REVIEW

Trichomonas vaginalis as a Cause of Perinatal

Morbidity: A Systematic Review and Meta-Analysis
Bronwyn J. Silver, MPH,* Rebecca J. Guy, PhD, John M. Kaldor, PhD,
Muhammad S. Jamil, MPH, and Alice R. Rumbold, PhD
Abstract: Trichomonas vaginalis is the most common curable sexually
transmissible infection worldwide, with high rates in women of reproductive age. There have been inconsistent findings about the impact of
infection and its treatment in pregnancy. We conducted a meta-analysis
to determine the association between T. vaginalis and perinatal outcomes.
Electronic databases were searched to May 2013. Included studies reported perinatal outcomes in women infected and uninfected with T.
vaginalis. Meta-analysis calculated a pooled relative risk (RR) and 95%
confidence interval (CI) using either a fixed- or random-effects model.
Study bias was assessed using funnel plots. Of 178 articles identified,
11 studies met the inclusion criteria. The study populations, outcomes,
and quality varied. T. vaginalis in pregnancy was associated with an increased risk of preterm birth (RR, 1.42; 95% CI, 1.15Y1.75; 9 studies;
n = 81,101; I2 = 62.7%), preterm premature rupture of membranes
(RR, 1.41; 95% CI,1.10Y1.82; 2 studies; n = 14,843; I2 = 0.0%) and small
for gestational age infants (RR, 1.51; 95% CI,1.32Y1.73; 2 studies;
n = 14,843; I2 = 0.0%). Sensitivity analyses of studies that accounted for
coinfection with other sexually transmissible infection found a slightly
reduced RR of 1.34 for preterm birth (95% CI, 1.19Y1.51; 6 studies;
n = 72,077; I2 = 11.2%), and in studies where no treatment was confirmed, the RR was 1.83 (95% CI, 0.98Y3.41; 3 studies; n = 1795;
I2 = 22.3%). Our review provides strong evidence that T. vaginalis in
pregnancy is associated with an increased risk of preterm birth. Based
on fewer studies, there were also substantial increases in the risk of preterm premature rupture of membranes and small for gestational age
infants. Further studies that address the current gaps in evidence on
treatment effects in pregnancy are needed.

richomoniasis is a sexually transmissible infection (STI)

caused by the parasite Trichomonas vaginalis. It is the most
common curable STI worldwide.1 Prevalence of T. vaginalis is
consistently higher in women than in men and varies substantially across populations, showing a strong association with health
and social disadvantage.2,3 It affects women in their peak

reproductive years and has been estimated that up to 25 million

pregnant women globally are infected with T. vaginalis.4 In
women, common symptoms of trichomoniasis include vaginal
discharge and itching; however, many will have no symptoms.2
Research conducted in the 1980s found associations between trichomoniasis during pregnancy and adverse pregnancy
outcomes, including preterm birth,5 low birth weight (LBW),5,6
and premature rupture of membranes (PROM).7 This research
led to clinicians being encouraged to screen and treat infections
in pregnancy.8 However, findings were not consistent across all
studies. Also, in a randomized trial9 conducted in the late 1990s,
asymptomatic women assigned to treatment with metronidazole
found an increased risk of preterm birth than in the placebo
group. As a result of these studies, practice changed. Currently,
screening of asymptomatic women is not routinely recommended
during pregnancy, except in endemic or high-risk populations;
diagnostic testing is recommended in women who are symptomatic.10 Treatment with metronidazole in pregnancy is currently only advised in symptomatic cases or if asymptomatic,
after 37 weeks gestation.10
Questions still remain about the role of trichomoniasis
in perinatal morbidity. If the infection is indeed associated with
preterm birth or other morbidities, strategies need to be found to
detect and safely treat it. The studies that have found a relationship may have been compromised by confounding due to
one of the many factors that determine pregnancy outcome. On
the other hand, the apparently negative studies may have suffered from methodological problems such as misclassification
of infection status or outcome, both of which would have diluted any real effect. Given the diversity in research findings,
we undertook a systematic review of studies that investigated
preterm birth and other perinatal outcomes in pregnant women
infected with T. vaginalis and women who were uninfected.

METHODS
From the *Epidemiology and Health Systems Division, Menzies School of
Health Research, Darwin, Northern Territory, Australia; The Kirby
Institute, University of New South Wales (UNSW) Australia, Sydney,
New South Wales, Australia; and Robinson Institute, The University of
Adelaide, Adelaide, South Australia, Australia.

Conicts of Interest and Source of Funding: No conicts declared. This

work was nancially supported by the Australian National Health and
Medical Research Council, Grant No. 568971. The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript. The views expressed in this publication
are those of the authors and do not reect the views of National Health
and Medical Research Council.
Correspondence: Bronwyn Silver, MPH, PO Box 4066, Alice Springs, Northern
Territory 0870, Australia. E-mail: bronwyn.silver@menzies.edu.au.
Received for publication December 16, 2013, and accepted February 8, 2011.
Supplemental digital content is available for this article. Direct URL
citations appear in the printed text, and links to the digital les are
provided in the HTML text of this article on the journals Web site
(http://www.stdjournal.com).
DOI: 10.1097/OLQ.0000000000000134
Copyright * 2014 American Sexually Transmitted Diseases Association
All rights reserved.

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This review used the Preferred Reporting Items for Systematic Reviews and Meta Analyses guidelines,11 the Metaanalysis of Observational Studies in Epidemiology criteria,12
and the National Institute for Health and Clinical Excellence
guidelines.13

Search Strategy
We searched Medline, EMBASE, and BioMedCentral
to 16th May 2013 using the following terms: Trichomonas or
Trichomonas vaginalis AND adverse pregnancy outcome
or premature birth or premature delivery or premature labour or premature rupture of membranes or low birth weight
or intrauterine growth retardation or small for gestational age
or gestational age.

Study Selection
Studies were included if they were published before 16th
May 2013 and assessed 1 or more of the specified outcomes
in women with T. vaginalis and a control group of women
without the infection. The following perinatal outcomes were

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Silver et al.

considered: preterm birth, preterm PROM (PPROM), PROM,

LBW, small for gestational age (SGA) infant, stillbirth, neonatal
death, and postpartum endometritis. Only full-text Englishlanguage articles were included. Studies were excluded if they
did not present original data.
The titles and abstracts of all articles were reviewed. If
the abstract seemed to meet the inclusion criteria, the full-text
article was obtained and reviewed. Reference lists of publications were checked for other potentially relevant studies. Two
reviewers (B.S. and A.R.) undertook this process independently and then reached consensus on the final set of studies
for inclusion.

Data Collection, Synthesis, and

Statistical Analysis
For each study that met the inclusion criteria, information
was extracted on the year of study, study design, setting, study
population, methods of determining T. vaginalis status, study
outcomes, and statistical methods, including adjustment for potential confounders. Where relevant, authors were contacted to
provide missing or additional information.
For outcomes reported by 2 or more studies, we pooled
data to generate combined estimates of relative risk (RR). The
I2 test was used to estimate the proportion of total variability in
point estimates that could be attributed to heterogeneity other
than that due to chance. If the I2 value was less than 25%, we
used a fixed-effects meta-analysis to estimate the combined RR
(and 95% confidence interval [CI]), assuming that most between
study variability was due to chance.14 If the I2 value was 25%
to 75%, a random-effects meta-analysis was used. If the I2 value
was greater than 75%, the heterogeneity was considered too
great for a summary estimate to be calculated.15 Data were analyzed using STATA 11.2.16
The initial analyses included all studies. For the outcome
preterm birth, sensitivity analyses were carried out, which involved excluding studies with very low numbers of T. vaginalis
infection. Sensitivity analyses were also carried out to explore
the effect of coinfection with other STI and treatment of trichomoniasis. This involved analysis based on studies that had adjusted for STI coinfection, and separately, studies that specified
that no treatment was given during pregnancy.

Quality Appraisal and Assessment of

Publication Bias
The methodological quality of each study was independently reviewed by 2 authors (B.S. and A.R.) using the National
Institute for Health and Clinical Excellence guidelines.13 This
involved completing a checklist for each study design that evaluates 4 potential sources of bias: selection bias, performance
bias, attrition bias, and detection bias. For each type of bias,
the reviewers classified the study as one of the following: low,
high, or unclear/unknown risk of bias. An overall risk of bias
was determined independently by assessing the major direction
of bias and was then discussed and agreed on by 2 authors
(B.S. and A.R.). The potential presence of publication bias was
assessed using a funnel plot; asymmetry was evaluated visually.
We undertook a sensitivity analysis to investigate the impact of
removing any studies that seemed to be outliers in the funnel plot
analysis.

RESULTS

Study Characteristics
Table 1 describes the characteristics of included studies.
Briefly, the size of studies varied from 115 to 60,296 (median,
1038), with data collection spanning from 1973 to 2003. Only
one study focused on adolescents (defined as 13Y17 years),
the remaining studies recruited women of any reproductive
age (e.g., 13Y49 years).
Most (n = 7) studies were conducted in general antenatal clinics. Four studies classified their population as being
at high risk for adverse pregnancy outcomes, based on the presence of one or more of the following risk factors: young age
(G18 years), African American or Hispanic ethnicity, unmarried,
of low socioeconomic status, uninsured, or had a low income.
For the remaining studies, the study population included women
who were unselected in regard to risk of adverse pregnancy
outcome. Most (n = 8) studies excluded women with multiple pregnancies, and 4 studies included statistical adjustments
for a previous preterm birth. Of the 9 studies that reported on
preterm birth, 8 excluded multiple pregnancies, 2 excluded
women with an existing obstetric or medical condition known
to predict preterm birth, and 5 made adjustments to account
for differences in smoking and/or other recognized risk factors
for preterm birth.
The most frequently reported outcome was preterm
birth. Eight studies defined preterm birth as gestation less than
37 weeks and one study as gestation less than 36 weeks. Only
one study reported on preterm and very preterm birth. Four
studies reported on PROM and LBW. The remaining outcomes
were reported by 1 or 2 studies each. The methods used to estimate gestational age varied across the 11 studies (see Table S1,
http://links.lww.com/OLQ/A85), with the most frequently used
method being based on the date of the last menstrual period and
ultrasound (where available). Five studies did not provide any
information on method used.
The risk of methodological bias was rated as unclear for
most (n = 7) studies (Table S1, http://links.lww.com/OLQ/A85),
mostly due to a lack of information regarding performance and
detection bias. Three studies17Y19 were rated as being at low risk
for bias and one rated at high risk.20 A key issue was potential
confounding by other STI; coinfection was considered in the
analyses of 6 studies, no statistical adjustment was made in 4
studies, and it was unclear in 1 study. Three studies reported that
treatment was given to women with trichomoniasis (although
none reported the specific regimen), 4 studies stated that no
treatment was given, and a further 4 studies stated that it was
unclear whether treatment was given.
The timing of screening for trichomoniasis varied, with
2 studies collecting specimens during the first trimester only, 3
in the second only, 1 in the third trimester, 3 allowing for screening in any trimester, and 2 not stating when screening was done. In
2 studies, repeat specimens were collected on all women closer
to birth regardless of infection status, and in 1 study, positive
women only were repeat tested. The method of diagnosis was
microscopy in 4 studies, culture in 1, a combination of both in 5,
and unspecified in 1.

Perinatal Outcomes

Selection of Studies
The literature search identified 178 articles, of which 127
were excluded on the basis of information conveyed by the title

370

and abstract (Fig. 1). The remaining 51 articles were reviewed,

and of these, 12 reporting on 11 separate studies met the inclusion criteria (Fig. 1).

Nine studies (n = 81,001), including 4 cohort studies, reported on the RR of preterm birth. Because heterogeneity was
moderate (I2 = 62.7%, P = 0.006), a random-effects analysis

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T. vaginalis as a Cause of Perinatal Morbidity

Figure 1. Study selection process.

was used, giving a summary RR of 1.42 (95% CI, 1.15Y1.75;

P = 0.001; Fig. 2).
In the sensitivity analysis that excluded 2 studies21,22 with
very low numbers of women with trichomoniasis, the summary
RR for preterm birth was slightly lower, at 1.28, but remained
statistically significant (95% CI, 1.09Y1.51; P = 0.003; 7 studies;
n = 79,674; I2 = 45.2%). In the analyses that included the
6 studies (n = 20,646) that adjusted for STI coinfection (Table S1,
http://links.lww.com/OLQ/A85), the summary RR was 1.34 (95%
CI, 1.19Y1.51; P e 0.001; I2 = 11.2%). Restricting analyses to
the 3 studies (n = 1795) in which no treatment was provided for
trichomoniasis (Table S1, http://links.lww.com/OLQ/A85) gave
a summary RR of 1.82, which was not statistically significant
(95% CI, 0.98Y3.41; P = 0.058; I2 = 22.3%). A RR was not
calculated for studies of treated women, because in the included
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studies, it was unclear if all or only some participants were

treated.
Two cohort studies (n = 14,843) reported on PPROM. Because there was negligible heterogeneity (I2 = 0.0%, P = 0.859),
a fixed-effects analysis was used, giving a summary RR of 1.41
(95% CI, 1.10Y1.82; P = 0.007; Fig. 3). Four cohort studies
(n = 14,754) reported on PROM including 2 that found a statistically significant increase in risk and 1 that did not. For the
fourth study, the 2 women who were positive for T. vaginalis
both had PROM,21 so the RR could not be calculated. A summary RR could not be calculated because of a high level of
heterogeneity (I2 = 93.9%, P e 0.001).
Four studies reported on LBW (n = 16,908), including
2 that found a statistically significant increase in risk, but a summary RR was not calculated because of significant heterogeneity

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372

19

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India (hospital)

NR

Iran (hospital)

2001Y2003 Tanzania/Zambia/
Malawi (NR)
1996Y02 USA (STI clinic)

Sweden (Pap
smear registry)
2001Y2002 Austria
(community)
2002Y2003 Iran (hospital)
1985Y1993 USA (community
hospital/health
center)

1973Y00

NR

Secondary analysis
of RCT
Retrospective case
control
Prospective cohort

Population-based
data linkage
Subgroup analysis
of RCT
Prospective cohort
Secondary analysis
of RCT and cohort

250

115

PROM, PTB

PTB, LBW,

PTB, LBW

PPROM, PTB
PTB

PTB

PTB, SB, SGA

PROM

450

1531

2661

1223
1038

877

60,296

300

LBW, NND, PE,

13,816
PPROM, PROM,
PTB, SGA

PROM, PTB

LBW, PTB, SB

Outcomes

NR

24.2/21.7 (13Y49)

24/25* (21Y28)

24.5/25* (NR)
24/23.8 (13Y47)

28.9 (NR)

NR (915)

23.3/23.8* (NR)

NR

27 T 5.7 (17Y39)

16.6/16.5* (13Y17)

Mean Age
(Target population)

NR

Underserved, uninsured

95% received public

assisted health care
Ed: 7 y (mean)

NR
56/76% unmarried

NR

Ed: 30% 910 y, 19%

G5 y
NR

85% unmarried, all

poor SES
Predominately
lower SES
57% unmarried; Ed:
38% secondary,
20% college.

SES

93% black

Race and/or
Ethnicity

NR

NR

NR

NR
70% Non-Hispanic
white or Asian
30% African American

NR

NR

NR

38% Black
30% Hispanic
32% White

Predominately black

*Infected/Uninfected.
Author provided missing information.
Non-Hispanic white women/African American.
With outcome/without outcome.
NR indicates not reported; RCT = randomized controlled trial; PTB, preterm birth; SB, stillbirth; Ed, education; PE, postpartum endometritis; NND, neonatal death.

Rasti et al.21

Johnson et al.17

Stringer et al.43

Azargoon et al.
French et al.42

Kiss et al.22

Buchmayer et al.

18

Prospective cohort

Minkoff et al.

Mathai et al.20

Prospective cohort

Prospective cohort

USA (hospital)

Study
Design

Vaginal Infections 1984Y1989 USA (hospital)

and Prematurity
Study (VIPS)5,41

1982

1982

Country
(Setting)

Prospective cohort

Study
Year

Characteristics of Included Studies

USA (hospital)

Hardy et al.

Author(s)

TABLE 1.

G1

14.9

21.4

5.5
6.7

G1

G1

6.4

12.6

14.6

34.0

TV, %

Silver et al.

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T. vaginalis as a Cause of Perinatal Morbidity

Figure 2. Meta-analysis of the association between T. vaginalis and preterm birth.

(I2 = 77.5%, P = 0.004). Two studies reported on SGA infants (n =

72,077) with negligible heterogeneity (I2 = 0.0%, P = 0.631), so a
fixed-effect analysis was used, giving a summary RR of 1.51 (95%
CI, 1.32Y1.73; P e 0.001; Fig. 4).
Two studies (n = 74,569) reported on stillbirth including one that found a significant increase in risk, but no summary RR was calculated because of significant heterogeneity
(I2 = 90.0%, P = 0.002). One cohort study reported on the association between T. vaginalis and neonatal death and reported
a significant association (1.6% vs. 0.8%; P = 0.005; 13,816
women). One cohort study (n = 13,814) reported on the association between T. vaginalis and postpartum endometritis and
reported a significant difference between rates of 6.9% in infected women compared with 4.7% in uninfected women.

Publication Bias
A funnel plot to assess publication bias is presented in
Figure S1, http://links.lww.com/OLQ/A85. The graph plots the
log risk ratios for preterm birth against trial size as measured by
standard error of the log risk ratio. One study21 was removed
before the analysis due to small exposure numbers (n = 2). In
the bottom right quadrant, there is one small study with a large
standard error suggesting that the point estimate in this study
may be inflated, possibly because of poor methodological quality.
Of note, this study was removed in the sensitivity analyses
presented earlier. The plot also shows some asymmetry around
the log of the pooled estimate, with fewer studies with point
estimates below the pooled estimate and no studies in the bottom
left quadrant. This indicates that small studies demonstrating
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no association between trichomoniasis and preterm birth may

be missing.

DISCUSSION
To our knowledge, this is the first comprehensive review
and meta-analysis of the relationship between the presence of
infection with T. vaginalis and perinatal morbidity. The most
commonly reported end point, preterm birth, was 42% more
likely (95% CI, 15%Y75%) to occur in infected women. Based
on much fewer studies, there were also substantial increases in
the risk of PPROM (increase in risk, 41%; 95% CI, 10%Y82%)
and having a SGA baby (increase of 51%; 95% CI, 32%Y73%).
Because of insufficient data and/or concerns about heterogeneity, we were unable to draw reliable conclusions about the
impact of T. vaginalis on other outcomes including PROM,
LBW, still birth, neonatal death, or postpartum endometritis.
We followed a systematic process to identify studies and
extract data. It is nevertheless possible that we missed 1 or more
studies. Data were abstracted by 2 independent reviewers, to
minimize any subjectivity in coding. We also undertook a detailed assessment of the quality of each study.
There are several limitations. Moderate heterogeneity was
detected for the outcome preterm birth, and significant heterogeneity prevented a summary measure being calculated for several
important outcomes. The statistical heterogeneity found may
reflect differences in the design of eligible studies as well as
the characteristics of participants. The proportion of preterm
births in the control groups ranged from 5% to 33%, suggesting a
range in baseline maternal risk in eligible studies. There was

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Silver et al.

Figure 3. Meta-analysis of the association between T. vaginalis and preterm PROM.

Figure 4. Meta-analysis of the association between T. vaginalis and SGA.

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T. vaginalis as a Cause of Perinatal Morbidity

variation in the degree to which studies accounted for maternal

and fetal characteristics that predict preterm birth and other
potential confounders, either through the exclusion criteria or
through statistical adjustment.
The funnel plot generated for preterm birth (Figure S1,
http://links.lww.com/OLQ/A85) indicated that there may be
publication bias, such that small studies that failed to show an
association between trichomoniasis and preterm birth remain
unpublished. However, it is also possible that the asymmetry
seen in the plot could be due to differences in the characteristics
of women enrolled in the smaller and larger studies rather than
publication bias.
A major limitation in all of the eligible studies is the
potential misclassification of exposure to T. vaginalis (Table S1,
http://links.lww.com/OLQ/A85). All studies were conducted at
least 10 years ago and therefore depended on diagnostic techniques such as wet mount microscopy, which may have resulted
in an underdetection of T. vaginalis. The more recently developed
nucleic acid amplification assays have been shown to almost
double the detection of T. vaginalis compared with wet mount
microscopy.23 Further misclassification of exposure could arise
because of the timing of swab collection, which was mostly at
first visit or first trimester, and may have missed infection acquired subsequently.
Several of the included studies did not rule out coinfection with other STIs. In particular, bacterial vaginosis24 and
chlamydia25 have both been found to be strong risk factors for
preterm birth, and their presence is likely to be correlated with T.
vaginalis. However, in the sensitivity analyses that excluded
studies that did not account for STI coinfection, the pooled estimate for preterm birth did not change substantially. Therefore,
we believe that the observed effect for preterm birth is unlikely
to be explained by confounding due to the presence of other
infections.
Despite these potential limitations, the finding of a strong
relationship between trichomoniasis and preterm birth has very
substantial public health implications. Preterm birth is a leading
cause of infant mortality26 and has enduring consequences for
the health and development of surviving infants.27 The magnitude of the association between preterm birth and trichomoniasis
is similar to estimates for other major preventable risk factors
such as maternal smoking (odds ratio, 1.27; 95% CI, 1.21Y1.33)28
for which interventions have become routine in antenatal care.
The mechanisms underlying the association between trichomoniasis and preterm birth are not well understood but are likely
to be linked to a maternal innate immune inflammatory response
after infection. Elevated concentrations of cervical interleukin8 and vaginal defensins have been demonstrated in pregnant
women with asymptomatic trichomoniasis.29 Both are markers
of neutrophil activation, which has been associated with amniotic fluid infection, preterm birth, and preterm PROM.30Y32
In particular, cervicovaginal interleukin-8 is considered to
play a critical role in triggering cervical ripening and dilatation, by recruiting neutrophils to cervical tissue resulting in
the release of collagenase and elastase.33 Our study also found
an increased risk of SGA infants, of which the pathogenesis is
unknown and may be quite different to preterm birth. Although speculative, we suggest that trichomoniasis may result
in chronic low-grade intrauterine inflammation that interferes
with uteroplacental circulation.
Our findings raise important questions about the management of trichomoniasis in pregnancy. First, in settings of high
endemnicity, should all women be screened in pregnancy? If
so, should symptomatic and asymptomatic infected women be
treated? The importance of these questions becomes more
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pronounced with higher levels of T. vaginalis prevalence. To determine the ideal policy for screening in pregnancy, we must
consider prevalence, outcome, and treatment safety.
A single dose of 2 mg metronidazole provides parasitological cure34 and has not been associated with any teratogenic
effects in pregnancy,35 even when given in the first trimester.
However, concerns about the safety of treatment in pregnancy
arose after the publication of 2 studies a decade ago that reported
an increased risk of preterm birth and/or LBW associated with
metronidazole treatment. Both studies had potential methodological limitations. Klebanoff and colleagues9 administered a dose
4 times higher than the recommended regimen and the trial was
stopped early after reaching a third of the target sample when
an interim analysis revealed an increased risk of preterm birth in
the treatment arm. Kigozi and colleagues36 reported on a small
subgroup of women with trichomoniasis participating in a trial
of a combination of antimicrobials to prevent perinatal HIV transmission. Conversely, a recent chart review37 of metronidazole use
in pregnancy among 2829 women found no association with
preterm birth or LBW. There has been very little subsequent
research investigating appropriate strategies for managing trichomoniasis in pregnancy with most treatment studies focusing on
bacterial vaginosis,38 which is likely to elicit a different immunological response to T. vaginalis. Therefore, whether there are
indeed risks or benefits associated with treatment in pregnancy
remains unclear,39 and further studies are needed to answer this
important question40 to ensure clinical practice and guidelines are
supported by a solid evidence base.
Future research should be conducted in a high-prevalence
setting, where the impact of policy change will be greatest, and
there will be adequate numbers of infected women to provide
statistical accuracy. It is recommended that a trial of routine screening and treatment of T. vaginalis is conducted that includes either
a strict exclusion criteria for known confounders or, where unfeasible, statistical adjustment. Using a highly sensitive diagnostic technology such as nucleic acid amplification assays
would ensure all infections were detected. Swab collection at
multiple time points throughout pregnancy and measurement
of organism load would also need to be considered. Data should
be collected on a comprehensive range of perinatal outcomes,
and statistical approaches should be used to take account of
treatment of T. vaginalis and STI coinfection, in particular bacterial vaginosis.

CONCLUSIONS
Although our review provides strong evidence that T.
vaginalis in pregnancy is associated with preterm birth, there
remains a gap in evidence on treatment effects in pregnancy. If
treatment is found to be effective, this represents a significant
opportunity to make inroads into the prevention of perinatal
morbidity in populations where trichomoniasis is endemic. Preventing the acquisition of T. vaginalis, as well as early detection
and treatment, should remain a priority.
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