E. coli belongs to a large group of bacteria called Escherichia coli. Many E. coli are harmless and they live in the intestines of animals and humans as they contribute to intestinal health. However, eating or drinking food or water contaminated with certain types of E. coli can cause mild to severe illness. Some are even life-threatening.
An estimated 150 million UTIs occur each year worldwide, accounting for $6 billion in healthcare costs, according to the American Urological Association. The bacterium E. coli is responsible for the majority of them. Antibiotics are the standard treatment, but often the infection returns when treatment is stopped.
Pooja Balani, a doctoral student at Northeastern University works on studying E. coli in urine samples from some 500 patients suffering from relapsing urinary tract infections. She aims to find an exact same mutation in the pathogens’ genes that could probably put people with relapsing UTIs on the fast track for a new therapeutic regimen.
“We took a large collection of E. coli isolates from patients with relapsing UTIs,” explains Balani. “And we found that quite a number of those isolates had exactly the same mutation—in a gene called hipA—that we and other scientists have seen in test-tube experiments.” After hours of tests poring over both test-tube cultures of E. coli and patients’ UTI isolates, in search of hipA mutations, she was delighted by what she saw: hipA leapt to the fore in both populations.
Her research also focuses on certain bacteria achieving antibiotic tolerance. Bacteria are one-cell organisms. To reproduce, they simply divide: One cell becomes two cells, and so on, until an army of progeny infects the host—here, a person’s urinary tract. Sometimes the division results in one active bacteria cell which continues to grow and divide and one that is alive but stops growing—it is dormant, and which eventually escapes the onslaught of active bacteria by the antibiotic.
Knowing this genetic mechanism could enable clinicians to customise treatment for relapsing UTIs. “You can track whether your patient has E. coli with a hipA mutation, and if so, introduce a pulse-dosing regimen,” says Balani, citing his earlier paper about pulse dosing and the pathogen that causes Lyme disease. Pulse dosing, he says, is straightforward: You give the patient an antibiotic and it kills all the growing cells. Then the persister cells start “waking up.” However, before they can divide to form a new population, you hit them with the antibiotic again. “In a test tube, if you repeat this process a couple of times, you can completely eradicate the population,” Balani says. “I believe that the same thing can be done in people.”
Anisha Naidu
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