Epidemiological and clinical trends of sexually transmitted infections. Literature review





chlamydial infection, gonorrhea, trichomoniasis, peak incidence, polymerase chain reaction, culture methods, microscopy


This article presents modern data on epidemiological trends, pathogenesis, and mechanisms of persistence and acquisition of antibiotic resistance of the most common sexually transmitted infections (STIs): chlamydial infection, gonorrhea, trichomoniasis. Data on the frequency of chlamydial infection, gonorrhea, trichomoniasis detection in the DILA medical laboratory in the period from 2018–2020 are also presented.
Analysis of epidemiological and microbiological studies indicates a significant increase in the STIs incidence in countries with high economic development and the need for constant revision of diagnostic and treatment approaches, based on new data on the pathogens physiology, mechanisms and levels of antibiotic resistance, possibilities of laboratory diagnostics. Analysis of the DILA data on the chlamydial infection, gonorrhea, trichomoniasis detection is coinciding with the world trends in the increase of their prevalence. At the same time, the analysis of the DILA data demonstrated an interesting clinical phenomenon as a presence of 2 STIs peaks in women: the first at 21–25 years and the second at 51–55 years old.
Clinical manifestations of STIs are increasingly losing their typical features today. This indicates the need for a laboratory search for all common STIs in the region. Knowledge of the etiological factor of the inflammatory process allows choosing the correct antibiotic therapy and preventing the further development of antibiotic resistance. This article presents data on the various methods of STIs laboratory tests. Regular visits of women for cervical cancer screening are a good opportunity to screen for STIs. The ability to detect STIs in biomaterial in liquid cytology makes this option more accessible.
Thus, since vaccines against common bacterial and protozoa STIs pathogens have not yet been developed, the promotion of hygiene of sexual behavior and timely detection of infected persons during examination or screening with subsequent etiopathogenetic treatment are the basis of the STIs control systems and their consequences prevention.

Author Biographies

T.M. Tutchenko, SI “O.M. Lukyanova IPOG of the NAMS of Ukraine”; SSI “CIMT of the NAS of Ukraine»; “DILA” Medical Laboratory

PhD, senior researcher of the Endocrine Gynecology Department;

Department of Reproductive Health;

scientific consultant of “DILA”

O.A. Burka, Bogomolets National Medical University; “DILA” Medical Laboratory

PhD, associate professor at the Obstetrics and Gynaecology Department No. 1; 

scientific consultant

I.F. Boyarchuk, City clinical maternity hospital No. 2


A.V. Trampolska, City Clinical Endocrinology Center


V.V. Iavniuk, City Clinical Endocrinology Center


L.S. Ostroukh, Municipal non-profit enterprise “Maternity Hospital No. 3”

Head of the woman’s clinic


  1. World Health Organization. Sexually transmitted and reproductive tract infections. WHO (2020). Available from: [http://www.who.int/reproductivehealth/publications/rtis/policy/en], last accessed May 1, 2021.
  2. USA National Prevention Information Network. Sexually Transmitted Infections National Strategic Plan for the United States: 2021–2025. Available from: [https://npin.cdc.gov/publication/sexually-transmitted-infections-national-strategic-plan-united-states-2021–2025], last accessed April 13, 2021.
  3. World Health Organization. Sexually transmitted and other reproductive tract infections: a guide to essential practice. Geneva. WHO (2005).
  4. Di Pietro, M., Filardo, S., Romano, S., Sessa, R. “Chlamydia trachomatis and chlamydia pneumoniae interaction with the host: Latest advances and future prospective.” Microorganisms 7 (2019): 140. DOI: 10.3390/microorganisms7050140
  5. Geisler, W.M. “Duration of untreated, uncomplicated chlamydia trachomatis genital infection and factors associated with chlamydia resolution: A review of human studies.” J Infect Dis 201 (2010). DOI: 10.1086/652402
  6. Omsland, A., Sixt, B.S., Horn, M., Hackstadt, T. “Chlamydial metabolism revisited: Interspecies metabolic variability and developmental stage-specific physiologic activities.” FEMS Microbiol Rev 38 (2014): 779–801. DOI: 10.1111/1574-6976.12059
  7. Elwell, C., Mirrashidi, K., Engel, J. “Chlamydia cell biology and pathogenesis.” Nat Rev Microbiol 14 (2016): 385–400. DOI: 10.1038/nrmicro.2016.30
  8. Hybiske, K., Stephens, R.S. “Mechanisms of host cell exit by the intracellular bacterium Chlamydia.” Proc Natl Acad Sci USA 104 (2007): 11430–5. DOI: 10.1073/pnas.0703218104
  9. Peeling, R.W., Brunham, R.C. “Chlamydiae as Pathogens: New Species and New Issues.” Emerg Infect Dis 2 (1996): 307–19. DOI: 10.3201/eid0204.960406
  10. Rodel, J., Groh, A., Vogelsang, H., et al. “Beta interferon is produced by Chlamydia trachomatis-infected fibroblast-like synoviocytes and inhibits gamma interferon-induced HLA-DR expression.” Infect Immun 66 (1998): 4491–5. DOI: 10.1128/iai.66.9.4491-4495.1998
  11. Chen, A.L., Johnson, K.A., Lee, J.K., et al. “CPAF: A Chlamydial Protease in Search of an Authentic Substrate.” PLoS Pathog 8 (2012): e1002842. DOI: 10.1371/journal.ppat.1002842
  12. Al-Zeer, M.A., Xavier, A., Abu Lubad, M., et al. “Chlamydia trachomatis Prevents Apoptosis Via Activation of PDPK1-MYC and Enhanced Mitochondrial Binding of Hexokinase II.” EBioMedicine 23 (2017): 100–10. DOI: 10.1016/j.ebiom.2017.08.005
  13. Fan, T., Lu, H., Hu, H., et al. “Inhibition of apoptosis in chlamydia-infected cells: Blockade of mitochondrial cytochrome c release and caspase activation.” J Exp Med 187 (1998): 487–96. DOI: 10.1084/jem.187.4.487
  14. Gao, L.Y., Kwaik, Y.A. “The modulation of host cell apoptosis by intracellular bacterial pathogens.” Trends Microbiol 8 (2000): 306–13. DOI: 10.1016/S0966-842X(00)01784-4
  15. Akers, J.C., Tan, M. “Molecular mechanism of tryptophan-dependent transcriptional regulation in Chlamydia trachomatis.” J Bacteriol 188 (2006): 4236–43. DOI: 10.1128/JB.01660-05
  16. Leonhardt, R.M., Lee, S.J., Kavathas, P.B., Cresswell, P. “Severe tryptophan starvation blocks onset of conventional persistence and reduces reactivation of Chlamydia trachomatis.” Infect Immun 75 (2007): 5105–17. DOI: 10.1128/IAI.00668-07.
  17. Brunham, R.C., Rey-Ladino, J. “Immunology of Chlamydia infection: Implications for a Chlamydia trachomatis vaccine.” Nat Rev Immunol 5 (2005): 149–61. DOI: 10.1038/nri1551
  18. Bavoil, P.M. “What’s in a word: the use, misuse, and abuse of the word ‘persistence’ in Chlamydia biology.” Front Cell Infect Microbiol 4 (2014): 27. DOI: 10.3389/fcimb.2014.00027
  19. Wyrick, P.B. “Chlamydia trachomatis Persistence In Vitro: An Overview.” J Infect Dis 201 (2010): 88–95. DOI: 10.1086/652394
  20. Eleutério, J., Teles, R.A., Linhares, I.M., et al. “Interferon-gamma gene polymorphism influences the frequency of a Chlamydia trachomatis cervical infection in young women.” Int J STD AIDS 26 (2015): 960–4. DOI: 10.1177/0956462414563627
  21. Ziklo, N., Huston, W.M., Hocking, J.S., Timms, P. “Chlamydia trachomatis Genital Tract Infections: When Host Immune Response and the Microbiome Collide.” Trends Microbiol 24 (2016): 750–65. DOI: 10.1016/j.tim.2016.05.007
  22. McClarty, G., Caldwell, H.D., Nelson, D.E. “Chlamydial interferon gamma immune evasion influences infection tropism.” Curr Opin Microbiol 10 (2007): 47–51. DOI: 10.1016/j.mib.2006.12.003
  23. Aiyar, A., Quayle, A.J., Buckner, L.R., et al. “Influence of the tryptophan-indole-IFNγ axis on human genital Chlamydia trachomatis infection: Role of vaginal co-infections.” Front Cell Infect Microbiol 4 (2014). DOI: 10.3389/fcimb.2014.00072
  24. Nasioudis, D., Linhares, I., Ledger, W., Witkin, S. “Bacterial vaginosis: a critical analysis of current knowledge.” BJOG An Int J Obstet Gynaecol 124 (2017): 61–9. DOI: 10.1111/1471-0528.14209
  25. Sasaki-Imamura, T., Yoshida, Y., Suwabe, K., et al. “Molecular basis of indole production catalyzed by tryptophanase in the genus Prevotella.” FEMS Microbiol Lett 322 (2011): 51–9. DOI: 10.1111/j.1574-6968.2011.02329.x
  26. Sziller, I., Babula, O., Ujházy, A., et al. “Chlamydia trachomatis infection, Fallopian tube damage and a mannose-binding lectin codon 54 gene polymorphism.” Hum Reprod 22 (2007): 1861–5. DOI: 10.1093/humrep/dem107
  27. Raulston, J.E. “Response of Chlamydia trachomatis serovar E to iron restriction vitro and evidence for iron-regulated chlamydial proteins.” Infect Immun 65 (1997): 4539–47. DOI: 10.1128/iai.65.11.4539-4547.1997
  28. LaVerda, D., Kalayoglu, M.V., Byrne, G.I. “Chlamydial heat shock proteins and disease pathology: New paradigms for old problems?” Infect Dis Obstet Gynecol 7 (1999): 64–71. DOI: 10.1002/(SICI)1098-0997(1999)7:1/2<64::AID-IDOG13>3.0.CO;2-I
  29. Henderson, B., Fares, M.A., Lund, P.A. “Chaperonin 60: a paradoxical, evolutionarily conserved protein family with multiple moonlighting functions.” Biol Rev 88 (2013): 955–87. DOI: 10.1111/brv.12037
  30. Rodgers, A.K., Budrys, N.M., Gong, S., et al. “Genome-wide identification of Chlamydia trachomatis antigens associated with tubal factor infertility.” Fertil Steril 96 (2011): 715–21. DOI: 10.1016/j.fertnstert.2011.06.021
  31. European Centre for Disease Prevention and Control. Annual epidemiological report 2018 – chlamydia. Available from: [https://www.ecdc.europa.eu/sites/default/files/documents/AER-for-2018-STI-chlamydia.pdf], last accessed May 07, 2021.
  32. Huai, P., Li, F., Chu, T., et al. “Prevalence of genital Chlamydia trachomatis infection in the general population: A meta-analysis.” BMC Infect Dis 20 (2020): 589. DOI: 10.1186/s12879-020-05307-w
  33. Manavi, K. “A review on infection with Chlamydia trachomatis.” Best Pract Res Clin Obstet Gynaecol 20 (2006): 941–51. DOI: 10.1016/j.bpobgyn.2006.06.003
  34. Workowski, K.A., Bolan, G.A. “Centers for Disease Control and Prevention, Sexually transmitted diseases treatment guidelines, 2015.” MMWR Recomm Reports Morb Mortal Wkly Report Recomm Reports 64 (2015): 1–137. Available from: [http://www. ncbi.nlm.nih.gov/pubmed/26042815], last accessed May 07, 2021.
  35. Sherrard, J., Wilson, J., Donders, G., et al. “European (IUSTI/WHO) International Union against sexually transmitted infections (IUSTI) World Health Organisation (WHO) guideline on the management of vaginal discharge.” Int J STD AIDS 29 (2018): 1258–72. DOI: 10.1177/0956462418785451
  36. Caruso, G., Giammanco, A., Virruso, R., Fasciana, T. “Current and Future Trends in the Laboratory Diagnosis of Sexually Transmitted Infections.” Int J Environ Res Public Health 18 (2021): 1038. DOI: 10.3390/ijerph18031038
  37. Lovett, A., Duncan, J.A. “Human Immune Responses and the Natural History of Neisseria gonorrhoeae Infection.” Front Immunol 9 (2019): 3187. DOI: 10.3389/fimmu.2018.03187
  38. Unemo, M., Seifert, H.S., Hook, E.W., et al. “Gonorrhoea.” Nat Rev Dis Prim 5 (2019): 1–23. DOI: 10.1038/s41572-019-0128-6
  39. Ann Melly, M., Gregg, C.R., McGee, Z.A. “Studies of toxicity of neisseria gonorrhoeae for human fallopian tube mucosa.” J Infect Dis 143 (1981): 423–31. DOI: 10.1093/infdis/143.3.423
  40. Lenz, J.D., Dillard, J.P. “Pathogenesis of neisseria gonorrhoeaeand the host defense in ascending infections of human fallopian tube.” Front Immunol 9 (2018). DOI: 10.3389/fimmu.2018.02710
  41. Unemo, M., Golparian, D., Eyre, D.W. “Antimicrobial Resistance in Neisseria gonorrhoeae and Treatment of Gonorrhea.” In: Methods Mol Biol. Humana Press Inc. (2019): 37–58. DOI: 10.1007/978-1-4939-9496-0_3
  42. Wi, T., Lahra, M.M., Ndowa, F., et al. “Antimicrobial resistance in Neisseria gonorrhoeae: Global surveillance and a call for international collaborative action.” PLOS Med 14 (2017): e1002344. DOI: 10.1371/journal.pmed.1002344
  43. Kenyon, C., Kenyon, C., Manoharan-Basil, S.S., Van Dijck, C. “Gonococcal resistance can be viewed productively as part of a syndemic of antimicrobial resistance: an ecological analysis of 30 European countries.” Antimicrob Resist Infect Control 9 (2020): 97. DOI: 10.1186/s13756-020-00764-z
  44. US Centers for Disease Control. Antibiotic Resistance Threats in the United States, 2019. DOI: 10.15620/cdc:82532
  45. St. Cyr, S., Barbee, L., Workowski, K.A., et al. “Update to CDC’s Treatment Guidelines for Gonococcal Infection, 2020.” MMWR Morb Mortal Wkly Rep 69 (2020): 1911–6. DOI: 10.15585/mmwr.mm6950a6
  46. European Centre for Disease Prevention and Control. Gonorrhoea – Annual Epidemiological Report for 2018. Available from: [https://www.ecdc.europa.eu/en/publications-data/gonorrhoea-annual-epidemiological-report-2018], last accessed May 07, 2021.
  47. Siracusano, S., Silvestri, T., Casotto, D. “Sexually transmitted diseases: epidemiological and clinical aspects in adults.” Urologia 81 (2014): 200–8. DOI: 10.5301/uro.5000101
  48. Bamberger, D.M. “Trends in Sexually Transmitted Infections.” Mo Med 117 (2020): 324–7. Available from: [http://www.ncbi.nlm.nih.gov/pubmed/32848268], last accessed Apr 13, 2021.
  49. Papp, J.R., Schachter, J., Gaydos, C.A., Van Der Pol, B. “Recommendations for the laboratory-based detection of Chlamydia trachomatis and Neisseria gonorrhoeae – 2014.” MMWR Recomm Reports 63 (2014). Available from: [https://jhu.pure.elsevier.com/en/publications/recommendations-for-the-laboratory-based-detection-of-chlamydia-t-4], last accessed Apr 26, 2021.
  50. Rein, M.F. “Trichomoniasis.” In: Hunter’s Trop Med Emerg Infect Dis. Elsevier (2020): 731–3. DOI: 10.1016/B978-0-323-55512-8.00100-9
  51. Mercer, F., Johnson, P.J. “Trichomonas vaginalis: Pathogenesis, Symbiont Interactions, and Host Cell Immune Responses.” Trends Parasitol 34 (2018): 683–93. DOI: 10.1016/j.pt.2018.05.006
  52. Kissinger, P. “Trichomonas vaginalis: A review of epidemiologic, clinical and treatment issues.” BMC Infect Dis 15 (2015): 307. DOI: 10.1186/s12879-015-1055-0
  53. Nemati, M., Malla, N., Yadav, M., et al. “Humoral and T cell-mediated immune response against trichomoniasis.” Parasite Immunol 40 (2018): e12510. DOI: 10.1111/pim.12510
  54. Yang, S., Zhao, W., Wang, H., et al. “Trichomonas vaginalis infection-associated risk of cervical cancer: A meta-analysis.” Eur J Obstet Gynecol Reprod Biol 228 (2018): 166–73. DOI: 10.1016/j.ejogrb.2018.06.031
  55. Sutton, M., Sternberg, M., Koumans, E.H., et al. “The prevalence of Trichomonas vaginalis infection among reproductive-age women in the United States, 2001–2004.” Clin Infect Dis 45 (2007): 1319–26. DOI: 10.1086/522532
  56. Kreisel, K.M., Spicknall, I.H., Gargano, J.W., et al. “Sexually Transmitted Infections Among US Women and Men: Prevalence and Incidence Estimates, 2018.” Sex Transm Dis 48 (2021): 208–14. DOI: 10.1097/OLQ.0000000000001355
  57. Alcaide, M.L., Feaster, D.J., Duan, R., et al. “The incidence of Trichomonas vaginalis infection in women attending nine sexually transmitted diseases clinics in the USA.” Sex Transm Infect 92 (2016): 58–62. DOI: 10.1136/sextrans-2015-052010
  58. Meites, E., Llata, E., Braxton, J., et al. “Trichomonas vaginalis in selected US sexually transmitted disease clinics: Testing, screening, and prevalence.” Sex Transm Dis 40 (2013): 865–9. DOI: 10.1097/OLQ.0000000000000038
  59. Stemmer, S.M., Mordechai, E., Adelson, M.E., et al. “Trichomonas vaginalis is most frequently detected in women at the age of peri-/premenopause: an unusual pattern for a sexually transmitted pathogen.” Am J Obstet Gynecol 218 (2018): 328.e1-328.e13. DOI: 10.1016/j.ajog.2017.12.006
  60. Van Der Pol, B. “Clinical and laboratory testing for trichomonas vaginalis infection.” J Clin Microbiol 54 (2016): 7–12. DOI: 10.1128/JCM.02025-15



How to Cite

Tutchenko, T., Burka, O., Boyarchuk, I., Trampolska, A., Iavniuk, V., & Ostroukh, L. (2021). Epidemiological and clinical trends of sexually transmitted infections. Literature review. REPRODUCTIVE ENDOCRINOLOGY, (58), 55–62. https://doi.org/10.18370/2309-4117.2021.58.55-62



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