On Aug. 1, 2002, a 12-year-old Tennessee Walking Horse gelding was observed in the field for the primary complaints of pyrexia,
inappetence and colic.
Eleanor Lenher, DVM
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.)
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.
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.
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.
At this point, initial differential diagnoses included Eastern equine encephalitis (EEE), West Nile Virus (WNV), equine protozoal
myeloencephalitis (EPM), equine herpes virus, type-1 (EHV-1), Western equine encephalitis (WEE), rabies virus, botulism, and
other infectious encephalitides.
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.
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).