Letter | Published:

Antibiotic resistance increases with local temperature

Nature Climate Changevolume 8pages510514 (2018) | Download Citation

Abstract

Bacteria that cause infections in humans can develop or acquire resistance to antibiotics commonly used against them1,2. Antimicrobial resistance (in bacteria and other microbes) causes significant morbidity worldwide, and some estimates indicate the attributable mortality could reach up to 10 million by 20502,3,4. Antibiotic resistance in bacteria is believed to develop largely under the selective pressure of antibiotic use; however, other factors may contribute to population level increases in antibiotic resistance1,2. We explored the role of climate (temperature) and additional factors on the distribution of antibiotic resistance across the United States, and here we show that increasing local temperature as well as population density are associated with increasing antibiotic resistance (percent resistant) in common pathogens. We found that an increase in temperature of 10 °C across regions was associated with an increases in antibiotic resistance of 4.2%, 2.2%, and 2.7% for the common pathogens Escherichia coli, Klebsiella pneumoniae and Staphylococcus aureus. The associations between temperature and antibiotic resistance in this ecological study are consistent across most classes of antibiotics and pathogens and may be strengthening over time. These findings suggest that current forecasts of the burden of antibiotic resistance could be significant underestimates in the face of a growing population and climate change4.

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Acknowledgements

D.R.M. is supported by a Canadian Institute for Health Research Fellowship Grant and the Clinician Scientist Program at the Department of Medicine, University of Toronto. J.S.B. is supported by the National Library of Medicine NIH R01 LM011965. Thank you to the developers and data analysts at HealthMap for their support. Thank you to M. Kramer for his thoughtful and insightful review and feedback.

Author information

Author notes

  1. These authors contributed equally: Derek R. MacFadden and Sarah F. McGough.

  2. These authors jointly supervised this work: Mauricio Santillana and John S. Brownstein.

Affiliations

  1. Division of Infectious Diseases, Department of Medicine, University of Toronto, Toronto, Canada

    • Derek R. MacFadden
    •  & David Fisman
  2. Harvard Chan School of Public Health, Harvard University, Boston, MA, USA

    • Derek R. MacFadden
    •  & Sarah F. McGough
  3. Computational Epidemiology Group, Boston Children’s Hospital, Boston, MA, USA

    • Derek R. MacFadden
    • , Mauricio Santillana
    •  & John S. Brownstein
  4. Computational Health Informatics Program, Boston Children’s Hospital, Boston, MA, USA

    • Sarah F. McGough
    • , Mauricio Santillana
    •  & John S. Brownstein
  5. Department of Pediatrics, Harvard Medical School, Harvard University, Boston, MA, USA

    • Mauricio Santillana
    •  & John S. Brownstein

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Contributions

D.R.M., S.F.M. and M.S. contributed to the data analysis. All the authors (D.R.M., S.F.M., D.F., M.S. and J.S.B.) contributed to development of the manuscript, discussion and preparation of final versions. All the authors approved the final version of the manuscript.

Competing interests

The authors declare no competing interests.

Corresponding authors

Correspondence to Derek R. MacFadden or Mauricio Santillana or John S. Brownstein.

Supplementary information

  1. Supplementary Information

    Supplementary figures 1–8, Supplementary tables 1–4

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DOI

https://doi.org/10.1038/s41558-018-0161-6

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