William Hepburn Russell Lumsden Scotland Has a Proud History of Nurturing Distinguished Contributors to Our Understanding of Disease in the Tropics

William Hepburn Russell Lumsden Scotland has a proud history of nurturing distinguished contributors to our understanding of disease in the tropics. Among these must be numbered Russell Lumsden, medical entomologist, virologist and parasitologist, but above all a man with boundless enthusiasm for the entire natural world. Russell became a keen naturalist while still at school. Born in Forfar on 27 March, 1914, he moved with his family to Darlington in 1919 when his father became Schools’ Medical Officer for Durham County. He was educated at the Queen Elizabeth Grammar School there, but in 1931 he was awarded a Carnegie Scholarship to read Zoology at Glasgow University under Sir John Graham Kerr. Russell took part in successive student expeditions to Canna in the Inner Hebrides and wrote detailed reports on the entomology of these and on various projects in marine biology. His dedication to natural history is splendidly illustrated by a paper in The Entomologist’s Monthly Magazine, recounting how, while sunning himself on a jetty at Lake Windermere after swimming, he found an old nail and kept a tally of the different prey of pond skaters by making scratches on the woodwork. After graduation with First Class Honours, Russell went on to qualify in medicine at Glasgow and wrote articles for Surgo, the Glasgow University Medical Journal, acting as its editor in 1938. His companion in all his student activities was Alexander J Haddow, (later FRSE, FRS): both were later to become world authorities on mosquito- borne disease. After receiving his medical degree in 1938, Russell was awarded a Medical Research Council Fellowship for work at the Liverpool School of Tropical Medicine. The MRC wished to promote research on drug treatment (chemotherapy) of tropical diseases, an endeavour in which the Liverpool School under Warrington Yorke was particularly distinguished. So, after taking the Diploma in Tropical Medicine and Hygiene, Russell began to look at the effect of antimalarial drugs on the development of mosquito-infecting stages of the malaria parasite in the laboratory. But with the outbreak of World War II in 1939, of necessity his interest in malaria became more directed to mosquito transmission of the disease in the field. In 1941 he joined the Royal Army Medical Corps on the staff of No 3 Malaria Field Laboratory, later becoming its commanding officer and rising to the rank of Lieutenant Colonel. The main task of the Laboratory was to investigate the malaria hazard to troops advancing into new territory. As a threat to health and survival, malaria assumes even greater importance in times of war. Russell saw active service in the Eastern Mediterranean, North African and Italian Campaigns, ending up in India in preparation for the Allied landings in Malaysia. His duties required extensive travel, often on solitary expeditions to remote places, and on dangerous ones to forward areas; in Sicily he miraculously survived when the truck in which he was travelling was blown to pieces by a land mine. The extensive London School of Hygiene and Tropical Medicine Memoir Anophelism and Malaria in Transjordan and in the neighbouring parts of Palestine and Syria that he later (1950) published (with Jacob Yofe), exemplifies Russell’s inexhaustable capacity for amassing relevant data and the thoroughness of his ecological approach to vector-borne disease transmission. The report that he wrote for Advanced Headquarters on Malaria in Malaya, in anticipation of the 14th Army attack, was equally breathtaking in its scholarship, but never put to use as Allied landings were cancelled when the Japanese surrendered following the bombing of Hiroshima and Nagasaki in August 1945. After demobilisation in 1946, Russell took up a MRC Senior Research Fellowship in Medical Entomology at the London School of Hygiene and Tropical Medicine. Here he met and married Pamela Bartram, a librarian at the School, who was to be his devoted companion for the rest of his life. He continued work he had started in Liverpool on factors affecting the biting activity of Aedes aegypti, the mosquito transmitting the virus of yellow fever in the urban environment. A year later he entered the Colonial Medical Research Service and joined the staff of the East African Virus Research Institute (EAVRI) in Entebbe, Uganda, as entomologist, alongside his friend of Glasgow student days, Alex Haddow, who later became its Director. Yellow fever wreaks havoc in urban populations when Aedes aegypti is around to transmit it. EAVRI had originally been set up by the Rockefeller Foundation to answer the question “Where does the virus of yellow fever hide between epidemics?” Based in Entebbe and a field station in Bwamba, just to the west of the Ruwenzori, the Institute was largely concerned with the investigation of the cycles of maintenance of the yellow fever virus in the forest environment and the avenues by which it entered the human population. Russell was soon in his element as a naturalist investigating possible transmission routes for the virus. He studied the biting patterns of forest canopy mosquitoes in relation to the behaviour of monkeys and bush babies which, he demonstrated, served as reservoirs of the human disease. He also sorted out those mosquitoes that had a predilection for humans - and Aedes africanus emerged as the main culprit. The Rockefeller had their answer! Over time, however, his interests became more virus-centred. He learned techniques for the isolation and identification of viruses, and in the laboratory, he isolated and characterised several viruses of medical importance. A WHO Fellowship for visiting virus laboratories in Canada and the USA assisted his conversion. He came to regard concepts of purification, standardisation and preservation of infective agents as essential prerequisites for critical study of their epidemiology - conclusions that profoundly influenced the rest of his career as a scientist. In 1957, while serving as Assistant Director of EAVRI, Russell was appointed Director of the East African Trypanosomiasis Research Organisation (EATRO) and forsook viruses for protozoan parasites. He embarked immediately on a radical revision of the Organisation’s activities. These covered the diseases caused by the tsetse fly-transmitted trypanosomes, blood-dwelling protozoa responsible for sleeping sickness in humans and the wasting disease nagana in livestock. For a start he did not like EATRO’s activities being split discipline-wise between three stations geographically distant from one another. His EAVRI experience had taught him that research on vector-borne disease demands close interaction of experts on pathogen, host and vector, not their isolation from one another, so he concentrated all the Organisation’s staff at Tororo in Uganda. In addition, despite his entomological background, he believed that the time had come to break away from preoccupation with the tsetse fly vector and expand research on the trypanosome itself and on the mammalian host’s immune response to it. This was a brave move. In medical science, understanding of the mammalian immune response was currently deepening rapidly. But since pioneering work at the beginning of the century, it had been known that while trypanosomes induce a powerful antibody response to their presence, these parasites can repeatedly change the nature of the antigen inducing the response and so evade immune destruction. In this way they give rise to a chronic relapsing infection in the blood. This ability of the parasite to undergo ‘antigenic variation’ was seen as an insurmountable barrier to much-needed vaccination against trypanosomiasis in both man and beast. The nature of this variation was a complete mystery. What little recent research had been done on it had been conducted on old laboratory isolates, syringe-passaged through rodents for decades with ever-increasing virulence. Such parasites bore about as much resemblance to their wild ancestors as a chihuahua does to a wolf. In addition there was the problem of standardising test materials to compare the antigens of trypanosomes at different points in an infection. At EATRO, however, Russell had ready access to recent trypanosome isolates from patients and sick animals, and he quickly introduced the novel practice of cryopreservation (deep freezing of living material) to set up a bank of such isolates, later termed ‘stabilates’. He devoted much time to developing the technique so as to ensure that stabilate populations were truly frozen in time, thus preserving their antigenic character and infectivity indefinitely. In this way he solved the standardisation problem. He became fascinated by the variable infectivity of trypanosomes and, drawing on his experience in virology, suggested that their infective properties should be measured as if they were invisible viruses. As a visiting researcher at EATRO in 1960, the writer was enthralled by the atmosphere of excitement and enthusiasm that the new director had generated in the laboratories. In 1962 Russell became a Member of the Expert Advisory Panel on Parasitic Diseases of the World Health Organisation. But Ugandan independence was looming, and in 1963 he had to make way for a native African director. He returned to the UK and accepted a lectureship in the Department of Bacteriology of the Medical School, Edinburgh University. Here he met the veterinarian John Herbert and they struck up an alliance to pursue the nature of trypanosome antigenic variation further. This was made possible by Sir Alex Robertson inviting Russell to head an Applied Protozoology Unit in his new Centre for Tropical Veterinary Medicine at Easter Bush. A basic question concerning trypanosome antigenic variation was whether it was due to survival of genetic mutants in the face of host antibody attack, or was the result of phenotypic change in a genetically constant population of trypanosomes, possibly induced by host antibody. Study of the pattern of switching from one antigenic type to another in relapsing clone infections was an obvious start to answering this question.

Load more