunoglobulin production combined with blood-brain barrier disturbance, blood-brain barrier disturbance, and unaltered CSF. These patterns correlated with the observed clinical and pathologic conditions. Seemingly, agarose electrophoresis of CSF is a simple and reliable technique that aids in the diagnosis of CNS disorders of dogs.     

High mortality and lesions of the central nervous system in trypanosomosis by Trypanosoma vivax in Brazilian hair sheep

Here, we report an outbreak of Trypanosoma vivax-induced trypanosomosis in Brazilian hair sheep on a farm in Paraíba state, a non-endemic region in northeastern Brazilian. Of 306 total sheep, 240 showed clinical signs and 216 died. Clinical signs included anorexia, lethargy, anemia, rough hair coat, weight loss, submandibular edema, abortion, and in some cases, neurological signs such as head pressing, lateral recumbence, paddling movements and muscle tremors. T. vivax was identified by blood smear analysis and polymerase chain reaction (PCR). At necropsy, animals exhibited watery blood, pale tissue coloring, and the presence of liquid in the peritoneal cavity and pericardial sac. Histologically, nonsuppurative myocarditis and meningoencephalitis with areas of malacia were observed. After treatment, no parasites were detected by blood smear analysis or PCR. Cattle and buffalo that remained in the same pasture were also infected but presented with asymptomatic infections. Epidemiological data suggest that T. vivax was introduced to the farm and the susceptible flock by buffalos that were asymptomatic carriers of the infection; T. vivax was most likely transmitted by Tabanus spp. bites and also iatrogenically.     

Viral antigen distribution in the central nervous system of cattle persistently infected with bovine viral diarrhea virus

Distribution of viral antigens in the central nervous system of 25 cattle with a persistent bovine viral diarrhea virus (BVDV) infection was studied. Using a polyclonal antiserum produced in pigs and the direct immunofluorescence and immunoperoxidase technique, BVDV antigen was located exclusively in neurons. Predilection sites for viral persistence were cerebral cortex and hippocampus; in other areas of brain and spinal cord, viral antigens were in single neurons or small groups of neurons. There was no morphological evidence of cellular alteration due to viral persistence. Perivascular lymphocytic infiltrations were in affected nervous tissue. It is concluded that the central nervous system is an important location for persistence of BVDV.     

Inflammatory disease of the central nervous system

Inflammatory diseases involving the central nervous system can be difficult to diagnose and frustrating to treat. The clinician can maximize successful treatment of these patients by recognizing the clinical signs in the early stages of disease, following a logical diagnostic plan to identify the specific etiologic agent involved, and formulating an appropriate and aggressive therapeutic plan. Treatment will not always be successful owing to lack of effective treatments and irreversible neurologic damage.     

Effects of tolazoline and yohimbine on xylazine-induced central nervous system depression, bradycardia, and tachypnea in sheep

We compared the ability of tolazoline and yohimbine to antagonize xylazine-induced central nervous system depression, bradycardia, and tachypnea in 9 ewes and 5 rams. Once a week for 3 weeks, each sheep received one IV treatment of 0.4 mg xylazine/kg, 0.4 mg xylazine/kg followed in 10 minutes by 2 mg tolazoline/kg, or 0.4 mg xylazine/kg followed in 10 minutes by 0.2 mg yohimbine/kg. The order of the 3 treatments in each sheep was randomized. Xylazine alone caused recumbency for 41.0 +/- 3.7 minutes (mean +/- SEM). Tolazoline and yohimbine shortened the xylazine-induced recumbency to 12.1 +/- 0.9 minutes and 18.1 +/- 1.5 minutes, respectively. Sheep given xylazine alone had head droop for 34.0 +/- 5.4 minutes after rising. Head drooping of sheep given tolazoline or yohimbine was reduced to 10.1 +/- 1.7 minutes and 14.2 +/- 1.7 minutes, respectively. Both tolazoline and yohimbine reversed the bradycardia and tachypnea that followed xylazine administration. No statistical differences in the rate and magnitude of the reversal were observed between the 2 drugs.