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Trichomonas vaginalis (T. vaginalis) infection is extremely contagious and ubiquitous worldwide. According to the World Health Organization (WHO), there are roughly 276 million new cases per year, with women having a higher frequency than men. The frequency of T. vaginalis infection varies dramatically between areas, with low- and middle-income countries having greater rates. This is due to a lack of regional health education and the low usage of contraception in these communities. Gender differences demonstrate that women have greater infection rates, which could be attributed to the anatomical and physiological aspects of their reproductive system. Additionally, asymptomatic male carriers increase the chance of disease transmission among sexual partners.
The largest occurrence occurs between the ages of 16 and 35, a period of sexual activity during which frequent sexual partners and risky sex practices are key risk factors, increasing the possibility of infection and spread. Lower socioeconomic position, a lack of education, and insufficient health resources are all connected with greater rates of T. vaginalis infection. These areas frequently lack efficient sexually transmitted disease preventive methods, which makes infection more likely to spread. T. vaginalis infection is not only a personal health concern, but also a huge public health risk, as its broad occurrence and possible sequelae endanger world health.
The detection, treatment, regulation, and issues related to co-infection & persistent infection of T. vaginalis are key factors in controlling the spread of this parasite.
Techniques for identifying T. vaginalis infection have evolved throughout time. Traditional wet mount microscopy is the most widely used diagnostic approach since it is simple and inexpensive, but its sensitivity is just 40%-60%, especially in asymptomatic women.
Figure 1. Trichomonas vaginalis in a fresh wet mount examination × 40
(Source: Mahmoud A, et al. 2015)
Other more sensitive diagnostic procedures are frequently employed in conjunction. Nucleic acid amplification tests (NAATs), such as APTIMA T. vaginalis testing and other PCR technologies, have recently emerged as the gold standard for detecting T. vaginalis infections, with sensitivity and specificity ranging from 95% to 100%. However, these approaches are typically more expensive and need specialist equipment, making them unsuitable for on-site testing. It is crucial to remember that NAATs can yield false-positive results after therapy due to leftover Trichomonas DNA. Therefore, testing is recommended 2-3 weeks after treatment to ensure that most residual DNA has been cleared.
Figure 2. Characteristics of diagnostic methods for Trichomonas vaginalis detection.
(Source: Van Der Pol B, 2016)
Metronidazole (MTZ) has been the most widely used therapy for nearly four decades. MTZ, a 5-nitroimidazole medication, and comparable treatments such as tinidazole (TNZ) and secnidazole (TCZ), have a success rate of about 95% in treating T. vaginalis infections. The World Health Organization (WHO) and the Centers for Disease Control and Prevention (CDC) recommend a single dose of 2 grams of MTZ or 400-500 milligrams of MTZ taken twice a day for 7 days. MTZ is categorized as a Category B drug in pregnant women, and studies have demonstrated that it is safe throughout pregnancy; however, TNZ has not been adequately tested in pregnant women and is still classified as a Category C drug. For breastfeeding women, it is advised to stop breastfeeding during the MTZ treatment period and for 12-24 hours after the last dose to reduce infant exposure. Despite MTZ's high effectiveness, the reinfection rate after a single dose is high. Resistance cannot entirely explain this phenomenon, as in vitro resistance is only 2-5%. Some studies indicate that treatment failure in HIV-positive women can be as high as 7-10%, potentially related to changes in vaginal ecology. Thus, the origins of reinfection need further exploration, and better treatment options are required. Current research suggests that treatment for persistent infections should consider multiple doses of MTZ or TNZ. Additionally, alternative therapies such as acetohydroxamic acid, boric acid, furazolidone, and paromomycin must be explored for patients allergic to MTZ or TNZ.
Monitoring and managing T. vaginalis infections pose significant challenges. Although T. vaginalis infection has important implications for human reproductive health and HIV transmission, it remains a non-notifiable disease with a lack of formal monitoring systems. Global surveillance of T. vaginalis infections faces many challenges. First, some T. vaginalis strains exhibit resistance to metronidazole, leading to decreased cure rates. Additionally, in developing countries, due to a shortage of medical resources and a high rate of asymptomatic infections, many infected individuals cannot receive timely treatment, creating reservoirs of infection within communities. The global prevalence of T. vaginalis infection is approximately 8.1% in women and 1.0% in men. These figures may be underestimated, as they primarily come from microscopy rather than more sensitive nucleic acid amplification tests (NAATs).
T. vaginalis and Mycoplasma hominis form a symbiotic interaction that influences their biological features and pathogenic mechanisms.
Mycoplasma hominis is a bacterial parasite with a tiny genome and no solid cell wall, relying heavily on the host for its ecological niche and nutrients. It is widely distributed in the human urogenital tract, with infection rates ranging from 1.3% to 51% depending on the research group. Although most infections are asymptomatic, they are linked to alterations in the vaginal microbiota and extra-genital disorders, especially during pregnancy, when they can cause serious difficulties like premature birth and chorioamnionitis. Although the exact pathogenic processes of Mycoplasma hominis remain unknown, it is known that the bacteria's surface lipoproteins interact with Toll-like receptor 2 (TLR-2) to significantly increase the inflammatory response. Furthermore, Mycoplasma hominis contains nuclease activity, which allows it to bypass the host's immune system. Mycoplasma hominis can localize and multiply within T. vaginalis cells, creating a protective "sanctuary" against the host immune response and potentially interfering with the trichomonad's physiological functions. This internal environment shields Mycoplasma hominis from immunological responses and may increase T. vaginalis' pathogenicity and hemolytic activity on host epithelial cells.
Figure 3. Schematic representation of the impact of intracellular Mycoplasma hominis on immune pathogenic mechanisms in T. vaginalis
(Source: Henriquez FL, et al. 2021)
This symbiotic relationship provides numerous obstacles in the treatment and control of T. vaginalis infections. To begin, the presence of Mycoplasma hominis can make T. vaginalis more resistant to routinely used medications such as metronidazole. Second, co-infection with Mycoplasma hominis complicates infection control since it is found among T. vaginalis cells. Mycoplasma hominis infection can disturb the natural vaginal microbiota, increasing infection rates and recurrence. Furthermore, the symbiosis may cause T. vaginalis to become more hemolytic and pathogenic during infection. These variables combine to make current treatment choices less effective at eliminating co-infections, complicating illness management.
T. vaginalis infection does not provide long-term immunity, leaving patients susceptible to reinfection following therapy. The virus has the potential to spread within communities, particularly among asymptomatic male patients who frequently do not obtain appropriate treatment. Partner therapy is critical in preventing reinfection, but because of social stigma and cultural considerations, many patients are reluctant to disclose their infection status to their partners, resulting in high rates of reinfection. The significant recurrence rate following single-dose MTZ treatment implies that the current treatment strategy is not completely effective. The high rate of persistent infections indicates that single treatments may be insufficient to address all infection issues, necessitating enhanced health education for patients and their sexual partners and promoting the development of more effective detection and treatment methods. Furthermore, the high transmission rate of T. vaginalis between female sex workers (FSWs) and their clients exacerbates the spread of T. vaginalis in high-risk populations, requiring more effective screening and treatment strategies, especially in high-risk groups.
To summarize, chronic T. gondii infection is a complex pathological process that involves a variety of mechanisms, including host immunological responses, parasite immune evasion, and pathogen reactivation. Although persistent T. gondii infection seldom causes severe disease in most immunocompetent people, in immunocompromised people, latent T. gondii can reactivate, resulting in devastating clinical signs. Future studies should look at T. gondii's immune evasion mechanisms as well as chronic infection control tactics in order to develop effective treatment and prevention methods, minimizing the threat of persistent T. gondii infection to public health. Creative Diagnostics provides a wide choice of high-quality T. vaginalis research equipment, such as antigens, antibodies, and assay kits, to ensure the accuracy of your experiments. Please visit the product page for additional information.
References
| Target | Cat. No. | Product Name | Size | Species | Application | Detection Sample | |
| T. vaginalis | DTS054 | Trichomonas Vaginalis (T.V) Rapid Test Kit (Device/Cassette) | 20T | Quantitative | vagina secretion sample | Inquiry |
| Target | Cat. No. | Product Name | Host | Isotype | Application | |
| T. vaginalis | DMAB4429 | Anti-T. vaginalis Monoclonal antibody, Clone C986M | Mouse | IgG3 | LFIA | Inquiry |
| DMAB4430 | Anti-T. vaginalis Monoclonal antibody, Clone C987M | Mouse | IgG3 | IF, ELISA | Inquiry | |
| DMAB4431 | Anti-T. vaginalis Monoclonal antibody, Clone C988M | Mouse | IgG3 | IF, ELISA | Inquiry | |
| DMAB4432 | Anti-T. vaginalis Monoclonal antibody, Clone C990M | Mouse | IgG3 | IF, ELISA | Inquiry | |
| T. vaginalis p65 | DMAB4433 | Anti-T. vaginalis P65 Monoclonal antibody, Clone CDI676 | Mouse | IgG1 | IF, ELISA | Inquiry |
| T. vaginalis type 1 | DMABT-51617MT | Anti-T. vaginalis type 1 Monoclonal antibody, Clone 2407/267 | Mouse | IgG1 | IHC, ELISA, FC, WB | Inquiry |
| Target | Cat. No. | Product Name | Expression System | Tag/Conjugate | Application | |
| T. vaginalis | DAG218 | Native T. vaginalis | N/A | KLH | ELISA | Inquiry |
| DAG-P2204 | T. vaginalis (full length) | N/A | KLH | N/A | Inquiry | |
| T. vaginalis p65 | DAGC591 | Recombinant T.Vaginalis P65 Antigen | E. coli | KLH | SDS-PAGE | Inquiry |
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