Proof that a patient is suffering from sulfone-resistant leprosy depends on demonstrating that his bacilli can multiply in the mouse foot pad even when the mice are fed sulfone in the diet. Hitherto the maximal dose of DDS tolerated by the mouse has been used in such tests. This paper concerns a patient whose bacilli multiplied in mice fed lower doses of DDS, but were inhibited when the maximal dose was used . His clinical features are distinctive and probably characteristic of this type of "partial" resistance. It is likely that more cases of this type will be found . Recommendations are made concerning the investigation of possible DDS-resistant leprosy patients and their treatment.
Using a trial design previously evolved at Sungei Buloh Leprosarium, a pilot trial was performed of B.663, in the dosage of 100 mgm. twice weekly, in eight patients with previously untreated lepromatous leprosy. The therapeutic results, as measured by clinical, bacteriologic and histologic assessment, and especially by the rate of fall of the morphologic index, were similar to those obtained with sulfone therapy or with 0.663 in the dosage of 300 mgm. daily. Although B.663 pigmentation was produced in all eight patients, it developed more slowly and was less intense than with standard dosage. Difficulties resulting from skin discoloration in assessing the clinical progress of patients on B.663 are discussed.
The fluorescent antibody (FA) technique was used to detect the presence of malarial antibody in populations living in 3 different ecological areas of Malaysia. Serum samples were tested using Plasmodium falciparum, P. vivax, P. malariae and P. fieldi antigens. An area of hyperendemic malaria had a good correlation between the antibody responses and active parasitaemias. The percentage and intensity of responses increased with the age of the individuals. In an area of hypoendemic malaria, each of 17 sites had ecological conditions which would favour or discourage the transmission of malaria. The reasons for high FA responses in some villages and low responses in others were readily apparent. The effect of even limited control programmes on the malarial ecology could be measured by an examination of the antibody responses. An aboriginal population receiving suppressive drugs had FA responses indicating both past experience and the effect of the drug programme.