According to the new study, the antibacterial response of white blood cells to the flu virus fails to target the S. aureus bacteria and instead causes inflammatory injury to the lungs and damage to surrounding tissue, creating a higher susceptibility to secondary bacterial infections such as MRSA pneumonia.
A new study from researchers at the University of Nebraska Medical Center and Albany Medical College explains how influenza sufferers may become susceptible to pneumonia from Methicillin-resistant Staphylococcus aureus (MRSA). According to the new study published in The Journal of Experimental Medicine, the antibacterial response of white blood cells to the flu virus fails to target the S. aureus bacteria and instead causes inflammatory injury to the lungs and damage to surrounding tissue, creating a higher susceptibility to secondary bacterial infections such as MRSA pneumonia.
A typical course of antibiotics often proves ineffective for coinfection of influenza and the MRSA “superbug” and more than half of patients don’t survive. In a previous study, author Keer Sun, PhD found that mice infected with influenza had a higher susceptibility to MRSA because of suppressed ability of their macrophages and neutrophils to kill bacteria by releasing hydrogen peroxide and other reactive oxygen species. However, that research did not find a reason for the severe rate of morbidity and mortality from coinfection.
In this new study, the researchers’ experiments indicated that the inefficacy of antibiotics against coinfection is attributable to oxidative stress-associated inflammatory lung injury. Macrophages and neutrophils of mice co-infected with influenza and MRSA did not effectively kill the bacteria, and reactive oxygen species induced the death of inflammatory cells within the lungs, with lethal damage to surrounding tissue. Sun and colleagues observed that inhibiting NADPH oxidase 2 (Nox2), the enzyme that produces reactive oxygen species in macrophages and neutrophils, reduced the extent of this damage and, when combined with antibiotic treatment, increased the survival of mice with coinfection.
The researchers concluded that the key to improving the survival rate from flu and MRSA coinfection is preventing the severe lung damage caused by white blood cells, writing that “treatment strategies that target both bacteria and oxidative stress will significantly benefit patients with influenza-complicated S. aureus pneumonia.”
"Our results demonstrate that influenza infection disrupts the delicate balance between Nox2-dependent antibacterial immunity and inflammation," said Sun in the study. "This not only leads to increased susceptibility to MRSA infection but also extensive lung damage. Treatment strategies that target both bacteria and reactive oxygen species may significantly benefit patients with influenza-complicated MRSA pneumonia."
According to the Centers for Disease Control and Prevention, two in 100 people carry MRSA and those who carry the bacteria can do so without having any signs of infection. It is spread in healthcare settings through direct contact with an infected wound or from contaminated hands, usually those of healthcare providers. The drug-resistant “superbug” can cause a range of difficult-to-treat infections, such as sepsis, pneumonia, skin infections and blood infections. Symptoms of MRSA pneumonia include cough, fever and difficulty breathing and can be more severe due to the antibiotic resistance of the bacteria. To prevent a MRSA infection, the CDC recommends good hygiene practices such as washing your hands regularly and disinfecting frequently touched surfaces.