Dataset Information

Normal procalcitonin, C-reactive protein, and negative blood cultures in infective endocarditis with a massive residual vegetation: a case report.

ABSTRACT:

Background

Infective endocarditis (IE) is a serious infection with high morbidity and mortality that involves the endocardial lining of the heart. Most cases of IE are due to bacteria although other atypical micro-organisms can also be involved. Procalcitonin (PCT) is a biomarker that is used in the diagnosis of bacterial infections.

Case summary

We present the case of a 54-year-old patient with bacterial endocarditis who has been regularly visiting his cardiologist for follow-up on a mitral valve prolapse and moderate mitral regurgitation (MR) for the last 11 years. During his last visit, transthoracic echocardiography (TTE) showed a previously non-existent structure on the posterior mitral valve leaflet with severe MR. Blood cultures were positive for Streptococcus viridans. On admission, he had elevated levels of PCT and C-reactive protein which returned to normal values after 4 weeks of intravenous antibiotic therapy. His follow-up blood cultures, taken after normalization of PCT, did not show bacterial growth; however, on TTE he had severe mitral regurgitation and a persistent vegetation which had slightly increased in size after completion of the full antibiotic course. He was referred for mitral valve replacement surgery.

Discussion

Normalization of procalcitonin levels may correlate with negative blood cultures in cases of IE with residual vegetations. The optimal time for surgery in such patients is difficult to define but even in circumstances with less infective organisms such as S. viridans and late in the course of the disease residual vegetations remain a serious risk factor for embolic events. Randomized controlled clinical trials are needed in order to have better recommendations with solid evidence regarding prophylaxis and treatment in IE.

SUBMITTER: Farandzha D

PROVIDER: S-EPMC8491057 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:AIMS: Infective endocarditis (IE) is characterized by septic thrombi (vegetations) attached on heart valves, consisting of microbial colonization of the valvular endocardium, that may eventually lead to congestive heart failure or stroke subsequent to systemic embolism. We hypothesized that host defense activation may be directly involved in tissue proteolytic aggression, in addition to pathogenic effects of bacterial colonization. METHODS AND RESULTS: IE valve samples collected during surgery (n = 39) were dissected macroscopically by separating vegetations (VG) and the surrounding damaged part of the valve from the adjacent, apparently normal (N) valvular tissue. Corresponding conditioned media were prepared separately by incubation in culture medium. Histological analysis showed an accumulation of platelets and polymorphonuclear neutrophils (PMNs) at the interface between the VG and the underlying tissue. Apoptotic cells (PMNs and valvular cells) were abundantly detected in this area. Plasminogen activators (PA), including urokinase (uPA) and tissue (tPA) types were also associated with the VG. Secreted matrix metalloproteinase (MMP) 9 was also increased in VG, as was leukocyte elastase and myeloperoxidase (MPO). The presence of neutrophil extracellular traps (NETs) associating MPO and externalized nucleosomes, was shown by immunostaining in the VG. Both MPO and cell-free DNA were released in larger amounts by VG than N samples, suggesting bacterial activation of PMNs within the vegetation. Finally, evidence of proteolytic tissue damage was obtained by the release of fragments of extracellular matrix components such as fibrinogen and fibronectin, as well as protease-sensitive receptors such as the uPA receptor. CONCLUSION: Our data obtained using human IE valves suggest that septic vegetations represent an important source of proteases originating from massive leukocyte recruitment and activation of the host plasminergic system. The latter forms a potential therapeutic target to minimize valvular tissue degradation independently from that induced by bacterial proteases.