Strangles

Streptococcus equi, subsp equi

• First reported in 1251

• Biochemically different from S. zooepidemicus

Sweeney, et al, JVIM, 2005:19:123-134

• Streptococcus equi infections in horses: guidelines for treatment, control and prevention of strangles

• Consensus statement of the American College of Veterinary Internal Medicine

Pathogenesis

S. equi enter horse via mouth or nose

• Attach to cells in lingual/palatine tonsils & epithelium of pharynx

• Translocates within hours to mandibular and suprapharyngeal lymph nodes that drain the pharynx and tonsillar areas

Molecular pathogenesis

• Neutrophils fail to phagocytose & kill bacteria

• Hyaluronic acid capsule

• Antiphagocytic SeM protein

• Mac protein

• Bacteria accumulate extracellularly in lymph nodes

• Streptolysin S & streptokinase damage cell membranes and activate proteolytic properties of plasminogen

• Contributes to abscess formation

Pathogenesis

Bacteria spread via blood or lymphatics

• Metastatic abscesses in thorax, abdomen, or other lymph nodes

• "Bastard strangles"

• Bacteremia occurs during days 6-12 in experimentally infected horses

• First clinical sign = fever

• 3 to 14 days after exposure

• Increase in WBC, neutrophils, fibrinogen

• Abscess development is rapid

• Nasal shedding begins at 2-3 days after onset of fever and persists for 2-3 weeks in most animals

• New cases can be isolated before they shed.

Chronic Shedders

• Guttural pouch infection ± chondroids

• Persistent/intermittent shedding for months-years

• Uncommon

Post-infection immunity

• Systemic & mucosal immunity is apparent 2-3 weeks after infection

• 75% of horses develop enduring immunity following recovery

Colostral immunity

• Milk from mares that have recovered from strangles contains IgGb & IgA that protect foal

• Foals that suckle immune mares are resistant until weaning.

Epidemiology

• Highly contagious

• Occurs in outbreaks

• Morbidity = 30 - 100%

• Mortality = 0 - 10%

• Morbidity highest in young (1-5 yo) horses