If your horse survives one of these 5 infections, he might still suffer lasting effects.
Every day a passel of pathogens pokes and prods at your horse’s immune system, trying to find a breach in the barrier. Even when horses look like they’re simply grazing peacefully in their paddocks, their bodies are on full defense. On a daily basis, for instance, they might encounter:
- Soil-borne bacteria such as Rhodococcus equi in foals;
- Bacteria such as Leptospira (which causes leptospirosis), which live in pasture puddles, ponds, and streams;
- Mosquito-borne viruses such as West Nile virus and Eastern equine encephalitis;
- Other insect-borne bacteria, such as those that cause Lyme, piroplasmosis, and anaplasmosis from ticks;
- Bacteria or viruses from herdmates or horses coming and going from equine facilities, including herpesviruses, equine influenza virus, coronavirus, Salmonella, and Streptococcus equi subspecies equi (strangles); and
- Parasites such as tapeworms and the causative agents of equine protozoal myeloencephalitis (EPM).
- And as if the pathogens weren’t enough of a threat, there’s also the toxins some can produce—and might be found in forage—that can cause diseases such as botulism.
Your horse often can’t avoid these merciless microbes, which makes an optimally functioning immune system imperative. Luckily, most horses have fully functional immune systems; they just need a boost from time to time, in the form of vaccination, or help from antibiotics or from supportive care such as intravenous fluids, anti-inflammatory drugs, etc. After simple, straightforward infections such as rainrot or run-of-the-mill upper respiratory tract issues, most horses fully recover. In other cases patients potentially suffer long-term effects that negatively impact their performance and quality of life.
In this article we’ll learn which diseases most commonly cause post-infection illnesses, why some linger far past their welcome, and how they can impact long-term health, use, and quality of life.
West Nile Virus (WNV)
This virus crosses the blood-brain barrier and enters the central nervous system (CNS), where the brain and spinal cord lie. The resulting inflammation in these delicate structures can lead to neurologic abnormalities. Typical clinical signs can be as mild as colic, lameness, lack of interest in feed, and fever or as severe as ataxia (wobbly gait) and paresis (weakness from nerve damage or disease) that can render the horse unable to rise, facial and tongue paralysis, behavioral changes/severe mental depression, convulsions, and coma.
Clinical signs of WNV infection in horses that recover can last anywhere from one day to several weeks, but improvement usually occurs within seven days of onset of clinical signs.
“Although 80% to 90% of owners report that the horse returns to normal function one to six months after disease, at least 10% of owners report long-term deficits that limit athletic potential and resale value,” says Maureen T. Long, DVM, PhD, Dipl. ACVIM, professor of virology and microbiology at the University of Florida’s College of Veterinary Medicine, in Gainesville. “Deficits include residual weakness or ataxia in one or more limbs, fatigue with exercise, focal or generalized muscle atrophy (wasting), and changes in personality and behavioral aberrations.”
Eastern Equine Encephalitis (EEE)
Like WNV, EEE can develop when an infected mosquito introduces the virus while having an equine blood meal. But horses infected with EEE have an even worse prognosis than those with WNV. Fifty to 90% of infected horses showing clinical signs of EEE do not survive, with many victims dying within two to three days of disease onset.
After the virus invades the central nervous system, encephalitis (inflammation of the brain) occurs, characterized by signs such as:
- Severe depression and behavior changes;
- Impaired vision;
- Circling or head-pressing;
- Muscle-twitching, paralysis of the cranial nerves that control the facial muscles (frequently apparent as an inability to swallow); and
- Convulsions, paralysis, recumbency, and death.
Veterinarians have noted a high incidence of residual neurologic deficits among horses that do recover from EEE—more than what is seen in horses that have had West Nile virus. In fact, Long says most horses surviving EEE infection exhibit long-term neurologic signs, such as those listed above. When these are severe enough, the horses are often deemed unfit for riding.
Equine Protozoal Myeloencephalitis
Horses pick up the protozoan parasites (Sarcocystis neurona or, less commonly, Neospora hughesi) responsible for this neurologic disease after ingesting contaminated food or water; the parasites’ definitive host, the opossum, sheds them in its feces. The parasites then migrate to the brain and spinal cord and cause inflammation there. While all horses are at risk of infection, not all infected horses develop disease. How many parasites are at play and whether the horse’s immune system is functional or suppressed are key to determining which horses succumb to infection.
Due to the causative agents’ unpredictable travel itinerary through the horse’s CNS and our inability to guesstimate where they might damage the brain and/or spinal cord, there are no “classic” clinical signs of disease. Instead, signs and their severity vary considerably depending on what regions of the central nervous system the parasites damage.
For example, if they damage the brain and cranial nerves, the horse can develop a head tilt, depression, facial nerve paralysis, difficulty swallowing, upper airway dysfunction, dorsal displacement of the soft palate, and even laryngeal hemiplegia (paralysis of the nerve that controls one of the arytenoid cartilages in the airway, which causes roaring). When the brainstem and spinal cord are involved, damage to their gray matter (which processes impulses that, in turn, control muscle movement) and resulting gait abnormalities that can easily be confused with lameness might result in asymmetric muscle atrophy. Often, this degeneration occurs in the quadriceps muscles, which are responsible for extending the stifle joint; gluteal muscles, which control hip motion and limb rotation in the hind end; and the temporal muscles that help close the jaw.
The more damage the parasites cause in a horse’s central nervous system, the higher his chances of either a poor outcome or failure to recover fully following treatment.
“There is a direct link between severity of pathological changes and outcome, including the presence of residual clinical signs despite treatment,” says Nicola Pusterla, DVM, PhD, Dipl. ACVIM, professor of equine internal medicine in the University of California, Davis, Department of Veterinary Medicine and Epidemiology.
Current treatment recommendations include:
- Marquis and Protazil, which both contain the benzene acetonitrile agents diclazuril or toltrazuril. Studies show that 62-67% of horses receiving these drugs might improve one neurologic grade or test negative for antibodies against S. neurona in cerebrospinal fluid (CSF). An estimated 10% of horses relapse following the standard 28-day treatment (Pusterla, 2017).
- ReBalance, a sulfadiazine/pyrimethamine oral suspension that inhibits DNA formation in the parasites. Treatment is long-term (approximately 90 days or more) and might result in an improvement of at least two neurologic function grades in 60-70% of treated horses. Approximately 10% of horses relapse following treatment (Pusterla, 2017).
Pusterla and other EPM researchers say these products’ efficacy is comparable, treatment should continue until no further clinical improvement occurs, and relapse can occur.
“Research in this field is focusing on the impact of extending treatment times, combining the use of these FDA-approved products, using higher doses, prophylactic (preventive) and prolonged/maintenance therapy, and the concurrent use of immunomodulators,” he says.
At this time, however, “there are insufficient data to support any recommendations regarding these strategies,” Pusterla adds. “Owners should follow the products’ and veterinarian’s instructions to achieve the best possible outcome.”
The persistent and tenacious corkscrew-shaped Leptospira bacteria live in water and soil and also reside in infected horses’ reproductive fluids and urine. Horses inadvertently ingest the bacteria, which gain access to the body through the gums and lips. Once they’ve penetrated tissues and accessed the bloodstream, they run amok like unsupervised children at an amusement park. Initial signs of infection include abortion in pregnant mares and kidney disease or jaundice in foals born to infected mares. Many horses, however, show nonspecific mild signs of disease (described by owners as simply fever and malaise) that resolve without veterinary intervention.
Leptospira organisms, predominantly Leptospira interrogans serovars Pomona and Grippotyphosa, have an affinity for the equine eye. Therefore, veterinarians sometimes detect live leptospires in the ocular tissues of horses with recurrent uveitis (ERU), an immune-mediated process that threatens otherwise healthy horses’ vision.
“Ocular manifestation is the most important clinical disease we see in horses with leptospirosis, with over 60% of equine recurrent uveitis cases attributable to this pathogen,” says Ann Dwyer, DVM, a private equine practitioner at Genesee Valley Equine Clinic, in Scottsville, New York.
Examples of typical ERU signs include a “hot,” painful eye (evidenced by the horse holding the eye closed) with light sensitivity, excessive constriction of the pupil (miosis), prominent blood vessels on the surface of the eye, and a green/orange hue in the posterior segment (the back of the eye).
Appaloosas and Warmbloods are genetically predisposed to ERU, but all horses living in temperate climates, particularly river valley regions, are at risk for developing leptospiral ERU.
Researchers don’t yet understand exactly when horses with leptospiral-associated ERU get infected and how long it takes for ocular disease to develop.
“I have always thought it takes months for ocular disease to develop following infection, but I do not have a specific number of months to suggest,” says Dwyer. “In some cases it might take years.
“The problem with identifying the interval from infection to ocular disease is that acute leptospirosis is often a very mild disease,” she continues. “Unless it causes abortion or renal (kidney) disease, leptospirosis is very rarely diagnosed in the primary stage. When I have diagnosed acute disease in practice in horses that are not pregnant, usually the horse has just been a ‘little sick’ and has gotten better quickly.”
Following abortion due to Leptospira infection, some mares have gone on to develop ocular disease, whereas others have not.
Dwyer admits that treatment options, even with the availability of systemic antibiotics, remain limited, making this an extremely frustrating disease to manage.
“Based on my experiences, prognosis for vision loss is probably around 50%,” she says.
Researchers at Auburn University have reported that a very low dose of the antibiotic gentamicin injected into the vitreous (back of the eye) might be promising in some cases. Dwyer warns, however, that “this is not a procedure for untrained practitioners to try.”
A master of disguise, this tick-borne disease continues to burden the equine community. Clinical signs of Lyme disease (borreliosis) can be frustratingly vague because the causative bacteria, Borrelia burgdorferi, can set up camp anywhere in the body, including the eyes and the central nervous system, where they essentially hide from the immune system. This explains why two of the clinical presentations veterinarians associate with Lyme disease in horses are uveitis and neuroborreliosis, the neurologic form.
Signs of uveitis caused by borreliosis include bilateral aqueous flare (cloudy eyes) and miosis. While these might sound similar to leptospirosis-associated ERU, the infections are quite distinct, says Tom Divers, DVM, Dipl. ACVIM, ACVECC, the Steffen Professor of Veterinary Medicine and section chief of large animal medicine at Cornell University’s College of Veterinary Medicine, in Ithaca, New York.
“One cannot actually distinguish between the two infections clinically without testing intraocular fluid samples,” he says. “Nonetheless, Lyme uveitis appears to be more severe and aggressive, causing more rapid blindness, whereas leptospirosis causes recurrent episodes that may eventually lead to blindness.”
Further, leptospirosis-associated uveitis appears to have a genetic component, with some horses more predisposed to developing it than others, while Lyme-associated uveitis does not.
Neuroborreliosis might cause signs of spinous muscle atrophy, difficulty swallowing, respiratory distress, paresis, ataxia, behavioral changes, hypersensitivity to touch and sound, involuntary muscle twitching, and neck and back stiffness and pain. Veterinarians have also reported joint effusion (fluid accumulation), cranial nerve dysfunction, meningitis (inflammation of the membranes surrounding the brain and spinal cord), and irregular heartbeat. These clinical signs can be difficult to interpret because other diseases can cause similar signs.
“Luckily, neither Lyme uveitis nor neuroborreliosis are particularly common,” says Divers. “That being said, many horses are infected with B. burgdorferi but never develop clinical disease. Why only a small number of infected horses develop clinical disease is not well-understood but appears somewhat reminiscent of EPM.”
While veterinarians frequently attribute shifting intermittent lameness and stiffness to Lyme disease, little data exist supporting these signs as part of the clinical disease syndrome. Nonetheless, we know joint involvement is possible because researchers have found B. burgdorferi in synovial membranes inside joints.
Due to a lack of reliable tests to clearly diagnose clinical Lyme disease, predicting whether a horse suspected of having it will respond to antibiotic therapy remains nearly impossible. In many presumptive Lyme cases treated with antibiotics, the vague clinical signs resolve. That said, cases involving neuroborreliosis have a poor outcome, and Lyme-induced uveitis bodes poorly for a horse’s vision. The duration of time from infection to treatment appears to affect case outcome—the longer that gap, the poorer the prognosis, say our sources.
Researchers have demonstrated that horses do suffer from chronic infection, and owners must be aware that horses can be reinfected even after antibiotic treatment.
As miraculous as it is, the immune system can’t be expected to wage its daily war unassisted. Fortunately, many sidekicks exist to help. Reducing stress—a risk factor for most infectious diseases—can improve immune function and decrease a horse’s chance of getting sick. Avoid exposing your horse to mosquitoes and ticks, keep opossums out of your barn and feed in covered containers, and keep up with your horse’s core and risk-based vaccinations to stimulate and prepare his immune system. These approaches are particularly effective when implemented alongside appropriate biosecurity protocols (TheHorse.com/BiosecurityTips).
A healthy and functional immune system helps a horse fully clear infections. Still, some diseases prove more challenging to treat, occasionally resulting in life-altering post-infection disabilities.