New study addresses why some of us get so many UTIs, while others of us do not

3 min read

About the Author

Kate graduated with a B.A. in Journalism from San Diego State University. She is the Content Manager at Uqora and is responsible for Uqora's social media, newsletters and contributing to the UTI Learning Center.

More about this author

About the author

Kate graduated with a B.A. in Journalism from San Diego State University. She is the Content Manager at Uqora and is responsible for Uqora's social media, newsletters and contributing to the UTI Learning Center.

More about this author

Why only some people get UTIs

Here’s a scenario: you and your friend have similar hygiene habits, are having a similar amount of sex, and have a similar post-sex and post-workout regimens, yet you get slammed with UTI after UTI, and she is cruising through life oblivious to your suffering. You may be asking yourself — why is this happening to me?

Well, it’s complicated. And, according to a study recently conducted by Annals of Translational Medicine, there are a bunch of gaps in our understanding preventing us from fully answering the age-old “why me?” question.

The team of researchers focused their study on the bacteria that most often causes UTIs, Escherichia coli, known collectively as uropathogenic E. coli (UPEC). The aim of the study was to develop a better understanding of the sometimes murky UTI space with the hopes of potentially offering new therapeutic strategies. The team of researchers analyzed 43 strains of E. coli sampled from 14 women with recurrent UTIs. The researchers took a subset of these strains (21) and injected them into mice in order to determine how well the sampled UPEC could infect hosts in a controlled setting.

Ultimately, they found that the results varied widely within the same strains. According to Broad Institute's coverage of the study, some mice would develop a UTI from the bacteria known to cause UTIs and some would not:

"Additionally, when tested in a second mouse model, some of the UPEC strains that successfully infected the first caused a less severe outcome. Based on these findings, the research team proposed a new pathogenesis model in which each combination of host and UPEC strain is a unique pairing of bacterial urovirulence potential and host susceptibility — and the compatibility of that pairing ultimately determines UTI outcome, including severity.”

What this research means

The research seems to suggest that you could actually transplant the bacteria that caused your UTI into your friend’s urinary tract, and it might not impact them. In other words, the relationship between your body and the bacteria may be more like a lock-and-key — where the bacteria is the key but it won’t find a fit with every body. So comparing hygiene habits, post-sex routine, etc, could be completely useless. More from Broad Institute:

“Thus, two women with UTIs could have infections caused by similar or radically different bacteria, and an E. coli strain that causes a UTI in one person may not make a different person sick at all due to differences in genetics, behavior, medical history, or other environmental features.”

Conclusion

It’s too early to draw definitive answers from this research, but the integrative approach is encouraging and the early findings are fascinating. If you find yourself comparing your urinary health journey to someone else’s, it’s important to use this research as a reminder that you are not doing anything wrong, but the simple fact that bacteria affects each of our bodies differently and to a different level of severity.

References

1. Henry L Schreiber, Matt S Conover, Wen-Chi Chou, Michael E Hibbing, Abigail L Manson, Karen W Dodson , Thomas J Hannan, Pacita L Roberts, Ann E Stapleton, Thomas M Hooton, Jonathan Livny, Ashlee M Earl, Scott J Hultgren. Bacterial virulence phenotypes of Escherichia coli and host susceptibility determine risk for urinary tract infections. Sci Transl. Med. 2017 Mar 22;9(382):eaaf1283.

2. Zusi K. Urinary tract infections reveal the importance of interactions between host susceptibility and bacterial gene expression. Broad Institute. 2017 Mar.


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