Pathogen Safety Data Sheets: Infectious Substances – Trichomonas vaginalis

PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Trichomonas vaginalis

SYNONYM OR CROSS REFERENCE: Trichomoniasis, vaginitis.

CHARACTERISTICS: Trichomonas vaginalis is a parasitic protozoan flagellate, and organisms vary in size but are usually around 10 μm in length and 7 μm in width(1,2). It usually has an oval or pear-like shape, but can assume an amoeboid form when attached to vaginal epithelial cells. T. vaginalis has a total of 5 flagella, four of which are located at its anterior portion. The fifth flagellum is incorporated within the undulating membrane(1,3). The anaerobic parasite can only exist as a trophozoite and lacks a cystic stage, reproducing by longitudinal binary fission. Growth is optimized at 37°C at pH 6.0 - 6.3, but can survive at up to pH 7(4).

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: T. vaginalis is generally restricted to the genitourinary tract by the host's immune system, and is the etiological agent of human trichomoniasis(2). Infection has been associated with an increased risk of human immunodeficiency syndrome in both sexes(4).

In women: Symptoms of infection include vaginal secretion that is scanty and mixed with mucus; malodorous discharge that is frothy, yellow or green, mycopurulent, and copious(4). The protozoan can be found in the vagina, cervix, bladder, Bartholin's, Skene's, and periurethral glands. Complications may result in cervical erosion, cervical cancer, infertility, adnexitis, pyosalpinx, and endometritis. Premature rupture of the placental membranes can occur in pregnant women, resulting in premature birth and low-birth weight(5). Acute infections are characterised by severe pruritus, vaginitis, vulvitis with dysuria and dyspareunia, and hemorrhagic spots on the mucosa (in 2% of patients) which results in colpitis macularis or petechiae (strawberry cervix). In females, 50% of cases are asymptomatic. Infection can persist for long periods of time in the urogenital tract of women. 25 - 50% are asymptomatic for the first 6 months of infection, and organisms can survive indefinitely in the lower urogenital tract if left untreated(1,6).

In men: Prevalence is lower in men, and infection is often asymptomatic(7). Infection in men can be present in the prostate, seminal vesicles, and epididymis. Complications are rare, but can potentially lead to genitourinary inflammation disease, sterility, scanty, clear to mucopurulent discharge, dysuria, non-gonococcal urethritis, prostatitis, balanoposthitis, epididymitis, and urethral disease(4). Infection is usually mild with no symptoms, thus making men potential carriers. Spontaneous resolution of infection is common as the oxidative nature of the male genital tract is speculated to be inhibitory to pathogenic factors of infection, which usually remains for 10 days or less(1).

EPIDEMIOLOGY: Worldwide - trichomoniasis caused by T. vaginalis is one of the most common non-viral sexually transmitted diseases with an estimated 170 million cases occurring annually (no seasonal variability)(1), and incidence has been found to be high in non-hispanic black women(5). Infection usually occurs in women during reproductive years, and occurrence before menarche or after menopause is rare(4). Fourteen to 60% of male infections are associated with known infected female partners(1).

HOST RANGE: Humans(1).

INFECTIOUS DOSE: Experimental studies have shown that urogenital inoculation with 10,000 to 120,000 organisms has resulted in transmission, although epidemiological examinations have shown that the infective dose in women is low and the infection rate is high(8-10).

MODE OF TRANSMISSION: Commonly spread through sexual contact with vaginal or urethral discharges of infected persons(1), and transmission of organisms via artificial insemination of infected cryobanked semen is also possible(11). Non-sexual transmission is rare but has been observed in cases involving contaminated douche nozzles, moist wash-clothes, specula, or toilet seats(1,12,13). Transmission to newborn infants from infected mothers is possible and is observed in 2 - 17% of cases, and can result in urinary tract or vaginal infections(1).

INCUBATION PERIOD: Ranges from 3 - 28 days with an average of 7 days(4,14).

COMMUNICABILITY: Infection can persist for a significant period of time in asymptomatic cases(14), from months to years.

SECTION III - DISSEMINATION

RESERVOIR: Humans, typically females, while men may act as a reservoir for infection(4).

ZOONOSIS: None.

VECTORS: None.

SECTION IV - STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: The only drugs that have been approved by the FDA for use in the United States are metronidazole (although the use of this drug can increase the incidence of preterm birth)(15), and Tinidazole (trade name known as Tindamax)(16). Ornidazole, secnidazole, and nimorazole can be used in countries outside of the US. In vitro testing has shown that nitroimidazole EU11100 also has similar efficacy as metronidazole(15).

DRUG RESISTANCE: Studies have shown that at least 5% of clinical cases of trichomoniasis are caused by metronidazole-resistant T. vaginalis, and cross-resistance to tinidazole is a concern as the two drugs are similar in modes of action (4).

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 1% sodium hypochlorite, and 70% ethanol(17).

PHYSICAL INACTIVATION: Inactivated below pH 5(4). Organisms cannot survive long (several hours) in dry conditions(1).

SURVIVAL OUTSIDE HOST: The organism grows best at 37°C, and specimens in urine should be considered viable for only 30 minutes to avoid false negatives (2 hours if PCR is used)(18). Live T. vaginalis have been found in swimming pool water, in urine, and semen after up to 6 - 24 hours, and up to 30 - 45 minutes when exposed to air(1,19,20). Studies have also shown that T. vaginalis organisms are able to survive through the cryopreservation process of human semen, making infection via artificial insemination possible(11).

SECTION V - FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Current laboratory diagnoses include direct microscopic observation, cell culture, immunological techniques, PCR assay, nucleic acid probe test, immunochromatographic capillary-flow dipstick technology, DNA probing and gene amplification, and in situ hybridization(2,9,16).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Topical vaginal medications and pessaries (such as clotrimazole, povidone-iodine, nonoxynol-9, and arsenical pessaries) may be prescribed for treatment in women to lessen the effects of symptoms; however, these do not consistently cure disease(4). Topical paromycin has been found to be effective, but side effects can be mild to severe(21). There are no topical medications available for men. Metronidazole can be administered orally or intravenously, with cure rates of 85-95%(1); Metronidazole should not be used by pregnant women in their first trimester as it has been linked to higher prevalence of preterm birth(22).

IMMUNISATION: No vaccinations are currently available. Two vaccines have progressed to the human clinical trials stage in the past 50 years (a heat-killed T. vaginalis vaccine, and SolcoTriovac), although they have not been proven to be effective against T. vaginalis(4).

PROPHYLAXIS: Since many males are asymptomatic and may be carriers, it is important to concurrently treat male partners of infected women to prevent re-infection(4).

SECTION VI - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: None reported to date.

SOURCES/SPECIMENS: Vaginal and urethral secretions, urine, human semen(4,11,18).

PRIMARY HAZARDS: Droplet exposure to mucous membrane, accidental parenteral inoculation and sexual transmission(1,23).

SPECIAL HAZARDS: None.

SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2(24).

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infected or potentially infected materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes(25).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities(25).

SECTION VIII - HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, while wearing protective clothing, cover spill with absorbent paper towel. Apply appropriate disinfectant, and starting from perimeter and wipe towards the center. Allow sufficient contact time with the disinfectant before cleaning up.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration(25).

STORAGE: Properly labelled and sealed containers.

SECTION IX - REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: November 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©
Public Health Agency of Canada, 2010
Canada

REFERENCES:

  1. Petrin, D., Delgaty, K., Bhatt, R., & Garber, G. (1998). Clinical and microbiological aspects of Trichomonas vaginalis. Clinical Microbiology Reviews, 11 (2), 300-317.
  2. Muresu, R., Rubino, S., Rizzu, P., Baldini, A., Colombo, M., & Cappuccinelli, P. (1994). A new method for identification of Trichomonas vaginalis by fluorescent DNA in situ hybridization. Journal of Clinical Microbiology, 32 (4), 1018-1022.
  3. Garber, G. E. (2005). The laboratory diagnosis of Trichomonas vaginalis. The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien Des Maladies Infectieuses Et De La Microbiologie Medicale / AMMI Canada, 16 (1), 35-38.
  4. Cudmore, S. L., Delgaty, K. L., Hayward-McClelland, S. F., Petrin, D. P., & Garber, G. E. (2004). Treatment of infections caused by metronidazole-resistant Trichomonas vaginalis. Clinical Microbiology Reviews, 17 (4), 783-93, table of contents. doi:10.1128/CMR.17.4.783- 793.2004
  5. Sutton, M., Sternberg, M., Koumans, E. H., McQuillan, G., Berman, S., & Markowitz, L. (2007). The prevalence of Trichomonas vaginalis infection among reproductive-age women in the United States, 2001-2004. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 45 (10), 1319-1326. doi:10.1086/522532
  6. Swygard, H., Sena, A. C., Hobbs, M. M., & Cohen, M. S. (2004). Trichomoniasis: clinical manifestations, diagnosis and management. Sexually Transmitted Infections, 80 (2), 91-95.
  7. Van der Pol, B. (2007). Trichomonas vaginalis infection: the most prevalent nonviral sexually transmitted infection receives the least public health attention. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 44 (1), 23-25. doi:10.1086/509934
  8. Hesseltine, H. C., Wolters, S. L., & Campbell, A. (1942). Experimental Human Vaginal Trichomoniasis. The Journal of Infections Disease, 71 (2), 127-130.
  9. Shaio, M. F., Lin, P. R., & Liu, J. Y. (1997). Colorimetric one-tube nested PCR for detection of Trichomonas vaginalis in vaginal discharge. Journal of Clinical Microbiology, 35 (1), 132- 138.
  10. Lossick, J. G. (1990). Epidemiology of urogenital trichomoniasis. In B. M. Honigberg (Ed.), Trichomonads parasitic in humans (pp. 311-323). New York, NY: Springer-Verlag.
  11. Sherman, J. K., Hostetler, T. L., McHenry, K., & Daly, J. J. (1991). Cryosurvival of Trichomonas vaginalis during cryopreservation of human semen. Cryobiology, 28 (3), 246- 250.
  12. BURCH, T. A., REES, C. W., & REARDON, L. V. (1959). Epidemiological studies on human trichomoniasis. The American Journal of Tropical Medicine and Hygiene, 8 (3), 312- 318.
  13. Peterson, K., & Drame, D. (2010). Iatrogenic transmission of Trichomonas vaginalis by a traditional healer. Sexually Transmitted Infections, 86 (5), 353-354. doi:10.1136/sti.2010.043125
  14. Webber, R. (2009). Communicable Disease Epidemiology and Control (3rd ed.). Cambridge, UK: Cambridge Univeristy Press.
  15. Okun, N., Gronau, K. A., & Hannah, M. E. (2005). Antibiotics for bacterial vaginosis or Trichomonas vaginalis in pregnancy: a systematic review. Obstetrics and Gynecology, 105 (4), 857-868. doi:10.1097/01.AOG.0000157108.32059.8f
  16. Wendel, K. A., & Workowski, K. A. (2007). Trichomoniasis: challenges to appropriate management. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 44 Suppl 3 , S123-9. doi:10.1086/511425
  17. Laboratory Safety Manual (1993). (2nd ed.). Geneva: World Health Organization.
  18. Shafir, S. C., & Sorvillo, F. J. (2006). Viability of Trichomonas vaginalis in urine: epidemiologic and clinical implications. Journal of Clinical Microbiology, 44 (10), 3787- 3789. doi:10.1128/JCM.01287-06
  19. Feigin, R. D. (Ed.). (2004). Textbook of Pediatric Infectious Diseases (5th ed.). Philadelphia, USA: Elsevier, Inc.
  20. BURGESS, J. A. (1963). Trichomonas Vaginalis Infection from Splashing in Water Closets. The British Journal of Venereal Diseases, 39 , 248-250.
  21. Aggarwal, A., & Shier, R. M. (2008). Recalcitrant Trichomonas vaginalis infections successfully treated with vaginal acidification. Journal of Obstetrics and Gynaecology Canada : JOGC = Journal d'Obstetrique Et Gynecologie Du Canada : JOGC, 30 (1), 55-58.
  22. Kigozi, G. G., Brahmbhatt, H., Wabwire-Mangen, F., Wawer, M. J., Serwadda, D., Sewankambo, N., & Gray, R. H. (2003). Treatment of Trichomonas in pregnancy and adverse outcomes of pregnancy: a subanalysis of a randomized trial in Rakai, Uganda. American Journal of Obstetrics and Gynecology, 189 (5), 1398-1400.
  23. SCHNITZER, R. J., KELLY, D. R., & LEIWANT, B. (1950). Experimental studies on trichomoniasis: 1. The pathogenicity of trichomonad species for mice. The Journal of Parasitology, 36 (4), 343-349.
  24. Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
  25. Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.
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