Taking azithromycin for as little as one day triggers antibiotic resistance in the respiratory tract, according to a first-of-its kind look by scientists at UC San Francisco of the changes that occur in the microbiome of hospitalized patients with COVID-19.
Azithromycin is one of the most widely used antibiotics in the world, and it is essential for treating certain classes of bacterial infections that cause strep throat, pneumonia, and sexually transmitted diseases. But it does not work against viruses.
Early in the pandemic, azithromycin was widely used after small studies suggested it might have therapeutic benefits. Randomized clinical trials later showed it did not work, but the drug continued to be prescribed to patients with respiratory illnesses.
"We've known for years that antibiotics don't treat viral infections, but these results were striking," said Chaz Langelier , MD, PhD. "That we could see resistance genes turning on in the respiratory tract within a day tells us the consequences of unnecessary antibiotic use aren't theoretical or long-term. They're immediate, measurable, and biologically real."
The results, published March 16 in Nature Microbiology , are from a multi-center genomic study that was funded in part by the National Institute of Allergy and Infectious Diseases (NIAID).
Researchers followed 1,164 COVID-19 patients who had been hospitalized at more than 20 U.S. hospitals between May of 2020 and March of 2021, before COVID vaccines were widely available.
They compared the patients who were given azithromycin to those who received no antibiotics, as well as to patients who were given other antibiotics.
Azithromycin changed the mix of microbes in the upper airway. Some normally harmless bacteria decreased, while potentially harmful bacteria became more common. These changes persisted for more than a week.
Next, the researchers will look at whether other widely used antibiotics, such as amoxicillin and ceftriaxone, exhibit similar effects in hospitalized patients.
Authors: Other authors associated with UCSF and/or the Chan Zuckerberg Biohub include co-first author Abigail Glascock, PhD, and co-authors Hoang Van Phan, PhD, Emily C. Lydon, MD, Carolyn S. Calfee, MD, MAS, John Greenland, MD, PhD, David J. Erle, MD, and Victoria T. Chu, MD. Other authors are affiliated with the University of Texas at Austin, UCLA, Baylor College of Medicine in Houston, Brigham and Women's Hospital in Boston, Case Western Reserve University and University Hospitals of Cleveland, Drexel University and Tower Health Hospital in Philadelphia, Stanford University School of Medicine, Icahn School of Medicine at Mount Sinai in New York City, Oklahoma University Health Sciences Center, Oregon Health & Science University in Portland, Ore., University of Arizona in Tucson, University of Florida in Gainesville, Yale School of Medicine and Yale School of Public Health, the Broad Institute of MIT & Harvard Medical School in Cambridge, Mass., National Institute of Allergy and Infectious Diseases (NIH), La Jolla Institute for Immunology, Precision Vaccines Program, Boston Children's Hospital, Boston Children's Hospital, Medical University of Vienna in Vienna, Austria, Emory School of Medicine in Atlanta, and the University of Washington in Seattle, Wash.
Funding and disclosures: Funding for this study was provided through the following U.S. NIH grants: (5R01AI135803-03, 5U19AI118608-04, 5U19AI128910-04, 4U19AI090023-11, 4U19AI118610-06, R01AI145835-01A1S1, 5U19AI062629-17, 5U19AI057229-17, 5U19AI125357-05, 5U19AI128913-03,3U19AI077439-13, 5U54AI142766-03, 5R01AI104870-07, 3U19AI089992-09, 3U19AI128913-03, 5T32DA018926-18, and K0826161611); NIAID, NIH (3U19AI1289130, U19AI128913-04S1, R01AI122220, and 1K23AI185326-01); NCATS (UM1TR004528), and National Science Foundation (DMS2310836). Funding sources did not have a direct role in the design, analysis, or approval of the manuscript. Please refer to the study for additional disclosures.
