CASE

A 28 y/o female, complained of vaginal pruritus, dysuria

and dyspareunia. On physical exam, copious frothy
discharge was noted in the vaginal introitus. A smear was
done revealing flagellated organisms with rapid jerky

Differential Diagnosis
Diagnosis:
Pathogenesis
T. vaginalis is the most intensively studied trichomonad and one of the
leading causes of nonviral STDs, but the exact mechanism of its pathogenesis
has not been clearly elucidated. This can be attributed lack of good animal
model which has limited the ability to conduct standardized, controlled
research on transmission, pathogenesis, immune response, and drug and
vaccine development.
The interaction of T. vaginalis with the members of the resident flora of
the vagina may be an important factor, and, like many other protozoans, T.
vaginalis has demonstrated many mechanisms which are used to evade the
host immune system (Alderete et al., 1992; Alderete et al., 1995). This
includes:
Adherence and adhesion
The first step in pathogenesis of T. vaginalis is adherence. It has been
observed that the side opposite the undulating membrane and the recurrent
flagellum of the parasite attaches itself to the epithelial cells.
Hemolysis
T. vaginalis is an obligate parasite in that it lacks the cell-cell contact
required for a more stable and efficient parasitism. The nutrients needed are
acquired from the vagina secretions or through phagocytosis of host and
bacterial cells (Huggins and Preti, 1981). Erythrocyte seems to be the prime
source of fatty acids that are needed by the parasite (Petrin et al., 1998). In
addition to lipid, iron is an important nutrient for T. vaginalis and may also be
acquired via the lysis of erythrocytes (Lehker et al., 1990)
Proteinases

T. vaginalis has between 11 and 23 distinct cysteine proteinase (CP)

activities, most of which are lysosomal (Neale and Alderete, 1990). The CPs of
T. vaginalis is by far the most abundant of the parasitic protozoa. It is not
surprising that these enzymes play a role in the pathogenesis of the parasite.
CP has been implicated as possible lytic factors in the haemolysis of
erythrocytes. In addition, CP activity is required for the adherence to
epithelial cells (Arroyo and Alderete, 1989). T. vaginalis CPs also have the
ability to degrade host immnoglobulins G and A (IgG and IgA) (Provenzano
and Alderete, 1995) both of which present in the vagina.
Cell detaching factor (CDF)
CDF is a 200 KDa glycoprotein, which is heat and acid labile. It has
been shown that a cell-product of T. vaginalis, CDF, causes cytopthic effects
in cell culture (Pindak et al., 1986). CDF is probably a factor in pathogenesis,
since Pentatrichomonas hominis, a nonpathogenic species does not show CDF
activity (Garber et al., 1989). Garber et al. (1989) found that purified CDF was
active within pH 5.0 - 8.5 with the optimum activity at pH 6.5 and inactivity
below 4.5. This is of clinical relevance since the normal pH of the vagina is
4.5 but is greater than 5.0 during trichomoniasis. The rise in vagina pH during
trichomoniasis may therefore be crucial in the pathogenesis of this disease
(Petrin et al., 1998).
Immune system evasion
In a hostile changing environment, T. vaginalis can survive and flourish.
Its ability to evade the host immune system is an important aspect of
pathogenesis. Avoidance of complement is a strategic tactic, which is used by
T. vaginalis to overcome the human immune system (Petrin et al., 1998).
Resistance to complement is dependent upon a high concentration of iron
(Alderete et al., 1995), a nutrient which indeed abundant during menses. It
seems that iron upregulate the expression of CPs which has been found to
degrade the C3 portion of the complement on the surface of the organism;
this allows the organism to evade complement-mediated destruction
(Alderete et al., 1995).
This parasite also secretes copious amounts of highly immunogenic
soluble antigens. A continuous release of these antigens may neutralize
antibody or cytotoxic T lymphocytes, thus short-circuiting specific anti-T.
vaginalis defense mechanisms As well, T. vaginalis can coat itself with host
plasma proteins. This coating does not allow the hosts immune system to
recognize the parasite as foreign (Peterson and Alderete, 1982).
T. vaginalis is a very complex organism, from its biochemistry to the
mechanisms of pathogenesis. Areas of pathogenesis that should be pursued
include defining soluble factors, further elucidating the contact-dependent
relationship between the vaginal epithelium and T. vaginalis, and defining
how the organism can establish itself in a normally inhospitable and changing
environment. It will also be important to further define the role of the human
immune system in trichomoniasis in order to develop targeted intervention
strategies.

Life Cycle
Trichomonas vaginalis is a
sexually-transmitted
genitourinary flagellate with a
simple life cycle. Infective T.
vaginalis trophozoites reside in
the female lower genital tract
and in the male urethra and
prostate
(Smith,
2014).
Trophozoites
replicate
by
longitudinal binary fission and
unlike other flagellates, does not
have a cyst form (Schwebke and
Burgess, 2004). During sexual
intercourse, the trophozoites are
transmitted via vaginal and
prostatic
secretions.
The
presence of the trophozoite form
of T. vaginalis in urine and
vaginal and prostatic secretions
is
confirmatory
for
trichomoniasis (Smith, 2014). Humans are the only known host of T.
vaginalis, and the parasite does not survive well in the external
environment.
Figure 1.
Life cycle of T. vaginalis
Though transmission is primarily via sexual intercourse,
contaminated towels, douche equipment, examination instruments,
and other objects may be responsible for some infections (Brooks, et
al, 2013). However, this transmission is limited by the lability of the
trophozoite form. Infants may also be infected during birth through
vertical transmission (Murray, et al, 2013).
The risk of acquiring T. vaginalis infection is based on the type of
sexual activity. Women who engage in higher-risk sexual activity are at
a greater risk of infection. Risk factors for T. vaginalis infection include
(Smith, 2014):
New or multiple partners

A history of sexually-transmitted infections (STIs)

Current STIs
Sexual contact with an infected partner
Not using barrier contraception (eg, oral contraceptives)

Treatment
The drug of choice is metronidazole for Trichomonas Vaginalis. The
mechanism of action target organisms preferentially reduce the 5-nitro group,
and active metabolites likely disrupt the helical structure of the DNA within
them, preventing nucleic acid synthesis and eventually leading to cell death.
The advantages of single-dose therapy of metronidazole or tinidazole
for trichomoniasis are better patient compliance, lower total dose, and,
possibly,
decreased
subsequent
candidal
vaginitis.
Patients
in
pharmacotherapy therapy should be advised to avoid alcohol consumption
during the course of treatment and for an appropriate amount of time after
the completion of their medication. Resistance to metronidazole has been
reported and may require retreatment with higher doses. More recently,
tinidazole has approval for treatment of trichomoniasis in adults and may be
used as a first-line agent or for cases refractory to metronidazole. Pregnant
women can take this oral medication as well. Because trichomoniasis is an
infection of multiple sites, systemic treatment is needed.
Both male and female sex partners must be treated to avoid
reinfection. Patient-delivered partner therapy is a safe and effective means of
treating the sexual partners of patients diagnosed with trichomoniasis. Both
patient and partner should abstain from sex until pharmacological treatment
has been completed and they have no symptoms. Thereafter, consistent use
of condoms and other barrier contraceptives reduces the chance of infection.
In clinical practice, repeat testing is rarely performed unless symptoms
do not improve with drug treatment. However, the CDC recommends
rescreening at 3 months post therapy for sexually active women, as they
have a high rate of reinfection. Currently, no data are available on
rescreening men.

Prevention
Personal hygiene, avoidance of shared toilet articles and clothing, and

safe sexual practices are important preventive actions. Elimination of

carriage in men is critical for the eradication of disease.
Abstinence from sexual intercourse prevents trichomoniasis. Limiting
the number of sexual partners decreases the risk of trichomoniasis. Male
condoms can protect against the transmission of trichomoniasis. Although the
efficacy of female condoms is undefined, they may also provide some
protection. Diaphragms have been shown to protect against trichomoniasis
but should not be used as the primary source of protection against HIV.
Spermicides that contain nonoxynol-9 are not recommended for the
prevention of sexually transmitted diseases. Frequent use is associated with
disruption of the genital epithelium, which may be associated with an
increased risk of HIV infection and other sexually transmissible agents.

Answers to the Questions

1. Explain the life cycle of the parasite that caused the disease. Give
the infective and diagnostic stages. Explain the most probable
cause, mechanism of infection of the patient.

T. vaginalis is primarily sexually-transmitted. The trophozoite

form inhabits the genitourinary tract where it replicates by
longitudinal binary fission; the parasite does not exhibit a cyst form.
Trophozoites in vaginal and prostatic secretions are both the
infective and diagnostic stage of T. vaginalis.
2. What is the treatment ?

Trichomanas Vaginalis is treated with a single dose

Metronidazole and Tinidazole. Both patient and partner are treated
to avoid reinfection. A 3-month post therapy resrcreening for
sexually active women is recommended.
3. How can it be prevented?

Personal hygiene, avoidance of shared toilet articles and

clothing, and safe sexual practices such as using male condoms are
important preventive actions.