To the Editor Dr van Vught and colleagues explored whether hypoinflammation/immune paralysis rather than hyperinflammation in the wake of a septic insult could predispose patients to secondary infection and higher mortality.1 The negative findings of this study cast doubt on the clinical implications of the immune suppression theory.
Even though their primary and secondary study findings did not support the importance of secondary infections after sepsis and their genetic analysis did not support the notion of immunosuppression, the authors introduced unnecessary reservations regarding these findings when they stated that “patients with sepsis on admission developed more ICU [intensive care unit]–acquired infections with opportunistic pathogens like enterococci, Pseudomonas aeruginosa, and viruses, hinting at possible immune suppression.” A more plausible explanation is that, compared with patients who are not septic, secondary infections in patients with sepsis are more likely to be due to multidrug-resistant bacteria, fungi, and viruses because of more frequent exposure to broad-spectrum antibiotics and an overall higher severity of disease.
Daniel A. Sweeney, Andre C. Kalil. Secondary Infection in Patients With Sepsis. JAMA. 2016;316(7):771–772. doi:10.1001/jama.2016.9272