SUPPLEMENT ARTICLE

Candida Urinary Tract Infections—Treatment

John F. Fisher,1 Jack D. Sobel,2 Carol A. Kauffman,3 and Cheryl A. Newman1
1Section of Infectious Diseases, Medical College of Georgia, Augusta, Georgia; 2Division of Infectious Diseases, Wayne State University School of

Medicine, Detroit, Michigan; and 3Division of Infectious Diseases, Veterans Affairs Ann Arbor Healthcare System, University of Michigan, Ann Arbor,
Michigan

Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024

In many instances a report from the clinical laboratory indicating candiduria represents colonization or
procurement contamination of the specimen and not invasive candidiasis. Even if infection of the urinary tract
by Candida species can be confirmed, antifungal therapy is not always warranted. Further investigation may
reveal predisposing factors, which if corrected or treated, result in the resolution of the infection. For those with
symptomatic urinary tract infections (UTIs), the choice of antifungal agent will depend upon the clinical status
of the patient, the site of infection, and the pharmacokinetics and pharmacodynamics of the agent. Because of
its safety, achievement of high concentrations in the urine, and availability in both an oral and intravenous
formulation, fluconazole is preferred for the treatment of Candida UTIs. Flucytosine is concentrated in urine
and has broad activity against Candida spp, but its use requires caution because of toxicity. Low-dose
amphotericin B may be useful for Candida UTIs in selected patients. The role of echinocandins and azoles that
do not achieve measurable concentrations in the urine is not clear. Small case series note some success, but
failures have also occurred. Irrigation of the bladder with antifungal agents has limited utility. However, with
fungus balls, irrigation of the renal pelvis through a nephrostomy tube can be useful in combination with
systemic antifungal agents.

The presence of candiduria represents a therapeutic candiduria. An algorithm summarizing an approach to

challenge for a physician because the patients in whom it the management of these groups of patients with can-
may be encountered range from asymptomatic and diduria is provided in Figures 1 and 2.
ambulatory to desperately ill. Accordingly, a classifica-
tion scheme might permit an orderly approach to
management. It is logical to group the patients whose ASYMPTOMATIC CANDIDURIA,
urine has yielded Candida species as follows: (1) those PREVIOUSLY HEALTHY PATIENT
with asymptomatic candiduria (previously healthy pa-
The presence of candiduria should be verified with
tients); (2) those with asymptomatic candiduria (pre-
a second, clean-voided urine culture. Many times it is
disposed outpatients); (3) those with asymptomatic
found that the first culture was contaminated, especially
candiduria (predisposed inpatients); (4) those with
in samples from female patients. Once the presence of
symptomatic candiduria (cystitis, pyelonephritis, pros-
candiduria is confirmed, a careful history and physical
tatitis, epididymo-orchitis, or urinary tract fungus
examination and screening laboratory studies to look
balls); and (5) clinically unstable patients with
for symptoms or signs of predisposing factors (Table 1)
are essential because occult diabetes mellitus, genito-
urinary structural abnormalities, diminished renal
Correspondence: John F. Fisher, MD, Infectious Disease Section, Medical function, and metabolic abnormalities may be discov-
College of Georgia, CB 1831, Augusta, GA 30912 (jfisher@mcg.edu).
ered [1–3]. If no explanation for candiduria is found,
Clinical Infectious Diseases 2011;52(S6):S457–S466
Ó The Author 2011. Published by Oxford University Press on behalf of the
a follow-up examination of the urine is generally all that
Infectious Diseases Society of America. All rights reserved. For Permissions, is necessary because candiduria can be expected to re-
please e-mail: journals.permissions@oup.com.
1058-4838/2011/52S6-0005$14.00
solve within weeks to months without therapeutic in-
DOI: 10.1093/cid/cir112 tervention in the vast majority of individuals [4].

Treatment d CID 2011:52 (Suppl 6) d S457


Figure 1. Algorithm for the management of asymptomatic candiduria.
ASYMPTOMATIC CANDIDURIA,
PREDISPOSED OUTPATIENT
The management of outpatients who have candiduria and who
have a predisposing condition is more complicated because
yeast in the urine may reflect an invasive infection that requires
an antifungal agent for cure. The presence of candiduria can also
be a marker for a process that requires urgent intervention, such
as the treatment of a urologic abnormality and associated ob-
struction. Imaging of the kidneys and collecting system as
a baseline in patients with diabetes mellitus or repeating imaging
studies in those with known abnormalities of the kidney and
collecting system is recommended so that the appropriate
treatment can be given.
Antifungal therapy can be avoided in most instances because
the long-term consequences of candiduria are generally benign,
even among predisposed patients [5]. For example, yeast in the
urine of an asymptomatic, elderly, diabetic patient with heavy
glycosuria may well disappear with tighter control of serum
glucose levels. Candiduria that complicates antibiotic therapy
frequently resolves shortly after antibiotics are stopped. If benign
prostatic hyperplasia and mild obstruction have resulted in
asymptomatic candiduria, a peripherally acting a-adrenergic
blocking agent may be all that is required for resolution. Close
follow-up of such predisposed patients is prudent.
One double-blind, randomized, placebo-controlled trial se-
riously challenged the wisdom of treating asymptomatic
S458 d CID 2011:52 (Suppl 6) d Fisher et al
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
candiduria. In a study designed to test the efficacy of fluconazole
in asymptomatic or minimally symptomatic candiduria, Sobel
and colleagues found that fluconazole was superior to placebo in
eradicating Candida from the urine in both catheterized and
uncatheterized patients in the short term [6]. However, 2 weeks
after discontinuation of the study drug or placebo, candiduria
had recurred in 40% of the catheterized subjects and 30% of
those without a bladder catheter. None of these mostly elderly,
female patients with multiple comorbid conditions developed
candidemia. Ironically, this drug trial demonstrated not only the
lack of long-term efficacy but the futility of treating the majority
of predisposed but asymptomatic patients even with an agent
with optimal pharmacokinetics for the kidney and collecting
system.
ASYMPTOMATIC CANDIDURIA,
PREDISPOSED INPATIENT
In an era of increasing acuity of illness among hospitalized pa-
tients, many are predisposed to candiduria for 1 or more reasons
and are unaware of or unable to complain of any associated
symptoms. This is especially true if an indwelling bladder
catheter is present and the patient is being cared for in an in-
tensive care unit (ICU). Hospitalized patients who have an in-
dwelling bladder catheter are at risk of acquiring yeast in the
urine. Platt and colleagues reported that 26.5% of all catheter-
associated UTIs (defined as the recovery of .105 organisms per

Figure 2. Algorithm for the management of symptomatic candiduria.
mililiter) were due to Candida species [7]. However, the authors
provided no distinction of infection from colonization of the
catheterized urinary tract among the patients, and no con-
clusions about the need for therapy can be assumed from these
data. Indeed, candiduria in this setting most likely represents
colonization of the bladder and catheter by Candida spp.
The possibility of disseminated candidiasis should be con-
sidered in all hospitalized patients with candiduria, especially in
patients in the ICU. Candidemia is common in this setting, and
46%–80% of persons with candidemia will have accompanying
candiduria [8–10]. Moreover, Candida spp are the fourth most
common isolates from blood cultures among hospitalized pa-
tients [11]. Despite these observations, candidemia is encoun-
tered in ,5% of patients in most ICUs [12–16]. Thus, most
patients with candiduria probably do not have disseminated
infection.
Since many patients in the ICU have an indwelling bladder
catheter to monitor urine output, when candiduria is found,
changing or removing the catheter can be anticipated to clear the
candiduria in 20%–40% of individuals [6]. When possible,
discontinuing antibiotics that are no longer necessary and
treating other predisposing conditions simultaneously should
also be done. If candiduria fails to resolve despite these meas-
ures, a more deep-seated infection should be suspected, and
imaging of the kidneys and collecting system is indicated. Such
studies may reveal renal abscess, fungus ball, or other urologic
abnormality accounting for the persistent funguria and that may
require an invasive procedure for management.
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
Antifungal treatment of candiduria in an inpatient should be
reserved for those patients who have solid clinical evidence of
infection of the kidney or collecting system or disseminated
candidiasis [6, 17]. Until reliable methods for detecting invasive
candidiasis in predisposed patients become available, antifungal
agents will continue to be used empirically and, many times,
inappropriately in this setting. This is unfortunate because for
many of these individuals, control or elimination of predis-
posing factors likely would have resolved candiduria [4, 5, 18].
SYMPTOMATIC CANDIDURIA, CYSTITIS,
PYELONEPHRITIS, PROSTATITIS, EPIDIDYMO-
ORCHITIS, and URINARY TRACT FUNGUS
BALLS
Cystitis
Assuming that predisposing factors have been eliminated or
managed to the extent possible, the in vitro activity and phar-
macokinetics of fluconazole make it the drug of choice for
cystitis due to most species of Candida, with the exception of
resistant Candida glabrata, Candida krusei, and other less
common resistant yeasts. A dose of 200–400 mg orally, daily, for
2 weeks should be adequate because fluconazole, which is highly
water soluble, is primarily excreted into the urine as active drug
[19–21]. Expected concentrations in urine exceed the minimal
inhibitory concentration (MIC) not only for susceptible yeasts
(MIC, <8 lg/mL) but also for organisms that are susceptible
but dose-dependent (MIC, 16–32 lg/mL) and sometimes even
Treatment d CID 2011:52 (Suppl 6) d S459
Table 1. Predisposing Factors for Candiduria and Candida
Urinary Tract Infections
Predisposing Factors
Diabetes mellitus
Renal transplantation
Extremes of age
Instrumentation of the urinary tract
Female sex
Concomitant bacteriuria
Prolonged hospitalization
Congenital abnormalities of the urinary tract
Intensive care unit admission
Structural abnormalities of the urinary tract
Broad-spectrum antibiotics
Indwelling urinary tract devices
Bladder dysfunction
Urinary stasis
Nephrolithiasis
those that are resistant (MIC, >64 lg/mL) [22]. Such levels can
be achieved because the drug is concentrated in the urine,
yielding urine levels .100 lg/mL, which is 10-fold the simul-
taneous plasma levels. Given its safety profile and efficacy, flu-
conazole is clearly the agent of choice for the initial treatment of
most patients with symptomatic Candida cystitis.
Other azoles that could serve as alternative choices for re-
sistant isolates are not useful for cystitis because of minimal
excretion of the active compound into the urine (itraconazole
concentration, ,1%; voriconazole concentration, ,5%; pos-
aconazole concentration, ,1%) [23–26]. For patients who are
allergic to fluconazole or for those in whom therapy clearly fails
despite maximum doses and optimal management of urologic
abnormalities and other predisposing conditions, other agents
such as oral flucytosine and parenteral amphotericin B (AmB)
or local AmB bladder instillations may be necessary.
Candida isolates are usually susceptible to flucytosine (,1.25
lg/mL), and this agent is concentrated in urine to levels of
.30 lg/mL [27, 28]. Approximately 25% of Candida albicans
isolates are resistant to flucytosine, but most C. glabrata isolates
are susceptible [29]. Eradication of Candida bladder infections
with flucytosine can be expected in 70% of symptomatic in-
dividuals [30], but the duration of therapy has not been estab-
lished. Generally, therapy is given for only 7–10 d because
resistance develops quickly when this agent is used alone for an
extended period. A dose of 25 mg/kg every 6 h is recommended,
with adjustment of the dose or dosing interval in patients with
renal insufficiency. Treatment with flucytosine is limited by
toxicity and has been associated with detectable serum levels of
5-fluorouracil [31]. As expected, normal tissues with a high rate
of cellular turnover, such as the bone marrow and gastrointes-
tinal mucosa, are vulnerable [32]. Frequent complete blood
S460 d CID 2011:52 (Suppl 6) d Fisher et al
cell counts and close monitoring of patients for rash, diarrhea, or
other gastrointestinal complaints are essential. Hepatotoxicity
has also been associated with flucytosine treatment in up to 41%
of patients, warranting monitoring of liver-associated enzyme
levels, but the mechanism by which liver injury occurs is not
known [33].
The toxicity of AmB would seem to militate against the use of
this agent for cystitis. However, in an occasional patient with
a refractory infection or unusually severe symptoms, AmB
should be considered. C. albicans isolates are susceptible to AmB
at concentrations ranging from .05–1 lg/mL, and the MIC for
most other Candida species ranges between .25 and 3 lg/mL [34,
35]. Although reports of AmB-resistant strains exist, the phe-
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
nomenon is rare and has been most often observed among non–
C. albicans organisms, such as Candida lusitaniae [36, 37].
The dose and duration of treatment have not been estab-
lished, but animal studies have revealed pharmacokinetic fea-
tures of AmB that allow the compound to be used in humans
with greater safety and increased cost-efficacy. Craven and col-
leagues previously demonstrated in dogs that a single in-
travenous dose of AmB was followed by prolonged urinary
excretion [38]. Urine concentrations exceeded MICs reported
for most Candida species for days to weeks following a single
1-mg/kg dose. Pilot studies substantiated the feasibility of this
approach in humans [39, 40]. Reports of the results in 35 pa-
tients with persistent candiduria are available, including the
results of a randomized, controlled, comparative trial that
showed that single-dose AmB was more cost-efficacious than
other modalities of treatment [41]. The studies showed a success
rate of 72% in eradicating yeast from the urine with a single
intravenous dose of AmB, suggesting that the delayed urinary
excretion of AmB might be used to advantage in Candida cystitis
as well as other forms of refractory Candida UTIs.
The lipid formulations of AmB were designed to decrease
renal toxicity. The 3 lipid formulations that are available are less
nephrotoxic but do not achieve appreciable levels in the kidneys
or in urine. Efficacy in Candida cystitis would not be predicted.
Indeed, failure to eradicate yeast from the urinary tract has al-
ready been reported despite the efficacy of lipid formulations of
AmB in disseminated candidiasis [42].
Another approach to the treatment of Candida cystitis has
been to irrigate the bladder with AmB. The dosage most com-
monly used is 50 mg AmB diluted in 1 L of sterile water to give
a concentration of 50 lg/mL [43]. A dosage of 10 lg/mL has
been noted to be less efficacious [44]. Continuous irrigation of
the bladder with this suspension for 5–7 d resolves Candida
cystitis in .90% of patients [45]. However, the relapse rate after
local bladder irrigation is high [46]. Unless patients with
symptomatic infections require a bladder catheter for other
clinical indications, it is wise to avoid bladder irrigation. Cath-
eter-induced bacteriuria can be expected in 20%–70% of these
individuals, which poses a serious risk in itself [47, 48]. A recent
review of the evidence for the therapeutic use of bladder irri-
gation concluded that ‘‘the use of amphotericin B bladder irri-
gation is a strategy rarely needed in our present clinical
armamentarium’’ [49, p. 1469].
However, in the unusual patient who has C. krusei or fluco-
nazole-resistant C. glabrata cystitis, AmB bladder irrigation can
sometimes prove useful [50]. This approach should be done in
concert with surgical correction of urinary tract obstruction or
other mechanical abnormalities. In patients who have severe
cystitis noted at cystoscopy, bladder irrigation can be given in
conjunction with parenteral treatment using an agent to which
the organism is susceptible, usually AmB or an echinocandin.
Pyelonephritis
Renal parenchymal infection is generally the result of candide-
mia, but retrograde infection of the kidneys can occur under
conditions of urinary tract obstruction, concomitant bacteri-
uria, or profound immunosuppression [51]. Fluconazole is the
agent of choice for pyelonephritis. A dose of 400 mg daily is
ordinarily given, for 2 weeks. For most patients, the oral for-
mulation is appropriate. Fluconazole is effective for a majority of
cases of Candida UTIs, since C. albicans accounts for 40%–65%
of yeast isolates from urine and Candida tropicalis and Candida
parapsilosis account for 25%; all 3 species are susceptible to
fluconazole [6, 52–56]. However, infection due to C. glabrata is
now more common than that caused by C. tropicalis and C.
parapsilosis in some geographic areas, accounting for 20% of
urine isolates [3, 17]. The susceptibility of C. glabrata to fluco-
nazole is highly variable; MICs range from .25 to 256 lg/mL.
The MIC90 and MIC50 for fluconazole are reported to be 16 lg/
mL and 4 lg/mL, respectively [57, 58].
It should be remembered that resistant organisms are classi-
fied as such on the basis of achievable serum concentrations.
Renal parenchymal levels of fluconazole are probably more
relevant and have been studied. Walsh and colleagues found that
tissue concentrations in the kidney ranged from 18 to 27 lg/g of
tissue in rabbits given a dose of fluconazole of 25 mg/kg body
weight [20]. The ratio of tissue to plasma concentrations was
consistently ..8, and trough levels in tissue were .3-fold higher
than those of simultaneously collected serum samples, con-
firming accumulation of fluconazole in the kidney. Reported
urine concentrations of .100 lg/mL provide additional confi-
dence that fluconazole should be effective in the treatment of
most Candida pyelonephritis including that caused by C. glab-
rata and the other common non-C. albicans species [59].
However, failures of fluconazole for the treatment of C. glabrata
renal infection have been reported with increasing frequency
[60].
Perfect and colleagues observed that itraconazole was equiv-
alent to fluconazole in a rabbit model of hematogenous renal
parenchymal candidiasis [61]. No details were provided by the
authors as to involvement or clearance of infection from the
lower urinary tract by itraconazole in these animals. There are
few data in humans for the use of this agent for Candida py-
elonephritis, and given its low excretion into the urine, it is
unlikely to be efficacious for patients with Candida UTIs.
Posaconazole has potent activity against C. albicans and
a variety of non-C. albicans species, including C. glabrata and C.
krusei, that are resistant to fluconazole and itraconazole [55].
Posaconazole has demonstrated efficacy in a murine model of
hematogenous renal parenchymal candidiasis [62]. However,
only 10% of active drug can be recovered in urine [25, 26].
Thus, like that of itraconazole, its antifungal activity in the renal
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
parenchyma and other deep tissue sites would be expected to be
adequate, but that in the urinary collecting system would be
doubtful.
Because it is a fluconazole congener with excellent activity
against most fluconazole-resistant Candida species, voriconazole
might be considered the ‘‘heir apparent’’ for Candida UTIs re-
fractory to fluconazole therapy. The efficacy of voriconazole in
renal parenchymal candidiasis was found to be superior to that
of either AmB or fluconazole in an animal model of hematog-
enous C. krusei infection, establishing its potential in eradicating
Candida species from the kidney [63]. Unfortunately, urine
voriconazole levels are low, with ,5% of active drug excreted,
and its usefulness in Candida UTIs is minimal [24].
Candida renal parenchymal infections as a component of
disseminated candidiasis in various experimental models have
been readily cleared with the echinocandins caspofungin, ani-
dulafungin, and micafungin [64–68]. Given the high frequency
of renal involvement in humans with disseminated candidiasis,
efficacy of the echinocandins in pyelonephritis could be ex-
pected. However, all the echinocandins are extensively metab-
olized, and very little active drug can be recovered in the urine
[69]. Therefore, eradication of Candida in the vascularized
cortex and interstitium of the kidney by echinocandins is more
likely than in the collecting system, and clinical experience is
minimal [68]. In a retrospective review of data from the cas-
pofungin database, this agent was found to be efficacious in 3
patients who had Candida pyelonephritis of ascending origin
and in whom other antifungal therapy had failed [70].
The favorable pharmacokinetics of flucytosine in the urinary
tract [28] and proven efficacy in a variety of forms of urinary
tract candidiasis make it a consideration for patients who are
able to take oral medications and for whom fluconazole cannot
be used [27]. A dose of 25 mg/kg every 6 h with adjustment for
renal insufficiency is standard. Since in some instances pro-
longed treatment may be required, the potentially serious tox-
icity of the compound mandates close follow-up of patients, and
in these cases, this agent should be given with another antifungal
agent, such as amphotericin B, to avoid the development of
Treatment d CID 2011:52 (Suppl 6) d S461
resistance [32]. Particular attention needs to be given to bone
marrow depression when both flucytosine and AmB are given
together.
AmB deoxycholate has demonstrated efficacy in virtually all
forms of invasive candidiasis and remains the choice of some
clinicians for systemic and severe forms of urinary tract candi-
diasis in seriously ill patients. However, the lipid formulations of
AmB should not be used for treating renal candidiasis. The
reduced nephrotoxicity of these agents suggests that their tissue
penetration in the renal parenchyma is reduced. Decreased
clearance of renal foci of C. albicans in leukopenic mice has been
demonstrated when liposomal AmB was compared with AmB
deoxycholate, and failure to eradicate Candida from the urinary
tract has been reported in humans [42, 71].
Treatment in Patients With Renal Failure
Given the above therapeutic considerations for the management
of Candida cystitis and pyelonephritis, the concomitant pres-
ence of renal insufficiency will affect the selection and dosing of
antifungal compounds and most likely treatment outcome as
well. It was shown in one study that the likelihood of eradicating
Candida from the urinary tract with fluconazole was inversely
proportional to the degree of renal impairment [6]. A study of
the pharmacokinetics of fluconazole in pediatric patients with
renal failure demonstrated that the drug was almost completely
cleared by peritoneal dialysis, making it likely that urine con-
centrations of the compound would most likely be sub-
therapeutic in this patient population [72]. However, urine
levels were not measured in those patients who were still pro-
ducing urine. In a single report in the literature documenting
urine concentrations of fluconazole in patients with renal dis-
ease, Debruyne and Ryckelynck administered fluconazole orally
or intraperitoneally to 3 groups, each with 5 patients, who were
receiving continuous ambulatory peritoneal dialysis (CAPD):
group 1 received an oral dose of 100 mg; groups 2 and 3 received
50 mg or 150 mg, respectively, in the dialysis bag [73]. These
investigators then measured fluconazole levels in urine, di-
alysate, and serum at intervals for 144 h. The mean urine flu-
conazole concentrations 48 h following the 100-mg oral dose
ranged from 1.8 to 1.9 lg/mL. During the 96 h following the
50-mg intraperitoneal dose, mean urine concentrations of flu-
conazole ranged from 1.15 to .66 lg/mL. Following the 150-mg
intraperitoneal dose, the mean urine concentrations ranged
from 2.2 and 1.4 lg/mL (as estimated from the graph) for the
same time period. The focus of this publication was the thera-
peutic potential of fluconazole in peritoneal fluid during CAPD
for Candida peritonitis and not candiduria. Nevertheless, the
study demonstrates that a measurable amount of fluconazole
continues to be excreted in urine for days in some patients with
end-stage renal disease after relatively small doses. The authors
gave no information about the causes of renal failure in the 15
S462 d CID 2011:52 (Suppl 6) d Fisher et al
patients. Therefore, it is possible that the pharmacokinetics of
fluconazole could vary widely among patients with diseased
kidneys with respect to urine concentrations.
Additional studies focusing on urine concentrations of flu-
conazole in patients with renal failure could prove to be ex-
tremely useful since many predisposed individuals with
candiduria have impaired kidney function. Studies correlating
urine concentrations of fluconazole with clinical outcome of
Candida cystitis and pyelonephritis in patients with varying
degrees of renal impairment would be of interest but to our
knowledge have not been done. Consequently, fluconazole
dosing in patients with marginal kidney function must be
chosen empirically with the expectation that concentration of
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
the azole in the nephron and subsequent urine levels will be
reduced. While lowering the dose of fluconazole for a decreased
creatinine clearance may be appropriate for systemic infection,
such a change may lead to failure of therapy in Candida UTIs.
Hence, we believe that, in general, patients with symptomatic
candiduria should be given at least 400 mg of fluconazole daily
regardless of renal function in an attempt to achieve therapeutic
urine concentrations. An oral 400-mg dose should produce a
peak serum concentration of 9 lg/mL at steady state, whereas
an intravenous dose yields a mean level of 16.7 lg/mL [74, 75].
In light of the efficacy and tolerability of high-dose fluconazole
in cryptococcal meningitis and other severe fungal infections in
daily doses of up to 1,600 mg with peak concentrations above
50 lg/mL, adverse events should be minimal [76–79]. Never-
theless, careful monitoring of hepatic function during therapy
is indicated.
Prostatitis
Because Candida prostatitis is uncommon, approaches to ther-
apy have been derived from individual case reports over the past
25 years and not from randomized clinical trials. Over this pe-
riod, new antifungal agents have been introduced, none of which
have been adequately studied in this unusual form of candidiasis.
Wise recently summarized the approach to the diagnosis and
treatment of Candida prostatitis [80]. He and his coauthor
suggested that fungal prostatitis should be treated with incision
and drainage of any abscess that is present or resection of
prostate tissue in addition to antifungal agents. Most case reports
have emphasized the role of surgery in conjunction with an
antifungal agent for the treatment of Candida prostatitis [80, 81].
AmB has been the antifungal agent most commonly used [80,
82], but fluconazole has also been given successfully [83]. Levels
of fluconazole in prostatic tissue and prostatic fluid in both
humans and experimental animals are 29%–89% that of serum
concentrations [84–86]. In a study by Finley and colleagues,
peak and trough serum levels were measured in 8 patients with
benign prostatic hyperplasia who were scheduled to undergo
elective transurethral prostate resection [84]. The participants
had received 200 mg of fluconazole for 5 d after a loading dose of
400 mg on the first day. Prostate tissue concentrations were then
obtained 12–15 h after the last dose. Mean (6 SD) peak and
trough serum levels for the patients were 6.5 6 .7 and 5.2 6 .6
lg/mL, respectively, and the mean (6 SD) serum concentration
at the time of surgery was 6.6 6 .7 lg/mL. Prostate tissue levels
at surgery were 1.9 6 .3 lg/g, or 29% of the mean serum
concentration. These data suggest that the drug does not accu-
mulate in the prostate and perhaps the concentrations achieved
will not be sufficient to eradicate some strains of C. albicans and
many non-C. albicans species. However, none of these patients
had acute Candida prostatitis, in which inflammation might
result in better penetration of fluconazole. Nevertheless, the data
make a circumstantial case for daily doses of the azole of .200
mg to treat proven Candida prostatitis.
In a preliminary report that has never been published in full,
Dimitrakov and Rawadi compared fluconazole and itraconazole
for the treatment of 147 patients with Candida prostatitis [87].
The majority of infections were caused by C. albicans (48%);
other species included C. glabrata (24%), C. tropicalis (19%),
and C. parapsilosis (7%). Success of therapy with fluconazole
was related to in vitro susceptibility of the isolates. More than
90% of infections resolved when the MICs were <8 lg/mL, and
only 76% resolved when the MICs were >16 lg/mL. Resolution
occurred in 81%, 50%, and 44% of itraconazole-treated subjects
with MICs of ,.12, .25–.5, and >1 lg/mL, respectively. While
results are promising for both agents, data such as these should
be interpreted with caution because little clinical information
was provided by the authors and the data have been published
thus far only in abstract form. The lower activity level of itra-
conazole likely reflects the lipophilic properties and poor water
solubility of this agent. Prostatic secretions have a high water
and minimal lipid content. The failure of itraconazole to erad-
icate a focus of cryptococcal prostate infection in a patient with
AIDS and the persistence of Aspergillus prostatitis in a renal
transplant recipient given itraconazole provide further anecdotal
evidence that this compound is not an optimal choice for fungal
prostatitis [88, 89]. No data are available regarding the pene-
tration of voriconazole, posaconazole, or the echinocandins into
prostatic tissue or secretions, and their efficacy is unknown.
In summary, successful treatment has uniformly involved
surgical intervention combined with the use of AmB or fluco-
nazole for Candida prostatitis [80]. There are no convincing
data that itraconazole should be used. Additional studies of the
appropriate dosage and duration of therapy of fluconazole and
other agents are warranted.
Epididymo-orchitis
Treatment recommendations for Candida epididymo-orchitis
are based entirely upon anecdotal experience from case reports
[90–95]. Most patients have required surgical drainage of
abscesses and/or orchiectomy for cure, in conjunction with
fluconazole or AmB with or without flucytosine [91–93, 95]. A
single patient who responded to ketoconazole alone has been
reported, but this agent is rarely used now [96].
Fungus Balls (Bezoars and Mycetomas) of the Urinary Tract
The location of the Candida fungus ball will determine the ap-
proach to therapy. Systemic treatment with AmB, with or
without flucytosine, or fluconazole has been used in the majority
of patients [2, 97–102]. Systemic therapy is reasonable because
these luminal fungal aggregates most often result from dissem-
inated candidiasis or deeply seated parenchymal infection. Al-
though treatment with antifungal agents may result in
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
spontaneous disruption and passage of the mass of hyphal fil-
aments and debris, this is unusual [2, 103]. Almost always, an
invasive procedure will need to be performed to relieve ob-
struction and to remove the bulk of the mass. If the urologic
procedure required (eg, percutaneous nephrostomy) provides
a portal of access to the renal pelvis, ureters, or bladder, local
irrigation with intermittent or continuous AmB or fluconazole
can be considered, but studies to determine optimal dosage and
duration have not been done [97–100]. Other methods to fa-
cilitate the breakdown and passage of fungus balls have included
intermittent irrigation with saline, insertion of thrombectomy
devices through a percutaneous nephrostomy, percutaneous
endoscopic disruption and drainage, and percutaneous irriga-
tion with streptokinase [104–109].
CANDIDURIA IN CLINICALLY UNSTABLE
PATIENTS
For critically ill patients, candiduria, whether symptomatic or
not, should initially be regarded as a harbinger of disseminated
candidiasis [10], since the kidney is the target of candidemia in
80% of patients [8]. Indeed, the finding of yeast in the urine
may be the only clue that the patient has a life-threatening in-
fection. It follows that an astute physician will immediately
consider disseminated candidiasis in such a patient and examine
the optic fundi, the skin, and vascular access devices and obtain
fungal blood cultures. Fortunately, most patients are not fun-
gemic even when desperately ill, and their urinary tract is simply
colonized by Candida, especially if an indwelling bladder cath-
eter is present.
If the candiduric patient’s clinical condition is too unstable to
permit an incremental approach to determine its cause or if
clinical evidence for disseminated candidiasis is sufficiently
compelling, systemic antifungal chemotherapy should be given
immediately with fluconazole in a loading dose of 800 mg fol-
lowed by 400 mg daily or with appropriate adjustment for renal
insufficiency. An echinocandin is preferred if the patient has had
recent azole exposure (caspofungin, 70-mg loading dose, then
Treatment d CID 2011:52 (Suppl 6) d S463
50 mg daily; anidulafungin, 200-mg loading dose, then 100 mg
daily; or micafungin, 100 mg daily) [21]. The reader is reminded
that an echinocandin has proven efficacy in disseminated can-
didiasis but cannot be expected to completely eradicate resultant
lower urinary tract foci of infection. In the unusual circumstance
in which the collecting system is the source of candidemia (eg,
obstruction), relapse could occur.
Acknowledgments
Supplement sponsorship. The supplement was sponsored through re-
search funds of Georgia Health Sciences University, Medical College of
Georgia, Augusta, Georgia.
Potential conflicts of interest. J. F. F. serves on the speaker’s bureaus
for Continuing Education Company and Southern Medical Association.
C. A. K. has received grant support from Merck, royalties from Springer
Publishing and UpToDate, and payment from Pfizer for chairing the Data
Adjudication Committee for an Aniduafungin study. J. D. S. serves on the
speaker’s bureaus for Astellas and Pfizer; his institution has received grant
support from Merck.
References
1. Fisher JF, Chew WH, Shadomy S, Duma RJ, Mayhall CG, House WC.
Urinary tract infections due to Candida albicans. Rev Infect Dis 1982;
4:1107–18.
2. Fisher JF, Mayhall CG, Duma RJ, Shadomy S, Shadomy HJ, Watlington
C. Fungus balls of the urinary tract. South Med J 1979; 72:1281–4.
3. Kauffman CA. Candiduria: diagnostic and treatment conundrums.
Curr Treat Opinions Infect Dis 2002; 4:513–9.
4. Schonebeck J. Studies on Candida infection of the urinary tract and
on the antimycotic drug 5-fluorocytosine. Scand J Urol Nephrol 1972;
11(Suppl):7–48.
5. Sobel JD. Management of asymptomatic candiduria. Int J Antimicrob
Agents 1999; 11:285–8.
6. Sobel JD, Kauffman CA, McKinsey D, et al. Candiduria: a random-
ized, double-blind study of treatment with fluconazole and placebo.
Clin Infect Dis 2000; 30:19–24.
7. Platt R, Polk BF, Murdock B, Rosner B. Risk factors for nosocomial
urinary tract infection. Am J Epidemiol 1986; 124:977–85.
8. Louria DB, Stiff DP, Bennett B. Disseminated moniliasis in the adult.
Medicine (Baltimore) 1962; 41:307–37.
9. Alvarez-Lerma F, Nolla-Salas J, Leon C, et al. Candiduria in critically
ill patients admitted to intensive care medical units. Intensive Care
Med 2003; 29:1069–76.
10. Nassoura Z, Ivatury RR, Simon RJ, Jabbour M, Stahl WM. Candiduria
as an early marker of disseminated infection in critically ill
surgical patients: the role of fluconazole therapy. J Trauma 1993;
35:290–5.
11. Wisplinghoff H, Bischoff T, Tallent SM, Seifert H, Wenzel RP,
Edmond MB. Nosocomial bloodstream infections in US hospitals:
analysis of 24,179 cases from a prospective nationwide surveillance
study. Clin Infect Dis 2004; 39:309–17.
12. Beck-Sague’ C, Jarvis WR. Secular trends in the epidemiology of
nosocomial fungal infections in the United States, 1980–1990. Na-
tional Nosocomial Infections Surveillance System. J Infect Dis 1993;
167:1247–51.
13. Vincent JL, Bihari DJ, Suter PM, et al. The prevalence of nosocomial
infection in intensive care units in Europe. Results of the European
Prevalence of Infection in Intensive Care (EPIC) study. EPIC Advisory
Committee. JAMA 1995; 274:639–44.
14. Macphail G, Taylor GD, Buchanan-Chell M, Ross C, Wilson S,
Kureishi A. Epidemiology, treatment, and outcome of candidemia: a
five-year review at three Canadian hospitals. Mycoses 2002; 45:141–5.
S464 d CID 2011:52 (Suppl 6) d Fisher et al
15. Blumberg HM, Jarvis WR, Soucie JM, et al. Risk factors for candidal
bloodstream infections in surgical intensive care unit patients: the
NEMIS prospective multicenter study. The National Epidemiology of
Mycosis Study. Clin Infect Dis 2001; 33:177–86.
16. Petri MG, Konig J, Moecke HP, et al. Epidemiology of invasive
mycosis in ICU patients: a prospective multicenter study in 435 non-
neutropenic patients. Paul-Ehrlich Society for Chemotherapy, Divi-
sions of Mycology and Pneumonia Research. Intensive Care Med
1997; 23:317–25.
17. Kauffman CA, Vasquez JA, Sobel JD, et al. Prospective multicenter
surveillance study of funguria in hospitalized patients. The National
Institute for Allergy and Infectious Diseases Mycoses Study Group.
Clin Infect Dis 2000; 30:14–8.
18. Fisher JF. Candiduria: when and how to treat it. Curr Infect Dis Rep
2000; 2:523–30.
19. Lazar JD, Hilligoss DM. The clinical pharmacology of fluconazole.
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
Semin Oncol 1990; 17:14–18.
20. Walsh TJ, Foulds G, Pizzo PA. Pharmacokinetics and tissue pene-
tration of fluconazole in rabbits. Antimicrob Agents Chemother 1989;
33:467–9.
21. Pappas PG, Kauffman CA, Andes D, et al. Clinical practice guidelines
for the management of candidiasis: 2009 update by the Infectious
Diseases Society of America. Clin Infect Dis 2009; 48:503–35.
22. Pfaller MA, Diekema DJ, Sheehan DJ. Interpretive breakpoints for
fluconazole and Candida revisited: a blueprint for the future of an-
tifungal susceptibility testing. Clin Microbiol Rev 2006; 19:435–47.
23. Stevens DA. Itraconazole in cyclodextrin solution. Pharmacotherapy
1999; 19:603–11.
24. Johnson LB, Kauffman CA. Voriconazole: a new triazole antifungal
agent. Clin Infect Dis 2003; 36:630–7.
25. Herbrecht R. Posaconazole: a potent, extended-spectrum triazole
anti-fungal for the treatment of serious fungal infections. Int J Clin
Pract 2004; 58:612–24.
26. Courtney R, Sansone A, Smith W, et al. Posaconazole pharmacoki-
netics, safety, and tolerability in subjects with varying degrees of
chronic renal disease. J Clin Pharmacol 2005; 45:185–92.
27. Schonebeck J, Polak A, Fernex M, Scholer HJ. Pharmacokinetic
studies on the oral antimycotic agent 5-fluorocytosine in individuals
with normal and impaired kidney function. Chemotherapy 1973;
18:321–36.
28. Schonebeck J. 5-fluorocytosine treatment of candidosis of the urinary
tract Candida infection localized elsewhere. 5th Congress of the In-
ternational Society for Human and Animal Mycology. Paris: ISHAM,
1971; 299.
29. Auger P, Dumas C, Joly J. A study of 666 strains of Candida albicans:
correlation between serotype and susceptibility to 5-fluorocytosine.
J Infect Dis 1979; 139:590–4.
30. Wise GJ, Wainstein S, Goldberg P, Kozinn PJ. Flucytosine in urinary
Candida infections. Urology 1974; 3:708–11.
31. Diasio RB, Lakings DE, Bennett JE. Evidence for the conversion
of 5-fluorocytosine to 5-fluorouracil in humans: possible factor in
5-fluorocytosine toxicity. Antimicrob Agents Chemother 1978;
14:903–8.
32. Kauffman CA, Frame PT. Bone marrow toxicity associated with flu-
orocytosine therapy. Antimicrob Agents Chemother 1977; 14:903–8.
33. Vermes A, Guchelaar HJ, Dankert J. Flucytosine: a review of its
pharmacology, clinical indications, pharmacokinetics, toxicity and
drug interactions. J Antimicrob Chemother 2000; 46:171–9.
34. Rippon JW. Antimycotic agents. In: Rippon JW, eds. Medical my-
cology, 2nd ed. Philadelphia: W. B. Saunders, 1982; 728.
35. Uzun O, Kocagoz S, Cetinkaya Y, Arikan S, Unal S. In vitro activity of
a new echinocandin, LY303366, compared with those of amphotericin
B and fluconazole against clinical yeast isolates. Antimicrob Agents
Chemother 1997; 41:1156–7.
36. Bodey GP, Fainstein V. Antifungal agents. In: Bodey GP, Fainstein V,
eds: Candidiasis. New York: Raven Press, 1993; 376.
37. Odds FC. Antifungal agents and their use in Candida infections. In: Odds
FC ed: Candida and candidosis. London: Baillière Tindall, 1988; 288.
38. Craven PC, Ludden TM, Drutz DJ, Rogers W, Haegele KA, Skrdlant HB.
Excretion pathways of amphotericin B. J Infect Dis 1979; 140:329–41.
39. Fisher JF, Hicks BC, DiPiro JT, Venable J, Fincher R-M. Efficacy of
a single intravenous dose of amphotericin B in urinary infections
caused by Candida. J Infect Dis 1987; 156:685–7.
40. Fisher JF, Woeltje K, Espinel-Ingroff A, Stanfield J, DiPiro JT. Efficacy
of a single intravenous dose of amphotericin B for Candida urinary
tract infections: further favorable experience. Clin Microbiol Infect
2003; 9:1024–7.
41. Leu H-S, Huang C-T. Clearance of funguria with short-course anti-
fungal regimens: a prospective, randomized, controlled study. Clin
Infect Dis 1995; 20:1152–7.
42. Augustin J, Raffalli J, Aguerro-Rosenfeld M, Wormser GP. Failure of
a lipid amphotericin B preparation to eradicate candiduria: pre-
liminary findings based on three cases. Clin Infect Dis 1999; 29:686–7.
43. Goldman HJ, Littman ML, Oppenheimer GD, Glickman SI. Monilial
cystitis—effective treatment with instillations of amphotericin B.
JAMA 1960; 174:359–62.
44. Nesbit SA, Katz LE, McClain BW, Murphy DP. Comparison of two
concentrations of amphotericin B bladder irrigation in the treatment
of funguria in patients with indwelling urinary catheters. Am J Health
Syst Pharm 1999; 56:872–5.
45. Wise GJ, Kozinn PJ, Goldberg P. Amphotericin B as a urological irrigant
in the management of non-invasive candiduria. J Urol 1982; 128:82–4.
46. Fan-Havard P, O’Donovan C, Smith SM, Oh J, Bamberger M, Eng
RHK. Oral fluconazole versus amphotericin B bladder irrigation for
the treatment of candidal funguria. Clin Infect Dis 1995; 21:960–5.
47. Warren JW. Nosocomial urinary tract infections. In: Mandell GL,
Bennett J, Dolan R, eds. Principles and practice of infectious diseases.
5th ed. Vol 2. Philadelphia: Churchill Livingstone, 2000; 3029.
48. Alvaren HF, Lim JA, Antonio-Velmonte M, Mendoza MT. Urinary
tract infection in patients with indwelling catheter. Phil J Microbiol
Infect Dis 1993; 22:65–74.
49. Drew RH, Arthur RR, Perfect JR. Is it time to abandon the use of
amphotericin B bladder irrigation? Clin Infect Dis 2005; 40:1465–70.
50. Sobel JD. When and how to treat candiduria. Infect Dis Clin Pract
2006; 14:125–6.
51. Odds FC. Candidosis of the urinary tract. In: Odds FC, eds. Candida
and candidosis: a review and bibliography. London: Baillière Tindall,
1988; 169–74.
52. Jacobs 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.
53. Gubbins PO, Occhipinti DI, Danziger LH. Surveillance of treated and
untreated funguria in a university hospital. Pharmacotherapy 1994;
14:463–70.
54. Gubbins PO, McConnell SA, Penzak R. Current management of
funguria. Am J Health Syst Pharm 1999; 56:1929–36.
55. Espinel-Ingroff AV. Comparison of the in vitro activities of the new
triazole SCH56592 and the echinocandins MK-0991, L-743,872, and
LY303366 against opportunistic filamentous and dimorphic fungi and
yeasts. J Clin Micrbiol 1998; 36:2950–6.
56. Lozano-Chiu M, Arikan S, Paetznick VL, Anaissie EJ, Rex JH. Opti-
mizing voriconazole susceptibility testing of Candida: effects of in-
cubation time, endpoint rule, species of Candida, and level of
fluconazole susceptibility. J Clin Micrbiol 1999; 37:2755–9.
57. Pfaller MA, Diekema DJ, Jones RN, et al. International surveillance of
bloodstream infections due to Candida species: frequency of occurrence
and in vitro susceptibilities to fluconazole, ravuconazole, and vor-
iconazole of isolates collected from 1997 through 1999 in the SENTRY
Antimicrobial Surveillance Program. J Clin Micrbiol 2001; 39:3254–9.
58. Yamaguchi H, Uchida K, Kawasaki K, Matsunaga T. In vitro activity
of fluconazole, a novel bistriazole antifungal agent. Jpn J Antibiot
1989; 42:1–16.
59. Grant SM, Clissold SP. Fluconazole: a review of its pharmacodynamic
and pharmacokinetic properties and therapeutic potential in super-
ficial and systemic mycoses. Drugs 1990; 39:877–916.
60. Ansari SH, Levin MH, Lipshitz S. Fluconazole treatment in Torulopsis
glabrata upper urinary tract infection causing ureteral obstruction. J
Urol 1995; 154:1870.
61. Perfect JR, Savani DV, Durack DT. Comparison of itraconazole and
fluconazole in the treatment of cryptococcal meningitis and Candida
pyelonephritis in rabbits. Antimicrob Agents Chemother 1986;
29:579–83.
62. Andes D, Marchillo K, Conklin R, et al. Pharmacodynamics of a new
triazole, posaconazole, in a murine model of disseminated candidia-
sis. Antimicrob Agents Chemother 2004; 48:137–42.
63. Ghannoum MA, Okogbule-Wonodi I, Bhat N, Sanati H. Antifungal
activity of voriconazole UK-109,496, fluconzole, and amphotericin B
against hematogenous Candida krusei infection in neutropenic guinea
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
pig model. J Chemother 1999; 11:34–9.
64. Abruzzo GK, Flattery AM, Gill CJ, et al. Evaluation of the echino-
candin antifungal MK-0991, L-743,872: efficacies in mouse models of
disseminated aspergillosis, candidiasis, and cryptococcosis. Anti-
microb Agents Chemother 1997; 41:2333–8.
65. Abruzzo GK, Gill CJ, Flattery AM, et al. Efficacy of the echinocandin
caspofungin against disseminated aspergillosis and candidiasis in cy-
clophosphamide-induced immunosuppressed mice. Antimicrob
Agents Chemother 2000; 44:2310–8.
66. Petraitiene R, Petraitis V, Groll AH, et al. Antifungal activity of
LY303366, a novel echinocandin B, in experimental disseminated
candidiasis in rabbits. Antimicrob Agents Chemother 1999;
43:2148–55.
67. Ikeda F, Wakai Y, Matsumoto S, et al. Efficacy of FK 463, a new
lipopeptide antifungal agent in mouse models of disseminated can-
didiasis and aspergillosis. Antimicrob Agents Chemother 2000;
44:614–8.
68. Petraitis V, Petraitiene R, Groll AH, et al. Comparative antifungal
activities and plasma pharmacokinetics of micafungin, FK 463,
against disseminated candidiasis and invasive pulmonary aspergillosis
in persistently neutropenic rabbits. Antimicrob Agents Chemother
2002; 46:1857–69.
69. Groll AH, Walsh TJ. FK-463. Curr Opin Anti-Infect Invest Drugs
2000; 2:405–12.
70. Sobel JD, Bradshaw SK, Lipka CJ, Kartsonis NA. Caspofungin in the
treatment of symptomatic candiduria. Clin Infect Dis 2007; 44:e46–9.
71. van Etten EW, van den Heuvel-de Groot C, Bakker-Woudenberg IA.
Efficacies of amphotericin B-desoxycholate (Fungizone), liposomal
amphotericin B (Ambisome), and fluconazole in the treatment of
systemic candidosis in immunocompetent and leucopenic mice. J
Antimicrob Chemother 1992; 32:723–39.
72. Wong SF, Leung M, Chan MY. Pharmacokinetics of fluconazole in
children requiring peritoneal dialysis. Clin Ther 1997; 19:1039–47.
73. Debruyne D, Ryckelynck JP. Fluconazole serum, urine, and dialysate
levels in CAPD patients. Perit Dial Int 1992; 12:328–9.
74. Cousin L, Le Berre M, Launay-Vacher V, Izzedine H, Deray G. Dosing
guidelines for fluconazole in patients with renal failure. Nephrol Dial
Transplant 2003; 18:2227–31.
75. Buijk SLCE, Gyssens IC, Mouton JW, Verbrugh HA, Touw DJ,
Bruining HA. Pharmacokinetics of sequential intravenous and enteral
fluconazole in critically ill surgical patients with invasive mycoses and
compromised gastro-intestinal function. Intensive Care Med 2001;
27:115–21.
76. Nussbaum JC, Jackson A, Namarika D, et al. Combination flucytosine
and high-dose fluconazole compared with fluconazole monotherapy
for the treatment of cruptococcal meningitis: a randomized trial in
Malawi. Clin Infect Dis 2010; 50:338–44.
77. Longley N, Muzoora C, Taseera K, et al. Dose response effect of high-
dose fluconazole for HIV-associated cryptococcal meningitis in
southwestern Uganda. Clin Infect Dis 2008; 47:1556–61.
Treatment d CID 2011:52 (Suppl 6) d S465
 78. Voss A, de Pauw BE. High-dose fluconazole therapy in patients with
severe fungal infections. Eur J Clin Microbiol Infect Dis 1999;
18:165–74.
79. Anaissie EJ, Kontoyiannis DP, Huls C, et al. Safety, plasma concen-
trations, and efficacy of high-dose fluconazole in invasive mold in-
fections. J Infect Dis 1995; 172:599–602.
80. Wise GJ, Shteynshyuger A. How to diagnose and treat fungal in-
fections in chronic prostatitis. Curr Urol Rep 2006; 7:320–8.
81. Bartkowski DP, Lanesky JR. Emphysematous prostatitis and cystitis
secondary to Candida albicans. J Urol 1988; 139:1063–5.
82. Wise GJ. Genitourinary fungal infections: a therapeutic conundrum.
Expert Opin Pharmacother 2001; 2:1211–26.
83. Tashjian JM, Coulam CB, Washington JAI. Vaginal flora in asymp-
tomatic women. Mayo Clin Proc 1976; 51:557–61.
84. Finley RW, Cleary JD, Goolsby J, Chapman SW. Fluconazole pene-
tration into the human prostate. Antimicrob Agents Chemother 1995;
39:553–5.
85. Luzzati R, Gatti G, Lazzarini L, Limonta D, Vento S, Concia E. Flu-
conazole penetration into the prostatic fluid of patients with AIDS-
associated cryptococcal meningitis [Letter]. J Antimicrob Chemother
1998; 41:423–4.
86. Schramm P, Wildfeuer A, Sarnow E. Determination of fluconazole
concentrations in the prostatic and seminal vesicle fluid (split ejacu-
late). Mycoses 1994; 37:417.
87. Dimitrakov J, Rawadi G. Fungal prostatitis experience at a single
institution. Presented at the IPCN Prostatitis Meeting, Baltimore
November, 4–5, 1999.
88. Staib F, Seibold M, L’age M. Persistence of Cryptococcus neoformans in
seminal fluid and urine under itraconazole treatment. the urogenital
tract (prostate) as a niche for Cryptococcus neoformans. Mycoses 1990;
33:369–73.
89. Banks FCL, Kelkar A, Harvey CJ, Williams G. Aspergillus prostatitis
post renal transplantation. Nephrol Dial Transplant 2005; 20:2865–6.
90. Gordon DL, Maddern J. Treatment of Candida epididymo-orchitis
with oral fluconazole. Med J Aust 1992; 156:744.
91. Jenks P, Brown J, Warnock D, Barnes N. Candida glabrata epi-
didymo-orchitis: an unusual infection rapidly cured with surgical and
antifungal treatment. J Infect 1995; 31:71–2.
92. Lyne JC, Flood HD. Bilateral fungal epididymo-orchitis with abscess.
Urology 1995; 46:412–4.
93. Pimentel M, Nicolle LE, Qureshi S. Candida albicans epididymo-or-
chitis and fungemia in a patient with chronic myelogenous leukemia.
Infect Dis Med Microbiol 1996; 7:332–4.
94. Jenkin GA, Choo M, Hosking P, Johnson PDR. Candidal epididymo-
orchitis: case report and review. Clin Infect Dis 1998; 26:942–5.
S466 d CID 2011:52 (Suppl 6) d Fisher et al
95. Giannopoulos A, Giamarellos-Bourboulis EJ, Adamakis I, Georgo-
poulou I, Petrikkos G, Katsilambros N. Epididymitis caused by
Candida glabrata [Letter]. Diabetes Care 2001; 24:2003–4.
96. Swartz DA, Harrington P, Wilcox R. Candidal epididymitis treated
with ketoconazole. N Engl J Med 1988; 319:1485.
97. Chung BH, Chang SY, Kim SI, Choi HS. Successfully treated renal
fungal ball with continuous irrigation of fluconazole. J Urol 2001;
166:1835–6.
98. Pappu LD, Purohit DM, Bradford BF, Turner WRJ, Levkoff AH.
Primary renal candidiasis in two preterm neonates. Report of cases
and review of literature on renal candidiasis in infancy. Am J Dis
Child 1984; 138:923–6.
99. Bartone FF, Hurwitz RS, Rojas EL, Steinberg E, Franceschini R. The
role of percutaneous nephrostomy in the management of obstructing
candidiasis of the urinary tract in infants. J Urol 1988; 140:338–41.
100. Baetz-Greenwalt B, Debaz B, Kumar ML. Bladder fungus ball: a re-
Downloaded from https://academic.oup.com/cid/article/52/suppl_6/S457/285164 by guest on 31 January 2024
versible cause of neonatal obstructive uropathy. Pediatrics 1988;
81:826–9.
101. Laufer J, Reichman B, Graif M, Brish M . Anuria in a premature in-
fant due to ureteropelvic fungal bezoars. Eur J Pediatr 1986; 145:125–7.
102. Yoo SY, Namkoong MK. Acute renal failure caused by fungal bezoar:
a late complication of Candida sepsis associated with central cathe-
terization. J Pediatr Surg 1995; 30:1600–2.
103. Vasquez-Tsuji O, Campos-Rivera T, Ahumada-Mendoza H, Rondan-
Zarate A, Martinez-Barbabosa I. Renal ultrasonography and detection
of pseudomycelium in urine as means of diagnosis of renal fungus
balls in neonates. Mycopathologia 2005; 159:331–7.
104. Abraham M, Mampilly T, Paul JP, Johny VF. Renal failure from ob-
structive fungal mycetoma and fungal sepsis in an infant. Indian
Pediatr 2002; 39:769–72.
105. Ming-Chen PS, Leung DA, Roth JA, Hagspiel KD. Percutaneous ex-
traction of bilateral renal mycetomas in premature infant using me-
chanical thrombectomy device. Urology 2005; 65:1226.e1–3.
106. Chitale SV, Shaida N, Burtt G, Burgess N. Endoscopic management of
renal candidiasis. J Endourol 2004; 18:865–6.
107. Thanka J, Kuruvilla S, Abraham G, Shroff S, Kumar BA, Ranjitham M.
Bilateral renal papillary necrosis due to Candida infection in a diabetic
patient presenting as anuria. J Assoc Physicians India 2003;
51:919–20.
108. Babu R, Hutton KAR. Renal fungal balls and pelvi-ureteric junction
obstruction in a very low-birth-weight infant: treatment with strep-
tokinase. Pediatr Surg Int 2004; 20:804–5.
109. Kabaalioglu A, Bahat E, Boneval C. Renal candidiasis in a 2-month-
old infant: treatment of fungus balls with streptokinase. AJR Am J
Roentgenol 2001; 176:511–2.