Changing host profile and microbiology of infective endocarditis across the COVID-19 pandemic: an 8-year single-centre cohort study
This single-centre cohort study reveals that following the withdrawal of non-pharmaceutical interventions during the COVID-19 pandemic, infective endocarditis cases shifted toward younger, more comorbid patients with more severe presentations and a higher prevalence of *Staphylococcus aureus*, yet the post-pandemic period itself was not an independent predictor of in-hospital mortality.
Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer
In the human body, the heart is a relentless pump, but its inner lining is not immune to invasion. When bacteria or other germs enter the bloodstream and latch onto the heart valves, they can form destructive clumps of infection known as infective endocarditis. This condition is a medical emergency that often requires long courses of antibiotics and sometimes urgent surgery to replace damaged valves. For decades, doctors have tracked who gets sick with this disease, what germs are causing it, and how likely patients are to survive. The landscape of these infections is not static; it shifts with changes in how people live, how they access healthcare, and how germs spread through communities.
The global response to the COVID-19 pandemic created a unique, unintended experiment in public health. Strict measures like staying home, wearing masks, and closing businesses dramatically reduced the spread of many common viruses and bacteria. At the same time, hospitals saw a surge in infections linked to medical equipment and heavy use of antibiotics to treat patients with COVID-19. When these restrictions were eventually lifted, the world watched to see if the patterns of disease would simply return to normal or if something permanent had changed. Researchers wanted to know if the pause in normal life had altered the nature of heart infections, making them more common, more dangerous, or caused by different germs once society reopened.
A team of doctors at a major hospital in Grosseto, Italy, set out to answer these questions by looking back at eight years of patient records. They examined every adult admitted with a confirmed case of infective endocarditis between early 2017 and early 2025. They divided these patients into three groups based on when they were diagnosed: before the pandemic began, while strict restrictions were in place, and after the restrictions were lifted. By comparing these groups, the researchers could see how the profile of the typical patient and the behavior of the infection had evolved over time.
The study revealed a striking shift in who was getting sick. Before the pandemic, the typical patient was an older adult, often in their late seventies, with a moderate number of other health problems. After the pandemic restrictions ended, the average age of patients dropped significantly to the late sixties. However, these younger patients were not healthier; in fact, they carried a much heavier burden of chronic illness. The researchers found that the post-pandemic group had more than double the number of serious health conditions, such as kidney failure requiring dialysis or a history of intravenous drug use, compared to the pre-pandemic group. This combination of being younger but sicker was a reversal of the usual pattern seen in heart infections.
The germs causing the infections also changed. The most significant shift was a rise in infections caused by Staphylococcus aureus, a common bacterium that can be very aggressive. This type of bacteria became the leading cause of infection in the post-pandemic period, appearing in nearly half of all cases, up from about one-quarter before the pandemic. Interestingly, the increase was driven by strains that were still sensitive to standard antibiotics, not by drug-resistant "superbugs." Another type of bacteria, Enterococcus, also became more common, doubling in frequency. These changes suggest that the infection was increasingly entering the body through medical devices or procedures rather than through the community at large.
The severity of the illness at the moment of hospital arrival also increased. Patients diagnosed after the pandemic were more likely to be in sepsis, a life-threatening reaction to infection that causes the body to attack its own organs. They arrived with higher scores indicating organ stress and were far more likely to require emergency surgery rather than a planned procedure. While the raw number of deaths in the hospital appeared higher in the later years, the researchers dug deeper to understand why. When they accounted for the fact that these patients were older, sicker, and arrived in a more critical state, the time period itself no longer predicted who would die.
The study concluded that the pandemic did not make the disease itself more lethal. Instead, it changed the population at risk. The people arriving at the hospital with heart infections after the pandemic were a different group: younger, but with more complex health issues and more severe symptoms upon arrival. The higher death rate observed in the later years was a direct result of this sicker patient population, not a change in the virulence of the germs or a failure of medical treatment. The findings suggest that the true impact of the pandemic on heart infections lies upstream, in the changing health of the community and the way patients access care, rather than in the hospital room itself.
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