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
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.
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
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
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
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