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Introduction: Strangles is an infectious, transmissible, world-wide disease of horses, donkeys and mules.  It continues to rank among the three most significant respiratory diseases of horses.  Its widespread distribution is favored by its highly contagious mode of spread and a mobile horse population.

Etiology: The causal agent, Streptococcus equi subspecies equi, is a gram-positive, beta-hemolytic coccobacillus organism.  Si. iequi is highly host adapted to equids and demonstrates no genetic or phenotypic variation although there is variation in virulence related to factors such as hyaluronic acid capsule, the M-like proteins SeM and SzPSe, streptolysin S, and pyrogenic superantigenic exotoxins.

Epizootiology: An obligate parasite of equids, S. equi relies on its host for survival and interepizootic maintenance.  Strangles may affect animals of all ages, but it is most common in horses less than two years old (except foals under four months of age, which are usually protected by colostrum-derived passive immunity).  Although the majority of animals with strangles are subsequently immune, some may contract the disease a second, or even third, time.  Horses that have recovered from the clinical disease may have persistent infection of S. equi in the pharynx and guttural pouches for many months and are an important source of infection.  Horses with clinically inapparent disease, such as some cases of guttural pouch empyema, may shed the organism for over three years.

  Strangles is highly contagious, with transmission occurring by the oral and nasal routes.  Communal drinking sources, population density, and mobility are important risk factors.  S. equi may survive for several weeks in water troughs, but dies quickly in soil and on pasture.  It will remain viable in frozen discharges; otherwise survival requires moisture and protection from sunlight.

Pathogenesis: Following entry into a new host, S. equi attaches primarily to the cells on the tonsillar crypts and the ventral surface of the soft palate.  The organism slowly multiplies in the lymph node.  Subsequent migration of neutrophils into the lymph nodes causes swelling and abscessation.  Nasal shedding usually begins 4-7 days after infection.  Resistance to phagocytosis mediated by a combination of the hyaluronic acid capsule and SeM protein is the key feature of S. equi virulence.

Clinical findings: After an incubation period of 1-3 weeks, the disease develops suddenly with complete anorexia, depression, fever, and a serous nasal discharge which rapidly becomes copious and mucopurulent.  Retropharyngeal lymph node enlargement may cause obstruction of the oro- and nasopharynx with subsequent dyspnea and dysphagia.  Death by asphyxiation may occur at this time in severe cases.

  An atypical form of the disease can occur in older animals with residual immunity to S. equi, which is characterized by a transient fever, profuse nasal discharge, and anorexia.  Lymphadenopathy is  seen in approximately half of the affected horses.

Sequelae and complications: Complications occur in about 20% of the cases.  The most common fatal complication is the development of suppurative necrotic bronchopneumonia secondary to the aspiration of pus from internal ruptured abscesses or metastatic infection of the lungs.  Guttural pouch infection with empyema may also result from rupture of abscesses in the retropharyngeal lymph node.  Metastatic infection, also known as “bastard strangles”, results in the formation of abscesses in any organ or body site, but most commonly in the lungs, mesenteric lymph nodes, liver, spleen, kidneys and brain.  Purpura hemorrhagica may occur as sequelae of S. equi infection as well.

Necropsy findings: In the rare fatalities that occur, necropsy examination usually reveals suppuration in internal organs, especially in liver, spleen, lungs, pleura, and peritoneum.  When the latter is involved, it is usually due to extension from abscesses in the mesenteric lymph nodes.

Diagnosis: Culture of nasal swabs, nasal washes or pus from abscesses is essential for confirming the presence of S. equi.  However, culture may fail to detect the organism during the incubation period, in early clinical phases, and in the guttural pouch carriage in apparently normal horses following recovery from strangles.  PCR, combined with culture, increases the carrier detection rate while serology is not very useful in the detection of S. equi infection.

  Hyperfibrinogenemia is characteristic of both the acute and chronic disease.  Leukocytosis with neutrophilia and hyperproteinemia attributable to a polyclonal gammaglobulinemia is characteristic of metastatic and chronic abscessation.

Differential diagnosis: Strangles should be differentiated clinically from other upper respiratory tract diseases of horses.  Chronic weight loss due to metastatic infection should be differentiated from equine infectious anemia, parasitism, inadequate nutrition, and neoplasia.

Treatment and control:  There is considerable debate about the antibiotic treatment of strangles.  It has been suggested that antibiotic treatment of horses with strangles is contraindicated because it promotes the development of metastatic infection.  Since there is no evidence to support this contention, horses with strangles should be treated with therapeutic doses of an appropriate antibiotic, such as procaine penicillin, for a period of time sufficient to effect a cure.  The very contagious nature of strangles requires rigorous control measures.

  Newly arrived animals, including nurse mares, should be observed for signs of strangles for three weeks before admission to the resident population.  Rectal temperature should be monitored twice daily.  Horses with elevated temperatures should have nasopharyngeal or guttural pouch swabs cultured.  Affected horses should be promptly isolated.  All potential fomites, including pails, brooms and grooming brushes, should be thoroughly cleaned and disinfected.  Nasopharyngeal swabs or washes from recovered animals should be cultured or tested by PCR to demonstrate cessation of nasal shedding.

Immunity and vaccination: Foals that receive adequate high quality colostrums from exposed or vaccinated mares have serum and nasopharyngeal mucosal immunoglobulins that provide resistance to S. equi infection.  The efficacy of vaccination of adult horses with S. equi bacterins or M protein extracts is controversial.  A common vaccination protocol involves the administration of an M protein vaccine intramuscularly for an initial course of 3 injections at 2-week intervals, with further administration of the vaccine every 6 months in animals at increased risk of contracting the disease.  On breeding farms, the vaccination of mares during the last 4-6 weeks of gestation and of the foals at 2-3 months of age may reduce the incidence of the disease.

  The intramuscular vaccine frequently causes swelling and pain at the injection site.  Injection into the cervical muscles may cause the horse to be unable to lower its head to eat and drink for several days.  Injection into the pectoral muscles is preferred for this reason.  Purpura hemorrhagica has been reported associated with administration of the S. equi vaccine.

  An intranasal vaccine of an avirulent, live strain of S. equi has recently been reported and appears useful.  However, its efficacy in field situations, safety in the face of an outbreak, in pregnant mares, incidence of adverse effects, and risk of reversion to virulence have not been reported.

-by Dhana Natarajan, ECFVG Student

-edited by Dr. Ingeborg Langohr, ADDL Graduate Student


1. Newton JR et al: 1997.  Strangles: long term carriage of Streptococcus equi in horses.  Equine Vet Educ 9:98-109.

2.  Radostits OM et al:  2000.  Strangles, in A textbook of the diseases of cattle, sheep, pigs, goats and horses, 9th ed.  W.B. Saunders.  p 703-706.

3.  Smith BP: 2002.  Streptococcus equi infection (strangles).  in Large animal internal medicine, 3rd ed.,  Mosby.  p. 1394-1395.

4.  Susan EA, Ed.: 1998.  Strangles, in the Merck veterinary manual, 8th ed. Merck and Co., in cooperation with Merial Limited.     pp 1020-1022.

5. Sweeney CR:1996.  Strangles: Streptococcus equi infections in horses.  Equine Vet Educ 8:317-322.

6.  Timoney JF: 1999.  Equine strangles.  Am Assoc Equine Practice Proc 45:31-37.


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