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Two hundred forty-one strains of Salmonella typhi isolated in Lima, Peru, from October 1981 through February 1983were tested for susceptibility to antimicrobial agents. Seventytwo strains (29.9%) were resistant to chloramphenicol and other antibiotics, including ampicillin, sulfonamides, and trimethoprim. The minimal inhibitory concentrations of 17 antimicrobial agents were determined for all of these chloramphenicol-resistant strains. Sch 25393, new β-lactams, new quinolones, and the formulation clavulanic acid-amoxicillin were effective against all the strains. Four different resistance patterns distributed among eight phage types were observed. The 72 resistant S. typhi could transfer the resistance marker into Escherichia coli ell and all the plasmids belonged to the incompatibility group H1. [ABSTRACT FROM PUBLISHER]

A “suicide” system based on thymidine kinase-ganciclovir combination was developed and tested in a Leishmania major experimental model. Susceptible BALB/c mice were infected with L. major expressing the thymidine kinase gene of herpes simplex virus type 1 and treated for 2 consecutive weeks with 7.5 mg/kg/day ganciclovir at different times from the initial infection. Ganciclovir treatment at varying times after infection had different effects on the outcome of disease. A complete inhibition of intracellular parasites was obtained in mice treated 1 or 4 days after infection, whereas ganciclovir administration 2 weeks later resulted in the control of infection only when the drug was provided. Variable levels of protection, from partial to total, against challenge infection with virulent L. major were observed, depending on the timing of ganciclovir treatment. The thymidine kinase-ganciclovir approach represents an excellent experimental model to control Leishmania infection and to evaluate the immunologic response of the host. [ABSTRACT FROM PUBLISHER]

DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin) binds human immunodeficiency virus type 1 (HIV-1) and facilitates transfer of virus to permissive cells. Leishmania parasites also exploit DC-SIGN as a receptor. Here, we report that transfer of HIV-1 to target cells is markedly reduced when DC-SIGN(+) cells are preincubated with Leishmania amastigotes before pulsing with virions. Moreover, binding of HIV-1 to DC-SIGN(+) cells is diminished by the presence of Leishmania amastigotes. Our findings provide novel insight into the complex interactions between HIV-1 and Leishmania parasites. The ability of both HIV-1 and Leishmania parasites to bind to the same cell-surface constituent to gain entry into dendritic cells might have an impact on the immunological and pathological events associated with HIV-1 infection.