Although there are diverse opinions on the proportion of acute salpingitis caused by Neisseria gonorrhoeae, most workers agree that other agents can be responsible for this condition. The authors have shown previously that Chlamydia trachomatis and Mycoplasma homonis are agents that may cause nongonococcal pelvic inflammatory disease. In the present study, they tested paired sera from 60 consecutive patients with acute salpingitis for antibodies to C. trachomatis by an indirect immuno-fluorescence test, and for antibodies to M. hominis and N. gonorrhoeae by indirect hemagglutination tests. Sera from 50 pregnant women attending consecutively from the same hospital catchment area served as controls. Antibodies (lgG or lgM or both) to C. trachomatis were detected in 80 per cent of the patients, and antibodies to M. homonis and N. gonorrhoeae were found in 40 per cent and 18 per cent, respectively. lgM antibodies to C. trachomatis occurred in 12, and lgG antibodies to the same organism occurred in all 48 seropositive patients. A significant change in antibody titre to C. trachomatis occurred in 40 per cent of the patients (21 with lgG, one with lgM, and two with both antibodies), to M. homonis in 12 per cent, and to N. gonorrhoeae in 5 per cent. The predictive values for a positive and a negative microimmunofluorescence test result were 44 per cent and 83 per cent, respectively; those for the indirect hemagglutination gonococcal pilar antibody test were 36 and 100 per cent, respectively. These calculations were based on the assumption that the diagnosis of a current infection was equivalent to a positive culture result for the organism. None of the 12 patients with lgM antibodies to C. trachomatis was culture positive for chlamydia. Evidence of a current infection (culture positive or significant change of antibody titer or both) with C. trachomatis and N. gonorrhoeae occurred in 35 (58 per cent) and five (8 per cent), respectively. Of the 23 patients with positive cultures for chiamydia, 17, 5, and 1 had titres of less than 64, from 128 to 156, and greater than 512, respectively. Ten had a significant rise in the titre of antichla-mydial lgG antibodies. The four patients who harbored gonococci were in the group of 11 patients who had indirect hemagglutination pilar antibodies to N. gonorrhoeae. Two of the three patients with a significant rise in titre harbored gonococci. There was a correlation between the severity of the tubal changes and the results of the microimmunofluorescence tests (P < 0.005) and between the duration of pelvic pain before attendance and the results of serological tests (P < 0.009). Four (7 per cent) of the 60 patients had a significant rise in antibody titres to both C. trachomatis and M. hominis. The three patients with a significant rise in the titre of indirect hemagglutination pilar antibodies had no evidence of current infection with chlamydia or mycoplasmas. Antibodies to C. trachomatis, M. hominis, and N. gonorrhoeae were demonstrated in 8, 8, and 6 per cent, respectively, of the sera from the control group of pregnant women. The study showed that acute salpingitis in Lund is associated with a current genital chlamydial infection in at least 40 per cent of the patients, whereas gonococcal infections at present occur in only a small proportion of all cases of salpingitis (8 per cent). Acute infections with M. hominis could be detected in 10 to 15 per cent of the patients with acute salpingitis in the area.
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