**2. Gastrointestinal chlamydial infections in humans**

York and Baker reported for the first time in cattle that *Chlamydia* was present in the gastrointestinal (GI) tract but did not cause a pathological response [21]. Later, Storz and Thornley reported that sheep have low levels of complement-fixing antibodies despite being infected. Antibody levels were found to be high in some sheep with positive fecal isolation but were observed as returning to low levels in the follow-up [22]. Cordy, Storz, and Dungworth stated that the presence of chlamydia in the intestine does not create a resistance against parenteral and respiratory tract infections [23–25]. Perry and Hughes observed that genital chlamydial infection may be somewhat protective against respiratory tract infections, but it does not prevent infection in the GI tract [26]. The reason why chlamydial GI infection could not be eliminated is the inability of the gastrointestinal tract to produce an adequate immune response. However, there are also data showing that oral infection is a potent immunization. Oral infection with live chlamydia has been shown to elicit a strong systemic immune response and a partial protective response in the genital area in both rat and guinea pig models [27, 28]. Nichols et al. showed that oral infection may be somewhat protective against conjunctival infection in the guinea pig [29]. Although these data suggest that GI chlamydial infection may trigger immunity, this immune response is insufficient. The absence of pathological findings may also indicate the complete absence of a local host response to chlamydial GI infection. In addition to the lack of pathology seen at various times after oral infection with *C. muridarum*, Igietsme et al. were unable to detect expression of VCAM-1 associated with the inflammatory response after oral infection and did not observe an increase in the number and density of intraepithelial lymphocytes. Hyperplasia of Peyer's patches was the only

finding for a local immune response [30, 31]. Yeruv L et al. examined whether a local and systemic response developed as a result of *C. muridarum* gastrointestinal infection in rats. They showed that IgG was produced at a level similar to the serum IgG level that occurs in chlamydia genital infection and remained high during the 75-day observation period, while anti-chlamydia IgA appeared in the intestine 2–3 weeks after the infection, peaking on the 50th day and decreasing on the 75th day [32]. Since it has been determined that the natural site of infection for chlamydia in many animal hosts is the gastrointestinal tract, it comes to mind that the natural site of infection in humans is the gastrointestinal tract as well. Apart from direct infection with anal intercourse, there are indications that both men and women can be infected orally. There is evidence that chlamydia can pass through the stomach and small intestine and settle in the large intestine after oral infection of rats [32]. Dunlop et al. found that both cervical and rectal cultures were positive in 5 (13.2%) of 38 women who had intercourse with men with ocular chlamydial infection or urethritis [33, 34]. Rectal cultures were also positive in 7 of 11 women with ocular infection only, and rectum and cervix were infected simultaneously in 6 of them. LGV serotypes were not found in rectal isolated cases. For this reason, it was thought that the rectum also serves as a reservoir, same as the genital tract, for chlamydial infection in women [34]. It has been shown by Jones et al. that men and women can be orally infected. They took pharyngeal samples from 706 heterosexual men and 686 women and rectal samples from 1223 women at risk for chlamydia infection. *C. trachomatis* was isolated in the pharynx of 3.7% of men and 3.2% of women. *C. trachomatis* was also isolated in the rectal culture of 5.2% of women at risk. However, they could not find a statistical relationship between positive rectal isolation and anal intercourse [35]. A strong correlation was found between positive genital and rectal cultures. While 11% of genital culture-positive women were positive in the rectum, rectal swab was positive in only 2.7% of genital culture-negative women. Positive rectal cultures having been detected in homosexual men were not surprising. Stamm et al. found a positive rectal culture in 33 of 155 heterosexual women with STDs. A high percentage of these women were having anal intercourse. However, 16 of 29 asymptomatic women with positive rectal cultures did not report anal intercourse [36]. Another source of information on persistent gastrointestinal chlamydia infection comes from studies on neonates exposed to chlamydia infection at birth. A 5-year prospective study by Schachter et al. followed 131 infants born to mothers infected with chlamydia. Inclusion conjunctivitis was confirmed by culture in 18% of infants and chlamydial pneumonia in 16%. Serological response was present in 60% of the infants. Interestingly, asymptomatic rectal and vaginal infections were detected in 14% of infants at risk. Conjunctival infections were detected in the first 22 days of life, while rectal cultures were positive after 2–3 months, and vaginal cultures after 70–154 days. This suggested that the vaginal infection was due to possible fecal contamination. A high titer IgM increase was also detected in positive rectal cultures [37].
