Strangles: Identifying the chronic shedder
Kate Hepworth-Warren is an equine internal medicine specialist who currently works as a clinical assistant professor of equine medicine at North Carolina State University in Raleigh. Outside of work, she enjoys traveling, reading, running and the beach.
Clients are often quick to place blame on the new horse for introducing strangles to a herd, but veterinarians who provide appropriate client education can control the pandemonium before it begins.
Strangles is an infectious condition of the upper airway caused by Streptococcus equi subsp equi that can wreak havoc on even the most organized and well-managed equine facility. So named because of the severe upper airway compression that can occur when the retropharyngeal lymph nodes become enlarged, strangles targets younger horses more frequently but can affect horses of any age. It can also be harbored in chronic shedders without clinical evidence of disease.
Up to 10% of horses in a strangles outbreak can become chronic, asymptomatic carriers.1 Chronic shedders are often the culprit in new outbreaks when horses suddenly develop signs of strangles with no known exposure; a chronic shedder also can make it difficult to end an outbreak once it begins.1,2
Strangles and shedding
Strangles occurs when Streptococcus equi subsp equi, a gram-positive, aerobic coccal bacteria, enters the mouth or nose and attaches to the tonsillar crypts. Within a few hours of attachment, bacteria can be found inside the nasal epithelial cells; shortly thereafter the bacteria translocate to the submandibular and retropharyngeal lymph nodes. Fever and lethargy usually develop within three to 14 days of infection, preceeding abscessation of the lymph nodes. Lymphadenopathy occurs in most cases, often concurrently with a painful pharyngitis. Abscesses usually rupture anywhere from seven days to four weeks after the initial infection. Abscesses rupture either externally or internally into the guttural pouch.
Nasal shedding begins two to three days after the initial fever and persists for at least two to three weeks past the resolution of clinical signs, although it can last as long as 6 weeks in uncomplicated cases. Most horses clear the infection on their own, but some become persistent carriers and continue to shed bacteria despite being asymptomatic for months or years after infection.1,2 In a group of 25 horses infected for more than 40 days, nearly 50% showed no clinical evidence of strangles but were still shedding the bacteria.3 In two other outbreaks, 12% and 37% of horses were classified as carriers 10 and 14 months, respectively, after the index case was identified, with no clinical signs of strangles.4
Identifying the shedder
A scenario that may suggest the presence of a chronic shedder in a herd may be one in which a new horse is brought into the boarding barn and quarantined for four weeks before being introduced into the herd. A week after being turned out with the previous residents of the farm, the new horse develops bilateral nasal discharge and a fever, consistent with strangles. Given that this horse was quarantined for longer than is usually recommended, there are a few possible explanations for the sudden development of clinical signs. Abscess development generally occurs within two weeks of initial exposure. Therefore, if the horse had an active infection when it was moved, it would probably have developed outward evidence of disease before the end of the quarantine period. A probable scenario would be that another horse in the group is a chronic shedder, and the other animals may already have immunity against S. equi subsp equi infections. If a more longstanding member of the herd had developed strangles after the new individual was introduced, the new horse should be ruled out as a chronic shedder.
Initially, when one horse on a farm develops signs of strangles, appropriate biosecurity measures should be taken regardless of the initial source of infection. The affected animal should be isolated so that it does not have nose-to-nose contact with any other horse, and it should be fed and cared for last to decrease the risk of caretakers spreading the bacteria. Personal protective equipment should be worn to minimize the risk of transmission via clothes, shoes and hands.
The temperature of unaffected animals should be monitored twice daily, and any horse that develops a fever should be separated from the herd and tested.1,2 Washes of the nasal passages, pharynx or guttural pouch; swabs; or aspirates taken directly from abscessed lymph nodes should be submitted for either polymerase chain reaction (PCR) testing or culture. It is important that samples for PCR be taken with rayon swabs, as cotton contains PCR inhibitors. For the same reason, culture transport media should not be used for samples on which PCR will be performed.
If test results are negative when there is high clinical suspicion, then retesting is recommended with a new sample as handling may affect final results. It is important to remember that dead bacteria will still lead to positive PCR results, so test selection can affect results. In horses without purulent nasal discharge, a deep pharyngeal or guttural pouch lavage is more likely to yield a positive result as intermittent shedding can lead to false negatives from samples taken more rostrally.2
In strangles outbreaks that do not have an obvious source of infection (i.e. no new horses introduced to herd, no recent travel with exposure to outside horses), it is important to examine all animals that have come in contact with the affected horses to identify the presence of chronic shedders. Upper airway endoscopy is often recommended to examine the guttural pouches for the presence of chondroids, although in one group only 25% of horses that were identified via culture to be shedding S. equi subsp equi actually had visible chondroids on endoscopy.5 The presence of S. equi subsp equi M protein antibody titers of 1:12,500 or greater has 67% sensitivity and 43% specificity in an outbreak for identification of persistent guttural pouch infections eight weeks after infection.5 While S. equi subsp equi M protein titers may be suggestive of a carrier state, the recommended method of sampling when looking for carrier animals is an endoscopically guided guttural pouch lavage and subsequent quantitative PCR of the fluid.2
After identifying the carriers
Once carrier animals have been identified, they need to be isolated from the herd and treated. Depending on the amount and character of the purulent material in the guttural pouches, treatment may consist of lavage, surgery and/or antimicrobials. While antimicrobial therapy is generally not recommended in uncomplicated “classic” cases of strangles, it may be warranted in the case of a chronic carrier. Foley catheters can be placed into the guttural pouches and isotonic fluid used to lavage purulent material and chondroids from the pouches. Animals are generally sedated for this procedure as sedation allows for better drainage due to a lower head position. Systemic penicillin, topical penicillin, or a combination have also been used. Penicillin can be mixed into a gelatin product that solidifies at body temperature, thus allowing for prolonged antimicrobial effect within the guttural pouch. Acetylcysteine has been administered into the pouches as a mucolytic in an attempt to break up the empyema. Endoscopic removal of chondroids with either snares or endoscopic forceps is required in some cases, and in severe cases surgical removal of chondroids may be warranted.1,2,6,7
While a number of factors play a role in propagating and controlling strangles outbreaks, identification of chronic carriers is a crucial task that can aid in ending a current outbreak and preventing future outbreaks and reinfection within a herd. Studies have shown that a variable proportion of horses—ranging from 0.3% to 37% of affected animals—can become chronically infected after an outbreak.2-4,7 Through use of appropriate biosecurity measures, endoscopic examination and sampling of the guttural pouches, chronic carriers can be identified and treated so that they no longer pose a risk to the rest of the herd.
1. Mallicote M. Update on Streptococcus equi subsp equi infections. Vet Clin North Am Equine Pract 2015;31(1):27-41.
2. Boyle AG, Timoney JF, Newton JR, et al. Streptococcus equi infections in horses: Guidelines for treatment, control, and prevention of strangles—revised consensus statement. J Vet Intern Med 2018;32(2):633-647.
3. Duffee LR, Stefanovski D, Boston RC, et al. Predictor variables for and complications associated with Streptococcus equi subsp equi infection in horses. J Am Vet Med Assoc 2015;247(10):1161-1168.
4. Pringle J, Venner M, Tseschlok L, et al. Long term silent carriers of Streptococcus equi ssp. equi following strangles; carrier detection related to sampling site of collection and culture versus qPCR. The Veterinary Journal 2019;246:66-70.
5. Delph KM, Beard LA, Trimble AC, et al. Strangles, convalescent Streptococcus equi subsp equi M antibody titers, and presence of complications. J Vet Intern Med 2019;33(1):275-279.
6. Freeman D. Update on disorders and treatment of the guttural pouch. Vet Clin North Am Equine Pract 2015;31(1):63-89.
7. Waller AS. New perspectives for the diagnosis, control, treatment, and prevention of strangles in horses. Vet Clin North Am Equine Pract 2014;30(3)591-607.
Dr. Hepworth-Warren is an equine internal medicine specialist who currently works as a clinical assistant professor of equine medicine at North Carolina State University College of Veterinary Medicine in Raleigh, NC. Outside of work, she enjoys travelling, cooking, reading, running and the beach.