Abstract

An account is given of the investigation of 300 cases of kala-azar in the Fung Province of the Sudan. The area is inhabited by Arabs, negroids and Fellata whose habits and mode of life are fairly primitive. Diet, though sufficient in calorie value, is ill-balanced and probably deficient in Vitamins A and C. The disease is truly endemic and liable to periodic increase in endemic foci One such increase involving twenty-one cases is described. Cases probably originated mostly between August and February. There is no particular racial predisposition; individuals in a state of malnutrition and lowered resistance generally being most prone to infection. The disease affected mainly children and young adults, and was commonest in males. A history of contact or familial infection was common, especially in children. Children appeared to develop the disease more quickly than adults—the usual interval being several months after exposure to infection. The parasite was always present in the spleen; in 1 per cent. only in the peripheral blood, and in 7·5 per cent. in nasal smears. The parasite demonstrated was morphologically the same as that described in India. On postmortem examination inflammation of the bowel was usually present. Concomitant infections found were malaria, intestinal helminths, schistosomiasis, dysentery, syphilis and tuberculosis. The disease was usually a chronic infection characterized by periodic or terminal acute exacerbations. The most prevalent symptoms were fever, splenic and hepatic enlargement, emaciation, epistaxis and diarrhoea. Blood examination showed anaemia and leucopenia with a relative increase in lymphocytes and large mononuclears. Diagnosis was always confirmed by splenic puncture. The course of the disease varied under treatment. The chief complications were septic conditions of the buccal cavity and upper respiratory passages. Pneumonia, dysentery, agranulocytosis and acute intestinal haemorrhage also occurred. Several cases of antimony poisoning occurred, especially in adults. Prognosis depended primarily on the stage of the disease at which treatment commenced. Ultimate cure was always associated with splenic shrinkage in addition to disappearance of all other symptoms. Children responded to treatment more favourably than adults. Cases peculiarly resistant to antimony therapy occurred. Routine specific treatment consisted of one course of neostibosan followed if necessary by one or two courses of antimony tartrate. Treatment was controlled by splenic puncture.

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