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The coronavirus has already killed nearly 6,5 million people. But it turns out that “many COVID-19 deaths are not caused by the virus itself”. The source of the devastating consequences in this case is different. It can be said that the coronavirus has an accomplice in the deadly trial, as does the flu virus. What exactly is going on, explains immunologist Haley Muendlein.
- Many COVID-19 deaths are not caused by the coronavirus itself, but the bacterial infections that develop afterwards
- Estimates from 2021 show that 16 to 28 percent. adults hospitalized for COVID-19 also had a bacterial infection
- “These patients stayed in hospital twice as long, needed mechanical ventilation four times more, and were three times more likely to die compared to patients with covid alone,” says Haley Muendlein
- Muendlein gives an example of how exactly viruses and bacteria can “work together”
- More information can be found on the Onet homepage
“Viruses and bacteria join forces”
«The 1918 flu pandemic caused a loss of more than 3 percent. world population – at least 50 million people. But it wasn’t the flu virus that caused most of these deaths, ”begins Haley Muendlein in his article in The Conversation. It turns out that the pathogen had an “accomplice” – bacteria.
Analysis of lung samples taken during the flu pandemic showed that most of the deaths were likely caused by bacterial pneumonia, the immunologist explains. A similar phenomenon, although not on such a scale, was observed, for example, during the so-called pandemic. Of the “swine flu” in 2009 As Muendlein explains, “almost 18 percent. patients with viral pneumonia had additional bacterial infections which increased the risk of death ». It’s not everything. Almost a quarter of patients admitted to the ICU with severe flu also have a bacterial infection. “The COVID-19 pandemic is no different,” he emphasizes.
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Understanding the “cooperation” between microbes is of paramount importance. And not only in the diagnosis and treatment process, but also in developing an effective plan to combat the current pandemic and prevent a future one.
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How do viruses and bacteria “work together”?
Simply put, “many flu and COVID-19-related deaths are not due to the virus alone.” In the opinion of the specialist, “it is a secondary bacterial infection, which is often the source of devastating consequences attributed to the initial viral infection”. Recall that secondary infections occur after the initial infection. As Haley Muendlein notes, they are often caused by pathogens resistant to antibiotics used to treat the primary infection.
Muendlein points out that the way viral and bacterial infections interact with each other magnifies the possible damage these microbes can cause. “Viral respiratory infections can increase the likelihood of bacterial infections and lead to aggravation of the disease,” he explains. There are several reasons for this.
Muendlein gives an example: “The epithelial cells that line the airways and lungs are the first line of defense against inhaled pathogens and pollutants. However, viruses can kill these cells and weaken this protective barrier, allowing inhaled bacteria to invade. They can also change the surface of epithelial cells, making it easier for bacteria to adhere to them ».
COVID-19 and secondary bacterial infections are three times more likely to die
The immunologist emphasizes that secondary bacterial infections are exacerbating the COVID-19 pandemic. «In a review from 2021, it was estimated that 16 to 28 percent. adults hospitalized for COVID-19 also had a bacterial infection. These patients stayed in hospital twice as long, needed mechanical ventilation four times more often, and were three times more likely to die compared to patients with covid alone ».
So how do you prevent secondary infections? In June, Haley Muendlein and her colleagues published a work that gives some clue. Scientists have identified a molecule (ZBP1) that regulates the immune system’s response to the flu (for example, it signals infected cells in the lungs to self-destruct). “This induced cell death kills the virus and favors the recruitment of additional immune cells to the site of infection,” explains the immunologist. But that’s not all.
Scientists have found that this molecule initiates the death of cells infected with bacteria that cause foodborne disease (Yersinia pseudotuberculosis). This limits the replication of bacteria and triggers processes that facilitate the removal of the pathogen from the body.
These findings suggest that ZBP1 may play a dual role in the body’s response to viral and bacterial infections. This gives hope for the development of new therapies.