West Nile virus infection in reindeer (Rangifer tarandus).

West Nile virus (WNV) infection in 4 reindeer (Rangifer tarandus) resulted in lymphohistiocytic encephalomyelitis within the medulla oblongata and cervical spinal cord. Immunohistochemistry revealed WNV antigen within neurons and among mononuclear cell infiltrates. These represent the first known cases of clinical WNV infection in Cervidae. Clinical signs and lesions were similar to those described in horses. Nucleotide sequence of a 768-bp region of the WNV E-glycoprotein gene revealed 1 nucleotide mutation, which resulted in a single amino acid substitution from a serine to a glycine (position 227 of E-glycoprotein) when compared with the prototype WNV-NY99 strain (isolated from Bronx zoo flamingo 382-99).     

Efficacy, duration, and onset of immunogenicity of a West Nile virus vaccine, live Flavivirus chimera, in horses with a clinical disease challenge model

REASON FOR PERFORMING STUDY: West Nile virus (WNF) is a Flavivirus responsible for a life-threatening neurological disease in man and horses. Development of improved vaccines against Flavivirus infections is therefore important. OBJECTIVES: To establish that a single immunogenicity dose of live Flavivirus chimera (WN-FV) vaccine protects horses from the disease and it induces a protective immune response, and to determine the duration of the protective immunity. METHODS: Clinical signs were compared between vaccinated (VACC) and control (CTRL) horses after an intrathecal WNV challenge given at 10 or 28 days, or 12 months post vaccination. RESULTS: Challenge of horses in the immunogenicity study at Day 28 post vaccination resulted in severe clinical signs of WNV infection in 10/10 control (CTRL) compared to 1/20 vaccinated (VACC) horses (P<0.01). None of the VACC horses developed viraemia and minimal histopathology was noted. Duration of immunity (DPI) was established at 12 months post vaccination. Eight of 10 CTRL exhibited severe clinical signs of infection compared to 1 of 9 VACC horses (P<0.05). There was a significant reduction in the occurrence of viraemia and histopathology lesion in VACC horses relative to CTRL horses. Horses challenged at Day 10 post vaccination experienced moderate or severe clinical signs of WNV infection in 3/3 CTRL compared to 5/6 VACC horses (P<0.05). CONCLUSIONS: This novel WN-FV chimera vaccine generates a protective immune response to WNV infection in horses that is demonstrated 10 days after a single vaccination and lasts for up to one year. POTENTIAL RELEVANCE: This is the first USDA licensed equine WNV vaccine to utilise a severe challenge model that produces the same WNV disease observed under field conditions to obtain a label claim for prevention of viraemia and aid in the prevention of WNV disease and encephalitis with a duration of immunity of 12 months.     

Clinical signs of West Nile virus encephalomyelitis in horses during the outbreak in Israel in 2000

Between August and October 2000, 76 horses were reported by veterinary practitioners as having signs of a neurological disorder, varying from an involvement of the spinal cord alone to the entire central nervous system; 15 of the horses died or were euthanased as a result of their grave prognosis or secondary complications. At the same time, an outbreak of West Nile virus infection affected people and birds, principally domestic geese. West Nile virus was isolated from four of the horses with encephalomyelitis and five other horses seroconverted, indicating that the virus was the probable cause of the outbreak in horses. Three of the cases from which the virus was isolated are described briefly and one case is described in detail. This horse behaved abnormally and had general proprioceptive deficits in all four limbs. Its neurological condition deteriorated after two days and severe inspiratory dyspnoea due to a failure to abduct the arytenoids necessitated a tracheostomy. It died on the fourth day and histological lesions were observed in the brain stem and grey matter of the spinal cord.     

Use of magnetic motor-evoked potentials in horses with bilateral hind limb ataxia

OBJECTIVE: To determine the usefulness of magnetic motor-evoked potentials (MMEPs) for assessing the integrity of the cervical, thoracic, and thoracolumbar spinal cord in horses with bilateral hind limb ataxia. ANIMALS: 9 horses and 1 donkey with bilateral hind limb ataxia of various degrees. PROCEDURE: The motor cortex was stimulated magnetically, and MMEPs were recorded bilaterally from the extensor carpi radialis and cranial tibial muscles. RESULTS: In 5 horses and 1 donkey, MMEPs with normal onset latencies and peak-to-peak amplitude were recorded from the extensor carpi radialis muscles, whereas abnormal onset latencies and peak-to-peak amplitudes were recorded from the cranial tibial muscles. In these animals, a spinal cord lesion in the thoracic or thoracolumbar segments was suspected. In 4 horses, onset latencies and peak-to-peak amplitude of MMEPs recorded from the extensor carpi radialis and cranial tibial muscles were abnormal. In these horses, a cervical spinal cord lesion was suspected. CONCLUSIONS AND CLINICAL RELEVANCE: Transcranial magnetic stimulation can be considered a valuable diagnostic tool for assessing the integrity of the spinal cord, and MMEPs may be used for differentiating thoracic or thoracolumbar spinal cord lesions from mild cervical spinal cord lesions that cause ataxia in the hind limbs only.     

Clinical and neuropathological features of West Nile virus equine encephalomyelitis in Italy

West Nile (WN) virus infection is a mosquito-borne flavivirosis endemic in Africa and Asia. Clinical disease is usually rare and mild and only in a few cases the infection causes encephalomyelitis in horses, fever and meningoencephalitis in man. We report here the clinical and pathological findings in an epidemic of the disease involving 14 horses from Tuscany, Italy. All cases were observed from August to October 1998. Affected horses showed ataxia, weakness paresis of the hindlimbs and, in 6 cases, there was paraparesis progressing to tetraplegia and recumbency within 2 to 9 days. Eight animals recovered without any important consequences. Serological investigations revealed positivity to WN virus in all the 14 horses and the agent was isolated from the cerebellum and spinal cord of an affected horse. Postmortem examination was carried out on 6 horses. The neuropathological pattern was that of a mild to moderate, nonsuppurative polioencephalomyelitis with constant involvement of the ventral horns of the thoracic and lumbar spinal cord, where focal gliosis and haemorrhage were also apparent in some cases. Differential diagnoses with other equine viral encephalomyelitides are discussed. Climatological and environmental characteristics of the geographic area in which the outbreaks occurred suggest the existence of suitable conditions for the development of the disease. This is the first report of WN virus equine encephalomyelitis in Italy.     

Clinical findings, lesions, and viral antigen distribution in great gray owls (Strix nebulosa) and barred owls (Strix varia) with spontaneous West Nile virus infection

West Nile Virus (WNV) infection manifests itself clinically a nd pathologically differently in various species of birds. The clinicopathologic findings and WNV antigen tissue distribution of six great gray owls (Strix nebulosa) and two barred owls (Strix varia) with WNV infection are described in this report. Great gray owls usually live in northern Canada, whereas the phylogenetically related barred owls are native to the midwestern and eastern United States and southern Canada. Naturally acquired WNV infection caused death essentially without previous signs of disease in the six great gray owls during a mortality event. Lesions of WNV infection we re dominated by hepatic and splenic necrosis, with evidence o f disseminatedintravascular coagulation in the great gray owls. WNV antigen was widely distributed in th e organs of the great gray owls and appeared totarget endothelial cells, macrophages, and hepatocytes. The barred owls represented two sporadic cases. They had neurologic disease with mental dullness that led to euthanasia. These birds had mild to moderate lymphoplasmacytic encephalitis with glial nodules and lymphoplasmacytic pectenitis. WNV antigen was sparse in barred owls and only present in a few brain neurons and renaltubular epithelial cells. The cause of the different manifestations of WNV disease in these fairly closely related owl species is uncertain.     

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.     

Bilateral laryngeal paralysis in the horse

Four two-year-old Thoroughbreds suffered an acute gastrointestinal illness shortly after dosing with mineral oil which was thought to have been contaminated with an organophosphate compound. Three weeks later all four were noted to be dyspnoeic and endoscopic examination showed that they had developed bilateral laryngeal paralysis. Two of the horses died during severe bouts of dyspnoea six and eight months later and the third was killed shortly thereafter. Examination of the left and right recurrent laryngeal nerves from these horses showed a severe loss of myelinated fibres distally, especially in the left nerve. A similar but less severe lesion was seen in other long peripheral nerves, including the phrenic and digital nerves of the third horse. The spinal cord in two horses showed evidence of mild axonal degeneration which was not related to a particular tract or location. The fourth horse had bilateral laryngeal paralysis two years later. The acute clinical signs and delayed neurological sequelae seen in these horses were strongly suggestive of accidental organophosphate toxicity.     

Seroprevalence and molecular characterization of West Nile Virus in Egypt

West Nile Virus (WNV) is a flavivirus, mosquito-borne infection and have public health importance worldwide. WNV infection have highly significant impact on animal and human health. The virus has been detected serologically in Egypt among equids. Therefore, the aim of the present study to investigate the serological situation of WNV among horse in north of Egypt and identification of WNV in vector. The serological survey was conducted on 500 serum samples that collected from horses from four governorates at north of Egypt. The infection rate was non-significant differed between four localities and the highest rate was reported in Qalyubia governorate (25.5 %) in comparison with other areas. Moreover, the WNV RNA was detected in mosquitoes and the obtained WNV sequence showed high similarity with Eg101 strain and characterized as lineage 1. The obtained findings confirm the circulation of WNV in mosquitoes and animals in Egypt.     

Contrast-enhanced computed tomography and myelography in six horses with cervical stenotic myelopathy.

The cervical spines of 6 horses with cervical stenotic myelopathy (CSM) were examined using myelography and contrast-enhanced computed tomography (CECT). Histopathology of the spinal cord of these horses identified 10 neurologically significant compressive lesions. Myelography and CECT were both able to demonstrate all 10 spinal cord compressive lesions, but myelography falsely identified 2 sites and CECT falsely identified 1 site as compressive lesions of the spinal cord which were not supported by histopathology. Additional qualitative information was obtained by CECT regarding the source, severity and location of spinal cord compression. Computed tomography identified stenosis of the vertebral canal with circumferential loss of contrast agent and documented lateral compressive lesions of the spinal cord due to malformed articular facets. Compression of the peripheral nerve roots by malformed articular facets encroaching on the intervertebral foramen was easily identified by CECT in the axial plane. No compressive lesions were identified in 3 unaffected horses by either method. Minimum sagittal diameter (MSD) values obtained from CECT images were strongly correlated with necropsy measurements, validating CECT as an accurate method of obtaining MSD values. The MSD values in the CSM-affected horses were significantly narrowed (P less than 0.05) from C3C6 regardless of the site of spinal cord compression, when compared with the unaffected controls. This finding supports previous reports suggesting that generalised stenosis of the vertebral canal is an important feature in the pathogenesis of cervical stenotic myelopathy.     

Myelopathy and vitamin E deficiency in six Mongolian wild horses

Degenerative myelopathy was diagnosed in six Mongolian wild horses. Three of the horses had a history of ataxia dating from birth to 3 months of age. The clinical signs were uncoordinated movement of the hindlimbs and an abnormally wide-based gait and stance. The other 3 horses had mild ataxia. There were no gross lesions in the brain, vertebrae, or spinal cord. Histologic examination revealed degeneration of the neural processes in the ventral and lateral funiculi of all 6 horses. Myelin sheaths were dilated and vacuolated, and there were swollen, fragmented, or lysed axons. Neuronal degeneration, phagocytosis, and accumulation of periodic acid-Schiff-positive, xylol-insoluble lipopigment were observed in the affected neurons of the dorsal root ganglia. The plasma alpha-tocopherol values of 5 of the affected horses ranged from less than 0.03 to 0.08 (mean, 0.04 +/- 0.01) mg/dl. Seven clinically normal horses from the same herd had a range of less than 0.03 to 0.3 (mean, 0.11 +/- 0.02) mg/dl, which was low enough to be considered deficient.     

Chronic cervical compressive myelopathy in horses: patterns of astrocytosis in the spinal cord

The distribution and morphology of fibrous astrocytes in the cervical spinal cord of normal horses and horses with chronic compressive myelopathy were demonstrated using immunohistochemical staining for glial fibrillary acidic protein. In the spinal cord from normal horses, astrocytes with stellate cell bodies and short processes were irregularly distributed in grey matter. In the white matter, their cell bodies were small and angular in areas adjacent to grey matter and larger and more stellate-shaped in the subpial area. Astrocyte processes were fine, and evenly distributed in a predominantly radial pattern in transverse sections of cord. Gliosis was marked in the spinal cords of horses with cervical compressive myelopathy. In the grey matter at the level of compression astrocytes were often enlarged and rounded, with short, blunt processes, but the gliosis was generally mild. In the white matter, gliosis was obvious in areas of nerve fibre swelling and degeneration at the level of compression and in areas of ascending and descending Wallerian degeneration. The fine radial pattern of astrocyte fibres was replaced by a dense, irregular arrangement. Gliosis persisted in the cords of chronically affected horses after active nerve fibre degeneration had subsided. The areas of gliosis coincided with the areas of Marchi staining for degenerating myelin and with areas of myelin loss in osmium tetroxide post-fixed tissue. Histological observations were consistent with astrocytes replacing areas of extracellular space that remained after nerve fibre degeneration. it is concluded that astrocytic gliosis is a prominent and persistent alteration of the spinal cord of horses with chronic cervical compressive myelopathy.     

Polioencephalomyelitis in cats.

Six cats with chronic progressive neurologic signs of ataxia, paresis, tremors, pupillary abnormalities and seizures had polioencephalomyelitis of probable viral origin. Lesions were most severe in the spinal cord. The uniformity in distribution and nature of the lesions in all six cats strongly suggested a common cause. The condition was compared with other viral infections of known and unknown cause.     

West Nile virus infection in horses,Indian ocean

The circulation of West Nile virus (WNV) in horses was investigated in the Southwest Indian ocean. In 2010, blood samples were collected from a total of 303 horses originating from Madagascar, Mauritius, Reunion and the Seychelles and tested for WNV-specific antibodies. An overall seroprevalence of 27.39% was detected in the Indian Ocean with the highest WNV antibody prevalence of 46.22% (95% CI: [37.4–55.2%]) in Madagascar. The age and origin of the horses were found to be associated with the WNV infection risk. This paper presents the first seroprevalence study investigating WN fever in horses in the Southwest Indian Ocean area and indicates a potential risk of infection for humans and animals. In order to gain a better understanding of WN transmission cycles, WNV surveillance needs to be implemented in each of the countries.