Understanding Strangles in Horses: A Comprehensive Guide to Prevention, Diagnosis, and Treatment

What is Strangles?

Strangles is a highly contagious bacterial infection of the upper respiratory tract in horses, characterized by severe inflammation of the lymph nodes in the head and neck region, often resulting in the formation of large abscesses that may rupture and drain thick pus. The disease derives its dramatic name from the characteristic clinical sign of severely affected horses—the swollen lymph nodes in the throat area can become so enlarged that they compress the pharynx and larynx, causing difficulty breathing that sounds like strangulation, though actual suffocation is rare.

The causative agent is Streptococcus equi subspecies equi (commonly abbreviated as S. equi or Strep equi)—a highly host-adapted bacterium that has evolved specifically to infect horses. This gram-positive coccus (spherical-shaped bacterium) produces numerous virulence factors enabling it to evade immune defenses, colonize the upper respiratory tract, and cause the characteristic lymph node infections that define the disease.

Strangles represents one of the most common infectious diseases affecting horses worldwide, occurring in virtually every country where horses are kept. The disease has been recognized for centuries—one of the earliest detailed descriptions dates to 1251, making it one of the oldest recorded equine diseases. Despite its long history and extensive research, strangles remains a significant problem in the equine industry, causing substantial economic losses through treatment costs, quarantine requirements, lost training and competition time, and occasionally, mortality.

The disease primarily affects young horses, with the highest incidence in animals between one and five years of age, though horses of any age can be infected if they lack immunity. Outbreaks commonly occur in facilities housing large numbers of horses—particularly boarding stables, training centers, breeding farms, racetracks, and show grounds—where close contact between animals facilitates transmission. The introduction of a single infected horse into a susceptible population can trigger explosive outbreaks affecting the majority of exposed horses within days to weeks.

Understanding strangles—its transmission, clinical signs, diagnosis, treatment, prevention, and management of outbreaks—proves essential for anyone involved with horses, as prompt recognition and appropriate response can minimize disease spread and complications.

The Causative Bacterium: Streptococcus equi

Streptococcus equi subspecies equi possesses several characteristics that make it a particularly successful equine pathogen and challenging disease to control.

Bacterial Characteristics

S. equi is a gram-positive coccus that appears in chains when viewed under microscopy. The bacterium is:

Beta-hemolytic: Produces complete hemolysis (destruction) of red blood cells when cultured on blood agar plates
Catalase-negative: Lacks the catalase enzyme, a characteristic used in laboratory identification
Lancefield Group C: Based on specific carbohydrate antigens in the cell wall

The bacterium produces a polysaccharide capsule—a thick, gelatinous coating that helps it evade phagocytosis (engulfment by immune cells) and resist destruction by the horse’s immune system. This capsule represents a critical virulence factor enabling the bacterium to survive long enough to establish infection.

Virulence Factors

S. equi produces numerous proteins and enzymes that contribute to its pathogenicity:

M-protein (SeM): A major surface protein that:

Prevents phagocytosis by binding host immune proteins
Enables adhesion to respiratory epithelial cells
Triggers strong antibody responses (important for immunity and diagnosis)

Hyaluronic acid capsule: Mimics host tissues, helping the bacterium evade immune recognition

Streptococcal pyrogenic exotoxins: Contribute to inflammation and tissue damage

Streptolysin S: A toxin that damages cell membranes and destroys immune cells

DNases, hyaluronidases, and other enzymes: Facilitate tissue invasion and bacterial spread

Host Specificity

S. equi demonstrates remarkable host specificity, infecting only equids (horses, ponies, donkeys, mules, zebras). Humans and other animals are not susceptible to infection with S. equi, though people can mechanically transmit the bacteria on contaminated hands, clothing, or equipment. This host specificity reflects millions of years of co-evolution between the bacterium and equine hosts.

Environmental Survival

Understanding how long S. equi survives outside the horse influences biosecurity and disinfection strategies:

In the environment:

Survives in water for up to four weeks
Persists in moist organic material (feed, bedding contaminated with nasal discharge or abscess drainage) for 4-6 weeks or longer
Survives on dry surfaces for shorter periods (days to weeks depending on conditions)
Killed by freezing and thawing cycles, reducing survival in winter in cold climates
Killed by direct sunlight and desiccation within hours to days
Sensitive to most common disinfectants when used properly

The bacterium’s ability to persist in the environment for weeks means that facilities, equipment, and areas where infected horses have been housed can serve as sources of infection long after sick horses are removed.

Transmission and Spread

Strangles spreads highly efficiently through horse populations via multiple transmission routes:

Direct Contact Transmission

Horse-to-horse contact represents the most important transmission route:

Nose-to-nose contact: Infected horses shed massive numbers of bacteria in nasal discharge; direct nasal contact with susceptible horses transmits infection efficiently
Social grooming: Horses nuzzling each other’s heads and necks can spread bacteria
Close proximity: Horses housed in adjacent stalls with shared air space can transmit infection through aerosol droplets from coughing or snorting

Indirect Contact Transmission

Fomites—inanimate objects contaminated with bacteria—serve as important transmission vehicles:

Shared water buckets and troughs: Probably the most important fomite; infected horses contaminate water sources that subsequently infect others
Shared feed buckets and hay nets
Grooming equipment: Brushes, combs, and other tools used on multiple horses
Tack: Bridles, bits, halters shared between horses
Handlers’ hands and clothing: People moving between horses without changing clothes or washing hands
Veterinary equipment: Nasogastric tubes, endoscopes, or other equipment used on multiple horses without proper disinfection

Environmental Contamination

Contaminated facilities and pastures:

Fence lines, gates, and posts that horses touch with their noses
Pastures where infected horses have grazed (particularly around water sources and feeding areas)
Barn aisles, stall walls, and any surfaces contacted by infected horses
Trailers used to transport infected horses

“Silent Carriers”

An important and challenging aspect of strangles epidemiology involves asymptomatic carriers—horses that harbor S. equi in their guttural pouches (air-filled compartments connected to the back of the throat) without showing clinical signs. These carriers:

Represent 1-10% of horses that have recovered from strangles
Intermittently or continuously shed bacteria for months to years after recovery
Appear completely healthy, making identification difficult
Serve as sources of new outbreaks when introduced into susceptible populations
Can only be reliably identified through specialized testing (guttural pouch endoscopy and culture or PCR)

The carrier problem makes strangles particularly difficult to eradicate from some facilities and contributes to the disease’s persistence in horse populations globally.

Incubation Period

After exposure, the incubation period—time from infection to development of clinical signs—typically ranges from 3-14 days, with most horses showing signs within 4-8 days. However, some horses may not develop signs for up to three weeks after exposure.

During the late incubation period, horses begin shedding bacteria before obvious clinical signs develop, enabling disease spread before owners recognize infection is present.

Pathophysiology: How Strangles Develops

Understanding what happens during strangles infection helps explain the clinical signs and complications.

Initial Infection

When S. equi enters a horse’s upper respiratory tract (typically through nasal inhalation or oral contact with contaminated sources), the bacteria:

Colonize the nasopharynx (back of the nasal passages and throat), adhering to epithelial cells lining the respiratory tract
Penetrate the mucosal barrier, crossing through or between epithelial cells to access underlying tissues
Resist immune defenses using their capsule and other virulence factors to avoid destruction by local immune cells

Lymph Node Involvement

The bacteria are picked up by the lymphatic system—the network of vessels that drains tissue fluid and transports it to lymph nodes where immune responses occur. S. equi is carried to the regional lymph nodes that drain the head and neck region, particularly:

Submandibular lymph nodes: Located under the jaw, between the branches of the mandible
Retropharyngeal lymph nodes: Located in the throat area behind the pharynx
Sometimes parotid lymph nodes: Near the ear base

Within the lymph nodes, the bacteria multiply rapidly, triggering intense inflammatory responses. The immune system attempts to contain the infection by forming abscesses—localized collections of pus (dead bacteria, dead white blood cells, and inflammatory debris) walled off by fibrous tissue.

Abscess Formation and Maturation

Over days to weeks, the infected lymph nodes:

Swell dramatically, becoming hot, firm, and painful
Develop central areas of liquefaction as tissue breaks down and pus accumulates
Gradually “mature” as the abscess becomes more superficial
Eventually rupture spontaneously, draining thick, creamy yellow-white to greenish pus through the skin or into the guttural pouches

Resolution

After abscess drainage, most horses begin recovering:

Fever resolves
Appetite returns
Lymph nodes gradually shrink
Drainage sites heal over weeks

The immune system, stimulated by intense exposure to bacterial antigens during active infection, produces strong immunity that protects most recovered horses from reinfection for months to years (though immunity is not always permanent or complete).

Clinical Signs and Symptoms

Strangles produces a characteristic clinical presentation, though severity varies considerably among affected horses.

Typical Clinical Course

Early signs (Days 1-3):

Fever: Temperature elevation to 103-106°F (39.4-41.1°C), often the first detectable sign
Depression and lethargy: Affected horses appear dull, depressed, and uninterested in surroundings
Decreased appetite: Reluctance to eat, particularly hard feeds
Nasal discharge: Initially watery and clear, rapidly becoming thick and mucopurulent (containing mucus and pus)

Progressive signs (Days 3-10):

Continued fever and malaise
Profuse nasal discharge: Thick, purulent discharge streaming from both nostrils, often yellow-white or greenish
Lymph node swelling: The submandibular and/or retropharyngeal lymph nodes become noticeably enlarged, creating visible and palpable swellings under the jaw and in the throat area
Pain and difficulty swallowing (dysphagia): Swollen lymph nodes and throat inflammation make swallowing painful; horses may drop food from their mouths or discharge feed material and saliva through their noses
Extended head and neck: Horses hold their heads extended and lowered to ease breathing and swallowing discomfort
Coughing: May be soft and moist, sometimes bringing up purulent material
Respiratory distress: In severe cases, swelling may narrow the airway, causing increased respiratory rate, flared nostrils, and loud breathing sounds

Abscess maturation and rupture (Days 7-21):

The swollen lymph nodes become increasingly enlarged and may feel fluctuant (fluid-filled) rather than firm
The overlying skin may appear stretched, shiny, and develop moist discharge or small openings
Spontaneous rupture typically occurs 1-3 weeks after initial signs, with sudden drainage of large volumes (sometimes cupfuls) of thick pus
Many horses show dramatic improvement within 24-48 hours after abscess drainage—fever resolves, appetite returns, attitude improves

Recovery (Weeks 3-6):

Drainage gradually decreases over days to weeks
Drainage tracts heal, usually leaving small scars
Lymph nodes gradually shrink to near-normal size
Most horses return to normal health

Severity Variations

Clinical severity ranges from mild to life-threatening:

Mild cases:

Low-grade fever
Modest nasal discharge
Minimal lymph node swelling
Little systemic illness
Rapid recovery

These mild cases may be missed entirely or attributed to minor respiratory infections, yet affected horses shed bacteria and can transmit disease.

Severe cases:

High fever (105-106°F)
Profound depression
Complete anorexia
Massive lymph node abscesses
Significant respiratory distress
Potential for serious complications

Peracute cases (rare):

Overwhelming infection
Death within days before abscesses form
Occurs primarily in very young foals or immunocompromised horses

Age-Related Differences

Young horses (weanlings to 3-year-olds) typically show more severe disease than adults, likely reflecting lack of previous exposure and naïve immune systems.

Adult horses with previous exposure often show milder signs or may resist infection entirely due to residual immunity.

Very young foals (under 3 months) rarely develop strangles, protected by maternal antibodies received through colostrum.

Complications of Strangles

While most horses recover uneventfully, approximately 20-30% develop complications, some of which can be life-threatening.

Respiratory Obstruction

Severe swelling of retropharyngeal lymph nodes can cause critical airway narrowing:

Progressive respiratory distress with labored breathing
Stridor (harsh breathing sounds)
Inability to get adequate air
Requires emergency intervention—tracheostomy (surgical creation of breathing opening in the trachea) may be necessary

Guttural Pouch Empyema

The guttural pouches—paired air-filled diverticula of the Eustachian tubes located in the throat region—can become infected when retropharyngeal abscesses drain into them:

Pus accumulates in the guttural pouches (empyema)
Creates persistent infection site
Causes chronic nasal discharge
May develop into carrier state if not treated
Requires specialized treatment including guttural pouch lavage (flushing)

Chondroids

Chondroids are inspissated (dried, hardened) masses of pus that form in guttural pouches when pus accumulates and loses moisture:

Range from small pellets to masses several inches in diameter
Create chronic infection and drainage
Can obstruct Eustachian tube function
Require surgical removal

Metastatic Abscessation

In some horses, S. equi spreads beyond the head and neck lymph nodes to form abscesses in distant locations:

Abdominal abscesses:

Form in mesenteric lymph nodes or abdominal organs
Cause chronic weight loss, recurrent fever, colic episodes
Often difficult to diagnose
May require prolonged antibiotic treatment
Can be fatal

Thoracic (chest) abscesses:

Form in mediastinal lymph nodes
Cause respiratory difficulty and weight loss

Brain abscesses (rare):

Cause neurological signs
Often fatal

Other locations:

Liver, spleen, kidneys
Muscles
Essentially any organ can be affected

Purpura Hemorrhagica

Purpura hemorrhagica represents a serious immune-mediated complication occurring in approximately 1-5% of strangles cases:

Pathophysiology: An excessive immune response produces immune complexes (antibodies bound to bacterial antigens) that deposit in blood vessel walls, causing vasculitis (blood vessel inflammation) and hemorrhage.

Clinical signs (typically developing 2-4 weeks after initial strangles infection):

Sudden development of extensive subcutaneous edema (swelling under the skin), particularly affecting the head, limbs, and ventral abdomen
Petechiae and ecchymoses (pinpoint to larger hemorrhages) visible on mucous membranes
Swelling can be so severe that the head becomes grossly distorted and limbs swell to several times normal size
Fever, depression, loss of appetite
Protein loss from damaged vessels can cause hypoproteinemia
Can be life-threatening

Treatment: Requires aggressive therapy with corticosteroids to suppress the immune response, plus supportive care. Prognosis is guarded; some horses die despite treatment, while others recover fully.

Myocarditis

Heart muscle inflammation occasionally occurs as a complication, causing:

Irregular heart rhythms
Exercise intolerance
Potentially sudden death

Laryngeal Hemiplegia (Roaring)

Damage to the nerves supplying the larynx (voice box) can result from:

Direct pressure from enlarged lymph nodes
Inflammation affecting adjacent structures
Guttural pouch mycosis (fungal infection) developing as a sequela

This causes permanent paralysis of the larynx, creating abnormal breathing sounds (roaring) during exercise and reduced athletic performance.

Other Complications

Aspiration pneumonia: From difficulty swallowing
Sinusitis: Extension of infection into sinus cavities
Bastard strangles: Old term for metastatic abscessation
Chronic carrier state: Persistent guttural pouch infection

Diagnosis

Diagnosing strangles combines clinical assessment with laboratory confirmation.

Clinical Diagnosis

Classic presentation—fever, purulent nasal discharge, swollen submandibular lymph nodes, and occurrence in young horses in outbreak situations—creates strong clinical suspicion. However, definitive diagnosis requires laboratory confirmation, as other respiratory diseases can produce similar signs.

Sample Collection

Nasopharyngeal swabs or washes:

Collecting samples from the back of the nasal passages or nasopharynx
Best performed early in disease (during first 2-3 days of fever/nasal discharge)
Sensitivity decreases once abscesses have walled off bacteria

Abscess aspirates or drainage:

Collecting pus from abscesses (via needle aspiration before rupture or from drainage after rupture)
Provides excellent samples when available
Highest diagnostic yield

Guttural pouch samples:

Obtained via endoscopy
Useful for identifying carriers
Requires specialized equipment

Laboratory Testing

Bacterial culture:

Growing S. equi from samples on blood agar plates
Provides definitive diagnosis
Takes 24-48 hours for results
Allows antimicrobial sensitivity testing if needed
Sensitivity limitations: Culture may be negative even in infected horses if samples taken at wrong time or bacteria are deep within abscesses

PCR (polymerase chain reaction):

Detects S. equi DNA in samples
More sensitive than culture—detects bacteria even when culture is negative
Faster results (often same day to 24 hours)
Can distinguish S. equi from closely related S. zooepidemicus
Increasingly becoming the preferred diagnostic method
Quantitative PCR (qPCR) provides information about bacterial numbers, helping distinguish active infection from small numbers of dead bacteria

Serology (antibody testing):

Measures antibodies against S. equi in blood
Useful for:
- Confirming recent infection in horses with compatible signs but negative cultures
- Screening for exposure in outbreak situations
- Assessing immune status before vaccination
Does NOT distinguish active infection from previous infection or vaccination
Not useful for diagnosing acute strangles but helpful in specific situations

Diagnostic Challenges

Early sampling before bacteria are established or when bacteria are walled off in developing abscesses may yield false-negative results.

Distinguishing S. equi from S. zooepidemicus: These closely related bacteria can be confused; S. zooepidemicus is a common commensal (normal resident) bacterium that occasionally causes opportunistic infections but is not the true strangles organism.

Carrier identification: Requires specialized testing (guttural pouch endoscopy with sampling), as carriers appear healthy.

Treatment

Strangles treatment remains controversial, particularly regarding antibiotic use. Management approaches must be individualized based on disease severity, stage, and specific circumstances.

Supportive Care (Cornerstone of Treatment)

Supportive care benefits all affected horses:

Isolation: Immediate separation from healthy horses to prevent disease spread

Rest: Strict rest avoiding any work or stress

Environmental management:

Comfortable, well-ventilated housing (not drafty but good air circulation)
Soft, dust-free bedding
Easy access to feed and water without having to move excessively

Nutritional support:

Soft, palatable feeds: Soaked hay cubes, bran mashes, soaked pelleted feeds that are easier to swallow
Warm food: Slightly warming feed may increase palatability and comfort
Small, frequent meals: Multiple small feedings rather than large meals
Ensure adequate hydration: Fresh water always available; may need intravenous fluids if horse won’t drink

Analgesics (pain relief):

NSAIDs like phenylbutazone or flunixin meglumine reduce pain, fever, and inflammation
Improve comfort and encourage eating

Topical therapy:

Hot packing abscessed lymph nodes may encourage maturation and drainage
Hydrotherapy (warm water bathing) of affected areas
Poulticing materials applied to encourage drainage

Tracheostomy if needed:

Emergency procedure creating surgical opening in trachea
Necessary for horses with severe respiratory obstruction
Maintains airway until swelling resolves

Antibiotic Therapy (Controversial)

The role of antibiotics in strangles treatment is hotly debated among veterinarians, with valid arguments on both sides.

Arguments FOR antibiotic use:

May reduce disease severity in early stages
May prevent complications including metastatic abscesses
Reduces bacterial shedding duration
Appropriate for severe cases, horses with complications, or valuable horses

Arguments AGAINST routine antibiotic use:

May delay abscess maturation, prolonging disease course
Bacteria walled off in abscesses may be protected from antibiotics
May interfere with development of natural immunity
Risk of purpura hemorrhagica may be increased (controversial)
Most horses recover without antibiotics

Current consensus:

Withhold antibiotics in uncomplicated cases where:

Abscesses are forming normally and expected to drain spontaneously
Horse is eating and drinking adequately
No respiratory distress
No evidence of complications
Allow natural disease course and development of strong immunity

Use antibiotics in:

Very early stages (first 24-48 hours) before abscesses form—may abort disease
Severe respiratory distress requiring intervention
Confirmed or suspected complications (metastatic abscesses, pneumonia)
Immunocompromised horses
Very valuable horses where even small risk of complications is unacceptable
Situations where quarantine/isolation not possible to reduce shedding duration

Antibiotic selection:

Penicillin remains the drug of choice (S. equi is typically susceptible)
Potassium penicillin G: 22,000 IU/kg IV every 6 hours
Procaine penicillin G: 22,000 IU/kg IM every 12 hours
Treatment duration: At least 7-10 days, sometimes longer if complications present
Alternative antibiotics: Ceftiofur, trimethoprim-sulfonamides, or others based on culture/sensitivity if penicillin resistance or allergy

Surgical Drainage

Lancing abscesses (surgical drainage) was historically common but is now generally discouraged in favor of allowing spontaneous drainage:

Reasons to avoid surgical drainage:

May spread infection to surrounding tissues
Creates wounds requiring management
Risks spreading bacteria to new areas
Drainage tracts may persist longer
Most abscesses drain spontaneously within reasonable timeframes

Occasional indications for surgical intervention:

Abscesses failing to drain after prolonged maturation
Large abscesses causing significant obstruction
Guttural pouch empyema requiring lavage
Chondroid removal

Treatment of Complications

Guttural pouch empyema:

Guttural pouch lavage (flushing) via endoscopic approach
Installation of antimicrobial solutions
May require repeated treatments
Surgical drainage in refractory cases

Chondroids:

Surgical removal via guttural pouch approach

Purpura hemorrhagica:

High-dose corticosteroids (dexamethasone or prednisolone)
Supportive care including IV fluids
Hydrotherapy for limb swelling
Controlled walking to reduce edema
Intensive monitoring

Metastatic abscesses:

Prolonged antibiotic therapy (weeks to months)
Supportive care
Surgical drainage if accessible

Biosecurity and Outbreak Management

Managing strangles outbreaks requires strict biosecurity protocols to minimize disease spread.

Isolation and Quarantine

Immediate isolation of sick horses:

Move to dedicated isolation facility as far from other horses as possible
Ideally separate building or at minimum 50+ feet from healthy horses
No shared air space, equipment, or personnel

Quarantine exposed horses:

Horses that had contact with sick horses but aren’t yet showing signs
Monitor twice daily for fever (any temperature >101.5°F warrants further investigation)
Maintain separate from both sick horses and unexposed horses
Three groups: sick (isolation), exposed (quarantine), unexposed (clean)

Duration:

Maintain isolation/quarantine until all horses have been fever-free and without nasal discharge for at least 3 weeks
Perform testing (culture or PCR) before releasing horses from quarantine
Minimum 4-6 weeks typically required

Movement Restrictions

Complete lockdown of affected facilities:

No horses in or out
No shared equipment with other facilities
No participation in shows, competitions, or events
Notify neighboring facilities, show organizers, and regulators as appropriate

Personnel and Equipment Hygiene

Dedicated personnel:

Ideally, separate people caring for sick, quarantined, and healthy horses
If not possible, care for clean horses FIRST, then quarantine, then sick horses last
Change clothes and boots between groups

Personal protective equipment (PPE):

Coveralls or dedicated outer clothing
Gloves
Boot covers or dedicated boots
Consider masks when handling sick horses

Hand hygiene:

Wash hands thoroughly with antimicrobial soap
Alcohol-based hand sanitizers as adjunct

Equipment:

Dedicate equipment (water buckets, feed tubs, pitchforks, wheelbarrows, grooming supplies, tack, etc.) to sick horses—do NOT share with healthy horses
Disinfect thoroughly after outbreak resolution before returning to general use
Disposable items preferred when practical

Facility Disinfection

Effective disinfectants against S. equi:

1:10 dilution of household bleach (sodium hypochlorite)
Accelerated hydrogen peroxide products
Quaternary ammonium compounds
Phenolic disinfectants
Commercial products labeled effective against Streptococcus species

Disinfection protocol:

Remove organic matter: Thoroughly clean surfaces to remove bedding, feed, manure, and discharge—disinfectants don’t work well in presence of organic material
Apply disinfectant: Follow manufacturer’s instructions for dilution and contact time
Allow adequate contact time: Most disinfectants require 10+ minutes of wet contact
Rinse if needed: Some products require rinsing before horse contact

Areas requiring disinfection:

Stalls, including walls, floors, feeders, waterers
Barn aisles, grooming areas, wash stalls
Trailers used to transport sick horses
Fencing, gates, posts that horses contacted
All equipment and tools

Water sources:

Drain and disinfect automatic waterers
Replace or disinfect water buckets
Ensure pasture water sources aren’t contaminated

Environmental Management

Pasture management:

Rest pastures used by sick horses for at least 4 weeks (longer is better)
Sunlight and desiccation help kill bacteria
Cold climate freezing helps eliminate bacteria
Remove or treat feed waste and areas of heavy contamination

Manure management:

Properly compost manure from sick horses (heat generated by composting kills bacteria)
Keep isolated from clean horse areas

Testing and Surveillance

Testing recovering horses:

Perform nasal swabs or washes for PCR/culture 3 weeks after clinical signs resolve
Three negative tests (collected at least 1 week apart) confirm the horse is not shedding
Some protocols require guttural pouch endoscopy to definitively rule out carrier state

Identifying carriers:

Consider screening horses that have recovered from strangles for carrier state
Guttural pouch endoscopy with sampling represents gold standard
Particularly important for horses that will join new herds

New Horse Protocols

Prevent introduction of strangles:

Quarantine all new arrivals:

Isolate for at least 2 weeks (3-4 weeks preferred)
Monitor for any signs of illness
Consider testing (nasal swab PCR) before introducing to resident horses

Obtain health history:

Recent exposure to sick horses?
Recent attendance at shows, sales, or events where exposure possible?
Vaccination history?
Previous strangles history?

Vaccination

Vaccines are available for strangles but have limitations and controversies regarding efficacy and appropriate use.

Available Vaccines

Intramuscular (injectable) vaccines:

Modified-live or killed bacterial products
Administered in the muscle
Multiple products available worldwide (specific products vary by country)

Intranasal vaccine:

Modified-live attenuated S. equi
Administered into the nostrils
Stimulates local mucosal immunity

Vaccine Efficacy

Strangles vaccines provide incomplete protection:

Reduce disease severity rather than preventing infection entirely
May reduce clinical signs if infection occurs
May decrease shedding duration
Efficacy estimates vary (approximately 50-75% reduction in clinical disease)
Do not reliably prevent infection, particularly with high infectious doses

Adverse Reactions

Strangles vaccines, particularly injectable products, have higher adverse reaction rates than many other equine vaccines:

Local reactions (common):

Swelling, pain, and abscess formation at injection sites
Can be severe, creating large muscle abscesses
Particularly problematic in the neck

Systemic reactions:

Fever, lethargy, decreased appetite
Purpura hemorrhagica (rare but serious)

Intranasal vaccine reactions:

Generally milder than injectable vaccines
Occasional mild nasal discharge or lymph node swelling
Very rare reports of abscess formation

Vaccination Recommendations

Consider vaccination for:

Horses at HIGH RISK of exposure (training barns, show horses, horses frequently traveling)
Young horses entering higher-risk environments
Facilities with endemic strangles problems

Generally NOT recommended for:

Low-risk horses (home horses with limited exposure to outside horses)
During active outbreaks (don’t vaccinate exposed or sick horses)
Horses that have recently recovered from strangles (already have natural immunity)

Vaccination protocols:

Initial series: typically 2-3 doses spaced 2-4 weeks apart
Boosters: annually or semi-annually for high-risk horses
Many experts prefer intranasal vaccine due to better side effect profile

Important considerations:

Vaccination may cause positive antibody titers, complicating serological testing
Never vaccinate sick horses or horses exposed during outbreak (may exacerbate disease or trigger purpura)
Discuss risks and benefits with veterinarian for individual situations

Immunity and Reinfection

Natural immunity following strangles infection is generally strong but not always permanent:

Most recovered horses develop robust immunity lasting months to several years
Some horses appear protected for life after single infection
Others can be reinfected, though subsequent infections are typically milder
Immunity appears stronger after natural infection than after vaccination

Factors affecting immunity:

Severity of initial infection (more severe = stronger immunity)
Age at first infection
Individual immune response variations
Time since infection (immunity gradually wanes)

Prognosis

Overall prognosis for horses with uncomplicated strangles is generally good:

Mortality rate: Less than 10% overall (approximately 1-2% in uncomplicated cases)
Recovery rate: 90%+ of affected horses recover fully
Return to full function: Most horses return to previous activities without long-term effects
Recovery timeline: 4-6 weeks for uncomplicated cases

Factors worsening prognosis:

Development of complications (metastatic abscesses, purpura hemorrhagica)
Severe respiratory obstruction
Very young or very old horses
Concurrent health problems
Delayed or inadequate treatment

Complications significantly worsen outcomes:

Purpura hemorrhagica: 30-50% mortality despite treatment
Metastatic abscesses: Guarded prognosis; some fatal
Severe respiratory obstruction: Can be fatal if not managed

Economic Impact

Strangles creates substantial economic costs:

Direct costs:

Veterinary care and medications
Laboratory testing
Facility cleaning and disinfection
Dedicated equipment and supplies
Increased labor for isolation and biosecurity

Indirect costs:

Lost training time
Inability to compete or sell horses during quarantine
Long-term sequelae requiring ongoing care
Facility reputation damage
Decreased business during and after outbreaks

Industry-wide impacts:

Estimated millions of dollars annually in losses globally
Event cancellations
Movement restrictions affecting commerce

Zoonotic Potential

Humans are NOT susceptible to infection with S. equi. However, people can:

Mechanically transmit bacteria on contaminated hands, clothing, equipment
Play important role in disease spread if biosecurity not practiced
Very rare reports of human skin infections after extensive contact with infected material (likely opportunistic infections rather than true strangles)

Personnel should:

Practice good hygiene to avoid spreading bacteria between horses
Wash hands thoroughly
Change clothing between infected and healthy horses
Follow biosecurity protocols

Future Directions and Research

Ongoing research focuses on:

Developing more effective vaccines with fewer side effects
Better understanding immune responses and duration of immunity
Molecular epidemiology to track outbreak sources and transmission patterns
Improved diagnostic tests for rapid, sensitive detection
Better identification of carrier horses
Alternative treatment approaches
Understanding factors affecting disease severity and complications

Conclusion

Strangles, caused by Streptococcus equi subspecies equi, represents one of the most important infectious diseases affecting horses worldwide. This highly contagious bacterial infection of the upper respiratory tract characteristically produces fever, profuse purulent nasal discharge, and abscessation of lymph nodes in the head and neck region. While most horses recover fully with supportive care, approximately 20-30% develop complications ranging from minor (guttural pouch empyema) to life-threatening (purpura hemorrhagica, metastatic abscesses).

The disease spreads efficiently through direct horse-to-horse contact, contaminated equipment and facilities, and insidiously through asymptomatic carriers harboring bacteria in their guttural pouches. This efficient transmission, combined with prolonged environmental survival of the bacterium, makes strangles outbreaks challenging to control once introduced into horse populations.

Diagnosis requires laboratory confirmation through bacterial culture or PCR testing of samples from the nasopharynx or abscess material. Treatment centers on supportive care including isolation, nutritional support, pain management, and allowing abscesses to mature and drain naturally. Antibiotic therapy remains controversial, generally reserved for specific situations rather than routine use in uncomplicated cases.

Prevention and outbreak management demand rigorous biosecurity protocols including immediate isolation of sick horses, quarantine of exposed horses, strict movement restrictions, meticulous hygiene and disinfection, and careful screening of new horses before introduction to resident populations. Vaccination provides partial protection but should be reserved for high-risk horses due to incomplete efficacy and relatively high adverse reaction rates.

Understanding strangles—its transmission, clinical presentation, diagnosis, treatment, and particularly the critical importance of biosecurity—enables horse owners, farm managers, and equine professionals to respond effectively when faced with this common but serious disease. Early recognition, appropriate isolation, supportive care, and strict biosecurity minimize disease spread, prevent complications, and optimize outcomes for affected horses while protecting healthy horses from this highly contagious infection.