Needle exchange programs (NEPs) are designed to prevent human immunodeficiency virus (HIV) transmission among injection drug users. Although most studies report beneficial effects in terms of behavior modification, a direct assessment of the effectiveness of NEPs in preventing HIV infection has been lacking. A cohort study was conducted to assess the association between risk behaviors and HIV seroprevalence and seroincidence among injection drug users in Montreal, Canada. The association between NEP use and HIV infection was examined in three risk assessment scenarios using intensive covariate adjustment for empirical confounders: a cross-sectional analysis of NEP use at entry as a determinant of seroprevalence, a cohort analysis of NEP use at entry as a predictor of subsequent seroconversion, and a nested case-control analysis of NEP participation during follow-up as a predictor of seroconversion. From September 1988 to January 1995, 1,599 subjects were enrolled with a baseline seroprevalence of 10.7%. The mean follow-up period was 21.7 months. The adjusted odds ratio for HIV seroprevalence in injection drug users reporting recent NEP use was 2.2 (95% confidence interval 1.5-3.2). In the cohort study, there were 89 incident cases of HIV infection with a cumulative probability of HIV seroconversion of 33% for NEP users and 13% for nonusers (p < 0.0001). In the nested case-control study, consistent NEP use was associated with HIV seroconversion during follow-up (odds ratio = 10.5, 95% confidence interval 2.7-41.0). Risk elevations for HIV infection associated with NEP attendance were substantial and consistent in all three risk assessment scenarios in our cohort of injection drug users, despite extensive adjustment for confounders. In summary, in Montreal, NEP users appear to have higher seroconversion rates then NEP nonusers.

We studied the role of the P-lactamase of Campylobacterjejuni in resistance to ,B-lactam agents. ,B-Lactamasepositive strains were more resistant than ,B-lactamase-negative strains to amoxicillin, ampicillin, and ticarcillin (P < 0.05). With penicillin G, piperacillin, imipenem, and six cephalosporins, the susceptibility levels were similar for both P-lactamase-positive and -negative strains. By using spectrophotometric and microbiological assays, the ,B-lactamase from three strains hydrolyzed ampicillin, amoxicihlin, penicillin G, cloxacillin, and, partially, cephalothin. Ticarcillin and piperacillin were partially hydrolyzed in the microbiological assay. There was no activity against five other cephalosporins or imipenem. Isoelectric focusing of the enzyme showed a pl of 8.8.Tazobactam was the best inhibitor of the enzyme, followed by clavulanic acid, sulbactam, and cefoxitin, while EDTA and p-chloromercuribenzoate had no activity. All P-lactamase-positive strains became susceptible to amoxicillin and ampicillin with 1 ,ug of clavulanic acid per ml. With the same inhibitor, there was a reduced but significant effect for ticarcillin but no effect for penicillin G or piperacillin. Sulbactam had no effect and tazobactam was effective only at 2 ,ig/ml on amoxicillin and ampicillin. The 1-lactamase of C. jejuni seems to be a penicillinase with a role in resistance for only amoxicillin, ampicillin, and ticarcillin.

No abstract

The percentages of susceptibility of 28 strains of Campylobacter coli to 1-lactam agents were 96% for amoxicillin and ampicillin, 57% for ticarcillin, 4% for cefoxitin and cefuroxime, 61% for cefotaxime, and 11% for ceftazidime. None of the strains were susceptible to penicillin G, piperacillin, cefazolin, cephalothin, cefamandole, and cefoperazone. All strains were susceptible to imipenem and ciprofloxacin, and 21% were susceptible to erythromycin. A 13-lactamase was detected in 68% of the strains by cefinase disks and by the nitrocefin method. The 13-lactamase-positive strains were significantly less susceptible to amoxicillin, ampicillin, and ticarcillin than the 13-lactamase-negative strains (P < 0.003). Clavulanic acid (0.25 ,ug/ml) but not sulbactam and tazobactam (2 jg/ml) lowered to susceptible levels the amoxicillin and ampicillin MICs of the only strain of C. coli resistant to amoxicillin, ampicillin, and ticarcillin.Campylobacter coli has been recognized as a cause of human bacterial diarrhea and represents between 3 and 7% of Campylobacter human infections (1,8). Little is known about the ,B-lactam susceptibility pattern of C. coli. A few studies have reported data about ampicillin (4,12,14), amoxicillin (6, 14), cefotaxime (4, 6, 15), cephalothin (4, 10, 15), cefoperazone (14), and cefuroxime and penicillin G (15) susceptibility. ,B-Lactamase production was reported in 29 of 31 C coli tested by Fliegelman et al. (4). The purpose of this study was to determine the susceptibility pattern of C. coli to 3-lactam agents and to investigate the role of the ,-lactamase in the resistance to these antibiotics. The effect of clavulanic acid, sulbactam, and tazobactam on amoxicillin, ampicillin and ticarcillin was also studied.Ten strains of C. coli were obtained from a collection of 160 human thermophilic Campylobacter strains isolated in five hospitals in the Montreal area. Eighteen other human strains of C coli were obtained from the Laboratoire de Sante Publique du Quebec. Identification was done by the methods of the Centers for Disease Control, Atlanta, Ga. (8)

A retrospective study was conducted to assess the relationships between clindamycin resistance in members of the Bacteroides fragilis group, previous antimicrobial therapy, and the context for the development of infection, whether in the community or during hospitalization. Eighty-five clindamycin-resistant clinical strains (one isolate per patient) isolated from January 1988 to October 1994 were matched (one to one) with clindamycin-susceptible isolates recovered during the same period, and the charts of the patients from whom the isolates were recovered were reviewed retrospectively. Of the clindamycin-resistant strains, 65% were recovered from patients with hospital-acquired infections compared with 40% of the clindamycin-susceptible strains (odds ratio [OR], 2.75; 95% confidence interval [CI], 1.41-5.38; P = .002). Prior antimicrobial therapy for > or = 48 hours was also associated with clindamycin resistance (OR, 2.33; 95% CI, 1.16-4.70; P = .02). However, clindamycin resistance remained associated with hospital-acquired infections independent of prior antimicrobial therapy (Mantel-Haenszel weighted average OR, 2.22; 95% CI, 1.03-4.89; P = .04). Clinicians should consider the risks for clindamycin resistance when treating hospital-acquired infections caused by members of the B. fragilis group.