Equine Strangles Study Guide

Overview and Clinical Importance

Strangles is the most frequently diagnosed infectious disease of horses worldwide, caused by the gram-positive, beta-hemolytic bacterium Streptococcus equi subspecies equi (S. equi). This highly contagious upper respiratory tract infection is characterized by lymphadenopathy and abscessation of the submandibular and retropharyngeal lymph nodes. The disease derives its name from the potential for enlarged lymph nodes to compress the pharynx and upper airway, causing respiratory distress. Strangles became a reportable disease in the United States in 2017.

Etiology and Microbiology

Streptococcus equi subspecies equi is a gram-positive, capsulated, beta-hemolytic, Lancefield group C coccoid bacterium. Unlike S. equi subspecies zooepidemicus, which is a commensal organism that can cause opportunistic infections, S. equi is considered an obligate parasite and primary pathogen in equids. The organism is highly host-adapted and produces clinical disease only in horses, donkeys, and mules.

Key Microbiological Characteristics

Transmission and Pathogenesis

Routes of Transmission

Direct transmission: Nose-to-nose contact with infected horses or subclinical shedders

Indirect transmission: Contact with contaminated water troughs, feed buckets, tack, grooming equipment, handler clothing/hands, or insects. Shared housing and fomites play a critical role in disease spread.

Carrier transmission: Outwardly healthy convalescent horses may harbor S. equi in the guttural pouches and intermittently shed bacteria for months to years. Approximately 10% of recovered horses develop persistent guttural pouch infection.

Pathogenesis

The bacteria attach to the pharyngeal and lingual tonsils, penetrate the mucous membranes, and drain via lymphatic vessels to regional lymph nodes (submandibular, retropharyngeal, and occasionally parotid). Large abscesses form within the lymph nodes. Retropharyngeal abscesses may rupture internally into the guttural pouches, leading to empyema and formation of chondroids (inspissated pus concretions that harbor viable bacteria).

Incubation Period and Shedding

Clinical Signs and Presentation

Classic (Typical) Strangles

Disease severity varies with immune status - younger horses exhibit more severe clinical signs with lymph node abscessation, while older horses with residual immunity may have a milder, atypical presentation.

Atypical (Catarrhal) Strangles

Older horses with partial immunity or vaccinated animals may exhibit a milder form with mucoid nasal discharge, cough, mild fever, and lymph node enlargement without abscess formation. This form resembles viral upper respiratory infections and is frequently missed without appropriate diagnostic testing.

Diagnosis

Clinical signs alone are often sufficient to make a presumptive diagnosis of strangles. However, definitive diagnosis requires laboratory confirmation via culture or PCR testing of appropriate samples.

Sample Collection

Diagnostic Testing Methods

Serology Interpretation (SeM Antibody Titers)

Titer greater than 1:1,600: DO NOT VACCINATE - high risk of purpura hemorrhagica

Elevated titers without clinical signs: May indicate recent exposure, carrier state, or metastatic infection

Titers peak: ~5 weeks post-exposure, remain elevated for at least 6 months

Exam Focus: PCR of a guttural pouch lavage (ideally endoscopically guided) is the gold standard for carrier detection. For release from quarantine, use either: (1) One negative bilateral guttural pouch PCR, OR (2) Three negative nasopharyngeal washes at 7-day intervals. Screening should not begin until 3 weeks after resolution of clinical signs.

Treatment

Treatment of strangles is stage-dependent and controversial. The primary goals are to control disease spread, eliminate infection, and support development of protective immunity.

Treatment by Disease Stage

Antimicrobial Selection

Drug of Choice: Procaine penicillin G - 22,000 IU/kg IM every 12 hours

Alternatives: Cephalosporins, macrolides

Duration for metastatic infection: Average 2 months (mean 72 days in one study)

Supportive Care

• Warm, dry, dust-free environment
• Palatable feed (soft, soaked)
• Hot compresses/poultices to abscessed lymph nodes to facilitate maturation
• Surgical lancing of mature abscesses once area of thinning develops
• Flush ruptured abscesses with dilute povidone-iodine solution
• Judicious NSAIDs for pain and fever (flunixin meglumine, phenylbutazone)
• Emergency tracheotomy if severe upper airway obstruction

Complications

Complications occur in approximately 10-20% of strangles cases and increase mortality from 8% to 40%.

Metastatic Strangles (Bastard Strangles)

Occurs when S. equi spreads beyond the head and neck via hematogenous or lymphatic routes to form abscesses in distant organs including: lungs, liver, spleen, kidneys, mesenteric lymph nodes, mediastinum, brain, synovia, and myocardium.

Clinical signs: Weight loss, intermittent fever, colic, dependent edema, variable signs based on organs affected

Diagnosis: Rectal examination, abdominocentesis, ultrasound, radiographs, transtracheal wash

Treatment: Long-term antimicrobial therapy (average 2 months); prognosis fair (40% long-term survival with treatment)

Purpura Hemorrhagica

An aseptic, Type III hypersensitivity (immune-complex) necrotizing vasculitis caused by deposition of antigen-antibody complexes in blood vessel walls. Occurs 2-4 weeks after S. equi infection OR after vaccination in previously sensitized horses.

Clinical signs: Pitting edema of limbs, ventral abdomen, and head; petechial/ecchymotic hemorrhages on mucous membranes and sclera; skin sloughing in severe cases; may affect lungs, muscles, kidneys, GI tract

Treatment: Corticosteroids (dexamethasone) + antibiotics if concurrent infection present; intensive supportive care

Prognosis: Often severe; can be fatal due to tissue necrosis

Other Complications

Prevention and Control

Biosecurity Measures

• Quarantine new arrivals for 3 weeks with temperature monitoring
• Twice daily rectal temperature monitoring during outbreaks
• Isolate any horse with fever immediately
• Stop all horse movement to/from premises during outbreak
• Do not share tack, equipment, water buckets, or grooming supplies
• Disinfect water buckets daily; clean equipment with detergent then disinfect
• Designate personnel to work only with infected or only with healthy horses
• Screen recovered horses via guttural pouch lavage PCR before reintroduction

Vaccination

Strangles vaccines are considered risk-based vaccines. Vaccination cannot guarantee disease prevention but may reduce severity. There is no consensus on routine vaccination.

Critical Vaccination Precautions

• DO NOT vaccinate during an outbreak or within 1 year of strangles exposure
• DO NOT vaccinate horses with titers greater than 1:1,600 (purpura risk)
• DO NOT vaccinate horses with clinical signs of strangles
• DO NOT give intranasal vaccine to foals less than 9-12 months old
• Give intranasal vaccine AFTER all other IM injections to prevent abscess formation
• DO NOT perform joint injections or other invasive procedures on same day as intranasal vaccine

Prognosis

Uncomplicated strangles: Good to excellent; recovery typically 3-6 weeks with supportive care

Post-infection immunity: 70-75% of horses develop immunity lasting at least 5 years

Bastard strangles: Fair to guarded; 40% long-term survival with prolonged antibiotic therapy

Purpura hemorrhagica: Guarded to poor; often severe and potentially fatal