Surgical Infection Society position on vancomycin-resistant Enterococcus.

The risk of transfer of vancomycin resistance to staphylococci is a real possibility and has been achieved in the laboratory. Prolonged colonization occurs with vancomycin-resistant Enterococcus (VRE), and many more patients are colonized than infected. The failure to identify, isolate, and adhere to infection control measures when caring for VRE-colonized patients dooms to failure any means to control its spread. Control of vancomycin use alone is unlikely to greatly affect the number of patients at risk for VRE colonization. The global spread of VRE may be impossible to stop, but infection control measures are the most important line of defense inside hospitals.

Treatment of experimental visceral leishmaniasis in a T-cell-deficient host: response to amphotericin B and pentamidine.

In experimental visceral leishmaniasis, euthymic but not athymic (nude) BALB/c mice respond to conventional treatment with pentavalent antimony, indicating that the in vivo efficacy of antimony is T cell dependent. This finding correlates with frequent antimony treatment failures for T-cell-deficient patients with visceral leishmaniasis. To determine whether the in vivo efficacies of alternative antileishmanial agents also require T cells, Leishmania donovani-infected euthymic and nude BALB/c mice were treated with pentamidine or amphotericin B. Pentamidine induced leishmanistatic activity in euthymic mice but had little effect in nude mice. In contrast, amphotericin B exerted potent leishmanicidal activities in both euthymic and nude animals. These results suggest that amphotericin B may be of particular use for T-cell-deficient patients with visceral leishmaniasis.

Models of relapse of experimental visceral leishmaniasis.

To establish models for studying recurrence of visceral leishmaniasis, a growing problem in T cell-deficient patients, two approaches were investigated: treatment of euthymic BALB/c mice with quiescent Leishmania donovani infection with T cell-depleting or anti-cytokine antibodies and serial observation of acutely infected nude BALB/c mice after an initial antileishmanial response induced by amphotericin B treatment. In chronically infected euthymic mice, maintenance of acquired immunity and prevention of relapse required CD4 cells and a multicytokine-dependent mechanism involving endogenous interleukin-2, interferon-gamma, and tumor necrosis factor-alpha. Acutely infected nude mice responded to amphotericin B with a > or = 85% reduction in liver parasite burdens; however, after a brief lag, visceral infection readily recurred in the posttreatment period. Both models may be useful for testing experimental interventions designed to reduce relapse of previously controlled visceral leishmaniasis in T cell-deficient hosts.