0% found this document useful (0 votes)
156 views24 pages

Trichomoniasis - UpToDate

Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
156 views24 pages

Trichomoniasis - UpToDate

Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

23/3/2021 Trichomoniasis - UpToDate

Official reprint from UpToDate®


[Link] ©2021 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Trichomoniasis
Authors: Jack D Sobel, MD, Caroline Mitchell, MD, MPH
Section Editor: Robert L Barbieri, MD
Deputy Editor: Kristen Eckler, MD, FACOG

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Feb 2021. | This topic last updated: Dec 15, 2020.

INTRODUCTION

Trichomoniasis is a genitourinary infection with the protozoan Trichomonas vaginalis. It is the most common
nonviral sexually transmitted disease (STD) worldwide. Women are affected more often than men. Trichomoniasis is
one of the three common infectious causes of vaginal complaints among reproductive-aged women, along with
bacterial vaginosis and candidal vulvovaginitis, and a cause of urethritis in men; however, the infection is often
asymptomatic.

Related topics on the approach to the evaluation of vulvovaginitis and urethritis are presented separately:

● (See "Approach to females with symptoms of vaginitis".)


● (See "Urethritis in adult men".)

BACKGROUND

Microbiology and transmission — The organism responsible for trichomoniasis is the flagellated protozoan T.
vaginalis, which principally infects the squamous epithelium in the urogenital tract: vagina, urethra, and
paraurethral glands [1]. Other less common sites include the cervix, bladder, Bartholin glands, and prostate.
Humans are the only natural host, and it is the most common nonviral sexually transmitted disease (STD) worldwide
[2,3]. The parasite is a pear- or round-shaped organism with four anterior flagella and an undulating membrane
that cause the characteristic motility seen on a diagnostic wet-mount slide [4]. (See 'Microscopy and pH' below.)

Trichomoniasis is virtually always sexually transmitted [5]. Although survival on fomites has been reported,
transmission by fomites has not been directly proven [6]. Women can acquire the disease from both women and
men, while men typically acquire the infection from women and do not usually transmit the infection to other men
[7-9]. The incubation period is unknown; however, in vitro studies suggest an incubation period of 4 to 28 days in
approximately 50 percent of patients [10]. Coexistence of T. vaginalis and bacterial vaginosis pathogens is common;
coinfection rates ranging from 20 to 60 to 80 percent have been reported [11,12]. (See "Bacterial vaginosis: Clinical
manifestations and diagnosis" and "Bacterial vaginosis: Treatment".)

Prevalence — Trichomonal infection does not need to be reported to public health authorities, so prevalence is
difficult to determine. Prevalence estimates vary according to the population studied and method used for
diagnosis. For example, a meta-analysis of 18 studies including over 37,000 women from low- and middle-income
African countries reported a prevalence rates of 2 to nearly 30 percent, depending on the age range and risk status

[Link] 1/24
23/3/2021 Trichomoniasis - UpToDate

of the population [13]. In 2008, the World Health Organization estimated that over 276 million new cases occurred
globally, and approximately 187 million people were infected at any one time [14].

The best estimate of the prevalence of trichomoniasis in reproductive-age women in the United States was provided
by the National Health and Nutrition Examination Survey (NHANES), in which a nationally representative sample of
3754 women ages 14 to 49 years self-collected vaginal swab specimens that were subsequently evaluated for T.
vaginalis by polymerase chain reaction (PCR) [15]. The overall prevalence of T. vaginalis was 3.1 percent and
increased with age. Prevalence was highest in non-Hispanic Black women (13.3 percent) and lowest in non-Hispanic
White women (1.3 percent). These estimates remained relatively stable in an analysis using urine samples from
4463 female participants in the 2013 to 2016 NHANES, which found a prevalence of 2.1 percent in women overall
and similar disparities between non-Hispanic Black women (9.56 percent) versus non-Hispanic White women (0.81
percent) [16]. Urine samples have a lower sensitivity than cervicovaginal swabs, which likely accounts for the slightly
lower prevalence estimates.

When nucleic acid amplification testing (NAAT) is used to detect T. vaginalis, the overall prevalence is higher than
that reported by the NHANES study and ranges from approximately 5 to 16 percent, depending on the clinical
setting (5 to 7 percent in family planning, internal medicine/family practice, and obstetrics and gynecology offices to
16 percent in prisons and sexually transmitted infection [STI] clinics) [17,18]. In contrast to the NHANES study, these
women were tested because of symptoms or the presence of risk factors for chlamydia or gonorrhea. Lastly, a study
in 15 STD clinics participating in the STD Surveillance Network reported the prevalence of T. vaginalis was 26 percent
among 17,952 symptomatic women tested, 6.5 percent among 3909 asymptomatic women screened, and 29
percent among 92 HIV-infected women tested/screened [19].

The age distribution of trichomoniasis infections in women appears to differ from other STIs. In a PCR study of
cervicovaginal samples obtained during gynecologic examinations, the peak rate of detection for T. vaginalis
occurred in women ages 47 to 53 years, compared with 14 to 20 years for Chlamydia trachomatis [20]. In addition,
while rates of chlamydia infection rapidly declined after peak detection, T. vaginalis infections had a bimodal
distribution with infection peaks occurring in women ages 21 to 22 years and 48 to 51 years.

T. vaginalis can be identified in 70 percent of the male sexual partners of infected women [21], although carriage in
men is often self-limited (see 'Treatment of sex partners' below). A study using an educational internet program to
offer sexually active men free NAATs for T. vaginalis on self-collected specimens reported an overall prevalence of 3.7
percent among the 1699 men, and the highest prevalence by age group was in men aged 40 to 49 years (5.2
percent) [22].

Prevention — The risk of acquiring T. vaginalis infection can be reduced by consistent use of condoms and limiting
the number of sexual partners. Spermicidal agents such as nonoxynol-9 reduce the rate of transmission [23].

● (See "Male condoms".)


● (See "Female condoms".)
● (See "Pericoital contraception: Diaphragm, cervical cap, spermicides, and sponge".)

SCREENING

In the United States, the Centers for Disease Control and Prevention recommend screening for T. vaginalis in all HIV-
infected women, annually and at their initial prenatal visits [7]. In addition, screening is reasonable for HIV-

[Link] 2/24
23/3/2021 Trichomoniasis - UpToDate

uninfected women at increased risk of Trichomonas infection, including those with new or multiple partners or a
history of sexually transmitted infections. Screening for men is not recommended.

Issues related to screening for T. vaginalis are discussed separately. (See "Screening for sexually transmitted
infections", section on 'Trichomonas'.)

CLINICAL FEATURES AND CONSEQUENCES

Women — In women, trichomoniasis ranges from an acute, severe inflammatory disease to an asymptomatic
carrier state. Common signs and symptoms of acute infection include a purulent, malodorous, thin discharge
associated with burning, pruritus, dysuria, frequency, lower abdominal pain, or dyspareunia [24]. However, in
women with proven infection, only 11 to 17 percent present with typical symptoms [25]. Symptoms may be worse
during menstruation [26]. Postcoital bleeding can occur. In chronic infection, signs and symptoms are milder and
may include pruritus and dyspareunia, with scanty vaginal secretion. As many as 70 to 85 percent of infected
women are asymptomatic, although many of these women eventually develop symptoms [7,27]. Asymptomatic
carriage can persist for prolonged periods of time (at least three months); thus, it is often not possible to ascertain
when or from whom the infection was acquired [28,29].

Physical examination often reveals erythema of the vulva and vaginal mucosa. The classically described green-
yellow, frothy, malodorous discharge occurs in 10 to 30 percent of symptomatic women. Punctate hemorrhages
may be visible on the vagina and cervix (ie, strawberry cervix) in 2 percent of cases ( picture 1) [30].

Consequences of trichomoniasis vary by population:

● Nonpregnant women – Untreated trichomonal vaginitis may progress to urethritis or cystitis. In addition, T.
vaginalis has been associated with a range of adverse reproductive health outcomes, including cervical
neoplasia [31,32], posthysterectomy cuff cellulitis or abscess [33], pelvic inflammatory disease [34,35], and
infertility [36]. It may also increase women's susceptibility to acquiring HIV infection by up to twofold [37-39].
Trichomoniasis in HIV-infected individuals is associated with an increased risk of HIV transmission to uninfected
partners [40-42]. There is some evidence that treatment of trichomoniasis reduces HIV shedding [40,41,43].

● Pregnant women – T. vaginalis infection during pregnancy is associated with adverse obstetric outcomes
including premature rupture of the membranes, preterm delivery, and delivery of a low birth weight infant
[27,44-47]. In a 2014 systematic review and meta-analysis of the association between T. vaginalis and perinatal
outcomes, the risk of preterm birth was increased by 42 percent among infected women (relative risk 1.42, 95%
CI 1.15-1.75; nine studies) [48]. The risks of premature rupture of membranes and delivery of a small for
gestational age infant were similarly increased, but each of these findings was based on only two studies.
Whether treatment in pregnancy affects these risks, positively or negatively, is unclear [7]. (See 'Pregnant
individuals' below.)

● Newborns – Infants born to infected mothers may contract infection during delivery. Signs and symptoms in
neonates may include fever, respiratory problems, urinary tract infection, nasal discharge, and, in girls, vaginal
discharge [49-52]. Treatment of asymptomatic infants is not necessary as spontaneous resolution will occur
when estrogen levels wane to normal prepubescent levels [53]. (See "Overview of vulvovaginal complaints in
the prepubertal child".)

[Link] 3/24
23/3/2021 Trichomoniasis - UpToDate

Men — In men, T. vaginalis infection is asymptomatic in over three-quarters of cases and often transient
(spontaneous resolution within 10 days) [21,53]. However, untreated infection can persist for months [54].
Symptoms, when present, are the same as those for urethritis from any cause and consist of a clear or
mucopurulent urethral discharge and/or dysuria. They may also have mild pruritus or burning sensation in the
penis after sexual intercourse. (See "Urethritis in adult men", section on 'Clinical manifestations'.)

T. vaginalis in men has been associated with prostatitis, balanoposthitis, epididymitis, infertility, and prostate cancer.
(See "Approach to infectious causes of dysuria in the adult man" and "Risk factors for prostate cancer", section on
'Trichomonas vaginalis infection'.)

DIAGNOSIS

For women and men, the diagnosis of T. vaginalis is based on laboratory testing (motile trichomonads on wet
mount, positive culture, positive nucleic acid amplification test, or positive rapid antigen or nucleic acid probe test)
that confirms T. vaginalis [55].

DIAGNOSTIC EVALUATION

Women — Microscopy is often the first step in the diagnostic evaluation for trichomoniasis because microscopy is
important in the evaluation of vaginal discharge. Microscopy is convenient and low cost, although less accurate
than other tests. If the microscopic evaluation is positive for trichomonads, no further trichomonal testing is
indicated. For women with nondiagnostic (or negative) wet-mount slides on microscopy, nucleic acid amplification
tests (NAAT) are performed. If NAAT is not available, rapid diagnostic kits, or culture are performed instead. The
choice of test is based on availability and cost.

Women undergoing testing for trichomoniasis are generally tested for chlamydia and gonorrhea infections as well.
The diagnostic approach to women with vaginal discharge is reviewed separately. (See "Approach to females with
symptoms of vaginitis" and "Screening for sexually transmitted infections", section on 'Screening
recommendations'.)

Preferred tests

Microscopy and pH — The presence of motile trichomonads on wet mount is diagnostic of infection, but they
are identified in only 60 to 70 percent of culture-confirmed cases ( picture 2) [56]. The motion is jerky and
spinning ( movie 1 and movie 2); organisms remain motile for 10 to 20 minutes after collection of the sample.
The slide should be evaluated soon after obtaining the specimen as sensitivity decreases over time, with up to 20
percent decrease reported one hour after collection [7,57,58]. Fixation and staining is not useful because T. vaginalis
may not have the typical pear-shaped flagellated form; instead, it may resemble polymorphonuclear leukocytes or
lose morphologic characteristics during fixation and staining, making the etiologic identification difficult [59].

Other findings that are typically present with T. vaginalis infection include an elevated vaginal pH (>4.5) and an
increase in polymorphonuclear leukocytes on saline microscopy. However, these additional findings are not
diagnostic as they can be found in other vaginal infections ( table 1).

Nucleic acid amplification test — NAATs detect RNA by transcription-mediated amplification (polymerase


chain reaction [PCR] or reverse transcriptase), are highly sensitive and specific, and have become the accepted gold

[Link] 4/24
23/3/2021 Trichomoniasis - UpToDate

standard for the diagnosis of T. vaginalis [60]. Test limitations include the need for instrumentation and laboratory
analysis. In a study of test samples from 303 female sex workers, test sensitivity was highest for vaginal samples
and lowest for first-voided urine specimens (86 versus 63 percent, all infections) [61].

One of the most commonly used tests, the Aptima T. vaginalis assay (Hologic), uses target capture and transcription
mediated nucleic acid amplification to detect species-specific ribonucleic acid (RNA) for T. vaginalis on a single
vaginal swab or urine specimen [62]. Reported sensitivity ranges from 95 to 100 percent and specificity ranges from
95 to 100 percent [7,63-65]. The Aptima T. vaginalis assay has demonstrated superior performance in side-by-side
comparisons with other diagnostic methods in all patient populations and specimen types tested (vaginal
discharge, urine). The Aptima T. vaginalis assay is approved by the US Food and Drug Administration (FDA) [65].
Because the prevalence of Trichomonas is equal to or greater than chlamydia and gonorrhea, there is an increasing
trend toward screening for all three infections simultaneously with NAAT [7,60]. A separate assay is currently
required for N. gonorrhoeae and C. trachomatis (eg, Aptima Combo 2).

Other available NAATs include Amplicor (Roche), AmpliVue (Quidel), BD ProbeTec TV Qx (BD Diagnostics), NuSwab VG
(LabCorp), Solana (Quidel), Xpert TV (Cepheid) assays. Few are approved by the FDA, but all are likely to be reliable.
The BD MAX vaginal panel, which is FDA approved, also tests for bacterial vaginosis and Candida species [66]. There
are no studies comparing one test with another. Amplicor (Roche) is a PCR assay for detection of N. gonorrhoeae and
C. trachomatis that has been modified to detect T. vaginalis in vaginal/endocervical swabs or urine; sensitivity and
specificity are 88 to 97 percent and 98 to 99 percent, respectively [28]. NuSwab VG (LabCorp) is a nucleic acid
amplification single specimen assay for the detection of trichomoniasis, bacterial vaginosis, and vulvovaginal
candidiasis.

Rapid antigen and DNA hybridization probes — Rapid diagnostic kits can be useful in areas of high
prevalence (eg, sexually transmitted disease [STD] clinics and clinics serving populations with high prevalence rates)
where microscopy or culture is not available. The following tests can be performed by the clinician at the point of
care and are commercially available.

● AFFIRM VPIII – The Affirm VPIII Microbial Identification System (Becton Dickinson) test uses a DNA
hybridization probe on a vaginal swab specimen. Results are available in 45 minutes. Although sensitivity and
specificity have been reported to exceed 95 percent, in side-by-side testing, this method was inferior to target
capture and transcription mediated amplification (sensitivity 63.4 versus 100 percent [63]).

● OSOM Trichomonas Rapid Test – The OSOM Trichomonas Rapid Test (Sekisui Diagnostics) is a rapid antigen test
that uses an immunochromatographic technology on a vaginal swab specimen. Testing can be done at the
point of care, and results are available in 10 minutes. It has sensitivity of 82 to 95 percent and specificity of 97 to
100 percent [67-70].

Test comparison — The excellent performance characteristics of the above tests are illustrated by the
following comparative studies, which compare performance of traditional and rapid testing methods:

● One study recruited 330 sexually active adolescent females seeking care at a teen health clinic or emergency
department and tested them for T. vaginalis using the four test methods discussed above: wet mount, culture
(InPouch TV), rapid antigen testing (OSOM TV), and transcription-mediated amplification testing (APTIMA TV)
[71]. The sensitivities of the four methods were 65, 96, 90, and 98 percent, respectively.

● Another study enrolled 296 female and 298 male subjects seeking care at a STD clinic [62]. Specimens from
each subject were tested for trichomoniasis using transcription-mediated amplification (APTIMA TV), wet mount

[Link] 5/24
23/3/2021 Trichomoniasis - UpToDate

microscopy, culture, and PCR tests. The subject was diagnosed with trichomoniasis if any of these tests were
positive. In women, vaginal swab APTIMA TV was more sensitive than wet mount or culture (96.6 versus 54.6
and 75.0 percent, respectively). In men, urethral swab APTIMA TV was more sensitive than culture or PCR (95.2
versus 28.6 and 54.8 percent, respectively).

● In a third study, specimens were retrieved consecutively from 766 patients with vaginal complaints and/or with
histories suggestive of a STD and tested by both the AFFIRM and the APTIMA T. vaginalis assays [63]. Overall, 5.1
percent of patients were positive for T vaginalis (defined as a specimen with two positive test results for T.
vaginalis by two different molecular assays). The APTIMA assay was statistically more sensitive than the AFFIRM
assay (100 versus 63.4 percent); specificity was similar (APTIMA 100 percent, AFFIRM 99.9 percent).

Less accurate

Culture — Culture of vaginal secretions on Diamond's medium was considered the gold standard method for
diagnosing T. vaginalis infection before the development of molecular detection methods [7]. Culture offers high
sensitivity (up to 95 percent) and specificity (>95 percent). However, this test is not widely available and takes up to
seven days to obtain a result. Culture is useful in patients with elevated vaginal pH and increased numbers of
polymorphonuclear leukocytes but an absence of motile trichomonads and clue cells on wet mount, when
microscopy is unavailable or yields ambiguous results, or when NAATs are not available. The "InPouch" T. vaginalis
culture system has high sensitivity (over 80 percent), takes ≤3 days to obtain results, and is commercially available
[72,73].

Cervical cytology — Trichomonads are sometimes reported as an incidental finding on tests performed for
cervical cancer screening. Liquid-based cervical cytology is not a sensitive test for diagnosis of trichomoniasis, but
treatment of women with trichomonads noted on liquid-based cervical cytology is reasonable since specificity is
high. In a study that performed both liquid-based cervical cytology and culture for T. vaginalis on 203 consecutive
women, 28 had a liquid-based smear positive for trichomonads, and 44 had positive cultures [74]. Although
sensitivity of liquid-based smears for Trichomonas infection was low (61 percent), specificity was high (99 percent),
resulting in a false-positive rate of only 1 percent.

Conventional Pap smears do not perform as well for diagnosis of trichomoniasis. Sensitivity is similar (51 to 63
percent) to liquid-based tests, but false-positive results are common (7 percent) [75]. This makes the positive
predictive value poor in a low prevalence population. Thus, a conventional Pap smear should not be used to
diagnose trichomoniasis. Asymptomatic women with trichomonads identified on a conventional Pap smear should
be evaluated by wet mount and then NAAT, culture, or rapid test if the wet mount is negative and treated only if the
diagnosis is confirmed.

Men — The most reliable methods for diagnosis of Trichomonas urethritis in the male are by culture or a NAAT (ie,
PCR or transcription-mediated amplification) of first fraction urine or a urethral swab specimen [62,76]. Saline
microscopy of a urethral swab specimen has low sensitivity and is not recommended. (See "Urethritis in adult men".)

DIFFERENTIAL DIAGNOSIS

For women, vaginal discharge is a nonspecific symptom that can be caused by vaginal infections, cervical infections,
and, less commonly, atrophy and irritation.

[Link] 6/24
23/3/2021 Trichomoniasis - UpToDate

● Vaginal infections – The most common infections responsible for vaginal discharge, odor, pruritus, and/or
discomfort are bacterial vaginosis (BV), Candida vulvovaginitis, and trichomoniasis; these infections account for
over 90 percent of cases [77]. The clinical features that distinguish among these infections are presented in the
table ( table 1). Detailed discussions of the clinical manifestations and management of BV and vulvovaginal
candidiasis are presented separately:

• (See "Bacterial vaginosis: Clinical manifestations and diagnosis".)


• (See "Bacterial vaginosis: Treatment".)
• (See "Candida vulvovaginitis: Clinical manifestations and diagnosis".)
• (See "Candida vulvovaginitis: Treatment".)

● Cervical infections – The sexually transmitted cervical infections gonorrhea and chlamydia also cause
symptomatic vaginal discharge, but less commonly than vaginal infections [78,79]. In two studies of women
presenting with symptomatic vaginal discharge in resource-limited countries, cervical infection with either
gonorrhea or chlamydia was present in 5 to 24 percent of women compared with vaginal infection (ie, BV,
vulvovaginal candidiasis, or trichomoniasis) in over 50 percent of women [78,79]. Organism-specific testing is
required to identify the infectious cause(s) of vaginal discharge. Clinical presentations and management of
cervical sexually transmitted infections are discussed elsewhere:

• (See "Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents".)
• (See "Treatment of uncomplicated Neisseria gonorrhoeae infections".)
• (See "Clinical manifestations and diagnosis of Chlamydia trachomatis infections".)
• (See "Treatment of Chlamydia trachomatis infection".)

● Other – Less common causes of vaginal discharge that could be mistaken for trichomoniasis include vaginal
atrophy/atrophic vaginitis in postmenopausal women, retained foreign body, irritants and allergens (ie,
dermatitis), desquamative inflammatory vaginitis, and several rarer entities, including some systemic medical
disorders. Targeted testing is performed to exclude infection, including T. vaginalis. Once infectious etiologies
have been excluded, then the evaluation continues to exclude noninfectious causes. (See "Approach to females
with symptoms of vaginitis", section on 'Women without a diagnosis after initial evaluation'.)

For men, urethritis is typically caused by a sexually transmitted pathogen. Similar to vaginal discharge in women,
urethritis is a nonspecific symptom in men and testing is performed to identify or exclude infectious organisms,
most commonly Neisseria gonorrhoeae, Chlamydia trachomatis, and Mycoplasma genitalium. The evaluation and
management of men with urethritis is presented elsewhere. (See "Urethritis in adult men".)

INITIAL TREATMENT

5-nitroimidazole drugs — The 5-nitroimidazole drugs (metronidazole or tinidazole) are the only class of drugs that
provide curative therapy of trichomoniasis. Most strains of T. vaginalis are highly susceptible to these agents [80].
Randomized trials using these drugs have generally reported cure rates of 90 to 95 percent [81-83].

For initial treatment, we suggest a seven-day course of either metronidazole or tinidazole, 500 mg orally twice daily.
While guidelines have recommended treatment with a single 2 g oral dose of either tinidazole or metronidazole (ie,
four 500 mg tablets), trials comparing the single- and multiple-day regimens of metronidazole in women with and
without HIV have demonstrated higher cure rates four weeks after treatment with the seven-day regimen [7,83,84].
An open-label trial comparing the two regimens among 623 enrolled women reported a significantly higher cure

[Link] 7/24
23/3/2021 Trichomoniasis - UpToDate

rate with seven-day versus single-dose treatment (89 versus 81 percent, respectively) [85]. Treatment success was
evaluated with nucleic acid amplification testing or culture. Reports of adverse events, including gastrointestinal
distress, were similar between the two treatment arms as was reported adherence (96 percent in the seven-day arm
and 99 percent in the single-dose arm).

Tinidazole generally causes fewer gastrointestinal side effects, but the cost is higher compared with metronidazole.
Although tinidazole was significantly more effective than metronidazole in several randomized trials, most of these
trials were subject to bias since outcome was assessed by clinicians who were not blinded to the patient's treatment
group [83]. Choice of agent is generally determined by availability and cost. Management of nitroimidazole-resistant
Trichomonas is discussed below. (See 'Refractory cases' below.)

Allergy to 5-nitroimidazole drugs — Therapy with drugs other than 5-nitroimidazoles is an option, but cure rates
are low (≤50 percent) [86,87]. Given the low efficacy of alternate drug therapies, we suggest patients with an IgE
mediated allergy to metronidazole or tinidazole be referred for desensitization rather than using an alternative
class of drugs [7]. Desensitization is very effective: In one series, all 15 women who underwent desensitization
subsequently eradicated their infections [88].

OUR APPROACH

Treatment is indicated for both symptomatic and asymptomatic women and men. Treatment reduces the
prevalence of T. vaginalis carriage in the population, relieves symptoms, and reduces the risk of sequelae (including
acquisition/transmission of HIV) [7].

Nonpregnant women — Treatment is indicated in all nonpregnant females diagnosed with trichomoniasis, even if
asymptomatic. The rationale for treatment of asymptomatic females is that, if left untreated, they continue to
transmit the infection to sexual partners and up to one-third of asymptomatic females become symptomatic within
six months [26]. As reviewed above, metronidazole 500 mg orally twice a day for seven days is the preferred
treatment. (See '5-nitroimidazole drugs' above.)

Treatment with a single 2 g oral dose of either tinidazole or metronidazole (ie, four 500 mg tablets) is associated
with lower rates of cure [7,83]. Although older studies reported similar cure rates for single- and multiple-dose
regimens (cure rate for single dose: 81 to 88 percent; cure rate for multiple dose: 85 to 90 percent) [81,83,85,89], a
meta-analysis of six trials reported a higher treatment failure rate for single-dose compared with multiple-dose
treatments (pooled risk ratio 1.80, 95% CI 1.07-3.03; p <0.03 in HIV-negative women) [84]. In combination with the
results of the randomized trial comparing single dose to multiple dose [85], these data suggest that females who
are able to complete the multiple-dose regimen appear to benefit from the longer treatment. By contrast,
advantages of single-dose therapy include better compliance and possibly decreased Candida superinfection
(although there is no evidence of decreased Candida superinfection). However, side effects (eg, nausea, vomiting,
headache, metallic taste, dizziness) appear to be dose-related and thus occur less frequently with the lower doses
used in multiple-dose, prolonged therapy [83]. The authors reserve single-dose therapy for those who are unable to
complete a multiple-dose treatment course.

Oral or vaginal therapy — Oral is preferred to vaginal therapy since systemic administration achieves higher
drug levels and therapeutic drug levels in the urethra and periurethral glands, which serve as endogenous
reservoirs of organisms that can cause recurrence. Cure rates for vaginal therapy with metronidazole gel are ≤50

[Link] 8/24
23/3/2021 Trichomoniasis - UpToDate

percent, which is significantly lower than with oral therapy, and therefore vaginal therapy with metronidazole is not
recommended [7,83].

Follow-up — We retest all women treated for a documented Trichomonas infection, regardless of whether they
believe their sex partners were treated. Repeat testing is ideally performed with a nucleic acid amplification test
(NAAT), which can be done as soon as two weeks after and within three months of completing treatment. This is
consistent with recommendations from the Centers for Disease Control and Prevention in the United States [7]. If
NAAT is not available, retesting with the same modality used to make the initial diagnosis (or a more sensitive test)
is advised. The rationale for repeat testing is that reinfection rates of up to 17 percent have been reported in
women treated for trichomoniasis.

Men with urethritis — The same treatment regimens are used in men as in nonpregnant women, with preference
given to single-dose treatment with either oral metronidazole or tinidazole, 2 g, to improve compliance. There are
no data to suggest that men would derive additional benefit from a longer course of therapy. The clinical evaluation
and management of men with urethritis are discussed in detail separately. (See "Urethritis in adult men".)

Treatment of sex partners — Treatment of sex partners is identical to that for nonpregnant females, with
preference for a single-dose regimen to maximize compliance (ie, single 2 g oral dose of either tinidazole or
metronidazole). Treatment of sex partners is indicated because maximal cure rates in infected women are achieved
when their sexual partners are treated simultaneously [7,90]. Concurrent treatment also prevents transmission to
other sexual contacts. After single-dose therapy of sexual contacts, patients should abstain from intercourse until
all partners have waited at least seven days since taking the last antibiotic dose. There are no studies on how long
trichomonads remain viable after treatment is initiated or completed.

It is not mandatory to identify the organism in a male partner before treating him (ie, Expedited Partner Therapy
[EPT]), given the high rate of concurrent carriage (30 to 70 percent [21]), difficulty of diagnosis in males, lower
compliance when the partner is asked to visit his health care provider, and the convenience, low morbidity, and low
cost of empiric treatment. Similarly, all female sex partners also should be treated. The rates of concurrent
trichomoniasis infections in women who have sex with women is not known.

Ideally, if possible, sexual partners should be referred for diagnostic evaluation because concurrent sexually
transmitted infections, such as chlamydia and gonorrhea, are common and should be diagnosed and treated, if
present [91,92]. However, if the one partner has been diagnosed with chlamydia or gonorrhea, EPT is also an option
for these infections [91].

Counseling — Previous guidelines have recommended avoiding alcohol due to a potential disulfiram-like reaction
associated with nitroimidazoles. However, several authors have reviewed the cases that are the basis of these
reports and have not identified any convincing data to suggest that this is a true association [93]. Disulfiram inhibits
acetaldehyde dehydrogenase, leading to increased concentrations of acetaldehyde, while in vitro experiments show
a decrease in acetaldehyde with addition of metronidazole [94]. Thus, we do not feel strongly that patients need to
be counseled to avoid alcohol while using metronidazole.

Patients should be instructed to avoid intercourse until they and their sex partners have completed treatment and
are asymptomatic, which generally takes approximately one week. (See 'Treatment of sex partners' above.)

SPECIAL POPULATIONS

[Link] 9/24
23/3/2021 Trichomoniasis - UpToDate

Pregnant individuals

Treatment and dosing options — Metronidazole 500 mg orally twice a day for seven days is the preferred
treatment for pregnant individuals. While both single- and multiple-dose regimens are acceptable, we reserve the
single-dose regimen for pregnant individuals who are unable to complete seven days of treatment or prefer single-
dose therapy. There are no specific data comparing single-dose and multiple-dose regimens in pregnant individuals.
However, there are no reasons to think that efficacy is different in pregnant patients, and, although tolerance may
be diminished because many pregnant women have significant nausea or vomiting, some clinicians have
historically preferred metronidazole 500 mg twice daily orally for five to seven days to lessen medication-induced
nausea and vomiting [95].

There is limited information on the safety of tinidazole in pregnancy; therefore, we avoid its use, especially in the
first trimester. Although clotrimazole 1% cream inserted vaginally often results in symptomatic relief, it does not
eradicate the organisms and therefore is not advised. For these reasons, oral metronidazole therapy is preferred.

Rationale for treatment — Given the association of T. vaginalis infection with adverse pregnancy outcomes [48],
symptomatic pregnant women with confirmed infection are treated [7]. Additionally, asymptomatic trichomoniasis
can be diagnosed during pregnancy with routine screening of HIV-infected or high-risk women. Although treatment
of asymptomatic pregnant women is not universal [7], we believe the benefits of treatment, including reduced
partner and perinatal transmission, outweigh potential risks. A historical concern regarding treatment of
asymptomatic pregnant women comes from one trial [96] and subsequent meta-analysis (based heavily on the trial)
[97], which reported an increased risk of preterm birth in women treated with metronidazole therapy compared
with untreated women. However, the trial had multiple limitations, including starting screening in the second
trimester, and subsequent studies have not reported adverse outcomes from treatment [48,98-100].

While metronidazole crosses the placenta [101], it appears to be low risk. Cross-sectional and cohort studies have
not reported teratogenicity or mutagenic effects in humans, although studies suggest the drug is mutagenic in
bacteria and carcinogenic in mice [97-99,102].

As with nonpregnant women, when T. vaginalis is confirmed and treated in a pregnant woman, we retest the
woman at a follow-up visit and treat all sexual partners. (See 'Follow-up' above and 'Treatment of sex partners'
above.)

Breastfeeding individuals — We treat breastfeeding individuals with metronidazole 500 mg orally twice a day for
seven days. This approach differs from the Centers for Disease Control and Prevention (CDC) guideline that
suggests 400 mg orally three times a day for seven days. While the study referenced by the CDC reported that three
times daily dosing produced a lower metronidazole concentration in breast milk [7,103], limitations include that the
study had data on only seven infants, more frequent dosing may be more challenging for patients, and 400 mg
tablets are not universally available. For those individuals who are unable or unlikely to complete a seven-day
treatment course, single-dose therapy is a reasonable alternative.

While metronidazole is secreted in breast milk, breastfed infants receive metronidazole doses that are lower than
those used to treat infections in infants. Nevertheless, some clinicians recommend deferring breastfeeding for 12 to
24 hours following maternal single-dose treatment because the relative infant dose of metronidazole is high (29
percent) with maternal administration of the 2 g one-time dose [104]. For women who wish to avoid any
metronidazole exposure to their infants, we advise pumping and expelling breast milk for 12 hours. There are no
data comparing 12- and 24-hour windows.

[Link] 10/24
23/3/2021 Trichomoniasis - UpToDate

There are no human data supporting an association between metronidazole exposure from breastfeeding and
cancer; however, an association with carcinogenesis in rodents has been demonstrated [105]. Outcomes data of
maternal metronidazole use did not show a significant increase in adverse events compared with use of other
antimicrobials, although a cohort study found a nonsignificant trend toward more loose stools and more candidal
colonization in metronidazole-exposed infants.

In mothers using tinidazole, which has a longer half-life than metronidazole, the CDC suggests interrupting
breastfeeding for three days after the last dose [7].

HIV-infected females — HIV-infected women with T. vaginalis are treated with metronidazole 500 mg twice per day
for seven days [7]. We do not use single-dose metronidazole for treatment of these women, given the high
prevalence of asymptomatic bacterial vaginosis (BV) coinfection and other factors that may render metronidazole
less effective in this population.

In a trial where 270 HIV-positive women with culture-confirmed T. vaginalis were randomly assigned to treatment
with metronidazole 2 g single dose or metronidazole 500 mg twice per day for seven days, single-dose therapy was
less effective than multiple-day therapy [106]. The seven-day treatment group had a lower rate of positive cultures 6
to 12 days after treatment completion (8.5 percent [11/130 women] versus 16.8 percent [21/125 women]; relative
risk [RR] 0.5, 95% CI 0.25-1.00) and at 3 months (11 percent [8/73 women] versus 24.1 percent [19/79 women]; RR
0.46, 95% CI 0.21-0.98). Of note, all women were given a 2 g metronidazole dose to deliver to their sex partners. In
another trial, HIV-infected women on antiretroviral therapy had 2.6-fold greater risk of persistent trichomoniasis
than HIV-infected women not on antiretroviral therapy, but this risk could be minimized by multiday dosing [107].

Additionally, there is a high prevalence of BV in HIV-infected/T. vaginalis-infected women, and there is an apparent
association between the presence of BV and early failure of single-dose metronidazole treatment of trichomoniasis
[108]. As with all women, the CDC suggests retesting HIV-infected women three months after completion of therapy
based on the high proportion of recurrent or persistent T. vaginalis infection in this population and the association
between HIV and this infection [7]. As with other populations, sexual partners of HIV-infected patients diagnosed
with Trichomonas infection should be treated as well. (See "HIV and women", section on 'Bacterial vaginosis, genital
ulcers, and pelvic inflammatory disease' and "Bacterial vaginosis: Treatment" and 'Treatment of sex partners'
above.)

REFRACTORY CASES

The most common causes of treatment failure are noncompliance and reinfection.

● Medication noncompliance – The most common cause of continued infection and symptoms is medication
misuse or noncompliance. Medication compliance is enhanced with single-dose therapy. Patients with recurrent
symptoms and likely medication misuse or noncompliance are retreated with the initial treatment above. (See
'Initial treatment' above.)

● Reinfection – Reinfection from untreated or undertreated sexual partners is another source of continued
infection. For patients with persistent symptoms in whom reinfection is likely, we repeat treatment with either
another seven-day course, or a single 2 g oral dose of metronidazole or tinidazole and retreat all sexual
partners as well.

[Link] 11/24
23/3/2021 Trichomoniasis - UpToDate

● Recurrent infection – Reinfection is unlikely if the sexual partners were treated concurrently and sexual
intercourse was avoided until both partners completed treatment. Women who fail a single dose of
metronidazole 2 g can be treated with oral metronidazole 500 mg twice daily for seven days (total dose 7 g) [7].
Sexual partner(s) should be treated as well. If this regimen fails, tinidazole or metronidazole is administered
orally at a dose of 2 g per day for seven days (total dose 14 g). These regimens can be effective in patients with
low levels of metronidazole resistance, which was noted in 4 percent of T. vaginalis isolates of women attending
sexually transmitted disease clinics in six cities in the United States [109].

● Refractory or resistant infection – If both of the above regimens fail, the Centers for Disease Control and
Prevention (CDC) recommends in vitro culture and drug susceptibility testing (available from the CDC Division of
STD Prevention, telephone 404-718-4141) and referral to a specialist. For patients with documented refractory
infection, therapeutic options include maximum tolerated doses of oral tinidazole (2 to 3 g daily in divided
doses) for 14 days. Considerable success with tinidazole in refractory disease has been reported, although the
optimal dose has not been established [110,111]. One woman with confirmed metronidazole and tinidazole
resistant trichomoniasis was successfully treated with high-dose tinidazole, 1 gm three time a day for 14 days,
and intravaginal boric acid, 600 mg, twice daily for 28 days [112].

Metronidazole-resistant T. vaginalis has been documented [113,114]. Cross resistance to tinidazole is frequent
but not inevitable [113,115]. Patients with high-level metronidazole resistance are usually successfully treated
by prolonged and high-dose tinidazole therapy. High-dose tinidazole has a better safety profile and is better
tolerated than high-dose metronidazole. Case reports have described successful use of nimorazole, ornidazole,
niridazole, furazolidone, and hamycin [53], whereas a trial of nitazoxanide in three women with difficult to
eradicate T. vaginalis reported lack of efficacy [116].

Rare patients who do not have a response to nitroimidazoles have been treated with topical paromomycin (250
mg daily for two weeks) [117]. Paromomycin is not available commercially in the United States as a cream and
has to be made by a compounding pharmacy. Little is known about this preparation, but severe local side
effects (pain, mucosal ulceration) can occur [118]. We advise not using it. Other topical agents that have a
limited (<50 percent) cure rate and therefore are not recommended by the CDC include intravaginal povidone-
iodine, clotrimazole, acetic acid, gentian violet, nonoxynol-9, and potassium permanganate [7].

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around the world are
provided separately. (See "Society guideline links: Sexually transmitted infections".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient
education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five
key questions a patient might have about a given condition. These articles are best for patients who want a general
overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.

[Link] 12/24
23/3/2021 Trichomoniasis - UpToDate

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: Trichomoniasis (The Basics)")

RESOURCES FOR PATIENTS AND CLINICIANS

The following organizations provide information for patients and clinicians at no cost.

● Division of STD Prevention (DSTDP) Centers for Disease Control and Prevention
● American Sexual Health Association (ASHA)
● Planned Parenthood

SUMMARY AND RECOMMENDATIONS

● Trichomoniasis is caused by the protozoa Trichomonas vaginalis. It is virtually always sexually transmitted and
can be identified in 70 percent of the male sexual partners of infected females. Coinfection with other sexually
transmitted diseases (STDs) and bacterial vaginosis is common. (See 'Microbiology and transmission' above.)

● Untreated trichomonal vaginitis may progress to urethritis or cervicitis. T. vaginalis has been associated with a
range of adverse reproductive health outcomes, including cervical neoplasia, posthysterectomy cuff cellulitis or
abscess, atypical pelvic inflammatory disease, infertility, and preterm birth. It may also increase females'
susceptibility to HIV-1 infection. (See 'Clinical features and consequences' above.)

● Clinical manifestations in females range from an asymptomatic carrier state to an acute, severe inflammatory
disease. Signs and symptoms include a purulent, malodorous, thin discharge with associated burning, pruritus,
dysuria, frequency, and dyspareunia. Males are often asymptomatic, but have developed urethritis.
Asymptomatic carriage can persist for prolonged periods of time (at least three months); thus, it is often not
possible to ascertain when or from whom the infection was acquired. (See 'Clinical features and consequences'
above.)

● The diagnosis of T. vaginalis is based on laboratory testing (motile trichomonads on wet mount ( picture 2),
positive culture, positive nucleic acid amplification test [NAAT], or positive rapid antigen or nucleic acid probe
test). None of the clinical features of trichomoniasis is sufficiently sensitive or specific to allow a diagnosis based
upon signs and symptoms alone. We suggest NAAT (if available) in patients with suggestive clinical findings (eg,
elevated vaginal pH, increased numbers of polymorphonuclear leukocytes but an absence of motile
trichomonads and clue cells on wet mount) or when microscopy is unavailable or unreliable. (See 'Diagnosis'
above.)

● If NAAT for trichomoniasis is not available, rapid antigen tests or DNA hybridization probes for diagnosis of T.
vaginalis are commercially available and can be used as an alternative to NAAT or culture. (See 'Rapid antigen
and DNA hybridization probes' above.)

● Treatment is indicated for both symptomatic and asymptomatic females and males. Treatment reduces the
prevalence of T. vaginalis carriage in the population, relieves symptoms, and reduces the risk of sequelae
(including acquisition/transmission of HIV). For nonpregnant females and their sex partners, we suggest a

[Link] 13/24
23/3/2021 Trichomoniasis - UpToDate

seven-day course of metronidazole, 500 mg twice daily (Grade 2C). The single-dose regimen is a reasonable
alternative for those who are unable to complete a seven-day treatment regimen or who prefer single-day
treatment. Oral administration is significantly more effective than topical administration. (See '5-nitroimidazole
drugs' above.)

● Patients should be screened for other sexually transmitted infections (STIs). (See "Screening for sexually
transmitted infections".)

● Although expedited partner therapy (EPT) is effective for treatment of Trichomonas infections, we prefer that
sexual partners be evaluated so they can be screened for other STIs. However, EPT is reasonable if compliance
is an issue. (See 'Treatment of sex partners' above.)

● We recommend treating symptomatic pregnant females with confirmed T. vaginalis infections (Grade 1B). In
addition, we suggest treating asymptomatic pregnant individuals with confirmed infection (Grade 2B). We
prefer the seven-day regimen and reserve the single-dose regimen for patients who are unable to complete a
seven-day treatment course. (See 'Pregnant individuals' above.)

● For HIV-positive females with T. vaginalis, we suggest metronidazole 500 mg twice per day for seven days rather
than single-dose therapy (Grade 2B). (See 'HIV-infected females' above.)

● For patients with refractory trichomoniasis, increasing the dose and duration of metronidazole or tinidazole are
the primary options. (See 'Refractory cases' above.)

● Patients should be instructed to avoid intercourse until they and their partners have completed treatment and
are asymptomatic, which generally takes approximately one week. (See 'Counseling' above.)

● Females treated for a documented trichomonal infection are retested within three months following treatment
regardless of whether they believe their sex partners were treated. Testing with NAAT can be done as soon as
two weeks after completing treatment. (See 'Follow-up' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Kissinger P. Epidemiology and treatment of trichomoniasis. Curr Infect Dis Rep 2015; 17:484.

2. Anderson MR, Klink K, Cohrssen A. Evaluation of vaginal complaints. JAMA 2004; 291:1368.
3. Maritz JM, Land KM, Carlton JM, Hirt RP. What is the importance of zoonotic trichomonads for human health?
Trends Parasitol 2014; 30:333.

4. Petrin D, Delgaty K, Bhatt R, Garber G. Clinical and microbiological aspects of Trichomonas vaginalis. Clin
Microbiol Rev 1998; 11:300.

5. Trichomoniasis- CDC Fact Sheet. Centers for Disease Control and Prevention. January 31, 2017. [Link]/st
d/trichomonas/[Link] (Accessed on March 05, 2018).

6. Crucitti T, Jespers V, Mulenga C, et al. Non-sexual transmission of Trichomonas vaginalis in adolescent girls
attending school in Ndola, Zambia. PLoS One 2011; 6:e16310.

7. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment
guidelines, 2015. MMWR Recomm Rep 2015; 64:1.

[Link] 14/24
23/3/2021 Trichomoniasis - UpToDate

8. Mayer KH, Bush T, Henry K, et al. Ongoing sexually transmitted disease acquisition and risk-taking behavior
among US HIV-infected patients in primary care: implications for prevention interventions. Sex Transm Dis
2012; 39:1.

9. Kelley CF, Rosenberg ES, OʼHara BM, et al. Prevalence of urethral Trichomonas vaginalis in black and white men
who have sex with men. Sex Transm Dis 2012; 39:739.

10. Hesseltine H. Experimental human vaginal trichomoniasis. J Infect Dis 1942; 71:127.

11. Sobel JD, Subramanian C, Foxman B, et al. Mixed vaginitis-more than coinfection and with therapeutic
implications. Curr Infect Dis Rep 2013; 15:104.

12. Gaydos CA, Beqaj S, Schwebke JR, et al. Clinical Validation of a Test for the Diagnosis of Vaginitis. Obstet
Gynecol 2017; 130:181.

13. Torrone EA, Morrison CS, Chen PL, et al. Prevalence of sexually transmitted infections and bacterial vaginosis
among women in sub-Saharan Africa: An individual participant data meta-analysis of 18 HIV prevention studies.
PLoS Med 2018; 15:e1002511.

14. Global incidence and prevalence of selected curable sexually transmitted infections - 2008. World Health Organi
zation. [Link] (Accessed on March 05, 201
8).

15. Sutton M, Sternberg M, Koumans EH, et al. The prevalence of Trichomonas vaginalis infection among
reproductive-age women in the United States, 2001-2004. Clin Infect Dis 2007; 45:1319.

16. Flagg EW, Meites E, Phillips C, et al. Prevalence of Trichomonas vaginalis Among Civilian, Noninstitutionalized
Male and Female Population Aged 14 to 59 Years: United States, 2013 to 2016. Sex Transm Dis 2019; 46:e93.

17. Ginocchio CC, Chapin K, Smith JS, et al. Prevalence of Trichomonas vaginalis and coinfection with Chlamydia
Trachomatis and neisseria gonorrhoeae in the United States as determined by the Aptima Trichomonas
vaginalis nucleic acid amplification assay. J Clin Microbiol 2012; 50:2601.

18. Schwebke J, Merriweather A, Massingale S, et al. Screening for Trichomonas vaginalis in a Large High-Risk
Population: Prevalence Among Men and Women Determined by Nucleic Acid Amplification Testing. Sex Transm
Dis 2018; 45:e23.

19. Meites E, Llata E, Braxton J, et al. Trichomonas vaginalis in selected US sexually transmitted disease clinics:
Testing, screening, and prevalence. Sex Transm Dis 2013; 40:865.

20. Stemmer SM, Mordechai E, Adelson ME, et al. Trichomonas vaginalis is most frequently detected in women at
the age of peri-/premenopause: an unusual pattern for a sexually transmitted pathogen. Am J Obstet Gynecol
2018; 218:328.e1.

21. Seña AC, Miller WC, Hobbs MM, et al. Trichomonas vaginalis infection in male sexual partners: Implications for
diagnosis, treatment, and prevention. Clin Infect Dis 2007; 44:13.

22. Gaydos CA, Barnes MR, Quinn N, et al. Trichomonas vaginalis infection in men who submit self-collected penile
swabs after internet recruitment. Sex Transm Infect 2013; 89:504.

23. d'Oro LC, Parazzini F, Naldi L, La Vecchia C. Barrier methods of contraception, spermicides, and sexually
transmitted diseases: A review. Genitourin Med 1994; 70:410.

24. Trichomoniasis- CDC Fact Sheet. National Center for HI/AIDS, Viral Hepatitis, STD, and TB Prevention. Division of
STD Prevention. Centers for Disease Control and Prevention. July 2017. [Link]/std/trichomonas/Trichom
[Link] (Accessed on March 05, 2018).

[Link] 15/24
23/3/2021 Trichomoniasis - UpToDate

25. Landers DV, Wiesenfeld HC, Heine RP, et al. Predictive value of the clinical diagnosis of lower genital tract
infection in women. Am J Obstet Gynecol 2004; 190:1004.

26. Heine P, McGregor JA. Trichomonas vaginalis: A reemerging pathogen. Clin Obstet Gynecol 1993; 36:137.

27. Cotch MF, Pastorek JG 2nd, Nugent RP, et al. Trichomonas vaginalis associated with low birth weight and
preterm delivery. The Vaginal Infections and Prematurity Study Group. Sex Transm Dis 1997; 24:353.

28. Van Der Pol B, Kraft CS, Williams JA. Use of an adaptation of a commercially available PCR assay aimed at
diagnosis of chlamydia and gonorrhea to detect Trichomonas vaginalis in urogenital specimens. J Clin Microbiol
2006; 44:366.

29. Van Der Pol B, Williams JA, Orr DP, et al. Prevalence, incidence, natural history, and response to treatment of
Trichomonas vaginalis infection among adolescent women. J Infect Dis 2005; 192:2039.

30. Fouts AC, Kraus SJ. Trichomonas vaginalis: Reevaluation of its clinical presentation and laboratory diagnosis. J
Infect Dis 1980; 141:137.

31. Zhang ZF, Begg CB. Is Trichomonas vaginalis a cause of cervical neoplasia? Results from a combined analysis of
24 studies. Int J Epidemiol 1994; 23:682.

32. Yap EH, Ho TH, Chan YC, et al. Serum antibodies to Trichomonas vaginalis in invasive cervical cancer patients.
Genitourin Med 1995; 71:402.

33. Soper DE, Bump RC, Hurt WG. Bacterial vaginosis and trichomoniasis vaginitis are risk factors for cuff cellulitis
after abdominal hysterectomy. Am J Obstet Gynecol 1990; 163:1016.

34. Moodley P, Wilkinson D, Connolly C, et al. Trichomonas vaginalis is associated with pelvic inflammatory disease
in women infected with human immunodeficiency virus. Clin Infect Dis 2002; 34:519.

35. Wiringa AE, Ness RB, Darville T, et al. Trichomonas vaginalis, endometritis and sequelae among women with
clinically suspected pelvic inflammatory disease. Sex Transm Infect 2020; 96:436.

36. Grodstein F, Goldman MB, Cramer DW. Relation of tubal infertility to history of sexually transmitted diseases.
Am J Epidemiol 1993; 137:577.

37. Laga M, Manoka A, Kivuvu M, et al. Non-ulcerative sexually transmitted diseases as risk factors for HIV-1
transmission in women: Results from a cohort study. AIDS 1993; 7:95.

38. Sorvillo F, Kerndt P. Trichomonas vaginalis and amplification of HIV-1 transmission. Lancet 1998; 351:213.

39. McClelland RS, Sangare L, Hassan WM, et al. Infection with Trichomonas vaginalis increases the risk of HIV-1
acquisition. J Infect Dis 2007; 195:698.

40. Wang CC, McClelland RS, Reilly M, et al. The effect of treatment of vaginal infections on shedding of human
immunodeficiency virus type 1. J Infect Dis 2001; 183:1017.

41. Kissinger P, Amedee A, Clark RA, et al. Trichomonas vaginalis treatment reduces vaginal HIV-1 shedding. Sex
Transm Dis 2009; 36:11.

42. Mostad SB, Overbaugh J, DeVange DM, et al. Hormonal contraception, vitamin A deficiency, and other risk
factors for shedding of HIV-1 infected cells from the cervix and vagina. Lancet 1997; 350:922.

43. Kissinger P, Adamski A. Trichomoniasis and HIV interactions: A review. Sex Transm Infect 2013; 89:426.

44. Mann JR, McDermott S, Gill T. Sexually transmitted infection is associated with increased risk of preterm birth in
South Carolina women insured by Medicaid. J Matern Fetal Neonatal Med 2010; 23:563.

45. Mann JR, McDermott S, Barnes TL, et al. Trichomoniasis in pregnancy and mental retardation in children. Ann
Epidemiol 2009; 19:891.

[Link] 16/24
23/3/2021 Trichomoniasis - UpToDate

46. Mann JR, McDermott S. Are maternal genitourinary infection and pre-eclampsia associated with ADHD in
school-aged children? J Atten Disord 2011; 15:667.

47. Mann JR, McDermott S, Gregg A, Gill TJ. Maternal genitourinary infection and small for gestational age. Am J
Perinatol 2009; 26:667.

48. Silver BJ, Guy RJ, Kaldor JM, et al. Trichomonas vaginalis as a cause of perinatal morbidity: A systematic review
and meta-analysis. Sex Transm Dis 2014; 41:369.

49. Smith LM, Wang M, Zangwill K, Yeh S. Trichomonas vaginalis infection in a premature newborn. J Perinatol
2002; 22:502.

50. Temesvári P, Kerekes A, Tege A, Szarka K. Demonstration of Trichomonas vaginalis in tracheal aspirates in
infants with early respiratory failure. J Matern Fetal Neonatal Med 2002; 11:347.

51. Hoffman DJ, Brown GD, Wirth FH, et al. Urinary tract infection with Trichomonas vaginalis in a premature
newborn infant and the development of chronic lung disease. J Perinatol 2003; 23:59.

52. Carter JE, Whithaus KC. Neonatal respiratory tract involvement by Trichomonas vaginalis: A case report and
review of the literature. Am J Trop Med Hyg 2008; 78:17.

53. Cudmore SL, Delgaty KL, Hayward-McClelland SF, et al. Treatment of infections caused by metronidazole-
resistant Trichomonas vaginalis. Clin Microbiol Rev 2004; 17:783.

54. LANCELEY F, MCENTEGART MG. Trichomonas vaginalis in the male; the experimental infection of a few
volunteers. Lancet 1953; 1:668.

55. Vaginitis in Nonpregnant Patients: ACOG Practice Bulletin, Number 215. Obstet Gynecol 2020; 135:e1.

56. Krieger JN, Tam MR, Stevens CE, et al. Diagnosis of trichomoniasis. Comparison of conventional wet-mount
examination with cytologic studies, cultures, and monoclonal antibody staining of direct specimens. JAMA 1988;
259:1223.

57. Stoner KA, Rabe LK, Meyn LA, Hillier SL. Survival of Trichomonas vaginalis in wet preparation and on wet
mount. Sex Transm Infect 2013; 89:485.

58. Kingston MA, Bansal D, Carlin EM. 'Shelf life' of Trichomonas vaginalis. Int J STD AIDS 2003; 14:28.

59. Perl G. Errors in the diagnosis of trichomonas vaginalis infections as observed among 1199 patients. Obstet
Gynecol 1972; 39:7.

60. Miller JM, Binnicker MJ, Campbell S, et al. A Guide to Utilization of the Microbiology Laboratory for Diagnosis of
Infectious Diseases: 2018 Update by the Infectious Diseases Society of America and the American Society for
Microbiology. Clin Infect Dis 2018; 67:e1.

61. Coorevits L, Traen A, Bingé L, et al. Identifying a consensus sample type to test for Chlamydia trachomatis,
Neisseria gonorrhoeae, Mycoplasma genitalium, Trichomonas vaginalis and human papillomavirus. Clin
Microbiol Infect 2018; 24:1328.

62. Nye MB, Schwebke JR, Body BA. Comparison of APTIMA Trichomonas vaginalis transcription-mediated
amplification to wet mount microscopy, culture, and polymerase chain reaction for diagnosis of trichomoniasis
in men and women. Am J Obstet Gynecol 2009; 200:188.e1.

63. Andrea SB, Chapin KC. Comparison of Aptima Trichomonas vaginalis transcription-mediated amplification
assay and BD affirm VPIII for detection of T. vaginalis in symptomatic women: Performance parameters and
epidemiological implications. J Clin Microbiol 2011; 49:866.
64. Chapin K, Andrea S. APTIMA® Trichomonas vaginalis, a transcription-mediated amplification assay for
detection of Trichomonas vaginalis in urogenital specimens. Expert Rev Mol Diagn 2011; 11:679.
[Link] 17/24
23/3/2021 Trichomoniasis - UpToDate

65. Schwebke JR, Hobbs MM, Taylor SN, et al. Molecular testing for Trichomonas vaginalis in women: Results from a
prospective U.S. clinical trial. J Clin Microbiol 2011; 49:4106.
66. Schwebke JR, Gaydos CA, Nyirjesy P, et al. Diagnostic Performance of a Molecular Test versus Clinician
Assessment of Vaginitis. J Clin Microbiol 2018; 56.

67. Huppert JS, Batteiger BE, Braslins P, et al. Use of an immunochromatographic assay for rapid detection of
Trichomonas vaginalis in vaginal specimens. J Clin Microbiol 2005; 43:684.
68. Jones HE, Lippman SA, Caiaffa-Filho HH, et al. Performance of a rapid self-test for detection of Trichomonas
vaginalis in South Africa and Brazil. J Clin Microbiol 2013; 51:1037.

69. Campbell L, Woods V, Lloyd T, et al. Evaluation of the OSOM Trichomonas rapid test versus wet preparation
examination for detection of Trichomonas vaginalis vaginitis in specimens from women with a low prevalence
of infection. J Clin Microbiol 2008; 46:3467.

70. Gaydos CA, Klausner JD, Pai NP, et al. Rapid and point-of-care tests for the diagnosis of Trichomonas vaginalis in
women and men. Sex Transm Infect 2017; 93:S31.

71. Huppert JS, Mortensen JE, Reed JL, et al. Rapid antigen testing compares favorably with transcription-mediated
amplification assay for the detection of Trichomonas vaginalis in young women. Clin Infect Dis 2007; 45:194.

72. Levi MH, Torres J, Piña C, Klein RS. Comparison of the InPouch TV culture system and Diamond's modified
medium for detection of Trichomonas vaginalis. J Clin Microbiol 1997; 35:3308.

73. Borchardt KA, Zhang MZ, Shing H, Flink K. A comparison of the sensitivity of the InPouch TV, Diamond's and
Trichosel media for detection of Trichomonas vaginalis. Genitourin Med 1997; 73:297.

74. Lara-Torre E, Pinkerton JS. Accuracy of detection of trichomonas vaginalis organisms on a liquid-based
papanicolaou smear. Am J Obstet Gynecol 2003; 188:354.

75. Wiese W, Patel SR, Patel SC, et al. A meta-analysis of the Papanicolaou smear and wet mount for the diagnosis
of vaginal trichomoniasis. Am J Med 2000; 108:301.

76. Bandea CI, Joseph K, Secor EW, et al. Development of PCR assays for detection of Trichomonas vaginalis in
urine specimens. J Clin Microbiol 2013; 51:1298.

77. Sobel JD. Vulvovaginitis in healthy women. Compr Ther 1999; 25:335.

78. Chirenje ZM, Dhibi N, Handsfield HH, et al. The Etiology of Vaginal Discharge Syndrome in Zimbabwe: Results
from the Zimbabwe STI Etiology Study. Sex Transm Dis 2018; 45:422.

79. Barry MS, Ba Diallo A, Diadhiou M, et al. Accuracy of syndromic management in targeting vaginal and cervical
infections among symptomatic women of reproductive age attending primary care clinics in Dakar, Senegal.
Trop Med Int Health 2018; 23:541.

80. Schwebke JR, Burgess D. Trichomoniasis. Clin Microbiol Rev 2004; 17:794.

81. Hager WD, Brown ST, Kraus SJ, et al. Metronidazole for vaginal trichomoniasis. Seven-day vs single-dose
regimens. JAMA 1980; 244:1219.

82. Manorama HT, Shenoy DR. Single-dose oral treatment of vaginal trichomoniasis with tinidazole and
metronidazole. J Int Med Res 1978; 6:46.

83. Forna F, Gülmezoglu AM. Interventions for treating trichomoniasis in women. Cochrane Database Syst Rev
2003; :CD000218.

84. Howe K, Kissinger PJ. Single-dose compared with multidose metronidazole for the treatment of Trichomoniasis
in women: A meta-analysis. Sex Transm Dis 2017; 44:29.

[Link] 18/24
23/3/2021 Trichomoniasis - UpToDate

85. Kissinger P, Muzny CA, Mena LA, et al. Single-dose versus 7-day-dose metronidazole for the treatment of
trichomoniasis in women: an open-label, randomised controlled trial. Lancet Infect Dis 2018; 18:1251.

86. Tidwell BH, Lushbaugh WB, Laughlin MD, et al. A double-blind placebo-controlled trial of single-dose
intravaginal versus single-dose oral metronidazole in the treatment of trichomonal vaginitis. J Infect Dis 1994;
170:242.

87. duBouchet L, Spence MR, Rein MF, et al. Multicenter comparison of clotrimazole vaginal tablets, oral
metronidazole, and vaginal suppositories containing sulfanilamide, aminacrine hydrochloride, and allantoin in
the treatment of symptomatic trichomoniasis. Sex Transm Dis 1997; 24:156.

88. Helms DJ, Mosure DJ, Secor WE, Workowski KA. Management of trichomonas vaginalis in women with
suspected metronidazole hypersensitivity. Am J Obstet Gynecol 2008; 198:370.e1.

89. Thin RN, Symonds MA, Booker R, et al. Double-blind comparison of a single dose and a five-day course of
metronidazole in the treatment of trichomoniasis. Br J Vener Dis 1979; 55:354.

90. Lossick JG. Treatment of sexually transmitted vaginosis/vaginitis. Rev Infect Dis 1990; 12 Suppl 6:S665.

91. Centers for Disease Control and Prevention. Expedited partner therapy in the management of sexually transmit
ted diseases. US Department of Health and Human Services; Atlanta, GA 2006.

92. Kissinger P, Schmidt N, Mohammed H, et al. Patient-delivered partner treatment for Trichomonas vaginalis
infection: A randomized controlled trial. Sex Transm Dis 2006; 33:445.

93. Williams CS, Woodcock KR. Do ethanol and metronidazole interact to produce a disulfiram-like reaction? Ann
Pharmacother 2000; 34:255.

94. Gupta NK, Woodley CL, Fried R. Effect of metronidazole on liver alcohol dehydrogenase. Biochem Pharmacol
1970; 19:2805.

95. National guideline for the management of Trichomonas vaginalis. Clinical Effectiveness Group (Association for
Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases). Sex Transm Infect 1999; 75
Suppl 1:S21.

96. Okun N, Gronau KA, Hannah ME. Antibiotics for bacterial vaginosis or Trichomonas vaginalis in pregnancy: A
systematic review. Obstet Gynecol 2005; 105:857.

97. Gülmezoglu AM, Azhar M. Interventions for trichomoniasis in pregnancy. Cochrane Database Syst Rev 2011;
:CD000220.

98. Mann JR, McDermott S, Zhou L, et al. Treatment of trichomoniasis in pregnancy and preterm birth: An
observational study. J Womens Health (Larchmt) 2009; 18:493.

99. Stringer E, Read JS, Hoffman I, et al. Treatment of trichomoniasis in pregnancy in sub-Saharan Africa does not
appear to be associated with low birth weight or preterm birth. S Afr Med J 2010; 100:58.

100. Koss CA, Baras DC, Lane SD, et al. Investigation of metronidazole use during pregnancy and adverse birth
outcomes. Antimicrob Agents Chemother 2012; 56:4800.

101. Drugs in Pregnancy and Lactation, 10, Briggs GG, Freeman RK (Eds), Wolters Kluwer Health, Philadelphia 2015.
p.905.

102. Goldenberg RL, Mwatha A, Read JS, et al. The HPTN 024 Study: The efficacy of antibiotics to prevent
chorioamnionitis and preterm birth. Am J Obstet Gynecol 2006; 194:650.

103. Passmore CM, McElnay JC, Rainey EA, D'Arcy PF. Metronidazole excretion in human milk and its effect on the
suckling neonate. Br J Clin Pharmacol 1988; 26:45.

[Link] 19/24
23/3/2021 Trichomoniasis - UpToDate

104. Drugs and Lactation Database (LactMed). Metronidazole. [Link]


~dNozos:1 (Accessed on February 13, 2013).

105. LactMed. [Link] (Accessed on June 15, 2017).

106. Kissinger P, Mena L, Levison J, et al. A randomized treatment trial: single versus 7-day dose of metronidazole for
the treatment of Trichomonas vaginalis among HIV-infected women. J Acquir Immune Defic Syndr 2010;
55:565.

107. Adamski A, Clark RA, Mena L, et al. The influence of ART on the treatment of Trichomonas vaginalis among HIV-
infected women. Clin Infect Dis 2014; 59:883.

108. Gatski M, Martin DH, Levison J, et al. The influence of bacterial vaginosis on the response to Trichomonas
vaginalis treatment among HIV-infected women. Sex Transm Infect 2011; 87:205.

109. Kirkcaldy RD, Augostini P, Asbel LE, et al. Trichomonas vaginalis antimicrobial drug resistance in 6 US cities, STD
Surveillance Network, 2009-2010. Emerg Infect Dis 2012; 18:939.

110. Sobel JD, Nyirjesy P, Brown W. Tinidazole therapy for metronidazole-resistant vaginal trichomoniasis. Clin Infect
Dis 2001; 33:1341.

111. Subramanian C, Sobel JD. A case of high-level metronidazole-resistant trichomoniasis in pregnancy successfully
treated. J Low Genit Tract Dis 2011; 15:248.

112. Salas A, Hamill MM, Tuddenham S. Nitroimidazole Resistance in Trichomonas vaginalis Infection: A Teachable
Moment. JAMA Intern Med 2019; 179:247.

113. Schwebke JR, Barrientes FJ. Prevalence of Trichomonas vaginalis isolates with resistance to metronidazole and
tinidazole. Antimicrob Agents Chemother 2006; 50:4209.

114. Dunne RL, Dunn LA, Upcroft P, et al. Drug resistance in the sexually transmitted protozoan Trichomonas
vaginalis. Cell Res 2003; 13:239.

115. Sobel JD, Nagappan V, Nyirjesy P. Metronidazole-resistant vaginal trichomoniasis--an emerging problem. N Engl
J Med 1999; 341:292.

116. Dan M, Sobel JD. Failure of nitazoxanide to cure trichomoniasis in three women. Sex Transm Dis 2007; 34:813.

117. Nyirjesy P, Weitz MV, Gelone SP, Fekete T. Paromomycin for nitroimidazole-resistant trichomonosis. Lancet
1995; 346:1110.

118. Poppe WA. Nitroimidazole-resistant vaginal trichomoniasis treated with paromomycin. Eur J Obstet Gynecol
Reprod Biol 2001; 96:119.
Topic 5453 Version 61.0

[Link] 20/24
23/3/2021 Trichomoniasis - UpToDate

GRAPHICS

Hemorrhages on cervix in trichomoniasis infection

Punctate hemorrhages on cervix.

Graphic 102398 Version 2.0

[Link] 21/24
23/3/2021 Trichomoniasis - UpToDate

Trichomonas vaginalis

High-power microscopy revealing Trichomonas vaginalis with easily identified flagella.

Courtesy of Jack D. Sobel, MD and William E. Secor.

Graphic 71667 Version 2.0

[Link] 22/24
23/3/2021 Trichomoniasis - UpToDate

Clinical findings in women with vaginitis

Vulvovaginal
Parameter Normal findings Bacterial vaginosis Trichomoniasis
candidiasis

Symptoms None or mild, transient Pruritus, soreness, Malodorous discharge, no Malodorous discharge,
dyspareunia dyspareunia burning, postcoital bleeding,
dyspareunia, dysuria

Signs Normal vaginal discharge Vulvar erythema and/or Off-white/gray thin discharge Thin green-yellow discharge,
consists of 1 to 4 mL fluid edema that coats the vagina vulvovaginal erythema
(per 24 hours), which is white Discharge may be white and
or transparent, thin or thick, clumpy and may or may not
and mostly odorless adhere to vagina

Vaginal pH 4.0 to 4.5 4.0 to 4.5 >4.5 5.0 to 6.0

Amine test Negative Negative Positive (in 70 to 80% of Often positive


patients)

Saline microscopy PMN:EC ratio <1; rods PMN:EC ratio <1; rods PMN:EC <1; loss of rods; PMN ++++; mixed flora;
dominate; squames +++ dominate; squames +++; increased coccobacilli; clue motile trichomonads
pseudohyphae (present in cells comprise at least 20% of (present in approximately
approximately 40% of epithelial cells (present in 60% of patients)
patients); budding yeast for >90% of patients)
nonalbicans Candida

10% potassium hydroxide Negative Pseudohyphae (in Negative Negative


microscopy approximately 70% of
patients)

Other tests – If microscopy nondiagnostic: Quantitative Gram stain (eg, If microscopy nondiagnostic:
Culture Nugent criteria, Hay/Ison Culture (eg, InPouch TV
DNA hybridization criteria) culture system)
probe (eg, Affirm VPIII) DNA hybridization probe (eg, Rapid antigen test (eg,
Affirm VPIII) OSOM Trichomonas
Rapid Test)
Culture of no value
Nucleic acid
amplification test (eg,
APTIMA Trichomonas
vaginalis test)
DNA Hybridization
probe (eg, Affirm VPIII)

Differential diagnosis Physiologic leukorrhea Contact irritant or allergic Elevated pH in Purulent vaginitis,
vulvar dermatitis, chemical trichomoniasis, atrophic desquamative inflammatory
irritation, focal vulvitis vaginitis, and desquamative vaginitis, atrophic vaginitis,
(vulvodynia) inflammatory vaginitis erosive lichen planus

PMN: polymorphonuclear leukocytes; EC: vaginal epithelial cells.

Graphic 68759 Version 14.0

[Link] 23/24
23/3/2021 Trichomoniasis - UpToDate

[Link] 24/24

You might also like