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SUPPLEMENT ARTICLE
Advances in the Understanding and Treatment of
Male Urethritis
Laura H. Bachmann,1Lisa E. Manhart,2David H. Martin,3Arlene C. Seña,4Jordan Dimitrakoff,5,6, 7 Jørgen Skov Jensen,8and
Charlotte A. Gaydos9
1
Division of Infectious Diseases, Department of Medicine, Wake Forest University Health Sciences, Winston-Salem, North Carolina;
2
Departments of
Epidemiology and Global Health, University of Washington, Seattle;
3
Division of Infectious Diseases, Department of Medicine, Louisiana State University,
New Orleans;
4
Division of Infectious Diseases, School of Medicine, University of North Carolina at Chapel Hill;
5
Division of Obstetrics/Gynecology and
Reproductive Biology, Beth Israel Deaconess Hospital, and
6
Harvard School of Public Health, Boston, Massachusetts;
7
Division of Bone, Reproductive and
Urologic Products, United States Food and Drug Administration, Silver Spring, Maryland;
8
Microbiology and Infection Control, Statens Serum Institut,
Copenhagen, Denmark; and
9
Division of Infectious Diseases, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland
Neisseria gonorrhoeae and Chlamydia trachomatis are well-documented urethral pathogens, and the literature
supporting Mycoplasma genitalium as an etiology of urethritis is growing. Trichomonas vaginalis and viral
pathogens (herpes simplex virus types 1 and 2 and adenovirus) can cause urethritis, particularly in specific sub-
populations. New data are emerging regarding the potential role of bacterial vaginosis–associated bacteria in
urethritis, although results are inconsistent regarding the pathogenic role of Ureaplasma urealyticum in men.
Mycoplasma hominis and Ureaplasma parvum do not appear to be pathogens. Men with suspected urethritis
should undergo evaluation to confirm urethral inflammation and etiologic cause. Although nucleic acid ampli-
fication testing would detect N. gonorrhoeae and C. trachomatis (or T. vaginalis if utilized), there is no US Food
and Drug Administration–approved clinical test for M. genitalium available in the United States at this time.
The varied etiologies of urethritis and lack of diagnostic options for some organisms present treatment chal-
lenges in the clinical setting.
Keywords.urethritis; men; Chlamydia trachomatis;Mycoplasma genitalium;Neisseria gonorrhoeae.
Urethritis is a common genitourinary syndrome en-
countered in men in clinical practice. This entity is
associated with a variety of etiologic agents including
Neisseria gonorrhoeae (GC), Chlamydia trachoma-
tis (CT), Mycoplasma genitalium (MG), Trichomonas
vaginalis (TV), Ureaplasma urealyticum (UU), herpes
simplex virus (HSV), and adenovirus [1]. Although
seemingly a minor condition, urethritis cases are esti-
mated to be 2.8 million in the United States each year
[2] and can be associated with complications including
acute epididymitis, orchitis, and prostatitis. This article
summarizes new data on the etiology of male urethritis
and its diagnosis and clinical management, using the
background material that informed the most recent
update of the US Centers for Disease Control and Pre-
vention (CDC) sexually transmitted diseases (STD)
treatment guidelines.
METHODS
A PubMed (US National Library of Medicine and the
National Institutes of Health) search was conducted
of all literature published between 2 February 2009
and 8 January 2013 using the search term “urethritis”
(249 articles), limited to human studies published in
English. Given the increasing recognition of MG as a
urethral pathogen, the search term “M. genitalium”was
also added (224 articles). Subsequent to the dates of the
literature review, the National Center for Biotechnology
Information sent notifications of all publications with
the keyword(s) “urethritis”and/or “M. genitalium.”Ab-
stracts from relevant conferences (conferences focused
on STDs, infectious diseases, and/or microbiology
Correspondence: Laura H. Bachmann, MD, MPH, Medical Center Blvd, Wake For-
est University Health Sciences, Winston-Salem, NC 27157 (lbachman@wakehealth.
edu).
Clinical Infectious Diseases
®
2015;61(S8):S763–9
© The Author 2015. Published by Oxford University Press on behalf of the Infectious
Diseases Society of America. All rights reserved. For Permissions, please e-mail:
journals.permissions@oup.com.
DOI: 10.1093/cid/civ755
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that took place during the defined dates above) were also iden-
tified, searching hard copies and online, using the search terms
“urethritis”and/or “M. genitalium.”All abstracts were reviewed,
and pertinent published articles (n = 95) were evaluated. After
each article was read, a determination was made as to whether
it provided data relevant to the scope of the CDC treatment
guidelines. Pertinent articles were summarized and entered
into a table of evidence that was used to inform the key ques-
tions (Table 1) addressed in the guidelines document. Due to
space limitations, not all of these questions are addressed in
this article.
Etiologies of Urethritis
The role of GC and CT as etiologic agents in symptomatic and
asymptomatic urethritis is well established. It is estimated that
approximately 5%–20% of urethritis is caused by gonococcal in-
fection, with prevalence varying by region of the United States,
testing venue, age, and symptom status of the patient [1]. Non-
gonococcal urethritis (NGU) in men may be caused by a variety
of different organisms. Chlamydia trachomatis causes a variable
percentage of NGU cases, depending on the population studied,
with ranges that vary from 15% to 40% in US populations.
Among NGU cases with an identified etiology, CT is responsi-
ble for the highest proportion, particularly among younger in-
dividuals [3]. However, a significant proportion of men with
NGU have no detectable pathogens [4,5].
Mycoplasma genitalium is now recognized as a common eti-
ologic agent of NGU; it is estimated in the published literature
to cause 15%–25% of NGU cases overall, ranging from 13% to
31% in more recent randomized controlled NGU treatment
studies [3,5,6]. Data support an association of the organism
with symptoms of NGU as well as an association with micro-
scopic evidence of inflammation (odds ratio > 4) [7]. Although
the role of MG in causing acute and persistent urethritis in men
is well established, the importance of this pathogen in causing
short- or long-term health complications in men is not clear.
For instance, MG was reported in 4% of men with prostatitis
in one uncontrolled study [8], but additional studies are clearly
needed to further define MG’s role in male genitourinary tract
complications. In contrast, Mycoplasma hominis is unlikely to
be an important etiology of NGU based on the literature to
date [1].
Studies of the role of Ureaplasma in the pathogenesis of ure-
thritis have been inconsistent. Ureaplasmas can be isolated by
culture from 30%–40% of asymptomatic men, and have been
associated with NGU in some studies but not others. After
the division of the ureaplasmas into 2 separate species (Urea-
plasma urealyticum [UU], formerly U. urealyticum biovar 2,
and Ureaplasma parvum [UP], formerly U. urealyticum biovar
1), it has become apparent that the inconsistencies may, to some
extent, be explained by differences in pathogenicity between
species. Newer studies suggest that UU is associated with non-
chlamydial NGU in some cases. Using quantitative polymerase
chain reaction (PCR), Frolund et al found UU in 13% of NGU
cases (>5 polymorphonuclear cells per high-power field
[PMNs/hpf]) and 12% of controls (<5 PMNs/hpf ) (P= not sig-
nificant). The median UU DNA load, however, was higher in
men with NGU vs no NGU (median, 223 vs 10 genome equiv-
alents; P= .002) [9]. Overall, UU as detected by species-specific
PCR has been weakly associated with NGU, particularly among
younger men and in men with fewer sexual partners [9]. UU
should be considered in men without other identifiable etiolo-
gies of NGU. However, UP does not appear to be a urethral
pathogen [9–12].
Rates of TV vary by age and geography, with ranges from 2%
to 13% in the United States [5,6,13,14]. For instance, a large
internet-based study of self-collected penile swabs for the diag-
nosis of TV among men reported a TV prevalence of 6% overall,
with higher rates among black men (9.2%) and men 30–39 years
of age (8%). Age >30 years, black race, younger age of sexual
debut, and the presence of urethral symptoms were all signifi-
cant predictors of TV infection in multivariate analyses [14].
Another study by Gaydos et al [13] found that TV was not as-
sociated with urethritis on multivariate analysis in a population
of men attending a Baltimore STD clinic.
There are few data on viruses, including HSV and adenovi-
rus, as an etiology of NGU. Urethritis is commonly seen
Table 1. Key Questions Addressed for the 2015 Centers for
Disease Control and Prevention Sexually Transmitted Diseases
Treatment Guidelines
1. How should the urethritis syndrome be characterized?
2. What are the specific microbial etiologies of urethritis/NGU and
associated epidemiology?
3. Should asymptomatic men be screened for evidence of NGU?
4. What are the criteria for a clinical diagnosis of urethritis/NGU (in
symptomatic men)?
5. What should be the recommended confirmatory diagnostic (and
screening) tests for Chlamydia trachomatis,Neisseria
gonorrhoeae,Mycoplasma genitalium, and Trichomonas
vaginalis?
6. What are the currently recommended treatment regimens for
NGU?
7. What should be the recommendations regarding empiric
treatment of urethritis (ie, in situations when point-of-care
diagnostic tools are unavailable)?
8. How should persistent/recurrent urethritis be managed?
9. What should be the partner management recommendations for
NGU?
10. Are there special considerations for the management of
urethritis in HIV-infected men?
11. What is the effect of medical male circumcision on urogenital
Mycoplasma genitalium among men?
Abbreviations: HIV, human immunodeficiency virus; NGU, nongonococcal
urethritis.
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(15%–30%) in patients with primary HSV and less common,
though documented, in recurrent HSV. In a recent study, Frol-
und and colleagues found HSV-1 in 3% of NGU cases and
HSV-2 in 2% of cases [9]. Adenovirus has been identified in
men with NGU associated with upper respiratory tract symp-
toms. Bradshaw et al [15] described 8 cases of adenovirus-
associated urethritis in which no other causative organism
was isolated. All of the cases reported recent insertive oral sex
(7 reported recent insertive vaginal sex as well) and were clus-
tered in autumn and winter of each year. The authors concluded
that adenovirus is an uncommon cause of urethritis in men but
should be considered in men presenting with dysuria, meatitis,
and associated conjunctivitis or constitutional symptoms.
There are some data on the role of enteric organisms in ure-
thritis, especially from rectal exposure. Gram-negative rods may
represent a urinary tract infection or be associated with insertive
anal sex. Insertive oral sex is the only exposure in some cases of
nonchlamydial NGU and respiratory tract pathogens such as
Haemophilus species, Neisseria meningitidis,Moraxella catar-
rhalis,andStreptococcus pneumoniae have been associated
with male NGU, although controlled studies are lacking [16].
Uncultured or fastidious organisms commonly found in bac-
terial vaginosis (BV) have also been associated with urethritis. For
instance, Leptotrichia/Sneathia was significantly associated with
nonchlamydial NGU in one study (25/157 [15.3%] vs 6/102
[5.9%]; P= .03), and BV-associated bacterium 2 (BVAB-2) was
detected more often in cases than controls [17]. Frolund et al
studied men (N= 58) with and without NGU (≥5PMNs/hpf),
without GC, CT, MG, UU, or UP and tested them for BV-
associated organisms by PCR (Atopobium vaginae,Sneathia
sanguinegens,Leptotrichia amnionii,Gardnerella vaginalis,
BVAB 1, 2, 3 and Megasphaera phylotype 1). They found G. vag-
inalis in 93% of cases with urethritis of unknown etiology vs 37%
controls (P< .0001), but there was no difference in organism
load between conditions [18]. Therefore, a small number of
studies have shown that specific organisms associated with
BV may be associated with urethritis, but further studies are
needed.
Recent studies utilizing high-throughput sequencing have
contributed to knowledge of the urethral microbiome. Ahrens
et al found a median of 60 genera in urethritis of unknown eti-
ology, 67 genera in CT-positive or MG-positive individuals, and
45 genera in controls [19]. Nelson and colleagues found that
urine from sexually active men often contains complex micro-
bial communities and that the composition of the communities
is related to sexually transmitted infections (STIs). Men with an
STIweremorelikelytohaveSneathia,Gemella,Aerococcus,
Anaerococcus,Prevotella,andVeillonella, for instance [20].
Aerococcus,Anaerococcus,Prevotella, and Veillonella have pre-
viously been detected in the prostate tissue of men with category
III chronic prostatitis/chronic pelvic pain syndrome [8]. These
findings suggest a role for urethral bacterial communities in the
natural history of urethritis and prostatitis. Unfortunately, de-
spite progress in determining the etiology of urethritis, many
cases of NGU (20%–40%) still have no identified pathogen [21].
Making the Diagnosis of Urethritis
The clinical presentation of urethritis is characterized by ure-
thral discharge, dysuria, urethral irritation, or meatal pruritus
and is confirmed by evidence of inflammation and/or the pres-
ence of a known pathogen. Objective evidence of inflammation
includes any of the following: (1) discharge on exam, (2) in-
creased number of PMNs on Gram stain smear of urethral ex-
udate, (3) positive leukocyte esterase on urine dipstick testing,
or (4) increased PMNs in the sediment of first-void urine
(with or without a Gram stain). Approximately 30%–50% of
men with microscopic evidence of urethritis are asymptomatic.
This proportion may be higher depending on the study setting
and methods for documenting inflammation. It is unclear
whether evidence of urethral inflammation in the absence of
symptoms and a known pathogen has clinical significance.
Traditionally, the urethral Gram stain has been utilized as the
point-of-care test to diagnose urethritis in many healthcare set-
tings. A new technique (methylene blue/gentian violet [MB/
GV] smear) has been reported as an alternative to Gram stain-
ing. MB/GV does not require heat fixation and has very similar
performance characteristics to Gram stain. Taylor et al [22]
found the sensitivity of both Gram stain and MB/GV to be
97.3% for the detection of gonococcal infection compared
with culture. The specificity of Gram stain and MB/GV was
99.6%, and 100% correlation was found between Gram stain
and MB/GV for the detection of GC.
Although the criteria for the clinical diagnosis of NGU are
well accepted and commonly used to define NGU for research
purposes, the high rates of CT and MG infection among those
with <5 WBCs (the historical cutoff for a significant number of
white cells required for the diagnosis of urethritis [23]) has been
a cause for concern. Given the fact that the sensitivity of the ure-
thral Gram stain is highly dependent upon collection technique
(experience of provider as well as device utilized [ie, swab vs
loop vs spatula with increasing yields in the same order]), sev-
eral studies have demonstrated that a substantial number of
pathogen-positive NGU cases are missed with current Gram
stain criteria.
An earlier study [24] found that treatment based on ≥5
PMNs on the Gram stain would treat 82% of CT cases and
94% of GC cases; among patients with <5 PMNs, treating
those with symptoms or contact to disease would treat an addi-
tional 6% of CT and 1% of GC identified using nucleic acid am-
plification tests (NAATs). Rietmeijer and Mettenbrink [25]
performed a recent study of 11 422 Gram stains for CT analysis
and 10 023 Gram stains for GC analysis. Samples were collected
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by directly collecting the discharge on a glass slide (if discharge
was present spontaneously or after manual expression) or using
calcium alginate swabs (if no obvious discharge was present).
CT positivity rates correlated strongly with the number of
PMNs/hpf in a stepwise fashion. Almost 5% of those with 0
PMNs/hpf had CT compared with 43.8% if there were >10
PMNs/hpf. There was a statistically significant increase in the
CT infection rate between 1 (6.6%) and 2 (16.2%) PMNs/hpf.
There was no trend in GC detection by PMN strata (only
2.3% had <10 PMNs). Couldwell et al [10], using rayon-tipped
swabs in an Australian STD clinic–based study, found that 35%
of CT, 60% of UU, and 50% of MG infections had <5 PMNs/
hpf. Similarly, Berntsson et al [26], using a plastic loop collec-
tion method in an STD clinic in Sweden, found that 15% of CT
cases and 12.5% MG cases had <5 PMNs/hpf. In contrast, Moi
et al [27] obtained samples for microscopy from 8468 men
using a spatula and detected 98% of all CT infections and
99% of all MG infections using a cutoff of ≥5PMNs/hpf.In
summary, depending on the sampling technique, the Gram
stain threshold for NGU (≥5 PMNs/hpf), when applied to
men in the STD clinic venue, may miss a significant proportion
of individuals with CT and MG. Given the recent data, a
threshold of ≥2 PMNs/hpf on the urethral Gram stain could
now be considered as a criterion to diagnose NGU in high-
risk settings, particularly in venues where the rate of loss to fol-
low-up is high.
Pathogen-Specific Screening Tests Among Men With Urethritis:
Rationale and Recommended Tests
Nucleic Acid Amplification Tests
The CDC released permissive guidelines for CT screening in
males in high-prevalence settings [28]. In general, males should
be screened for CT ± GC based on risk ( young age, sexual ori-
entation, sexual risk, sexual contact, other STI diagnosis). The
recent CDC laboratory testing guidelines now recommend the
use of NAATs for testing men for both CT and GC, unless cul-
ture is desired to perform susceptibility testing for GC. First-
void urine is the specimen of choice for NAATs in men, though
the urethral swab specimen remains an option [29]. In general,
most NAATs find more pathogens from urine than urethral
swabs, with no statistical difference in pathogen detection be-
tween urine and urethral swabs [29].
Microscopic tests for trichomonas in men (urine wet mount)
are neither sensitive nor specific. Culture can be used to test
males, but it has poor sensitivity and would require multiple
specimen types. Newer NAATs have superior test performance
for diagnosing TV in males [30], although none are cleared by
the US Food and Drug Administration (FDA) for use in men.
Several large reference laboratories have performed verification
studies for TV NAAT tests for men using NAAT assays that are
only FDA-cleared for use with female samples. However, the
low prevalence of TV in NGU does not warrant using such
tests in the initial workup, although consideration could be
given to utilizing them among male sexual partners to women
with trichomoniasis and in other male populations in high-
prevalence areas of the country. NAAT-based research tests
for MG have been developed and are both sensitive and specific
for identifying the organism, although there are no FDA-
cleared tests currently available in the United States. Several
large reference laboratories offer male testing for MG after hav-
ing internally validated NAAT assays previously restricted to re-
search use. Overall, the value of additional tests (eg, NAATs) for
other NGU etiologies such as the viral pathogens is unclear.
Urethritis Treatment: What Is New?
Despite the evolving data regarding the association of new path-
ogens with urethritis in men, the 2015 CDC-recommended
treatment for urethritis will remain the same as the regimens
recommended in 2010. The initial treatment for NGU should
include azithromycin 1 g orally in a single dose or doxycycline
100 mg orally twice a day for 7 days. Alternative regimens in-
clude erythromycin base 500 mg orally 4 times a day for 7
days, or erythromycin ethylsuccinate 800 mg orally 4 times a
day for 7 days, or levofloxacin 500 mg once daily for 7 days
or ofloxacin 300 mg twice a day for 7 days. In clinical settings
where diagnostic studies are not available to exclude GC (ie,
Gram stain or MB/GV stain), patients should be treated with
drug regimens effective against both GC and CT (Figure 1).
Prior studies demonstrated good efficacy for azithromycin
and doxycycline in the treatment of NGU caused by CT. How-
ever, recent data are conflicting regarding cure rates for CT in
men with NGU, utilizing NAATs for CT detection. These data
may be confounded by the use of clinical or microbiologic def-
initions of cure as well as by the timing of test of cure. Schwebke
and colleagues reported a 95% clearance rate for CT with dox-
ycycline compared to 77% for azithromycin [5], whereas Man-
hart found no differences based on microbiologic cure for CT
[6]. A more recent study that harmonized definitions of
NGU, time frames for follow-up test of cure, and controlled
for sexual reexposure found the CT treatment failure rate for
azithromycin to be only 6.6% [31].
The treatment of NGU is made more complicated by the
challenge of effective treatment for MG. Doxycycline is only
20%–35% effective against MG, whereas azithromycin is esti-
mated to be ≥70% effective. However, a recent US-based
NGU treatment trial found that cure rates for MG were ex-
tremely low for both azithromycin and doxycycline (40% vs
30%, respectively; P=.41)[5,6,32,33]. Unfortunately, there is
increasing evidence that suboptimal treatment of MG may se-
lect for rapid macrolide resistance in those who fail [34,35]. A
survey of 31 600 specimens in Denmark reported that almost
40% of MG specimens were resistant to macrolides, raising
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concerns about the future of azithromycin for NGU treatment
[36]. For patients with macrolide-resistant MG infections, mox-
ifloxacin is currently the only treatment option for which lim-
ited data are available [37–40]. In summary, MG treatment
failure following the currently recommended NGU regimens
is extremely common and NGU treatment should ideally be
guided by etiologic diagnosis [36,41]. In practice, this will be
difficult until affordable licensed assays are on the market.
Several recent studies have shed light on the question of
whether initial TV treatment is beneficial in men presenting
with NGU. Schwebke and colleagues [5] conducted an STD
clinic–based, multicenter randomized controlled trial to evalu-
ate the addition of tinidazole to azithromycin or doxycycline for
initial treatment of symptomatic men with NGU. The addition
of tinidazole did not lead to increased clinical cure rates for
NGU. Only 1 of 20 (5%) tinidazole-treated patients with TV
at baseline remained positive at follow-up and of those with
baseline TV who did not receive tinidazole, 5 of 16 (31%) re-
mained positive. Thus, 69% of men with TV who did not re-
ceive tinidazole spontaneously resolved their infection (73%
of these had cleared by first follow-up visit). At this time, the
accumulated evidence fails to support empiric treatment of
TV infection for an initial episode of NGU.
Persistent/Recurrent NGU: Recommended Approach
Persistent/recurrent NGU often represents a diagnostic and
therapeutic challenge. It is estimated that 20%–40% of NGU
does not respond to first-line treatment, with up to 20% of
men with chlamydial NGU and 30%–50% of men with non-
chlamydial NGU experiencing persistence/recurrence. These
high rates are derived from research studies and are defined
based on elevated white blood cells on urethral smear, often
in the absence of symptoms, thus accounting for why the clini-
cian does not encounter high numbers of men returning volun-
tarily complaining of persistent/recurrent disease [5,6,33]. The
differential diagnosis for recurrence includes reinfection, non-
adherence, drug resistance, a persistent postinfectious immuno-
logic response, and complicated infection. A good history can
guide the clinician’s assessment regarding the likelihood of
these scenarios. At the time of clinical presentation, the first pri-
ority is to determine whether or not reinfection is likely (in
which case the patient should be re-treated with a recommend-
ed regimen for NGU) or if clinical failure is a possibility, in
which case treatment approaches differ as discussed below.
These patients should be documented to have objective evi-
dence of inflammation on examination as described above. If
the patient is not likely to have been reinfected and he has
Figure 1. Treatment algorithm for nongonococcal urethritis (NGU). Abbreviations: BID, twice daily; PO, per oral; QD, once daily; QID, 4 times daily.
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evidence of inflammation on exam, evaluation and therapy for
persistent NGU are indicated.
Cross-sectional studies of men seeking evaluation for persistent/
recurrent NGU suggest that CT and TV are responsible for some
cases, while MG is responsible for 12%–41% of cases [38,42,43].
The contribution of viral pathogens to persistent/recurrent NGU is
unclear at this time. Seña et al [44] conducted a secondary data
analysis from a large NGU trial, and reported that 33 of 245
(13%) men with NGU who were reassessed at visit 2 (1 week
after posttreatment) had clinical failure—9% were CT infected,
33% MG infected, and 12% TV infected. Among the men who re-
turned for visit 3 (3–4 weeks posttreatment), 10% had CT, 25%
MG, 10% TV, and 56% no pathogen (Figure 2).
Therefore, CT and TV may be associated with persistent NGU,
the prevalence of which likely varies by subpopulation and is
based on the initial treatment regimen. Given the strong evidence
that MG is associated with NGU and that failure to eradicate MG
is associated with persistent urethritis, moxifloxacin 400 mg oral-
ly once daily for 7 days and treatment for TV with either metro-
nidazole or tinidazole are recommended in the CDC guidelines
for treatment of persistent NGU after initial azithromycin thera-
py. Men with persistent/recurrent NGU who received doxycy-
cline, ofloxacin, or levofloxacin as initial therapy should receive
azithromycin 1 g orally once and therapy for TV. Given the ex-
tremely low prevalence of TV in men who have sex only with
men, this population has a low likelihood of benefiting from
the addition of TV-directed therapy in this situation and should
be treated with MG-active agents only (Figure 1).
CONCLUSIONS
Urethritis is an extremely common problem encountered in a
variety of clinical settings. Knowledge regarding potential
etiologic agents continues to evolve as technology improves
and new diagnostic tests continue to be developed. The
evolving role of antibiotic-resistant MG as well as new data re-
garding the prevalence of TV and other new etiologic agents in
male urethritis will continue to impact therapeutic strategies for
this disease entity.
Notes
Disclaimer. The views and opinions expressed in the present manu-
script do not reflect the views and opinions of the United States Food and
Drug Administration or the United States Government.
Supplement sponsorship. This article appears as part of the supplement
“Evidence Papers for the CDC Sexually Transmitted Diseases Treatment
Guidelines,”sponsored by the Centers for Disease Control and Prevention.
Potential conflicts of interest. L. E. M. is a board member for Qiagen,
Inc, and Hologic/Gen-Probe and has received research supplies from Holo-
gic/Gen-Probe. J. S. J. receives funding from Cempra Pharmaceuticals and
NabrivaPharmaceuticals.D.H.M.isaconsultantforHologic,Inc.
C. A. G. receives research support from Hologic, Inc and Becton Dickinson.
All other authors report no potential conflicts.
All authors have submitted the ICMJE Form for Disclosure of Potential
Conflicts of Interest. Conflicts that the editors consider relevant to the con-
tent of the manuscript have been disclosed.
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