A 62-year-old man with a history of ulcerative colitis presented to our institution for evaluation of fever, dyspnea, and positive blood cultures. His ulcerative colitis had been controlled with a regimen of mesalamine and azathioprine. Three months prior to admission, he was unable to refill his medications and subsequently had an ulcerative colitis flare. During his flare, he noticed new dyspnea on exertion. Three days prior to admission, he had a fever of 39.2 ºC, prompting a visit to his primary care provider. The next day, the patient was instructed to present to the emergency department after his blood cultures grew gram-positive cocci in chains.
On admission, the patient’s exam was notable for a harsh, 3/6 systolic murmur at the right upper sternal border and a 1/4 decrescendo diastolic murmur at the right lower sternal border. His labs were notable for a white blood count of 12.4 thous/mcL with 87% neutrophils, and an ESR elevated to 47 mm/hr. A transesophageal echocardiogram showed a bicuspid aortic valve with an area of severe calcification suggestive of a vegetation. Blood cultures grew S. viridans sensitive to ceftriaxone. An STD screen was ordered because of a history of unprotected sexual intercourse and revealed a new diagnosis of hepatitis C. He was diagnosed with endocarditis and discharged to complete a course of intravenous ceftriaxone.
Endocarditis is an uncommon complication of ulcerative colitis. Bacteremia is caused by a number of organisms, including E. coli, S. bovis, Proteus spp, and C. perfringens. A combined retrospective and prospective case-control study showed a significant overrepresentation of inflammatory bowel disease among cases of native valve endocarditis. In this patient’s case, his endocarditis may have been the result of the combination of his bicuspid aortic valve, recent ulcerative colitis flare, and underlying hepatitis C infection. Chronic hepatitis C can lead to the suppression of the immune system by an IL-10 mediated pathway that inhibits IFN- α and decreases T cell effectiveness. In studies involving IL-10 knockout mice, high bacterial concentrations were found in the large intestine with visual changes that resembled inflammatory bowel disease. IL-10 has been hypothesized as having a role in maintaining the mucosal barrier in the gut. An abundance of IL-10 may have contributed to this patient developing endocarditis along with his underlying valvular defect and possible episode of transient bacteremia during his ulcerative colitis flare.
Ulcerative colitis should be considered an independent risk factor for developing endocarditis and the use of antibiotic prophylaxis in high-risk patients should be further explored. Hepatitis C may also contribute to the development of infections in patients with inflammatory bowel disease through an IL-10 mediated pathway.
To cite this abstract:Joseph P, Ma H, Adler N. A Triple Hit for Endocarditis. Abstract published at Hospital Medicine 2015, March 29-April 1, National Harbor, Md. Abstract 556. Journal of Hospital Medicine. 2015; 10 (suppl 2). https://www.shmabstracts.com/abstract/a-triple-hit-for-endocarditis/. Accessed April 7, 2020.