This is case of a 64‐year‐old male who presented to the rheumatologists office with a lower‐extremity purpuric skin rash. His past medical history included porcine mitral valve replacement 3 years ago for subacute bacterial endocarditis (SBE). At the rheumalologist's office, he had a complete autoimmune workup for the rash, which was negative except a very high sed rate and a high rheumatoid factor. He had a skin biopsy, which confirmed leukocytoclastic vasculitis. He was treated with empiric steroids without any improvement in the rash. Further, he had 2 blood cultures done in the office that came back positive for gram‐positive cocci, and he was admitted to the hospital for probable SBE. On admission, he was asymptomatic except for the vasculitic rash. He was afebrile with pulse of 97, BP of 141/75, respirations at 20/minute with O2 saturation of 98% on room air. On exam, he had a soft 1/6 systolic murmur in the mitral region and the vasculitic skin rash. SBE was suspected. He had a leukocytosis of 11,900 and hemoglobin of 9.7. He was started on IV vancomycin. Transesophageal echocardiogram was performed which revealed normal systolic function, mild leaflet thickening with some degree of restriction in leaflet mobility, as well as a 1‐ to 2‐mm echo reflective mobile structure on the left ventricular side of the mitral valve. Blood cultures identified the organism as Abiotropbia defectiva. He was clinically diagnosed with SBE with vasculitis. He was discharged home on IV vancomycin for 6 weeks, and prednisone was quickly tapered off. On follow‐up. patient reported resolution of the vasculitic rash on IV vancomycin. Repeat blood cultures remained negative, and the SBE and vasculitis resolved.
Leukocytoclastic vasculitis can be caused by infections such as SBE, and pathophysiology of vasculitis involves immune‐complex formation. It typically presents as palpable purpura, as was the case in our patient. Vasculitis is treated with steroids, but in our patient it did not improve until the underlying cause (endocarditis) was treated with antibiotics. Abiotropbia defecliva was previously known as nutritionally variant streptococci. Abiotropbia defectiva is found in approximately 5% of patients with SBE. They are difficult To grow in agar and require meTabolically active forms of vitamin B6 for growth. They are frequently associated with large vegetations and congestive heart failure. They respond poorly to antibiotics and have a high rate of posttreatment relapse. They are typically treated with penicillin and gentamicin, but vancomycin is an acceptable alternative.
Leukocytoclastic vasculitis can be an uncommon presentation of SBE and requires a high index of suspicion. Abiotropbia defectiva is a nutritionally variant streptococcus that is difficult to grow on blood cultures and can lead to a delay in diagnosis.
R. Rao, Holy Spirit Hospital, Camp Hill, PA, medical student rotation; T. Gajjar, Holy Spirit Hospital, Camp Hill, PA, employment.