The day prior, he, along with other horses on the property, was administered his first West Nile vaccine. That day he was noticeably quieter and did not exit his stall as readily as usual. The morning of Aug. 1, his owner noted he had not eaten his grain, his rectal temperature was 104 degrees F, and he was pawing and demonstrating signs of abdominal pain.
His vaccination history was unknown prior to purchase; since purchase he had only received the recent West Nile vaccination. (The horse was purchased in Florida and brought to North Carolina six months prior to examination.)
Vitals During his examination his mentation appeared obtunded, his heart rate was 60 bpm, his respiratory rate was 14 bpm, and his rectal temperature was 102 degrees F. His mucous membranes were dry, petechiated, dark red with a yellow hue, and injected with a toxic line. His capillary refill time was greater than 2 seconds. Gastrointestinal auscultation revealed decreased to absent borborygmi in all four quadrants. Digital pulses were within normal limits. Rectal palpation was unremarkable. Nasogastric intubation revealed no nasogastric reflux. Blood was collected for complete blood cell count and biochemical profile and colic treatment was initiated at this time.
Based on the physical exam, hospitalization and supportive therapy were recommended. The owner declined due to financial constraints.
Recommendations The owner was instructed to monitor closely the horse's attitude, comfort, rectal temperature, water consumption and appetite. The owner was urged to call immediately for further recommendations if the horse didn't improve or if it deteriorated. Shortly following treatment, the horse appeared to be more comfortable and less obtunded. Mild hypocalcemia, mild hyperglycemia, and evidence of moderate dehydration and anorexia were the only remarkable findings identified on bloodwork.
The owner reported that as the day progressed the horse seemed to deteriorate; he was subsequently admitted to the hospital at 10 p.m. that night for further treatment. More aggressive treatment was initiated and he seemed to improve.
However, the following morning he began to show signs of urinary incontinence and became severely ataxic, developed unilateral facial nerve paresis on his left side, and had intermittent episodes of facial muscle twitching. Although he appeared aware of his surroundings and responded to auditory and visual stimuli, his mentation was obtunded.
Revised treatment More blood work was performed and treatment was initiated to address his changing symptoms. He was offered a bran mash and hay but did not show interest in it. Upon recognition of neurological disease, standard isolation protocol was initiated and serum samples were collected for available diagnostics of suspected etiologies of acute onset neurological diseases.
Corporate support Although the WNV vaccine is a killed virus, communication with Fort Dodge was initiated because of the proximity of the WNV vaccination to the onset of clinical signs. Even though the likelihood of vaccine-induced encephalitis was very low and no vaccine reaction similar to this case had been reported, Ft. Dodge offered complete support for diagnosis and treatment of this case. This enabled hospital care to continue beyond the owner's financial limitations.
Clinically the horse deteriorated rapidly over the following 48 hours with progression of bruxism, recumbency and dementia. He continued to demonstrate intermittent pyrexia. Supportive therapy was continued until humane euthanasia was elected, and the corpse was submitted to Rollins State Laboratory for post-mortem examination. The post-mortem examination, conducted that day, revealed a definitive diagnosis of rabies.
Familiar signs This horse's clinical signs could have fit many neurologic diseases including rabies. Horses infected with rabies may present with any combination of clinical signs. Undulating fevers are not uncommon and colic is often the first noticed sign. Ataxia, visual deficits, hyperesthesia, hind limb paresis, lameness, extra ocular muscle spasms, hyperactivity, aggressive, and/or erratic behavior are some of the more common complaints. Hydrophobia is not common in equids.
Diagnosis is made by postmortem examination of the brain. Fluorescent antibody testing is used to identify rabies antigen in the brain tissue. If this test is negative, histopathology is performed and can be used to identify pathopneumonic intracytoplasmic inclusions (Negri bodies).
Horses have a very low incidence of rabies. CDC's 2000 surveillance report notes the incidence of rabies in horses declined 100 percent from 1999. Domestic animals account for a very low number of rabies cases per year, less than 10 percent. Cats have the highest incidence of rabies in all domestic species. Because of the statistics, rabies was low on the differential list in this case. However, it should never be ruled out in a neurological case with acute onset and rapid decline of the patient.
Clinical signs of EEE, WEE, and VEE are similar to each other. Acutely, the horse may have a fever or inappetence. WEE may not progress beyond this acute phase of the disease. In EEE signs become more severe and usually lead to death. These signs are consistent with central nervous system disease and can include undulating fever, behavioral changes, head pressing, aimless wandering, and blindness. Cranial nerve dysfunction may be seen as well.
Tricky diagnosis Antemortem diagnosis is difficult. Acute serum titers and convalescent serum titers can be used, as can complement fixation and cross-serum neutralization assays. Results must be considered with vaccination history. CSF analysis along with virus isolation can be used as well.
WNV has clinical signs similar to the encephalitides as well. Signs include listlessness, stumbling, incoordination, partial paralysis, weakness or ataxia of hind limbs and death. Many horses can be exposed without developing clinical signs. WNV can be diagnosed through serum or CSF, IgM, ELISA or PCR.
EPM has variable clinical signs. Acute infections with EPM can lead to recumbency. An insidious onset of the disease can be lameness, or signs of spinal cord disease. CSF sampling for Western blot analysis is necessary for diagnosis.
EHV-1 usually occurs in outbreaks. Alteration in rear limb gait is usually the first indication of the virus. Lesions of the caudal spine are most common, resulting in ataxia, urinary incontinence and paralysis. Diagnosis is usually made from clinical signs and number of horses involved in an outbreak. Virus isolation is required for antemortem diagnosis. Acute and convalescent serum titers may also be performed.
Prevention paramount Prevention is the best treatment for most of the neurological diseases mentioned in this case report. Efficacious vaccines are available for EEE, WEE, VEE, rabies virus, and EHV-1. The WNV vaccine is now available and initial studies are promising for efficacy.
As with management of any horse with neurological disease, this case was very labor intensive. Fort Dodge generously supported this case. To date the horse has shown no significant reactions to the WNV vaccine but Fort Dodge diligently pursues any cases that could be related to the WNV vaccination. (Editor's note: The FDA recently granted Fort Dodge an unconditional license for West Nile - Innovator.)
Other contributors to the case include Heather Burkhardt, DVM, attending clinician; Laura Kellam, DVM; and Ali Morton, DVM. Sarah Kohn, Michelle Martin, Cindy Hudson and Csaba Foldvari-Nagy provided technical support for the case.