Buruli disease, caused by Mycobacterium ulcerans, is the third most important mycobacterial disease in humans besides tuberculosis and leprosy. We have compared systemic and intralesional cytokine production in patients presenting with a nodular form and a necrotizing, ulcerative form of the disease. Gamma interferon (IFN-␥) levels in response to whole M. ulcerans and Mycobacterium bovis BCG bacilli and in response to purified Ag85 protein from BCG were lower in peripheral blood mononuclear cells (PBMC) cultures from Buruli disease patients than in PBMC from healthy purified protein derivative-positive contacts. Interleukin-4 (IL-4) and IL-13 content was below the detection threshold in these PBMC cultures. IFN-␥ production after stimulation with M. ulcerans was significantly lower (P < 0.05) in PBMC cultures from patients with ulcers than in those from patients with nodules. On the other hand, PBMC from Buruli disease patients produced significant levels of IL-10 in response to M. ulcerans (but not to M. bovis BCG) and production was highest in patients with the ulcerative form. Third, semiquantitative reverse transcription-PCR analysis demonstrated a similar difference in the local, intralesional cytokine profile for the two forms of the disease: high IFN-␥ but low IL-10 mRNA levels in nodular lesions and high IL-10 but low IFN-␥ mRNA levels in ulcerative lesions. Intralesional IL-4 and IL-13 mRNA levels were low and only detected in patients with the ulcerative form. Our results indicate, although they do not formally prove, that production of IL-10 rather than production of IL-4 or IL-13 by Th2-type T cells may be involved in the low M. ulcerans-specific IFN-␥ response in Buruli disease patients.

We aimed to identify prognostic factors for AIDS-associated disseminated histoplasmosis. In a multivariate analysis, we found that dyspnea, a platelet count of <100,000 platelets/mm3, and lactate dehydrogenase levels of >2 times the upper limit of the normal range were significantly independently associated with the death of the patient during the first 30 days of antifungal treatment.

Both preventive and therapeutic vaccine programs provided substantial benefit, but their relative merit depended on which outcome measures were assessed. Evaluation of HIV vaccine programs based solely on cases averted or on prevalence of HIV in the population underestimates the benefit associated with therapeutic vaccine programs. The effect of a therapeutic HIV vaccine on the epidemic outcomes depended markedly on whether the therapeutic vaccine reduced the infectivity of the vaccine recipient. The relative merits of preventive and therapeutic vaccines depend on the stage of the epidemic. Field vaccine trials should evaluate correlates of infectivity, such as HIV viral load. HIV vaccine implementation strategies should be tailored to the dynamics of the epidemic in specific populations.

Leishmania species can cause a wide spectrum of cutaneous disease in HIV-positive patients: asymptomatic, localized cutaneous, mucosal, muco-cutaneous, diffuse cutaneous or post-kala-azar leishmaniasis. In such cases, which are usually severely immunocompromised, the leishmanial parasites reach the skin of the human host by dissemination after either a new infection (resulting from the bite of infected sandfly or, probably, the sharing of contaminated syringes by intravenous-drug users) or the re-activation of a latent infection. Recent experience and past observations on the dermatology of leishmaniasis in those with Leishmania/HIV co-infection are reviewed here.