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Compendium March 2011 (Vol 33, No 3)

Streptococcus equi subspecies equi Infection (Strangles) in Horses

by Ashley G. Boyle, DVM, DACVIM

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    Streptococcus equi subspecies equi (strangles) is a highly contagious upper respiratory infection in horses. The infection is transmitted by inhalation or direct contact with mucopurulent discharge from an infective animal, resulting in fever, depression, and submandibular and retropharyngeal lymph node enlargement that can lead to respiratory distress. Complications include purpura hemorrhagica and metastatic abscessation. Control of outbreaks requires strict isolation protocols and hygiene measures. Detection of carriers is essential for preventing disease recurrence on a farm.

    Strangles is a worldwide, acute upper respiratory infection in horses, resulting in high morbidity but low mortality.1,2 The etiologic agent is the gram-positive coccus Streptococcus equi subspecies equi. The infection is characterized by fever, lethargy, purulent nasal discharge, and regional lymph node abscessation. Highly concentrated and transient populations are at greater risk of contracting the disease.1,2


    S. equi subsp equi is inhaled or ingested after direct contact with mucopurulent discharge from infected horses or contaminated equipment. The bacterium attaches to the crypts and epithelium of the lingual and palatine tonsils with the assistance of fibronectin binding protein.1,3 The organism does not colonize the mucosal surface but penetrates into deeper tissue and enters the mandibular and pharyngeal lymph nodes. The hyaluronic acid capsule and the SeM protein allow the bacterium to avoid phagocytosis by neutrophils. Clinical signs develop 3 to 14 days after exposure. In as many as 20% of cases, S. equi subsp equi spreads via the hematic or lymphatic systems or by close proximity to an existing abscess. This results in metastatic abscessation (also known as bastard strangles), which can affect any organ system.1,2

    Clinical Signs

    The first clinical sign of strangles is acute-onset fever (often >103°F [39.4°C]), followed by lethargy, depression, bilateral mucopurulent nasal discharge (FIGURE 1) , lymphadenopathy, and abscessation of the retropharyngeal and mandibular lymph nodes (FIGURE 2) . Occasionally, the parotid and cranial cervical lymph nodes are affected. Retropharyngeal lymph node enlargement can lead to narrowing of the pharynx, resulting in respiratory stridor, dysphagia, and neck extension. Empyema results when the retropharyngeal lymph nodes drain into the guttural pouches. This can sometimes result in the formation of chrondroids or inspissated pus (FIGURE 3; FIGURE 4). On endoscopic examination, drainage from the opening of the guttural pouch and difficult entry into the pouch are suggestive of guttural pouch empyema. In addition, horses may develop respiratory distress due to retropharyngeal abscesses that are not externally mature. Upper airway endoscopy often reveals a narrowed pharynx due to axial deviation of the guttural pouches and enlarged retropharyngeal lymph nodes that bulge through the respiratory mucosa on the floor of the guttural pouch. Clinical signs are more severe in immunologically naïve (1 through 5 years of age), geriatric (older than 20 years), and immunocompromised horses.1,2 Some horses may develop complications such as metastatic abscessation, purpura hemorrhagica, and myositis.

    Bastard Strangles (Metastatic Abscessation)

    In cases of bastard strangles, clinical signs depend on the organ system involved. Aspiration of mucopurulent discharge or hematogenous or lymphatic spread to the lungs can cause pneumonia. Abscessation in the mesentery, liver, spleen, and kidneys is common, leading to peritonitis and clinical signs of colic. Abscessation of the cranial mediastinal lymph nodes can cause tracheal compression and respiratory distress. Neurologic signs are present when abscessation occurs in the brain.1 The mortality rate of horses with strangles is less than 2%, but the presence of bastard strangles increases the mortality rate to as high as 62%, according to some reports.4

    Purpura Hemorrhagica

    Purpura hemorrhagica is an aseptic necrotizing vasculitis that can occur in mature horses after repeated natural exposure to infection or after vaccination of horses that have had strangles.1,5–7 Timoney and others1,8 have suggested that horses with high SeM-specific serum antibodies may be predisposed to purpura when vaccinated for S. equi subspequi with an attenuated live intranasal S. equi vaccine. The actual incidence of this type III hypersensitivity response secondary to strangles or vaccination is unknown.1,2 A report8 from 1999 noted two cases of purpura-like disease per 100,000 doses of attenuated live intranasal S. equi subsp equi vaccine sold. Clinical signs range from mild to life-threatening, including pitting edema of the head, trunk, and distal limbs as well as petechiae and ecchymoses of the mucous membranes. In some cases, antigen–antibody complexes affect other sites, including the gastrointestinal tract, muscles, lungs, and kidneys.1,5,6

    Transmission and Immunity

    Shedding of S. equi subsp equi begins 2 to 3 days after onset of fever. In most cases, shedding persists for a minimum of 2 to 3 weeks. Horses that have recovered from strangles have been shown to shed for an additional 6 weeks.1 If organisms are harbored in the guttural pouches, horses can shed S. equi subsp equi for months or years. These outwardly healthy horses (i.e., carriers) that still shed organisms are a source of infection when introduced into a new population of horses.9–11 Transmission occurs through nose-to-nose contact; close proximity of housing; shared equipment (e.g., water buckets, feed buckets, tack, twitches); clothing of people or horses; and equipment of owners, caretakers, farriers, and veterinarians.1 Under laboratory conditions, not field conditions, S. equi subsp equi has been shown to persist on wood for 63 days at 35.6°F (2°C) and for 48 days on glass and wood at 20°C (68°F).12 Moist environments (e.g., water buckets) allow the organism to persist for extended periods.1

    Seventy-five percent of horses that have been infected with S. equi subsp equi and have not been treated with antimicrobials develop lasting immunity for approximately 5 years or longer.1,13,14 Older horses that have had a milder form of the disease can shed virulent S. equi subsp equi that can produce significant disease in the naïve population.1 Foals of mares that have recovered from strangles are usually protected by maternal antibodies until weaning.1,14


    Early definitive diagnosis is essential for containing this highly infectious disease. Suspicion of disease can be supported but not confirmed if cytologic evaluation reveals gram-positive extracellular cocci in long chains. The gold standard for diagnosis is bacterial culture of S. equi subspequi. This can be performed on abscess aspirates. Culture can also be performed on nasopharyngeal swabs, nasopharyngeal washes (BOX 1 1,15 and FIGURE A) , and guttural pouch lavage samples. To be diagnostic, nasopharyngeal swabs must be long enough (e.g., unguarded uterine culture swabs, sterile human proctoscopic swabs) to enter the pharynx.11 To detect the DNA of the organism, polymerase chain reaction (PCR) testing can be used on nasopharyngeal swab and wash samples at the onset of disease and on guttural pouch lavage samples for weeks after the onset of disease.1 PCR testing is more sensitive than bacterial culture but detects both dead and live S. equi subsp equi DNA; thus, PCR testing does not confirm active infection. Therefore, positive PCR samples should be confirmed with bacterial culture of the guttural pouch lavage fluid.9

    Carriers can appear outwardly healthy but harbor S. equi subsp equi in their guttural pouches. Definitive determination of carrier status requires endoscopic examination of the guttural pouches as well as culture and PCR testing of guttural pouch fluid1,10,11 (FIGURE 5) .

    Serologic testing involves the use of ELISA to detect the SeM protein (BOX 2) . Serology is useful for detecting recent, but not current, infection; assessing the need for vaccination; identifying horses that may be predisposed to purpura hemorrhagica; and diagnosing S. equi subspequi–associated purpura hemorrhagica and metastatic abscessation.1,16

    A complete blood count reveals neutrophilia and hyperfibrinogenemia during the initial stages of the disease. Patients with acute cases may have temporary hemolytic anemia secondary to a high fever. Cases of metastatic abscessation may be characterized by anemia of chronic disease. Chemistry profiles reflect abnormalities indicative of the body system affected in bastard strangles and purpura hemorrhagica. The latter disease often produces an abnormal coagulation profile. Rectal examination, abdominal ultrasonography (using a 2.5-MHz probe), and rectal ultrasonography (using a 5-MHz probe) of patients suspected of having metastatic abscessation often reveal an intraabdominal mass.1,17


    The goal of treating strangles is to control transmission and eliminate infection while providing future immunity to the disease. Uncomplicated cases of strangles are often left to run their course with supportive care, providing lasting immunity. Affected horses should be isolated in a clean, dry stall and fed moist, palatable food. NSAIDs should be used judiciously to decrease swelling and promote eating. Hot compresses or topical 20% ichthammol can be used to accelerate maturation of abscessation. Mature external abscesses should be lanced to allow drainage, followed by daily lavage of open abscesses using 3% to 5% povidone iodine solution (FIGURE 6) . This expedites resolution of abscessation as well as alleviation of compression of surrounding structures, such as the pharynx.

    While the use of antimicrobials for treating strangles is controversial (BOX 3) , horses with complications such as metastatic disease or purpura definitely require the use of systemic antimicrobials for extended periods. In addition, horses with severely enlarged lymph nodes and dyspnea often require an emergency tracheostomy1,2,8 and intensive supportive care. The preferred antimicrobial is penicillin (procaine penicillin [22,000 to 44,000 IU/kg IM q12h] or aqueous potassium penicillin [22,000 to 44,000 IU/kg IV q6h]). The use of antimicrobials during the acute phase of fever and depression may prevent abscess formation but also the development of lasting immunity. It has been argued that antimicrobial use after abscess development may lead to metastasis based on the theory that protein synthesis by the organism is changed by antimicrobial treatment and that a decreased immunogen level results in a suboptimal immune response. However, there are no experimental or clinical data to support this theory.1 There are also reports of outbreaks in which no antimicrobials were used and the incidence of complications was high.1,18 In cases with complications such asS. equi subsp equi internal abdominal abscesses, the mean duration of antimicrobial treatment was 2 months in one study.17 Cases of purpura hemorrhagica also require the use of systemic corticosteroids (dexamethasone, 0.1 to 0.2 mg/kg IV or IM q12–24h; prednisolone, 0.5 to 1 mg/kg PO q24h) for an average of 3 weeks to reduce systemic vasculitis.19

    Elimination of guttural pouch empyema requires repeated lavage with a solution of 20% acetylcysteine in buffered saline via Penrose tubing through an endoscope or via a chambers catheter. Chondroids are particularly difficult to remove, possibly requiring manual removal with endoscopic equipment such as a memory helical polyp retrieval basket (FIGURE 7) , repeated lavage via indwelling catheters, or surgical removal.1,10,11,20 Successful elimination of S. equi subsp equi in these carriers requires local treatment of the guttural pouch with a gelatin/benzyl penicillin mixture(i.e., 20 mL of 3% gelatin in phosphate-buffered saline containing 5 × 106 IU of benzylpenicillin per guttural pouch) after removal of the material within the guttural pouch.1,10,11 Repeated local treatment and systemic treatment with procaine penicillin (22,000 to 44,000 IU/kg IM q12h) or potassium penicillin (22,000 to 44,000 IU/kg IV q6h) for 7 to 10 days are necessary for refractory cases.10


    The several available intramuscular vaccines do not provide complete protection against infection with S. equi subspequi. The immunity level provided by these vaccines is lower than that produced during recovery of natural disease. Due to potential complications associated with intramuscular strangles vaccines, advisement of vaccination is based on a risk assessment of the patient.1,21 These intramuscular vaccines tend to cause injection-site reactions; therefore, they are not administered routinely.1,21 An intranasal vaccine is also available and contains an attenuated live strain of S. equi subsp equi that is antigenic with low pathogenicity. Experiments performed by the manufacturer of the intranasal vaccine have shown a more significant reduction of clinical disease with the use of the intranasal vaccine than with the intramuscular vaccines.a The intranasal vaccine provides a strong mucosal antibody response and a weaker systemic antibody response.22,23 Two initial boosters for the intranasal vaccine are given 3 weeks apart, followed by annual boosters.24

    Complications associated with the intranasal vaccine include mild clinical signs such as coughing and nasal discharge for a few days after vaccination and S. equi subsp equi abscessation at the site of concurrent intramuscular vaccinations against other diseases. Because the intranasal vaccine is an attenuated live vaccine, it should not be given concurrently with other routine intramuscular vaccines in order to avoid contamination of the intramuscular injection site. In addition, the intranasal vaccine should not be given concurrently with invasive procedures such as joint injections and surgeries, such as routine castration. Severe, life-threatening complications such as purpura hemorrhagica have been associated with intranasal and intramuscular vaccines. Therefore, the 2005 American College of Veterinary Internal Medicine (ACVIM) Consensus Statement recommends measurement of SeM-specific antibody titers by ELISA before vaccination.1 Current recommendations state that horses with titers >1:3200 should not be vaccinated.1,16 A recent study evaluating risk factors of horses with SeM-specific antibody titers >1:1600 found that horses previously vaccinated with the intranasal vaccine, non-Thoroughbreds, non-Warmbloods, and older horses were significantly more likely to have higher titers.25 Currently, no strangles vaccine is licensed for use in Europe.26

    Methods of Outbreak Control

    Most outbreaks are thought to originate from introduction of an infected horse into a naïve population. All new horses should be isolated for 3 weeks and monitored for signs of disease, including fever. If cost is not prohibitive, horses should be screened for S. equi subsp equi infection using nasopharyngeal washes or swabs. Many farms with repeated infections have resorted to screening for infection by culture and PCR testing of guttural pouch lavage samples (BOX 4) . Once an outbreak has occurred, twice-daily monitoring of rectal temperatures of all horses on the farm is essential to contain the outbreak. Because febrile horses do not shed disease for the initial 2 days, immediate identification of febrile horses enables caretakers to isolate these horses before shedding occurs. All movement of horses to and from the farm should be stopped until they are determined to be noninfectious. All equipment (e.g., pitchforks, buckets, grooming tools) for an affected horse should be isolated and used only for that horse. Personnel handling infected horses should wear barrier precautions (i.e., gowns, gloves, plastic boots that cover shoes) and, ideally, should not handle noninfected horses or should handle infected horses last. Water buckets should be disinfected daily.1,9 Facilities and equipment should be cleaned first to remove all organic material and then disinfected with a phenol, an iodophor, a chlorhexidine compound, or steam cleaning.1,12 Surfaces and equipment must be allowed to dry thoroughly. Paddocks that hold infected horses should be rested for 4 weeks. Once all cases of strangles have resolved on a farm, three nasopharyngeal washes or swabs should be obtained from convalescing horses and their contacts at approximately weekly intervals and tested for S. equi subsp equi by culture and PCR testing to detect carriers. Because of the costliness of this testing, a minimum recommendation includes bacterial cultures on the first two samples and PCR testing on the third sample.1,11 If any of these samples has a positive result, the guttural pouch should be examined by endoscopy for evidence of guttural pouch empyema or chondroids and lavaged to perform culture and PCR testing. The percentage of carriers per outbreak could be as high as 10%.1,9–11 The SeM ELISA does not detect carrier status.27 Eradication of this disease will not be possible until the subpopulation of carriers is eliminated.28

    The use of vaccination during an outbreak is controversial. The 2005 ACVIM Consensus Statement recommends that live vaccine should be administered only to healthy animals with no known exposure to infected horses during an outbreak, but no published data show that vaccine use during an outbreak is detrimental.1 The AAEP Infectious Disease Committee does not recommend vaccination during an outbreak.29 It is suggested that horses recovering from infection should not be vaccinated for 1 to 2 years.21

    Future Directions/Research

    Strangles is a highly contagious upper respiratory disease that persists in nature due to the presence of silent carriers. Improved diagnostics are needed to detect infection earlier, more conveniently, and at less cost. Stall-side detection would accelerate identification of affected horses, which, in turn, would lead to faster quarantine protocols and reduced spread of disease.1,27,30 The Animal Health Trust in the United Kingdom recently developed a new serologic test that detects antigens differently than the SeM ELISA. This new test appears to be more sensitive for detecting animals with recent exposure (as little as 2 weeks) to S. equi subsp equi. However, this test is currently not available in the United States.31,32 Researchers are also working to develop new vaccines.1,33

    aHustead DR. Fort Dodge Animal Health Technical Information, February 19, 1998.

    Key Points

    • Twice-daily rectal temperature assessment and immediate isolation of febrile horses are essential for rapid control of an S. equi subsp equi outbreak.
    • Asymptomatic carriers are the most likely source of strangles.
    • Asymptomatic horses that test positive for S. equi subsp equi according to PCR testing and culture of a nasopharyngeal swab or lavage should undergo endoscopic examination of the guttural pouches for evidence of empyema or chondroids.
    • Seventy-five percent of horses that have been infected with S. equi subsp equi and have not been treated with antimicrobials develop lasting immunity for approximately 5 years or longer.
    • Carriers can appear outwardly healthy but harbor S. equi subsp equi in their guttural pouches. Definitive determination of carrier status requires endoscopic examination of the guttural pouches as well as culture and PCR testing of guttural pouch fluid.
    • Because the intranasal vaccine for strangles is an attenuated live vaccine, it should not be given concurrently with other routine intramuscular vaccines, to avoid contamination of the intramuscular injection site.
    • Once all cases of strangles have resolved on a farm, three nasopharyngeal washes or swabs should be obtained from convalescing horses and their contacts at approximately weekly intervals and tested for S. equi subsp equi by culture and PCR testing to detect carriers.

    Downloadable PDF

    Dr. Boyle discloses that EBI/IDEXX performed SeM-specific antibody titers at a discounted “research price” for her research project (Boyle AG. Factors associated with likelihood of horses having a high serum Streptococcus equi SeM-specific antibody titer. JAVMA 2009:235:973-977).

    1. Sweeney CR, Timoney JF, Newton JR, Hines MT. Streptococcus equi infections in horses: guidelines for treatment, control, and prevention of strangles. J Vet Intern Med 2005:19:123-134.

    2. Sweeney CR, Benson CE, Whitlock RH, et al. Description of an epizootic and persistence of Streptococcus equi infections in horses. JAVMA 1989;9:1281-1286.

    3. Lannergard J, Flock M, Johansson S, et al. Studies of fibronectin-binding proteins of Streptococcus equi. Infect Immun 2005:73:7243-7251.

    4. Ford J, Lokai MD. Complications of Streptococcus equi infection. Equine Pract 1980;4:41-44.

    5. Radostits OM, Gay CC, Blood DC, et al. Purpura hemorrhagica. In: Veterinary Medicine: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 8th ed. London: Balliere Tindall; 1999:1713-1714.

    6. Carlson GP. Diseases of the hematopoietic and hemolymphatic systems. In: Smith BP, ed. Large Animal Internal Medicine. 3rd ed. St. Louis: CV Mosby; 2002:1043.

    7. Galan JE, Timoney JF. Immune complexes in purpura hemorrhagica of the horse contain IgA and M antigen of Streptococcus equi. J Immunol 1985;135:3134-3137.

    8. Timoney JF. Equine strangles. Proc 45th Annu Meet AAEP 1999:31-37.

    9. Newton JR, Verheyen K, Talbot NC, et al. Control of strangles outbreaks by isolation of guttural pouch carriers identified using PCR and culture of Streptococcus equi. Equine Vet J 2000;32:515-526.

    10. Newton JR, Wood JN, Dunn KA, et al. Naturally occurring persistent and asymptomatic infection of the guttural pouches of horses with Streptococcus equi. Vet Rec 1997;140:84-90.

    11. Verheyen K, Newton JR, Talbot NC, et al. Elimination of guttural pouch infection and inflammation in asymptomatic carriers of Streptococcus equi. Equine Vet J 2000;32:527-532.

    12. Jorm LR. Laboratory studies on the survival of Streptococcus equi on surfaces. In: Plowright W, Rossdale PD, Wade JF, eds. Proceedings of Equine infectious Diseases VI. Newmarket, UK: R & W Publications;1992:39-43.

    13. Todd TG. Strangles. J Comp Path Ther 1910;23:212-229.

    14. Hamlen HJ, Timoney JF, Bell RJ. Epidemiologic and immunologic characteristics of Streptococcus equi infection in foals. JAVMA 1994;204:768-775.

    15. Holland RE, Harris DG, Monge A. How to control strangles infections on the endemic farm. Proc 52nd Annu Meet AAEP 2006:78-80.

    16. IDEXX. S. equi ELISA testing recommendations. Accessed June 2009 at www.idexx.com/equine/laboratory/sequi_elisa/sequi_elisarecommend.jsp.

    17. Pusterla N, Whitcomb MB, Wilson WD. Internal abdominal abscesses caused by Streptococcus equi subspecies equi in 10 horses in California between 1989 and 2004. Vet Rec 2007;160:589-592.

    18. Spoormakers TJ, Ensink JM, Goehring LS. Brain abscesses as a metastatic manifestation of strangles: symptomatology and the use of magnetic resonance imaging as a diagnostic aid. Equine Vet J 2003;35:146-151.

    19. Pusterla N, Watson JL, Affolter VK, et al. Purpura haemorrhagica in 53 horses. Vet Rec 2003;153:118-121.

    20. Freeman DE. Diagnosis and treatment of diseases of the guttural pouch (part 2). Compend Contin Educ Pract Vet 1980;2:S25-S31.

    21. Wilson JH. Vaccine efficacy and controversies. Proc 51st Annu Meet AAEP 2005;409-420.

    22. Timoney JF. Additional information on SeM-specific antibody titer levels, ELISA testing, and vaccination. J Equine Vet Sci 2007;27:471-472.

    23. Sheoran AS, Sponseller BT, Holmes MA, Timoney JF. Serum and mucosal antibody isotype responses to M-like protein (SeM) of Streptococcus equi in convalescent and vaccinated horses. Vet Immunol Immunopathol 1997;59:239-251.

    24. AAEP. Strangles (Streptococcus equi). Accessed June 2009 at www.aaep.org/strangles.htm.

    25. Boyle AG, Sweeney CR, Kristula M, et al. Factors associated with likelihood of horses having a high serum Streptococcus equi SeM-specific antibody titer. JAVMA2009;235:973-977.

    26. Intervet/Schering-Plough Animal Health. Recall of Equilis StrepE. Accessed June 2009 at www.equine-strangles.co.uk/News.asp.

    27. Davidson A, Traub-Dargatz JL, Magnuson R, et al. Lack of correlation between antibody titers to fibrinogen-binding protein of Streptococcus equi and persistent carriers of strangles. J Vet Diagn Invest 2008;20:457-462.

    28. Waller A, Robinson C, Newton JR. Further thoughts on the eradication of strangles in equids. JAVMA 2007;231:1335.

    29. AAEP. Vaccinations for adult horses. Accessed June 2009 at www.aaep.org/images/files/Adultvaccinationtablerevised108.pdf.

    30. Prescott JF, Timoney JF. Could we eradicate strangles in equids? JAVMA 2007;231:377-378.

    31. Animal Health Trust. Strangles blood test. Accessed June 2009 at www.aht.org.uk/bact_blood.html.

    32. Knowles EJ, Mair TS, Butcher N, et al.  Use of a novel serological test for exposure to Streptococcus equi subspecies equi in hospitalised horses. Vet Rec 2010;166:294-297.

    33. Waller AS, Jolley KA. Getting a grip on strangles: recent progress towards improved diagnostics and vaccines. Vet J 2007;173:492-501.

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