Equine vegetative endocarditis and vertebral osteomyelitis due to refractory Erysipelothrix rhusiopathiae infection
Erysipelothrix rhusiopathiae was the causative agent of vegetative endocarditis and vertebral osteomyelitis in a 24-year-old Irish draught gelding that presented with prolonged history of intermittent pyrexia and tachycardia. Clinical investigations revealed persistently reduced neck mobility, tachydysrhythmia and episodic pyrexia up to 41°C. Echocardiographic examinations demonstrated vegetative lesions on the tricuspid and mitral valve leaflets. Leucocytosis, hyperglobulinaemia and persistent elevation of serum amyloid A (SAA) were present. Prolonged antimicrobial treatment (enrofloxacin 7.5–10 mg/kg bwt PO s.i.d. and ceftiofur 2.2 mg/kg IM b.i.d.) was based on urine and blood culture and antimicrobial susceptibility testing. Additional therapies included antidysrhythmic treatment for ventricular tachycardia (sotalol 2 mg/kg bwt PO b.i.d) and articular process joint medication. Despite initial response to therapy, range of neck movement decreased further, and the gelding was euthanised 55 days after first admission. Postmortem examination revealed valvular endocarditis of the mitral valve and extensive osteomyelitis of the first thoracic vertebral body. Genomic analyses of the E. rhusiopathiae isolate revealed only intrinsic antimicrobial resistance or virulence genes. This is the first report of antemortem diagnosis of E. rhusiopathiae in an adult horse, highlighting the severe clinical sequelae of infection and the therapeutic challenges in preventing disease progression.
Erysipelothrix rhusiopathiae was the causative agent of vegetative endocarditis and vertebral osteomyelitis in a 24-year-old Irish draught gelding that presented with prolonged history of intermittent pyrexia and tachycardia. Clinical investigations revealed persistently reduced neck mobility, tachydysrhythmia and episodic pyrexia up to 41°C. Echocardiographic examinations demonstrated vegetative lesions on the tricuspid and mitral valve leaflets. Leucocytosis, hyperglobulinaemia and persistent elevation of serum amyloid A (SAA) were present. Prolonged antimicrobial treatment (enrofloxacin 7.5–10 mg/kg bwt PO s.i.d. and ceftiofur 2.2 mg/kg IM b.i.d.) was based on urine and blood culture and antimicrobial susceptibility testing. Additional therapies included antidysrhythmic treatment for ventricular tachycardia (sotalol 2 mg/kg bwt PO b.i.d) and articular process joint medication. Despite initial response to therapy, range of neck movement decreased further, and the gelding was euthanised 55 days after first admission. Postmortem examination revealed valvular endocarditis of the mitral valve and extensive osteomyelitis of the first thoracic vertebral body. Genomic analyses of the E. rhusiopathiae isolate revealed only intrinsic antimicrobial resistance or virulence genes. This is the first report of antemortem diagnosis of E. rhusiopathiae in an adult horse, highlighting the severe clinical sequelae of infection and the therapeutic challenges in preventing disease progression.