Clinical West Nile virus infection in 2 horses in western Canada

Abstract

Two horses had a history of ataxia and weakness or recumbency. One recovered and was diagnosed with West Nile virus (WNV) infection by serologic testing. The other was euthanized; it had meningoencephalomyelitis, WNV was detected by polymerase chain reaction. West Nile virus infection is an emerging disease. Year 2002 is the first year in which cases have been seen in Saskatchewan.

Case 1

A 9-year-old quarter horse gelding was presented to the Western College of Veterinary Medicine (WCVM) in October 2002, with a history of acute onset of ataxia. The horse was kept on pasture with another horse, which was apparently normal. The horse had been vaccinated against Eastern, Western, and Venezuelan equine encephalomyelitis and dewormed on regular basis. There was no history of travel outside Saskatchewan. No mosquitoes had been observed on the horse’s pasture for 10 d prior to the onset of clinical signs. The owner reported that the horse was unstable on all 4 limbs, stood with its neck arched, and showed muscle fasciculation on the face, especially the upper lip, but continued to eat and drink.

On physical examination, the horse was depressed, interspersed with periods of hyperresponsiveness. Vital signs were normal. Muscle fasciculation was noticed over the face, particularly the upper lip, the trunk, and the limbs. Neurological examination revealed normal cranial nerve function. The horse was very ataxic with both weakness and proprioceptive deficits affecting all 4 limbs. When he was circled, he pivoted on the hind limbs, crossed the fore legs, and occasionally stepped on himself. Based on these signs, a multifocal neurological lesion affecting both brain and spinal cord was diagnosed. The most likely differential diagnoses for these signs in the Saskatchewan area included West Nile virus (WNV), Western equine encephalomyelitis, equine herpes virus (EHV1) infection, rabies, and possibly hepatoencephalopathy.

A venous blood sample was submitted for a complete blood cell (CBC) count, serum biochemical analysis, immunoglobulin (Ig)M capture enzyme-linked immunosorbent assay (ELISA) for WNV, and measurement of the antibody titer to EHV1. The CBC count and serum biochemical analysis revealed no significant findings. The assay for WNV revealed a high serum titer of IgM antibodies to WNV, consistent with an acute infection. The antibody titer for EHV1 was not consistent with infection. Attempts at a lumbosacral cerebrospinal fluid tap were unsuccessful.

The horse was hospitalized in a stall with extra bedding. The clinical signs improved after the 2nd day and the horse maintained a good appetite. Twitches and hyperesthesia gradually disappeared and the horse became stronger on all 4 limbs. The horse recovered and was discharged 8 d later with mild weakness of the hind legs, which resolved 7 mo later.

Case 2

A 16-year-old quarter horse mare was admitted to the WCVM in September 2002 with a history of neurological signs. She had been vaccinated against tetanus and Eastern, Western, and Venezuelan equine encephalomyelitis. She was born and raised in Saskatchewan and kept on a pasture close to Regina in which there had been a mosquito problem during the late summer months. The only other horse on the pasture, a geriatric gelding thoroughbred, had been euthanized by the owner 10 d previously because of involuntary recumbency and suspected colic; no diagnostic testing had been performed.

The mare had been found in lateral recumbency with normal mentation early in the morning. She vocalized in response to the other horses on the premises and ate food when it was offered. During the next 12 h, the mare’s responsiveness to stimuli decreased and she began to thrash uncontrollably. She was heavily sedated with xylazine (Rompun; Bayer, Toronto, Ontario), 500 mg; acepromazine (Acepro-25; Bimeda-MTC, Cambridge, Ontario), 100 mg; and ketamine (Ketalean; Bimeda-MTC), 1 g, IV, and referred to the WCVM.

At presentation, the mare was in lateral recumbency and unable to maintain sternal recumbency, even with assistance. She was unresponsive to most stimuli. The right side of the face was badly bruised and swollen. Body temperature was 35.6°C, heart rate 68 beats/min, and respiratory rate 16 breaths/min. Because of the mare’s semicomatose state, only a rudimentary neurological examination could be performed. The pupils were mydriatic with a slight menace response. The tail was flaccid and the rectum full of feces, but some anal tone was present. The muscles of the hind end were tense and firm. The clinical signs could be explained by multifocal CNS dysfunction, which could be due to neurological disease, aggravated and intensified by iatrogenic anesthetic and tranquilizer administration.

Results from a CBC count indicated a left shift without neutrophilia and lymphopenia. There were elevated concentrations of serum creatine kinase, aspartate aminotransferase, sorbitol dehydrogenase, glucose, urea, and creatinine.

The mare did not respond to therapy and was euthanized about 24 h after the clinical signs had first been observed.

At necropsy, the mare was in good body condition, but the abdomen was gaunt. The only gross lesion was bruising on the right side of the face and swelling around the right eye, consistent with self-trauma when recumbent.

On histopathological examination of sections of brain and spinal cord, stained with hematoxylin and eosin, severe meningoencephalitis was observed. There was a moderate perivascular lymphocytic infiltration throughout the brain and in the cervical spinal cord. There were mild focal accumulations of glial cells in many areas. In the midbrain, there were more severe multifocal mononuclear cell infiltrations with variable numbers of neutrophils, as previously described (1). In the white matter of the cerebellum, there was a locally extensive area in which there was mineralization in the walls of blood vessels and in the brain parenchyma, which was considered an incidental finding associated with aging. There was congestion in the lung and spleen, consistent with barbiturate euthanasia. No other microscopic abnormalities were detected in other organs.

The results of testing brain samples sent to the Animal Disease Research Institute, Canadian Food Inspection Agency, Lethbridge, Alberta, for rabies by the fluorescent antibody technique (FAT) and tissue culture were negative. West Nile virus was detected in the brain tissue by the polymerase chain reaction (PCR) at the Manitoba Agriculture and Food Veterinary Services Laboratory in Winnipeg, Manitoba, and at the Prairie Diagnostic Services Laboratory in Saskatoon, Saskatchewan.

West Nile virus infection is an emerging disease in Canada. In North America, it was seen first in New York City in 1999 (2). These 2 cases of WNV infection in the late summer and early fall of 2002 are the first to be reported in western Canada.

West Nile virus is an arbovirus from the family Flaviridae. It is carried by mosquitoes and causes meningoencephalomyelitis in horses (2). However, infection with WNV can be subclinical (2). In WNV infection, weakness or ataxia is common; seizures, head pressing, and coma are rare clinical signs (4). Acute onset of ataxia, sometimes resulting in recumbency, muscle fasciculations, and changes in mentation are common in WNV infection (2,3,5–7). Results from a CBC count and serum biochemical analysis in cases of WNV infection are usually normal, but CSF examination may reveal mononuclear pleocytosis and a high protein concentration of protein; however, CSF examination findings can be normal (8).

The differential diagnoses of WNV infection in horses include equine protozoal myeloencephalitis, Western equine encephalomyelitis (WEE), rabies, equine herpesvirus (EHV1), and liver disease (hepatoencephalopathy) (3). Equine protozoal myeloencephalitis has not been seen in this geographical area, except in animals that have spent some time in the USA. Clinical signs of WNV infection can be similar to those of rabies; however, rabies is always progressive (2–4). The lesions of WEE are more severe in the cranial areas of the CNS; therefore, abnormal mentation and behavior, seizures, and cranial nerve signs are common clinical signs (4). In cases of hepatoencephalopathy, inappetence, jaundice, and periods of somnolence are common, and serum biochemical findings are indicative of liver failure (3). Specific serological tests are available to detect infection with EHV1, WEE, and WNV (4).

Recent exposure to WNV can be confirmed by using the IgM capture ELISA; other tests that may be used include plaque-reduction neutralization, complement fixation, or hemagglutination tests (6).

In case 2, recumbency and self-trauma were likely the cause of increased muscle enzymes, and the azotemia was consistent with dehydration. In case 1, the consistent good appetite and the fact that the horse did not progress to recumbency were favorable clinical signs. Different treatment protocols for WNV infection have not been compared; supportive care is generally used (1). Prevention and control of the disease can be accomplished by control of the mosquito vector and minimizing exposure of susceptible horses to mosquitoes (5). Administration of an inactivated virus vaccine 2 doses, IM, 3 to 6 wk apart is recommended, with the last dose about 4 wk before the 1st cases are expected that year (4). CVJ