Strangles (Streptococcus equi subsp. equi)

Strangles is a highly contagious, acute, and occasionally chronic bacterial disease of the upper respiratory tract of horses, donkeys, and mules, caused by the Lancefield group C beta-hemolytic bacterium Streptococcus equi subspecies equi (S. equi). The disease is characterized by fever, mucopurulent nasal discharge, and painful abscessation of the submandibular and retropharyngeal lymph nodes. The name 'strangles' derives from the characteristic respiratory distress and stridor caused by enlarged lymph nodes that can compress the pharynx, larynx, and trachea, potentially leading to asphyxiation. In the equine industry, strangles is a major biosecurity concern due to its high morbidity (up to 100% in naive populations) and significant economic impact from quarantine, treatment costs, and disruption of training and competition schedules. The disease affects all breeds and disciplines, including Thoroughbred racing, Standardbred racing, dressage, eventing, and pleasure horses, but is most prevalent in young horses (weanlings to 5 years old) and in populations with high turnover or commingling, such as breeding farms, boarding stables, and show grounds. Although mortality is generally low (1-10%), complications such as 'bastard strangles' (metastatic abscessation), guttural pouch empyema, and purpura hemorrhagica can be life-threatening and lead to chronic carrier states.

The primary causative agent is Streptococcus equi subspecies equi, a gram-positive, beta-hemolytic, catalase-negative coccus that forms chains. It is a host-adapted pathogen of equids, with no significant environmental reservoir outside of infected or carrier horses. The bacterium produces several virulence factors, including the antiphagocytic hyaluronic acid capsule, M-protein (SeM) which is antiphagocytic and immunogenic, streptolysins, streptokinase, and various exotoxins. The M-protein is a major virulence factor that inhibits phagocytosis and is used for serotyping and vaccine development. The bacterium is transmitted via direct contact with infected horses, fomites (e.g., water troughs, feed buckets, grooming equipment), or aerosolized respiratory secretions. It can survive in the environment for up to 6 weeks in organic material, but is susceptible to desiccation and common disinfectants. The incubation period is typically 3-14 days. The disease is not zoonotic, but humans can transiently carry the organism on skin or clothing.

Strangles is endemic worldwide, with higher prevalence in temperate climates and during cooler, wetter seasons. It affects horses of all ages, but the highest incidence is in young horses (1-5 years old) due to waning maternal immunity and increased exposure. Breed and sex predilections are not significant, but management factors such as high stocking density, frequent movement of horses, and poor biosecurity increase risk. Morbidity can reach 100% in naive populations, while mortality is typically 1-10%, but can be higher in foals or immunocompromised individuals. The disease has a significant impact on athletic careers, causing lost training days, delayed competition schedules, and potential long-term respiratory sequelae. Carrier horses, particularly those with guttural pouch empyema or chondroids, serve as reservoirs and can shed the organism intermittently for months to years, perpetuating outbreaks. The economic impact includes veterinary costs, quarantine, and loss of performance.

Following inhalation or ingestion of S. equi, the bacterium adheres to the tonsillar crypts and pharyngeal mucosa via M-protein and other adhesins. It then invades the submucosa and drains to the regional lymph nodes (submandibular and retropharyngeal). The bacteria multiply within the lymph nodes, causing acute suppurative lymphadenitis with abscess formation. The host inflammatory response, characterized by neutrophil infiltration and cytokine release, leads to tissue necrosis and abscessation. The abscesses enlarge over 1-3 weeks, eventually rupturing and draining externally (typically from the submandibular lymph nodes) or into the guttural pouches (from the retropharyngeal lymph nodes). The fever and systemic signs are due to bacteremia and release of exotoxins. In some cases, the bacteria disseminate hematogenously to other organs (lungs, liver, spleen, brain, joints, etc.), causing 'bastard strangles' or metastatic abscessation. Immunological complications, such as purpura hemorrhagica, are thought to be due to an immune-mediated type III hypersensitivity reaction to bacterial antigens, leading to vasculitis and edema.

Intrinsic factors include young age (1-5 years), immunocompromised status (e.g., concurrent disease, stress), and individual genetic susceptibility. Extrinsic factors include overcrowding, poor ventilation, contaminated water sources, shared equipment, high horse traffic, and inadequate biosecurity protocols. Stressful events such as transportation, weaning, or intense training can increase susceptibility. Lack of vaccination or incomplete vaccination protocols may also predispose to infection. The disease is more common in facilities with frequent introduction of new horses without proper quarantine.

Clinical signs typically appear 3-14 days after exposure. The classic presentation includes sudden onset of fever (103-106°F / 39.4-41.1°C), depression, anorexia, and a serous to mucopurulent nasal discharge. Within 24-48 hours, the submandibular and retropharyngeal lymph nodes become enlarged, painful, and warm. Abscessation may cause dysphagia, respiratory stridor, and a characteristic 'roaring' sound. In severe cases, airway obstruction can lead to respiratory distress and cyanosis. Some horses may develop guttural pouch empyema, which can cause chronic nasal discharge and cranial nerve deficits (e.g., dysphagia, laryngeal hemiplegia). Complications include bastard strangles (metastatic abscessation), purpura hemorrhagica (characterized by well-demarcated edema, petechial hemorrhages, and vasculitis), and agalactia in mares. Physical examination findings include elevated heart rate and respiratory rate, injected mucous membranes, and possibly petechiae in severe cases.

Differential diagnoses include other causes of upper respiratory infection and lymphadenopathy: 1) Equine influenza (EIV): acute onset of fever, dry cough, and nasal discharge, but lymph node enlargement is not typical; diagnosis via PCR or virus isolation. 2) Equine herpesvirus-1 and -4 (EHV-1/EHV-4): respiratory signs, fever, and possible neurological signs; lymph node enlargement is rare; PCR on nasal swabs. 3) Equine viral arteritis (EVA): fever, conjunctivitis, edema, and abortion; lymph node enlargement is not a feature; serology and PCR. 4) Streptococcus zooepidemicus: opportunistic pathogen causing respiratory disease, but lymph node abscessation is less common; culture and molecular typing. 5) Corynebacterium pseudotuberculosis (pigeon fever): external abscesses, particularly in the pectoral region, but can also cause lymph node abscessation; culture. 6) Rhodococcus equi (in foals): pneumonia with abscessation, but lymph node involvement is less prominent; culture and PCR. 7) Guttural pouch empyema or chondroids: chronic nasal discharge and retropharyngeal swelling, but often without acute fever; endoscopy. 8) Pharyngeal trauma or foreign body: acute dysphagia and swelling; endoscopy and radiography. 9) Neoplasia (e.g., lymphoma): chronic lymphadenopathy, but usually non-painful and progressive; biopsy. 10) Abscessation due to other bacteria (e.g., Staphylococcus aureus): culture and sensitivity.

The diagnostic approach for strangles should be systematic: 1) History and physical examination: assess for fever, nasal discharge, and lymph node swelling. 2) If lymph node abscessation is present, perform ultrasonography to confirm abscessation and guide aspiration. 3) Collect samples for laboratory confirmation: a) Swab of nasal discharge or abscess contents for bacterial culture and PCR (S. equi-specific PCR is highly sensitive and specific). b) Blood work: CBC may show leukocytosis with neutrophilia and hyperfibrinogenemia. c) Serology (anti-SeM antibodies) can be used for retrospective diagnosis or to identify carriers, but is not useful in the acute phase. 4) Endoscopy of the upper respiratory tract to evaluate the guttural pouches and pharynx for empyema or chondroids. 5) In cases of suspected bastard strangles, perform ultrasonography of the thorax and abdomen to detect metastatic abscesses. 6) For carrier detection, perform guttural pouch lavage and PCR or culture. 7) Rule out other respiratory pathogens via PCR panels. 8) In outbreak situations, implement biosecurity measures and quarantine.

Complete blood count (CBC) typically reveals leukocytosis due to mature neutrophilia, and hyperfibrinogenemia (elevated fibrinogen > 400 mg/dL). Serum amyloid A (SAA) is markedly elevated (often > 1000 mg/L) during the acute phase. Blood cultures may be positive in septicemic cases. Peritoneal fluid analysis is not typically performed unless there is suspicion of abdominal abscessation; in such cases, fluid may show increased nucleated cell count and protein. In cases of purpura hemorrhagica, serum protein may be low due to vasculitis. Guttural pouch lavage fluid may be turbid and contain neutrophils and bacteria. Culture and PCR of nasal swabs or abscess contents are the gold standard for diagnosis. PCR is highly sensitive and can detect S. equi even in chronic carriers.

Ultrasonography is the primary imaging modality for strangles. It can be used to evaluate submandibular and retropharyngeal lymph nodes for abscessation (hypoechoic to anechoic centers with surrounding hyperemia). Thoracic ultrasonography may reveal pulmonary abscesses or pleural effusion in cases of bastard strangles. Abdominal ultrasonography can detect metastatic abscesses in the liver, spleen, or mesenteric lymph nodes. Endoscopy is essential for evaluating the guttural pouches and pharynx; it can reveal empyema (purulent material) or chondroids (inspissated pus concretions) in the guttural pouches. Radiography of the throat region may show soft tissue swelling or gas within abscesses, but is less sensitive than ultrasound. CT and MRI are rarely needed but can be useful for evaluating deep abscesses or neurological complications.

Cytological examination of abscess contents or guttural pouch lavage typically shows degenerate neutrophils, intracellular and extracellular gram-positive cocci in chains, and cellular debris. Histopathology of affected lymph nodes reveals acute suppurative inflammation with abscess formation, necrosis, and edema. In cases of purpura hemorrhagica, skin biopsies may show leukocytoclastic vasculitis with fibrinoid necrosis of vessel walls. In chronic carriers, guttural pouch mucosa may show chronic inflammation and fibrosis.

Treatment of strangles depends on the stage and severity. For uncomplicated cases with external abscesses, the primary approach is supportive care and allowing abscesses to mature and rupture spontaneously. Hot compresses and hydrotherapy can promote maturation. Once the abscess has 'pointed' (softened), it should be lanced and drained under aseptic conditions. Systemic antibiotics are controversial; they are generally not recommended in uncomplicated cases because they may delay abscess maturation and immune response, potentially leading to chronic carriers. However, antibiotics are indicated in severe cases with systemic signs, dysphagia, respiratory distress, or in foals and immunocompromised animals. Penicillin G (22,000 IU/kg IV q6h or 44,000 IU/kg IV q12h) is the drug of choice, but oral antibiotics (e.g., trimethoprim-sulfamethoxazole 30 mg/kg PO q12h) may be used for less severe cases. Non-steroidal anti-inflammatory drugs (NSAIDs) such as flunixin meglumine (1.1 mg/kg IV q12-24h) or phenylbutazone (2.2-4.4 mg/kg PO q12-24h) are used to reduce fever and inflammation. For guttural pouch empyema, repeated lavage with isotonic fluids via indwelling catheters is recommended, and in some cases, surgical drainage or removal of chondroids may be necessary. For purpura hemorrhagica, corticosteroids (e.g., dexamethasone 0.04-0.1 mg/kg IV q24h) are used to suppress the immune response, along with supportive care. In cases of severe airway obstruction, emergency tracheostomy may be required.

The prognosis for uncomplicated strangles is excellent, with most horses recovering within 2-4 weeks. Mortality is low (1-10%). However, complications such as bastard strangles, guttural pouch empyema, and purpura hemorrhagica carry a guarded to poor prognosis, with mortality rates up to 30% for purpura hemorrhagica. Chronic carriers may shed the organism intermittently, posing a risk to other horses. Return to athletic performance is generally good after full recovery, but horses with guttural pouch involvement may have residual cranial nerve deficits or chronic nasal discharge. Early diagnosis and appropriate management improve the prognosis.

Follow-up care is crucial to monitor for complications and prevent spread. Horses should be isolated for at least 4 weeks after clinical signs resolve. Recheck examinations should include: 1) Serial temperature monitoring twice daily for 2 weeks after resolution of clinical signs. 2) Endoscopic examination of the guttural pouches at 2-4 weeks post-recovery to rule out empyema or chondroids. 3) PCR testing of guttural pouch lavage or nasopharyngeal swabs at 2-4 week intervals until two consecutive negative results are obtained. 4) In horses with purpura hemorrhagica, monitor for recurrence and manage with corticosteroids as needed. 5) Gradual return to work after full recovery, typically 2-4 weeks after clinical resolution. 6) Implement biosecurity measures to prevent spread to other horses.

Clinical pearls: 1) Always consider strangles in any horse with fever and lymph node swelling, especially in young horses or after exposure to new horses. 2) Ultrasonography is invaluable for assessing lymph node abscessation and guiding drainage. 3) Do not routinely use antibiotics in uncomplicated cases; they may increase the risk of chronic carriers. 4) Guttural pouch lavage is essential for treating empyema and preventing carrier states. 5) Purpura hemorrhagica is a medical emergency; treat with corticosteroids and supportive care. Pitfalls: 1) Failure to isolate affected horses promptly can lead to widespread outbreaks. 2) Lancing abscesses prematurely can cause bacteremia and spread. 3) Using antibiotics without drainage can lead to chronic abscessation. 4) Overlooking guttural pouch involvement can result in chronic carriers. 5) Misdiagnosing purpura hemorrhagica as other causes of edema can delay appropriate treatment.

Based on Plumb's Veterinary Drug Handbook and ACVIM guidelines, the following protocols are recommended: 1) Antibiotics: Penicillin G procaine (22,000 IU/kg IM q12h) or Penicillin G potassium (22,000 IU/kg IV q6h) for severe cases; for oral therapy, trimethoprim-sulfamethoxazole (30 mg/kg PO q12h) or doxycycline (10 mg/kg PO q12h) may be used, but resistance is possible. 2) NSAIDs: Flunixin meglumine (1.1 mg/kg IV or PO q12-24h) or phenylbutazone (2.2-4.4 mg/kg PO q12-24h) for fever and inflammation. 3) Corticosteroids: Dexamethasone (0.04-0.1 mg/kg IV q24h) for purpura hemorrhagica or severe inflammation. 4) Guttural pouch lavage: Use 1-2 liters of sterile isotonic saline or balanced electrolyte solution per pouch, repeated daily or every other day until clear. 5) Supportive care: IV fluids (e.g., lactated Ringer's solution at 50-80 mL/kg/day) for dehydrated or septicemic horses. 6) For pain management, consider butorphanol (0.01-0.02 mg/kg IV) or morphine (0.05-0.1 mg/kg IM) in severe cases. 7) In cases of respiratory distress, oxygen supplementation and tracheostomy may be necessary.

Key literature on strangles includes: 1) Sweeney et al. (2005) 'Streptococcus equi Infections in Horses: Guidelines for Treatment, Control, and Prevention of Strangles' (ACVIM consensus statement) provides evidence-based recommendations for diagnosis, treatment, and biosecurity. 2) Newton et al. (2000) 'Control of strangles outbreaks by isolation of guttural pouch carriers identified using PCR and culture' demonstrated the importance of identifying carriers. 3) Waller et al. (2011) 'Strangles: A review of the literature' summarizes pathogenesis and management. 4) Boyle et al. (2018) 'Streptococcus equi subsp. equi: A review of the current understanding of the disease' highlights advances in molecular diagnostics and vaccines. 5) Studies on vaccination (e.g., modified-live vaccines) have shown reduced severity but not complete prevention. 6) Research on antimicrobial therapy suggests that early antibiotic treatment may increase the risk of chronic carriers, supporting the conservative approach in uncomplicated cases. 7) Meta-analyses of outbreak management emphasize the importance of biosecurity and carrier detection.