CONGRESS ABSTRACT

Background Abiotrophia defectiva (AD) is a nutritionally variant streptococcus (NVS) found in the normal flora of the oral cavity, urogenital, and intestinal tracts. Along with other NVS, it accounts for 5-6% of infective endocarditis (IE) cases, with 1-2% due to AD alone. It is a major cause of blood culture-negative IE, as it requires media enriched with pyridoxine and L-cysteine. AD endocarditis represents a real challenge for the cardiologist. Case A 11-year-old boy affected by Criss-cross heart with Blalock-Taussig-Shunt presented with fever that began 11 days after a dental extraction performed without antibiotic prophylaxis. Transthoracic echocardiogram showed no clear signs of endocarditis, except for thickening of the tricuspid subvalvular apparatus. The Blalock-Taussig shunt presented normal function. Serial blood cultures tested negative. Despite the absence of a clear valve involvement, after exclusion of alternative diagnosis, the high pre-test probability suggested the diagnosis of endocarditis. Antigen tests resulted positive for AD. In the absence of antibiogram, empirical treatment with ampicillin and gentamicin was administered but after completion of antibiotic regimen fever restarted. New blood cultures sent to a specialized center showed the persistence of AD suggesting incomplete eradication. Despite the antibiogram showed a sensitivity to the previous antibiotic regimen, the persistent infection led to a revision of the antibiotic regimen with a combination of daptomycin (10 mg/kg) and amoxicillin (200 mg/kg) for 6 weeks. The patient’s condition improved gradually with normalization of inflammatory markers. During the antibiotic regimen extraction of several teeth with destructive caries was made to remove potential source of reinfection. A pre-discharge echocardiogram showed normalization of the tricuspid subvalvular thickening. Sequential antibiotic therapy with dalbavancin (480 mg, single week dose for two weeks) followed. Strict follow-up for several months showed eradication of the disease. Conclusion This case highlights the challenges in managing endocarditis caused by AD, particularly in pediatric patients with congenital heart disease. It emphasizes the need for specialized diagnostic and therapeutic approaches, including non-standard antibiotics and consideration for aggressive source control. Negative result of the blood cultures in a high risk clinical situation mandates the search for fastidious germs like AD.