Streptococcus equi subsp. equi is the etiological agent of strangles
Strangles Epidemiology
Highly contagious disease affecting horses of all ages
More common in younger animals
S. equi only causes disease in equids
Strangles Clinical Findings
Acute onset of fever, anorexia, and depression
Submandibular and pharygneal lymphadenopathy with abscessation and rupture
Copious purulent nasal discharge
Metastatic infection in other organ systems
Strangles Lesions
Caseous lymphadenopathy with rhinitis and pharyngitis, pneumonia, and metastatic infection in severe cases
Strangles Diagnostics
Culture of S. equi, or PCR
Strangles Treatment
Systemic administration of Penicillin and local treatment of abcesses
Strangles Control
Isolation and testing; Vaccination
Streptococcus equi subsp. equi
Gram positive, cocci
Facultative anaerobe
Catalase and coagulase negative
Beta-Hemolytic
Highly adapted to Equids
Strangles Species
Horses
Ponies
Donkeys
Mules
Strangles can affect horses of any age, although morbidity is higher in younger horses.
Strangles fatality without treatment is about 9%; with adequate treatment it may be 1-2%
Outbreaks frequent on breeding farms, and in polo and racing stables, where infection is introduced by asymptomatic newarrivals or horses taken to fairs/riding schools.
Strangles transmission
Obligateparasite of horses
All infections attributable to transmission from infected horses directly or by fomites
Source of Strangles
Nasal and abscess discharges from infected animals
From infected pastures, tracks, stalls, feed/water troughs, grooming equipment, or hands/clothes of groomers and veterinarians.
Strangles survival
Less than 3 days in environment; prolonged quarantine not required.
Persistent Strangles Infection
About 10-40% of recovered horses have persistent infection and are important sources for infection.
Detection of Strangles Carriers
PCR on nasal swabs or gutturalpouch lavage fluid
Resistance to Strangles
Associated with production of serum and mucosal antibodies to streptococcal M protein (SeM)
Animals that had disease less likely than naive animals to develop disease on subsequent exposure
Around 25% of horses do NOT develop protective immunity
Immunity after natural exposure wanes over time
Virulence of Strangles
M proteins on the surface of bacteria
Hyaluronicacid capsule
Production of Leukocidal toxin
M proteins - Virulence
Adhere to oral, nasal, and pharyngeal tissue
Invade pharyngeal tonsils
Evade innate immune system
Strangles' viral capsule provides resistance to phagocytosis
Following adhesion, S. equi lodge and multiply in pharyngeal and tonsillar lymphoid tissue.
Strangles Pathogenesis
Toxins produced by S. equi cause direct cell damage
Migration of neutrophils into the lymph nodes causes swelling and abscessation
Swelling of retropharyngeal lymph nodes may interfere with respiration
Most abscesses eventually rupture and drain, resolving with effective immune response
Nasal shedding persists for 2-3 weeks, but longer in exceptional cases
Strangles mortality
Death is rare and associated with secondary infections
Due to pneumonia caused by aspiration of infected material
Due to asphyxiation secondary to upper airway obstruction
Due to organ failure by metastatic infection
Strangles Metastatic Infection
Bacteremia or lymph vessel spread
Heart Valves, brain, joints, eyes, and other vital organs affected
Can cause death
Strangles - Purpura hemorrhagica

Can occur as a sequela to S equi infection and is associated with high serum antibody titers to SeM.
Strangles - Acute disease
Varying severity, infection of retropharyngeal nodes and guttural pouches
Strangles - Chronic disease

Metastatic infection of organs distant from respiratory tract.
Strangles severity factors
Age
Immune Status
Size of inoculum
Duration of exposure
Strangles Etymology
Derived from the enlarged retropharyngeal lymph nodes and guttural pouches causing respiratory distress in severely affected animals.
Acute Strangles disease
Characterized by mucopurulent discharge and abscessation of submandibular and retropharyngeal lymph nodes
Incubation period of 1-3 weeks
Sudden onset of symptoms
Strangles Essential dates
Swelling of lymph nodes in 3-4 days
Serum exudate in 10 days, and subsequent rupture
The most common fatal complication of Strangles is the development of suppurative necrotic bronchopneumonia (aspiration of pus from ruptured abscesses).
Metastatic strangles infection is also know as Bastard Strangles, occuring in about 1% of affected animals.
Purpura hemorrhagica

Immune mediated disease occurring in a subset of Strangles affected horses 1-3 weeks after initial illness.
Gram positive cocci in chains = Strangles
Strangles Culture
Colonies usually mucoid, up to 4 mm, surrounded by zone of beta hemolysis
Control of Strangles
Penicillin to in-contact and infected horses before development of lymphadenopathy; limited benefit if abscesses already present.
Isolation of suspect animals
Quarantine horses for 3 weeks before introduction to herd; test negative before introduction.
Live Attenuated Intranasal vaccine
Avoid overcrowding and mixing age groups, clean building/equipment
Shipping Fever
Pneumonic Pastuerellosis of Cattle or Bovine Respiratory Disease
Characteristic of Pneumonic Pasteurellosis
Clinical signs of acute bronchopneumonia with toxemia