This high incidence of Chlamydia only in coronary arteries diseased by atherosclerosis suggests an etiologic role for Chlamydia infection in the development of coronary atherosclerosis that should be further studied.

No abstract

The outer surface lipoproteins of Borrelia burgdorfieri, OspA and OspB, stimulate the production of nitric oxide (NO) by murine bone marrow-derived macrophages from BALB/c, C3H/HeN, and C3H/HeJ mice. Gamma interferon (IFN-y) caused a threeto fivefold enhancement of this production of NO, and the L-arginine analog N-guanidino-monomethyl L-arginine inhibited it. Activation of transcription of the inducible NO synthase gene in stimulated macrophages was demonstrated by reverse transcriptase rapid PCR. Although IFN-y increased the amount of NO produced in macrophage cultures, it did not cause transcription of the inducible NO synthase gene greater than that seen with the Borrelia proteins. OspA and OspB also induced the production of high levels (40 to 150 ng/ml) of IFN-y in cultures of macrophages incubated with interleukin-2 (IL-2)-elicited cells from normal (T and NK cells) and scid (NK cells) mice but not in macrophages or IL-2-elicited cells cultured individually. This suggests that OspA stimulated macrophage production of cytokines, which, in turn, stimulated the production of IFN-y by NK and T cells. Reverse transcriptase rapid PCR demonstrated that OspA and sonicated B. burgdorferi stimulated production of several inflammatory cytokines in macrophage cultures, including IL-1, IL-6, IL-12, IFN-1l, and tumor necrosis factor alpha. As tumor necrosis factor alpha, IFN-I, and IL-12 are potent activators of IFN-y production by T and NK cells, their presence in these cocultures could be responsible for the IFN-y production. Lymphocytes from infected C3H mice also produced IFN-y when stimulated with B. burgdorferi; thus, immune cells may also modulate NO responses. The generation of NO during infection with B. burgdorferi may be important, as NO has potent antimicrobial properties. NO can also be involved in pathological inflammatory processes in which its generation is detrimental to the host. Thus, the colocalization of B. burgdorferi lipoproteins, NO-producing cells, and regulatory cytokines may determine the outcome of infection.

In order to assess the efficacy of 70% ethanol locks in addition to antibiotic therapy to treat tunnelled central venous catheter-associated bloodstream infections, a pilot study of 19 patients was performed prospectively using ethanol locks for 5 d in addition to antibiotic therapy to treat tunnelled central venous catheter-associated bacteraemia. 12 patients had mono-microbial infections and 7 had polymicrobial isolates. 17 of 19 patients completed ethanol lock therapy. 15 of 17 patients completing ethanol lock therapy had no recurrence of the original organism and retained their catheter for a median of 36 and an average of 47 d following initiation of ethanol lock therapy. These results demonstrate the safety and potential efficacy of this technique against a broad range of potentially virulent organisms. The intervention was acceptable to both staff and patients with no significant side-effects. These preliminary results from our prospective pilot study suggest that ethanol lock therapy is safe and easily integrated into clinical practice, and may have utility in treating central venous catheter-associated infections, avoiding removal of catheters in patients requiring long-term venous access.