Trichomoniasis
Trichomoniasis (n. pl. trich·o·mo·ni·a·ses) is the most common non viral sexually transmitted disease in the world.
According to the World Health Organization’s annual estimates, there are an estimated 7.4 million trichomoniasis cases each year in the United States, with over 180 million cases reported worldwide
Trichomoniasis is caused by the parasitic protozoan Trichomonas vaginalis, which infects both men and women. There has been a growing body of data implicating trichomoniasis as a contributor to health complications among both women and men.
Organism
Trichomonas vaginalis is a pear-shaped, flagellate, motile protozoan, with an undulating membrane. It is about 10-20µm wide, and is ovate. The organism is propelled by four anterior flagella with a flagellum attached to an undulating membrane (Heine, 1993). T. vaginalis is anaerobic and does not contain mitochondria in its cytoplasm, but instead contains specialized granules called hydrogenosomes throughout the region of the cytoplasm. The morphology of T. tenax and T. hominis differ from T. vaginalis in that the trailing flagellum of the protozoa extends past the organism’s undulating membrane
Pathogenesis
Although trichomoniasis is the most common non-viral sexually transmitted disease, the pathogenicity of T. vaginalis is not thoroughly understood. Trichomonads participate in a host-parasite relationship, causing them to adhere to epithelial cells. The ability of trichomonads to adhere is affected by time, temperature, and pH level. T. vaginalis grows best in an anaerobic environment with a pH > 6 (Diamond LS, 1986). T. vaginalis binding to vaginal epithelial cells for colonization and infection is dependent upon specific parasite surface proteins. Parasites treated with metronidazole or other nitroimidazoles lose their ability to adhere, making them ineffective disease agents. Hemolysis, the destruction of red blood cells such that hemoglobin is released, is also correlated with virulence. Trichomoniasis has been seen to increase in severity during or slightly after menstruation (Graves, 1993).
The relationship between T. vaginalis growth and protective lactobacilli is a complex one. It is currently unknown whether TV infection alters the vaginal environment by creating an anaerobic situation or if anaerobes in the vagina precede TV growth. The vagina contains glycogen, especially rich in reproductive aged women. Glycogen is broken down into glucose, a nutrient T. vaginalis requires for growth
Several risk factors for acquisition of the organism have been identified, including multiple sexual partners, black race, history of previous STD and coexistent infection with Neisseria gonorrhoeae (Sobel, 1997). Approximately 8% to 50% of patients with T. vaginalis have concomitant infections. T. vaginalis often coexists with Bacterial Vaginosis. Trichomoniasis was associated with the presence of bacterial vaginosis in a study of 871 HIV-seropositive women and 439 HIV-seronegative women in the HIV Epidemiology Research Study (Cu-Uvin, 2002). T. vaginalis was present in 74% of women with BV vs. 35% of women without BV (p=.02).
Due to T. vaginalis’ anaerobic characteristics, the organism’s growth is enhanced at elevated pH levels. T. vaginalis grows over a wide pH range of 3.5-8. However, a vaginal pH below 4.5 decreases motility. Therefore a vaginal pH above 4.5 would be conducive to infection (Thomason, 1989). Failure to use barrier contraceptives increases an individual’s susceptibility to infection.
MOT
nfection of the genitourinary tract occurs through sexual transmission. Evidence for sexual transmission of T. vaginalis is very strong as prevalence is highest among patients with increased sexual activity and multiple partners. Approximately 14-65% of male partners of infected females are also infected (Krieger, 1995, Sena, 2003). The incubation period before symptoms arise is 4-28 days in approximately 50% of infected women (Weston, 1963). Asymptomatically infected individuals are in important vector and act as a stealth factor in trichomoniasis transmission. Many studies have shown that treatment of the male partner(s) of infected women improves both cure rates and recurrence rates (Hager 1980, Lyng, 1981).
Live T. vaginalis organisms in urine and semen samples have been found after being exposed to air for several hours. Also, organisms are able to survive for hours on damp towels and clothes of infected women (Lossick, 1989). There have been no well-documented cases regarding transmission through the aforementioned means. Nonsexual transmission is extremely rare since T. vaginalis infection is generally restricted to a specific site, namely the urogenital tract (Thomason, 1989). The only known nonvenereal form of transmission is through perinatal acquisition. Approximately 5% of female babies born of infected mothers contract the infection (Bramley, 1976).
SITES
T. vaginalis infection is generally confined to the urogenital tract. There have, however, been rare reports of trichomonads being found in other sites such as the lungs and cerebrospinal fluid. These cases have usually been accompanied by a severe underlying disease. Rarely have the organisms been identified as T. vaginalis, but were most likely T. tenax or T. hominis (Rein, 1990).
Recently, a 41 year old HIV+ male was hospitalized due to fever and dyspnea. A cytologic examination of his bronchoalveolar lavage fluid revealed numerous T. vaginalis organisms. This is the first case where T. vaginalis was found in the lungs of an adult. Data collected suggest that trichomonads are overlooked parasites and may be implicated in various human pathologies (Duboucher, 2003).
T. vaginalis organisms may be isolated from the cervix, vagina, Bartholins glands, bladder, urethra and occasionally the upper reproductive/urinary tract (Rein, 1990). Over 95% of infections have been isolated from the vagina and only 5% from the urinary tract of adult women (Grys, 1964). The urethra and Skene’s glands are infected in 90% of cases. There have also been instances where organisms were isolated from bladder urine (Thomason, 1989). T. vaginalis may also act as a carrier for other pathogenic organisms. Keith conducted an in vitro study in 1986 to observe the attachment between T. vaginalis and other bacteria that inhabit the urogenital areas. Using scanning electron microscopy, one finding displayed a cluster of cocci attached to a trichomonad and two other demonstrated multiple cocci and E. coli attached to a T. vaginalis organism. Trichomonads have been shown to migrate to the fallopian tubes and peritoneal cavity. Thus, by carrying bacteria or viruses on their surfaces, it is possible that T. vaginalis organisms contribute to upper genital tract infections (Keith, 1986).
In 2003, Rendón-Maldonado, et al. cited that STDs caused by bacteria and protozoa are important factors in the epidemiology of HIV-1. The research team incubated three subtypes of HIV-1 (A, B, and D) with HIV-1 infected lymphocytes and observed the interactions with immunofluorescence microscopy and transmission electron microscopy. Results showed that trichomonads may internalize HIV-1 particles for a short time period. Under in vitro conditions, trichomonads ingest and digest HIV-1 infected lymphocytes (Rendón-Maldonado, et al., 2003).
Results of a study by Pindak (1989), also indicate that viruses may be transmitted by T. vaginalis. Virus containing cell fragments were engulfed by trichomonads and internalized in vacuoles. Viable reoviruses were recovered from the trichomonads for nine days and genital herpes simplex virus for six days, suggesting the possibility of transmission of viruses by T. vaginalis (Pindak, 1989).
In men the urethra is the most common site for T. vaginalis infection. Organisms can also be detected in the epididymis, semen, and urine (Krieger, 1981). T. vaginalis was first located in prostatic fluid by Drummond who examined prostatic secretions from husbands of infected women (Drummond, 1936).
S/S FM
In women, the infection is often characterized by a yellow-green, frothy vaginal discharge, vaginal odor, pain with sexual intercourse, pain with urination, and vulvovaginal soreness and itching (Rein, 1990). Common clinical signs include vulvar erythema, inflammation, excess of white blood cells seen on a wet mount preparation of vaginal discharge, motile trichomonads in the wet mount preparation, and a vaginal pH above 5, most of which overlap with BV signs and symptoms, complicating diagnosis. The following is a differential diagnosis chart comparing several vaginal infections.
S/SM
In men, the infection is more difficult to detect as the majority of infections remain asymptomatic and readily available diagnostic techniques are inadequate. This is problematic since long term carriage of T. vaginalis in asymptomatic men has been documented up to 4 months (Krieger, 1993). Most men seeking treatment do so because of an infected partner (Hager, 1994).
Symptoms in men typically include urethral discharge, dysuria, mild pruritis, or burning after intercourse. Forty percent of symptomatic males have infected prostate glands. Men who are unresponsive to antimicrobial therapy for nonspecific urethritis should be tested for T. vaginalis since 15-20% will be infected with the organism (Thomason, 1989, Schwebke, 2003). The following table summarizes common symptoms found in T. vaginalis infected men.
RISK
Recently, a growing body of literature has linked T. vaginalis infection to a variety of health complications among both men and women. Among both women and men, T. vaginalis is emerging as one of the most important factors in transmission and acquisition of HIV infection (Sorvillo, 1998). In women, the health complications include increased risks for the following: infertility, development of atypical pelvic inflammatory disease, infection following gynecologic surgery, and cervical inflammatory neoplasia. There have also been high rates of correlation between trichomoniasis and pregnancy complications in women. In men, T. vaginalis has been linked to male factor infertility and as a common cause of non-gonococcal urethritis (NGU) (Schwebke, 2002, Soper, 2004).
Trichomoniasis as a Risk Factor for Cervical Neoplasia
The association between T. vaginalis and cervical neoplasia has been reported in many studies since the early 1950s. It has been suggested that this organism is responsible for the induction of changes in the human cervical mucosa resulting in dysplasia or carcinoma (Bechtold, 1952). A prospective, longitudinal cohort study followed over 19,000 women in Finland in a mass cervical cancer screening program for up to a 10 year period, to determine if women with cytologically diagnosed infections (T. vaginalis, herpes, or HPV) preceded development of cervical neoplasia. T. vaginalis was shown to be associated with a high relative risk (OR 6.4) of subsequent CIN. This was similar to risks found with either HPV (OR = 5.5) or herpes infection (OR = 12) and development of subsequent CIN (Viikki, 2000).
Zhang (1994) conducted a combined analysis of 2 cohort and 22 case-control studies examining the association between T. vaginalis infection and cervical neoplasia. The results from the analysis indicated that T. vaginalis is associated with increased risk of cervical neoplasia. The following table is a summary of the 24 studies used in Zhang’s data analysis.