The same bug infects different people. Most bounce back, some languish, while a few perish. What makes the difference? Can we predict and target more aggressive treatment to those who may need it more?
It sounds almost paradoxical: current immunosuppressive treatment with biologics (most commonly an anti-TNF agent) increases the risk of severe infections, but seems to protect against the worst life-threatening complications in sepsis, like shock, multi-organ failure and death.
While being on a biologic understandably increases susceptibility to infection, it may attenuate a dysregulated and unbridled immune response to the infection, which could otherwise result in a cytokine storm, called the Systemic Inflammatory Response Syndrome (SIRS). Survival is touch and go in this situation. This is the main mechanism of mortality: it's the immune system, not the infection, that kills. We are indeed our worse enemy.
Treating severe sepsis should perhaps be a close collaboration between ID physicians and immunologists.
Can vaccines kill?
No, I'm not fear-mongering about excipients in some older vaccines possibly causing autism (which has been roundly debunked), or even the newly described but rare ASIA (Autoinflammatory/Autoimmunity Syndrome Induced by Adjuvants).
It's about ADE (Antibody-Dependent Enhancement), whereby flaviviruses (Dengue, Zika, Yellow Fever) latch onto cross-reacting antibodies produced against a different flavivirus strain to gain entry into Antigen-Presenting Cells. From there on, the viruses replicate unrestrained, while the immune response goes nuclear.
As such, a Zika or a Dengue vaccine can potentially set a population up for a far more catastrophic epidemic when a different flavivirus strain comes along in future.