Although funguria is a relatively common finding in some patient populations, there is uncertainty about its importance. This is because funguria might be present for one of several reasons, and differentiating colonization from true infection is difficult. Unfortunately, there are no established criteria that reliably differentiate the two entities.3 Most patients with funguria have no symptoms suggestive of a UTI (e.g., dysuria, suprapubic tenderness, or hematuria).1,6,7,10
For bacterial UTIs, the presence of pyuria, and a defined minimum number of colony-forming units (CFUs), is helpful in establishing this diagnosis.1,2,3,6 However, with funguria, neither of these parameters is helpful in distinguishing between colonization, contamination, or a true UTI. The reason is that pyuria commonly develops as a result of either coexistent bacteriuria or local irritation caused by the presence of an indwelling urinary catheter.1,7 Large numbers of fungal CFUs might indicate colonization only, which has no clinical significance.6,14
Candida spp often live as saprophytes on the skin in the genital and perineal areas.13 Women have a 10% to 65% rate of colonization of the vulvovestibular area with Candida spp.7 This readily allows for contamination of urine specimens during the collection process, and facilitates the introduction of organisms into the urinary bladder, particularly through the use of indwelling urinary catheters.6
Colonization of indwelling urinary devices universally occurs, as long as they remain inserted for substantial periods of time.6 Funguria is commonly observed with the use of either urethral or suprapubic catheters.4,7 Fortunately, intermittent urinary catheterization rarely is associated with the development of funguria.15 Additional substrates for the development of colonization include ureteral stents and nephrostomy tubes.7,14
UTIs due to fungi can present in several ways, including asymptomatic funguria, lower-tract UTIs, upper-tract UTIs, and renal candidiasis.7 Asymptomatic funguria is most commonly found in hospitalized patients who have indwelling urinary catheterization devices. Fungal lower-tract UTIs (i.e., cystitis) resulting in symptoms are uncommon in both catheterized and noncatheterized patients.15 Fungal upper-tract UTIs, which usually manifest as pyelonephritis or sepsis due to a UTI, cannot be distinguished from those with a bacterial etiology because their clinical presentations are similar.7 Upper-tract UTIs tend to occur in patients who have either urinary obstruction or a disorder that results in urinary stasis.7 Fungal balls (bezoars) might develop as a serious complication of an upper UTI, and can result in obstruction. Renal candidiasis usually develops as a result of hematogenous dissemination of a fungal infection.7,14
Funguria generally does not predispose to the development of fungemia, but when it does occur, it usually is due to the presence of an upper-urinary-tract obstruction.3,4,6,8,12,14
It has been estimated that disseminated infection can be expected to occur in 1.3% to 10.5% of immunosuppressed patients with funguria.1,3,6,10,15
Until fairly recently, it was thought that renal transplant patients with funguria were at increased risk for developing fungemia, but this assertion is now known to be false.5
In deciding whether to treat funguria, it is important to consider the clinical setting in which it occurs. For example, when funguria occurs in asymptomatic patients with an indwelling urinary catheter, it often is due to colonization of the catheter. In such instances, simply removing the catheter will result in the resolution of between 33% and 40% of funguria cases.1,12 For most patients with asymptomatic funguria, it has been shown that the administration of antifungal therapy has no significant effect on morbidity or mortality.6,16