A New Plan
American malariologists also launched a malaria project, but on a different trajectory. It began in April 1939, when Lowell Coggeshall attended his first meeting of a special committee created by the National Research Council to examine the problem of malaria and war.
The Nazis had invaded and occupied Austria and Czechoslovakia. This was just five months from when Germany would send troops, planes, and tanks to slaughter Poles and encircle Warsaw—and Great Britain and France would finally declare war on Germany.
The NRC’s job was to anticipate research needs of the War Department, should the United States be dragged into hostilities in Europe. A chief concern on the health care front was vicious endemic malaria in the Pacific, Asian, and Mediterranean regions—all areas mapped out by war planners as likely battle zones. The fevers would attack and disarm occupying troops indiscriminately. A magic-bullet cure would be great. But a good prophylactic would do, as it would allow troops to sit out engagements in a defensive posture and just wait for the enemy to fall back with fever. Then U.S. forces would go on attack in a much stronger position, resulting in overall fewer battle casualties and no malaria-related troop attrition. As far as anyone knew, no government had developed a true prophylactic against malaria, not even Germany.
The Allies at least had Holland and the Dutch East Indies’ vast cinchona plantations, which would provide enough quinine to mitigate the intensity of infections. But quinine stopped working when used for too long or in regions with abundant infectious mosquitoes—conditions war created. A drug that could stop infections completely would be as potent a weapon as any in the military’s arsenal, and would most certainly shorten the war in favor of the Allies, maybe even by years—which would reduce military and civilian casualties by millions.
But first it had to be developed. The question of how such a drug could be made was brought up at the April 1939 NRC meeting.
For the first time, Lowell found himself on a project with chemists, which was exactly where he wanted to be. His work at Rockefeller proved to him that a malaria vaccine—a preparation with proteins derived from the pathogen—would not come anytime soon, and certainly not in time for war. He steered the NRC from a broad discussion of finding a wide range of chemically derived compounds to treat diseases, which they called chemotherapy, to finding a chemical prophylactic for malaria. This would be a pill troops took daily or weekly to block malaria transmission while they slept under the stars unprotected from thirsty malarial mosquitoes. At the meeting were renowned chemists, including Marston T. Bogert, professor of organic chemistry at Columbia University; Lyndon F. Small, chief chemist at the U.S. Public Health Service; Herbert R. Moody, director of the chemical laboratories at the College of the City of New York and of chemical technology at the NRC; Leonard H. Cretcher of the Mellon Institute of Industrial Research; and Torald H. Sollmann, dean of Western Reserve University School of Medicine.1
From this initial meeting grew the NRC-sponsored Committee on Chemotherapy. Lowell and the others invited additional experts—parasitologists, entomologists, hematologists, and medical researchers. For support and funding, they recruited high-end sponsors, including Surgeon General Thomas Parran, who chaired a symposium on malaria in May 1940, and the American Association for the Advancement of Science (AAAS), which was about to run another symposium coming up in December 1940. The group received endorsements and promises of support from the War Department, the U.S. Department of Commerce, the Tennessee Valley Authority, the Pasteur Institute, Harvard, and the American Drug Manufacturers Association, to name only a few.
Lowell undertook the Herculean task of surveying top university labs and commercial pharmaceutical and chemical companies to gauge their willingness to participate.2 He also recruited other malariologists to bring to the group a deep knowledge of the disease. Others compiled bibliographies, reviews, and digests of all work done thus far to develop antimalaria chemotherapies. The landscape was pretty stark, and almost entirely originating in Germany and centering on Bayer’s two synthetic quinines: plasmochin and atabrine.
In August 1940, Lowell and his colleagues wrote a piece for Science magazine—the prestigious journal of the AAAS—calling for a national campaign with a media strategy designed to encourage research investments in drug development, specifically for malaria. They argued for a strong national program that put “chemistry in the service of medicine” so that all citizens would benefit. U.S. chemical companies, which were quite small, would grow in size as they filled druggists’ shelves with new treatments for everything from the flu to cancer.3 But anyone watching world events knew the impetus really was the war, and that the United States would soon be in it and in need of battlefield remedies, especially for malaria.
Committee members also canvassed colleagues and spoke and wrote about efforts to bring more experts on board. And they all pressed the War Department, Congress, and the Roosevelt administration to provide needed funds. “Speed is urgently needed,” Lowell and his colleague wrote in Science, “for the medical profession confidently predicts a malaria peak this year or next.”4 They were, of course, talking about American troops fighting battles across Great Britain’s vast colonial empire—most of which lay in tropical malaria zones.
They all, especially Lowell, assumed the Roosevelt administration would open the funding spigot. How could it not back the plan? Top administrators were on board. Key leaders in the army and navy medical corps were on board. The NRC was recommending it. And it was visionary, innovative, solution based, and science driven.
But it was also ahead of its time. The big money didn’t materialize. And the group remained isolated with only limited resources.
Nonetheless, Lowell and his NRC colleagues forged ahead using Rockefeller’s fever therapy lab at the state hospital in Tallahassee; the Public Service’s lab at the South Carolina State Hospital in Columbia; and smaller affiliated labs at North Carolina University at Chapel Hill and Emory University in Atlanta. To synthesize new compounds they recruited the chemical labs at Parke-Davis and Company in Detroit; Eli Lilly and Company in Indianapolis; Merck & Co. in Rahway, New Jersey; E. R. Squibb and Sons, in New Brunswick; and, of course, Winthrop Chemical Company in Rensselaer, New York.
LOWELL forged relationships with these burgeoning commercial companies, which made what they could and imported the rest. From Winthrop, for example, Lowell obtained German-made samples of Bayer’s two antimalarials, the odd yellow drug atabrine and its oxygen-choker cousin, plasmochin.
DuPont gave him samples of sulfa-based compounds, which in 1939 had won German pathologist and chemist Dr. Gerhard Domagk a Nobel Prize. Domagk was a university professor and brilliant researcher Bayer had hired in the late 1920s to find drug remedies amid I.G. Farben’s huge catalog of already made chemical compounds. In that short time he took off the shelf an old substance from 1908 and turned it into a magic bullet that cured his mice and rabbits of deadly bacterial infections. He gave the formula to Bayer’s chief chemist, Heinrich Hörlein, who recognized the sulfa-based compound as something for which Bayer already held a patent that was more than twenty years old—which meant the patent was worthless. What happened next was described by award-winning science journalist Milton Silverman in his book Magic in a Bottle. According to Silverman, Hörlein had two company chemists camouflage this simple sulfa compound with hard-to-make molecules from a red tar-coal derivative. He then patented that compound, called it Prontosil, and sent it out for clinical testing—which showed a near 100 percent cure rate against a broad spectrum of bacteria, including the sepsis-causing streptococci germs that killed a million and half Americans and Europeans every year. French chemists deciphered Hörlein’s “trick.” They broke Prontosil into its component parts and tested each against bacteria, quickly seeing that the sulfa compound—a simple mix of aminos, benzene, and sulfonamide (called sulfanilamide)—did all the work. They ran a patent check and discovered that Hörlein himself filed for it in 1909. What a treat for the French. They spoiled Hörlein’s deception and robbed Bayer of a potential blockbuster drug. With an expired patent, this amazing antibacterial belonged to the world, license-free!5
Lowell thought that if sulfa worked so well against really bad bacteria—like the hideous flesh-destroying rods of gangrene and deadly skin- and blood-poisoning spheres of streptococci, staphylococci, and the other coccis—maybe it would work against malaria. Maybe, just maybe, sulfa-based drugs could be made to kill all types of malaria, and every stage of this shape-shifting germ—from the sticks delivered in mosquito saliva, to the rings that destroyed red blood cells, to the wrigglers that sexually reproduced in the mosquito’s gut. If any of the above panned out, sulfa would make treating and preventing the disease much, much easier. If all of the above panned out, the world would have a magic bullet for malaria—a miracle.
Also intriguing to Lowell was this new antibacterial the British brought to the United States for testing, called penicillin. He was among the first, and may have been the first, malariologist to hypothesize that this microbe killer might be broad enough to destroy malaria’s Plasmodia. The medication was still under development and hard to obtain. Nonetheless, Lowell requested 6.0 grams from Merck & Co. He was told that amount was “unprocurable,” but, with the help of A. N. Richards and the White House, Lowell finally got 2.0 grams of it in May 1942. Under heavy secrecy he saw, anecdotally, that it worked well against sporozoites (the stage transmitted by mosquitoes).6 But further studies would have to wait.
For the time being, he and the others had to learn more about malaria and decided to use their hundreds of state hospital patients for basic research. The infections would help researchers understand why and how the microbes responded to drugs, and why and how they seemingly disappeared so quickly after being delivered by a mosquito—completely undetectable—until they launched their attack on red cells a week or ten days later. What were they doing and why did they do it? Lowell and his colleagues presumed the germs hid in soft tissue—but where? And after an acute attack, where did the parasites disappear to, and why would they suddenly, without warning or provocation, reappear to launch another acute attack? Presumably the initial attack created antibodies against the invaders, yet the body seemed to have no power against the second, third, fourth, and so on, rounds of attack. Why?
Lowell felt that these questions, if answered, might lead the way to a whole new class of treatments, and away from the toxic standards—quinine and Germany’s quinine look-alikes, the 8-aminoquinolines. The madmen they worked on, however, weren’t ideal. The induced infections to treat syphilis produced only normal concentrations of microbes that were difficult to capture in a blood draw. When caught, there were usually only a few swimming around for study. The culprit was the spleen, the body’s filter that caught and killed germs as the heart pumped blood through it. Malarial parasites caused the spleen to swell, which gave doctors a simple diagnostic tool for gauging a community’s malaria infection rate. For researchers, however, this organ was a hindrance, because it caught and killed a majority of germ specimens.
A clever Indian doctor, B. M. Das Gupta, came up with an answer. He removed the spleen from a monkey, then infected the animal with P. inui, creating a rapid buildup of parasites in the animal’s blood and intense concentrations of P. inui for study. The concentrations were so high that he could even use it to launch malaria in man—something no one had been able to do, because small amounts of these microbes were insufficient to cause human infection.7
Das Gupta inspired Lowell. Scientists, including him, had already used P. knowlesi to infect man, finding it wasn’t as deadly as, say, falciparum. The P. inui innovation added great value to researchers, because this type of malaria appeared to resemble vivax. Scientists now had two close cousins of human malaria, both of which could be used to study the potential for a drug or be used in vaccine preparations—maybe P. inui would be the one to induce immunity against them all.
As it turned out, it wasn’t and couldn’t. Still, here was another animal malaria for screenings—which allowed work to progress without state hospital patients.
* * *
THIS shift in focus brought immediate satisfaction. Lowell tried the Germans’ sulfa-based compound on rhesus monkeys infected with P. knowlesi and P. inui, and cured them completely! There was no need to run toxicity tests in lower animals, because this sulfa compound had been rigorously tested as an antibacterial and showed no sign of untoward effects—with the exception of what appeared to be an allergic reaction to sulfa in a small percentage of the population. Otherwise it was completely safe. He tried it on his syphilis patients at Manhattan State Hospital, but their vivax infections were unchanged. His chemist friends were moving molecules around to make analogues of sulfanilamide, which he hoped would work better.
For him, sulfa presented the highest potential, in terms of drug development for military use—much better than atabrine or plasmochin, because sulfa clearly was not toxic, and it was much easier to make. The other two required medical supervision, which wouldn’t work on the battlefield. A safe sulfa drug could be included in medical kits, along with sulfa powders every man would soon carry to stop war wounds from going septic.
But sulfa was just a possibility. Lowell and the others wanted it and other possibilities fully explored. In the big picture, making compounds for the sake of making them would give American chemists needed practice in drug making, and potentially propel them and U.S. medicine into the twentieth century. American drug companies were decades behind the British and French, and what felt like light-years behind the crafty chemists at I.G. Farben. In any case, better drugs were desperately needed. Atabrine, plasmochin, and quinine were poisons. They attacked the malaria germs while poisoning the body at levels that were somewhat tolerable. Their value was in their ability to stop infections from turning fatal by reducing parasite counts in the blood. But studies suggested that they were unsafe to take for long periods—which, if true, meant they were no good as a prophylactic. Each was known for triggering severe side effects: atabrine and its intense stomach and intestinal pains, as well as psychosis; plasmochin and its potentially deadly depletion of oxygen in the blood; and quinine and its cardiac disturbances, partial blindness, severe headaches, loud ringing in the ears, confusion, and, when overused, dreaded blackwater fever.
For the United States to find its own new drug would be a godsend. Though funding for a full-blown, federally sponsored malaria project failed to materialize right away, the need was clearly there and the outbreaks were only a matter of months away, depending on the timing of America’s entry into the war. This was a medical Manhattan Project that sought to build on basic principles devised by the Germans, but perfected and improved upon by way of American innovation and sheer scientific will. Lowell got support from his University of Chicago friends and former bosses, especially William Hay Taliaferro, dean of the Division of Biological Sciences and the School of Medicine, and editor of the Journal of Infectious Diseases.8 Taliaferro had been elected to the National Academy of Sciences and the American Philosophical Society. He brought great weight to the effort and helped recruit other giants in their fields.
With Lowell, Taliaferro pressed the point that a better lab animal would make things a lot easier—like a mouse, but one that could be infected with malaria.
Lowell already knew from other scientists that dogs, cats, rats, and many other animals could not be infected with malaria (scientists have since found a malaria parasite of tree rats called P. berghei, and another one called P. yoelii that can infect mice). Monkeys worked well—extremely well—but they were expensive to keep and hard to come by, especially with half the world at war. Even canaries—which Bayer used for preliminary drug screenings—were too expensive at a dollar each. The committee envisioned all the major drug companies feeding experimental compounds into university labs, which would then run large controlled tests on lower species. They needed an animal they could raise for next to nothing and infect with lethal malaria—some small creature that could be shoveled by the thousands into incinerators—until that one drug materialized to save them all.
Studies out of the Pasteur Institute in Paris by Émile Brumpt showed that the bird malaria used in Germany, P. gallinaceum, came from a Southeast Asian pheasant—that is, it occurred naturally in the pheasant and could be used experimentally in canaries. The French tried it on chicks to see what would happen, and it killed them all. Perfect! This parasite didn’t always kill the canaries, which meant lab technicians had to take blood to see under a microscope whether or not a drug acted against the parasites—which was labor intensive. With chicks, technicians just had to look inside the cages. If the birds were dead, the drug had failed. If they were alive, it had worked. This was ideal. For only pennies each, the Americans would have a cheap, easy-to-work-with animal on which to run countless drug screenings. Lowell made it his mission to import this fantastic chick-killing bird malaria.9
The big catch, however, was that P. gallinaceum was lethal to adult chickens. The U.S. Bureau of Animal Industry banned its use for fear it would escape malaria labs, by way of mosquitoes, and destroy America’s industrial chicken farms—which Lowell’s uncle Don helped launch. Lowell wrote letters trying to pry permission out of the bureau, using national security and the impending war as a hook, but got nowhere. He couldn’t sleep thinking about the possibilities this parasite offered the malaria project, and he bugged the executives at Rockefeller to help. He was so persistent, the foundation’s director of international programs told him, “If you don’t quit annoying me, you’ll have to go someplace else and work, not here.”
Lowell felt hemmed in.
* * *
THEN, one day while he strolled through the Bronx Zoo, a favorite pastime, Lowell had an epiphany.10 What if he could find P. gallinacium in the zoo’s exotic bird collection? What if there was a bird in New York infected with this malaria? Obtaining permission from the zoo’s ornithologist to take blood samples from every Asian bird in captivity, Lowell found his treasure in the blood of a Borneo fireback pheasant. There swam what Lowell thought was P. gallinaceum. But soon he realized he’d discovered a never-before-seen type of bird malaria that could infect standard American ducklings. And it didn’t harm chickens—posing no threat to the U.S. poultry industry. Squibb Institute for Medical Research was the first commercial firm to use it in antimalaria drug screening. It was named Plasmodium lophurae, for the taxonomical name of its pheasant host—Lophura igniti igniti11—but most people called it the Coggeshall strain. Labs across the continent, from Johns Hopkins to the Gorgas Memorial Hospital in the canal zone, soon asked for samples. The Coggeshall strain filled an important gap.
But it had shortcomings. It couldn’t infect lab-raised anopheline mosquitoes, so they used the yellow fever mosquito, Aedes aegypti, which also carried a type of encephalitis that killed many of Lowell’s monkeys. These setbacks he observed and wrote about for prestigious science journals, sharing every detail in this slow march forward in a hunt for a cure. Patient, persistent, and highly competent, he just kept raising ducklings and screening compounds, assigning each a number so they could be cataloged and filed.
One day in 1940 he received a substance from Winthrop. Lowell could tell it was a variation on plasmochin (the oxygen-depriving 8-aminoquinoline). His assistant, John Maier, injected it into ducklings infected with the Coggeshall strain. To their surprise the ducklings lived! Lowell recommended to Winthrop that they do toxicity tests on mice and dogs. If those animals lived, he asked that it be sent back for testing on syphilitics at Manhattan State Hospital, on Wards Island.
* * *
MEANWHILE, all-out war hit Europe. In the spring, Germany bombed Belgium and Holland. By June 14, 1940, Nazi tanks rumbled down the Champs-Élysées, taking their revenge for the Treaty of Versailles. French premier Paul Reynaud begged the free world to save his country, while Hitler made a pact with Vichy leader Henri-Philippe Pétain, signing away French independence and her colonial holdings. This put Germany closer to ruling Europe, the Gold Coast of Africa, and the Suez Canal—England’s gateway to a vast colonial empire and huge oil reserves.
That same month Italy declared war on France and England. The move sealed an uneasy alliance with Hitler that Italian king Victor Emmanuel III objected to—because he didn’t want Hitler waging battles on Italian soil. But Benito Mussolini needed Hitler to oust Great Britain from North Africa, a necessary piece of his plan to rebuild the Roman Empire around the Mediterranean rim. Mussolini neither liked nor trusted Hitler, maybe because the two had much in common. They both led riots and masterfully exploited their country’s postwar economic disasters to seize power. Hitler was stronger and forced Mussolini to choose sides—to either fall like France or join him. So Mussolini joined him and sent Italy’s ill-equipped troops to march on southern France, East Africa, and Libya—on their way to Egypt.
On the other side of the world, Japan used its control of Manchuria to drive deep into China. Then, in the fall of 1940, Japanese forces set up military bases and naval ports in Indochina, and prepared for attacks on Ceylon, Burma, India, Thailand, Malaya, Singapore, the East Indies, Kuala Lumpur, Manila, and more. The Japanese military’s long-term goal of leading an all-Asian economic and military empire was, like Mussolini’s ambitions, linked to Hitler’s ability to destroy Great Britain. With the Royal Navy gone from the South China Sea and Indian Ocean, all Asian governments would fall in line behind Japan.
As war spread across the globe, Bayer labs couldn’t obtain basic supplies, let alone sparrows, canaries and monkeys for screening new experimental compounds. But the company had its new top-secret series, the one it made before Germany invaded Poland; the one company chemists discovered while playing around with the 8-aminoquinolines, trying to make less toxic versions of the partially successful drugs plasmochin and atabrine; the series they made when they experimentally rotated a key side chain to the theoretical fourth position and then cleverly eliminated the yellow dye to produce a series of colorless, tasteless compounds they called 4-aminoquinolines. At first the drugs made from this series appeared too toxic, including one called resochin. But Bayer’s chemists kept teasing out different molecules until they added a methyl group to the toxic resochin and arrived at an exciting one they called sontochin. It cured Bayer’s canaries. Then it worked on Sioli’s syphilitics in Düsseldorf, and on larger groups in Romania.
Bayer had done it again—they had a new drug with new patents. If all went well, this new Bayer concoction would supplant quinine and absorb its worldwide market.
But the world was at war. Bayer made barely enough of the stuff to distribute to Werner Schulemann, who ran preliminary tests on canaries and then tried it on soldiers sick with relapsing malaria, infected during the Greece campaign.12 Everywhere this drug went it produced great results, and the momentum around it continued to grow.
Making it, however, became impossible.
* * *
ABOUT that time, Frederick Russell, who five years earlier had recruited Lowell back to Rockefeller from the University of Chicago, called again. He was now at Harvard and offered Lowell a prestigious professorship there named for Theobald Smith—who first discovered insects as disease carriers in 1889, presaging Ronald Ross’s proof that mosquitoes carried malaria. Fred Russell warned that a formal offer would take time but told Lowell to sit tight; his next job would be at Harvard.
While Lowell waited for Harvard’s official offer, Thomas Francis—developer of the flu vaccine—offered him a job as chair of a new school of tropical diseases at the University of Michigan, complete with a malaria-therapy lab at a nearby state hospital.
Harvard was expected to pay in the low “five figures” and, with some reluctance, the University of Michigan agreed to meet it. Lowell’s new salary would be $10,000 ($160,000 in 2014 dollars).13 The day after he wired his acceptance, a call came from Harvard offering him the Theobald Smith professorship. But Lowell had accepted Michigan. So, for the second time, he passed up Boston’s Ivy League for a solid Midwestern university (the first time being his decision to pass up Harvard’s medical school for IU). He moved his family to Ann Arbor that summer and set up a malaria therapy unit at the former Battle Creek Sanitarium less than an hour away. Then he put together what is today one of the country’s top schools of infectious diseases. From there he flew into DC for the monthly meetings of the malaria project.
On September 11, 1941, at one of the most important malaria conferences up to that point, there appeared an unmistakable sign of things to come. In attendance was Colonel James Simmons, a decorated Medical Corps physician and tropical disease expert who held many degrees—including a doctorate and medical degree—from several top universities, including Harvard. The conferees all knew him at once by his pressed uniform, large square shoulders, slick comb-over, and kind but piercing eyes. He was one of the few high-ranking military officers who actually spoke their language of malaria. His presence changed the tenor of the meeting. It meant the War Department was preparing for troop deployments, and indeed, Colonel Simmons said as much. How and where remained undisclosed. But Colonel Simmons said troops would fight in highly malarious areas and that the War Department wanted the committee to speed up its work. He asked questions about mosquito vectors in West Africa and the Far East. And he disclosed that the army had already run preliminary experiments to see if atabrine or quinine could be used dependably to prevent infections—as a true prophylactic. Their experiments, he said, were inconclusive. Then he declared that the War Department’s highest priority on malaria was to “get a field prophylactic which can be given without too much administrative difficulty.”14
Committee members must have been thrilled. According to the minutes, they brought him up to speed in rapid succession—talking over one another, as they were just so damn enthusiastic to be getting real attention from the War Department. They described the setup: Clinical trials at state hospitals were stamped “secret”; promising compounds were stamped “confidential”; and everything else was stamped “restricted.” In general, no information could be published without permission from the committee. And they said they expected to have up to 150,000 new chemical compounds or derivatives worth exploring for antimalarial activity.
Several project members, including Lowell, talked of the dire need for basic research, which was not what Simmons wanted to hear. What he wanted to hear was that they had good drugs to work with and that they’d have reports on potential prophylactics shortly. But Taliaferro from the University of Chicago argued that the program would be on shaky ground if it failed to find a cure—a drug that could, in fact, eliminate the blood- and tissue-stage parasites. Without a 100 percent effective prophylactic—which no one in the room felt plausible, given their limited knowledge of the microbes—troops would still fall from infections. The goal should be finding a radical cure.
By the end of a long and sometimes tedious day of malaria talk, conferees ended up split on this and other smaller issues. But they all agreed on one strategic point: Atabrine would never do; something better had to be found—preferably before U.S. troops shipped out for war.
Colonel Simmons knew something they didn’t: that time had run out. He shut down the group’s notion that they could move molecules around other molecules until luck produced a magic cure. Such luxuries belonged to peacetime research. Not while Axis troops marched on North Africa, attacked Russia, and occupied Europe. Not while Japan attacked and occupied nearly all of Southeast Asia on its way to claiming China and India, and maybe even Australia. Yes, he agreed that fundamental research was needed. He even announced that the War Department and the White House were prepared to make necessary funds available for a broad research program. But with that money came an expectation that the group would focus efforts on a prophylactic and, first and foremost, figure out how the heck to use this strange yellow drug atabrine.
This, of course, upset the pack. No scientist worth his or her salt took directions well. They preferred to let the science guide them.
But the message Lowell heard—the one that mattered most—was that the malaria project’s political stock had just shot up. Lowell was quick to exploit it. Just weeks after the meeting he secured permission to finally import from Mexico City his long-sought-after, chicken-killing bird malaria, P. gallinaceum. The victory over the poultry industry’s strong lobby was achievable only with the help of President Roosevelt’s science advisory team, especially A. N. Richards, who oversaw all medical research linked to war preparations.
At the October 13, 1941, meeting, Lowell announced that he had P. gallinaceum, which “created considerable excitement.”15
The White House help came at a cost, of course. Lowell would not enjoy carte blanche with this dangerous microbe. He was told to keep a lid on it, which he apparently didn’t do well, for on October 16, 1941, Lowell received a terse letter from Richards reprimanding him for being too loose with his new chicken-killing germ. “The permit was granted upon my assurance that the precautions described in the report signed by you and Taliaferro would be rigidly carried out,” wrote Richards. In that report, they promised to keep tight control of the germ’s distribution, limiting it to lead malaria investigators at Johns Hopkins, the University of Michigan, the University of Chicago, the University of Tennessee, and John Maier at Rockefeller, Lowell’s colleague there before he left for Michigan. How did G. Robert Coatney at the South Carolina state hospital somehow get his hands on it? Richards learned of the breach and instructed Coatney to kill and burn all chicks and remaining cultures immediately.16
“Now, as far as the future is concerned,” Richard’s letter to Lowell continued, “it seems to me that you as Chairman of the Malaria Conference should inform me officially of the names of the persons to whom the culture may rightly go. . . . I propose also to write to Maier to say that he is to give the culture to no one except on my authorization and that that authorization will be given only on your recommendation. . . . I take it for granted that every effort will be made to impress the workers with the responsibility we all are accepting.” The Department of Agriculture had stipulated that all labs using P. gallinaceum be located in areas protected from air raids, and have armed guards to keep watch twenty-four hours a day.17
Lowell didn’t take the reprimand personally. He knew the tight hold on gallinaceum would loosen once the U.S. went to war. But for the time being, he would comply with Richards’s demands. For Lowell, what mattered most was that he had all the tools he needed to catch up to Germany: ample money, buy-in from the military and the White House, and P. gallinaceum.