Horses usually pick up the virus that causes rabies via bites from infected (rabid) wild animals, such as raccoons, skunks, bats, or foxes. The incubation period varies from a few weeks to several months. The virus likely multiplies at the site of bite and, when it reaches peripheral nerves, rapidly reaching the horse’s brain. Once there it spreads to other organs and tissues and, through cranial nerves, reaches salivary glands and possibly nasal secretions. Once the virus becomes established, its effects are devastating—and irreversible. Clinical signs described in horses are highly variable, but common signs can range from lameness, poor athletic performance, and lethargy to depression, aggressiveness, convulsion, and recumbency (lying down or falling and being unable to rise). With the onset of clinical signs, there’s no effective treatment, and horses should be euthanized. If you see a wild animal exhibiting unusual behavior, contact your local animal control agency immediately to remove the animal. Due to the potential risk of virus transmission from horses and other infected animals to humans, animals suspected of having rabies should be handled by individuals who have been appropriately vaccinated against rabies.

West Nile virus is an infectious agent transmitted via mosquito bites. It infects birds, humans, and horses and other mammals such as dogs. The virus enters the bloodstream and travels to the central nervous system, where it causes brain and spinal cord inflammation and leads to clinical signs within three to 15 days. These include ataxia (incoordination), muscle trembling, depression, lethargy, weakness, and sometimes fever. Disease severity varies, and not all horses develop clinical signs. Among those that do, one-third die from the disease. Among the survivors, 40% have lasting neurologic effects, mainly weakness and ataxia. Thanks to an aggressive vaccination program, the number of WNV cases has dropped in the U.S. An additional way to reduce risk of all mosquito-borne diseases is to control mosquito populations on the farm, by eliminating or reducing mosquito breeding habitats, and in conjunction with your local mosquito control authority.

Dr. Angela Bordin

Angela Bordin, PhD, is assistant professor of immunology and infectious disease in the Department of Large Animal Medicine at Texas A&M University’s School of Veterinary Medicine, in College Station. She specializes in infectious diseases in neonatal foals.

Eastern equine encephalomyelitis is a viral disease that’s also transmitted through mosquito bites. The incubation period can vary from a few days to a few weeks. Clinical signs include high fever; colic; anorexia; and neurologic signs as depression; blindness; ataxia; head-pressing or tilt; recumbency; seizures; sleepiness; circling; and paralysis of the pharynx, larynx, and tongue. Zero to 15% of affected equids survive EEE infection, and those that do usually have lifelong neurologic impairments, such as loss of full control over bodily movements. In the United States EEE occurs mainly in the East, especially in the South, but it has occurred as far west as Texas and as far north as Wisconsin in the Midwest. Birds harbor the virus silently—showing no signs—and act as reservoirs. Mosquitoes that feed on infected birds and mammals transmit the virus from birds to horses and humans.

Like EEE, WEE develops after exposure to the virus transmitted via bites from infected mosquitoes. It causes clinical signs similar to those of EEE. Fortunately, its effects are not quite as devastating: 50% of affected horses can survive a WEE infection. It is important to note, however, that at least half of all WEE cases end in death and neurologic deficits are common among survivors. The WEE geographical region extends west of the Mississippi River. The good news is there have not been recent reports of WEE in horses. The bad news, though, is this doesn’t mean the virus isn’t present. Scientists have detected the virus in birds (which, as with EEE, don’t develop clinical signs but act as inapparent carriers), so the threat of infection in horses still exists.

Tetanus is caused by a potent neurotoxin produced by Clostridium tetani, an anaerobic (not requiring oxygen) bacterium living in soil and feces. Bacterial spores get into the horse’s body through injuries to the skin, both simple—cuts, scrapes, and small punctures—and more serious, such as surgical incisions. (Though we often think of wounds from rusty objects, such as nails and barbed wire, as the source of the bacterium that causes tetanus, it’s the injuries they create that are the offenders. Rust itself isn’t the problem; rather, rusty objects are often found in places that harbor anaerobic bacteria.) Once they gain entry into the boy, the spores produce toxins that reach peripheral nerves (via the bloodstream) and, ultimately, the central nervous system. Clinical signs include muscle spasms, stiffness, extended neck and head, third eyelid prolapse, retracted lips, and an elevated tail. Some horses have difficulty breathing and can become recumbent. Treatment includes muscle relaxants, padding stalls for animals that have difficulty rising, removing infection (surgically and with antibiotics), neutralizing unbound toxin with antitoxin, and ensuring horses stay hydrated and receive appropriate nutrients. Despite treatment, up to 75% of affected horses die.

Dr. Claudia True agrees. “Those horses definitely suffer,” she says. “With encephalitis, for example, they are in such horrible pain, they push their heads into the walls and just don’t even seem to know where they are. One horse with EEE in our practice pushed his head into all four walls of his stall and had rubbed his skin down to raw tissue.” That horse was eventually euthanized, True says. The suffering is particularly tragic knowing how preventable the diseases are, she adds. “After seeing what it looks like for a horse to have one of the diseases, I just can’t imagine why you wouldn’t vaccinate,” she says.