An Eastern Equine Encephalomyelitis outbreak in Quebec in the fall of 2008 

Eastern Equine Encephalomyelitis (EEE) virus is a rare but highly pathogenic arthropod-borne viral encephalitis caused by an Alphavirus, Togaviridae. In humans and equines, EEE is particularly lethal and survivors are left with neurological impairment. EEE is thought to occur primarily in an enzootic transmission cycle with birds acting as a reservoir host and several species of mosquitos acting as vectors. The Culiseta melanura mosquito is vital in maintaining this cycle (Soghigian et al., 2010). C. melanura is an ornithophilic species that primarily feeds on passerine birds but recent studies indicate that up to 11% of C.

melanura bloodmeals have a mammalian origin, suggesting that it may also act as a principal vector for mammalian species (Soghigian et al., 2010). Historically, this disease has occurred intermittently across the eastern United States, but recent climate change may be responsible for an increase in vector species and more frequent equine outbreaks in Canada (Chenier et al., 2010).

The 2008 Quebec outbreak began in September with an 8-year-old mare being presented to the Equine Hospital of the Centre Hospitalier Universitaire Vétérinaire de l’Université de Montréal for weakness.

Before onset, the mare had no clinical signs. When found that morning she was found, “weak, with head down and tilted to the left” (Chenier et al., 2010, 1011). On arrival, the mare was ambulatory but weak and uncoordinated. Physical examination revealed irregular breathing (28 breaths/min) and heart rate (52 beats/min). Her body temperature and other physical aspects were unremarkable. Neurological tests revealed dorsal strabismus of the left eye and absent menace response, but other reflexes were normal.

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Additional CBC, serum biochemistry, abdominal ultrasonography, and urine analysis diagnostics revealed no abnormalities. Based on poor neurological responses, ofa neurological disease was suspected. Vertebral and skull radiographs, CSF tap, and protein concentration were all normal but “Cytological examination of the fluid showed a strong neutrophilic pleocytosis [618 X 10^6 leukocytes/L: reference range: 0 to 6 X 10^6 Leukocytes/L] without evidence of microorganisms” (Chenier et al., 2010, 1012). The mare eventually became extremely agitated despite support and sedatives and was eventually euthanized due to her continuously deteriorating condition. A necropsy was performed, revealing diffuse flattening of cerebral gyri, which suggested cerebral edema, and multiple hemorrhages were found in the thalamus and along the spinal cord (Chenier et al., 2010). Microscopic examination of the brain revealed necrosis, satellitosis, gliosis, and spongiosis. Cerebral and visceral tissues were later found positive for EEE by the immunoperoxidase test and culture, ruling out any diagnosis for West Nile or rabies. Between September 1st and October 14th, 19 cases of EEE were confirmed in Quebec, by viral culture, PCR, immunohistochemistry, and/or serology tests. In each case, the horses had similar microscopic lesions of varying degrees but not all had evidence of neutrophils in the brain. Of the 19 affected horses, only one survived with almost no issues following symptomatic treatment. None had been vaccinated against EEE. During this same period, a local emu farm reported a loss of half of its population. Infected emu exhibited similar neurological signs. A necropsy was performed on 3 of the emus, revealing severe necrosis and hemorrhaging. PCR and viral isolation confirmed EEE in all three birds. An entomological survey was attempted in October of 2008 but only 118 specimens were captured due to the freezing conditions (Chenier et al. 2010). Quebec’s freezing climate no longer provided hospitable conditions for the vector species and most likely led to the end of the 2008 outbreak.

Despite a rise in EEE outbreaks, there is no known cure for EEE, only symptomatic treatment consisting of corticosteroids, anticonvulsants, intravenous fluids, tracheal intubation, and antipyretics (Kumar et al., 2018). Vaccines containing the killed virus are available and are frequently used in the United States but were not used in Quebec (Chenier et al., 2010) which may have led to the outbreak of 2008. Elimination of mosquito breeding sites and insecticides are also common preventative measures taken in areas that a susceptible to EEE.

Reference:

1. Chénier, S., Côté, G., Vanderstock, J., Macieira, S., Laperle, A., & Hélie, P. (2010). An eastern equine encephalomyelitis (EEE) outbreak in Quebec in the fall of 2008. The Canadian veterinary journal = La revue veterinaire canadienne, 51(9), 1011-5.
2. Chénier, S., Côté, G., Vanderstock, J., Macieira, S., Laperle, A., & Hélie, P. (2010). An eastern equine encephalomyelitis (EEE) outbreak in Quebec in the fall of 2008. The Canadian veterinary journal = La revue veterinaire canadienne, 51(9), 1011-5.
3. Kumar, B., Manuja, A., Gulati, B. R., Virmani, N., & Tripathi, B. N. (2018). Zoonotic Viral Diseases of Equines and Their Impact on Human and Animal Health. The open virology journal, 12, 80-98. doi:10.2174/1874357901812010080