The author carried out a rapid survey of coastal and inland malaria in Sarawak in December 1946. Before recording the results of that survey, he summarizes previous reports concerning malaria in that country. [For information concerning malaria in Borneo, see this Bulletin, 1946, v. 43, 516 & 1, 000.] From May till November 1946, simultaneous epidemics of malaria occurred along the coast of Sarawak at the mouth of the Kuching River, Bintulu, Miri, Lutong, and at Kuala Bêlait and Seria in Brunei. These were aggravated by migrations of population. The epidemics were severe in type; the Kuching area had to be evacuated. In Miri and Lutong, malaria was epidemic to some degree in 1945 but the incidence fell to a low level in December and remained low until April 1946. Thereafter there was a very rapid rise until October, when the disease was reported as being out of control; the entire population was sick. The epidemic here was almost entirely due to P. falciparum. In the Kuala Bêlait and Seria epidemics, P. vivax was most in evidence. The Malay communities suffered much more than the Chinese; the latter are said to have become ' mepacrine conscious ' to the extent that they are willing to purchase the drug. Malays made no attempt at self protection. Spleen and parasite rates of Malay school children were found by the author to be more than twice as high as the Chinese school rates. Low rainfall in July, August and September allowed brackish water to infiltrate far up the Miri and Lutong Rivers and their tributaries; intense A. sundaicus breeding resulted. Moreover in 1946 spring tides flooded an area ravaged by war, with defective drainage, broken tidal gates, ponds and swamps. It is suggested that while A. leucosphyrus and A. umbrosus may transmit malaria along the coast, A. sundaicus is responsible for epidemic manifestations and this by reason of intense breeding rather than of its high infectivity. Further investigation is necessary to determine the importance of A. leucosphyrus and A. umbrosus as vectors. Norman White.
Plasmodium knowlesicauses severe malaria, but its pathogenesis is poorly understood. Retinal changes provide insights into falciparum malaria pathogenesis but have not been studied in knowlesi malaria.