BIOGRAPHICAL MEMOIRS

William Percy Rogers 1914-1997

This memoir was originally published in Historical Records of Australian Science, vol.13, no.2, 2000.

Numbers in brackets refer to the bibliography at the end of the text.

William Percy Rogers was elected a Fellow of the Australian Academy of Science in 1954, and served as a member of the Council (1958-1960) and as Vice-President (1971-1973). He received a DSc from the University of London in 1956, and was a Fellow of the Institute of Biology (UK) and of the Australian Society for Parasitology, of which he served as president in 1966-1967. He was a member of the Australian National Research Council, of which he was a Fellow, and of five other National Committees. For fifteen years he was a member of the WHO Expert Committee on Parasitic Diseases. A member and for three years chairman of the Board of Standards of Journals of the Australian Academy of Science and CSIRO, he was also on the editorial boards of seven Australian and international journals. He was known affectionately as 'Buddy' by friends and colleagues, a nickname borrowed from a well known American actor of the early decades of the twentieth century, Charles 'Buddy' Rogers.

Rogers was born on 23 November 1914 in Katanning, Western Australia. His father, Percy Nunn Rogers and his mother, Agnes Fanny Rogers (née Bishop), were both born in England. William Rogers was the last and, by eleven years, the youngest in a family of four children. The eldest was Dorothy, born in England on 10 October 1900; Leslie was born in Australia on 6 January 1902; and Gladys was born on 23 November 1903.

His father was a storekeeper who at various times ran general grocery stores in several West Australian country towns, including Meekatharra, Wickepin, Woodanilling and Katanning. He recalled his parents as 'kind, generous people', well-educated and well-read and possessing many books. His father's favourite authors included Shakespeare, Emerson and Dickens. Rogers remembered this 'because, an avid reader myself, my father's choice of books surprised me. However, there was a wide choice of books in our house and I was allowed to buy lots myself.' He retained a love of reading for the rest of his life. He also developed a lasting interest in field biology and became involved in amateur radio.

At the age of eleven it seems likely that his parents decided that he needed a better education than was available locally, so he was sent to school in Perth, where he lived in private lodgings. In 1927 he won an Entrance Scholarship for secondary education and attended Perth Modern School, from which he matriculated to the University of Western Australia in 1933. Aided by a Commonwealth Bursary, he studied zoology, chemistry, physics and mathematics and obtained his BSc in 1936. The subsequent grant of a Commonwealth Post-graduate Scholarship enabled him to study for an MSc, which was awarded in 1938. His thesis was in parasitology and his supervisor was Dr H.W. ('Bill') Bennetts, who held degrees in veterinary science from the University of Melbourne and was the first veterinary pathologist in Western Australia's Department of Agriculture. Highly respected for his understanding of both field and laboratory work, Bennetts was an important influence on Rogers' early years, and parasitologists generally owe a great debt to him for introducing Rogers to the subject.

Two papers were published from Rogers' thesis (1, 5). Here we see those qualities that are so much a hallmark of his research. The problems were defined with masterly clarity, special apparatus developed, and findings and conclusions expressed with precision and imagination. The paper (5) on the effect of the environment on availability of infective stages of parasites for sheep was and remains an outstanding contribution.

Rogers was awarded a Hackett Scholarship from the University of Western Australia to enrol for a PhD at the University of London in the School of Hygiene and Tropical Medicine. His supervisor was the distinguished parasitologist Professor R.T. Leiper, FRS, 'who first encouraged me to undertake research work on the physiology of parasites' (49). Rogers later wrote: 'I doubt if I spoke to him about my work after the first week. But he did allow me to follow my own interests in research and to submit my thesis as a collection of papers or “galleys” which ranged from taxonomy…to physiology (2, 3, 4, 6, 7, 8, 9, 10, 11, 12) – looking back it seems terrible stuff'. Nowadays no supervisor could or would have so little involvement with a student. Yet Leiper recognized that Rogers was outstanding and suggested the general direction of his research. No doubt Rogers would have seen much more of his supervisor had his research floundered.

Of great significance was Leiper's selection of Professor David Keilin, FRS, to be examiner. The degree of PhD was awarded in 1940. There were however, other important consequences. Keilin was not only a distinguished biologist but also director of the Molteno Institute at Cambridge and one of the foremost biochemists of his day – the discoverer of cytochrome. In Roger's words, 'He was a brilliant lecturer and stimulating research worker'. Keilin invited Rogers to the Molteno as a post-doctoral student. This was perhaps the most important event in shaping Rogers' future as a scientist and teacher, because it allowed him to meet and work with some of the most outstanding biochemists of the day. However, he confessed to one of us (RIS) that he was none-the-less astonished, within a few hours of arriving at the Molteno, to witness Keilin hurl a flask across the laboratory, apparently in disgust with the experimental results.

In addition to his appointment to the Molteno, another event of great consequence took place at this time. In 1939, at St Albans, Rogers married Lillian Edith Readhead Taylor, daughter of George Taylor of Gloucester, England and Elizabeth Readhead, of Greta, New South Wales. It is appropriate to give more than a passing reference to this marriage, because Lillian Rogers was not only her husband's equal intellectually, but a scientist in her own right. A graduate in physics (MSc 1940) of the University of Western Australia, she commenced work for a PhD at Leeds University, but with the outbreak of war this was abandoned and she worked on range tables and ballistic missiles, finally becoming an assistant crystallographer at the Cavendish Laboratory, Cambridge. When she and Rogers returned to Australia, Mrs Rogers joined the staff of the Australian Council for Scientific and Industrial Research (CSIR), which subsequently became the Commonwealth Scientific and Industrial Research Organization, or CSIRO. Her background enabled her to appreciate and discuss with Rogers his research and she was, as those who knew her could testify, a strong source of advice, criticism and support.

Rogers remained at the Molteno Institute through the war years. Rejected on medical grounds for service in the RAF, he remained there until 1946. He was concerned with work on parasitic diseases, which were given special emphasis during the war, and his list of publications includes papers on trichinosis and anthelmintics (11, 12, 13, 15, 17). But a greater benefit to generations of university students and to research in Australia arose from Keilin's insistence that Rogers take the Part II Tripos in biochemistry. This gave Rogers 'a basis on which I was able to build much of the knowledge and biological understanding I use in research and teaching'. Rogers confessed that the course was hard work and 'remarkable for its intensity and standards'. There were only four students and some twenty or so lecturers, including such well-known names as Baldwin, Chibnall, Danielli, Dixon, Gale, Hill, Keilin, Mann, Sanger and Stephenson. It is clear that this experience was profoundly important for Rogers' future work.

In 1946 Rogers and his wife returned to Australia to enable him to take up an appointment as leader of the Parasite Physiology and Toxicology Unit at the McMaster Laboratory of CSIR, then located in the grounds of the University of Sydney. He soon gathered a group of outstanding young people in the Unit and made a strong impact, not only on the McMaster Laboratory but also on the study of parasites and parasitism generally in Australia. He introduced the study of physiological and biochemical aspects of parasites, and directed attention to the parasite rather than to the host. This was a change in thinking which, in Australia at least, was almost revolutionary. Hitherto, and for excellent economic reasons, parasites – particularly parasites of ruminants – were viewed only as pests. Rogers was among the first to see the parasite as an interesting organism in its own right. Of course, pest control had to be faced, but it was Rogers' view that this desirable outcome could be best addressed by first clearly understanding the biology of the animal. He sought out model systems within which to work and introduced the experimental organisms Nippostrongylus brasiliensis and Plasmodium berghei to Australia. In the search for techniques of greater resolution – for work with parasites is both labour intensive and bedevilled by scarcity of material – he was one of the earliest in the country to use radioactive chemicals in biological research.

At the McMaster Laboratory he was exposed to practical as well as theoretical questions. He often related how a senior member of the scientific staff sought his opinion on the design of some new sheep yards. Although astonished, it seems he lodged no objection: he heard later that the designer of the pens reported of the plan: 'If it's good enough for the “professor”, it's good enough for me'!

In 1952 Rogers accepted appointment to the Chair of Zoology in the University of Adelaide in succession to Professor T. Harvey Johnston, who had also been a keen student of parasites. This appointment was viewed with some astonishment by his colleagues: universities were impoverished compared with CSIRO, overcrowded and short of staff. Rogers apparently did not offer, at least in public, a reason for his move, saying only that his reasons were 'imponderable'. Examination of his publications offers a clue. There was a reduction in output, not unexpected in view of his new duties, but there was also a change in direction, and it may be that he felt free to determine the course of his research without the obligations associated with an organization like CSIRO. In later years, when writing about his work on the control of growth and infection in nematode parasites he said 'it was not until I got a university job that I felt secure enough to tackle that, as I thought, difficult problem'. It is ironical that within a year of his resignation from the McMaster Laboratory, research on this very problem began there.

The first hints of this change in direction can be found in his address as President of Section D of ANZAAS (38) and in his paper with A.F. Bird on the cuticle of the infective stage of parasitic nematodes (42). But a clear statement of his interests appeared in Nature in 1957 with a paper entitled 'Physiology of exsheathment in nematodes and its relation to parasitism' (44). This paper appears at about the mid-point in his list of publications. It formed the central theme of both his book, The Nature of Parasitism, published in 1962, and virtually all his subsequent papers.

Rogers faced a heavy workload when he became professor and head of the Zoology Department. Numbers of students were growing and more staff were needed. It was not uncommon in those days for heads of departments in Australian universities to travel on personal recruiting drives for academic staff. One of the authors (CB) was interviewed in London in 1962 by no fewer than three such heads, including Rogers. The Rogers interview was particularly harrowing. The London underground was delayed because of an accident on the line and after a sprint up the Strand to South Australia House CB arrived at Rogers' desk, breathlessly incoherent. Rogers glared from under his bushy eyebrows, stroked his luxuriant moustache and harrumphed. After explanations, the atmosphere thawed somewhat and a glass of sherry was offered. Even so, it may be significant that Rogers was the only one of the three heads who did not offer CB a job. Some two years later, at a conference in Canberra they met again. CB was about to introduce himself when Rogers produced another harrumph. 'Ha! You were the chap who was an hour late for interview!' Happily, subsequent relations were much more cordial.

In those early years he gathered an outstanding staff, and ensured that a wide range of interests was represented. The department was both lively and democratic. Everyone, from junior laboratory assistant up, came to the common room for tea, and discussion was stimulating. Rogers often introduced controversial topics, and encouraged debate: his wide reading and deep interest in social questions helped him to select and preside over provocative topics. For honours and graduate students these discussions were particularly valuable.

One his students from the early 1960s, Dr Val Kempster, recalls that Rogers' gruff manner alienated some students but she further comments that:

I hope my memories of him as one of the brightest minds I have had the privilege to work with will counterbalance that … Most of us students never called him Buddy – always Prof – not that we were scared of him, just a mark of respect. I only reluctantly called him Buddy when I met him again in 1994 on coming back to Australia. I think of him as a very lateral thinking man, inspiring to work for, but a very well-rounded man. He was quite a gourmet, loved good food and wine and prided himself on his knowledge of Australian and other wines. I was thus most flattered when he asked me to arrange the menu, including the wines, for the dinner that he held for senior people from Park-Davis & Co. who funded his Chair of Parasitology.

At the Sixth International Congress of Parasitology in Brisbane in 1986,

it was a sign of the man that he insisted that two of his former students, Alison Bailey and me, were seated either side of him at the Conference Dinner.

In 1962 the late Professor H.G. Andrewartha, FAA, became head of the Department of Zoology and Rogers was appointed to a personal chair of parasitology, a post supported by the United States Public Health Service for five years and by Parke, Davis & Co. for three. In 1966 he transferred to the Department of Entomology at the Waite Agricultural Research Institute of the University of Adelaide, where the teaching load was comparatively light, and space and facilities more suited to his work. He reached the statutory age for retirement in 1979, and was appointed Professor Emeritus. Although an outstanding teacher, his real interest was in research, and he continued to be very productive for a further ten years.

Rogers displayed a very broad understanding of modern science. He claimed he was not a biochemist, although many thought him such, but his interests were wider. The claim implied a very narrow view of what biochemistry is, and we feel sure that Rogers had his tongue firmly in his cheek. No-one who had been taught by Danielli, the elucidator of membrane structure, or Keilin, who first demonstrated the presence of haemoproteins in the nematode Ascaris, or Hill, famous for his studies on muscle physiology, or Baldwin, the founder of comparative biochemistry (adaptive biochemistry, as it is now called) could reasonably claim not to be a biochemist and we show later how empty that disclaimer is! He not only had a deep appreciation of modern biology and its wider implications, but was able to apply chemistry and physics – aided here by Lillian Rogers – to biological problems. He was adept at modifying apparatus to suit his particular purposes, for which his early interest in amateur radio was important. He impressed on students 'never be afraid of techniques', and set the example in his own work.

Rogers was especially interested in the social implications of science and believed it was his duty to encourage informed discussion on such topics as atomic energy. After the atomic bomb tests at Maralinga in South Australia in 1956, he tried to influence public opinion by organizing demonstrations and making speeches. He was interested in the aims of the Pugwash Conferences, and spoke publicly about the dangers of nuclear warfare as well as other topics, including conservation and environmental problems, science and antiscience and the problems of human populations. In more recent years he became less sympathetic to what he regarded as extreme views, particularly about the use of uranium as a fuel. He wrote, 'I doubt if my actions had any influence on public opinion: there was only one tangible result – the establishment at the University of Adelaide of a masters course in Environmental Studies'. This was the precursor of what is now a substantial course that includes both undergraduate and doctoral students. Yet the views he held, which were largely disregarded in the past, are now more widely appreciated and understood. He was one of a small band of pioneers whose collective influence has been profound and is continuing. A list, almost certainly incomplete, of his non-scientific papers is given in an Appendix to the bibliography below.

One of Rogers' great assets was his capacity to introduce and explain a problem to students in ways that induced an ordered yet constrained enthusiasm. Yet he was unusual, for an outstanding scientist and professor, in that he has not left a large body of postgraduate students. Perhaps this came about because he came to science before team-work became the vogue. Certainly he preferred to do his own research, and made no serious attempt to enlist a body of graduate students. Of a total of 95 papers and one book, more than half – 54 papers and the book – are sole publications. He was also an intensely private person, a little known facet of his character that may in some way have contributed to the paucity of graduate students. Yet his consideration and kindness to, and defence of, graduate students was exemplary. Dr Alison Bailey reported arriving at the Adelaide railway station to hear her name called over the loudspeaker to go to 'the man in grey', who turned out to be Professor Rogers accompanied by the departmental secretary. She was then to be driven to her digs. His advice to her on writing a thesis was 'to go home at night, have one glass of wine (but never two), and write seven pages'!

An obvious feature of Rogers' character was a dislike of ceremony and pomp. He tried to avoid formal occasions, whether at the University or in private. A nephew recalls that his uncle, after a walk across the farm with the dogs, insisting that he need not change for a concert in Adelaide, put on an overcoat but retained his muddy boots which were visible to all. He was very democratic and became irritated if staff or students had no views of their own to express. In politics he was left of centre, although not markedly so. It was not without friendly amusement, however, that his friends and relations noticed how with retirement and a dependence on investment income, his outlook on economics moved to the right of the political spectrum.

The desire for privacy perhaps influenced the purchase of a farm in the Adelaide Hills where he and Lillian Rogers lived for some thirty years. The property was named 'Lirra Lirra' after the aboriginal name for the superb blue wren, a common bird on the property. Here he was able to indulge in his deep love of natural history and the countryside. He bred cattle and his wife kept horses. Curiously for a private person, he did not ignore other aspects of rural life. Perhaps he saw it as his duty to become a member of the Oakbank-Balhannah brigade of the Country Fire Service of South Australia, and he served at various times as radio officer, brigade and regional secretary. The farm played a large part in his life, although even after retirement he continued for a time to go each day to the laboratory. But in later years this became more difficult. There were no children, and he and Lillian Rogers made provision to transfer the title of the property to the University of Adelaide Student Union. They continued to live on and to manage the property. When failing health made this difficult, the property was eventually sold and the proceeds supported the construction of a student refectory at the Waite Institute, named, appropriately 'Lirra Lirra', after the property that he and Lillian Rogers loved so much.

Lillian Rogers had been troubled by ill-health for many years, and died on 20 September 1992. Rogers married his second wife, Marjorie Howley, née MacWilliam, on 24 April 1994. Declining health forced him to move, in March 1996, to a retirement village in Stirling in the Adelaide Hills, where he died a year later, on 28 April 1997.

Scientific research

Rogers as biochemist

It is often interesting to attempt to evaluate a man's work in the light of his own assessment. Rogers claimed he was not a biochemist; he certainly made the disclaimer to both of us at different times. Above, we have argued that, for anyone exposed to the influences to which he had been exposed, to make such a case would be disingenuous. The reason probably lies in the definition of biochemist that was current at the time. The 1940s and 1950s was a period when almost the whole of biochemistry was defined by rat liver, yeast and Escherischia coli. It was a time when standard metabolic pathways were being elucidated and interest was on the similarity of those pathways in different organisms. Glycolysis (in full or in part) is almost universally distributed in the living world; attention was focused on its regulation. The tricarboxylic acid (Krebs) cycle had almost been defined, but people were still seeking the mythological 7-carbon intermediate and 'active acetate'. Oxidative phosphorylation was easily observed but the chemiosmotic theory was ten years away; meanwhile huge effort went into the hunt for a hypothetical 'high energy intermediate'. It was a period of reductionism.

Rogers was certainly not a reductionist. What characterizes his work is his interest in the parasite, in the process of parasitism. The question that he wanted to ask of the biochemists about each newly discovered metabolic intermediate or regulatory control point was 'what does it mean in the life of the organism?' This emphasis on the whole animal is a characteristic frequently encountered in biochemists who have been trained in zoology. As mentioned above, Rogers' holistic view is today frequently called 'adaptive biochemistry'. Almost all his work on nematode development falls into that category.

He was, however, ahead of his time in this. Rogers carried out most of his research before 1970. In the field of parasite biochemistry, the thirty years leading up to 1970 were largely concerned with mapping the unknown continent. Parasites are notoriously difficult to work with so that biochemists of the time were concerned more with structural than with functional biochemistry. A very few researchers were attempting to tackle simple problems of function but their work was dominated by what could be measured rather than what should be measured. Succinate dehydrogenase was the most studied enzyme in intestinal helminths because it was rugged and survived all the insults of isolation procedures to which other enzymes succumbed.

These endeavours – very necessary if not intellectually stimulating – achieved their apotheosis in the two heroic compendia on the biochemistry of parasites by the great German-American biochemical parasitologist, Theodor von Brand. These two volumes are monuments to the assiduous compilation of data about parasites; they describe the constitution of parasites but reveal remarkably little about the nature of parasitism. This was why Rogers' book, The Nature of Parasitism, was a breath of fresh air to those of us who were following the trail that he had blazed.

In the preface, Rogers states that his intention is seminal, to generate interest in the peculiar problems of parasites and the evolution of parasitism:

A consideration of host-parasite relationships raises a number of basic problems. What are the features of the parasite and the host that allow infection to occur? What are the physiological characters that distinguish a parasite from its free-living relatives? What are the features of the environments of parasites which affect specificity? To these sorts of questions our present knowledge provides only general answers. Until we have more precise answers we cannot begin to understand the basic features of the host-parasite relationship and the nature of parasitism… I have been concerned not so much to summarize our knowledge as to stimulate research on parasitism.

The book itself actually provides an excellent summary of research to that point. More important, it is a unique attempt to see the parasite as a whole organism, with an evolutionary history, an ecology and a life.

We have dwelt on this point because we believe it explains something about Rogers' attitude to his science and, in particular, illuminates his transfer from the comparatively wealthy CSIRO to the relatively impoverished university sector. His personal philosophy was at odds with the policy of directed research necessarily espoused by the CSIRO. His goal was not the control of parasites but that of understanding them as the products of evolutionary processes.

This journey is well illustrated in his early papers. Thus the first fourteen in the bibliography and paper 16 may fairly be described as physiological studies. But paper 15 is concerned with the anthelmintic effect of two organic compounds while numbers 17 and 20 are concerned with the theoretical approach to drug design. It is as if he has made one excursion into the field, become appalled by the drudgery involved and has attempted to think his way through the problem. It is notable that he made only one other excursion into the study of drug action (33, 34) and that was because opportunities offered by radioactive tracers had become available.

His paper 17, in a series entitled 'Scientific Method in the Evolution of New Drugs', clearly states Rogers' position. It takes the form of a mini-review of comparative (adaptive?) biochemistry remarkably succinct and complete for its time (1946). It is worth quoting the discussion in full.

In this article, emphasis has been laid on comparative biochemistry and physiology rather than on chemotherapy and pharmacology, and this with definite reason, for though the chemical development of new drugs is being pressed forward, comparative biochemistry and biophysics (so important in relation to cell permeability) lag far behind. The outline of the fundamental ground-plan is but barely visible, and the special biochemistry of phyla has hardly been touched upon. Much of the little evidence now available is based on such poor experimental procedure that it needs re-examination. Further, the academic flavour of this work reduces its rate of advance. And yet comparative biochemistry is one of the important approaches to the logical evolution of new drugs! (our emphasis)

This theme is revisited in paper 20:

the field of helminth therapy is greatly limited by the lack of knowledge concerning helminth physiology; a great deal of research in this field is needed before a logical approach to the problem will be possible.

It is clear that, over the next forty years, Rogers attempted to remedy this deficiency.

The evidence that a change had taken place in Rogers' thinking is manifest in papers published over the next few years. With few exceptions, they are concerned with attempts to elucidate the respiratory and nitrogen metabolism of parasitic nematodes. Central to his work is the comparative approach. He makes comparisons both within and without phyla. In re-evaluating his work in the light of knowledge fifty years later it is impressive to see what he achieved. His basic findings have been confirmed and have been built on by adaptive biochemists using modern techniques.

Thus, Rogers concluded that the cytochrome system plays some role in oxygen transport in parasitic nematodes in vitro but is careful not to assume that same is necessarily true in vivo (19). He established that glycolysis was similar to that in yeast and mammalian muscle (22); concluded that oxygen uptake may (always the caveat) play a part in their metabolism (23); and worried over the fact that, while there were similarities in the tricarboxylic acid cycle, there were important differences (24, 29, 30, 32, 35). This led him to take a detailed look at the environments in which the adult parasite lived (25, 26), remarking that there was some oxygen available and concluding that nematodes were well adapted to live in low oxygen tensions. Rogers attacked the problem again in papers 27 and 28, examining the properties and seeking a role for nematode haemoglobin. All this was a tremendous achievement, given the paucity of microtechniques in the fifth decade of the last century.

Almost certainly this need for techniques of much higher resolution fuelled Rogers' interest in the use of radioactive isotopes in biological experiments (31). He made another foray into the field of anthelmintics, this time phenothiazine labelled with radioactive sulphur (33, 34), and later followed up this work with a colleague (40, 41, 43). Shortly after this began his major preoccupation with the developmental processes surrounding hatching and exsheathment of nematodes (42, 44), the outcome of which is described below.

The nature of the infectious process

We have already mentioned that Rogers' move to the university was associated with a change in the direction of his research. His address to Section D at the 1954 meeting of ANZAAS (38) reveals something of this change. Rogers made it clear that he wanted to understand parasitism as a biological phenomenon, and that, in spite of the increasing interest in the study of the physiology of parasites, 'the real problems have yet to be formulated'. He proposed that the answers he sought lay in the transition from a free-living to a parasitic mode of life, that is, in the nature of the infectious processes and the concomitant physiological changes in the parasite. Because the study of parasitology is bedevilled by a vast array of examples, derived from many phyla and frequently of great complexity, he elected to study those nematodes which live as parasites in the alimentary tract of vertebrates. In these the morphological changes that accompany infection are relatively simple, thus avoiding the complexities associated with such phyla as the platyhelminthes, parasitic molluscs and arthropods.

The infective stage of these nematodes is commonly in the third larval stage of development. The first of four moults has been completed but the second is incomplete, so that the worm has retained the uncast cuticle of the second stage. When a susceptible host is infected, the moult is completed and the old cuticle discarded, a process known as ecdysis or exsheathment. It was the mechanism of exsheathment and the initial developmental changes that succeeded it that were to become the principal theme of Rogers' research for the next thirty years. Indeed, these initial events in the transition to parasitism are the subject of nearly half his scientific publications, and include almost all those published after 1962.

The first paper in this series was a joint publication with A. F. Bird on the chemical constitution of the discarded second-stage cuticule (42). The cuticle must be discarded before infection can proceed, and an understanding of its structure offers clues to its breakdown. The paper also recognised that the worm completes the moult because it has received a stimulus provided by the host. This was followed in 1957 by a paper entitled 'The physiology of exsheathment in nematodes and its relation to parasitism' (44). Rogers said publicly that he regarded this as his most important paper. Its genesis was strongly influenced by the publication, in 1954, of V.B. Wigglesworth's monograph, The Physiology of Insect Metamorphosis. The paper proposed that 'moulting in nematodes is controlled by endocrine systems, and that, in parasitic species, the delayed exsheathment of the second stage is due to the suspension of the normal endocrine mechanism'. Some component of the host's alimentary tract was needed to enable moulting to be resumed and infection to be established.

At that time this was an unusual paper in the field of parasitology. It directed attention to the parasite as an animal in its own right, rather than as an appendage of the host. It asked some original questions about the biology of these animals and about the particular and special features of the host that were essential requisites for successful infection. Over the ensuing years Rogers devoted himself to three facets of this problem. The first was to define the stimulus from the host for oral infection, the second, to trace the physiological consequences of stimulation, and the third to determine the enzymic basis of moulting. We consider his work on these three aspects in turn.

The stimulus for oral infection

Early work (44) showed that nematode parasites of sheep, such as Haemonchus contortus and Trichostrongylus axei, exsheathed readily in the rumen of the host, an observation that prompted attempts to chemically analyse rumen fluid for an active substance. Rogers argued against this: intuitively he believed, and later showed, that the stimulus was a physical process that induced a change in the internal pH of the worm.

Soon after the 1957 paper was published, Rogers took study leave at the Institute of Parasitology in McGill University, Montreal. Here Donald Fairbairn and a student, B. I. Passey, had begun to study the hatching mechanism in vitro of eggs of the nematode Ascaris lumbricoides. In their work Rogers found support for his views on the physical nature of the stimulus. The important components in vitro for the hatching of eggs of this species were carbon dioxide and temperature (46), findings that he later extended not only to eggs of another species, Ascaridia galli (49), but also to exsheathment of nematode infective stages such as H. contortus, T. axei and Trichostrongylus colubriformis (47).

It became evident that a great number of parasites that infect the host by the oral route responded to carbon dioxide. Under physiological conditions more than 99% of the carbon dioxide in aqueous solution is in its original gaseous form. The balance, consisting of carbonic acid, bicarbonate and carbonate ions and protons, thus forms a very small proportion of the whole. The reaction whereby carbonic acid is converted to bicarbonate and protons is very rapid, but is readily reversed if the concentration of carbonic acid falls. This ensures that bicarbonate and protons provide what Rogers referred to as a 'readily available' source of carbonic acid.

In his early work, Rogers described the stimulus for hatching and exsheathment as a function of the sum of the concentration of dissolved carbon dioxide and carbonic acid: direct experimental methods to distinguish between their effects were not available. However, in a later paper (88), he presented evidence that undissociated carbonic acid, or, put in another way, undissociated carbonic acid plus protons plus bicarbonate are the critical factors. As he said, 'it is the physical chemistry of the overall system which is important in assessing the biological roles of the components' (94).

The major products of the hydration of carbon dioxide, that is, protons, bicarbonate and carbonate ions, do not readily pass across biological membranes, and are not in themselves the stimulus. But dissolved gaseous carbon dioxide and undissociated carbonic acid are able to pass freely through biological membranes. It is well known that in most biological systems the uptake of carbonic acid or carbon dioxide leads to a reduction in the internal pH. Rogers therefore proposed that the initial event in the worm, which starts development of the parasitic stage, is a sudden reduction in the internal pH, brought about by the dissociation of carbonic acid to produce protons and bicarbonate ions.

It should be added that, for species which live in the acid stomach, the signal from the host is provided by undissociated hydrochloric acid (90). At low pH values, very small amounts of undissociated acid would be available, and Rogers proposed that this would be rapidly taken up by the worm and immediately dissociated. In this way a change in the internal pH would be expected.

Rogers' analysis of the role of carbon dioxide shows that it is not an isolated stimulus for a few species. Carbon dioxide is the stimulus for the resumption of development in numerous species of nematodes that infect the host by the oral route (66, 90), but its activity is not limited to nematodes. Infective stages of the platyhelminth Fasciola hepatica and of some acanthocephalids and parasitic protoza are also dependent on carbon dioxide to initiate oral infection of the mammalian host. Rogers constantly stressed to his students and colleagues the importance of seeking generalizations in science, and he was delighted to find this example. However, we do not know whether subsequent events, such as a change in the internal pH, also follows exposure of these infective stages to carbon dioxide as it does in nematodes.

The physiological consequences of stimulation

Rogers described the infective stage as being in a state of 'hypometabolic dormancy' (92). Exposure to 'readily available' undissociated carbonic acid, or, less commonly, undissociated hydrochloric acid, terminates dormancy, and the obvious changes that ensue, exsheathment or hatching, may take place within thirty minutes. These changes, it was proposed, depend on both the activation of an endocrine system, set up in the previous (second) stage, which controls moulting or hatching, as well as much slower changes involving DNA transcription of the gene set of the first parasitic stage (third stage).

Significance of the change in internal pH. Experimental evidence showed that the change in internal pH was not slow and steady, but fast and diphasic. Within thirty minutes of exposure to the stimulus, the internal pH fell and then recovered quickly, overshooting the initial pH before returning close to the original value. The significance of these changes lies in the demonstration that they were associated with the release of calcium ion, which as a 'second messenger', was proposed in turn to activate systems that direct development of the early stages of the parasite (94).

Involvement of an endocrine system in ecdysis. In 1982 Rogers and his colleague T. Petronijevic drew attention (86) to the work of K. G. Davey and colleagues at McGill University, who had been largely responsible for establishing the form of an endocrine system governing ecdysis in nematodes. The Canadian group used the cod-worm Pseudoterranova decipiens. Worms in codfish are infective for seals. The early changes they undergo when eaten by a seal can be reproduced in vitro and involve the formation of a new cuticle followed by ecdysis of the old. This moult is preceded by a cycle of activity in catecholaminergic cells in the nervous system that synthesises noradrenaline. Some of these cells are in close association with peptidergic cells, and it was proposed that noradrenaline modulated the release of a hypothetical peptide hormone which in turn controlled the release, from the excretory cell, of enzymes involved in ecdysis.

A link between the action of the stimulus for exsheathment and an endocrine system in H. contortus was suggested by Rogers' observation that there was a rapid increase in the noradrenaline content of worms within one hour of exposure to the stimulus (71). Moreover the neurosecretion Davey had reported in P. decipiens had been detected in comparable regions of H. contortus (65). Although the information about the sequence of events that leads to exsheathment in H. contortus was tenuous compared with that available for P. decipiens, Rogers argued that the same principles governed the terminal events of ecdysis. Thus, a stimulus from the host (not defined in P. decipiens), induces a sequence of changes in an endocrine system. These in turn induce the release of enzymes from the secretory cell that break down the old cuticle.

Gene activity and the initiation of development. Nematodes moult four times, and each of the five stages in the life cycle is different. Rogers (85, 86) suggested that, in addition to a set of genes that control continuous processes common to all stages, there must be a gene set characteristic of each stage. The infective juvenile of H. contortus is ready to enter the third stage. Expression of the gene set that controlled the formation of the infective stage would have been completed during the second-stage, but the gene set that controls the third (or first parasitic) stage is suppressed, and so is ecdysis. If this is correct, the formation of the infective stage involves the suppression of genetic activity, and this suppression is lifted when the host is infected. How these events are controlled was the problem Rogers set out to answer.

In the United States, two groups had shown that actinomycin-D, which inhibits DNA-dependent synthesis of RNA, prevented or delayed the development of infective stages both in vitro and in vivo. Rogers, using H. contortus, was able to show (85) that the antibiotic blocked the action of the stimulus that normally initiates the development of the first parasitic stage, but it did not prevent exsheathment. He concluded that the hypometabolic dormancy that is a characteristic of these infective stages, and that is normally reversed by the host, must be initiated at the point of DNA transcription. But the failure to stop exsheathment implied that here the control mechanism had developed beyond the point of transcription. Thus, when a parasite like H. contortus infects the host, exposure to the stimulus arising from carbon dioxide initiates transcription of the gene set of the next (third) stage, but also triggers exsheathment. The mechanism for exsheathment, including the formation and release of the enzymes concerned, was presumably set up by the gene set of the previous (second) stage.

Investigations with juvenile hormone. The similarity between the life cycles of apterygote insects and nematodes, particularly in the cycles of growth and moulting, had prompted a number of workers in North America to see whether the insect hormones ecdysone and juvenile hormone, and analogues of the latter, had an effect on development of nematodes. Some years previously Rogers (72) had already shown that the infective stage of H. contortus contained a substance with activity which resembled the activity of juvenile hormone in insects, and that hatching of the non-infective eggs of this species could be inhibited by analogues of juvenile hormone.

Non-infective eggs of H. contortus normally hatch when the embryo has attained the first stage of development. Rogers re-examined the effect of juvenile hormone on hatching of non-infective eggs of five different species, including H. contortus (78), and found that if the hormone or its analogues were present shortly prior to the expected commencement of hatching, the process was completely inhibited. Inhibition was assumed to arise because of failure of eggs to release enzymes that attack the egg membranes and so release the worm, a process that had already already been examined (75) in collaboration with F. Brooks.

However, the inhibition brought about by juvenile hormone was reversed by exposure of the eggs to undissociated carbonic acid (80). Of great significance was the finding that the relationship between pH and the optimum concentrations of carbonic acid for the reversal of inhibition was similar to that already recognised in the action of the stimulus on infective eggs and infective juveniles (81). For both non-infective and infective eggs, a sharp optimum concentration of undissociated carbonic acid was obtained at each pH level tested between pH 6 and 8: increase beyond the optimum decreased hatching. As the pH increased from 6 to 8, the optimum concentration of carbonic acid required for hatching fell. A similar relationship was observed between the effect of carbonic acid and pH on exsheathment of infective juveniles, although sharp optima for each pH tested were not obtained. Instead, exsheathment rose to a maximum with increase in the concentration of carbonic acid, but remained high as the concentration of carbonic acid was further increased (47). These results on the reversal of the inhibition imposed by juvenile hormone implied that the key to the formation of the infective stage may lie in the accumulation of a juvenile hormone-like substance.

Two additional observations are relevant. It was found that as the temperature rose from 20°C to 38°C, the capacity of exogenous juvenile hormone to inhibit hatching also rose (81). Therefore if endogenous juvenile hormone controlled hatching of non-infective eggs at 20°C, at higher temperatures it might be expected that these eggs would fail to hatch, a prediction that was confirmed. This observation may be extrapolated to other stages in the life cycle: perhaps the amount of juvenile hormone-like substance in non-infective stages determines the threshold to an internal stimulus that initiates their development.

Second, two specific inhibitors of the enzyme carbonic anhydrase prevented hatching of non-infective eggs and exsheathment of infective juveniles. These observations suggested that this enzyme was in some way critical for the developmental processes that juvenile hormone controls.

These apparently disparate observations led Rogers to propose a general hypothesis about the role of a juvenile hormone-like substance in nematodes (80, 81, 86). Nematodes have a uniform pattern of growth. All moult four times, and it is likely that the mechanisms that control the transition through four juvenile stages to the adult are similar throughout the group. He suggested that juvenile hormone plays a central role in these developmental processes. The similarity in the effects of carbonic acid on both infective and non-infective eggs, together with the observation that increase in temperature enhanced the inhibition of hatching by juvenile hormone, implied that this substance is present throughout development. In non-infective stages, and presumedly in non-parasitic species, the level of juvenile hormone would determine the threshold to an internal stimulus that initiates development of successive stages in the life cycle. But it is the accumulation of endogenous juvenile hormone above a normal level that is proposed to be the key to the pause in development characterizing the infective stage. The significance of the inhibition of carbonic anhydrase was, however, far from clear, but Rogers proposed that juvenile hormone acted directly or indirectly with carbonic anhydrase activity perhaps associated with a membrane protein, so affecting permeability 'which has consequences in the control of development' (81).

These investigations, culminating in the hypothesis that development of nematodes is regulated by a juvenile hormone-like substance, are important, and provide a significant advance, both in our understanding of nematode development and, more importantly, the nature of parasitism. The exact nature of the 'juvenile hormone-like' molecule that is proposed to control infection is unknown. It should be noted that Rogers was careful in his references to it, using such terms as 'JH-like substance' (80) and similar terminology elsewhere (72, 86). He was concerned about the need to use very high concentrations of juvenile hormone and its analogues in the experiments, and drew attention to the view expressed by K. G. Davey that under natural conditions, juvenile hormone itself may not be involved in nematode physiology.

Direct observations on stimulated worms. A different approach to the study of internal changes in the stimulated H. contortus came from collaboration with K. G. Davey (82, 83). An examination was made of changes in the volume of water associated with exsheath-ment, as measured by exchange in tritiated water, by changes in volume of the worm calculated from linear measurements and by quantitative interference microscopy. Of particular interest were examinations of changes within the oesophagus and the excretory cells by interference microscopy which, under the particular circumstances of this study, indicated changes in volume of water.

Exsheathment was shown to be associated with loss of water from both the excretory cell and the oesophagus, and ethoxyzolamide, which strongly inhibited exsheathment, also inhibited the loss of water from the excretory cells. An analogue of juvenile hormone had an effect like exsheathment on the water content of the excretory cells and this was also blocked by ethoxyzolamide. Although the enzyme carbonic anhydrase is specifically inhibited by ethoxyzolamide, very little is known about this enzyme in nematodes, and it cannot be ruled out that the inhibitor may function in other ways. However, in spite of these complexities, it was possible to propose a working hypothesis in which it is envisaged that both carbon dioxide and juvenile hormone act on the same receptor, an action which can be blocked by ethoxyzolamide. The receptor is envisaged to be in the nervous system, from which it triggers the release of noradrenaline. This in turn leads to the release of a peptide hormone from neurosecretory cells that acts on the excretory cells, promoting release of the contents, including enzymes capable of breaking down the old cuticle.

The involvement of enzymes in hatching and exsheathment

Early work had suggested that when the infective stage exsheathed, an 'exsheathing fluid', which included the enzymes responsible for loss of the old cuticle or sheath, was detectable in the medium and was apparently released from the excretory pore. It seemed likely that the site for storage of these enzymes was located in a region between the base of the oesophagus and the excretory pore (48). In this region lie the excretory cells that connect to the exterior through the excretory pore. Rogers identified three enzymes, an esterase, a lipase and a chitinase, in the hatching fluid of the eggs of A. lumbricoides (46), and he subsequently published similar results of an investigation of enzymes in exsheathing fluid (56, 60).

Rogers showed that exsheathing fluid contained an enzyme, leucine aminopeptidase, which he concluded 'is indeed the enzyme which completes the second moult of some species of nematodes' (60). It was clear however, both from the paper itself as well as from discussions with one of us (RIS), that he was troubled by the results. Exsheathing fluid from H. contortus attacked sheaths isolated from this species, but not those isolated from T. colubriformis. Similarly, fluid from the latter failed to attack sheaths isolated from H. contortus. More seriously, a purified preparation of mammalian leucine aminopeptidase had no significant effect on isolated sheaths of both species. There were other inconsistencies which it was not in Rogers' nature to ignore. Moreover between 1969 and 1974, doubt was cast on Rogers' conclusions about the role of leucine aminopeptidase by two groups of workers in the United States. This provided an additional stimulus to clarify the inconsistencies.

In one of the papers critical of his work, Rogers saw what he regarded, correctly, as fatal flaws in the techniques. His response was to publish paper 70, in which he described as his chief aim the simplification of methods to test for the presence and activity of the disputed enzyme. He saw no reason to change his views on the importance of leucine aminopeptidase, but modified his conclusions by proposing that it may be only one of the enzymes involved. He later confessed to one of us (RIS) that he wished he had expressed himself differently and been less impatient with his critics.

Further clues as to the identity of these enzymes came from an examination of the hatching of the non-infective eggs of H. contortus (75). These eggs hatch 'spontaneously' when the enclosed embryo has attained the first stage in the life cycle and is ready for life as a free-living worm. Working with F. Brooks, Rogers found that hatching fluid contained both a leucine aminopeptidase and a lipase. The hatching fluid was able to act on isolated sheaths in the same way as exsheathing fluid. The natural substrates were interchangeable, a demonstration that implied that hatching and the four subsequent moults in the life-cycle may be associated with similar enzymes throughout the life cycle. But more important in the present context was the recognition (76, 77) that leucine aminopeptidase 'cannot be the sole agent involved in exsheathment': a lipase may be necessary.

The cast cuticles of nematodes like H. contortus are composed chiefly of a protein that resembles a degraded collagen, with small amounts of lipid and carbohydrate (42). Leucine aminopeptidase alone had no effect on pieces of cast cuticles. Moreover combinations of this enzyme with a lipase were also without effect (84) and it became clear that some other enzyme was involved. Early attempts to locate a collagenase in exsheathing fluid had failed, but the problem was readdressed using a modified method of analysis and a pseudocollagenase was detected. Moreover, a highly purified preparation of bacterial collagenase was found to produce changes in the isolated cuticles like those seen in natural exsheathment, although the activity was substantially less than with the enzyme from exsheathing fluid.

Rogers concluded (84) that the active components in exsheathing fluid consisted of leucine aminopeptidase, a pseudocollagenase and a lipase. The probable role of the aminopeptidase was believed to be the breakdown of membranes within the excretory cell, so allowing water uptake and the discharge of cell contents. In eggs the lipase is probably necessary for breakdown of the lipid membrane, although pieces of sheaths were readily attacked by collagenase alone. But pieces of sheaths are not the same as intact sheaths: presumedly in these the lipase is important, although this aspect is not clear in his discussion.

This controversy is interesting. Rogers' critics were correct in their claim that leucine aminopeptidase was not the enzyme that attacked the sheath, but for the wrong reasons. Yet their criticisms were valuable because Rogers became cautious about his claim and investigated the matter further, with the consequence, as we have seen, that at least three enzymes were found to be concerned: exsheathment was more complicated than at first thought. Identification of the enzymes involved in exsheathing and hatching was particularly difficult, not only because of their instability but also because the organisms are small and not readily available in large numbers. Success depended in part on the development of new and the modification of old techniques for handling worms, concentrating exsheathing fluid and measuring enzyme activity (70, 74, 75, 84).

Epilogue

Rogers' real interests lay in research and, to a lesser extent, in teaching, which he saw as an extension of his research. Although a capable administrator, he avoided administrative chores when he could reasonably do so. In his later years, he was much consulted for his opinions in departmental reviews in his own and other Australian universities, and asked to provide advice on senior appointments. He seems to have favoured those with similar attributes to his own, which might not have been entirely appropriate for universities in the latter half of the twentieth century. Rogers himself held views about the roles and functions of universities that have become increasingly outmoded in these modern, entrepreneurial times.

These facets of his character are not uncommon in research workers of his generation. But in his chosen discipline, parasitology, Rogers was unique in his approach. For sound reasons, animal parasitology in the middle of the twentieth century was concerned primarily with pathology and chemotherapy, with immunity and to a lesser extent biochemistry in the ascendant. The parasite was not seen as an identity in its own right.

Rogers' views were the antithesis of this approach. As he made clear in his book The Nature of Parasitism, he was interested in the whole animal. He wanted to understand parasites and parasitism as products of the evolutionary process. He adopted a comparative approach within and across phyla, applying his outstanding technical skills and always trying to elucidate the fundamental features of the parasitic state. This work in the late forties and early fifties was remarkable. His technical ability enabled him to tackle problems that were inaccessible to scientists of lesser accomplishments. The organisms with which he worked do not lend themselves readily to the experiments imposed upon them, and a high degree of technical skill was required of Rogers to put the questions and obtain the answers. As we have pointed out, his findings of some fifty years ago have been confirmed and built upon by subsequent generations of adaptive biochemists.

These achievements alone ensured his place as a distinguished worker in the field. But more was to come with his investigations of developmental processes in parasitic nematodes and the insight these gave to the nature of parasitism. We have drawn attention to the conflict between Rogers' personal philosophy and the policy of directed research that characterized CSIRO. From his personal papers it is clear that he regarded the research on development as being both difficult to investigate and uncertain as to its outcome. In his view, only the environment of a university gave him the security he needed to take this new direction. These days it is argued that university research must be accompanied by commercialization, which seems to imply some limitations on what might and might not be studied. Yet it was the university that provided freedom to undertake the difficult and speculative research which enabled Rogers to develop his ideas, and to make an enlightened and original contribution to our understanding of parasitism.

In his examination of developmental processes and their relationship to parasitism, Rogers never confused host and parasite. Rather, he saw parasites as animals in their own right. He deciphered the sequences of transcription and translation that control both formation of the infective stage and the subsequent resumption of development that is the sequel to contact with the host. He showed that a physico-chemical state in the host animal's alimentary tract triggered development and began to analyse the role of the parasite's endocrine system in these events. Parasitic nematodes are difficult animals with which to work. Those who are familiar with them can appreciate that these investigations demanded substantial ingenuity in the invention and adaptation of appropriate techniques.

Rogers worked with parasitic nematodes partly because, compared with other parasitic metazoa, they are relatively simple animals. But it seems likely that the principles he has established will be found to apply to a wide range of parasitic invertebrates. Where a potential parasite enters a 'resting' stage in which it waits for the advent of a host, the suspension of development implies arrest of transcription or translation, or both. When a host is encountered, the response of the potential parasite must be prompt. Recognition of the host which involves response to a physico-chemical state is likely to be quicker than a process which involves, for example, ingestion of active components: infective stages do not feed. It remains to be seen whether the challenge Rogers' work offers is taken up in the future.

Acknowledgements

We particularly thank Mrs Marjorie Rogers for giving us access to private papers of her late husband. We are grateful to the following for information on aspects of Professor Rogers' life and family: Dr A. Bailey, Mr W. P. Haack, Mrs W. Cruse, and Dr V. N. Kempster. We are also pleased to acknowledge the assistance of Ms A. Brooks, Graduate Database Supervisor, University of Western Australia, for information about Mrs Lillian Rogers.

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79. Dr Theodor Von Brand – an appreciation of the man and his work. (Obituary). International Journal of Parasitology, 9 (1979), 164.
80. The interaction of insect juvenile hormone and carbon dioxide in the hatching of nematode eggs: its significance in the physiology of infective stages. Comparative Biochemistry and Physiology, 64A (1979), 77-80.
81. The action of insect juvenile hormone, on the hatching of eggs of the nematode, Haemonchus contortus, and its role in development of infective and non-infective stages. Comparative Biochemistry and Physiology, 66A (1980), 631-635.
82. (With K.G. Davey) Changes in water content and volume accompanying exsheathment of Haemonchus contortus. International Journal for Parasitology, 12 (1982), 93-96.
83. (With K.G. Davey and R.I. Sommerville) The effect of ethoxyzolamide, an analogue of insect juvenile hormone, nor-adrenaline and iodine on changes in the optical path difference in the excretory calls and oesophagus during exsheathment in Haemonchus contortus. International Journal for Parasitology, 12 (1982), 509-513.
84. Enzymes in the exsheathing fluid of nematodes and their biological significance. International Journal of Parasitology, 12 (1982), 495-502.
85. (With T. Petronijevic) Gene activity and the development of early parasitic stages of nematodes. International Journal for Parasitology, 13 (1983), 197-199.
86. (With T. Petronijevic) The infective stage and the development of nematodes. In: Symons, L.E.A., Donald, A.D. and Dineen, J.K. (Eds), Biology and Control of Endoparasites. McMaster Laboratory 50th Anniversary Symposium in Parasitology, University of Sydney, 5-6 November 1981. Sydney: Academic Press, Australia (1982), 3-28.
87. (With G.P. Jones and T. Petronijevic) The dynamics of the permeation of an analogue of insect juvenile hormone into nematodes. Comparative Biochemistry and Physiology, 76A (1983), 289-293.
88. (With T. Petronijevic and R.I. Sommerville) Carbonic acid as the host signal for development of parasitic stages of nematodes. International Journal for Parasitology, 15 (1985), 661-667.
89. Dormancy in nematode infections. Parasitology Today, 2 (1986), Australian Supplement, S17.
90. (With T. Petronijevic and R.I. Sommerville) Organic and inorganic acids as the stimulus for exsheathment of infective juveniles of nematodes. International Journal for Parasitology, 16 (1986), 163-168.
91. Advances in parasitology, 1886-1986. In: Howell, M.J. (Ed.), Parasitology – Quo vadit: Proceedings, 6th International Conference of Parasitology, 24-29 August, 1986, Brisbane, Australia. Canberra: Australian Academy of Science (1986), 1-13. (Also published in International Journal for Parasitology, 17(1987), 1-13.
92. (With T. Petronijevic) Undissociated bases as the stimulus for development of the early parasitic stages of nematodes. International Journal for Parasitology, 17 (1987), 911-915.
93. (With T. Petronijevic) The physiology of infection with nematodes: the role of intracellular pH in the development of the early parasitic stage. Comparative Biochemistry and Physiology, 88A (1987), 207-212.
94. (With R.I. Sommerville) The nature and action of host signals. Advances in Parasitology, 26 (1987), 239-293.
95. Centenary biographical note: David Keilin, 1887-1963. International Journal for Parasitology, 17 (1987), 1337-1379.

Appendix: Publications other than scientific*

1. Biological science in Australian universities. Vestes, 4 (1961), 13-16.
2. The scientific revolution and adult education. Australian Journal of Adult Education, 1 (1961), 12-16.
3. The function of research in universities. Vestes, 9 (1966), 23-27.
4. Education for our students in the 1980's. Journal of the South Australian Science Teachers Association, Special publication from Conference, Salisbury Teachers College, July 1971, 3-8.
5. Learning from experience. In 'Education '78', The Advertiser (Adelaide), 12 September 1978.
6. John Ellerton Becker, 1904-1979. Historical Records of Australian Science, 5 (3) (1982), 92-107.

*List almost certainly incomplete.