Infection and drug resistance · 2026
An Unusual Case of Streptococcus mitis-Associated Infective Endocarditis Triggered by Upper Gastrointestinal Bleeding Secondary to Superficial Gastritis.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Xu Hongxian, Xia Yun, Dai Anyin, Liu Changlong, Xu Lijian, Turdi Amina, Fang Lingli, Yang Zijian, Yang Bo
Аннотация
BACKGROUND: Streptococcus (S). mitis, a viridans group streptococci (VGS) typically colonizes the oral cavity, is a recognized cause of infective endocarditis (IE) and is primarily associated with dental risk factors. A review of the literature revealed a few reported cases of IE resulting from invasion of S. mitis into the bloodstream. However, we report a case of S. mitis-associated IE originating from upper gastrointestinal bleeding (UGIB) secondary to superficial gastritis (SG) with erosion in a patient without prior cardiac or active oral pathology. To our knowledge, no such case has been reported to date.
CASE PRESENTATION: A 59-year-old man with hypertension presented to the hospital 14 days after the onset of melena. Gastroscopy revealed SG with erosions, leading to his admission for treatment. Upon admission, the patient exhibited signs of bloodstream infection and an unexplained fever. Abdominal computed tomography revealed a wedge-shaped splenic infarction. Blood cultures were positive for S. mitis. Transthoracic echocardiography revealed vegetations on the aortic valve and severe regurgitation, meeting modified Duke criteria for IE. The clinical findings included multiple Osler's nodes, splinter hemorrhages under the nails, and Janeway lesions. The patient responded to empirical antibiotics and ultimately underwent aortic valve replacement.
CONCLUSION: We report a rare case of IE caused by S. mitis in a patient initially admitted for UGIB. This study suggests that the pathogenic invasion of S. mitis likely occurs through early mucosal erosions and ulcerations in the gastric lining, which facilitate bacterial entry into the bloodstream, resulting in IE. Clinicians should consider gastrointestinal mucosal injury in unexplained systemic infections and emphasize timely diagnosis and targeted therapy to mitigate IE risks.
CASE PRESENTATION: A 59-year-old man with hypertension presented to the hospital 14 days after the onset of melena. Gastroscopy revealed SG with erosions, leading to his admission for treatment. Upon admission, the patient exhibited signs of bloodstream infection and an unexplained fever. Abdominal computed tomography revealed a wedge-shaped splenic infarction. Blood cultures were positive for S. mitis. Transthoracic echocardiography revealed vegetations on the aortic valve and severe regurgitation, meeting modified Duke criteria for IE. The clinical findings included multiple Osler's nodes, splinter hemorrhages under the nails, and Janeway lesions. The patient responded to empirical antibiotics and ultimately underwent aortic valve replacement.
CONCLUSION: We report a rare case of IE caused by S. mitis in a patient initially admitted for UGIB. This study suggests that the pathogenic invasion of S. mitis likely occurs through early mucosal erosions and ulcerations in the gastric lining, which facilitate bacterial entry into the bloodstream, resulting in IE. Clinicians should consider gastrointestinal mucosal injury in unexplained systemic infections and emphasize timely diagnosis and targeted therapy to mitigate IE risks.