Can a Fungus Cause a Urinary Tract Infection (UTI)?

Fungi can and do cause urinary tract infections, though they are far less common than the bacterial UTIs most people are familiar with. The overwhelming majority of fungal UTIs are caused by Candida species, with Candida albicans leading the pack. These infections occur most often in hospitalized patients, particularly those with urinary catheters, diabetes, or a history of broad-spectrum antibiotic use. While a healthy person walking around in daily life is unlikely to develop a fungal UTI, the situation changes quickly in a hospital setting where multiple risk factors pile up.

How Common Are Fungal UTIs

Fungal UTIs are overwhelmingly a hospital problem. In one 10-year retrospective study, Candida showed up in the urine of less than 1% of outpatient samples but appeared in roughly 3.5% to over 10% of inpatient samples, depending on the year.¹ That gap reflects the concentration of risk factors in hospitals: catheters, weakened immune systems, and heavy antibiotic use all create conditions where fungi can gain a foothold.

The numbers have also been trending upward. A case series tracking fungal UTIs at a single hospital found a dramatic year-over-year increase in confirmed cases, with renal disease being the most common underlying condition.² Broader reviews have tied this rise to the expanding use of broad-spectrum antibiotics, corticosteroids, immunosuppressive drugs, and cytotoxic chemotherapy agents in modern medicine.³ In other words, as medicine has become more aggressive at treating serious illnesses, one side effect has been creating more opportunities for fungal infections.

Which Fungi Are Responsible

Candida albicans is the species most often found in fungal UTIs, accounting for anywhere from about 48% to 87% of cases depending on the patient population studied.² But non-albicans species are increasingly important. Candida glabrata is the second most common culprit, appearing in roughly 20% to 30% of cases in some hospital surveys, and its prevalence matters because it often responds differently to antifungal medications.¹

In people with diabetes, the balance shifts further toward non-albicans species. One study of 400 urine samples from diabetic patients found that C. albicans accounted for just under half the positive cultures, with C. glabrata close behind at about 38%.⁴ Other species like C. krusei and C. kefyr appear less frequently but can be even harder to treat. This species distribution matters because first-line antifungal drugs work well against C. albicans but may be ineffective against some of the others.

Beyond Candida, other fungi occasionally infect the urinary tract, usually as part of a body-wide infection that has spread to the kidneys. Blastomycosis, for example, has been documented in the urinary tract of immunocompromised individuals, sometimes mimicking a kidney tumor on imaging.⁵ These cases are rare, but they illustrate that fungal UTIs are not exclusively a Candida phenomenon.

How Fungi Reach the Urinary Tract

Fungal UTIs develop through two main routes. The more common path is retrograde, meaning the fungus enters through the urethra and travels upward into the bladder, the same direction bacteria typically invade. The less common route is antegrade, where Candida circulating in the bloodstream seeds the kidneys from above. Antegrade infection tends to happen in patients who already have candidemia, a dangerous fungal bloodstream infection.⁶

In the retrograde scenario, several things have to go wrong for the fungus to establish itself. In a healthy urinary tract, a protein called Tamm-Horsfall protein helps prevent fungal cells from sticking to the bladder wall, and the natural flow of urine washes Candida away before it can set up shop.⁷ When that flow is disrupted by a catheter, a structural abnormality, or anything that causes urine to pool, the fungus gets time to attach and grow.

Who Is at Risk

Urinary catheters are the single biggest risk factor. Some reports indicate that as many as 90% of patients with fungal UTIs were hospitalized and had a catheter in place.⁸ Catheters introduce foreign material into the urinary tract, disrupt the normal flushing mechanism, and provide a surface for fungi to cling to and form biofilms.

Diabetes is another major contributor. The reasons are layered: high blood sugar feeds fungal growth, diabetic patients often have impaired immune cell function, and complications of diabetes including nerve damage to the bladder and recurrent vaginal yeast infections create additional entry points and environments for Candida.⁹

Broad-spectrum antibiotics deserve particular mention. When you take antibiotics for a bacterial infection, those drugs don’t just kill the bacteria causing the problem. They also wipe out the normal bacterial populations in and around the urinary tract. Those resident bacteria normally compete with fungi for space and nutrients. Once the bacteria are cleared out, Candida and other fungi face less competition and can colonize more easily.¹⁰ This is one reason fungal UTIs often follow courses of antibiotics given for something else entirely.

Other risk factors include immunosuppressive drugs, corticosteroids, chemotherapy, and any condition that weakens the immune system.³ Age plays a role too, with older adults being disproportionately affected, partly because they accumulate more of these risk factors over time.

When Candida in Urine Is Not Actually an Infection

One of the trickiest aspects of fungal UTIs is figuring out whether the Candida in a urine sample represents a genuine infection or is just passing through. Finding yeast in the urine, a condition called candiduria, is common in hospitalized patients, but it frequently reflects colonization or even contamination of the sample rather than a true infection. This distinction matters enormously because treating a non-infection with antifungal drugs is not harmless: it drives resistance, can cause side effects, and wastes time.

Clinicians generally rely on a combination of how much yeast is present and whether the patient has symptoms. However, dismissing candiduria too casually carries its own risks, because it can be a sign of a deeper problem, whether that’s a brewing fungal infection or an underlying issue in the genitourinary system like a structural abnormality or a vaginal yeast infection contaminating the sample.⁸ The candiduria can also, in some patients, be the first signal that Candida has entered the bloodstream and is now being filtered out through the kidneys.

The clinical spectrum ranges from completely asymptomatic candiduria all the way to full-blown sepsis originating from the urinary tract.¹¹ Where a given patient falls on that spectrum depends on their immune status, how the fungus got there, and whether any structural issues in the urinary tract are trapping it.

The Biofilm Problem

One reason fungal UTIs are harder to treat than you might expect is biofilm formation. When Candida attaches to a surface in the urinary tract, particularly a catheter, the cells don’t just sit there individually. They form organized communities called biofilms: layered structures embedded in a protective matrix that shields the fungal cells from both the immune system and antifungal drugs.

In laboratory studies, C. albicans cells growing in biofilm form showed resistance to fluconazole and amphotericin B, two of the most commonly used antifungal agents, regardless of the growth conditions.¹² Animal catheter models have confirmed this pattern: Candida biofilms on catheter surfaces exhibit high tolerance to antifungal therapy, making treatment much more difficult than dealing with free-floating yeast cells.¹³

This is why removing the catheter, when medically possible, is often the single most effective step in managing a fungal UTI. The biofilm goes with it.

Treatment Approaches

For many patients with asymptomatic candiduria, the first step isn’t an antifungal prescription at all. Simply removing the urinary catheter and stopping any unnecessary antibiotics clears the Candida from the urine in roughly half of cases.¹⁴ Ruling out urinary obstruction and kidney stones is also part of the standard workup, since stagnant urine gives fungi more time to grow.¹⁵

When treatment is needed, fluconazole is the go-to drug for most Candida UTIs. There’s a pharmacological reason for this: about 80% of a fluconazole dose is excreted unchanged in the urine, producing urine concentrations roughly ten times the level in the blood.¹⁶ That means the drug concentrates exactly where you need it. Other antifungal drugs, like itraconazole, barely show up in the urine at all, making them poor choices for bladder infections even though they may work well in other parts of the body.

For patients who can’t take fluconazole or have kidney problems that change the math, bladder irrigation with amphotericin B is an alternative. This approach delivers the drug directly into the bladder through a catheter. Studies have found that it clears Candida from the urine at rates comparable to or better than fluconazole in the short term: in one comparison, clearance rates were about 92% for bladder irrigation versus 68% for fluconazole.¹⁷ The advantage was especially pronounced in patients with kidney dysfunction, where fluconazole dosing becomes more complicated. A meta-analysis found that continuous irrigation for more than five days produced the best sustained clearance.¹⁸

A persistent frustration in treating fungal UTIs is recurrence. Even after successful clearance, Candida often comes back if the underlying risk factors haven’t changed. A patient who still has a catheter, is still on broad-spectrum antibiotics, and still has poorly controlled diabetes will likely see the yeast return regardless of which antifungal was used.

When Fungal UTIs Turn Dangerous

Most fungal UTIs, when they are actual infections and not just colonization, are confined to the lower urinary tract and are more of an annoyance than an emergency. But in some cases, particularly in immunosuppressed patients, things can escalate.

One uncommon but serious complication is the formation of fungal balls, also known as fungal bezoars. These are clumps of fungal filaments, dead tissue, and debris that can grow large enough to obstruct the urinary tract. Fungal balls tend to lodge at the junction where the kidney meets the ureter and can block urine drainage, leading to hydronephrosis, which is swelling of the kidney from backed-up urine.¹⁹ They can cause symptoms ranging from flank pain and fever to decreased urine output, and they sometimes require surgical removal.²⁰

Diagnosis can be tricky. In one case report, a diabetic man with a fungal ball in his upper urinary tract was initially misdiagnosed with a bacterial kidney infection because the urine cultures were negative for fungi, likely because the obstruction prevented infected urine from draining into the sample.²¹ Cases like this are a reminder that a negative culture doesn’t always rule out a fungal process, especially when imaging shows something suspicious.

The Growing Concern Around Candida Auris

If the landscape of fungal UTIs wasn’t complicated enough, a relatively new player has been making headlines. Candida auris was first identified as a human pathogen in 2009 and has since been found on every inhabited continent. It is now recognized as a cause of UTIs worldwide, and the urinary tract is actually one of its most common isolation sites. An analysis of nearly 13,000 C. auris strains found that urine was the second most common source of C. auris isolates in the United States and the third most common globally.²²

What makes C. auris alarming is a combination of traits that set it apart from other Candida species:

Multidrug resistance: Many strains are resistant to one or more classes of antifungals. Genomic analysis of individual isolates has turned up resistance genes covering azoles, echinocandins, and polyenes, essentially the three main categories of antifungal drugs available.²³
Misidentification: Standard laboratory methods frequently confuse C. auris with other Candida species, delaying appropriate treatment.²⁴
Environmental persistence: C. auris sticks to surfaces in hospitals and is difficult to eradicate with standard cleaning protocols, facilitating spread between patients.
High mortality: Urinary isolates of C. auris are often associated with high mortality rates, partly because the patients who develop these infections tend to be critically ill and partly because treatment options may be severely limited.

Early data also suggest that C. auris strains isolated from the urinary tract may be developing resistance to echinocandins, which are often the last-resort treatment when azole drugs fail.²² Public health agencies around the world now consider C. auris a serious and urgent threat, and healthcare facilities are implementing screening and containment protocols specifically targeting it.

Why Healthy People Rarely Get Fungal UTIs

If you’re not hospitalized, don’t have a catheter, aren’t on long-term antibiotics, and don’t have diabetes or an immune-compromising condition, your chances of developing a fungal UTI are quite low. The urinary tract has multiple layers of defense: the physical flushing of urine, proteins in the urine that prevent fungal adhesion, and a local immune response that deals with the small numbers of yeast that might occasionally show up. A study on immune responses to Candida in the urinary tract found that Tamm-Horsfall protein, the most abundant protein in normal urine, actively prevents Candida from attaching to the bladder lining in healthy individuals.⁷

What researchers still don’t fully understand is how and when these defenses break down at a molecular level. There’s a recognized knowledge gap around the immune response to fungal urinary infections specifically, as opposed to the much more thoroughly studied bacterial UTIs. Most of what we know about urinary immunity has been built on research into E. coli and other bacteria, and fungal pathogens may interact with the urinary tract in fundamentally different ways that haven’t been mapped out yet. For now, the practical takeaway is straightforward: if you’re generally healthy and develop UTI symptoms, it’s almost certainly bacterial. If you’re in a hospital with several risk factors stacking up, fungi become a real possibility that your medical team should be considering.

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