Rhodococcus equi pneumonia - The Merck Veterinary Manual

Rhodococcus equi pneumonia

Rhodococcus equi is the most serious cause of pneumonia in foals 1-5 mo of age. It is not the most common cause of pneumonia in this age group; however, it has significant economic consequences due to mortality, prolonged treatment, surveillance programs for early detection, and relatively expensive prophylactic strategies. Clinical disease is rare in horses >8 mo of age. Compelling epidemiologic data indicate pulmonary infection probably originates within the first 2 wk of life.

Etiology and Pathogenesis:

R equi is a gram-positive, facultative intracellular pathogen that is nearly ubiquitous in soil. Only certain types (Vap A, B, C) are pathogenic. The organism is likely present on all premises to some degree; however, disease incidence may be enzootic, sporadic, or nonexistent for specific farms. High ambient summer temperatures, sandy soil, and dusty conditions favor multiplication and dissemination of the organism in the environment. Inhalation of dust particles laden with virulent R equi is the major route of pneumonic infection. The organism readily multiplies within the intestine of foals 3 mo of age. Foals with pulmonary infections swallow sputum laden with R equi, which replicates in their intestinal tract. Manure from pneumonic foals is a major source of virulent bacteria contaminating the environment. The pathogenicity is linked to the ability of R equi to survive intracellularly, which hinges on failure of phagosome-lysosomal fusion in infected macrophages and failure of functional respiratory burst upon phagocytosis of R equi .

Clinical Findings and Lesions:

Pneumonia due to Rhodococus equi, radiograph

R equi infection is slowly progressive with acute to subacute clinical manifestations. Clinical signs of disease are difficult to detect until pulmonary lesions reach a critical mass resulting in decompensation of the foal. Pulmonary lesions are relatively consistent and include subacute to chronic suppurative bronchopneumonia, pulmonary abscessation, and suppurative lymphadenitis. At the onset of clinical signs, most foals are lethargic, febrile, and tachypneic. Cough is a variable clinical sign; purulent nasal discharge is less common. Thoracic auscultation reveals crackles and wheezes with asymmetric/regional distribution. Pulmonary regions with marked consolidation lack breath sounds and exhibit dull resonance on thoracic percussion. Diarrhea is observed in many foals due to colonic microabscessation.

Intestinal and mesenteric abscesses are the most common extrapulmonary sites of infection. Foals with abdominal involvement often present with fever, depression, anorexia, weight loss, colic, and diarrhea. Intestinal lesion are characterized by multifocal, ulcerative enterocolitis and typhlitis involving Peyer’s patches with granulomatous or suppurative inflammation of the mesenteric and/or colonic lymph nodes. The prognosis for foals with abdominal forms of R equi is less favorable than for those with pulmonary disease. Septic physitis and osteomyelitis are less common extrapulmonary sites of infection. Vertebral osteomyelitis may result in pathologic vertebral fracture and spinal cord compression, and is a devastating manifestation of R equi osteomyelitis. Panophthalmitis, guttural pouch empyema, sinusitis, pericarditis, nephritis, nonseptic uveitis and synovitis, and hepatic and renal abscessation with R equi have been reported.

Diagnosis:

Rhodococcal pneumonia, foal

Routine laboratory evaluation of CBC and serum chemistry reveals nonspecific abnormalities consistent with infection and inflammation. Neutrophilic leukocytosis and hyperfibrinogenemia are common, and the severity of these findings relates to prognosis. Thoracic radiographic evaluation may reveal a pattern of perihilar alveolization, consolidation, and abscessation. The presence of nodular lung lesions and mediastinal lymphadenopathy in foals 1-5 mo of age is highly suggestive of R equi . Bacterial culture of transtracheal wash samples is required for definitive diagnosis. Cytologic evaluation of transtracheal wash samples reveals intracellular coccobacilli, identification of which indicates initiation of appropriate antimicrobial therapy pending culture results.

Treatment and Prognosis:

The combination of erythromycin (25 mg/kg, PO, qid; esters or salts) and rifampin (5 mg/kg, bid, or 10 mg/kg, sid) is the treatment of choice. These antimicrobials may be bacteriostatic, but their activity is synergistic, and the combination has markedly improved survival of foals. Idiosyncratic hyperthermia and tachypnea can occur with erythromycin administration during periods of warm environmental conditions, and anorexia, bruxism, and salivation may be observed. Life-threatening, antibiotic-induced enterocolitis, due to Clostridium difficile , has been observed in the dams of nursing foals treated with erythromycin. Azithromycin is a newer generation macrolide with greater bioavailability than erythromycin. Azithromycin is administered orally (10 mg/kg, sid) with rifampin until clinical signs stabilize, then every other day until resolution of disease. The duration of antimicrobial therapy typically ranges from 4-9 wk.

Supportive therapy includes provision of a clean, comfortable environment and highly palatable, dust-free feeds. Judicial IV fluid therapy and saline nebulization facilitates expectoration of pulmonary exudates. NSAID should be administered as needed to maintain rectal temperature <103.5°F (39.7°C). Nasal insufflation with oxygen is necessary in foals with severe respiratory compromise. Bronchodilator therapy may or may not improve arterial oxygenation. Prophylactic antiulcer medication is indicated in foals that are stressed by respiratory difficulty, pain, frequent handling, hospitalization, and transportation.

The survival rate of R equi pneumonia is approximately 70-90% with appropriate therapy. The case fatality rate without therapy (or with inappropriate antimicrobial therapy) is ~80%. Parameters for discontinuation of medical therapy include clinical signs, serum fibrinogen concentration, and radiographic resolution of pulmonary consolidation and abscessation.

Prevention:

There are 3 basic strategies to decrease the incidence of R equi pneumonia on endemic farms: decreased exposure to the organism, early detection of clinical cases, and enhanced passive immunity for neonatal foals. Foals should be maintained in well-ventilated, dust-free areas, avoiding dirt paddocks and overcrowding. Pneumonic foals should be isolated and their manure composted. Herd surveillance programs for early detection of pneumonic foals on endemic farms include twice weekly physical examination and auscultation, and monthly CBC and fibrinogen concentration. Foals with WBC count >14,000 cells/µL should be further evaluated for R equi . Administration of hyperimmune plasma might reduce the incidence and severity of R equi within the herd, but it is not completely effective in preventing disease. Hyperimmune plasma (1 L) is administered IV within the first week of life, followed by a second liter at approximately 25 days of age.