Understanding the pathophysiology of GBS urinary tract infections in diabetes

7/19/2021

Ritwij Kulkarni, MSc, PhD

About presenter

Dr. Ritwij Kulkarni received his PhD from SUNY Stony Brook studying the importance of type II secretion and type IV pilus systems in uropathogenic Escherichia coli. Following this Dr. Kulkarni received post-doctoral training in the Department of Pediatrics at Columbia University studying host-pathogen interactions in the respiratory and urinary tracts. Dr. Kulkarni is working as assistant professor of immunology at University of Louisiana at Lafayette where his research group is focused on examining the effects of diabetic urinary microenvironment on the physiology of UTI caused by various Gram positive and Gram negative uropathogenic bacteria.

Group B Strep International

7/19/2021 10:17:43 pm

Thank you for your excellent presentation, Dr. Kulkarni, and for your very important work to better understand the role of diabetes in GBS UTIs!

Megan

7/20/2021 08:59:18 am

Great presentation - very informative

Ritwij Kulkarni

7/20/2021 11:30:26 am

Thank you.

Marti Perhach

7/20/2021 09:28:30 am

Do you have any observations from your research about lower colony counts of GBS bacteriuria, not sufficient to be considered a UTI, and diabetes?

Ritwij Kulkarni

7/20/2021 11:29:46 am

That is a great suggestion. In our current model, presence of bacteria in the urinary tract (bacterial burden) at 24h post infection is indicative of acute UTI. To study chronic urinary carriage of GBS (bacteriuria) we will have to examine diabetic and non-diabetic mice over a period of 7 to 28 days (1 to 4 weeks). We have not done those experiments yet.

Amelia P

7/20/2021 10:05:29 am

You mentioned you were currently examining GBS physiology over time. When do you think that research will be completed? I am very interested to see the results.

Ritwij Kulkarni

7/20/2021 11:24:01 am

We are examining changes in GBS physiology following exposure to glycosuria for different lengths of time (early versus late). Currently we are in the standardization phase of these experiments. We hope to complete this work by next year!

James Mcgregor

7/20/2021 11:37:58 am

Thanks for your excellent explications of your work.. Hope you publish I journal read by clinicians so that appropriate clinical trials will be informed / inspired by your experiments, thanks

Ritwij Kulkarni

7/21/2021 07:11:18 pm

Thank you for your comments. Our paper describing effects of glycosuria on GBS physiology was published in the Journal of Infectious Diseases.

Josh Pak

7/22/2021 08:13:55 am

When applied to people, do you think that proactive insulin use could decrease virulence?

Ritwij Kulkarni

7/31/2021 05:25:11 am

That's a very interesting question, although I am a little confused about the defintion of "proactive" insulin use. So my answer refers to insulin treatment to regulate hyperglycemia and glycosuria. Our results indicate that the presence of glucose in urine is the principal driver of virulence phenotypes in GBS. Therefore, a treatment (insulin) that reduces glycosuria may affect GBS virulence.
BUT I would qualify my answer by pointing one major caveat that our work is "in vitro". In the future, we will compare GBS virulence gene expression in diabetic and non-diabetic urinary tracts, which will reveal (we hope!) how GBS may respond to both glycosuria and myriad host factors. In addition, we can test the effects of insulin administration on GBS virulence in mouse models of diabetes. Both these are on our "to do" list!
Meanwhile, I will draw your attention to an interesting paper that addresses role of insulin receptors on UTI pathophysiology: https://www.jci.org/articles/view/98595
Thank you.

Comments are closed.

Understanding the pathophysiology of GBS urinary tract infections in diabetes

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Understanding the pathophysiology of GBS urinary tract infections in diabetes

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