Sepsis-related multiple organ dysfunction is fundamentally driven by the host response to infection, rather than by the direct effect of the microorganism. This was accepted in the consensus conferences that coined the concept of sepsis [1] and remains in the Sepsis-3 definition [2]. Since the early days of its conceptualization, a dysregulated immune response to an infection is a key feature of sepsis’ pathophysiology. Therefore, important differences would be expected when comparing the presentation, evolution and outcomes in immunocompromised patients compared with their non-immunocompromised counterparts.
