Study: Antibiotics Can Cause Harm to Flu Patients

Newswise — LOS ANGELES (Nov. 12, 2024) -- Taking antibiotics during an influenza infection can be harmful and increases the risk of developing a bacterial pneumonia while sick with the flu, according to new research led by Cedars-Sinai. 

Antibiotics are often prescribed for patients experiencing a respiratory illness. But when tests reveal that a virus—such as influenza—is causing the illness, antibiotics should be stopped, Cedars-Sinai investigators say. That’s because antibiotics are not meant to treat a viral illness; they are only effective against bacterial infections.

Some flu patients continue taking antibiotics out of concern that they will also develop a bacterial pneumonia—a common “secondary” infection often seen in vulnerable patients with influenza and a leading cause of death in flu patients.

A team of investigators led by Cedars-Sinai found that when influenza patients take antibiotics, the drugs disturb the gut’s fungal microbiome. This results in an increase in immune cells called eosinophils in the lungs that hinder the function of alveolar macrophages—important immune cells that clear out pathogens from the lungs.

This chain of events actually makes it more likely that a flu patient taking antibiotics will develop a bacterial pneumonia rather than avoid one. The investigators also showed that increased levels of eosinophils are associated with poor clinical outcomes and more systemic inflammation. The results of the experimental study were published in The Journal of Clinical Investigation. 

“We need to be aware that antibiotics are not innocuous and can have harmful side effects,” said the study’s corresponding author, Peter Chen, MD, the Medallion Chair in Molecular Medicine and the interim chair of the Department of Medicine at Cedars-Sinai. “To be clear: When a flu patient has a confirmed bacterial infection, you definitely need to prescribe antibiotics. But when there is no direct evidence of such an infection, antibiotics should not be prescribed because they will not help, and could, in fact, be harmful.”

To conduct the study, investigators examined laboratory mice that had been infected with influenza followed by a bacterial infection caused by MRSA (methicillin-resistant Staphylococcus aureus), one of the most common causes of a secondary bacterial pneumonia. One group of mice received antibiotics prior to the onset of a bacterial infection; the control group did not receive any medication.

Compared with the control group, those treated with antibiotics experienced greater weight loss and showed evidence of greater lung damage after MRSA infection. The mice that were given antibiotics also had higher levels of MRSA bacteria in their lungs and higher levels of immune cells (macrophages and eosinophils). In other words, this data suggests that antibiotic treatment during an influenza infection actually impaired the body’s efforts to clear the MRSA bacteria rather than helping the body heal.

The investigators also evaluated a cohort of influenza patients at Cedars-Sinai and critically ill patients at Northwestern University and the University of Pittsburgh. They found that eosinophils increase with antibiotic use and are associated with a higher length of stay and systemic inflammation.

“Altogether, this research demonstrates that prescribing antibiotics during influenza infections may do more harm than good. This research also sheds light on the role that eosinophils play in regulating lung immunity,” said co-author David Underhill, PhD, chair of the Department of Biomedical Sciences and the Janis and William Wetsman Family Chair in Inflammatory Bowel Disease. “These results also support clinical trials using eosinophil-depleting strategies as a therapy to improve outcomes in patients admitted with influenza and other viral illnesses.”

Additional authors include Marilia Sanches Santos Rizzo Zuttion, Tanyalak Parimon, Stephanie A. Bora, Changfu Yao, Katherine Lagree, Catherine A. Gao, Richard G. Wunderink, Georgios D. Kitsios, Alison Morris, Yingze Zhang, Bryan J. McVerry, Matthew E. Modes, Alberto M. Marchevsky, Barry R. Stripp, Christopher M. Soto, Ying Wang, Kimberly Merene, Silvia Cho, Blandine L. Victor, Ivan Vujkovic-Cvijin, Suman Gupta, Suzanne L. Cassel, Fayyaz S. Sutterwala and Suzanne Devkota.

This work was supported by grants from the NIH (TP: K08HL1411590; CAG: F32HL162377; RGW: U19AI135964, U01TR003528,P01HL154998, R01HL14988, and R01LM013337; GDK: R03HL162655; AM: R01HL163646, R01HL164177; BJM: P01HL114453; PC: R01HL159953, R01HL155759). This research was also supported by NIH National Center for Advancing Translational Science (NCATS) UCLA CTSI Grant Number UL1TR001881.

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