Strangles is an infectious, contagious disease of Equidae characterized by abscessation of the lymphoid tissue of the upper respiratory tract. The causative organism, Streptococcus equi equi, is highly host-adapted and produces clinical disease only in horses, donkeys, and mules. It is a gram-positive, capsulated β-hemolytic Lancefield group C coccus, which is an obligate parasite and a primary pathogen.
Etiology and Pathogenesis
S equi equi is highly contagious and produces high morbidity and low mortality in susceptible populations. Transmission occurs via fomites and direct contact with infectious exudates. Carrier animals are important for maintenance of the bacteria between epizootics and initiation of outbreaks on premises previously free of disease. Survival of the organism in the environment depends on temperature and humidity; it is susceptible to desiccation, extreme heat, and exposure to sunlight, and must be protected within mucoid secretions to survive. Under ideal environmental circumstances, the organism can survive ~4 wk outside the host. Paddocks and barn facilities used by infected horses should be regarded as contaminated for ~1 mo after resolution of an outbreak.
The incubation period of strangles is 3–14 days, and the first sign of infection is fever (103–106°F [39.4–41.1°C]). Within 24–48 hr of the initial fever spike, the horse will exhibit signs typical of strangles, including mucoid to mucopurulent nasal discharge, depression, and submandibular lymphadenopathy. Horses with retropharyngeal lymph node involvement have difficulty swallowing, inspiratory respiratory noise (compression of the dorsal pharyngeal wall), and extended head and neck. Older animals with residual immunity may develop an atypical or catarrhal form of the disease with mucoid nasal discharge, cough, and mild fever. Metastatic strangles (“bastard strangles”) is characterized by abscessation in other lymph nodes of the body, particularly the lymph nodes in the abdomen and, less frequently, the thorax.
Diagnosis is confirmed by bacterial culture of exudate from abscesses or nasal swab samples. CBC reveals neutrophilic leukocytosis and hyperfibrinogenemia. Serum biochemical analysis is typically unremarkable. Complicated cases may require endoscopic examination of the upper respiratory tract (including the guttural pouches), ultrasonographic examination of the retropharyngeal area, or radiographic examination of the skull to identify the location and extent of retropharyngeal abscesses.
The environment for clinically ill horses should be warm, dry, and dust-free. Warm compresses are applied to sites of lymphadenopathy to facilitate maturation of abscesses. Facilitated drainage of mature abscesses will speed recovery. Ruptured abscesses should be flushed with dilute (3–5%) povidone-iodine solution for several days until discharge ceases. NSAID can be administered judiciously to reduce pain and fever and to improve appetite in horses with fulminant clinical disease.
Antimicrobial therapy is controversial. Most authors agree that initiation of antibiotic therapy after abscess formation may provide temporary clinical improvement in fever and depression, but it ultimately prolongs the course of disease by delaying maturation of abscesses. Antibiotic therapy is indicated in cases with dyspnea, dysphagia, prolonged high fever, and severe lethargy/anorexia. Administration of penicillin during the early stage of infection (≤24 hr of onset of fever) will usually abort abscess formation. The disadvantage of early antimicrobial treatment is failure to mount a protective immune response, rendering horses highly susceptible to infection after cessation of therapy. If antimicrobial therapy is indicated, procaine penicillin (22,000 IU/kg, IM, bid) is the antibiotic of choice.
Postexposure immunity is prolonged after natural disease in most horses, and protection is associated with local (nasal mucosa) production of antibody against the antiphagocytic M protein. The clinical attack rate of strangles is reduced by 50% in horses vaccinated with IM products that do not induce mucosal immunity. Local (mucosal) production of antibody requires mucosal antigen stimulation. An intranasal vaccine containing a live attenuated strain of S equi equi was designed to elicit a mucosal immunologic response. This attenuated strain is not temperature sensitive (inactivated by core body temperature), like the intranasal influenza vaccine. Reported complications include S equi equi abscesses at subsequent IM injection sites (live bacteria on hands of administrator), submandibular lymphadenophathy, serous nasal discharge, and purpura hemorrhagica.
Clinically affected horses should be physically separated from the herd and cared for by separate caretakers. The rectal temperature of all horses exposed to strangles should be obtained twice daily, and horses developing fever should be isolated (and potentially treated with penicillin). Contaminated equipment should be cleaned with detergent and disinfected using chlorhexidine gluconate or glutaraldehyde. Flies can transmit infection mechanically; therefore, efforts should be made to control the fly population during an outbreak. Farriers, trainers, and veterinarians should wear protective clothing or change clothes before traveling to the next equine facility. Additions to the herd should be carefully scrutinized for evidence of disease or shedding (nasopharyngeal culture) and quarantined for 14–21 days. Two negative nasal swab cultures should be obtained during the quarantine period.
Most horses continue to shed S equi for ~1 mo after recovery. Three negative nasopharyngeal swabs, at intervals of 4–7 days, should be obtained before release from quarantine, and the minimal isolation period should be 1 mo. Prolonged bacterial shedding (up to 18 mo) has been identified in a small number of horses. Guttural pouch empyema is the source of infection in most prolonged carrier states. Bacterial culture of nasopharyngeal swab and/or guttural pouch lavage is used to identify persistent carriers.
Last full review/revision March 2012 by Bonnie R. Rush, DVM, MS, DACVIM