5: Microbiological etiology of symptomatic versus subclinical pelvic inflammatory disease

5: Microbiological etiology of symptomatic versus subclinical pelvic inflammatory disease

IDSOG Abstracts ajog.org copper IUD, no highly effective method) were assessed as independent exposures using linear mixed models. Analyses were rep...

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IDSOG Abstracts

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copper IUD, no highly effective method) were assessed as independent exposures using linear mixed models. Analyses were repeated among the subset of women who used the same method throughout follow-up. RESULTS: Among 116 women enrolled in the placebo arm, 107 women were eligible for this analysis. The proportion of visits with BV differed by contraceptive method (BV+ at 24% of injectable visits versus 39% of non-method visits; p¼0.01). After adjusting for age, site, sex without a condom, and new sex partners, IUD users had an average -1.2 (95% CI -1.9, -0.4) log load of L. jensenii compared to women using no highly effective method; likewise, injectable users had an average -0.7 (95% CI -1.3, 0) log load of L. iners compared to women using no method. L. crispatus, Leptotrichia/Sneathia and G. vaginalis quantities were similar across all groups. The magnitude of the difference in bacterial loads was larger when restricted to consistent contraceptive users. However, there were no significant associations in this smaller population. CONCLUSIONS: While hormonal contraception is associated with reductions in prevalent and incident BV, we found few species-specific associations when comparing common contraceptive methods. The lower level of L. jensenii among IUD users is consistent with reports of possible increased BV risk among IUD users. Lower level of L. iners in injectable users is consistent with studies reporting decreased lactobacilli among women using injectables. Further work is needed to understand if there are larger changes in the vaginal microbiota upon initiation of highly effective contraceptive methods and with prolonged use.

5 Microbiological etiology of symptomatic versus subclinical pelvic inflammatory disease L. A. Meyn1, I. Macio2, T. Darville3, H. C. Wiesenfeld1,2, S. L. Hillier1,2 1 The University of Pittsburgh Department of Obstetrics, Gynecology and Reproductive Sciences, Pittsburgh PA, 2Magee-Womens Research Institute, Pittsburgh, PA, 3University of North Carolina at Chapel Hill Department of Pediatrics

OBJECTIVES: Many women with tubal factor infertility do not report a prior episode of pelvic inflammatory disease (PID). In many cases upper genital tract infection and inflammation are asymptomatic,

leading to lack of detection and treatment. Subclinical PID can lead to chronic sequelae. Our objective was to compare bacterial etiologies of endometritis in women with symptomatic versus subclinical PID. METHODS: Women presenting with symptoms meeting the CDC criteria for PID and women at risk for PID [mucopurulent cervicitis, endocervical C. trachomatis (CT), or a recent sex partner infected with N. gonorrhoeae (GC), CT, or non-gonococcal urethritis] but without signs or symptoms were enrolled. An endometrial biopsy was obtained from all women prior to treatment. Histologic assessment for endometritis, defined as >1 plasma cell per 100X microscopic field, was assessed independently by 2 pathologists blinded to the design. Women having symptoms of PID (n¼208) who had endometritis were defined as symptomatic PID cases, while women at risk of PID (n¼134) who had endometritis were defined as subclinical PID. Endometrial tissue was tested for GC, CT, and M. genitalium (MG) by NAAT and cultured for aerobic and anaerobic bacteria. Differences in bacterial prevalence were evaluated by Fisher’s exact test. RESULTS: Symptomatic PID was present in 70 women and subclinical PID was present in 46 women. As shown in Table 1, endometrial CT, MG, Gardnerella vaginalis and Atopobium vaginae were equally frequent among women with symptomatic vs subclinical PID (P>0.2). GC was recovered from the endometrium of 8 women, 3 as the sole pathogen, in 4 women co-infected with CT, and in 1 woman co-infected with CT and MG, while 5 women had H. influenzae recovered from the endometrium as the sole pathogen. Both GC and H. influenzae were recovered exclusively from women with symptomatic PID (Table 1), and were never recovered from the endometrium of women having subclinical PID. One quarter of women with symptomatic PID and 30% of women with subclinical PID had no pathogens detected from the endometrium (P¼0.67). CONCLUSIONS: In this study, only half of women with histologically confirmed PID associated with endometrial CT and MG have symptoms. Ascending infections due to GC and H. influenzae cause pain and symptoms leading to the diagnosis of PID. Signs and symptoms of PID are a poor surrogate for most upper genital tract infections. The etiology of endometritis among women lacking upper genital tract infection remains unclear.

Table 1 Endometrium microorganisms among women with histologic endometritis No. of Women with Microorgansim Detected in the Endometrium

Women with Symptomatic PID (N¼70) n (%)

Women with Sublinical PID (N¼46) n (%)

C. trachomatis

33

17 (51.5%)

16 (48.5%)

N. gonorrhoeae

8

8 (100%)

M. genitalium

21

12 (57.1%)

H. influenzae

5

5 (100%)

G. vaginalis

38

22 (57.9%)

Endometrial Microbiota

P-value* 0.29

0

0.02

9 (42.9%)

0.81

0

0.16

16 (42.1%)

0.84

A. vaginae

19

13 (68.4%)

6 (31.6%)

0.61

Anaerobic gram negative rods

19

8 (42.1%)

11 (57.9%)

0.12

Anaerobic gram positive cocci

18

10 (55.6%)

8 (44.4%)

0.79

Negative culture and negative NAAT

32

18 (56.2%)

14 (43.8%)

0.67

* Fisher’s exact test.

816 American Journal of Obstetrics & Gynecology DECEMBER 2016