It has happened to me and my colleagues far too often: watching a patient die from complications of COVID-19. While the ultimate cause of death is multiorgan failure – shock, respiratory failure, kidney failure, etc – the question is what caused this multiorgan failure?
Many have postulated that secondary bacterial infections may be one culprit. Indeed, as much as we try to avoid it, many patients suffering from COVID-19 do in fact get bacterial infections in the lungs and other organs. Are these infections – and the sepsis they may cause – the reason why some COVID-19 patients die? New research just published in Nature Microbiology challenges this assertion.
Researchers from New York studied samples from the lungs of 142 patients who underwent clinically indicated bronchoscopies (cameras tests in the lungs) during their course of treatment of COVID-19. They found that – in those patients who ultimately died – the amount of virus in the lungs, known as the viral load, was significantly higher than those that survived. Moreover, the immune response in the lungs themselves was also weaker in those patients who died as well.
They did not find bacterial infection to be associated with mortality, interestingly. And the researchers did extensive analysis on the bronchoscopic samples. These findings make sense.
The more virus you have in the lung, the more viral replication occurs, and the more virus-induced destruction of lung tissue occurs. This helps explain why many patients with severe COVID-19 develop collapse of the lung requiring chest tube placement. What surprised me was the fact that it was not an exaggerated immune response that did the destroying, but the immune response was actually not strong enough in those patients that ended up dying from COVID-19.
What are the implications of these findings?
First, does this mean that suppressing the immune response may be counterproductive? Yet, steroids are recommended as first-line therapy for COVID-19 pneumonia causing hypoxia, or low oxygen levels. And the anti-inflammatory drug tociluzimab has also been shown to provide beneficial outcomes as well. Why the disconnect?
Second, if there are fewer antibodies in the lungs of those who died from COVID-19, should be we giving them antibodies – either with monoclonal antibodies or convalescent plasma – to help the immune system along? Yet, when this very thing was studied, patients who were critically ill actually did worse, and these therapies are not recommended. Again, why the disconnect?
It remains unclear. Still, these findings are very important, and they help explain why some patients succumb to this horrible illness: there is so much virus in the lungs, and all that virus overwhelms the immune response and causes extensive, and ultimately irreversible, destruction in the lungs. Several other studies have also shown that mortality corresponds to viral load, and the current investigation is further confirmation of this.
The other major takeaways of this stud for me are that, first, we need to get vaccinated against COVID-19. The patients in this study were infected early on in the pandemic, before the vaccines were available. Now, we have no excuse. Vaccines are free and widely available, and they are extremely effective at preventing the very thing from which these study patients suffered: death and/or severe illness.
Second, wear a mask. A mask helps reduce viral particles that get into your upper airway (which is why leaving the nose uncovered is counterproductive). This is especially true if everyone is masked. With less viral particles, the chance of severe infection – or perhaps even any infection – goes down.
The science on SARS CoV-2 and COVID-19 is forever changing. We are constantly learning new things about this virus and the scourge it is causing. This is ultimately a good thing. Knowledge is power, and the more we know, the more we can learn about what this virus does and how we can effectively fight against it.
