6 Strangles Disease in Horses

• Strangles is caused by beta-hemolytic, Gram-positive cocci, which are highly host-adapted to Equidae.
• This disease exclusively affects horses, donkeys, and mules.
• Strangles is caused by an obligate parasite and a primary pathogen.

Transmission of Strangles

• Strangles is highly contagious through direct contact and fomites.
• Fomites can survive in the environment for up to one week.
• Water buckets and wood fencing can act as significant reservoirs during outbreaks.
• Nasal shedding typically ceases 2 to 3 weeks after the acute disease phase.
• Carrier animals are crucial for maintaining the disease between outbreaks.
• Persistent nasal shedding for over 6 months is rare.
• Young horses, overcrowding, mixing of horses, stress, and poor sanitation are high-risk factors.

Pathogenesis of Strangles

• Strangles enters through the oral cavity and translocates via the lingual and palatine tonsils to reach local lymphatics.
• Strangles evades neutrophil killing using a hyaluronic capsule, antiphagocytic M protein, and leucocidal toxin.

Clinical Signs of Strangles

• Incubation period: 3 to 14 days.
• Morbidity is high, while mortality is low.
• Clinical signs include fever (103 F), mucoid nasal discharge, depression, difficulty swallowing, and swelling of submandibular or retropharyngeal lymph nodes.
• The head and neck become extended
• Abscessation of submandibular and/or retropharyngeal lymph nodes occurs
• Diffuse, painful swelling of the intermandibular space is present.
• Compression of the dorsal pharyngeal wall or guttural pouch leads to respiratory noise (dyspnea)
• Swelling in the parotid region.
• Metastatic abscesses can occur in the thoracic region, mesentery, and brain (ELISA 1:12,800).
• Laboratory abnormalities include neutrophilic leukocytosis and hyperfibrinogenemia.

Diagnosis of Strangles

• Diagnosis can be confirmed by a bacterial culture of aspirate from abscess, nasal swab, or nasopharyngeal flush.
• PCR (bacterial DNA) of nasopharyngeal flush is used for confirmation, new horse introduction decisions, and carrier screening.
• ELISA (antibody titer SeM protein) indicates metastatic disease if > 12,800 and purpura, GN, or myositis if > 12,800.
• ELISA would indicate need for vacciantion if the titer is < 1,600
• ELISA cannot detect carriers
• Endoscopic examination of the guttural pouch reveals empyema and chondroids.
• Dorsal pharyngeal compression can be visualized via endoscopic examination and is an indication for tracheotomy.
• Ultrasound or skull radiography can detect retropharyngeal abscesses.

Treatment of Strangles

• Facilitate drainage with warm compresses twice a day to promote maturation.
• Mature abscesses can be ruptured by stab incision, followed by lavage of the submandibular cavity.
• Supportive therapy includes providing palatable feeds and a warm, dry environment.
• NSAIDs can address high fever, anorexia, and depression.
• Penicillin is a controversial antibiotic choice as it delays drainage and prolongs the disease course.
• Penicillin prevents a strong antibody response if given before abscess formation, making the horse susceptible to reinfection.
• Antibiotic administration may promote the development of "bastard strangles" related to unresolved abscesses.
• Avoid antibiotics in uncomplicated submandibular abscess formation.
• Penicillin is indicated for high fever (104 F), marked depression, anorexia, respiratory compromise, dyspnea, or early infection (3 days post-exposure).
• Surgical drainage is necessary for chondroids or retropharyngeal abscesses.
• Tracheotomy provides an alternative airway.

Prevention of Strangles

• Post-exposure immunity is prolonged (75% of horses are protected for more than 5 years).
• This immunity is associated with local nasal mucosa production of IgG and IgA against M protein.
• Serum IgG to M protein is present, but less important for protection.
• Intramuscular vaccine is contraindicated at 1:1,600.
• The vaccine does not confer a high level of protective immunity.
• The vaccine elicits serum IgG production.
• Injection site arthrus reaction is common.
• Vaccination is recommended only for farms with continued problems.
• Post-vaccinal purpura occurs more commonly with the IM vaccine.
• Intranasal vaccine is live attenuated bacterial culture, not temperature sensitive, and elicits a local immunologic response.
• Intranasal is contraindicated at 1:1,600
• Abscesses at other IM vaccine sites, lymphadenopathy, and serous nasal discharge can occur when administering live culture vaccines.
• The most important reason to quarantine incoming horses is for 21 days.
• Horses can be released from quarantine after three negative nasal swab cultures and/or PCR tests.
• During an outbreak, isolate affected horses, considering them shedders for 4 weeks with 3 negative nasal swab cultures and PCR tests.
• Use separate caretakers for affected and unaffected horses.
• Buckets, tack, and stalls should be washed with detergent and disinfected with chlorhexidine.
• Nasal swab cultures and PCR are used to determine release from quarantine.
• Guttural pouch culture and PCR are used to identify carrier horses with persistent shedding.
• Premises should be considered contaminated for up to one week.
• Sunlight creates unfavorable conditions for survival (<24 hours), versus dark and damp environments having longer survival (approximately 3 days).

Purpura Hemorrhagica

• Purpura hemorrhagica is an immune-mediated vasculitis occurring in 1-5% of horses exposed to Strep equi.
• Affected horses have a stronger antibody response to streptococcal proteins and unusually high plasma C3 concentrations.
• Purpura can occur after acute disease or post-vaccination in previously naive or immunologically experienced horses.
• Vaccination is contraindicated in horses with titers > 1,600.
• Purpura can occur in response to influenza and Strep zooepidemicus.
• Older horses, non-Thoroughbreds/Warmbloods, and horses receiving intranasal strangles within 3 years are more likely to have an M-protein titer > 1,600.

Clinical Signs of Purpura Hemorrhagica

• Limb swellings are painful, hot, symmetric/asymmetric; severely swollen limbs may crack/ooze serum.
• Painful plaques of edema on the ventral midline
• Discoloration of the nose, swelling of nares, petechial hemorrhage of mucous membranes
• Fever, depression
• Laboratory abnormalities include neutrophilic leukocytosis and elevated serum muscle enzymes
• Thrombocytopenia usually does not occur
• Severe cases may present with atypical clinical signs including dyspnea, colic, and myonecrosis (Henoch-Schonlein purpura).

Pathogenesis of Purpura Hemorrhagica (Leukocytoclastic Vasculitis)

• Type III hypersensitivity reaction in the vascular wall.
• Antigen-antibody complex deposition in the vascular wall
• C3 fragment
• Neutrophilic inflammation
• High serum IgA to M protein and high serum C3 concentrations

Diagnosis of Purpura Hemorrhagica

• Clinical signs are most common
• Skin biopsy shows neutrophilic vasculitis (leukocytoclastic inflammation)
• SeM > 1:12,800

Treatment of Purpura Hemorrhagica

• Supportive care, including hydrotherapy with lukewarm water
• Well-padded, pressure bandages required to stifle and elbow
• Hock and carpus support bandages may be required for 2-3 weeks
• Hand-walk when limb edema begins to resolve; do not force severely swollen limbs to walk
• Corticosteroids: administer dexamethasone until swelling decreases (1-2 days), gradually reduce dose over time
• Penicillin to treat unidentified Strep infection
• NSAIDs are used as anti-inflammatories, analgesics, to improve appetite and attitude
• Intravenous DMSO may reduce inflammation
• DIuretics are contraindicated

Sequela of Purpura Hemorrhagica

• Skin slough may be life-threatening
• Skin grafts may be necessary