Bit & Bridle

Equine Rhodococcosis

Other Names

  • Rhodococcus equi Infection
  • Equine Pneumonia (Rhodococcus)
  • Foal Pneumonia (R. equi)
  • Corynebacterium equi Infection (historical name)
  • Equine Lung Abscess

What is Equine Rhodococcosis?

Equine Rhodococcosis is a serious and potentially fatal bacterial disease caused by Rhodococcus equi, a Gram-positive soil bacterium. The disease primarily affects foals between one and six months of age, causing a distinctive suppurative (pus-forming) pneumonia characterised by the development of multiple large abscesses throughout the lungs. It is one of the most significant causes of mortality in foals in many horse-breeding regions worldwide, and managing it effectively represents a major challenge on breeding farms.

R. equi is an intracellular pathogen — it survives and replicates inside macrophages, the very immune cells normally responsible for destroying bacteria. This makes it inherently difficult to treat and means that conventional antibiotic approaches are less effective than combinations that penetrate within cells. The organism is ubiquitous in soil and horse faeces on most horse farms, and foals are inevitably exposed from birth; whether they develop disease depends on the bacterial virulence, the dose of exposure, and the foal’s developing immune capacity.

Causes

Rhodococcus equi is found in soil globally. Key aspects of its epidemiology in horses:

  • Route of infection: Foals primarily acquire infection by inhaling dust particles contaminated with R. equi. The organism is shed in faeces of infected foals and adult horses, enriches in soil with repeated horse contact, and becomes airborne in dusty conditions.
  • Virulence plasmid: Virulent strains of R. equi carry a virulence-associated plasmid (VAP) encoding proteins — particularly VapA — that allow the bacterium to survive intracellularly. Only VAP-positive strains cause typical equine pneumonia. Testing of isolates for VAP status is useful both diagnostically and for epidemiological monitoring on farms.
  • Farm prevalence: On endemic farms, R. equi concentrations in soil can be very high, and the majority of foals may be subclinically infected whilst only some develop clinical disease.
  • Predisposing factors: High bacterial load in the environment, dusty conditions, large foal groups, inadequate passive immunity transfer, and the natural immaturity of the foal’s cell-mediated immune response all increase disease risk.

The disease is not transmitted directly from foal to foal or from foal to adult horses through the respiratory route; indirect environmental transmission via soil is the dominant route.

Symptoms and Signs

Rhodococcosis is insidious — foals often appear relatively well in the early stages whilst extensive pulmonary abscesses develop. By the time overt respiratory signs are visible, the lungs may be severely compromised:

  • Coughing — initially mild and intermittent, progressively worsening
  • Increased respiratory rate and effort — nostril flaring, laboured breathing
  • Fever — often intermittent, sometimes spiking dramatically
  • Exercise intolerance and fatigue — foals tire easily and lag behind the mare
  • Mucopurulent nasal discharge
  • Weight loss and failure to thrive despite nursing
  • Generalised depression and lethargy
  • In some foals: extrapulmonary involvement — diarrhoea (intestinal abscessation), joint swelling (septic arthritis), eye disease (uveitis), or lymph node abscessation

The combination of subacute pneumonia in a 1–6 month old foal on a breeding farm with a history of the disease should always prompt immediate investigation for rhodococcosis.

Diagnosis

Early diagnosis is critical for treatment success. Several diagnostic approaches are used:

  • Thoracic ultrasonography: The most sensitive and practical tool for detecting early rhodococcal pneumonia. Allows visualisation of pulmonary abscesses, consolidation, and pleural changes. Regular ultrasonographic screening (every 2 weeks from 4–16 weeks of age) on endemic farms enables early detection before clinical signs develop.
  • Thoracic radiography: Reveals lung consolidation, abscesses, and the characteristic patterns of rhodococcal pneumonia. Requires appropriate equipment and sedation.
  • Tracheobronchial wash (TW) / bronchoalveolar lavage (BAL): Fluid collected from the airways is cultured for R. equi and cytology assessed. The gold standard for microbiological confirmation, though requires specialist equipment.
  • Blood work: Elevated fibrinogen, leucocytosis, and elevated SAA support active infection. Serial monitoring helps gauge treatment response.
  • PCR testing: Rapid detection of R. equi DNA in tracheal wash samples; also allows VAP plasmid status determination.
  • Serology: Antibody tests have been developed but are inconsistent in discriminating infected from exposed foals.

Treatment

Treatment relies on antimicrobials that achieve high intracellular concentrations, as R. equi lives within macrophages:

  • Rifampicin combined with a macrolide antibiotic: The standard treatment. Rifampicin is almost always used in combination to prevent rapid development of resistance. Macrolide choices include:
    • Azithromycin — convenient once-daily dosing, good palatability
    • Clarithromycin — twice daily dosing, excellent tissue penetration
    • Erythromycin — older, more GI side effects but still used in some protocols
  • Duration: Treatment is prolonged — typically four to nine weeks depending on response. Monitoring by serial ultrasonography guides the duration.
  • Supportive care: NSAIDs for fever and inflammation, nutritional support, and controlled exercise (to promote airway drainage) are part of comprehensive management.
  • Warning — macrolide-associated hyperthermia: Foals treated with macrolides in hot weather can develop life-threatening hyperthermia (overheating) — they must be kept in shade and cool environments, with body temperature monitored regularly. This is a significant management consideration on warm-weather farms.

Extrapulmonary disease (joint infection, intestinal abscessation) requires additional targeted management and typically carries a more guarded prognosis.

Prevention

Prevention on endemic farms is multi-pronged:

  • Hyperimmune plasma: Plasma from horses with high anti-R. equi antibody titres, given to foals at birth and repeated at 1–2 weeks of age, significantly reduces the severity of disease in endemic farms. This is the most effective preventive intervention currently available.
  • Ultrasonographic screening: Early detection enables treatment before disease becomes severe and before clinical signs develop. Mandatory on high-risk farms.
  • Reduce environmental contamination: Decrease stocking density, avoid overcrowding in paddocks, remove manure regularly, and reduce dust through pasture management and wetting of dry areas.
  • Ventilation: Ensure good airflow in foaling boxes and early paddock management to minimise aerosol concentrations of contaminated dust.
  • Avoid communal foal creches that concentrate foals in dusty conditions.

Prognosis

Prognosis depends critically on the severity of disease at diagnosis and how early treatment begins. Foals detected through screening before overt clinical signs and started on treatment promptly have a good prognosis for recovery and long-term soundness. Foals with advanced pneumonia, respiratory distress, or extrapulmonary disease have a guarded prognosis, and mortality rates can be significant in severely affected cases. On endemic farms with good screening and treatment programmes, overall survival rates are substantially improved compared to farms relying on clinical detection alone.

When to Call the Vet

Contact your vet immediately if:

  • A foal aged 1–6 months shows coughing, increased breathing rate, or lethargy
  • A foal has intermittent fever without obvious cause
  • You run a breeding farm with a history of rhodococcosis and have not established a screening programme
  • A foal is losing weight or failing to keep up with the mare during turnout

Frequently Asked Questions

Can adult horses get rhodococcosis?

Serious clinical disease in adult horses is rare, though R. equi infections in immunocompromised adults — including horses on immunosuppressive therapy or those with underlying disease — have been reported. Healthy adult horses generally have robust cell-mediated immunity that prevents the organism from establishing systemic infection.

Is rhodococcosis present on all horse farms?

R. equi is widely distributed in soil environments globally. Virulent strains are found on many horse farms, particularly those with a long history of horse management. Not all farms have sufficient environmental contamination levels or foal susceptibility to result in clinical disease. High-traffic, high-stocking-density breeding operations in warm climates are at greatest risk.

Can humans get rhodococcosis from horses?

R. equi is an opportunistic pathogen in severely immunocompromised humans (HIV/AIDS patients, those on immunosuppressive drugs). It does not cause disease in healthy individuals. However, immunocompromised people working with infected foals or highly contaminated environments should take precautions and discuss the risk with their physician.

How do I know if my farm is endemic for rhodococcosis?

A farm is considered endemic if one or more foals have been diagnosed with rhodococcal pneumonia in previous years. Environmental sampling for R. equi and VAP-positive strain quantification can assess farm contamination levels. Farms with a history of the disease should implement screening protocols and discuss prophylactic hyperimmune plasma with their vet. See also: Equine Foal Immunodeficiency Syndrome for another serious foal disease and intracellular pathogen for background on how organisms like R. equi evade normal immunity.