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O controle das doenças parasitárias do intestino demanda muitas ações: devemos levar em consideração o ciclo de vida do parasita, a higiene pessoal e os hábitos alimentares do hospedeiro, bem como as condições econômicas, educação, serviços de saúde pública e atendimento médico da comunidade. Além disso, os fatores biológicos e ecológicos e, as condições gerais de saúde de animais domésticos e silvestres do local, devem igualmente compor o quadro (LEVENTHAL, 2009).

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Artigo: Infecção por Trichomonas vaginalis aumenta o risco de aquisição de HIV-1.

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Artigo: Infecção por Trichomonas vaginalis aumenta o risco de aquisição de HIV-1.

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Realizamos um estudo prospectivo entre mulheres em Mombaça,
Quênia, para determinar se a infecção por Trichomonas vaginalis
foi associada a um risco aumentado de infecção
infecção pelo vírus da imunodeficiência tipo 1 (HIV-1). Mensalmente
visitas de acompanhamento, triagem laboratorial para HIV-1 e infecções do trato genital foram conduzidas. Entre 1335 mulheres soronegativas para HIV-1
monitoradas por uma média de 566 dias, 806 infecções incidentes por T. vaginalis (23,6 / 100 pessoas), e 265 mulheres soroconvertidas para HIV-1 (7,7 / 100 pessoas)
anos). A tricomoníase foi associada a 1,52 vezes (Intervalo de confiança de 95%, 1,04-2,24 vezes) aumentando do risco de
aquisição do HIV-1 após ajuste para possível confusão
fatores. Tratamento e prevenção da infecção por T. vaginalis
poderia reduzir o risco de HIV-1 em mulheres.

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Abstract

We conducted a prospective study among women in Mombasa, Kenya, to determine whether Trichomonas vaginalis infection was associated with an increased risk of human immunodeficiency virus type 1 (HIV-1) infection. At monthly follow-up visits, laboratory screening for HIV-1 and genital tract infections was conducted. Among 1335 HIV-1-seronegative women monitored for a median of 566 days, there were 806 incident T. vaginalis infections (23.6/100 personyears), and 265 women seroconverted to HIV-1 (7.7/100 person- years). Trichomoniasis was associated with a 1.52-fold (95% confidence interval, 1.04-2.24-fold) increased risk of HIV-1 acquisition after adjustment for potential confounding factors. Treatment and prevention of T. vaginalis infection could reduce HIV-1 risk in women.

Trichomonas vaginalis infects 173 million people each year worldwide, and 32 million of these infections occur in sub-Saharan Africa [ 1]. Although it is well accepted that sexually transmitted infections (STIs) in general increase susceptibility to HIV-1 [ 2], data exploring the association between T. vaginalis infection and HIV-1 acquisition have been inconclusive. Among the 7 prospective studies that have evaluated vaginal trichomoniasis as a risk factor for HIV-1, all found elevated point estimates [ 2]. However, only 1 study demonstrated a statistically significant increased risk (relative risk, 1.7 [95% confidence interval {CI}, 1.1-2.8]) [ 3]. The lack of statistical significance in many of the other studies may have been related to sample size constraints. We used data from an 11-year prospective study of female sex workers (FSWs) in Mombasa, Kenya, to test the hypothesis that infection with T. vaginalis increases the risk of HIV-1 acquisition in women.

Participants and methods. From February 1993 through March 2004, HIV-1-seronegative FSWs attending a municipal clinic in Mombasa were invited to participate in an open cohort study of risk factors for HIV-1 acquisition. Detailed procedures have been described elsewhere [ 4]. At enrollment and monthly follow-up visits, a standardized interview was conducted to ascertain medical, gynecological, and sexual history. A physical examination was performed, and specimens were collected for laboratory diagnosis of HIV-1 and STIs.

Women with signs or symptoms of a genital tract infection at an examination visit were given syndromic treatment in accordance with Kenya Ministry of Health guidelines. Syndromic management for vaginal discharge and for suspected pelvic inflammatory disease included oral metronidazole, which is effective as treatment for T. vaginalis infection. All women were asked to return for their laboratory results after 1 week. Additional treatment was provided at the results visit if the laboratory findings identified infections, including with T. vaginalis, that were not treated syndromically at the time of the examination. Individual HIV-1 risk-reduction counseling and free condoms were provided at each visit. This study was approved by the institutional review boards of the University of Washington and the University of Nairobi.

Screening for HIV-1 was performed using an ELISA (Detect- HIV; Biochem Immunosystems). Positive results were confirmed using a second ELISA (Recombigen; Cambridge Biotech) [ 5]. Light microscopy of a vaginal wet preparation at ×40 magnification was used to diagnose vaginal trichomoniasis and candidiasis on the basis of identifying motile trichomonads and yeast forms, respectively. Bacterial vaginosis (BV) was diagnosed using microscopic analysis of a vaginal Gram stain [ 6]. Neisseria gonorrhoeae cultures of cervical secretions were performed on modified Thayer-Martin medium. Cervicitis was defined as the presence of an average polymorphonuclear leukocyte count ⩾30 cells/high-power field of gram-stained cervical secretions.

Analyses were performed using SPSS (version 10; SPSS) and S-Plus (2000; Mathsoft). All HIV-1-seronegative women who enrolled in the cohort and had at least 1 follow-up visit were included. Women were censored at HIV-1 seroconversion or at their last follow-up visit.

The association between T. vaginalis infection and HIV-1 acquisition was evaluated using univariate and multivariateCox proportional hazards analysis. T. vaginalis infection was analyzed as a time-dependent variable. As we have done previously [ 4], we assumed that the effect of T. vaginalis infection on HIV- 1 susceptibility would persist for 15 days after the infection was detected at a clinic visit. We estimated that HIV-1 seroconversion would be detected 45 days after HIV-1 acquisition, under the assumption that infection would occur, on average, at the midpoint between visits and that visits occurred every 30 days. HIV-1 antibodies take 25 days to appear after infection [ 7], so antibodies would be detectable at a visit occurring 45 days after infection. Thus, we calculated that the total window of effect for T. vaginalis infection to influence HIV-1 susceptibility would be 60 days (15+45 days).

The multivariate model controlled for baseline educational level (⩽8 vs. ⩽8 years), parity (⩽2 vs. >2), alcohol use, workplace (bar vs. nightclub), and vaginal washing practices and included time-dependent adjustment for genital tract infections other than with T. vaginalis (BV, vaginal candidiasis, genital ulcer disease, cervicitis, and gonorrhea), contraceptive method (no contraception or tubal ligation, oral contraceptive pills, depot medroxyprogesterone acetate [DMPA], Norplant, or intrauterine device [ 4]), age (<25, 25-29, 30-34, 35-39, and ⩾40 years), duration of prostitution (<1, 2-4, 5-9, and ⩾10 years), number of sex partners per week (⩽1 vs. >1), sexual frequency per week (⩽2 vs. >2), and condom use (<100% vs. 100%).

Continuous measures were dichotomized at the median from the enrollment visit. Similar to our modeling of trichomoniasis, we assumed an effect window of 60 days to capture the influence of other genital tract infections on HIV-1 susceptibility. For the sexual behavior variables (number of sex partners, sexual frequency, and condom use), an average was calculated for each year of follow-up, to capture average behavior over time.

We also performed univariate and multivariate analyses of risk factors for T. vaginalis acquisition, using Andersen-Gill proportional hazards models. Variables associated with incident T. vaginalis infection in univariate analysis ( P⩽.1) were included in a multivariate model. As we have done previously [ 8], we assumed an effect window of 85 days to capture the effect of hormonal contraceptive use on T. vaginalis acquisition among women who changed contraceptive methods during follow-up (70 days of persistent effect of hormonal contraception after discontinuation of use +15 days from T. vaginalis acquisition to detection at a clinic visit, under the assumption of acquisition at the midpoint between monthly visits).

Results. A total of 1579 HIV-1-seronegative women were enrolled in the cohort, of whom 1335 (85%) returned for follow-up. Women who were lost to follow-up were generally similar to those included in the analyses, although they were slightly younger (median, 25 vs. 26 years; P=.002) and had a shorter duration of prostitution (median, 0.8 vs. 1 year, P=.01). Women who never returned for follow-up were not significantly different from those who returned in terms of number of sex partners per week, sexual frequency, condom use, contraceptive use, or baseline prevalence of T. vaginalis infection (data not shown).

Baseline characteristics of the 1335 women included in these analyses are provided in table 1. The median duration of followup was 566 days (interquartile range [IQR], 178-1330 days), and the median time between visits was 34 days (IQR, 28-54 days). A total of 3422 person-years of follow-up were accrued. There were 806 incident T. vaginalis infections (23.6/100 person-years), and 265 women seroconverted to HIV-1 (7.7/100 person-years).

In univariate analyses, infection with T. vaginalis was associated with a significantly increased risk of HIV-1 seroconversion (hazard ratio [HR], 1.60 [95% CI, 1.11-2.31]; P=.01). This association remained statistically significant after adjustment for sexual risk behaviors, STIs, and other potential confounding factors as detailed above (adjusted HR, 1.52 [95% CI, 1.04-2.24]; P=.03).

In an exploratory analysis evaluating risk factors for T. vaginalis infection, we found that shorter duration of prostitution, lower educational level, and use of alcohol were associated with a significantly higher risk of T. vaginalis infection ( table 2). Acquisition of trichomoniasis was also more common among women who had concurrent cervicitis or concurrent BV. By contrast, 100% reported condom use and use of progesterone-only contraceptives (DMPA and Norplant) were associated with a lower risk of vaginal trichomoniasis. The results were similar in multivariate analyses.

Discussion. In the present prospective study, infection with T. vaginalis was associated with a significantly increased risk of HIV-1 acquisition. To our knowledge, this is the largest study to date to examine this relationship and is only the second study to show a statistically significant association. This is also one of only a few studies to investigate correlates of incident trichomoniasis in women.

Several lines of evidence suggest the biological plausibility of a causal association between vaginal trichomoniasis and increased risk of HIV-1 acquisition. First, infection with T. vaginalis leads to an inflammatory response with recruitment of CD4-bearing lymphocytes and macrophages to the vaginal and cervical mucosa [ 9, 10]. Second, punctate mucosal hemorrhages can occur in trichomoniasis, which potentially compromise the mechanical barrier to HIV-1 infection [ 11]. Third, T. vaginalis has been shown to degrade secretory leukocyte protease inhibitor, which can block HIV-1 attachment to cells [ 12]. Finally, trichomoniasis could increase the risk of HIV-1 acquisition by increasing susceptibility to BV or persistence of abnormal vaginal flora [ 13].

A recent meta-analysis that included all previously published prospective studies of the association between T. vaginalis and HIV-1 acquisition found a 1.5-fold (95% CI, 1.2-2.0-fold) increased risk of HIV-1 acquisition among women with vaginal trichomoniasis [ 2]. Our results, which used data from >3400 person-years of follow-up, are in agreement with these findings and thus provide the strongest evidence to date that infection with T. vaginalis may increase women's risk of HIV-1 acquisition by ∼50%.

Given the high prevalence of vaginal trichomoniasis globally, even a modest increase in the risk of HIV-1 acquisition from T. vaginalis infection could account for a high attributable risk for HIV-1 acquisition. One study recently estimated that 6.2% of HIV-1 infections among US women might be attributed to T. vaginalis [ 14]. The incidence of vaginal trichomoniasis is thought to be 4-fold higher in sub-Saharan Africa than in the United States [ 1], so this infection could be responsible for an even greater percentage of HIV-1 infections in African women.

Several features of the study's design support the validity of its findings. Prospective, monthly data collection allowed precise estimation of the timing of the exposure ( T. vaginalis infection), the outcome (HIV-1 seroconversion), and potential confounding factors. The large sample size and long duration of follow-up allowed us to performcomprehensive multivariate analyses to adjust for potential confounding factors. The study was conducted in a population of women at high risk for both HIV-1 infection and STIs, making this an ideal setting in which both to identify this association and to consider possible intervention strategies.

The findings of the present study should be interpreted in the context of potential limitations. First, because T. vaginalis and HIV-1 share a common route of transmission, it is important to control for behaviors that simultaneously increase the risk for both infections. Accurate assessment of sexual risk can be difficult. We have previously shown that self-reported behavioral data from this population were associated with STIs, which may provide objective markers of sexual risk [ 15]. Nonetheless, there remains a potential for residual confounding. Second, if a causal association between trichomoniasis and HIV- 1 acquisition exists, then the insensitivity of microscopy (compared with that of culture or of nucleic acid amplification techniques) could lead to an underestimation of the true magnitude of the effect. Finally, some STIs (e.g., Chlamydia trachomatis and HSV-2 infections) were not tested or included in our analyses.

In this cohort of Mombasa FSWs, we identified recent entry into prostitution and lower educational level as correlates of incident T. vaginalis infection. These characteristics may be markers for other risk behaviors.We also found that T. vaginalis infection was associated with concurrent BV and cervicitis. Lower rates of trichomoniasis were seen among women using progesterone-only contraceptives, particularly Norplant. We have previously reported a significantly lower risk of trichomoniasis in women using DMPA [ 8]. The mechanism for a protective effect of progesterone-only contraceptives is not clear, but it has been suggested that exogenous hormones may interfere with binding to androgen and estrogen receptors that are present on T. vaginalis [ 16]. It will be important to determine whether this finding can be replicated in other settings.

Globally, there is a higher incidence of T. vaginalis infection than of any other curable STI [ 1]. Our finding associating this infection with increased risk of HIV-1 acquisition suggests that interventions targeted toward preventing vaginal trichomoniasis could reduce the spread of HIV-1. There is mounting evidence that other conditions that disrupt the normal vaginal milieu, including BV and vaginal candidiasis, also increase susceptibility to HIV-1 acquisition [ 4], but little attention has been given to the potential role of vaginal health as an HIV-1 prevention strategy. Interventions to prevent and treat trichomoniasis and to improve vaginal health in general could provide important female-controlled methods for reducing the risk of HIV-1 transmission to women.

Acknowledgments

We acknowledge the valuable contributions made to the study by our clinic staff, laboratory staff, and administrators. We thank the Mombasa Municipal Council, for allowing us to use their clinical facilities, and Coast Provincial General Hospital, for providing laboratory space.We are grateful to the women who participated in the study, without whose time and effort this research would not have been possible.

References

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Infection with Trichomonas vaginalis Increases the Risk of HIV-1 Acquisition

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We conducted a prospective study among women in Mombasa, Kenya, to determine whether Trichomonas vaginalis infection was associated with an increased risk of human immunodeficiency virus type 1 (HIV-1) infection. At monthly follow-up visits, laboratory screening for HIV-1 and genital tract infections was conducted.

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Ciclo Biológico Trichomonas Vaginalis

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Importância do conhecimento sobre parasitoses.

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Métodos e Diagnóstico de Trichomonas vaginalis
(Achei esse vídeo bem completo em relação a explicação, apesar de não mostrar o método, a explicação sobre o diagnóstico foi bem completa e direta.)

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Diagnóstico da Tricomoníase: algumas opções