She came to me with a manila folder stuffed with urine culture reports. 14 of them, spanning three years. Every one showed a different organism, or the same organism with a longer and longer list of resistances. Her most recent culture, the one that finally prompted her primary care physician to refer her to urology, showed an Escherichia coli (E. coli) resistant to 15 antibiotics. 15. She had been treated with trimethoprim-sulfamethoxazole, nitrofurantoin, ciprofloxacin, levofloxacin, cephalexin, augmentin, and several others I would rather not see used empirically in outpatient urology. Each course provided brief relief. Each course made the next infection harder to treat. Nobody had ever asked why she kept getting infected.
She is not unusual. In a busy urology practice, she is Tuesday afternoon.
The antibiotic reflex that is harming our patients
We have created a medical culture around recurrent urinary tract infections (UTIs) that is actively making patients sicker. It goes like this: patient calls with symptoms, nurse calls in an antibiotic, patient improves temporarily, infection returns, repeat. The threshold for prescribing keeps lowering. Patients learn to call at the first sign of cloudy urine, malodorous urine, or, in the case of our elderly demented patients, any behavioral change at all. Families call insisting their mother “always gets a UTI when she gets confused.” Nursing homes fax requests for antibiotics based on urinalysis findings that would be unremarkable in a younger patient.
The result is a population of patients arriving in my office carrying the cumulative antibiotic burden of years of reflexive prescribing, with organisms that have adapted to survive every drug we have tried, and a microbiome so disrupted that the very communities that once protected the bladder and vaginal tract have been eliminated. We did this. The medical system did this. And we need to stop.
What we are misdiagnosing
Let me address the clinical triggers directly, because this is where the antibiotic reflex begins. Cloudy urine is not a UTI. Malodorous urine is not a UTI. A positive dipstick for leukocyte esterase in a patient without symptoms is not a UTI. Confusion in a demented patient is not, by default, a UTI; yet this is one of the most persistent and damaging reflexes in all of geriatric medicine. Altered mental status in a demented patient has a broad differential diagnosis. Automatically attributing it to a UTI and prescribing an antibiotic treats a presumption, not a diagnosis, while contributing to resistance and leaving the actual cause of the behavioral change unaddressed.
The 2025 American Urological Association (AUA) guideline on recurrent UTIs was explicit on this point, moving away from microbial detection as the primary diagnostic criterion and toward clinician judgment that integrates symptoms, urinalysis, and culture together. Pyuria without symptoms does not equal infection. Bacteria in the urine of an asymptomatic patient, particularly an elderly woman, is often colonization, not infection, and treating colonization with antibiotics selects for resistance without benefiting the patient. When my patients ask for antibiotics based on the appearance or smell of their urine, I have a conversation. It is not always easy. But it is necessary.
The colonization problem nobody wants to discuss
Here is a clinical reality that is uncomfortable for patients and physicians alike: A significant proportion of men and women who believe they are suffering from recurrent UTIs are, in fact, chronically colonized. Colonization means bacteria are present in the bladder, sometimes in substantial quantities, sometimes producing a positive culture, without causing a true invasive infection. The urothelium is not breached. The immune response is not meaningfully activated. There is no fever, no systemic illness, no pyuria indicating active inflammation. The urine may be cloudy. It may smell different. A culture may grow an organism. But the patient does not have a UTI in the clinical sense that requires antibiotic treatment.
This distinction matters enormously, and it is one that the current system of reflexive antibiotic prescribing erases entirely. When a culture comes back positive, the instinct, for the patient, for the nurse, for the prescribing physician, is to treat. To prescribe. To do something. The idea of a positive culture that does not require antibiotics is genuinely difficult for patients to accept, particularly those who have spent years in the antibiotic cycle and associate a positive culture with immediate treatment.
What I tell these patients is this: A positive culture tells us bacteria are present. It does not automatically tell us those bacteria are making you sick. Your symptoms, your inflammatory markers, your clinical picture, those tell us whether you have an infection or a colonization. And for colonized patients, the most important thing I can offer is not an antibiotic. It is daily mechanical bladder hygiene. The most effective intervention for chronically colonized patients, men and women alike, is clean intermittent catheterization with daily bladder irrigation. By catheterizing once daily and flushing the bladder with 400 cubic centimeters (cc) of distilled or sterile water, we mechanically remove the bacterial load before it reaches the threshold and adherence level needed to establish a true infection. We are not treating colonization with drugs. We are physically removing the colonizing organisms, every single day, before they can cause harm.
This approach does not sterilize the bladder. It does not eliminate colonization permanently. But it interrupts the accumulation cycle consistently enough that many chronically colonized patients, patients who were receiving antibiotic courses every three to four weeks, go months without a clinical infection. The organisms are still there. They simply never reach the critical mass needed to become a problem. For these patients, the culture is not the target. The bacterial load is the target. And a catheter and 400 cc of sterile water addresses it more effectively than any antibiotic I have prescribed.
What I have learned after years of treating these patients
I want to share what actually works, not from a clinical trial, but from the lessons I have accumulated treating patients with multidrug-resistant recurrent UTIs who arrived in my office after years of failed antibiotic cycles.
Lesson one: Hydration is medicine, but only the right kind.
The single simplest intervention I offer every recurrent UTI patient is this: Drink more water. Plain water. Not juice, not sports drinks, not flavored water, not soda: water. Concentrated, high-osmolality urine is a favorable environment for bacterial growth. Dilute urine flushes the bladder more frequently, reduces bacterial contact time with the urothelium, and creates a less hospitable environment for uropathogens. The evidence for increased water intake reducing UTI recurrence is now strong enough that the 2025 AUA guideline formally recommends it for patients drinking less than 1.5 liters per day. The sugary drinks deserve specific mention. Glucose in the urine, whether from dietary sugar or uncontrolled diabetes, feeds bacteria. It is as simple as that. I tell patients: If you keep filling your bladder with sugar water, you are feeding the organisms you are trying to eliminate.
Lesson two: You cannot out-antibiotic a metabolic problem.
A significant proportion of my most difficult recurrent UTI patients have metabolic syndrome, insulin resistance, or poorly controlled diabetes, and no one treating their UTIs has addressed it. Elevated blood glucose creates glycosuria that provides a rich nutrient source for bacterial growth, impairs the immune response to infection, increases bacterial adherence to the urothelial cells, and, in patients with diabetic autonomic neuropathy, contributes to incomplete bladder emptying that creates a stagnant reservoir for bacterial proliferation. I cannot fix recurrent UTIs in a patient with a hemoglobin A1c (HbA1c) of 10 without also fixing the metabolic environment. Every antibiotic I prescribe in that context is fighting uphill. Optimizing glucose control, in collaboration with the patient’s primary care physician or endocrinologist, is not peripheral to my UTI management. It is foundational to it.
One nuance worth highlighting for clinicians: Glucosuria is not always a marker of poorly controlled diabetes. A growing number of patients are now taking sodium-glucose cotransporter-2 (SGLT-2) inhibitors, empagliflozin, dapagliflozin, canagliflozin, for diabetes, heart failure, or chronic kidney disease. These medications work precisely by causing the kidneys to spill glucose into the urine. That is their mechanism. It is intentional, it is therapeutic, and it also creates a persistently glucose-rich urinary environment that feeds uropathogens in exactly the way uncontrolled hyperglycemia does.
When I see a patient on an SGLT-2 inhibitor with recurrent UTIs, I do not assume their glucose is out of control. I recognize that the drug itself is creating the urinary environment driving their infections. The conversation then becomes whether the SGLT-2 inhibitor can be substituted for an alternative agent in collaboration with their cardiologist or endocrinologist, because no amount of Hiprex, estrogen cream, or bladder irrigation will fully overcome a medication that is actively depositing glucose into the bladder every single day. This is a conversation most prescribers of SGLT-2 inhibitors are not having with their patients. It needs to happen.
Lesson three: Hiprex works, and it does not create resistance.
Methenamine hippurate, sold under the brand name Hiprex, is a urinary antiseptic that has been used for nearly a century and is experiencing a well-deserved renaissance. Its mechanism is entirely distinct from antibiotics: It converts to bactericidal formaldehyde in acidic urine, destroying bacterial proteins and replication machinery. Because it is not an antibiotic, bacteria cannot develop resistance to it in the way they develop resistance to fluoroquinolones or nitrofurantoin. I prescribe Hiprex 1 gram twice daily for appropriate patients. The 2025 AUA guideline now formally recommends methenamine hippurate as a prophylaxis option, specifically to reduce antibiotic dependence. The ALTAR trial demonstrated non-inferiority to antibiotic prophylaxis over 12 months. For patients with multidrug-resistant organisms, Hiprex is often the most powerful tool I have precisely because resistance is irrelevant to its mechanism. The key to efficacy is maintaining acidic urine. I counsel patients to avoid alkalinizing agents and to ensure adequate hydration. Hiprex is not a cure, but for patients who commit to it, it substantially reduces infection frequency without touching the antibiotic arsenal.
Lesson four: Topical vaginal estrogen is underused.
For postmenopausal and perimenopausal women with recurrent UTIs, topical vaginal estrogen cream is one of the most evidence-backed, lowest-risk, highest-impact interventions available, and it is prescribed at a fraction of the rate it should be. The vaginal and urethral tissues depend on estrogen to maintain the Lactobacillus-dominant microbiome that creates the acidic, bacteria-hostile environment that protects the bladder. When estrogen declines, that environment collapses. The potential of hydrogen (pH) rises. The protective microbiome disappears. Uropathogens colonize tissues that were once inhospitable to them.
Published data shows that topical vaginal estrogen reduces UTI frequency by over 50 percent in postmenopausal women with recurrent infections. The 2025 AUA guideline strengthened its recommendation for vaginal estrogen in perimenopausal and postmenopausal women without contraindications. A small amount of topical cream applied vaginally two to three times per week restores the hormonal environment that no antibiotic can replicate. I start estrogen cream in virtually every eligible postmenopausal woman who walks into my office with recurrent UTIs. It is safe, inexpensive, effective, and ignored by most of the physicians who have been treating these patients.
Lesson five: For refractory patients, clean intermittent catheterization with daily bladder irrigation.
As described above in the colonization section, this is the intervention that surprises physicians most and delivers the most dramatic results in my most refractory patients. For patients who have optimized hydration, controlled their metabolic syndrome, started Hiprex, and used topical estrogen, and who still experience recurrent infections or remain chronically colonized with positive cultures, daily clean intermittent catheterization with 400 cc bladder irrigation is the next step. Patients catheterize themselves once daily using sterile technique and flush the bladder with distilled or sterile water. It takes five minutes. The results, for patients who commit to it consistently, are remarkable. Not because we have eliminated bacteria from the urinary tract, but because we have interrupted the daily accumulation cycle that converts colonization into clinical infection. I teach this in the office. Patients go home and do it themselves. For the right patient, it is the single most impactful thing I can offer.
The conversation I have to have, and so do you
Here is the hardest part of this protocol, and I want to be direct about it because it is the part that determines whether any of the above actually works. I tell my patients: You must stop asking for antibiotics for cloudy urine, smelly urine, or mild symptoms. I tell them: You may feel uncomfortable sometimes and that discomfort is not automatically an infection. I tell them: If you truly develop a fever, rigors, flank pain, or systemic symptoms, you call us immediately and we act. But a culture-positive, symptom-negative or minimally symptomatic episode is not an automatic indication for ciprofloxacin.
And I tell them something that is harder to hear: If we stay on this path, aggressive bladder hygiene, Hiprex, estrogen, daily irrigation, there is a small chance that at some point you may develop a more serious infection. You may need to be hospitalized. You may need intravenous (IV) antibiotics for a pyelonephritis or urosepsis episode. That risk exists. It is real. And for most patients, it is significantly lower than the trajectory they were on, cycling through oral antibiotics every few weeks, building resistance with each course, until the day arrives when no oral antibiotic works at all and the hospitalization is unavoidable.
Most of my patients, once they understand the alternative, choose the non-antibiotic path. They stay on it. Their cultures improve. Their infection frequency drops. The organisms, when they do emerge, are often susceptible to agents we have kept in reserve rather than the resistant monsters that frequent antibiotic exposure produces. It works. Not for every patient, not every time, but for most patients, most of the time, it works dramatically better than another prescription.
A call to change how we practice
Recurrent UTI management is broken. It is broken because we respond to patient pressure with prescriptions. It is broken because we treat dipstick results and positive cultures rather than patients. It is broken because we have conflated patient satisfaction with appropriate medical care. And it is broken because the downstream consequences, multidrug resistance, destroyed microbiomes, escalating resistance patterns, fall on the subspecialist who inherits the patient years later, not on the clinician who wrote the 10th antibiotic prescription.
We can do better. The tools are available. The evidence is there. The 2025 AUA guidelines support a non-antibiotic-first approach for appropriate patients. Hiprex, vaginal estrogen, optimized hydration, metabolic control, and, for the most refractory and chronically colonized patients, mechanical bladder hygiene through daily self-catheterization and irrigation represent a coherent, evidence-informed protocol that reduces antibiotic dependence without abandoning patient safety. What it requires is a different kind of conversation with patients. Longer, harder, and more honest than calling in a prescription. But the patients on the other side of that conversation, the ones with fewer infections, better quality of life, and organisms that are still treatable when they need to be, make every one of those conversations worth having.
Jitesh Patel is a urologist.
