Medicine: The Case of Japanese B

When U.S. forces invaded Okinawa on Easter Sunday in 1945, some divisions were assigned to hit the beaches and engage the known enemy, the Japanese army, while others were held aboard ships bobbing offshore, as replacements for men expected to be knocked out of battle by a second enemy, unseen and almost unknown. In that campaign, however, this unknown enemy held his fire. In Tokyo, later, occupation forces set up a special headquarters near the Imperial Palace to direct operations against the stealthy killer. By 1950 they thought they had him cornered, but then Red aggression gave him the chance he had been waiting for. As Allied forces were backed into the overcrowded, filthy Pusan perimeter of southern Korea, thousands were stricken. Most made good recoveries, but 307 U.S. soldiers suffered severely and 30 of them died.

Their enemy was "Japanese B," a form of encephalitis (inflammation of the brain) akin to those forms which plagued St. Louis in 1933 and recently centered in southern Indiana (TIME, Oct. 10). The nature of the illness has long been known, along with the fact that it breaks out every summer in most of Japan, parts of Manchuria and all of Korea, and a few weeks later in Russia's Maritime Prov ince. However, the most important questions could not be answered for years: How is the disease transmitted? Where does it come from? Who is susceptible? How can it be controlled?

Last week U.S. Army medics were confident that they had most of the answers to the first three questions, and had hopes of coping with the fourth. Along the way they had done some astute medical detective work from their 406th Medical General Laboratory in downtown Tokyo, and had pulled in expert virus sleuths from halfway round the world.

Guilty Birds. Primary clues: Japanese B breaks out regularly every June in Japan and Korea, subsides in September. Peak numbers of cases go with hot, wet weather. In southern Japan, up to 95% of all tested subjects over 20 have antibodies which give them immunity: they have had an undetected, mild case, as so often happens with polio. But in cold, northern Hokkaido, fewer than 10% have antibodies. Where the people have antibodies, so have horses, cattle, goats, sheep and chickens. So Japanese farmers who have brought chickens into their homes (and Koreans who have asked the cattle in) during the epidemic season were working on the right clue, though they naively hoped that the critters would take most of the bites.

For it soon developed that Japanese B is transmitted to humans by the bite of a mosquito, Culex tritaeniorhynchus. Only the females are venomous bloodsuckers; the gentle males stick to flower nectar. All well and good, but mosquitoes disappear in winter. Where did they fill up with encephalitis virus in the early summer to pump it into humans? The answer was an animal, no doubt, with seasonal habits—one easily infected with the virus but not made seriously ill or killed by it. That pointed to young animals, which would promptly develop antibodies. The only creatures that fitted these specifications were birds.