Trichomonas vaginalis
Marina Ferrari Klemm de Aquino,1,2
Annabel Sabine Hinderfeld,1,2
and Augusto Simoes-Barbosa1,2,
*
1
School of Biological Science, University of Auckland, New Zealand
2
All authors made equal contributions
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The extracellular protozoan parasite Trichomonas vaginalis colonizes the lower urogenital tract of
humans: the vagina, ectocervix, urethra, and prostate, where trophozoites divide asexually and the
transmission depends on sexual contact. Trichomoniasis is the most common, nonviral sexually transmitted
infection worldwide, accounting for ~270 million cases each year. Pathogenesis has been well
characterized in the female genital tract, where reproductive outcomes are clinically relevant, resulting
in vaginitis with discharge. T. vaginalis often carries endosymbionts (Mycoplasma and Trichomonasvirus
spp.) and is accompanied with vaginal dysbiotic microbiota containing mostly anaerobic bacteria. Host
cell adhesion, phagocytosis, and lysis are the major virulence traits of T. vaginalis, with levels varying
among strains. Immunopathogenesis is modulated by endosymbionts and the associated microbiota.
Despite drug resistance being documented for decades, 5-nitroimidazoles remain the only treatment
option.
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KEY FACTS:
While parasite colonization is inhibited by
protective lactobacilli in the vaginal
microbiota, T. vaginalis and the bacteria
causing bacterial vaginosis amplify
disease synergistically.
Metabolic interactions with Mycoplasma
enhance the growth and weaken the
macrophage-mediated killing of
T. vaginalis.
5-Nitromidazole treatment of
trichomoniasis neither eliminates
Mycoplasma nor counteracts the vaginal
microbiome disturbances; hence novel
therapies are necessary.
Despite hurdles of genome size
(~160 Mbp and 60 000 protein-coding
genes) and repetitiveness, CRISPR/Cas9
editing should advance genetic studies.
DISEASE FACTS:
Trichomoniasis is associated with poor
birth outcomes and increased risks of
HIV transmission and cervical cancer.
Parasite clumping is strain dependent.
Size-variable microcolonies dysregulate
epithelium permeability or promote its
destruction.
Parasite extracellular vesicles are
immunomodulatory, ‘priming’ host cells
and parasites for adherence.
T. vaginalis-induced immunomodulation
contributes to pathology, HIV spread,
and immune evasion.
Neutrophils kill the parasites by
trogocytosis, but reinfections are
common due to insufficient immunity.
TAXONOMY AND CLASSIFICATION:
KINGDOM: Protozoa
PHYLUM: Parabasalia
CLASS: Trichomonadea
ORDER: Trichomonadida
FAMILY: Trichomonadidae
GENUS: Trichomonas
SPECIES: T. vaginalis
*Correspondence:
a.barbosa@auckland.ac.nz
(A. Simoes-Barbosa).
646 Trends in Parasitology, July 2020, Vol. 36, No. 7 © 2020 Elsevier Ltd. All rights reserved. https://doi.org/10.1016/j.pt.2020.01.010
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Acknowledgment
A.S.-B. thanks the Health Research Council of New Zealand for funding of the original research proposal on T. vaginalis and the vaginal microbiota (HRC 11/314); this led to many of the
findings summarized here. The authors are grateful for the technical support on microscopy from Dr Adrian Turner and Ms Catherine Hobbis, University of Auckland.
Resources
www.cdc.gov/dpdx/trichomoniasis/
www.who.int/news-room/fact-sheets/detail/sexually-transmitted-infections-(stis)
https://trichdb.org/
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