Despite improvements in health care, the incidence of infective endocarditis has not decreased over the past decades. This apparent paradox is explained by a progressive evolution in risk factors; while classic predisposing conditions such as rheumatic heart disease have been all but eradicated, new risk factors for infective endocarditis have emerged. These include intravenous drug use, sclerotic valve disease in elderly patients, use of prosthetic valves, and nosocomial disease. Newly identified pathogens, which are difficult to cultivate--eg, Bartonella spp and Tropheryma whipplei--are present in selected individuals, and resistant organisms are challenging conventional antimicrobial therapy. Keeping up with these changes depends on a comprehensive approach, allying understanding of the pathogenesis of disease with the development of new drugs for infective endocarditis. Infection by staphylococci and streptococci is being dissected at the molecular level. New ideas for antimicrobial agents are being developed. These novel insights should help redefine preventive and therapeutic strategies against infective endocarditis.

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BackgroundThe coronavirus infectious disease (COVID-19) pandemic is an ongoing global health care challenge. Up to one third of hospitalised patients develop severe pulmonary complications and ARDS. Pulmonary outcomes following COVID-19 are unknown.MethodsThe Swiss COVID-19 lung study is a multicentre prospective cohort investigating pulmonary sequela of COVID-19. We report on initial follow-up 4 months after mild/moderate or severe/critical COVID-19 according to the WHO severity classification.Results113 COVID-19 survivors were included (mild/moderate 47, severe/critical 66). We confirmed several comorbidities as risk factors for severe/critical disease. Severe/critical disease was associated with impaired pulmonary function, i.e. diffusing capacity (DLCO) %-predicted, reduced 6-MWD, and exercise-induced oxygen desaturation. After adjustment for potential confounding by age, sex, and BMI, patients after severe/critical COVID-19 had a 20.9 (95% CI 12.4–29.4, p=0.01) lower DLCO %-predicted at follow up. DLCO %-predicted was the strongest independent factor associated with previous severe/critical disease when age, sex, BMI, 6MWD, and minimal SpO2 at exercise, were included in the multivariable model (adjusted odds ratio [OR] per 10%-predicted 0.59 [95% CI 0. 37–0.87], p=0.01). Mosaic hypoattenuation on chest computed tomography at follow-up was significantly associated with previous severe/critical COVID-19 including adjustment for age and sex (adjusted OR 11.7 [95%CI 1.7–239), p=0.03).ConclusionsFour months after SARS CoV-2 infection, severe/critical COVID-19 was associated with significant functional and radiological abnormalities, potentially due to small airway and lung parenchymal disease. A systematic follow-up for survivors needs to be evaluated to optimise care for patients recovering from COVID-19.