A look back at seven eye-opening equine epidemics in the past 100 years
Outbreak. The word itself can be terrifying, sounding like some kind of prison escape involving dangerous inmates. And in a way, that’s exactly what it is—but on a much larger scale. Billions of pathogens escape their hosts and slip into farms, barns, stalls, tack, equipment, and, inevitably, horses. Worse, they reproduce, sending out more of their destructive kind, wreaking havoc at alarming rates and causing illness, death, and financial losses.
Getting outbreaks under control can be tricky, costly, and frustrating. Some happen because of biosecurity oversights; others occur due to a lack of understanding of how diseases function. Some even occur as a result of malicious intent.
The history of equine science is full of stories about devastating outbreaks. While their trails of destruction are tragic, their tales of management and resolution are heroic. Join us as we look back at some of the world’s most legendary equine outbreaks and what we’ve learned from them.
S. zooepidemicus in Iceland
When it comes to keeping diseases out, Iceland leads the planet. The isolated country of fewer than 500,000 inhabitants benefits from hundreds of miles of surrounding ocean to keep it free of diseases that are endemic elsewhere. And its import rules are strict, clear, and simple: No horses enter. Ever. That’s it. No horses have been allowed into Iceland in the past 1,000 years. The country has one breed of horse—the Icelandic—and it’s a product of historical local development, with no outside influences from any other breed. In fact, the import rule is so strict, even horses leaving Iceland for an international competition can never come home.
In addition to this rigid closed-door import policy, the government has set up tight control measures to keep diseases out. If you’ve been on a farm before traveling to Iceland, you must disinfect any clothes or equipment you bring with you. Better yet, leave it at the farm and buy new ones that have never touched a horse. Iceland doesn’t have many of the most common equine infectious diseases. And they aim to never get them.
But 2010 was a strange year for Iceland. In mid-April, the Eyjafjallajokull volcano erupted, spreading ash and gases across the island. Researchers warned that hydrogen sulfide and ash could provoke bronchial constriction, cough, and bronchitis among the country’s horses. So when horses started coughing and having snotty noses, some owners suspected volcanic ash was to blame.
But the signs didn’t add up. Stabled horses were more seriously affected than horses living outdoors. And horses beyond the ash cloud’s path were getting sick. By early May competitions were being canceled to contain what was clearly an infectious disease.
“Initially, the Icelandic vets thought that a virus, such as equine herpesvirus (EHV), was causing the disease,” says Andrew Waller, PhD, head of bacteriology at the Animal Health Trust (AHT), in Newmarket, U.K. “Samples were sent to labs all over the world to screen for different viral pathogens (disease-causing organisms), but none matched up with cases of disease.”
Clinical signs of Iceland’s “mystery disease” included a dry cough, weakness, shortness of breath, nasal discharge, and, rarely, fever, all lasting up to six weeks. Only a few cases were fatal.
It wasn’t until Waller’s team received isolates from which they were able to finally confirm a diagnosis. The bacteria were about 97% identical to Streptococcus equi, which causes strangles. But Iceland’s sick horses didn’t have strangles. They had “strep zoo,” or Streptococcus equi subsp zooepidemicus.
Worse, they were spreading it among each other at epic rates because they were stabled in close quarters and working in indoor arenas over the country’s long, dark winter.
“Full genome sequencing of 257 isolates of Iceland’s S. zooepidemicus, in collaboration with the Wellcome (Trust) Sanger Institute, showed very few changes in the pathogen across the country,” Waller says. “This close identity confirmed there’d been rapid spread of a single strain,” which they named ST209.
Researchers have also identified ST209 in Scandinavian horses, a person in Finland, an Icelandic cat, and a woman in Iceland who miscarried. “The pathogen could have come into Iceland inside a human,” he says. “But the most likely scenario is that it traveled on clothing or riding equipment that hadn’t been properly cleaned according to the biosecurity rules.”
Scientists used the information from laboratory testing to manage the epidemic, which was “extremely interesting from a scientific perspective,” says Waller. They were particularly curious about how one pathogen could quickly spread across an entire country of naive (never previously exposed) horses. But the experience also reminded officials about Iceland’s vulnerability to such diseases and the importance of upholding its stringent biosecurity policies.
“This epidemic highlighted just how susceptible the special population of horses in Iceland are to new diseases that they have not encountered before,” he says. “The import regulations in Iceland were already tough, but these measures have been further tightened to avoid more dangerous diseases, such as strangles, from making the trip to this incredible land of fire and ice.”
Flu in Australia
Three years before Iceland’s strep zoo outbreak, another island country full of naive unvaccinated horses fell victim to a devastating epidemic. This time it was Australia, when equine influenza slipped past its tough biosecurity firewalls.
In early August 2007 imported horses from the U.S., Japan, the U.K., and Ireland arrived in two quarantine stations in Australia for their mandatory two-week stay. Per protocol, they were all tested for specific antibodies (blood proteins horses produce in response to vaccination and exposure that the immune system uses to fight disease), including those against equine influenza—which is critical because Australia is one of only three officially equine-flu-free countries (the other two are Iceland and New Zealand). One of the imported horses at the Eastern Creek Quarantine Facility, in Sydney, New South Wales (NSW), had no evidence of antibodies against equine influenza, even though he’d been properly vaccinated prior to arrival (which is required for incoming horses).
Within days the horse fell sick with fever and respiratory signs, and testing showed he’d seroconverted to positive (developed antibodies) for flu while in the quarantine station. That meant he’d picked up the disease from another imported horse. Two other horses in the same quarantine stable were also sick, says Martyn Jeggo, PhD, director of the Australian Animal Health Laboratory, in Newcomb, Victoria.
Then the flu virus popped up a few days later at an equestrian event 100 miles away in Maitland, New South Wales. With spring’s emergence in the Southern Hemisphere, riders and horses were heading into the competition season in enthusiastic droves. And the virus took full advantage of that movement. Horses that had attended the Maitland event were falling sick in their home stables, spreading the virus to their stablemates, which were transported to other events before owners realized the risk. Equine influenza spread through NSW and south into Victoria like a bushfire.
What happened? How could this country in the middle of an ocean that hadn’t encountered equine influenza in recorded history suddenly have such widespread disease in less than two weeks? Where did it come from? And how did it get out of quarantine?
Those are questions researchers investigated for years. Their best guess is the virus was imported with Japanese horses—since Japan had its own epidemic (its first since 1977) at the same time. If the horses imported from Japan in August 2007 were infected, they would have picked up the virus about a week before Japanese officials discovered the epidemic. But it’s also possible the virus came into Australia with American horses, because the Japanese flu epidemic came from horses imported from the U.S. into Japan. Either way, even if the Japanese and U.S. horses were vaccinated according to protocol, they could have picked up a strain the vaccine didn’t prevent, Jeggo says.
“Grievous” biosecurity breeches—such as a farrier not washing his equipment between horses—could have led to the disease’s spread within the quarantine facility and beyond, says Debra C. Sellon, DVM, PhD, Dipl. ACVIM, director of the Veterinary Teaching Hospital at Washington State University, in Pullman.
Australian authorities did blame biosecurity oversights within the Eastern Creek facility for the outbreak after comparing that facility to the country’s other quarantine station, where the flu virus was contained. Horses there had been exposed to the virus, as testing showed, but did not fall ill or spread the disease. However, researchers were never able to determine exactly how the virus got out of the Eastern Creek quarantine station.
What followed was mobilization of the largest animal health emergency effort in Australian history. As soon as veterinarians diagnosed the first horses from the Maitland show, authorities shut down all equine movement. Wherever horses were, they stayed—even if they were away from home. Absolutely zero movement was allowed, with strict enforcement.
“Extraordinary efforts were taken to contain the outbreak … and to prevent it from reaching the wild Brumby population,” says Anne Jackson, MA, VetMB, PhD, MRCVS, of the Australian Veterinary Association. “Drivers of horse floats or small trucks who seemed to think that the movement restrictions either didn’t apply to them or that a quick trip home into Victoria wouldn’t be noticed, were highly surprised to find that all 32 border crossings at the Murray River between NSW and Victoria were manned 24/7 with armed guards. Nothing equine was going to cross that river.”
Meanwhile, the country initiated a vaccine campaign, inoculating 140,000 horses in an emergency effort. As the world’s horse industry watched, wondering if Australia would ever recover its flu-free status, veterinarians and authorities kept going full force—quarantining, enforcing movement restrictions, vaccinating, tracing, keeping records, washing and sterilizing, and educating.
Their program worked. By December 2007, just four months after the first case diagnosis, disease spread had ceased. In February 2008 the World Organization for Animal Health (OIE) officially declared Australia once again free of equine influenza. In all, the disease had hit 10,000 properties, infecting around 50,000 horses and covering 100,000 square miles.
“This epidemic led to real lessons in biosecurity,” Sellon says. “People weren’t paying attention to the details. It’s phenomenal to see how just little mistakes in biosecurity can impact so many horses in the entire country. And the tiniest little lapse can cause this kind of economic devastation to an industry. When they were in the middle of that epidemic, I honestly had my doubts as to whether they would get it eradicated again, but they did. That was a pretty amazing effort.”
Equine Viral Arteritis in North America
Scientists at the University of Kentucky’s (UK) Department of Veterinary Science, in Lexington, first isolated the equine arteritis virus (EAV) in 1953 after an extensive outbreak in Ohio that caused mares on a Standardbred breeding farm to abort and other horses to develop respiratory disease. The disease—equine viral arteritis (EVA)—subsequently spread to farms in Pennsylvania, California, and Kentucky. However, it attracted little attention nationally or internationally for 31 years, says Peter Timoney, PhD, FRCVS, professor and former department chair and director of UK’s Gluck Equine Research Center and an OIE-recognized expert on EVA.
In 1984 EVA mysteriously resurfaced, this time in Central Kentucky. The virus appeared on a Thoroughbred breeding farm housing 17 stallions, though no one has ever figured out where it came from. All 17 stallions became infected—some with severe clinical signs—but none died. However, the disease spread via the stallions’ semen to 41 Thoroughbred breeding farms throughout the region. The industry was hit hard, with hundreds of sick horses and aborted foals that season.
“This outbreak resulted in an unprecedented response from the international horse community and national veterinary authorities around the world,” says Timoney. “The uncertainty over how far this infection would spread led to a unique action, taken by France, the U.K., and Ireland, to impose an embargo on the import of all horses from the U.S. into their countries, until the industry in Kentucky had the opportunity to bring the situation under control.”
One month later the countries lifted the embargo. “But that was succeeded by some of the most stringent import requirements seen yet in the international breeding industry, and other countries followed suit,” he adds.
Until then, the only country that required EAV testing was Japan, as it had tested its horse population in the 1960s and found it to be entirely seronegative for the virus. Timoney says it took the 1984 outbreak to make international breeders impose strict requirements for EAV testing in imported horses.
This outbreak was a landmark event for another, equally significant reason. It was the first time researchers understood that stallions could become carriers of the disease.
“We tested a significant number of Standardbred stallions between 1984 and 1998 and found that 69% were seropositive for antibodies to the virus,” Timoney says. “Where it was possible to obtain sequential semen samples over time, it was found that the majority were long-term carriers. Some were likely lifelong carriers.”
There’s no treatment for the carrier status, aside from castration.
“This event helped us understand the significance of the carrier state and importance of the carrier stallion as the reservoir of EAV,” he says. “We’re talking about the ability of the long-term carrier animal, showing no clinical signs of disease, to serve as a highly effective means of dissemination of the virus during a breeding season, and also to ensure its perpetuation for years and years.”
Because of this discovery, the OIE made EVA “one of its most regulated diseases,” Timoney says.
A subsequent outbreak at the Arlington Park racetrack, in Chicago, in 1993 exposed more than 1,600 horses to the disease, resulting in at least 200 clinical cases, he says. “What was significant about that outbreak was that, unlike the 1984 outbreak that was spread via the venereal route, this outbreak spread almost exclusively via the respiratory route.”
Equine viral arteritis hit the North American breeding industry on a large scale once again in 2006, when one of the most sought-after Quarter Horse sires contracted the disease in New Mexico. “Within two to three weeks, the virus had spread through shipped fresh-cooled semen to 18 American states, as well as Canadian provinces,” Timoney says. “That event was associated with clinical outbreaks of EVA, outbreaks of abortion, deaths in neonatal foals, and exposure and infection of stallions, a percentage of which became long-term carriers. It was an event of major importance and significant economic impact.”
Contagious Equine Metritis in Ireland
In the 1970s in Ireland, the Thoroughbred horse racing industry was in full swing, having developed out of a long and rich cultural history of gallop and hunt racing that began more than 2,000 years ago. But starting in 1975, Thoroughbred mares on an Irish stud farm developed signs of a venereally transmitted disease. They had purulent (containing pus) vaginal discharge, reproductive tract inflammation, and temporary infertility.
Researchers sought an explanation for a disease that seemed very different from other known infections of the mare’s reproductive tract. They collected endometrial swabs and cultured them in standard laboratory conditions. But nothing revealing grew out of those cultures. For two years the industry struggled with this curious infection, which became known as contagious equine metritis (CEM), all the while spreading it unknowingly within Ireland and the U.K. and introducing it into Australia.
“The main infectious agent that showed up on cultures was Proteus mirabilis, a very common environmental contaminant,” Timoney says. Proteus is an opportunistic bacterium that can cause urinary tract infections in humans and horses. But it likely wouldn’t cause the discharge and infertility these breeders were dealing with.
It took the insight of a sexually transmitted disease specialist (Dr. Eddie Taylor, in Cambridge, U.K.) to recognize the similarities between the mares’ signs and those of women suffering from gonorrhea. “What was especially telling was that it was the mare that was infected and became clinical (showed signs of disease) following exposure to the bacterium, but not the stallion,” Timoney says. “The stallion was an asymptomatic carrier of whatever the causal agent was.”
So Taylor tried a different culture technique, using “more enriched media” for the genital swabs and an environment that included 5 to 10% carbon dioxide, in hopes of bringing out a different bacterial growth. The outcome was a game changer, says Timoney. Under such conditions a small, delicate bacterium grew on cultures from clinically affected mares in three to four days. “The true cause of CEM was identified and subsequently classified as Taylorella equigenitalis, in recognition of the person who first discovered it,” says Timoney.
Targeted antibiotic treatment cured the mares easily. In 1978 the Thoroughbred breeding industries in the U.K., France, and Ireland developed a Code of Practice to prevent and control CEM, which was eliminated from those countries’ Thoroughbred breeding populations within several years.
African Horse Sickness
Deadly African horse sickness (AHS) devastates working equids every year. Endemic in sub-Saharan Africa, it has mortality rates as high as 95% in naive populations. Vaccines exist; treatments don’t.
The AHS virus spreads via biting midges that thrive in the sub-Saharan climate—a fact that, for a long time, reassured researchers that AHS was unlikely to become established in Europe. We now know that’s not true due to factors such as climate change and the globalization of animal movement and trade. But even before this became apparent, a devastating AHS outbreak in southern Spain alerted scientists to a frightening reality: It’s not just African midges that can carry the virus.
“The transmission did not just occur with its regular midges from Africa; it looks like there were other species, more common in Northern Europe, that were involved,” says Simon Carpenter, PhD, head of the Entomology Group at the U.K. Biotechnology and Biological Sciences Research Council Pirbright Laboratory, in Woking, Surrey.
It happened when a central Spanish zoo received a shipment of imported zebras from Africa in 1987. The zebras had likely been recently bitten by infected midges and were carrying the virus when they entered Spain. But unlike horses, zebras show no clinical signs of infection. They don’t get sick, and they don’t die. They just act as healthy reservoirs, with midges feeding on their blood, then transmitting the virus to susceptible horses, which do get sick and die.
Shortly after the zebras arrived, Spanish riding horses in the area started getting seriously ill and dying. Their owners were shocked and devastated, helplessly watching their horses struggle with painful clinical signs ranging from pulmonary distress to heart failure and die as foam discharged from swollen lungs through the horses’ nostrils. Veterinarians were confused, distraught, and frustrated, unable to cure or even treat their clients’ show horses and beloved companions.
“While the disease was identified relatively rapidly, most vets had no experience in combating the virus and had no idea what they were up against,” Carpenter says. “The main hope was that AHS would die out over winter, as it had done in previous outbreaks, although there was also a concerted vaccination campaign.”
Authorities managed as best they could under the circumstances, he says, holding out for when, theoretically, the midges would die or hibernate through the cold season.
Despite that outbreak being quite localized and more than 38,000 horses being vaccinated in 1987, AHS re-emerged in 1988 far to the south of the initial cases. “This may have been a consequence of a horse movement and then local transmission,” Carpenter says. “It’s a very visual disease, lots of hemorrhaging, very traumatic to see, and the first thing an owner wants to do is get his horse as far away from the disease as possible. But if their horse was already exposed and just wasn’t symptomatic yet, he was carrying that virus to wherever his owner tried to take him, spreading it more.”
African horse sickness reached Portugal and Morocco that year, bringing the total number of horses killed to approximately 2,000 by winter.
Despite vaccination, it took two more years—and cost the lives of 3,000 Spanish horses—but Spain finally eradicated AHS from its territories. “The real lesson of the outbreak was to realize that, contrary to what we thought, virus could overwinter consistently, over extended periods of time,” says Carpenter. “Even with effective vaccines, these outbreaks were incredibly challenging to deal with.
“This outbreak gave the worldwide veterinary community a real lesson in the importance of recognizing diseases that aren’t typical to your home area,” he adds. “Certainly in 1987 the number of people in Europe with experience in AHS was limited, and that led to serious limitations in our efforts to control it.”
Major equine disease outbreaks are extremely rare. But when they happen, they serve as unforgettable lessons in biosecurity and disease management. Prevention includes strict adherence to vaccination, screening, and disinfection protocols. Containing the outbreak requires good communication and education in local—as well as foreign—diseases.
“You don’t want to be the veterinarian that saw that case and didn’t recognize it for what it was,” says Sellon.