Sexually transmitted microorganisms, such as HPV and C.trachomatis are asymptomatic infections in approximately 90% and 80% of women worldwide respectively and they could produce persistent infection and progress to cervical cancer [15]. Therefore, potential mechanisms have been hypothesized about this coinfection: C.trachomatis infection may lead to epithelial disruption and facilitate HPV entry, or it can affect the immune response favoring the persistence of HPV [16].
When cervical HPV infection is investigated, different sites such as the oral cavity is not investigated, except in the presence of visible lesions, as well neither C.trachomatis infection [17]. The frequency of C.trachomatis in the oral cavity varies widely among published studies. This variability can be explained by the varied biological samples, the lack of global standardization techniques and the diversity of population study groups [18,19].
Although knowledge of HPV related tumor is clear, the prevalence of oropharyngeal HPV and C.trachomatis infection in unclear [8,17]. Both microorganisms are important to public health, because of the high risk of asymptomatic genital or oral infections could lead to complications like cervical and/or oral cancer [16].
The present results showed a prevalence of 27% for HPV, 14% for oral mucosa. In reference to oral HPV, in asymptomatic patient is still a matter of debate. Kreimer reported that asymptomatic oral HPV 16 infection was found in 1.3% [20] and Ciccarese detected 37% oral HPV DNA in women without signs of HPV infection [21]. In a previous local study, HPV was not detected in oral mucosa without lesion or injury [9]. Likewise, in a study conducted in the same region among randomly selected healthy subjects, HPV was detected in 3% (13/401) and all the identified genotypes were low risk [22]. So, our prevalence detected is higher than previous studies. Other study conducted by our group, detected 34% of oral HPV in patients with oral lesions [3], while in this present study only one patient had visible oral lesion. However, the absence of clinical signs of lesions in the oral cavity could show a subclinical infection which can be transmitted [17].
For C.trachomatis, our results show a prevalence of 49%, 31% in oral mucosa. These results are higher in comparison with other study conducted by our group, in which we detected 17% C.trachomatis DNA positive in oral lesions [3]. Our results are similar to a study from Japanese population, in which 44% of C.trachomatis was detected in pharyngeal smears and 61% in oral fluid in sex workers [18]. This frequency was higher too than a study conducted in the Netherlands, which pharyngeal C. trachomatis was detected in 2.3% of women [19]. A review that described extra genital C.trachomatis infections, showed a prevalence of 0.2 to 3.2% in pharyngeal swabs from asymptomatic women [23].
In reference to cytology status, we found a HPV detection rate of 36% in women with normal cytology and more prevalent in genital area. These results are in concordance with a study published from Brazil in which a prevalence of 36.09% was detected in women with normal cytology [24] and lower than other study, in which the prevalence of genital HPV in normal cytology was 49%. Patients with normal cytology tests and HPV HR types must be followed up because are at a high risk of having HPV induced lesions in the future[14]. In women with abnormal cytology we detected 18% HPV DNA positive, surprisingly prevalence lower than women with normal cytology but in agreement with Ji, who detected 18.4% HPV in abnormal cytology [5]. To difference with our results, Beyazit detected 51% of genital HPV [14], Ssedyabane 63.4% [25] and a local study conducted by Venezuela detected 51.6% in women with abnormal cytology [26].
Although HPV18 genotype is the second more frequent high risk type detected worldwide, in this study, we not detected HPV18 genotype in genital as well as oral mucosa. This is in agreeing with previous studies in oral mucosa in Argentina [3,9,22,27]. Reference to genital mucosa, the Brazilian study not detected HPV18 genotype in normal mucosa [1,24]. The more frequent HPV genotype detected was type 16; this result is in concordance with others studies in oral as well as genital mucosa [3,5,9,14,22,24,26,27]. The coinfection detected in this work was high risk genotypes 16 and 31 in genital mucosa. However, previous reports suggest that HPV genotypes coinfection do not increase the risk of acquiring a new infection but may impair the immune response [5].
We detected a C.trachomatis prevalence of 38% in women with normal cytology and 60% in abnormal cytology, being more frequent in genital area. These results are in concordance with a study from India, which detected more prevalence of C.trachomatis in patients with abnormal cytology (31.5%) in comparison with normal cytology (5.8%) [28]. On the other hand, other studies showed different results, such as local studies: Jordá, detected 8.5% C.trachomatis prevalence in symptomatic and asymptomatic women [29] and Kiguen, 6.9% in pregnant women [30], all results lower than our prevalence detected. Other studies, conducted by Ji, detected similar prevalence of C.trachomatis in women with normal and abnormal cytology, 7.1% and 7.2%, respectively [5] and Costa Lira, detected to genital C.trachomatis in 9.02% [24]. Asymptomatic women are untested for C.trachomatis so this may account for the high number of positive women in our study.