Israel Medical Association Journal

Background: Although the presence of bacteria in the cervix is not a sign of disease, the majority of pathogens involved in pelvic inflammatory disease originate from this "normal" flora.

Objectives: To assess the distribution of cervical non-gonococcal and non-chlamydial bacteria in hospitalized women with PID[1] and the bacteria's antibiotic sensitivity.

Methods: We retrospectively evaluated the cultures obtained from the uterine cervix over a 1 year period (2008) at Wolfson Medical Center, Holon. The distribution of cervical non-gonococcal and non-chlamydial bacteria in women with PID and the bacteria's antibiotic sensitivity was compared to that in our previous 1 year study that was performed at Kaplan Medical Center, Rehovot (1988–89). 

Results: In 2008, a total of 412 cultures were obtained of which 126 (30.5%) were sterile. The prevalence of negative cultures was similar in 2008 and in 1988, namely, 30.5% and 33.7%, respectively (P = 0.23). PID was finally diagnosed in 116 patients with positive cultures. The most prevalent bacteria in the 2008 study were Enterococcus species and Escherichia coli – 24.0 % and 26.4% respectively compared to 18.0% and 38.1% in the 1988 study, with the decrease in E. coli isolates being significant (P = 0.0003). In 2008 the antimicrobial sensitivity for various antibiotics ranged from 44.3% to 100.0% (median 90.2%) while in 1988 it ranged from 2.9% to 80.1% (median 51.9%).

Conclusions: The cervical bacterial flora in hospitalized women with PID did not vary significantly between 1988 and 2008. However, antimicrobial sensitivity of the isolated bacteria increased dramatically, probably due to a decrease in resistance to antibiotics.

Background: Chlamydia pneumoniae has previously been associated with higher prevalence of valvular and cardiac calcifications.

Objectives: To investigate a possible association of seropositivity for C. pneumoniae and the presence of cardiac calcifications (mitral annular or aortic root calcification, and aortic valve sclerosis).

Methods: We retrospectively analyzed serological data (immunoglobulin G TWAR antibodies) from the AZACS trial (Azithromycin in Acute Coronary Syndromes), and correlated the serological findings according to titer levels with the presence of cardiac calcifications as detected by transthoracic echocardiography.

Results: In 271 patients, age 69 ± 13 years, who underwent both serological and echocardiographic evaluation, we found no significant association between the "calcification sum score" (on a scale of 0–3) in seropositive compared to seronegative patients (1.56 ± 1.15 vs.1.35 ± 1.15, respectively, P = 0.26). The median "calcification sum score" was 1 (interquartile range 0–3) for the seronegative group, and 2 (interquartile range 0–3) for the seropositive group (P = 0.2757). In addition, we did not find a significant correlation of any of the individual sites of cardiac calcification and Chlamydia pneumoniae seropositivity.

Conclusion: Our findings suggest that past C. pneumoniae infection may not be associated with the pathogenesis of valvular and cardiac calcifications.
 

Objectives: To determine whether there is an association between the presence and severity of adult calcific aortic stenosis and Chlamydia pneumoniae seropositivity

Methods: Forty adult patients (23 women, 17 men) were divided into three groups according to echocardiographic aortic valve area: Group A – 7 symptomatic subjects (age 67 ± 7 years) with normal aortic valve and normal coronary angiogram, Group B – 16 patients (age 73 ± 6) with moderate ACAS[1] (AVA[2]> 0.8 £ 1.5 cm²), and Group C – 17 patients (age 76 ± 7) with severe ACAS (AVA £ 0.8 cm²). We tested for immunoglobulins M, G and A as retrospective evidence of C. pneumoniae infection using the micro-immunofluorescence method. Past C. pneumoniae infection was defined by IgG titer > 16 £ 512.

Results: No patients in Group A showed positive Ig[3] for C. pneumoniae. IgM was not detected in any of the patients with ACAS (groups B and C) while 2 of 17 patients (12%) in group C showed IgA for the pathogen. High titers of IgG were found in 14 of 33 (42%) of the patients with moderate or severe ACAS: 5 of 16 (31%) in group B and 9 of 17 (53%) in group C (P = 0.2). Both groups had the same prevalence of coronary artery disease (66%). AVA was lower in IgG-seropositive patients than in the seronegative group (0.88 ± 0.3 cm² vs. 1.22 ± 0.4 cm², respectively, P = 0.02).

Conclusions: Past C. pneumoniae infection may be associated with a higher prevalence and greater severity of ACAS.

Objectives: To determine the prevalence of different pathogens in patients presenting to our sexually transmitted disease clinic with hematospermia.

Methods: Between January 1999 and January 2000, 16 patients presented to our STD[1] clinic with hematospermia after other non-infectious pathologies had been excluded by a referring physician. After obtaining informed consent, subjects completed a questionnaire addressing symptoms and sexual behavior. First void urine samples, as well as genitourinary and serum specimens were tested for Chlamydia trachomatis, Ureaplasma urealyticum and Herpes simplex virus. Standard bacterial cultures were also performed.

Results: Laboratory testing detected a pathogen in 12 of the 16 males presenting with hematospermia. The sexually transmitted pathogens detected were Herpes simplex virus in 5 patients (42%), Chlamydia trachomatis in 4 (33%), Enterococcus fecalis in 2 (17%), and Ureaplasma urealyticum in 1 (8%). In all cases in which a pathogen was identified, the appropriate antimicrobial agent was administered. Symptoms resolved for each patient following antimicrobial therapy. During a 1 year follow-up, all 12 patients remained free of disease.

Conclusions: Recent advances in microbiologic diagnostic techniques have facilitated the detection of pathogens in patients with hematospermia, thereby enhancing the efficacy of treatment.

____________________

[1] STD = sexually transmitted disease

Background: Non-gonococcal urethritis is the most common clinical diagnosis for men seeking care at sexually transmitted disease clinics.

Objective: To identify the pathogens involved in NGU[1] among males attending an Israeli STD clinic.

Methods: During 19 months spanning September 1996 to July 1998 we investigated a cohort of 238 male patients attending the Bnai Zion Medical Center STD[2] clinic with a clinical presentation of urethritis. Intraurethral swab specimens were tested for Neisseria gonorrhea, Ureaplasma urealyticum, Mycoplasma hominis, and Trichomonas vaginalis by culture and for herpes simplex virus by antigen detection. First voiding urine for Chlamydia trachomatis was done by polymerase chain reaction. The specific seropositivities of HSV[3] types 1 and 2 were tested by enzyme-linked immunosorbent assay.

Results: From among 238 males with dysuria or urethral discharge an etiology for urethritis was found for 71 (29.8%). N. gonorrhea was recovered in only three men (4.2%). In the remaining 68 NGU patients C. trachomatis (35/68, 51.5%) and U. urealyticum (31/68, 45.6%) were the most common infecting and co-infecting pathogens (P < 0.0001). M. hominis and T. vaginalis were found in 9/68 (13.2%), and 1 patient, respectively. HSV was recovered from the urethra in 7/68 males (10.3%) – 3 with HSV-1, 2 with HSV-2, and 2 were seronegative for HSV. None of these males had genital lesions. Although a single etiologic agent was identified in 45/68 infected men (66.2%), co-infection was common: 2 organisms in 15 (22%) and 3 organisms in 8 (11.8%).

Conclusion: C. trachomatis and U. urealyticum were the most common infecting and co-infecting pathogens in this cohort of men with NGU. Unrecognized genital HSV infections are common in males attending our STD clinic and symptomatic shedding of HSV occurs without genital lesions. Still, the microbial etiology in this group remains unclear in many patients despite careful microbiologic evaluation.

Background: Recent studies have suggested a possible association between Chlamydia pneumoniae infection and coronary heart disease.

Objectives: To determine titers of antibodies to Chlamydia pneumoniae in patients with acute  myocardial infraction compared with titers in several control groups.

Methods: This prospective case-control study investigated 209 individuals. We assessed the serum IgG antibody titers to Chlamydia pneumoniae in 57 consecutive patients admitted with AMI to our intensive coronary care unit during a 4 month period. A serum sample was drawn upon admission after 6 weeks. Results were compared with those of four control groups: a) patients admitted with community-acquired pneumonia (n=18), b) patients with community-acquired urinary tract infection (n=42), c) patients with angiographically normal coronary artery disease (n=44), and d) patients with stable coronary artery disease (n=48). Serum immunoglobin G antibody titers to C. pneumoniae were determined using standard micro-immunofluorescene technology.

Results: Of 57 patients with AMI, 32 (56%) had a high lgG titer to C. pneumoniae (>=1:256) on the initial test, which remained unchanged (62%) after 6 weeks. The percentage of patients with high titers was significantly lower in the control groups: 5 of 18 patients (28%) in the pneumonia group (P<0.01), 11 of 42 (26%) in the urinary tract infection group (P<0.01), 11 of 44 (25%) with normal coronary arteries (P<0.01), and 17 of 48 (35%) with stable chronic ischemic heart disease (P<0.05).

Conclusion: The detection of high titers of lgG antibodies to C. pneumoniae in many patients with AMI, compared to control groups, suggest that chronic Chlamydia pneumoniae infection plays a role in the pathogenesis of atherosclerosis and acute ischemic events.

Objectives: To evaluate the association between chronic infection with C. pneumoniae, as measured by a high titer of IgG antibody, and CAD. Our study was designed to explore the relationship between seropositivity to C. pneumoniae and serious coronary events, and to assess whether or not there may be an additional association between established cardiovascular factors and infection with this organism.

Methods: The serum of 130 patients with proven CAD was tested for the presence of IgG antibodies to C. pneumoniae using an ELISA test. A titer ≤1:64 using the microinfluorescence method, the recognized "gold standard," correlates with a positive result when using the ELISA method. The mean age was 57 (40-65 years). The patients, 82% male and 18% female, had either myocardial infarction (n=109) or unstable angina (n=21) 6 months before the investigation (range 3-24 months). The serum for the control group was obtained from 98 blood donors from the same area matched for age 52 (40-58 years) and sex. The donors had no known cardiac history.

Results: In the CAD group 75% of patients were positive for C. pneumoniae compared to 33% in the control group (P=0.001). No increased correlation could be demonstrated between traditional risk factors and C. pneumoniae infection, except in those patients with diabetes mellitus. We found a lower prevalence of IgG antibody to C. pneumoniae in the diabetes subgroup than in other subgroups (P<0.006), but a higher prevalence than in the control group.

Conclusions: We demonstrated a more than twofold increase in seropositivity to C. pneumoniae among patients suffering serious coronary events, and this trend was independent of gender, age or ethnic group. These findings suggest that chronic C. pneumoniae infection may be a significant risk factor for the development of CAD, but this correlation should be investigated further.

_______________________________________

CAD= coronary artery disease