Flu and superbug combo causes fatal lung damage

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As if having the flu wasn’t bad enough – the virus increases susceptibility to secondary bacterial infections by turning your own immune cells against your lungs.
Credit: Lester V. Bergman / Getty Images

A golden staph infection during or after catching the flu ends up killing more patients because the virus urges white blood cells to attack patients’ lungs, a new study claims.

The work, which traced how the virus and bacteria act in mice, was published in the Journal of Experimental Medicine.

Strains of golden staph (Staphylococcus aureus) have developed immunity to commonly used antibiotics. Methicillin-resistant Staphylococcus aureus (MRSA) is one such superbug.

When patients are infected with influenza – a virus – they’re more susceptible to bacterial infection. But post-influenza patients that contract MRSA can end up with severe cases of S. aureus pneumonia.

In more than half these cases, the patient will die, even if they take a course of antibiotics that usually win out against MRSA.

The reason antibiotics are ineffective, according to researchers led by Keer Sun at the University of Nebraska in the US, is the patient’s wayward white blood cells.

Sun and colleagues examined how flu infection tinkers with macrophages and neutrophils, two types of white blood cell that usually mobilise against infections.

In normal cases, these cells release atoms or molecules called reactive oxygen species that help to destroy pathogens. But when a patient is infected with influenza, this process is altered – the white blood cells end up targeting cells in the lung area, causing inflammation and damage to the surrounding tissue that can give MRSA an easy infection route.

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The lungs of mice co-infected with influenza and MRSA appear much healthier after combined treatment with antibiotics and a Nox2 inhibitor (right) than they do after antibiotic treatment alone (left).
Credit: Sun et al., 2016

According to studies on flu-infected mice, stopping white blood cells from releasing of NADPH oxidase 2 (Nox2), the enzyme that produces reactive oxygen species in macrophages and neutrophils, can reverse this potentially lethal effect.

“Our results demonstrate that influenza infection disrupts the delicate balance between Nox2-dependent antibacterial immunity and inflammation,” the researchers write.

“Treatment strategies that target both bacteria and oxidative stress will significantly benefit patients with influenza-complicated S. aureus pneumonia.”

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