ArticlePDF Available

Trichomonas vaginalis in Sub-Saharan Africa: occurrence and diagnostic approaches for the male partner

26 | ISSN 1011 5528
Volume 27 No. 1 | June 2013
Medical Technology SA
Before the turn of the century, the World Health Organisation
(WHO) reported that amongst the set of curable sexually trans-
mitted infections (STI’s), there was an estimated 340 million
new cases annually amongst which, Trichomonas vaginalis was
recognised as the most common, with an overwhelming inci-
dence of approximately 174 million reported cases.[1] In 2010,
it was estimated that 32 million individuals suffering from tri-
chomoniasis were localised to Sub-Saharan Africa.[2]
Developing countries face the challenge of increasing rates
in the transmission of microorganisms causing asymptomatic
STI’s. Influential factors that have led to an increase in STI’s
amongst populations of developing countries have been identi-
fied as a combination of behavioural, socio-demographic and
economic. Inadequate health facilities[3], a lack of education[4],
alcohol and drug abuse, as well as multiple sexual partners[5]
have been recognised as significant contributing factors to the
increasing rate of trichomoniasis.[6] An additional cause behind
the increased rate of STI’s, specifically within South Africa, is
the common phenomenon of migration by men from rural to
urban areas for employment.[7] Male migrant workers have been
shown to have high levels of contact with sex workers, as well
as a greater number of casual sexual partners.[8] Over a three
year period, 50% of the male subjects attending the Steve Biko
Academic Hospital, Johannesburg, for an Assisted Reproduc-
tive Technology programme had semen samples which showed
significant levels of positive bacterial cultures.[9] In a study
which observed the occurrence of sexually transmitted bacteria
amongst 367 black South African men, it was shown that al-
most half of the subjects presented urine samples that displayed
infectious microorganisms.[10] Amongst African populations, T.
vaginalis is one of the top four most common bacteria identi-
fied in both male and female subjects which include; Candida
albicans, Neisseria gonorrhoea and Chlamydia trachomatis.[11]
T. vaginalis is an extracellular flagellated protozoan that can be
found in both the male and female urogenital tracts, whereby
it primarily infects the squamous epithelium. Trichomonal
cytopathogenicity has been recognised as a causative factor
behind nongonococcal urethritis and prostatitis in male sub-
jects.[12] The organism is localised to the genitourinary system
and the pathogen has been found in practically all sites of the
genitourinary systems in both sexes infected with T. vaginalis.[13]
Despite the fact that the clinical implications of trichomoniasis
in sexually active women are well known, the significance of
the pathogen T. vaginalis for the male partner is still relatively
uncertain.[14] Infection in the female is a causative factor behind
a number of conditions which include: pelvic inflammatory dis-
ease, cervicitis, urethritis, vaginitis as well as adverse pregnancy
outcomes and preterm delivery.[15, 16, 17] Bacterial colonisation of
the male genital tract (MGT) can result in a variety of clinical
manifestations such as; painful ejaculation, testicular sensitivity
and urethral discharge.[18] It is furthermore regarded as a con-
tributor of male factor infertility.[19] However, infection with T.
vaginalis complicates the diagnostic and treatment approach as
it presents asymptomatically in male subjects. A study which
isolated females with trichomoniasis and examined the sexual
partner’s urine and semen samples, showed that an overwhelm-
ing 72% of the men also tested positive for T. vaginalis despite
the fact that the majority showed no symptoms of the urethral
A link between trichomoniasis and the subsequent increased
risk for human immunodeficiency virus (HIV) infection has
sparked an increased focus on T. vaginalis.[21] With focus on the
infection and HIV amongst high risk population groups in Sub-
Saharan Africa, a bidirectional relationship has been shown to
exist.[22, 23] Research into the management of urethritis amongst
Malawian men showed that treatment of trichomoniasis with
metronidazole resulted in a decrease in the viral shedding of
HIV ribonucleic acid in semen samples.[24] Concomitant treat-
ment of sexual partners with metronidazole offers an avenue
of decreasing the transmission rate of the STI.[13] Considering
that trichomoniasis is asymptomatic, the need for an efficient
screening method in male partners is crucial in the public health
sector.[25] The efficacy of this approach was demonstrated by a
study in Tanzania, which showed that with rapid and aggressive
STI treatment intervention, a decrease in the transmission rate
of HIV was observed.[26] With Sub-Saharan Africa’s distressing
Peer reviewed 
Trichomonas vaginalis in Sub-Saharan africa: occurrence
and diagnoStic approacheS for the male partner
(BSc, HSc, MSc) |  (BSc, HSc, MSc, MBA, PhD)
Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, Tygerberg, South Africa
Corresponding author: Margot Flint | email: | +(27) 72 122 2111
The article aims to focus on trichomoniasis as to highlight the prevalence of this sexually transmitted infection (STI) within Sub-
Saharan Africa, and to introduce an alternative means of diagnosing the infection. Globally, trichomoniasis is the STI with the
highest burden in resource limited countries such as those in Sub-Saharan Africa; however, it is also the most common curable
condition. With challenges faced particularly in the context of South Africa’s public health sector, the implementation of affordable
and rapid point-of-care diagnostic tests could allow for a more effective strategy in recognising asymptomatic STI’s, where labora-
tory infrastructure is lacking.
Trichomonas vaginalis; trichomoniasis; sexually transmitted infections; human immunodeficiency virus; South Africa.
ISSN 1011 5528 | 27
Volume 27 No. 1 | June 2013
Medical Technology SA
increase in HIV, the identification and management of STI’s
has been postulated as the most effective means of slowing the
transmission rate.[27]
Over the past 150 years, the most common diagnostic method
employed for the identification of aerobic and microaerophilic
bacterial pathogens present in the MGT remains semen cul-
tures.[28, 29] The classification of semen samples as positive for
specific bacterial species is defined with a culture of >1 x 103
colony forming units/millilitre.[30] Agar plates which have been
utilised in studying bacterial species in semen include; MacCo-
nkey agar, blood agar, chocolate agar and Thayer Martin agar.
[31] Culture media, in particular the Diamonds’ medium deemed
the “gold standard”[13], has been considered as the reference
testing for T. vaginalis.[32] However, shortcomings in the tradi-
tional culture process have been recognised, which has led to
the development of enhanced methods of detecting bacterial
pathogens in the MGT.[29] A variety of techniques have since
been developed, for example: direct fluorescent antibody assay
(DFA), enzyme-linked immunoabsorbent assay (ELISA), nucleic
acid amplification test (NAAT) with polymerase chain reaction
(PCR), dot-immunobinding assay (DIBA) and the agglutination
test (AT).[33] With the application of sensitive molecular assays
amongst a group of asymptomatic men seeking fertility as-
sessment, a study showed an unpredicted high occurrence of
pathogens in the semen samples that were analysed.[34] Based
on past research reports such as the above, it is recognised that
there is a necessity for further investigations into more reliable,
inexpensive and convenient diagnostic approaches.
Diagnostic kits
The increasing focus on the pathogen’s involvement in the trans-
mission of HIV[35] and conditions such as perinatal morbidity
and preterm labour in the female subject[36, 37], led to the devel-
opment of more reliable, inexpensive and convenient diagnostic
tests which include: the InPouch® TV (BioMed Diagnostics), as
well as the immunochromatographic XenoStrip-Tv™ (Xenotope
Diagnostics). Research into the efficacy and sensitivity of the
XenoStrip-Tv™ has promoted the kit as a valuable approach
to identify possible trichomoniasis in settings whereby there
is a lack of resources and a need for “rapid point-of care” for
patients.[38, 39] These commercially available diagnostic kits offer
a minimally invasive manner in which to test for T. vaginalis as
urine can replace a urethral swab as the medium.[40] A study
which investigated the stability of T. vaginalis deoxyribonucleic
acid (DNA) for molecular testing when the urine samples were
exposed to varying time delays, showed that the DNA remained
stable over a period of 3 days when stored at 4°C[41], demon-
strating the relative stability of the DNA of the bacteria.
Molecular techniques
The use of PCR in comparison to cultures has been shown to
be significantly more sensitive as a diagnostic approach.[42] To
circumvent the time- and labour-intensive use of cultures to
diagnose a patient with a specific STI, PCR kits were devised
which utilize DNA hybridisation. The use of NAAT is an ex-
tremely sensitive and effective means of diagnosing infection
on several different clinical specimens.[13] It allows for an ELISA-
like system to detect the amplified plasmid DNA particular to a
pathogen.[43] This diagnostic alternative has been proven to have
a high sensitivity (92.7%) and specificity (88.6%) for detecting
T. vaginalis in urine samples from male subjects.[44] The advanta-
geous element to the use of PCR’s to detect the presence of a
cell is the sensitivity of the test, whereby a single nucleated cell
can be detected from a medium allowing for an efficient and
reliable test for possible pathogens.[45]
Despite a decrease in the incident rate in African populations[46,
47], South Africa still remains a populace with a high incident
rate of STI’s.[35] In resource-poor regions, the absence of labora-
tory diagnostic services furthers the predicament of the negative
impacts of STI’s.[3] It has been noted that the absence of routine
screening of patients for STI’s is a fundamental reason.[48] This
highlights the significant need for a logistical and user-friendly
approach to decrease the rate of STI contamination between
partners[9] which may also circumvent the related complica-
tions such as compromised fertility.[48] Within the South African
context, the predominant racial group of black and coloured
citizens also represent the sector of the population that are con-
strained by financial and other limitations which don’t allow for
easy access to health facilities.[48]
Despite comprehensive global studies on the incidence and
effects of STI’s, South Africa remains a country with a consider-
ably low number of studies and publications, highlighting the
need to urgently address the concern.[9] With the findings that
T. vaginalis facilitates the sexual transmission of HIV, a need
has arisen for a rapid and cost-effective detection method to
circumvent an increase in the infection rate in resource-limited
settings. As the STI is commonly asymptomatic amongst males,
there is a need for a reassessment of the identification of the
pathogen to decrease the transmission rate between partners.
1. W.H. Organisation. Global Prevalence and Incidence of
Selected Curable Sexually Transmitted Infections. Geneva: W.H.
Organisation Press; 2001.
2. W.H. Organisation. The world health report 1999: making a
difference. Geneva: W.H. Organisation Press; 2010.
3. Sena AC, Miller WC, Hobbs MM, Schwebke JR, Leone PA,
Swygard H, et al. Trichomonas vaginalis infection in male sexual
partners: implications for diagnosis, treatment, and prevention.
Clin Infect Dis 2007; 44(1):13-22.
4. Golshani M, Eslami G, Mohhammadzadeh Ghobadloo SH,
Fallah F, Goudarzi H Detection of Chlamydia trachomatis,
Mycoplasma hominis and Ureaplasma urealyticum by Multiplex
PCR in Semen Sample of Infertile Men. Iranian J Publ Health
2007; 36(2) 50-57.
5. Helms DJ, Mosure DJ, Metcalf CA, Douglas JM Jr, Malotte
CK, Paul SM, et al. Risk factors for prevalent and incident
Trichomonas vaginalis among women attending three sexu-
ally transmitted disease clinics. Sex Transm Diseases 2008;
6. Bowden FJ & Garnett GP. Trichomonas vaginalis epidemiology:
parameterising and analysing a model of treatment interven-
tions. Sex Transm Infect 2000; 76, 248–256.
7. Colvin M, Abdool Karim SS, Wilkinson D. Migration and AIDS.
Lancet 1995; 346(8985):1303-1304.
8. Carael M, Cleland J, Ingham R. Extramarital implications of
survey results for STD/HIV transmission: AIDS impact and pre-
vention in developing world: demographic and social science
perspectives. Health Transit Review 1994; 4:153-171.
9. Huyser C, Fourie J. Sperm only please: Prevention of infections
in an assisted reproduction laboratory in a developing country.
F, V & V in ObGyn 2010; 1:97-106.
10. Taylor-Robinson D, Horner PJ. The role of Mycoplasma
genitalium in non-gonococcal urethritis. Sex Transm Infect 2001;
11. Bambra CS. Current status of reproductive behaviour in Africa.
Hum Reprod Update 1999; 5(1):1-20.
28 | ISSN 1011 5528
Volume 27 No. 1 | June 2013
Medical Technology SA
12. Carlton JM, Hirt RP, Silva JC, Delcher AL, Schatz M, Zhao Q, et
al. Draft genome sequence of the sexually transmitted pathogen
Trichomonas vaginalis. Science 2007; 315(5809):207-212.
13. Swygard H, Sena AC, Hobbs MM, Cohen MS. Trichomoniasis:
clinical manifestations, diagnosis and management. Sex Transm
Infect 2004; 80(2):91-95.
14. Krieger JN, Ross SO, Riley DE. Chronic prostatitis: epidemiology
and role of infection. Urology 2002; 60(6):8-12
15. Pastorek JG, Cotch MF, Martin DH, Eschenbach DA. Clinical
and microbiological correlates of vaginal trichomoniasis during
pregnancy. Clin Infect Dis 1996; 23(5):1075-1080.
16. Cotch MF, Pastorek JG, 2nd, Nugent RP, Hillier SL, Gibbs RS,
Martin DH, et al. Trichomonas vaginalis associated with low
birth weight and preterm delivery. The Vaginal Infections and
Prematurity Study Group. Sex Transm Dis 1997; 24(6):353-360.
17. Minkoff HL, Eisenberger-Matityahu D, Feldman J, Burk R, Clarke
L. Prevalence and incidence of gynecologic disorders among
women infected with human immunodeficiency virus. Am J
Obstet Gynecol 1999; 180(4):824-836.
18. Bar-Chama N, Fisch H. Infection and pyospermia in male
infertility. World J Urol 1993; 11(2):76-81.
19. Lloyd G, Case JR, De Frias D, Brannigan RE. Trichomonas
vaginalis orchitis with associated severe oligoasthenoteratosper-
mia and hypogonadism. J Urol 2003; 170(3):924.
20. Hobbs MM, Lapple DM, Lawing LF, Schwebke JR, Cohen
MS, Swygard H, et al. Methods for detection of Trichomonas
vaginalis in the male partners of infected women: implica-
tions for control of trichomoniasis. J Clin Microbiol 2006;
21. Rothenberg RB, Wasserheit JN, St Louis ME, Douglas JM. The
effect of treating sexually transmitted diseases on the transmis-
sion of HIV in dually infected persons: a clinic-based estimate.
Ad Hoc STD/HIV Transmission Group. Sex Transm Dis 2000;
22. Buve A, Weiss HA, Laga M, Van Dyck E, Musonda R, Zekeng L,
et al. The epidemiology of gonorrhoea, chlamydial infection and
syphilis in four African cities. AIDS 2001; 15(4):S79-88.
23. Mavedzenge SN, Pol BV, Cheng H, Montgomery ET, Blanchard
K, de Bruyn G, et al. Epidemiological synergy of Trichomonas
vaginalis and HIV in Zimbabwean and South African women.
Sex Transm Dis 2010; 37(7):460-466.
24. Price MA, Zimba D, Hoffman IF, Kaydos-Daniels SC, Miller WC,
Martinson F, et al. Addition of treatment for trichomoniasis to
syndromic management of urethritis in Malawi: a randomized
clinical trial. Sex Transm Dis 2003; 30(6):516-522.
25. Schwebke JR, Lawing LF. Improved detection by DNA amplifica-
tion of Trichomonas vaginalis in males. J Clin Microbiol 2002;
26. Grosskurth H, Mosha F, Todd J, Mwijarubi E, Klokke A, Senkoro
K, et al. Impact of improved treatment of sexually transmitted
diseases on HIV infection in rural Tanzania: randomised control-
led trial. Lancet 1995; 346(8974):530-536.
27. Grosskurth H, Gray R, Hayes R, Mabey D, Wawer M. Control of
sexually transmitted diseases for HIV-1 prevention: understand-
ing the implications of the Mwanza and Rakai trials. Lancet
2000; 355(9219):1981-1987.
28. Keck C, Gerber-Schafer C, Clad A, Wilhelm C, Breckwoldt M.
Seminal tract infections: impact on male fertility and treatment
options. Hum Reprod Update 1998; 4(6):891-903.
29. Lacroix JM, Jarvi K, Sukhsatej BD, Heritz DM, Mittelman MW.
PCR-based technique for the detection of bacteria in semen and
urine. J Microbiol Methods 1996; 26:61-71.
30. W.H. Organisation. WHO, WHO laboratory manual for the
examination and processing of human semen. 5th ed. Geneva.
2010. 5th ed. Geneva: W.H. Organisation Press
31. Gardner WA, Jr, Culberson DE, Bennett BD. Trichomonas
vaginalis in the prostate gland. Arch Pathol Lab Med 1986;
32. Lawing LF, Hedges SR, Schwebke JR. Detection of trichomonosis
in vaginal and urine specimens from women by culture and
PCR. J Clin Microbiol 2000; 38(10):3585-3588.
33. Patel SR, Wiese W, Patel SC, Ohl C, Byrd JC, Estrada CA.
Systematic review of diagnostic tests for vaginal trichomoniasis.
Infect Dis Obstet Gynecol 2000; 8:248-257.
34. Bezold G, Politch JA, Kiviat NB, Kuypers JM, Wolff H, Anderson
DJ. Prevalence of sexually transmissible pathogens in semen
from asymptomatic male infertility patients with and without
leukocytospermia. Fertil Steril 2007; 87(5):1087-1097.
35. Johnston VJ, Mabey DC. Global epidemiology and control of
Trichomonas vaginalis. Curr Opin Infect Dis 2008; 21(1):56-64.
36. Gram IT, Macaluso M, Churchill J, Stalsberg H. Trichomonas
vaginalis (TV) and human papillomavirus (HPV) infection and
the incidence of cervical intraepithelial neoplasia (CIN) grade III.
Cancer Causes Control 1992; 3(3):231-236.
37. Petrin D, Delgaty K, Bhatt R, Garber G. Clinical and microbio-
logical aspects of Trichomonas vaginalis. Clin Microbiol Rev
1998; 11(2):300-317.
38. Pillay A, Lewis J, Ballard RC. Evaluation of Xenostrip-Tv, a
rapid diagnostic test for Trichomonas vaginalis infection. J Clin
Microbiol 2004; 42(8):3853-3856.
39. Maraghi S, Khosravi A, Kardooni T, Razi T, Feiz-Haddad MH.
Evaluation of an Immunochromatographic Strip (Xenostrip –Tv)
Test for Diagnosis of Vaginal Trichomoniasis Compared with Wet
Mount and PCR Assay. Iranian J Parasitol 2008; 170(3):11-17.
40. 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(2):366-373.
41. Ingersoll J, Bythwood T, Abdul-Ali D, Wingood GM, Diclemente
RJ, Caliendo AM. Stability of Trichomonas vaginalis DNA in
urine specimens. J Clin Microbiol 2008; 46(5):1628-1630.
42. Pillay A, Radebe F, Fehler G, Htun Y, Ballard RC. Comparison
of a TaqMan-based real-time polymerase chain reaction with
conventional tests for the detection of Trichomonas vaginalis.
Sex Transm Infect 2007; 83(2):126-129.
43. Karch H, Schwarzkofk A, Schmidt H. Amplification methods in
diagnostic bacteriology (selected examples). J Microbial Method
1995; 23(1):55-73.
44. Kaydos-Daniels SC, Miller WC, Hoffman I, Banda T, Dzinyemba
W, Martinson F, Cohen MS, Hobbs MM. Validation of a urine-
based PCR-enzyme-linked immunosorbent assay for use in
clinical research settings to detect Trichomonas vaginalis in
men. J Clin Microbiol 2003; 41:318-323.
45. Gdoura R, Kchaou W, Chaari C, Znazen A, Keskes L, Rebai T, et
al. Ureaplasma urealyticum, Ureaplasma parvum, Mycoplasma
hominis and Mycoplasma genitalium infections and semen
quality of infertile men. BMC Infect Dis 2007; 7:1-9.
46. Taha TE, Dallabetta GA, Hoover DR, Chiphangwi JD, Mti-
mavalye LA, Liomba GN, et al. Trends of HIV-1 and sexually
transmitted diseases among pregnant and postpartum women in
urban Malawi. AIDS 1998; 22; 12(2):197-203.
47. Creek TL, Thuku H, Kolou B, Rahman M, Kilmarx PH. Declin-
ing syphilis prevalence among pregnant women in northern
Botswana: an encouraging sign for the HIV epidemic? Sex
Transm Infect 2005; 81(6):453-5.
48. Pham-Kanter GB, Steinberg MH, Ballard RC. Sexually transmit-
ted diseases in South Africa. Genitourin Med 1996; 72(3):160-
... Sub-Sahara Africa (SSA) is burdened with a high incidence of parasitic infections, including schistosomiasis, trypanosomiasis, trichomoniasis, and leishmaniasis [1][2][3]. Currently, there is a rapid widespread development of resistance to prescription drugs for these parasitic neglected tropical diseases (pNTDs) [4][5][6][7][8]. The available number of drugs for treatment is exceptionally low and each of these has been under prescription for periods of no less than 30 years [9]. ...
Full-text available
A new alkaloid paenidigyamycin A (1) was obtained from the novel Ghanaian Paenibacillus sp. isolated from the mangrove rhizosphere soils of the Pterocarpus santalinoides tree growing in the wetlands of the Digya National Park, Ghana. Compound 1 was isolated on HPLC at tR = 37.0 min and its structure determined by MS, 1D, and 2D-NMR data. When tested against L. major, 1 (IC50 0.75 µM) was just as effective as amphotericin B (IC50 0.31 µM). Against L. donovani, 1 (IC50 7.02 µM) was twenty-two times less active than amphotericin B (IC50 0.32 µM), reinforcing the unique effectiveness of 1 against L. major. For T. brucei brucei, 1 (IC50 0.78 µM) was ten times more active than the laboratory standard Coptis japonica (IC50 8.20 µM). The IC50 of 9.08 µM for 1 against P. falciparum 3d7 compared to artesunate (IC50 36 nM) was not strong, but this result suggests the possibility of using the paenidigyamycin scaffold for the development of potent antimalarial drugs. Against cercariae, 1 showed high anticercaricidal activity compared to artesunate. The minimal lethal concentration (MLC) and minimal effective concentration (MEC) of the compound were 25 and 6.25 µM, respectively, while artesunate was needed in higher quantities to produce such results. However, 1 (IC50 > 100 µM) was not active against T. mobilensis.
Full-text available
Microorganisms residing in the male or female genital tracts cause sexually transmitted infections (STIs) and are generally transmitted through unprotected intercourse or other sexual acts. The increasing prevalence of STIs as a whole, and curable STIs in particular, has become a global challenge. A total of 498.9 million cases of curable STIs were reported by the World Health Organization (WHO) in 2008 compared to 448.3 million in 2005 indicating an 11.3 % increase in the incidence rate (Fig. 11.1) (WHO 2008).
Full-text available
Colonization with Trichomonas vaginalis is a possible cause of poor pregnancy outcome. To facilitate the diagnosis of this condition during pregnancy, we conducted a prospective, multicenter study of 13,816 gravid women who were between the 23rd and 26th week of gestation. Findings significantly associated with T. vaginalis colonization included a yellow, green, or bloody discharge from the vagina or cervix; abnormal odor after KOH was added to a vaginal specimen; a vaginal pH of >5.0; and cervical friability. The amount of vaginal discharge and abnormal consistency of the discharge were also associated with T. vaginalis colonization. These findings (except for cervical bleeding and odor after the addition of KOH to a vaginal specimen, which may be influenced by the presence of other flora) are consistent with those reported elsewhere. The clinical usefulness of these features is minimal, and it is more significant that other microorganisms are markers for trichomoniasis; therefore, controlling for other flora is important in the investigation of T. vaginalis colonization.
Full-text available
Background: The aim of this study was to detect Chlamydia trachomatis, Mycoplasma hominis and Ureaplasma urealyti-cum from semen samples of infertile men by Multiplex PCR and investigation of influence of bacteriospermia on semen parameters. Methods: Semen samples of 200 infertile men were evaluated by Multiplex PCR. In addition, analysis of semen parameters was performed according to the WHO guidelines. Results: All the patients were without clinical symptoms of urogenital tract infection. Thirty three percent of cases showed at least one bacterium. We found a noticeable relation between the presence of bacteriospermia and the rate of non motile and morphologically abnormal sperms (P< 0.0001). In addition, sperm concentration was lower in positive cases (P< 0.04). There was no relation between leukocytospermia and bacteriospermia (P> 0.05). Conclusion: Asymptomatic existence of Chlamydia and Mycoplasmas in urogenital tracts might play an important role in sperm impairment due to infertility. Bacteriospermia can influence sperm's motility, morphology and concentration.
Background: Trichomoniasis, caused by Trichomonas vaginalis, is one of the most common sexually transmitted infections in the world. Diagnosis of T. vaginalis is performed by different methods, including wet mount, culture, serological methods and PCR, which required laboratory equipments and expert laboratory personnel. The aim of this study was evaluation of immunochromatographic strip test (Xenostrip-Tv) for diagnosis of vaginal trichomoniasis compared with wet mount and PCR assay. Methods: In this prospective study vaginal swabs were obtained from 100 women with genital complaints demanding a speculum examination, referred to Imam Khomeini and Amir Kabir hospitals in Ahwaz, Khuzestan Province. Samples were first examined by wet mount and Xenostrip-Tv. PCR assay was performed in the next step using TVK3 and TVK7 primers initially. The positive samples were then confirmed by the second PCR assay using TVA5-1 and TVA6 primers. Results: PCR with TVA5-1 and TVA6 primers was determined as gold standard. The wet mount as well as Xenostrip-Tv sensitivity and specificity were 73.3% and 100%, respectively in comparison with gold standard. The sensitivity and specificity of PCR with primers TVK3 and TVK7 were also determined as 100% and 96.6%, respectively. The infection rates were 14% for wet mount and Xenostrip-Tv, 21% for PCR with primers TVK3 plus TVK7 and 19% with the gold standard PCR using TVA5-1 and TVA6 primers. Conclusion: Xenostrip- Tv could be used for diagnosis of vaginal trichomoniasis in regions with no laboratory diagnostic facilities.
Objectives: To examine rates of HIV-1 and sexually transmitted disease (STD) among pregnant and postpartum women in urban Malawi, Africa. Design: Serial cross-sectional surveys and a prospective study. Methods: Three major surveys were conducted in 1990, 1993 and 1994/1995. Consecutive first-visit antenatal women and women giving birth at the Queen Elizabeth Central Hospital were tested for HIV and STD after counseling and obtaining informed consent. Unlinked, anonymous HIV testing was also conducted on smaller samples of antenatal women in the same hospital to provide annual prevalence data. HIV-seronegative postpartum women from the 1990 and 1993 surveys were enrolled in a prospective study to determine HIV incidence. Results: HIV seroprevalence rose from 2.0% in 1985 to 32.8% in 1996, a 16-fold increase. The highest age-specific HIV prevalence was in the following age-groups: 20-24 years during 1990, 25-29 years during 1993, and 30-34 years during 1996. Among 1173 women followed for a median of 30.9 months, HIV incidence was 5.98 per 100 person-years in women aged < 20 years and declined steadily in older women. The prevalence of STD significantly declined among both HIV-positive and negative women. This decline in STD prevalence, however, was not accompanied by increased condom use over time. Conclusions: Among urban childbearing women in Malawi, incidence of HIV is highest among young women while, currently, prevalence is highest among older women. Recent declines in STD prevalence suggest that HIV prevention programs are having an impact either through improved STD diagnosis and treatment or reduced risk behaviors. Sequential cross-sectional STD prevalence measures may be useful in monitoring effectiveness of STD and HIV prevention activities.
This paper will review the significance of results obtained by DNA amplification methods performed on clinical materials for the detection of bacterial pathogens. They will be compared with conventional culture, antigen detection or serological methods with respect to speed, sensitivity and specificity. PCR has provided promising results in the identification of Bordetella pertussis, Chlamydia pneumoniae, Legionella pneumophila, Streptococcus pneumoniae, Mycoplasma pneumoniae and the various pathogroups of diarrheagenic Escherichia coli. PCR and LCR have also shown encouraging results when used in the diagnosis of sexually transmitted diseases caused by Chlamydia trachomatis. In patients with Lyme disease, the sensitivity of PCR is still insufficient, when compared to serological methods. Here PCR is an adjunct in the diagnosis and no substitute for clinical judgement and serology. PCR applications for the detection of bacterial pathogens in clinical materials have also proved to be both problematic and challenging. Problems in using the PCR include determining the optimal target selection, quantifying the sample volume necessary for analysis, determining a standard for sample preparation, and optimizing amplification reactions. There are also difficulties with PCR inhibitors present in the clinical material and with monitoring the performance of the technique. PCR results are highly reliable and reproducible between laboratories when standardized reagents and protocols are used. An important step in this direction is the commercial availability of PCR kits. Such kits also simplify the handling of PCR, thus requiring less technical expertise, and allowing broader use for diagnosis. In the near future, additional studies must provide a correlation between PCR results and conventional methods with larger numbers of samples. Moreover, as a final evaluation, PCR detection methods must prove their benefit with respect to clinical management.
Microorganisms associated with genito-urinary tract infections are often difficult to detect due to limitations associated with culture techniques. We have applied PCR-based detection of clinical isolates to complex sample matrices. Clinical isolates of Chlamydia trachomatis, Escherichia coli, Proteus vulgaris and Pseudomonas aeruginosa were grown, diluted and used to spike human urine and human semen. The urine and semen samples were centrifuged and the bacterial pellet was kept. A lysis buffer containing proteinase K, 8-methoxypsoralen and lauryl alcohol polyether was exposed to UV light to remove the bacterial DNA in the proteinase K, and was added to the bacterial pellet. After digestion, the proteinase K was destroyed and the lysates were subjected to 35 cycles of 16S rDNA amplification using a hot-starts technique and two primer pairs specific for eubacterial 16S rDNA: 8FPL-806R and 515FPL-13B. After amplification, the amplicons were cloned and sequenced to confirm amplification of the bacteria used to spiked the samples. We were able to detect as few as 105 bacteria per ml of urine or semen. Thirty unspiked semen samples were tested by PCR, and 17 were positive, including 10 samples negative by routine culture. The amplicons were cloned and sequenced for four PCR-positive/culture-negative semen samples: the 16S rDNA sequences obtained were mainly from strict anaerobes, including Prevotella spp. and Peptostrep-tococcus spp. Some 16S rDNA sequences were obtained that did not match any other 16S rDNA sequences available in various nucleic acid databases. Half of 14 unspiked urine sample tested were positive by PCR, including four samples negative by routine culture. Amplicons were cloned and sequenced for one urine sample showing only Lactobacillus spp. by routine culture, and sequences from Bacteroides ureolyticus, Clostridium spp., Corynebacterium urealyticum, Peptostrep-tococcus spp., and Lactobacillus acidophilus were found. These methods have great promise for the rapid detection of viable, but non-culturable bacteria in semen and urine. We are currently applying this technique for the detection of bacteria associated with idiopathic inflammatory conditions.
Trichomonas vaginalis (T. vaginalis) is the most common nonviral sexually transmitted infection in the world. Despite the coexisting global epidemics of T. vaginalis and HIV, little attention has focused on the emerging evidence that T. vaginalis increases susceptibility to, and potentially transmission of, HIV. We evaluated T. vaginalis infection in the context of a multisite, randomized controlled trial amongst women in South Africa and Zimbabwe, to determine first, if risk of HIV acquisition was increased among women recently infected with T. vaginalis, and second, if risk of T. vaginalis acquisition was increased among women infected with HIV. After controlling for potential confounders, participants infected with T. vaginalis were more likely to test positive for HIV at their following visit, compared to participants uninfected with T. vaginalis (adjusted hazard ratio = 2.05; 95% CI, 1.05-4.02). Similarly, HIV-positive participants were twice as likely to have acquired T. vaginalis infection at the following visit, compared to HIV-negative participants (adjusted hazard ratio = 2.12; 95% CI, 1.35-3.32). We found an increased risk of both HIV acquisition associated with T. vaginalis infection and risk of T. vaginalis acquisition associated with HIV infection. This bidirectional relationship represents a potentially important factor in sustaining the HIV epidemic in populations where T. vaginalis is endemic.
The temporal relationship between cervical infection with Trichomonas vaginalis (TV) or human papillomavirus (HPV) and the incidence rate of cervical intraepithelial neoplasia grade three (CIN III) was examined in a cohort of 43,016 Norwegian women. From 1980 to 1989, a cervico-vaginal infection from TV and HPV was diagnosed cytologically in 988 and 678 women, respectively. During the 181,240 person-years of observation, 440 cases of CIN III/cervical cancer developed. The age-adjusted incidence rates (IR) of CIN III were 225 per 100,000 person-years among women with no cytologic evidence of infection, 459 among women with TV infection, and 729 among women with HPV infection. A multiple regression model yielded a relative rate (RR) of CIN III of 2.1 (95 percent confidence interval [CI] = 1.3-3.4) among women with TV infection and 3.5 (CI = 1.9-6.6) among women with HPV infection, compared with women with neither infection. As CIN can be misclassified as HPV infection, the entry Pap-smears of 10 women with HPV infection who later developed CIN III were re-examined. Excluding the four discordant cases with the corresponding person-years decreased the RR of CIN III to 2.1 (CI = 0.9-4.8). Our report demonstrates the limitations of studies that rely only on cytologic detection of HPV infection. Nevertheless, the results support the hypothesis that HPV is a causal factor for CIN III lesions, and also display an association between TV infection and cervical neoplasia.
Although the prostate gland is believed to serve as a parasite reservoir in trichomoniasis in men, and clinical association of trichomonads with prostatitis is common, there has been, to our knowledge, no unequivocal demonstration of Trichomonas vaginalis within the prostate gland. Using established immunoperoxidase procedures, we have positively identified trichomonads in the prostatic urethra, glandular lumina, submucosa, and stroma. Foci of nonspecific acute and chronic inflammation, as well as intraepithelial vacuolization, were associated with the infection. The finding of trichomonads within and beneath glandular epithelium necessitates reevaluation of the traditional view of T vaginalis as a strictly surface-dwelling organism.