Year : 2008 | Volume
: 19 | Issue : 3 | Page : 350--360
Candiduria: A Review of Clinical Significance and Management
Zakeya Abdulbaqi Bukhary
Division of Infectious Diseases, Department of Medicine, Medical College, Taibah University, Medina, Saudi Arabia
Zakeya Abdulbaqi Bukhary
Consultant Internist and Infectious Diseases, Medical College, Taibah University, P.O. Box 2953, Medina
Candiduria is a common nosocomial infection afflicting the urinary tract. This review is aimed at providing an updated summary of the problem in hospitalized adult patients. A review of English Medline literature published between Jan 1970 until June 2007 was performed. Reviews, clinical trials and case-controlled studies in adult patients were included. Risk factors for candiduria included urinary indwelling catheters, use of antibiotics, elderly age, underlying genitourinary tract abnormality, previous surgery and presence of diabetes mellitus. Presence of candiduria may represent only colonization and there are no consistent diagnostic criteria to define significant infection. Candiduria may not be associated with candidemia and most cases are asymptomatic. Asymptomatic candiduria is usually benign, and does not require local or systemic antifungal therapy. Physicians need to confirm the infection by a second sterile urine sample, adopt non-pharmacologic interventions and modify risk factors. Mortality rate can be high particularly in debilitated patients and awareness to validate candiduria is necessary to stratify treatment according to patient status. Appropriate use of anti fungal drugs, when indicated, should not replace correction of the underlying risk factors. Treatment of symptomatic candiduria is less controversial and easier.
|How to cite this article:|
Bukhary ZA. Candiduria: A Review of Clinical Significance and Management.Saudi J Kidney Dis Transpl 2008;19:350-360
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Bukhary ZA. Candiduria: A Review of Clinical Significance and Management. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2019 Nov 12 ];19:350-360
Available from: http://www.sjkdt.org/text.asp?2008/19/3/350/40493
Candida urinary tract infections are an increasingly prevalent nosocomial problem with uncertain significance.  The presence of Candida species (Spp) in urine samples presents the physician with a challenge as to whether the candiduria represents colonization or, lower or upper urinary tract infection including ascending pyelonephritis and renal candidiasis with sepsis. ,,, Management has been inconsistent because of lack of information about the natural history of candiduria, which has not been studied properly. ,,,,, The aim of this review is to give an update on the problem in hospitalized adult patients and try to answer the three challenging classical questions in managing candiduria which are: whom to treat?, when to treat? and, for how long to treat?
A review of English Medline literature published between 1970 and June 2007 was performed, including the guidelines for treatment of candidiasis by the Infectious Diseases Society of America (IDSA). Articles related to selected populations such as critically ill patients, pediatric age-group, neonates, renal transplant recipients, and studies on candidemia were excluded.
Candiduria is rarely seen as a community acquired infection in a structurally normal urinary tract, and in healthy people. ,, It is increasingly becoming an important subgroup of nosocomial urinary tract infections (10-15%) and almost all are caused by Candida spp. ,,, The prevalence of candiduria varies in the hospital setting and is most prevalent among patients in intensive care units (ICU), more specifically surgical ICU and in leukemia and bone marrow transplant units. [,5],,
A review of the epidemiology of candiduria including all retrospective reviews, case-controlled studies and a large prospective surveillance study on candiduria, showed that the common risk factors include urinary tract instrumentation, prior surgical procedures, recent use of antibiotics, advanced age, female sex, diabetes mellitus, immunosuppressive therapy and prolonged hospital stay. ,,,,,,, In a recent case-controlled study, it was shown that that the risk to develop candiduria was increased by 12-fold after urinary catheterrization, six-fold each after the use of broad spectrum antibiotics and urinary tract abnormalities, four-fold following abdominal surgeries, two-fold in the presence of diabetes mellitus, and one-fold in association with corticosteroid administration.  However, no significant difference was found between the compared groups in terms of female sex, and age.
Candida was the causative pathogen in 27% of all urinary tract infections related to indwelling catheters.  Use of Foley's catheters was associated with candiduria in 78% of the patients although a variety of other devices such as suprapubic catheters and nephrostomy tubes were also noted. These catheters serve as a portal of entry for microorganisms into the urinary system where they colonize if left in place long enough. ,
Use of antibiotics was a major risk factor to develop Candida urinary tract infection; it is likely to contribute to colonization by Candida spp by suppressing endogenous bacterial flora, primarily in the gut and lower genital tract and possibly in the superficial area adjacent to the urethral meatus. It may interfere with phagocyte function and antibody formation with subsequent impaired host defense mechanisms against Candida infection. ,,
Previous surgery was a factor associated with candiduria and more than half of the patients who had a surgical procedure performed within the preceding month developed candiduria.  Whether surgery per se, or the need for a urinary drainage devices in the peri-operative period was the most important factor, could not be determined.
In a large multicenter study of candiduria in hospitalized patients, only 11% had no underlying illness recorded, 90% of patients had received antibiotics in the month preceding documentation of candiduria and 83% had urinary drainage devices in place. Other predisposing factors were present in most patients including surgical procedures, diabetes mellitus, urinary tract abnormallities such as neurogenic bladder and obstruction, and malignancy. Diabetes mellitus was the most common underlying disease seen in 39% of the patients.  It was the most common underlying disease noted in almost every study of candiduria. ,, It was proposed that diabetes predisposes to Candida colonization of the vulvo-vestibular area in women by enhancing urinary fungal growth in the presence of glycosuria, by lowering host resistance to invasion by Candida spp. as a consequence of impaired phagocyte activity, and promoting stasis of urine in a neurogenic bladder with more likelihood to undergo urinary tract instrumentation and to receive antibiotics. , However, the exact mechanism to for its contribution to candiduria is still not clear.  Clinical presentation in diabetic patients with candiduria range from lower urinary tract colonization to asymptomatic infection, cystitis, emphysematous cystitis, pyelonephritis and perinephric abscess.  Interestingly, men and women were equally represented among the diabetic population.  However, in large surveys in terms of gender difference in candiduria, women outnumbered men. ,
Most observational studies of candiduria have reported Candida albicans (C. albicans) as the predominant causative organism seen in more than 51 % cases, followed by C. glabrata (16 %) and C. tropicalis. ,, The candida species varies depending on the site of infection. Non-albicans Candida spp are common and more prevalent than C. albicans in sites such as oropharynx and vagina. ,,,,, It has been suggested that Candida spp causing candiduria might also be shifting to non-albicans Candida, the most prevalent of which was C. tropicalis (43%). These differences in the microbiological pattern of candiduria remain unexplained currently , [Table 1]. Mixed isolates were found in 10% of patients with nosocomial candiduria. 
Strain persistence was exceedingly frequent in candiduria and was documented in both persistent and recurrent infections. Therefore, species identification is not useful in differentiating persistent from recurrent infections. However, molecular methods would certainly be useful in this regard. 
The significance of systemic factors in the defense against urinary candida infection is unknown, but secretions from the prostate gland in men and from periurethral gland in women have been reported to be fungistatic. In addition, other normal flora may suppress growth of Candida at sites on mucous membranes. Lower urinary tract candidiasis is usually the result of a retrograde infection, while renal parenchymal infection often follows candidemia. ,
Although it is the most common route for bacterial infection of the urinary tract, the pathogenesis of ascending infection with Candida spp is not clearly known.  Catheterization can cause infection by introducing organisms during the catheterization process or by allowing migration of the organisms into the bladder along the surface of the catheter from the external peri-urethral surfaces. Ascending infection that originates in the bladder can lead to upper urinary tract infection, especially if vesicoureteric reflux or obstruction of urinary flow occurs.
Recently, experimental studies have indicated that multiple micro-abscesses develop through out the renal cortex following which the yeast penetrates through the glomeruli into the proximal tubules and are then shed into the urine. Hematogenous spread of Candida spp to the kidney was the most common route in renal candidiasis and was well verified in majority of patients with disseminated candidiasis who had renal involvement at autopsy. ,,,
The presence of Candida spp in urine, on examination or culture, does not necessarily imply clinical significance. The determination of the significance of candiduria can be blurred and difficult. Unfortunately, clinical criteria are insufficient to distinguish reliably among the clinical types. The finding of Candida spp in the urine could mean that the patient has cystitis or pyelonephritis or most likely it may reflect only colonization of the perineum, indwelling urinary catheter or the bladder. Currently, neither sensitive nor specific laboratory diagnostic tests are available to reliably distinguish infection from colonization.
Contamination is common, especially if the specimen is suboptimal urine collection from a catheterized patient or a woman who has heavy Candida colonization of the perineum. A small amount of the organisms that may find their way into the collected urine sample can grow and may multiply quickly. Usually, a second sterile urine sample should be clear. ,
Colonization is usually asymptomatic adherence and settlement of the Candida spp on the drainage catheters or foreign bodies in the urinary tract and, may result in high concentration of Candida colonies in urine cultures. Confirmation of candiduria by a second sterile urine examination after changing the catheter or a clean catch or suprapubic sample is required, before further investigations and initiation of treatment. ,
Most patients with candiduria are asymptomatic and there are no associated signs or symptoms.  Quantitative cultures with colony counts of > 100,000 cfu/ml of urine are associated with infection in patients without indwelling urinary catheters. In contrast, clinically significant renal candidiasis has been reported even with low colony counts of 1000 cfu/ml of urine. 
Pyuria usually supports the diagnosis of infection. , However, it may be a result of coexistent bacteriuria or mechanical injury of the bladder mucosa caused by the presence of an indwelling catheter. Absence of pyuria and low colony counts tend to role out Candida infection. The low specificity of pyuria as well as low colony counts of 1000 cfu/ml of urine, requires careful interpretation and proper clinical correlation. Quantitative Candida test in urine has little value in localizing the anatomic site of the infection. Rarely, finding a granular cast containing Candida hyphal elements localizes the infection to renal parenchyma with low sensitivity but high specificity. ,
Candida Cystitis is symptomatic lower urinary tract infection and presents with symptoms and signs of bladder irritation including dysuria, hematuria, frequency, urgency and suprapubic tenderness. A symptomatic patient with local invasive fungal infection of the bladder rarely requires cystoscopy unless obstruction or presence of a fungus ball is suspected.
Candida pyelonephritis can be associated with candidemia, sepsis and/or septic shock. It is uncommon and seen in hospitalized patients with diabetes and renal insufficiency with papillary necrosis and obstructive uropathy. It is indistinguishable from bacterial pyelonephritis and urosepsis. Often, it is complicated by suppurative disease, resulting in pyonephrosis and focal abscess formation. Fungus ball is a major complication, and consists of yeast, hyphal elements, epithelial and inflammatory cells and sometimes, renal medullary tissue secondary to papillary necrosis. It may complicate ascending or descending infections; especially in the presence of obstruction and stasis.
Candiduria and fever may be the only clues and the first indications of systemic invasive candidiasis in high-risk patients. They include patients with neutropenia and renal, liver or bone marrow transplant recipients as well as those who have undergone invasive urologic procedures. For patients with candiduria who have fever and/or sepsis, it is necessary to obtain blood cultures and perform radiological investigations to determine the anatomic source of candiduria. ,
Candiduria does not cause candidemia in most of the patients unless urinary tract obstruction is present.  An understanding of the anatomic site of infection along with patient's condition (elderly, catheterized) would determine the nature of treatment. There is a lot of controversy about whether, and when to treat, the most appropriate anti fungal agents to be used, as well as systemic versus local bladder irrigation. ,,,
Strategies for management are based on presence or absence of genitourinary tract abnormalities, risks for systemic infection or invasive candidiasis and the potential to develop complications from infection. As an initial intervention, removal of an indwelling catheter is recommended.  Current available evidence shows that the discontinuation of catheter use alone might result in eradication of candiduria in almost 40% of asymptomatic patients. After a new catheter was inserted, untreated candiduria resolved in 20% of patients. ,, Systemic therapy demonstrated that clinical benefits were less apparent in elderly, debilitated or minimally symptomatic patients without catheter removal, and were unable to document continued eradication of the Candida in the urine two weeks after the discontinuation of the anti fungal therapy. Not surprisingly, candiduria was more common at two weeks follow-up visit in those patients whose catheters remained in place.  Persistent candiduria, despite treatment, may warrant ultrasonography or CT scan of the kidney. ,
Based on evidence from clinical experience, descriptive studies and other reports, asymptomatic candiduria is usually benign and self-limiting, if the predisposing factors are corrected. Although properly designed randomized controlled studies are lacking, available data indicates that routine treatment is not indicated. However, treatment is indicated in patients at high-risk for invasive candidiasis.  Nevertheless, asymptomatic candiduria may be considered as a marker of high morbidity/mortality in elderly and debilitated patients with underlying diseases including diabetes mellitus. ,,
If treatment is considered in symptomatic patients, fluconazole is the anti fungal drug of choice provided the organism isolated is not C. glabrata or C. krusei. Treatment with fluconazole, 200 mg/day, for 7-14 days or with intravenous amphotericin B deoxycholate at doses of 0.3-1.0 mg/kg/day for 1-7 days has been successful based on moderate evidence from a randomized clinical trial. Short courses of therapy are not recommended; therapy for 7-14 days is more likely to be successful. , In a randomized controlled trial of 22 patients, candiduria persisted in 68% patients who received no anti fungal therapy versus 39% among individuals who received fluconazole therapy. 
Fluconazole is potentially useful because of the high concentrations of active drug in the urine, is better tolerated and is less likely to be associated with the emergence of resistance during therapy. It is advocated as a safe and effective alternative to amphotericin B for the treatment of serious Candida infections in organ transplant recipients, especially those receiving cyclosporine.  Treatment of Candida can be guided by in vitro susceptibility testing. Individual isolates do not necessarily follow the general pattern. For example, C. albicans is usually susceptible to all major agents. However, azole resistance for this species is well described especially among HIV-positive patients. , The greatest concern for fluconazole resistance is related to C. glabrata and C. krusei isolates which require maximal doses of amphotericin B. Amphotericin B resistance appears uncommonly among isolates of C. tropicalis and C. parapilosis. 
Nevertheless, susceptibility testing of Candida is not considered a routine procedure in many laboratories, it is not always available and is not universally considered as the standard of care. The new anti fungal drug voriconazole can be used, especially in severe sepsis or septic shock but its use is determined by the renal function.  Echinocandin anti fungal agents (caspofungin, micafungin, and anidulafungin) can be used although low sub-therapeutic levels are achieved in the urine because the drug has poor glomerular filtration with subsequent diminished tubular secretion. ,
The alternative choice for C. glabarata is flucytocine with excellent activity against non-albicans candida. The drug achieves high concentrations in the urine of patients who do not have renal failure. Its limitations included bone marrow, hepatic and gastrointestinal toxicity and de novo resistance which is seen in 25% of C. albicans strains, particularly when used as monotherapy. ,,
There are few case series and prospective studies that have compared the various therapeutic agents. Oral fluconazole has a more delayed but more lasting effect on candiduria than amphotericin B bladder irrigation. Patients receiving amphotericin B bladder irrigation had higher rates of eradication two days after the beginning of therapy than those receiving oral fluconazole but the cure rates were similar one month after the beginning of the therapy. Although amphotericin B bladder irrigation has been highly effective in the eradication of Candida cystitis, it is inconvenient to insert a catheter in non-catheterized patient and a 5-day course of localized bladder therapy is inconvenient. Such therapy may be necessary in patients with renal insufficiency. ,,,,
Continuous amphotericin B bladder irrigation was superior to intermittent treatment in terms of efficacy, ease of administration and patient comfort.  Recurrence was more common with amphotericin B bladder irrigation compared to fluconazole therapy. , The rate of eradication seven days after therapy was higher in patients who received oral fluconazole for four days or single dose of intravenous amphotericin B than in those who underwent bladder irrigation with amphotericin B for three days.  A single intravenous injection of amphotericin B causes persistent and sustained urinary excretion of the drug in levels that inhibit Candida spp. and thereby may permit successful single or pauci dose therapy of candiduria in some patients with a minimum toxicity. ,
In patients with Candida pyelonephritis, systemic therapy together with adequate drainage of the upper urinary tract is essential. Treatment with systemic antifungal agent (oral or intravenous) is indicated to eradicate the infection. Long-term antifungal therapy and drainage is needed after relieving the obstruction and identifying local complications by prompt imaging. Systemic anti fungal therapy used for treatment of systemic candidiasis is with either parenteral amphotericin B >0.6 mg/kg/day or fluconazole 6 mg/kg/day. 
No data is available regarding the efficacy of the less nephrotoxic lipid formulations of amphotericin B in treatment of patients with ascending Candida pyelonephritis or renal candidiasis. Given the favorable ratio of therapeutic effectiveness of fluconazole to toxicity, maintaining conventional doses of the drug in presence of renal insufficiency may achieve therapeutic concentrations in the urine necessary for eradicating non-albicans Candida. ,
Removal of the nephrostomy tube or a replacement by a new one as well as surgical removal of the obstructing fungus ball is the most important part of the management. The nephrostomy tube also serves as a route for local administration of high doses of amphotericin B or fluconazole, when renal insufficiency exists with the resultant decreased therapeutic urine concentrations of the drug.
Renal candidiasis is usually due to hematogenous seeding to the kidneys, and associated with candidemia, which may present with sepsis, hemodynamic instability and renal insuffeciency. Treatment should be with high dose systemic amphotericin B (0.6 mg/ kg/day) or parenteral fluconazole (6 mg/kg/ day). The optimal duration of therapy has not been determined. ,, Candidemia is rarely the consequence of candiduria and usually occurs in the presence of upper urinary tract obstruction. ,
Nosocomial urinary tract infection resulting in candiduria more common in patients with indwelling urinary catheters, systemic antibiotic use, underlying genitourinary abnormality, previous surgery and diabetes mellitus. Most cases are asymptomatic and require no treatment. Progression to candiedmia is rare unless patients are at high-risk for invasive disease. Mortality with candiduria can be high in debilitated patients and those in advanced age. If treatment is indicated, the drug of choice is fluconazole. Identification of Candida spp may be necessary in complicated cases to decide on the anti fungal drug of choice and response to therapy.
The approach to patients with candiduria needs to be individualized and the two important determinants of decision to treat include the extent of genitourinary tract involvement and renal function. Physicians are urged to have an early validation of candiduria considering the status of the patient by stratifying their risks  [Figure 1].
Large-scale surveys of candiduria are needed in certain populations at risk to find the true incidence of the disease and compare the microbiology patterns, which will help in further understanding of the problem in our population.
For Hail Al-abdely who supported to compose the review and for Carol A. Kauffman from University of Mitchigan and Peter G pappas from University of Alabama for their permission .
|1||Guler S, Ural O, Findik D, Arslan U. risk factors for nosocomial candiduria. Saudi Med J 2006;27(11):1706-10.|
|2||Kauffman CA. Candiduria. Clin Infect Dis 2005;41(suppl 6):S371-6.|
|3||Lundstorm T, Sobel JD. Nosocomial candiduria: A review. Clin Infect Dis 2001; 32(11):1602-7.|
|4||Sobel JD, Vazaquez JA. Fungal infections of urinary tract. World J Urol 1999;17(6): 410-4.|
|5||Pappas PG, Rex JH, Sobel JD, et al. Guidelines for treatment of candidiasis. Clin Infect Dis 2004;38(2):161-9.|
|6||Sobel JD, Kauffman CA, Mckinsey D, et al. Candiduria: A randomized, double-blind study of treatment with fluconazole and placebo. Clin Infect Dis 2000;30(1):19-24.|
|7||Fisher JF, Newma CL, Sobel JD. Yeast in the urine: Solution for a budding problem. Clin Infect Dis 1995;20(1):183-9.|
|8||Wong-Beringer A, Jacobs RA, Guglielmo BJ. Treatment of funguria. JAMA 1992; 267(20):2780-5.|
|9||Johnson JR. Should all catheterized patients with candiduria be treated? Clin Infect Dis 1993;17(4):814-6.|
|10||Kauffman CA, Vazaquez JA, Sobel JD, et al. Prospective multicenter surveillance study of funguria in hospitalized patients. Clin Infect Dis 2000;30(1):14-8.|
|11||Strofer SP, Medoff G, Fraser VJ, Powderly WG, Dunagan WC. Candiduria: Retrospective review in hospitalized patients. Infect Dis Clin Pract 1994;3:23-9.|
|12||Shoenbeck J, Einsehn S. The occurance of yeast-like fungi in the urine under normal conditions and in various types of urinary pathology. Scand J Urol Nephrol 1972;6 (2):123-8.|
|13||Weber DJ, Rutala WA, Samsa GP, Wilson MB, Hoffman KK. Relative frequency of nosocomial pathogens at a university hospital during the decade 1980-1989. Am J Infect Control 1992;20(4):192-7.|
|14||Schaerg DR, Culver AH, Gaynes RP. Major trends in the microbial etiology of nosocomial infection. Am J Med 1991;91(Suppl 3B):72S-4S.|
|15||Revitt AG, Perry JA, Cohen J. Urinary candidiasis: A prospective study in hospital patients. Urol Res 1986;14(4):183-6.|
|16||Gubbins PO, McConnell SA, Penzak SR. Current management of funguria. Am J Health Syst Pharm 1999;56(19):1929-35.|
|17||Hedderwick S, Kauffman CA. Opportunistic fungal infections: Superficial and systemic candidiasis. Geriatrics 1997;52(10):50-4.|
|18||Kobayashi CC, de Fernandes OF, Miranda KC, de Sousa ED, Silva Mdo R. Candiduria in hospital patients: A study prospective. Mycopathologia 2004;158(1):49-52.|
|19||Platt R, Polk BF, Murduok B, Rosner B. Risk factors for nosocomial urinary tract infection. Am J Epidemiol 1986;124(6):977-85.|
|20||Joshi N, Caputo GM, Weitekamp MR, Karchmer AW. Infections in patients with diabetes mellitus. N Engl J Med 1999;341 (25):1906-12.|
|21||de Oliveria RD, Maffei CM, Martinez R. Nosocomial urinary tract infections by candida species. Rev Assoc Med Bras 2001;47(3):231-5.|
|22||Paul N, Mathia E, Abraham OC, Mathia D. Emerging microbiological trends in candiduria. Clin Infect Dis 2004;39(11):1743-4.|
|23||Khatib R, Ayeni O, Riederer KM, Briski LE, Wilson FM. Strain relatedness in persistent and recurrent candiduria. J Urol 1998;159(6):2054-6.|
|24||Fisher JF, Chew WH, Shadomy S, Duma RJ, Mayhall CG, House WC. Urinary tract infections due to candida albicans. Rev Infect Dis 1982;4(6):1107-18.|
|25||Kozinn PJ, Taschdjian CL, Goldberg PK, Wise GJ, Toni EF, Seelig MS. Advances in the diagnosis of renal candidiasis. J Urol 1978;119(2):184-7.|
|26||Navarro EE, Almario JS, King C, Bacher J, Pizzo PA, Walsh TJ. Detection of candida casts in experimental renal candidiasis: Implications for the diagnosis and pathogenesis of upper urinary tract infection. J Med Vet Mycol 1994;32(6):415-26.|
|27||Schoenbeck J. Asymptomatic candiduria: Prognosis, complications and other clinical considerations. Scand J Urol Nephrol 1972;6(2):136-46.|
|28||Sobel JD, Lundstrom T. Management of candiduria. Curr Urol Rep 2001;2(4):321-5.|
|29||Binelli CA, Moretti ML, Assis RS, et al. Investigation of the possible association between nosocomial candiduria and candidemia. Clin Microbiol Infec 2006;12(6): 538-43.|
|30||Malani AN, Kauffman CA. Candida urinary tract infections: Treatment options. Expert Rev Anti Infect Ther 2007;5(2):277-84.|
|31||Jackobs LG. Fungal urinary tract infections in the elderly: Treatment guidelines. Drug Aging 1996;8(2):89-96.|
|32||Como JA, Dismukes WE. Oral azole drugs as systemic antifungal therapy. N Engl J Med 1994;330(4):263-72.|
|33||Xu JP, Ramos AR, Vilgalys R, Mitchell TG. Clonal and spontaneous origin of fluconazole resistance in candida albicans. J Clin Microbiol 2000;38(3):1214-20.|
|34||Johson LB, Kauffman CA. Voriconazole: A new triazole antifungal agent. Clin Infect Dis 2003;36(5):630-7.|
|35||Denning DW. Echinocandin antifungal drugs. Lancet 2003;362(9390):1142-51.|
|36||McCormack PL, Perry CM. Caspofungin: A review of its use in the treatment of fungal infections. Drugs 2005;65(14):2049-68.|
|37||Schoenbeck J. Studies on candida infection of the urinary tract and on the antimycotic drug 5-flurocytocine. Scand J Urol Nephrol 1972;11(Suppl I):7-48.|
|38||Jacob LG, Skidmore EA, Freeman K, Lipschultz D, Fox N. Oral fluconazole compared with bladder irrigation with amphotericin B for treatment of fungal urinary tract infections in elderly patients. Clin Infect Dis 1996;22(1):30-5.|
|39||Jacob LG, Skidmore EA, Cardoso LA, Ziv F. Bladder irrigation with amphotericin B for treatment of fungal urinary tract infections. Clin Infect Dis 1994;18():313-8.|
|40||Trinh T, Simonian J, Vigil S, Chin D, Bidari M. Continuous versus intermittent Bladder irrigation of amphtericin B for the treatment of candiduria. J Urol 1995;154(6): 2032-4.|
|41||Leu HS, Huang CT. Clearance of funguria with short-course antifungal regiemen: A prospective, randomized, controlled. Clin Infect Dis 1995;20(5):1152-7.|
|42||Fisher JF, Woeltje K, Espinel-Ingroff A, Stanfield J, Dipiro JT. Efficacy of a single intravenous dose of amphtericin B for candida urinary tract infection: Further favorable experience. Clin Microbiol Infect 2003;9(10):1024-7.|
|43||Fisher JF, Hicks BC, Dipiro JT, Venable J, Fincher RM. Efficacy of a single intravenous dose of amphotericin B in urinary tract infections caused by candida. J Infect Dis 1987;156(4):685-7.0|
|44||Agustin J, Lacson S, Raffalli J, AgueroRosenfeld ME, Wormser GP. Failure of a lipid amphotericin B preparation to eradicate candiduria: Preliminary findings based on three cases. Clin Infect Dis 1999;29 (3):686-7.|
|45||Rex JH, Walsh TJ, Sobel JD, et al. Practice guidelines for the treatment of candidiasis. Clin Infect Dis 2000;30(4): 662-7.|
|46||Ang BS, Telanti A, King B, Steckelberg JM, Wilson WR. Candidemia from a urinary tract source: Microbiological aspects and clinical significance. Clin Infect Dis 1993;17(4):662-6.|
|47||Ayeni O, Riedere KM, Wilson FM, Khatib R. Clinicians` reaction to positive urine culture for candida organisms. Mycoses 1999;42(4):285-9.|