The Threat of Infectious Disease in Americans Returning from Operation Desert Storm

Acute visceral leishmaniasis is associated with an antigen-specific immunosuppression of mononuclear cells as evidenced by defective in vitro production of interferon gamma. We evaluated treatment with recombinant human interferon gamma in combination with conventional pentavalent antimony therapy in patients with visceral leishmaniasis. Six of eight patients with visceral leishmaniasis (mean duration, 17 months) that had been unresponsive to multiple courses of pentavalent antimony responded to treatment with recombinant human interferon gamma (100 to 400 micrograms per square meter of body-surface area per day) in addition to pentavalent antimony (20 mg per kilogram of body weight per day) for 10 to 40 days. The other two patients improved initially but then relapsed and required treatment with amphotericin B. Eight of nine additional patients with previously untreated severe visceral leishmaniasis were also successfully treated with the combination of interferon gamma and pentavalent antimony. The 14 patients who responded to this regimen had marked improvement in symptoms and in measures of anemia and leukopenia, as well as weight gain, a decrease in spleen size, and an absence or reduction of leishmanias in splenic aspirates. These patients had no recurrence of illness after a mean (+/- SE) follow-up of 8 +/- 1 months. Fever was the only major side effect of interferon gamma. We conclude that the combination of interferon gamma and pentavalent antimony is effective in treating seriously ill patients with refractory or previously untreated visceral leishmaniasis.

Electrophoretic enzyme typing revealed that a single group A Neisseria meningitidis clonal complex, designated III-1, was responsible for recent epidemics in Nepal, Saudi Arabia, and Chad. Epidemiological investigations and enzyme typing profiles indicated that this clone was brought from South Asia to the Middle East by Muslims making their pilgrimage (haj) to Mecca, Saudi Arabia, in 1987. Pilgrims who became group A carriers introduced this clonal group into sub-Saharan Africa on their return from the haj. The introduction of this clonal group into sub-Saharan Africa may be responsible for the current wave of epidemics affecting the region. Although the findings suggest that clonal virulence is an important factor in the development of epidemics of meningococcal disease, other factors also seem to be necessary for the development of an epidemic.