The epidemiology, clinical patterns, and risk factors for visceral leishmaniasis were prospectively studied in an endemic area of Brazil. The prevalence of disease was 3.1% for children less than 15 years of age, and the annual incidence was 4.3 cases per 1,000 children. The number of children with disease fluctuated yearly and seasonally, and distribution of the disease varied within the endemic area. Risk factors included young age (median, three years) and malnutrition before the onset of disease. Intestinal parasitism, recent migration into the area, and house location within the area did not influence the progression of infection to disease. Serological testing indicated that 7.5% of children were infected with Leishmania each year and that the ratio of disease to infection was 1:18.5 for the whole area and 1:6.5 for the section with the highest prevalence of disease. Early diagnosis and therapy altered clinical patterns of the disease.

Leishmaniasis, caused by infection with the protozoan parasite

No abstract

Cell-mediated immunity was assessed in 14 Brazilian patients with acute untreated American visceral leishmaniasis (AVL) and in 11 healthy patients successfully treated 1 to 14 years previously. The diagnosis of AVL was established by demonstration of leishmania in bone marrow aspirates. The responsiveness of peripheral blood mononuclear cells to Leishmania chagasi antigens and phytohemagglutinin was studied in vitro. Soluble preparations of L. chagasi antigens were obtained from frozen-thawed promastigote cultures. L. chagasi antigenstimulated lymphocytes from untreated AVL patients were unresponsive and incorporated a mean of 1.2 ± 0.5 X 10' cpm after a [3H]thymidine pulse. The cured AVL patients had 19.1 ± 7.2 cpm, and 15 normal control subjects had 0.8 ± 0.1 cpm. There was no difference in the response of controls and either untreated or cured AVL patients to phytohemagglutinin stimulation. Three of four untreated AVL patients responded to L. chagasi antigens when restudied 2 to 4 weeks after therapy. The impaired response of lymphocytes from untreated AVL patients could not be attributed to either reduced numbers of circulating T cells or the inhibitory effect of monocytes or serum factors. Leishmania are obligate intracellular protozoa which cause a spectrum of disease in man ranging from self-healing skin ulcers to fatal visceral infections (13). American visceral leishmaniasis (AVL) is caused by Leishmania chagasi and clinically is characterized by fever, hepatosplenomegaly, anemia, leukopenia, and marked hyperglobulinemia (13). AVL occurs primarily in children and is usually fatal if untreated. A similar disease caused by L. donovani is called kalaazar in Africa and Asia.