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      Clinical and Microbiological Aspects ofTrichomonas vaginalis

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      Clinical Microbiology Reviews
      American Society for Microbiology

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          Abstract

          Trichomonas vaginalis, a parasitic protozoan, is the etiologic agent of trichomoniasis, a sexually transmitted disease (STD) of worldwide importance. Trichomoniasis is the most common nonviral STD, and it is associated with many perinatal complications, male and female genitourinary tract infections, and an increased incidence of HIV transmission. Diagnosis is difficult, since the symptoms of trichomoniasis mimic those of other STDs and detection methods lack precision. Although current treatment protocols involving nitroimidazoles are curative, metronidazole resistance is on the rise, outlining the need for research into alternative antibiotics. Vaccine development has been limited by a lack of understanding of the role of the host immune response to T. vaginalis infection. The lack of a good animal model has made it difficult to conduct standardized studies in drug and vaccine development and pathogenesis. Current work on pathogenesis has focused on the host-parasite relationship, in particular the initial events required to establish infection. These studies have illustrated that the pathogenesis of T. vaginalis is indeed very complex and involves adhesion, hemolysis, and soluble factors such as cysteine proteinases and cell-detaching factor. T. vaginalis interaction with the members of the resident vaginal flora, an advanced immune evasion strategy, and certain stress responses enable the organism to survive in its changing environment. Clearly, further research and collaboration will help elucidate these pathogenic mechanisms, and with better knowledge will come improved disease control.

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          Author and article information

          Journal
          Clinical Microbiology Reviews
          Clin. Microbiol. Rev.
          American Society for Microbiology
          0893-8512
          1098-6618
          April 01 1998
          April 01 1998
          April 01 1998
          April 01 1998
          : 11
          : 2
          : 300-317
          Article
          10.1128/CMR.11.2.300
          106834
          9564565
          cc51141a-32ff-41b5-959d-a1dd101b8035
          © 1998
          History

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