West Nile virus (WNV) is a mosquito-borne arbovirus known to cause severe illness in humans, birds, and horses.

Affected horses can develop inflammation in the brain (encephalitis), as well as neurological symptoms such as head pressing, difficulty swallowing, and poor coordination. [1][2]

Although only 10% of horses infected with WNV show signs of the disease, the mortality rate can be as high as 57% in those with symptoms. [3]

There is no specific treatment for West Nile virus in horses. Management is primarily supportive, aiming to reduce symptoms and prevent complications. [11]

Every year, sporadic cases of West Nile virus are reported across North America. Fortunately, equine vaccines against WNV and mosquito control measures have helped reduce cases in horses. [4][5]

West Nile Virus (WNV) in Horses

West Nile virus (WNV) belongs to a family of RNA viruses known as Flaviviridae. [6] The virus was first isolated in 1937 from a Ugandan woman. Since then, it has spread worldwide and is now a leading cause of viral encephalitis. [6]

In 1999, the first equine case of WNV was reported in the United States, with thousands of cases reported in the following years. [18]

Mosquitoes are the primary vector for WNV, which means they are the main agents that transmit the disease between hosts. Mosquitoes contract the virus from infected birds, and then transmit it to humans, horses, and other animals.

All horses can contract this virus, but unvaccinated, young, and elderly horses face a heightened risk of severe illness. [4]

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Transmission

The transmission of West Nile Virus to horses is facilitated by mosquitoes that contract the virus by feeding on infected birds.

Wild birds are a reservoir for WNV, which means they carry the virus without getting sick. [2][6] Birds also act as amplifier hosts, allowing the virus to replicate. House sparrows (Passer domesticus) and other Passerine birds such as crows and robins have the highest levels of circulating virus in their blood. [3]

Mosquitoes, especially the Culex species spread the virus by carrying it from infected birds to other animals. [3] The virus replicates in the salivary glands of infected mosquitoes. When the mosquito feeds again, it transfers the virus to the next animal. [3]

Mosquitoes only contract the virus from viremic animals. When an animal is viremic, it has a high enough viral load in its blood that the mosquito ingests the virus and becomes a carrier. [3]

In horses and humans with WNV, the viral load in the blood is minimal, making them incapable of infecting mosquitoes. Both species are considered “dead-end” hosts, meaning they do not contribute to the transmission cycle of the virus. This also means that the virus cannot spread from horse to horse, or from horse to human and vice-versa. [1][3]

During the winter, WNV is thought to persist in mosquitoes, and remains at low levels in host species and/or migratory birds. [3] This keeps the virus endemic in the region, leading to new infections the following year.

Disease Outbreaks

West Nile Virus infections in horses can occur as sporadic cases or as outbreaks within a region. The most significant outbreak in North America took place between 1999 and 2002.

The virus was first detected in New York and rapidly spread to Canada, Mexico and the Caribbean. This WNV outbreak resulted in nearly 15,000 confirmed encephalitis cases in horses, 4,000 cases in humans, and the death of 16,500 birds. [3]

To reduce the risk of outbreaks, it is important to remain vigilant for signs of disease in your horse and implement preventative measures.

Pathogenesis of WNV Encephalitis

West Nile Virus infection in horses can lead to encephalitis, which is characterized by inflammation of the brain. Affected horses can develop inflammation throughout the nervous system, affecting the brain, spinal cord, and protective tissues. [5]

The virus is able to cross the blood-brain barrier, to access the central nervous system (CNS). Replication of the virus within the CNS and the ensuing immune response results in damage to neurons and surrounding cells.

The neurological symptoms associated with WNV, such as ataxia (incoordination), arise from infection of the pons and medulla of the brainstem, as well as the neighbouring cranial nerves. [7]

The virus can also replicate in other tissues including the spleen, liver, heart, lymph nodes, and lungs. [3] Although rare, WNV infections can also harm these tissues, as illustrated by a case of WNV-induced hepatitis