by Nancy S. Loving, DVM
Strangles is hardly a new disease, having been recognized as a contagious bacterial problem in horses since the late 18th century. Yet, it still remains a troublesome and persistent issue in the horse world and is identified worldwide. Research has been directed toward developing effective vaccines to control its spread through the horse population, but management strategies are equally important in limiting its presence.
What is Strangles?
Fortunately, most cases of strangles do not become this extreme. An affected horse may stand listless in the paddock and be inappetant. A fever may develop along with myalgia. Most horses that are sick with this disease eventually develop a mucopurulent nasal discharge and/or a cough. The submandibular and/or retropharyngeal lymph nodes often swell to varying degrees. There may be some edema around the face, and breathing may be labored or stertorous. At the onset, the lymph nodes may be very firm and painful to touch, long before they soften and break open to drain a creamy mucopurulent discharge. Typically the lymph node abscesses rupture within a couple of weeks subsequent to the horse showing initial clinical signs of infection. Only half the time do the draining lymph nodes culture positive for the Streptococcus equi organism.1 Identification of the disease is based on clinical signs and probabilities since few other illnesses infect the lymph nodes.
Who Is At Risk?
Strangles is a highly contagious disease, particularly in conditions of stress. This includes situations where horses are housed in crowded areas, or with poor hygiene, or with inadequate nutrition. Transmission occurs via direct contact with nasal secretions or saliva. Flies also spread the disease, as do contaminated fomites such as feed buckets, rakes, and human hands and clothing. The organism can survive in the environment for a couple of months, particularly if shielded from the sun inside of dark barns or within the soil.2 Once established on a property, another outbreak may occur on that farm a year or two later. The infection keeps cycling through horses to the environment and back to horses to become a persistent and frustrating management issue.
Once a horse has been infected with strangles, it is possible for him to continue to shed the organism through nasal secretions for months. Most horses stop shedding within about 6 weeks, but the potential exists for a previously sick horse to carry the infection to others despite appearing to be fully recovered. Nasopharyngeal swabs of suspected carriers or of previously infected horses can help identify those that may be shedding S. equi organisms yet are not exhibiting clinical signs. In one study, the average period of shedding from carriers was 9.2 months, with one horse shedding for as long as 42 months.3 Sixty-eight percent of horses continued to shed for at least four weeks following resolution of clinical signs.3 Seventy-five percent of horses infected by strangles develop a long-lived immunity once they recover from the disease.2
Antibiotics may actually be counter-productive, particularly in the early stages of disease. Antibiotics often suppress the bacteria within the lymph nodes sufficiently for a time, only to have a simmering infection flare when the antibiotics are discontinued. Then the abscesses return and the horse appears sick again. Antibiotic therapy is indicated in certain instances when an affected horse remains persistently off feed and is depressed despite other supportive care, or if the fever remains elevated (greater than 104 degrees Fahrenheit), or if the airway is being obstructed by lymph node swelling, contributing to dyspnea. Once the abscesses rupture, then antibiotic treatment is appropriate to enable the horse's immune system to eliminate the disease. Procaine penicillin (22,000IU/kg bid) still remains the drug of choice in addressing S. equi infections, although tetracyclines, erythromycin, and ampicillin may be useful.
Control and Prevention
In the face of an outbreak, it has been demonstrated that vaccinating non-sick animals can decrease the morbidity by half. This strategy may have limited usefulness in horses that have never before been vaccinated against strangles since in order to ensure the maximum protective effect, the non-sick horses need to receive the full protocol of two vaccines spaced 2-3 weeks apart. This may be too long a time-frame for the horses to develop sufficient protective immunity when directly challenged by the bacteria; it is possible that disease may occur before the second vaccine in the series is given. Horses that have been on a previous strangles vaccine program can be "boosted" with one dose of vaccine, and this should effect some immunity at least to limit the severity of the infection. Pregnant mares should be vaccinated with approved products about a month prior to foaling so the newborn foal will receive protective antibodies in the colostrum.
It is good common sense to isolate any newcomers to a farm for 2-3 weeks just in case they may be carrying a bacterial infection or virus to which the resident horses have not previously been exposed. This allows the new horses to incubate and break with disease before they've had a chance to co-mingle and infect all the others on the farm. Then a disease process can be identified and controlled before too much damage is done. This is especially important where foals, weanlings, and yearlings are involved. In managing herd health for any farm and to minimize casual spread of disease, it is prudent that a new horse be examined and given a health certificate prior to entry on the new premises. Rectal temperatures of new arrivals should be checked twice daily. If S. equi is suspected or is a concern, nasopharyngeal swabs are useful to identify a carrier horse. Ideally, a horse is considered to not be a carrier if it has three negative nasopharyngeal swabs for S. equi over a two to three week period. Nasopharyngeal swab bacterial cultures detect 60 percent of carrier horses while combining this test with PCR (polymerase chain reaction) testing increases detection of carriers to 90 percent. The PCR test detects DNA from both living and dead bacteria so is more sensitive than a bacterial culture which only detects live bacteria that grow on laboratory media.
One of the more difficult-to-identify complications is called bastard strangles. In these cases, the organism spreads to other internal lymph nodes (particularly those of the gastrointestinal tract) or to other organs like the spleen, liver, kidney, lungs, or even the brain. It is often hard to recognize that a horse has bastard strangles until there is an on-going problem with unthriftiness, continued weight loss, poor performance, and listlessness that cannot be explained by any other causes. The results of a complete blood count and fibrinogen level may strongly point to a systemic infection. A rectal exam, an abdominal ultrasound exam, or an abdominal tap may identify the location of an internal abscess. These are hard cases to treat, requiring long term antibiotic therapy.
Another complication that may not become apparent for a time is an infection of the guttural pouch with the development of empyema or chondroids. This could be a life-threatening problem if the infection erodes through the large blood vessels that course through the guttural pouch. Major nerve branches may also be affected in this area creating neurologic problems referable to the cranial nerves. Often the mucopurulent debris that accumulates within the guttural pouch is swallowed as it drains into the pharynx, but sometimes it is visible as a nasal discharge from one or both nostrils. An endoscopic exam and radiographs of the head are useful to detect this problem. Most asymptomatic carrier horses harbor S. equi within their guttural pouches.
Some horses infected with
strangles develop myocarditis. This can be a source of exercise
intolerance and poor performance. An EKG and ultrasound of the heart are
useful diagnostic tools to screen for this problem. Chronic anemia can
also be a complication of a strangles infection, but once the primary
disease is resolved, the heart problems usually resolve with time.
Previously, all vaccination strategies against strangles have relied on intramuscular injections that elicit a systemic immune response. These vaccines have had limited efficacy, only curtailing disease in 60-70 percent of those cases challenged by the organism. In addition, many times the intramuscular injections are accompanied by sore muscles, malaise, and a fever. These secondary vaccine reactions may last for as long as a week. Although these complications occur in a small percentage of horses, many horse owners are concerned by these adverse reactions. Having weighed the risks, many have considered that the intramuscular vaccine is seemingly as bad as the horse contracting the disease. For that reason, use of the strangles vaccine has been limited by horse owners until the advent of the intranasal form.
The intranasal strangles vaccine is given as a series of two doses spaced 2-3 weeks apart. The material is a live avirulent S. equi organism that is freeze dried and then reconstituted with a special diluent just prior to administration. The 2 ml dose is squirted through a nasal canula into a nostril to reach the local area of the upper respiratory tract. This provides the best protective response since it stimulates the production of locally produced antibody at the level of an infectious invasion into the system. This prevents attachment of the organism to tonsil receptors, and may prevent tissue invasion of the organism if it does manage to adhere to the receptive respiratory tissues.
In the clinical trials associated with this product, there was a reduction in the clinical disease observed in vaccinated horses. However, despite "protection" derived from the intranasal vaccine, 40 percent of horses challenged with the organism did still develop clinical signs of disease as opposed to 60 percent of unvaccinated horses that were challenged with the organism. Morbidity was decreased, and of those that did get sick, the clinical signs were reduced by 65 percent as compared to unvaccinated horses. Just as with the intramuscular vaccines, no horse can receive complete protection from the strangles organism when challenged. However the intranasal vaccine shows promise in reducing the number of horses affected and the severity of the infection if it occurs.
There is some concern that giving a modified live organism via the nasal passages could result in shedding from the vaccinated individuals to those who were not. The safety studies performed by Fort Dodge indicated that any slight shedding that may occur does so only during the first day and the organism is not shed to any significant degree. This company feels that "the use of the vaccine is safe in vaccinated horses and for those horses kept in contact with vaccinates." Currently, the vaccine is not yet approved for use in pregnant mares although preliminary data indicates there are as yet no problems.
It is recommended that the intranasal strangles vaccine be administered following vaccination of other intramuscular products during routine inoculations. This strategy may prevent inadvertent contamination of other intramuscular inoculation sites with the avirulent S. equi organisms that could result in the development of injection site abscesses.