8.8.14 Trichomoniasis 1475

8.8.14 Trichomoniasis 1475
8.8.14  Trichomoniasis
1475
Africa with pentavalent antimonials for 30–​60 days or liposomal
amphotericin B for 20 days.
Supportive treatment
Intercurrent infection must be sought and treated, and nutritional
deficiencies corrected. Blood transfusion is rarely needed.
Response to treatment
Fever, splenic size, haemoglobin, serum albumin, and body weight
are useful monitors of progress. Proof of parasitological cure is not
usually necessary. Reassessment at 6 weeks and 6 months will detect
over 90% of relapses. Serology is unhelpful in monitoring progress.
Relapse rates should be under 4%. Relapsed patients are slower to
respond and run a 40% chance of further relapses and of becoming
unresponsive to antimony.
Economic impact
Visceral leishmaniasis is a major economic burden on affected fam-
ilies. The direct costs of an episode of visceral leishmaniasis in rural
India or Bangladesh, where the drug is, in principle, provided free,
are equivalent to the household’s annual income.
Prevention and control of cutaneous and visceral
leishmaniasis
Prevention is a matter of controlling reservoir hosts and sandfly vec-
tors or of avoiding bites by vectors. Successful control requires an
accurate knowledge of transmission in each ecological focus.
In the Old World, urban cutaneous leishmaniasis is controlled by
case-​finding and treatment, better housing, and domestic spraying
with residual insecticides, while rural leishmaniasis is controlled in
the Middle East and North Africa by poisoning or destruction of
gerbil colonies. Mediterranean and urban visceral leishmaniasis in
South America can be controlled by the destruction or treatment of
dogs, but dogs are infectious to flies before they become symptom-
atic and screening of dogs is problematic. Dog collars impregnated
with permethrin reduce the numbers of flies that become infected.
In India, mass campaigns to spray houses and cattle sheds are needed
in addition to case-​finding and treatment. In the interepidemic
period, cases of PKDL should be sought and treated. Currently no
nation has an effective control programme in place.
In endemic populations, infection can be prevented during the
season of transmission by the use of insect repellent creams and of
fine mesh bed nets, top sheets or chadors (women’s outer garments
or cloaks) impregnated with permethrin during the hours of biting,
usually around dusk and dawn. In endemic foci, a higher level of
education in households is associated with lower rates of disease.
Vaccines have proved disappointing.
FURTHER READING
Blum J, et  al. (2014). LeishMan recommendations for treatment of
cutaneous and mucosal leishmaniasis in travellers. J Trav Med, 21,
116–​29.
den Boer M, Davidson RN (2006). Treatment options for visceral
leishmaniasis. Expert Rev Anti Infect Ther, 4, 187–​97.
Desjeux P (2001). The increase in risk factors for leishmaniasis world-
wide. Trans R Soc Trop Med Hyg, 95, 239–​43.
Lockwood DNJ, Sundar S (2006). Serological tests for visceral leish-
maniasis. Br Med J, 333, 711–​12.
Murray HW, et  al. (2005). Advances in leishmaniasis. Lancet, 366,
1561–​77.
Sundar S, et al. (2011) Comparison of short-​course multidrug treat-
ment with standard therapy for visceral leishmaniasis in India:
an open-​label, non-​inferiority, randomised controlled trial. Lancet,
377, 477–​86.
World Health Organization (WHO) (2010). Control of the leishman­
iasis:  report of a meeting of the WHO Expert Committee on the
Control of Leishmaniases. Geneva, 22–​26 March 2010. WHO tech-
nical report series; no. 949. World Health Organization, Geneva.
Websites
Centres for Disease Control. http://​www.cdc.gov/​parasites/​leishman-
iasis/​index.html
World Health Organization (WHO). Leishmaniasis. http://​www.who.
int/​leishmaniasis/​en/​
8.8.14  Trichomoniasis
Jane Schwebke
ESSENTIALS
Trichomonas vaginalis is a sexually transmitted protozoan pathogen
that may cause more than one-​half of all curable sexually trans-
mitted genital infections worldwide. Women with trichomoniasis
are often asymptomatic, but they may develop vaginal malodour,
discharge, erythema, or itching, and their male or female sexual part-
ners may also be infected, although urethritis in men is less likely
to cause symptoms. Women with trichomoniasis have an increased
risk of HIV acquisition, HIV shedding, pelvic inflammatory disease,
and preterm birth. For diagnosis, rapid antigen detection, culture,
and polymerase chain reaction methods have advantages over con-
ventional microscopy, but are more expensive. Oral metronidazole is
usually an effective treatment, with both sexual partners needing to
be treated to prevent reinfection.
Introduction
Trichomoniasis is an infection of the human urogenital tract caused
by the flagellated protozoan Trichomonas vaginalis. There are about
170 million new cases each year, making it the world’s most common
Acknowledgement: The editors acknowledge the inclusion of material from
Dr Sharon Hillier’s chapter in the previous edition of the Oxford Textbook
of Medicine.
section 8  Infectious diseases
1476
non​viral sexually transmitted infection and, according to the World
Health Organization (WHO), it accounts for more than one-​half
of all curable sexually transmitted infections worldwide. Pregnant
women who have trichomoniasis are at increased risk of preterm
delivery. Trichomoniasis is a risk factor for HIV acquisition and
shedding.
Aetiology
Although there are more than 100 species of this protozoan, only
T.  vaginalis parasitizes the human genital tract and has specific
tropism for this environment. Trichomonas tenax can be found in
the human oral mucosa and Pentatrichomonas homininis might be
found in the human gastrointestinal tract. In women, T. vaginalis
can be found in the vagina and the exterior cervix in over 95% of
infections, but is recovered from the endocervix in 13%. The urethra
and Skene’s glands are also commonly infected. In men, the urethra
is the most common site of infection but the organism has also been
recovered from epididymal aspirates and semen.
Epidemiology
Epidemiological evidence suggests that T. vaginalis is transmitted
almost exclusively by sexual intercourse, both during heterosexual
intercourse and in sexual activity between female sexual part-
ners. Although the organism can survive for many hours at room
temperature if kept damp, there is only limited evidence that this
pathogen is transmitted among household members in the absence
of sexual exposure. No cyst form of the organism is known to exist.
A very small proportion of female babies of infected mothers will
become infected during birth, but this infection is transient and
trichomoniasis discovered in a child should immediately raise the
suspicion of sexual abuse.
The recent availability of nucleic acid amplification tests (NAATS)
for women and men has provided newer and more accurate data on
the prevalence of infection. The US National Health and Nutrition
Examination Survey conducted 2001–​2004 projected that 3.1% of
US women are infected. Rates were higher among minority popu-
lations. HIV infection and illicit drug use are risk factors for infec-
tion. T. vaginalis has been reported in 18–​24% of women attending
sexual health clinics in the United States of America and in 3–​34%
of women in four African cities. The epidemiology of this pathogen
is less well understood among men, but has been reported in 3–​20%
of men attending sexual health clinics.
In several developed countries, there has been a steady decline in
the incidence of trichomoniasis in the past few decades, but this has
not occurred in less-​developed countries nor in deprived inner-​city
areas in industrialized nations. Human trichomoniasis is becoming
a disease of the underprivileged.
Pathogenesis
In vitro, T. vaginalis has a well-​defined, contact-​mediated, cytotoxic
effect, but its relationship to pathogenesis in vivo is unknown. It
activates complement and attracts neutrophils, which may kill the
parasite but, in large numbers, might also contribute to the pathology.
The organism produces several proteolytic enzymes which degrade
genital tract mucins. Several potential T. vaginalis adhesions have
been identified but, apart from its surface lipophosphoglycan, there
is little evidence supporting a role in adhesion. Availability of the
T. vaginalis genome sequence has allowed wider search for surface,
soluble, and secreted proteins involved in host–​parasite interactions.
Clinical features
In women, T.  vaginalis can infect the vagina, urethra, and the
Bartholin’s and Skene’s glands. From 10 to 50% of cases are asymp-
tomatic but acute inflammatory diseases can occur, with copious
and malodorous vaginal discharge, vulvovaginal soreness and ir-
ritation, dysuria, and dyspareunia. Trichomoniasis is significantly
associated with purulent yellow vaginal discharge, vulvar itching,
and colpitis macularis (strawberry cervix) detectable by colposcopy,
with vulvar and vaginal erythema. The discharge fluctuates with
time and, if untreated, might disappear spontaneously or persist for
months or even years.
Most men with trichomoniasis are asymptomatic, but the parasite
is responsible for a significant number of cases of non​gonococcal
urethritis.
Differential diagnosis
In women, vaginal discharge syndromes including bacterial vagin-
osis, yeast vulvovaginitis, and trichomoniasis should be considered
(see Chapter  9.4). Women who present with vaginal discharge,
vulvar itching, and/​or vaginal malodour might have no infection, or
could have any combination of these common vaginal infections. In
men, other causes of urethritis should be ruled out.
An accurate diagnosis cannot be made based upon signs or symp-
toms elicited during the clinical evaluation.
Trichomoniasis in women
The most commonly used method for diagnosis is identification
of the pathogen in vaginal (not endocervical) secretions examined
under the microscope at ×400 magnification. In clinical specimens
or culture, T. vaginalis is a motile and round or oval flagellate, 10–​
13 μm long and 8–​10 μm wide. Fixed and stained, it is about 25%
smaller (Fig. 8.8.14.1). Diagnostic features include the jerky motility,
undulating membrane, and microtubular rod (axostyle), which runs
through the body and projects as a thin spine from the posterior end.
Vaginal pH is usually elevated (>4.5) but can be normal.
Microscopy is inexpensive and can be used as a bedside diagnostic
test, allowing immediate treatment of infected people. However,
its sensitivity is only 65–​80% and it requires a microscope. Broth
culture methods for detection of T. vaginalis have the advantage of
greater sensitivity, but require up to 5 days’ incubation (Diamond’s
TYM and the InPouch system). Rapid antigen tests can be per-
formed within the clinic in a few minutes. Their sensitivity is 80%
compared to culture, with the advantage of providing results during
the clinic visit.
The current gold standard for diagnosis is NAATS testing which
can be performed on the same sample as collected for gonorrhoea
8.8.14  Trichomoniasis
1477
and chlamydia. These specimens include vaginal, endocervical,
urine, or liquid-​based Pap smears. Vaginal specimens can be
self-​collected. The sensitivity and specificity of NAATS testing
exceeds 95%.
Trichomoniasis in men
Although currently male testing with NAATS has not been pre-
sented to the US Food and Drug Administration (FDA) for poten-
tial approval, NAATS is the diagnostic test of choice for men and
has excellent sensitivity and specificity. The test can be run as an
analyte specific reagent test in laboratories which have internally
validated the assay in men. Urethral swab specimens or urine can
be tested.
Treatment
5-​nitroimidazoles are the first line therapy. A single 2 g dose of oral
metronidazole is most widely used. The alternative is 500 mg twice
daily for 7 days. The latter is the recommended dose for women in-
fected with HIV. Metronidazole is not contraindicated in pregnancy.
Recurrence occurs in 8 to 20% of women in the first month after
therapy. About half the occurrences are attributed to reinfection
by the same or a new sexual partner. Sexual partners must also be
treated. Only the 7-​day regimen has been extensively evaluated in
men, in whom it appears as effective as in women.
Treatment failures with metronidazole due to resistance occur 5–​
10% of the time. If reinfection can be ruled out, metronidazole for
a longer treatment course can be tried. However, tinidazole should
be considered due to its more favourable pharmacokinetic profile
against T. vaginalis. There is no standardized dose for treating metro-
nidazole resistant infections. One approach is 2 gm orally per day for
5–​7 days. In cases of continued treatment failure, the combination of
intravaginal paromomycin cream with high dose oral tinidazole has
been reported to be successful.
Because up to half of infected individuals are asymptomatic, the
only way to reduce the population prevalence of this pathogen is
through screening of individuals and providing treatment to in-
dividuals and their sexual partners. There is no effective vaccine
against T. vaginalis.
Prognosis
In most women who receive appropriate treatment, symptoms will
resolve but they are at increased risk of becoming infected with
Trichomonas in the future. About 50% of men will spontaneously
clear their infections, but unless both sexual partners are treated,
reinfection is common.
Complications
Trichomoniasis in women was previously regarded as unpleasant
but harmless; however, epidemiological studies have now linked it
with a modest increase in the risk of heterosexual HIV transmission,
and with complications in pregnancy.
Areas of uncertainty, controversy, and future
developments
Trichomonisis has been linked with preterm birth, pelvic inflamma-
tory disease (Chapter 9.8), and an increased risk of HIV. However,
metronidazole treatment failed to reduce the risk of preterm delivery
or acquisition of HIV in a limited number of previously conducted
clinical trials which used culture for diagnosis as opposed to the
currently available, more sensitive, NAATS. No study has yet docu-
mented that accurate diagnosis and treatment of trichomoniasis
provides a long-​term health benefit for men and women. In preg-
nant women, single-​dose metronidazole treatment achieves para-
sitological cure, but one trial suggested an increased risk of preterm
birth. Broader implementation of specific and sensitive screening
tests and additional prospective studies of treatment should reveal
whether routine screening and treatment of T.  vaginalis reduces
morbidity.
FURTHER READING
Kissinger P, et al. (2013). Trichomoniasis and HIV interactions: a re-
view. Sex Trans Infect, 89, 426–​33.
Meites E, et al. (2015). A review of evidence-​based care of symptomatic
trichomoniasis and asymptomatic Trichomonas vaginalis infections.
Clin Infect Dis, 61 (Suppl 8), S837–​48.
Nye MB, et al. (2009). Comparison of APTIMA Trichomonas vagina­
lis transcription-​mediated amplification to wet mount microscopy,
culture, and polymerase chain reaction for diagnosis of trichomon-
iasis in men and women. Am J Obstet Gynecol, 200, 188.e181–​7.
Sena AC, et al. (2007). Trichomonas vaginalis infection in male sexual
partners: implications for diagnosis, treatment, and prevention. Clin
Infect Dis, 44, 13–​22.
Fig. 8.8.14.1  Trichomonads in vaginal secretions (Giemsa stain).
Copyright J. P. Ackers.