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.
Objectives: To investigate the signs, symptoms and changes in the vaginal milieu that could be associated with cervical human papillomavirus infection (CHPI). Study design: Women (n = 972) attending for contraceptive advice were tested for human papillomavirus in cervical samples. Results of gynecological history, examination, and vaginal wet smear findings were compared between CHPI patients and negative women. Results: Sixty-six (6.8%) of the women had a CHPI. Bacterial vaginosis was more common among those with, than without, CHPI, but the significance of this association was abolished after adjustment for age and for markers of sexual risk-taking. Vaginal discharge with a fishy odor, a positive amine test, and genital fissures showed significant correlations with CHPI, which persisted after adjustments. Symptoms of proctitis also correlated with CHPI, and remained significant after adjustment for anal sex. Conclusion: Bacterial vaginosis is associated with the presence of CHPI, possibly due to sexual behavioral factors. However, several other features, in particular the presence of amines, may be independently associated with CHPI.
The L‐phase variants of three bacteria were at least 100‐fold more susceptible to lysolecithin than their corresponding parents. Other bacteria, a yeast and protozoa were relatively resistant to lysolecithin although some bacteria, notably anaerobes, were particularly sensitive. It seems that some of the differences in sensitivity to lysolecithin may be accounted for, in part, by differences in the cholesterol content of the cell membranes and walls. Preliminary observations indicate that the infectivity of lipid‐containing viruses, i.e. influenza B virus and Herpesvirus hominis type 1, but not of non‐lipid‐containing viruses, i.e. an adenovirus and a rhinovirus, was diminished by lysolecithin treatment. The possibility that lysolecithin production might interfere with the isolation of L‐phase variants is discussed. Also considered is the possibility that the differential sensitivity of mycoplasmas and stable L‐phase variants to lysolecithin might provide a means of distinguishing between them.
Urinary tract infection by Staphylococcus saprophyticus was provoked in two female grivet monkeys. A non-hemagglutinating strain of S. saprophyticus was injected into the renal pelvis of one of the animals (monkey I), while in the other (monkey II), a hemagglutinating strain of the same species was inoculated into the bladder by suprapubic puncture. In monkey I, massive hematuria and proteinuria were demonstrated during the post-inoculation (p.i.) week, after which the monkey was killed. In monkey II, which was killed after 2 weeks, hematuria and proteinuria were present during the first 5 p.i. days. In both monkeys, S. saprophyticus was isolated in numbers < 10(5) bacteria/ml bladder urine on each p.i. day. Autopsy of monkey I revealed acute pyelonephritis and inflammatory changes in the ureter on the same side on which S. saprophyticus had been inoculated. In monkey II, both kidneys were enlarged and there were signs of acute pyelonephritis. The histopathological examination revealed microabscesses, interstitial infiltration and numerous leukocytes in the tubules. Both the ureters of monkey II were congested and microscopically an acute inflammatory reaction was found. Inflammatory signs were also present in the bladder. Scanning electron microscopy revealed cocci adhering to the epithelial lining of the urinary tract.
From 75 children with primary acute otitis media middle ear exudate was collected by needle aspiration through the tympanic membrane and investigated with respect to the presence of bacteria, bacterial L forms and mycoplasmas. In 60 cases (80%) bacteria were found by cultivation. Diplococcus pneumoniae was isolated in 50.7%, Haemophilus influenzae in 14.7%, group A streptococci in 5.3% and Neisseria catarrhalis in 9.3%. From 2 cases D. pneumoniae was isolated only on media designed for the isolation of L forms. In 5 of the 15 cases with negative culture findings, evidence for a bacterial infection was obtained by microscopic examination of the exudate. Mycoplasma was not demonstrated in any of the exudates. The bacterial findings from the throat were of little value in assessing the aetiology of otitis media. On the other hand, the bacterium isolated from the middle ear exudate was isolated from the nasopharynx in all but one case. The bacterium that was isolated from the middle ear exudate was recovered from the nasopharynx in pure culture in about half the cases.
