Arthur William Turner 1900-1989
This memoir was originally published in Historical Records of Australian Science, Vol.9, No.1, 1992
- Parasitology & Protozoology
- Contagious Bovine Pleuropneumonia
- Bacterial Oxidation of Arsenite
- Biochemistry and Pharmacology
- Miscellaneous Papers
- Personal Details and Family
Before the Second World War, the veterinary profession in Australia was relatively small. The teaching of veterinary science began in Melbourne in 1888 and in Sydney in 1910 (Bull, 1972). Some early graduates of these two schools made scientific contributions to research on bacterial diseases of animals. One of the most outstanding among this distinguished group was Dr A.W. Turner, who worked for most of his life in Melbourne. Arthur William Turner was born on 17 August 1900, in Melbourne, the first of six children of Arthur Edwin Turner and Esther May Turner née Reynolds. From notes left by Turner, it appears that both his grandfathers had migrated from England, the paternal grandfather from Coventry and the maternal grandfather from London. As a small boy, Arthur learned that his father's father had been a teamster and his mother's father, a tin-smith. He has recorded that it is unlikely that there was any tradition of learning or scholarship in the families, otherwise it would have been known and talked about.
Turner's parents had only minimum primary education and limited financial resources. At the age of 14, Arthur Turner won a Junior Scholarship to proceed to secondary education, being placed third on the list in the State. He was offered a Free Place (similar to an entrance scholarship today) by Wesley and Scotch Colleges. However, he chose to go to Melbourne High School, believing that his parents could not possibly afford the unavoidable extra expenses that attendance at a Public School would entail. He has recorded that he never seriously regretted that decision. He suffered bouts of pleurisy and pneumonia during his time at Melbourne High School. Illness in his matriculation year so interfered with his studies and examination results that he missed out on a Senior Scholarship that would have allowed him to enter the medical course at the University of Melbourne. However, he was offered, and accepted, a 'Nominated Scholarship' to pursue the course for the Bachelor of Veterinary Science degree which had been established by the University in 1909.
Turner graduated B.V.Sc. in 1923 with honours and prizes for Parasitology, Pathology, Bacteriology, Veterinary Surgery, Veterinary Medicine and Veterinary Obstetrics. He joined the staff of the Department of Veterinary Science as a demonstrator while continuing his studies for the M.V.Sc. degree. He passed the examinations for this in 1924, but there is no evidence in the University records that he was admitted to the degree. Probably he felt he could not afford the fee required at that time for admission to this degree, a situation not unusual in those stringent times. He was appointed a Walter and Eliza Hall Fellow at the University Veterinary School in 1924 and commenced research work on infectious necrotic hepatitis or black disease of sheep with Harold E. Albiston, under Professor H.A. Woodruff, in the Veterinary Research Institute which was part of the University's Department of Veterinary Science.
He had some difficulty in obtaining access to field cases of black disease due to apathy or even hostility to this work by stock breeders, who feared that any association of their flocks with such a disease would reduce the value of their properties. Harold Albiston made available the organisms he had isolated in 1921-22, and Turner commenced work to study these.
Late in 1926, Turner
was awarded a fellowship by the Rockefeller Foundation that took
him to the Institut Pasteur, where he studied under Professor
M. Weinberg, a leading authority on anaerobic bacteria. He took
with him to France the organisms isolated by Albiston, that they
had been working on in Melbourne. He became very proficient in
handling and identifying anaerobic bacteria in the laboratory.
While there, he published six papers in French, which confirmed
the identity of the causal anaerobe of black disease as a special
type of Bacillus oedematiens. He also described
a possible method of controlling infections with this organism
in guinea pigs and sheep, by means of a formalin-killed culture.
In September 1927, he proceeded to the Cambridge Institute of
Animal Pathology to further his research experience. This completed
his overseas training, and in March 1928 he returned to Melbourne
at the invitation of (Sir) David Rivett to join the infant Council for Scientific and Industrial Research
(C.S.I.R.). He set up his laboratory in the Veterinary Research
Institute where he had made his first studies of black disease
Parasitology and Protozoology
Parasitology and Protozoology
Turner's first scientific papers described the use of the Schultz-Dale phenomenon (Dale, 1920), involving the specific sensitivity to proteins of the anaphylactic guinea pig's isolated uterus. The technique is very sensitive, detecting minute concentrations of specific proteins, but it requires a special bath and solutions for the isolated uterine tissue, and a kymograph for recording the contractions of the muscular tissue. He demonstrated the use of this technique to identify a range of parasites of veterinary interest including Ascaris equi, Ascaris suilla, Toxascaris limbata, Onchocerca gibsoni, Fasciola hepatica, Gasterophilus haemorrhoidalis, Gasterophilus nasalis and Gasterophilus intestinalis. In a short note, Turner made use of this technique to support the conclusion of Neil Hamilton Fairley (1925) that extracts of bilharzia cercariae, used in the complement fixation test for schistosomiasis, contained no protein. These papers describe the first use of a sensitive serological method now superseded by fluorescent, monoclonal antibody, and DNA finger printing techniques, for identifying specific parasites.
Somewhat later, with his veterinary colleague Daniel Murnane, Turner demonstrated the presence of a harmless trypanosome (T melophagium) in the blood of sheep in Victoria. They showed that splenectomy of infected sheep caused large numbers of the parasites to appear in the blood stream. They confirmed earlier work that demonstrated transmission of the parasite by sheep ingesting infected keds (Melophagus ovinus). This paper was followed by another describing the occurrence of Trypanosoma theileri in the blood of cattle in Victoria. Both T. melophagium and T. theileri were shown to be non-pathogenic. These two papers were reprinted with some additional comments in the Journal of C.S.I.R.
Turner and Murnane also described the presence of large numbers of a Giardia sp. in a sheep that had died after losing weight over a long period. This was apparently an unusual occurrence, since this parasite has not been described as the cause of disease in sheep since this first case. Turner and Murnane considered their parasite, on morphological grounds, to be different from Giardia lamblia, which is known to be a pathogen for human beings as well as occurring in monkeys and pigs.
There is one other short paper by Turner on protozoology describing
the preservation of the red-cell parasite, Anaplasma centrale at low temperature. This organism was imported into Australia
from South Africa to immunise cattle against anaplasmosis caused
by infection with Anaplasma marginale in northern Australia.
The technique required the serial passage of A. centrale in calves in southern Australia away from possible cross-infection
with the virulent A. marginale. To guard against the loss
of the immunising strain of A. centrale by death
or accident to the 'carrier' animals kept in southern Australia,
Turner showed that blood infected with A. centrale could
be safely stored in sealed ampoules, kept on solid carbon dioxide
for long periods.
Turner's first paper on bacteriology involved an investigation of the cause of mustiness in eggs.
Some hens' eggs may develop a very characteristic musty odour which makes them unsuitable for ordinary food manufacture, particularly of pastry and cake. The problem was referred to Turner at the Veterinary Research Institute by officers of the Victorian Department of Agriculture in 1926.
Turner examined some of these musty eggs and isolated a small gram-negative cocco-bacillus, in pure culture, from the egg-white of affected eggs. He established the morphological, cultural and biochemical characteristics of this organism, and decided it belonged to the genus Achromobacter, and that it was a previously undescribed species for which he proposed the name A. perolens from the Latin perolere, to emit a penetrating odour. This was a classical bacteriological study, establishing the causal organism of the condition. It indicated that penetration of the egg-shell by the causal organism, after the egg had been laid and stored for a time at room or lower temperatures, was the likely mode of infection, since A. perolens would not grow at the body temperature of hens.
Black disease, or infectious necrotic hepatitis, is a fatal toxaemia of sheep which was recorded in Australia as early as 1894. It may also occur in cattle, pigs and horses. Early investigators confused the disease in Australia with braxy, a similar disease known to occur in sheep in Scotland but caused by a different bacterium. Hence in the early Australian literature, it is called 'braxy-like black disease'. In 1930, black disease was considered to be the most serious infectious disease affecting sheep in Australia and was costing the sheep industry about one million pounds sterling each year.
Fresh from his overseas experience, Turner began a systematic study of the natural history of the disease that was designed ultimately to control its effect on the sheep industry of Australia. It was known that infection of sheep with the liver fluke (Fasciola hepatica) was often seen in cases of black disease (Dodd, 1921). It was also known that the spores of B. oedematiens could sometimes be found in the liver of sheep that showed no clinical signs of black disease (Edgar, 1929). Turner, by a series of careful and detailed experiments, demonstrated that, when the liver of a sheep is invaded by the wandering larvae of the liver fluke on its way through the liver tissue to a bile duct, the invaded tissue is damaged to such an extent that the oxygen tension of the tissue is lowered to the point where the latent spores of B. oedematiens can germinate, multiply, and produce the powerful toxin that results in the full clinical picture of black disease. Initially he used a guinea pig model, and then went on to show this sequence in the sheep.
It was brilliant work, undertaken with meticulous care and attention to scientific detail, which identified the natural history of the disease. It also demonstrated that a two-fold attack on the problem was possible. First, one could attack the intermediate host of the sheep liver fluke (which is the snail, Lymnaea tomentosa) by clearing water channels and treating these with copper sulphate at the rate of 25 to 30 pounds of 'bluestone' per acre. An alternative was the use of carbon tetrachloride in paraffin oil given to sheep as a drench. However, carbon tetrachloride in larger doses than recommended in the drench for sheep caused liver damage, which might initiate black disease in sheep carrying B. oedematiens spores as readily as did invasion of the liver by immature flukes.
The second line of attack was the development of a vaccine made from six field strains of B. oedematiens grown in a special V-F [V-F = viande-foie, a peptic digest of heart muscle, beef liver and pig stomach tissue] broth, developed by Weinberg for growing anaerobic bacteria. After growth, when maximum toxin production had occurred, the cultures were treated with 0.4% commercial formalin until sterile. Such anacultures are innocuous, and were found to produce good immunity to black disease when given in two doses subcutaneously. Extensive field trials showed the value of this vaccine, and many thousands of sheep were inoculated with vaccine produced by Turner and supplied, free of charge, by C.S.I.R. to sheep breeders throughout Australia in 1930.
Thereafter, the vaccine, made according to Turner's formula, was prepared and distributed by the Commonwealth Serum Laboratories (C.S.L.). Donald Thomas Oxer in 1937 modified Turner's vaccine by adding alum, to produce an alum-precipitated vaccine, which produces a greater and more prolonged response in sheep, following administration of a single dose. This is the type of vaccine now produced by C.S.L. and used throughout Australia and other parts of the world to control black disease.
The results of Turner's five years' work on black disease were published by C.S.I.R. in 1930. This work formed the basis of Turner's thesis submitted to the University of Melbourne early in 1930 for the D.V.Sc. degree. J.A. Gilruth, Chief of the C.S.I.R. Division of Animal Health at that time, wrote a foreword to this Bulletin. He indicated that the thesis had been accepted, and he quoted the following from the examiner's report:
The thesis of Mr A.W. Turner is, in the opinion of all the examiners, a remarkably fine piece of work of quite outstanding merit. The work reveals a profound knowledge of the subject in hand, its literature and its techniques, a critical sincerity combined with a breadth of outlook - an awareness of possibilities - which combination is the essential for any first class research work. The work embodied in this thesis is a comprehensive study, bacteriological, pathological, experimental, and, not only constitutes an elucidation of a problem of animal pathology, but is a valuable contribution to preventive veterinary medicine of great economic importance to Australia. The thesis is alike a credit to the author, to the University of Melbourne, and to the Commonwealth Council for Scientific and Industrial Research.
As might be expected from such a report, the University accepted Turner's thesis in July 1930, and he was admitted to the degree of D.V.Sc. in September of that year. The published papers on this work were submitted by Turner for the Syme Prize of the University of Melbourne which he received in 1932.
The work on anaerobic bacterial infections of livestock was interrupted when C.S.I.R. sent Turner to Townsville in late 1931, as dealt with in the section on contagious bovine pleuro-pneumonia which follows later in this memoir. On his return to Melbourne in 1936, Turner quickly re-established his work on anaerobic infections. With Catherine E. Eales as his assistant, he published further papers on Cl. oedematiens, two dealing with the interesting phenomenon of motile daughter colonies produced by several clostridial organisms, and another reporting a study of the 'H' and 'O' antigens of Cl. oedematiens. This latter paper, involving a study of 33 strains, required a considerable volume of careful work which led to the conclusion that a serological subdivision of the group was not possible. The cultural, biochemical and pathogenic relationships of these organisms were stated to form the subject of another communication which, however, was not published.
Clostridium welchii toxins
In addition to the work on B. oedematiens, now known as Clostridium novyi, Turner widened his scope to take in another anaerobe, Clostridium welchii, now known as Cl. perfringens. This species had been divided into four types on the basis of their exotoxins. Type A, involved in gas gangrene of human beings and animals, and type D, responsible for enterotoxaemia of sheep and cattle, were those of main interest to veterinarians. However, initially Turner and his colleagues investigated the alpha- and theta-toxins of Cl. perfringens, type A. The alpha-toxin was known to be a lecithinase, and they attempted to enhance the production of this toxin by passaging the organisms through growth medium containing added lecithin. They found no increase in the production of alpha-toxin, but there was complete loss of the production of the theta-toxin by both Type A and C strains of Cl. perfringens. These findings, published in Nature (150, 1942, pp.549-550), provided a method of producing large quantities of Cl. perfringens alpha-toxin free of theta-toxin.
Turner then focussed his attention on the epsilon-toxin, produced by Cl. welchii type D, since this was the toxin mainly responsible for toxaemia in sheep. It was known that the ileum of sheep affected by enterotoxaemia contained levels of type D toxin many times higher than could be obtained by growing Cl. welchii in bacteriological media. Bosworth and Glover (1934) had reported that the treatment of dried Cl. welchii type D toxin by small quantities of trypsin markedly increased its toxicity for mice. However, despite the increased toxicity, the antigenic combining power with anti-toxic sera was not changed.
Turner and his young assistant, Alan W. Rodwell, extended these observations by showing that the activation of the toxin of Cl. welchii type D could be obtained by treatment of cultures with a wide variety of proteolytic enzymes. They also found that most cultures of Cl. welchii type D contain, in addition to epsilon-toxin, an atoxic epsilon prototoxin with the same antigenic combining power as epsilon-toxin. This was followed by a detailed study of toxin production in cultures in the laboratory which showed that normally growing Cl. welchii type D organisms readily produced the prototoxin, which was excreted as such, into the medium, producing maximum combining power with anti-toxic serum, in 24 to 30 hours. Most strains also produced an intrinsic but weak proteinase so that after continued incubation of the cultures for four to five days, a variable proportion (depending on the intrinsic proteinase activity of the particular strain) of the prototoxin was converted to toxin. They suggested that the conversion of prototoxin to toxin might involve the proteolytic removal of part of the prototoxin molecule which 'masked' the toxicity of the molecule, a suggestion that was later shown to be correct. These observations provided two important facts. They explained the very rapid onset of enterotoxaemia in sheep infected with Cl. welchii type D, and also provided the vaccine manufacturer with a means of producing potent toxin preparations for conversion into toxoid vaccines for protection of animals in the field.
Turner, while a Walter and Eliza Hall Research Fellow, was introduced by Professor Woodruff to Charles H. Kellaway, Director of the Walter and Eliza Hall Institute of Medical Research. The Hall Institute group was interested in the physiology of neurotoxins and cardiac stimulants and depressants. In 1940, Turner collaborated with Kellaway and Everton Rowe Trethewie in a study of the neurotoxic and circulatory effects of the toxins of Cl. welchii type D. They produced two papers that described the first recorded investigations of the physiological effects of Cl. welchii toxin on guinea pigs and sheep. They found that the type D toxin, after intravenous injection, caused convulsions in lambs by direct action on the basal ganglia of the central nervous system. Death occurred mainly by failure of respiration, or by cardiac failure, complicated by oedema of the lungs and by pleural and pericardial effusions and anhydraemia. In the cat, type D toxin caused the liberation of histamine from oedematous perfused lungs as well as adenyl compounds. These were among the earliest observations on the physiological effects of type D toxin on animals and one is reminded of recent work on focal symmetrical encephalomalacia. This is a condition of adult sheep affected by Cl. perfringens, type D toxin, in which the main lesions are softening and haemorrhages in the internal capsule, the lateral thalamus, the substantia nigra and the cerebellum (Gay et al., 1975).
Before leaving the work on anaerobic organisms carried out by
Turner and his colleagues, mention should be made of a description
of Cl. botulinum type D from soil, and the high rate of
mutation towards loss of toxicity of some Australian strains of
this organism which were originally isolated by Bull in South
Australia (1921). The original cultures were found to be mixed
with sporing contaminants, and Eales and Turner described their
methods of separation and production of pure cultures of this
Contagious Bovine Pleuropneumonia
Contagious Bovine Pleuropneumonia
In 1932, the Empire Marketing Board and the Commonwealth Government of Australia provided a grant to C.S.I.R. to establish a research station in Queensland to study animal diseases in the tropical environment. Laboratory accommodation and animal stables were provided at Oonoonba, Townsville, on loan to the C.S.I.R. from the Queensland Department of Agriculture and Stock.
Turner, with several research assistants, was sent by John Anderson Gilruth, Acting Chief of the C.S.I.R. Division of Animal Health, to take charge of the Oonoonba Laboratory. Work began in December 1931, to investigate tick-borne disease of cattle, peg-leg disease, as well as the wide-spread cattle disease, contagious bovine pleuropneumonia (C.B.P.P.), known colloquially as 'pleuro'.
Contagious bovine pleuropneumonia was introduced into Australia in 1858 with the importation of an infected heifer in a group of cattle landed in Melbourne from England. Little was known about the aetiology or the epidemiology of this disease at the time and, although animals that became ill with this disease were destroyed and their owners compensated, the disease spread steadily throughout Victoria, New South Wales, Queensland, the Northern Territory and the Kimberley region of Western Australia. By 1926, 'pleuro' was enzootic throughout northern Australia and spread occasionally to the southern states. Turner, as Officer-in-Charge of the new laboratory, decided to concentrate his own research efforts on this disease.
Early studies by French bacteriologists had established that the causal organism of C.B.P.P. could be grown in cell-free, nutrient media. There was some confusion about the nature of this organism, which was shown to pass through filters that held back ordinary bacteria. It was therefore considered by some workers to be a filterable virus.
Turner quickly developed a culture medium for growing the C.B.P.P. organism, in pure culture, based upon his earlier success with the V-F medium used to cultivate anaerobic bacteria. He buffered the medium and added ox-serum. In this B.V-F.O.S. medium, the organism was shown to produce a rich growth in 24 hours of incubation at 37°C. Using this medium, Turner prepared very thin layers of inoculated cultures between a microscope slide and cover-slip sealed with paraffin wax. He mounted these preparations on a microscope stage in a constant temperature room and studied the growth of the organism in the thin layer of culture medium, using dark-ground illumination. He photographed the various stages of growth and revealed the morphology of the organism during growth - no mean feat for those days, especially in the relatively unsophisticated Oonoonba laboratory building with its wooden floor mounted on wooden stumps.
By this technique, Turner showed that the organism produced relatively long, branching, mycelium-like filaments, from which very small particles, that were filter-passing, were produced. He demonstrated five morphological forms of the organism in his cultures, three of which he could identify in the pleural exudate from active cases of the disease in bovine animals. Turner identified some of the structures he found in his cultures with the stained particles previously described by other workers. It was his use of a highly suitable medium for the growth of the organism that enabled him to study, by his technique, the progress of the organism from one morphological form to another.
This monumental work was carried out over a period of three years, using, as he put it, 'many scores of strains . . . all isolated by us in Queensland'. The work was published in The Journal of Pathology and Bacteriology, and was reprinted as C.S.I.R. Bulletin 93. In a foreword to this latter publication, L.B. Bull, the Chief of the C.S.I.R. Division of Animal Health, commended Turner's work, commenting that '...a thorough knowledge of the organism forms a necessary foundation on which to build our knowledge of its relationship to the host'.
This paper, on the morphology of the C.B.P.P. organism, was quickly followed by other important and practical papers on the complement fixation test to detect antibody in the serum of infected animals. The first attempts to use the complement fixation (C.F.) test for C.B.P.P. was described by Heslop (1921), but it proved to be too intricate and unreliable for routine use. Campbell and Turner published a detailed description of a reproducible complement fixation test, using an antigen extracted from infected pleuritic fluid, that was shown to be reliable by two other independent research workers from New South Wales and Victoria. This test became known as the Campbell-Turner C.F. test and was used worldwide for detection of infected animals. The antigen was later modified by Campbell (1938a) by the use of a cultured antigen using the B.V-F.O.S. medium developed earlier by Turner for growing the V5 strain of this organism. The use of the C.F. test, modified further was discussed in more detail by Campbell and Turner in 1953.
At Oonoonba, Turner established an infected herd of cattle at the laboratory. By regular testing of sera, it was possible to follow the rise and fall of complement fixing antibody during the whole period of infection and recovery. The routine testing, clinical observation, and subsequent post-mortem examinations, provided the basis for interpreting the complement fixation reaction for diagnoses of acute and chronic pleuro-pneumonia, and for detecting symptomless carriers. Vaccinated and unvaccinated calves were added at intervals to replenish the herd. All the cattle were eventually examined post-mortem - a total of 105 animals. This study yielded valuable information on the behaviour of the disease in an infected herd, and on the accuracy of the complement fixation test for detecting infected cattle as well as on the variety of lesions that may occur. The report on this study concluded with recommendations on the use of the complement fixation test, and of vaccination in the differing circumstances encountered in dairy herds, beef herds and travelling cattle.
At the end of 1936 the Oonoonba Laboratory was returned to the Queensland Department of Agriculture and Stock, and Turner and his staff were transferred to Melbourne, where new laboratories were being built for the headquarters of the C.S.I.R. Division of Animal Health under its newly appointed Chief, L.B. Bull. Turner initially became the Chief Bacteriologist in this laboratory and was later its Officer-in-Charge and Assistant Chief of the Division. A paper in 1935 described for the first time a method of staining the C.B.P.P. organisms in pathological tissue, and another short paper described an inflammatory oedema occurring in the epidural space, and around the sciatic nerve, in six cases of C.B.P.P. This latter was a hitherto unrecorded lesion associated with this condition. The causal organism of C.B.P.P. was readily isolated from these unusual lesions, which could be related to physical signs exhibited by the affected animals.
Turner continued his interest in C.B.P.P. and in the organisms later to become known as the Mycoplasmas, and a paper appeared in 1953, with Campbell, on studies on C.B.P.P. This heralded Turner's renewed interest in the whole problem. It was followed, the next year, by a study of the epidemiology of C.B.P.P, which set out the constraints for understanding the disease and its control in the field.
The live vaccine described by Campbell (1938b), utilizing the moderately virulent but stable V5 strain of Mycoplasma mycoides grown in B.V-F.O.S. medium, was in widespread use in Australia, having replaced the infected pleural fluid inoculated in the tip of the tail. The shelf-life of this vaccine was found to be about two months so frequent batches of vaccine needed to be prepared. In 1949 it became necessary to send this vaccine to Ethiopia to control a devastating epizootic of C.B.P.P. in that country. Gray and Turner investigated freeze-drying the vaccine for despatch overseas. They found a sharp fall in viability of the organisms in vaccine following freeze-drying, but the vaccine could be stored for up to 27 months before being reconstituted and used to immunise cattle effectively. As early as 1952, Turner investigated therapeutic agents likely to be useful in treating cattle affected adversely by the V5 vaccine, the so-called 'bad tails' syndrome. He published the results of growth-inhibition tests carried out on forty antibiotic substances then available. He found the broad-spectrum antibiotics (streptomycin, chloramphenicol and the tetracycline substances) to be useful in such cases. The other main interest in these results was the possible use of various sulphonamides, lysozyme, cyclo-heximide, cyanide and azide as inhibitors in selective media.
In 1961, three papers were published, two with his former colleague, E.R. Trethewie, on preventive tail-tip inoculation of calves against C.B.P.P. They examined the influence of age on the serological response of calves, and the incidence of swollen joints and the occurrence of myocarditis and subacute mycoplasma endocarditis in these animals. These were the first reports of such lesions in calves, and the first description of heart and joint lesions, due to a mycoplasma, in any animal. Turner completed these studies in 1961 with a description of the immune response of calves in relationship to age at inoculation. He concluded that, provided vaccination of calves was delayed until they were 5 to 9 months old, such heart or joint lesions could be avoided and good immunity could be expected in such animals.
In 1962 two papers appeared on work Turner had initiated before his retirement. The first detailed a tube precipitin test to detect C.B.P.P. antigen in acute and chronic lesions, as well as in old pathology specimens preserved in formalin solutions. The test was useful as a quick preliminary test for infection with M. mycoides, but was inferior to the standard complement fixation test on serum for C.B.P.P. described by Campbell and Turner in 1953.
The other 1962 paper discussed the cause of the observed loss of agglutination, and occasionally of the complement fixing reactivity, in acute cases of C.B.P.P. The latter was found to be due to the rapid production of Mycoplasma mycoides antigens entering the blood stream and neutralizing the specific antibody being produced by the animal. The work explained some false negative C.F. serological results being found occasionally with field cases of C.B.P.P. Such cases complicated the control programme. The precipitin test for antigen was recommended in these cases.
The next paper was a study of the efficacy of the standard V5 vaccine strain of M. mycoides grown in the liquid culture medium B.V-F.O.S. compared with M. mycoides grown in embryonated eggs. The senior author was John Richard Hudson, who had been appointed to take charge of the work on C.B.P.P. on the retirement of Turner. In this work, a challenge technique, more closely resembling natural challenge in the field, was used, namely the close and continued exposure of vaccinated and unvaccinated (control) animals to donor animals infected by intra-bronchial intubation with a virulent strain of M. mycoides. This paper bears the hallmarks of the senior author, who had a great regard for Turner's contributions to research on C.B.P.P., and he included him as a co-author even though, by this time, Turner had been retired for three years.
A paper was written in 1963 with Turner's long-time technician, John Richard Etheridge and described a slide agglutination test for C.B.P.P. It was a test that had been included in a panel of tests applied to acute cases of C.B.P.P. since about 1952. This test was found to be inferior to the complement fixation test for detecting field cases of C.B.P.P. A final paper rounded off Turner's work on the significance of the serological reaction of immune cattle to exposure to heat-killed, virulent M. mycoides organisms, and suggested that some of the complement fixation reactions observed in cattle after their exposure to killed aerosol may have been related to contact with cross reacting non-mycoides mycoplasmas.
The work by Turner and his collaborators that commenced in Oonoonba in 1932, established confidence in the accuracy of the complement fixation test for diagnosis and identified, also, the value of vaccination and its occasional shortcomings. This work was, indeed, the basis on which the veterinary administrators undertook the national eradication campaign commencing in 1961, that led to Australia being declared officially free of contagious bovine pleuro-pneumonia in 1973 after the last case was found in 1967. It is estimated that C.B.P.P. cost Australia many millions of dollars each year until it was eradicated.
In March 1960, the Expert Panel on Pleuro-pneumonia, appointed
by the Food and Agriculture Organization of the United Nations
(FAO), together with the Office International des Epizooties (Paris),
held its first meeting in the C.S.I.R.O. Animal Health Laboratories
in Melbourne. Turner had not travelled abroad since his work in
France and England in 1926-28, despite many invitations to attend
international scientific meetings, largely because of indifferent
health. Delegates to this Melbourne meeting came from Portuguese
West Africa, French Equatorial Africa, Kenya, Nigeria, the United
Kingdom and FAO headquarters in Rome. Turner contributed seven
papers to the conference outlining the use of vaccination and
serology to control C.B.P.P. in the field. The Expert Panel
resolved to accept, as the world standard serological method for
the diagnosis of C.B.P.P., the complement fixation test then being
used in Turner's laboratory. This meeting gave him much pleasure,
occurring as it did just before he retired from C.S.I.R.O. in
Bacterial Oxidation of Arsenite
Bacterial Oxidation of Arsenite
The cattle tick, Boophilus microplus, is a serious parasite of cattle and horses. It was probably introduced into Australia through Darwin, from Java, in 1872. It rapidly spread to the Kimberley region of Western Australia and to Queensland and New South Wales. Control of tick infestation by dipping cattle in a dilute bath of Stockholm tar and sodium arsenite solution was used in Queensland from 1895. This dip became known as the 'Australian Dip' for cattle tick and was used world-wide. Later it was shown that Stockholm tar was an unnecessary ingredient.
Spontaneous oxidation of arsenite to arsenate in cattle dipping fluids was first described by Brünnich (1909) in Queensland. It was in 1935 that Turner carried out some observations upon oxidation and reduction of arsenic in the dipping vat of his laboratory at Oonoonba. He recommended the addition of lactose to the fluid as having some advantage over casein or milk that was being used at this time to prevent oxidation. In a paper to Nature in 1949, Turner described the isolation of fifteen strains of heterotrophic bacteria which tolerated 0.1M arsenite, and which seemingly brought about its oxidation to arsenate through an arsenite dehydrogenase, coupled with the bacterial cytochromes. In 1954, Turner published three more papers, two of which were with J.W. Legge, describing, in detail, the bacteria isolated from dipping fluids and the biochemical pathways of bacterial oxidation of arsenite. The isolated bacteria were identified as new species of the genera Pseudomonas, Xanthomonas and Achromobacter. This was a careful, detailed, classical study of the classification and biochemistry of these organisms. Two further papers followed, outlining the chemical and physical factors affecting the arsenite-oxidizing activity of Ps. arsenoxydans-quinque, one of the organisms described in the first paper. This work confirmed that oxidation of arsenite involved a specific bacterial dehydrogenase and cytochromes, which could be extracted from washed bacteria that had been ground with powdered glass. These were early, original observations on the biochemical pathways for the bacterial oxidation of arsenite.
The widespread use of the chlorinated hydrocarbon DDT as an acaricide
resulted in the decline, and finally the abandonment, of arsenical
dips, and a decline in Turner's interest in bacterial oxidation
Biochemistry and Pharmacology
Biochemistry and Pharmacology
In times of drought, the feeding of sheep with wheat grain is a common practice. This is sometimes followed by extensive loss of animals. Some work was initiated by Turner to study this problem. He read the available literature and decided he needed an assistant with training in pharmacology. He chose a young graduate biochemist, Violet Elizabeth Hodgetts, who was working as a laboratory assistant, and sent her to take a postgraduate course in pharmacology.
Their first paper dealt with the effect, on ruminal digestion of sheep, of the administration of chlortetracycline ('Aureomycin') in feed supplements. For some time prior to their work, small amounts of this antibiotic were being fed to pigs and poultry since it caused them to grow faster. Turner wanted to know what effect his antibiotic would have on the bacterial flora in the rumen of sheep being fed large amounts of grain. He used doses at least ten times greater than those used as growth supplements in other animals, and found the number of bacteria in the rumen decreased sharply and ruminal digestion was greatly depressed, with consequent diminished appetite and loss of weight of the sheep.
Then followed two further papers on the buffer systems in the rumen of sheep. The first emphasised the importance of avoiding loss of carbon dioxide from ruminal fluid collected, either by suction tube inserted down the oesophagus into the rumen, or by withdrawal through a ruminal fistula. Equilibration with a sample of the animal's ruminal gas or with a mixture of equal volumes of CO2 and nitrogen was found to be suitable. The second paper confirmed that sheep ruminal fluid is relatively well buffered against addition of acid, but poorly against additions of alkali. Intervals after feeding, the nature of the diet and composition of the drinking water, all affected the total and relative concentrations of bicarbonate, phosphate and volatile fatty acids present. They found that after heavy consumption of wheat grain, lactic acid accumulates, and since this acid has a pk value of 3.8 compared with the usual volatile fatty acids present in the rumen, that have a pk value of 4.7 to 4.8, the pH of the ruminal fluid may fall to nearly 4. This would result in the production of acidosis and probably account for the death of sheep fed excess grain under drought conditions. Although this work was undertaken to ascertain the cause of losses due to drought feeding of wheat to sheep, no paper summarizing these findings in relation to the main problem was published. However, the Report of the Twenty-eighth Meeting of the Australian and New Zealand Association for the Advancement of Science, held in Brisbane in 1951, records that 'Dr A.W. Turner and Miss V.E. Hodgetts read a paper on "Effects of Excessive Wheat Consumption in Sheep" at the meeting of Section L - Veterinary Science'. No abstract or manuscript of this paper is available.
During the investigations into the toxic effects of excess consumption of wheat by sheep, Turner had observed fluctuations and anomalous increases in the haematocrit values of successive samples of blood taken from the jugular vein of sheep. He and Elizabeth Hodgetts investigated this phenomenon and showed that it is a consequence of splenic relaxation causing passive filling of the spleen, and segregation therein of an increased fraction of the total red cell mass in a state of dynamic equilibrium with the circulating blood. Although at this time it was known that, in dogs and cats, the spleen could act as a storage organ for red blood cells, there was no published information on this phenomenon in sheep.
In two detailed papers and a summary paper published in Nature in 1960, Turner and Hodgetts showed that gentle handling and soothing of sheep produced a fall of up to 24% in the haematocrit value compared with the value obtained from a sheep caught and bled immediately. They concluded that the soothing of the animal produced a diminution of the sympatho-adrenal flux from the cerebral cortex. Turner referred to this as 'tranquillization by holding'. [One of us (E.L.F.) remembers seeing, at the time of this work, one of Turner's young female assistants solemnly playing Brahms' 'Cradle Song', on her flute, to a pen of experimental sheep to 'soothe them' before taking blood samples! This specific method is not mentioned in the published paper, but gentleness and quietness is, and suggested to them the use of the ataractic drugs described in the paper.] They then tested the effects of tranquillization by chlorpromazine which was found to produce a profound fall in the haematocrit value in sheep. The effect was virtually abolished by splenectomy. Haematocrit falls also occurred after administration of sodium pentobarbitone which prevents sympatho-adrenal discharge by blocking nervous impulses within the central nervous system. This work was among the earliest observations on the haemo-dynamics of the sheep, and provided new pharmacological information regarding the use of tranquillizers and anaesthetics in the sheep.
The barbiturate sodium pentobarbitone ('Nembutal') has been used as a general intravenous anaesthetic in sheep since about 1939 with generally satisfactory results. However, during long operations, with repeated additional amounts of 'Nembutal' injected intravenously, sheep may die from respiratory failure. Turner and Hodgetts investigated the use of the barbiturate antagonists, 'Megimide' and 'Daptazole', in curtailing anaesthesia and the occasional apnoea encountered in sheep subjected to lengthy operations under 'Nembutal' anaesthesia.
These barbiturate antagonists were introduced into pharmacology by Professor F.H. Shaw of Melbourne in 1954 (Shulman et al. 1955) as the 'Shaw-Shulman' treatment of barbiturate intoxication in man. Turner's paper established the value of 'Megimide' and the combination of 'Daptazole' and 'Megimide' in terminating 'Nembutal' anaesthesia in sheep. It also demonstrated that these barbiturate antagonists function similarly in the ruminant animal to the way they do in monogastric animals. It was essentially a paper to assist the busy professional veterinarian.
Turner was also involved, though not as a senior author, in a study of the effect on cattle of long-continued cutaneous application of DDT. This work showed that cattle tolerated dipping with DDT, and that small amounts of this substance could be detected in milk and tissue of the test animals. It was some time later that the use of DDT as a dipping agent was banned in Australia and elsewhere.
There are a few general publications from Turner of varying length and significance.
He gave the Presidential Address to Section L - Veterinary Science of ANZAAS in 1947, on 'The Influence of Nutrition upon the Immune Response and upon Resistance to Infection'. This was a wide-ranging survey of nutrition relative to disease in animals, and included references to work on trace elements and phyto-toxins being undertaken by Western Australian workers.
Peg-leg of cattle was one of the conditions Turner investigated when he went to Townsville. It is a disease of cattle in north Queensland characterised by under-development, relative infertility, lameness and skeletal deformities, and is most common in pregnant and lactating females during long dry winters. Investigations by Turner and his colleagues showed it to be essentially an aphosphorosis due to a deficiency of phosphorus in the soil and herbage, aggravated by the absence of rain for long periods. Dosing cattle with dicalcium phosphate or by the administration of sodium phosphate in drinking water was found to produce significant body weight gain in recipient animals. This work can be considered the foundation of studies that continue in Queensland to the present day on the best practical method for correcting phosphorus deficiency on northern Queensland beef cattle properties.
Turner collaborated with C.W. Crane in a letter to Nature on the amino-acid patterns of urine and blood plasma in a dog exhibiting cystinuria, which they found to be similar to the human hereditary form of this condition. They suggested that such dogs may be useful experimental animals for studying the human disease.
In 1944, at a meeting of the Australian Veterinary Association, Turner read a paper on the use of the Brucella abortus strain 19 vaccine being investigated by C.S.I.R. at that time to reduce wastage of cattle from brucellosis (contagious abortion). It was wartime, and facilities and research personnel were in short supply. Promising results were indicated, but it would be many years before the present situation with this disease would be reached with brucellosis eliminated from cattle in Australia in July 1989.
For most of his scientific career, Turner worked with relatively small groups of scientists and technicians. They all received sound training in laboratory techniques, the design of experiments and the honest, critical assessment of results. He never sought to expand his department beyond the immediate scientific requirements needed to investigate the various problems for which he, as leader, had responsibility. He was named Officer-in-Charge of the C.S.I.R. Animal Health and Production Laboratory at Parkville and later Assistant Chief of Division, but he was over-shadowed by his Chief, Dr L.B. Bull, F.A.A.
Bull and Turner had respect for each other as scientists. Bull had designed and built the Parkville Laboratories as the headquarters of his Division, but he frequently issued instructions to various members of the staff without any prior consultation with the Officer-in-Charge. Bull was a dominant character, a leader who assumed control in nearly all his endeavours. Turner was more retiring, widely read, and with a gentler approach to those with whom he worked. He often found it difficult to accept Bull's direct dealings with the laboratory staff, and uneasiness existed in their relationships over their years together (French and Stewart, 1983).
On Bull's retirement in 1954, Turner was offered the position of Chief of the Division. He declined, believing he could be more useful actively working at the bench. He remained as Officer-in-Charge and Assistant Chief of the Division until July 1954, when he asked to be relieved of the position of Officer-in-Charge and Thomas Screen Gregory assumed this responsibility. Declining health led Turner to the decision to take early retirement in 1960. In retirement he took no active part in scientific or professional work. This was his deliberate decision.
It is worth recalling the names and achievements of Turner's various assistants who went on to make their own scientific reputations, based mostly on his careful training of them in their early scientific development.
First, there was A.T. Dick, who worked with Turner in Townsville. He went on to a distinguished career in chemical pathology to which he was directed by Bull on his return from Townsville. He became Dr A.T. Dick, O.B.E., F.A.A., and the last Chief of the C.S.I.R.O. Division of Nutritional Biochemistry, from which he retired in 1976.
Alan Wratislaw Rodwell joined Turner in 1939 as a research assistant and made significant contributions to the work on anaerobic infections and Brucella abortus. He, with his wife Edith Shirley Rodwell, then went on to make an international contribution to the biochemistry of mycoplasmas, which earned Alan Rodwell the first Kleineberger-Nobel Award in 1980 for work on this group of organisms.
In 1955, Geoffrey Selkirk Cottew came to work under Turner on the microbiology and classification of the bovine mycoplasmas. He eventually expanded his interests to include those mycoplasmas affecting sheep and goats. On several occasions he was appointed a consultant to the Food and Agriculture Organization of the United Nations on the mycoplasmas of sheep and goats. He retired from C.S.I.R.O in 1986.
Turner's work as an administrator can be summarized by saying
he disliked it intensely and sought to avoid it as often as possible.
He regarded it as interfering with the research work which was
his great love. He accepted, for only short terms, duties on the
Council of the Australian Veterinary Association (1939-40, 1946-47),
editorship of the Australian Veterinary Journal (1937-39),
and membership of some minor scientific committees. He was President
of Section L of ANZAAS in 1947 but generally he avoided such commitments.
Turner received many honours and awards for his scientific work. In addition to his D.V.Sc., D.Sc. and the Syme Prize from the University of Melbourne mentioned earlier, Turner was elected a Life Member of the Australian Veterinary Association. He was a Foundation Life Fellow of the Australian College of Veterinary Scientists.
In 1938 he was made an Officer of the Order of the British Empire (O.B.E.), in the Birthday honours for that year, by His Majesty the King, for outstanding services to Science and the Commonwealth. Initially he had some reservations about accepting this award because of his perception of the assistance of his colleagues. His mother, as well as his professional colleagues, encouraged him to accept the award. Characteristically, he left the ceremony with his O.B.E. insignia in his pocket rather than around his neck. He was in the first group of Fellows elected by the Foundation Fellows of the Academy of Science in 1954. Turner greatly valued this and all recognitions of his work, but he was always quick to acknowledge the debt he owed to his family, his teachers, his colleagues and those who had gone before.
In l958 Turner received the Gilruth Prize of the Australian Veterinary Association, the highest honour
his profession could confer on him.
Personal Details and Family
Personal Details and Family
In 1924, Turner married Grace Winifred Godfrey, the daughter of R.T. Godfrey. They had two sons and a daughter: Arthur Malcolm, born in 1925, Christopher Robin, born in 1929, and Jocelyn Merle, born in 1940. Arthur Malcolm Turner took a medical degree and is now in general practice in Nunawading, a suburb of Melbourne. The second son died suddenly in September 1990 having been employed in the Melbourne and Metropolitan Board of Works. Jocelyn married Jeffrey Dyson in 1959 and they have five children.
Arthur William Turner was a shy man who made few intimate friends. He had indifferent health for most of his working life being subject to bouts of pneumonia and pleurisy from an early age, and later from severe attacks of migraine often lasting for several days. Social activities had little attraction for him, although he was a regular attender of meetings of the Australian Veterinary Association and the Victorian Society of Pathology and Experimental Medicine. He was also a member of the Australian Association for the Advancement of Science (ANZAAS).
He loved music and had a good library of records and tapes of classical music. He particularly enjoyed chamber music and orchestral recitals, and often attended these with his sister, Mrs Ellen Bradshaw. However, his main recreation was reading and his library contained books in French, German, Spanish, Russian, Greek and Latin as well as in English. He is said to have surreptitiously taken a book with him when, as a child, he accompanied his father to football matches in Carlton. He had little interest in organized sport but continued an avid reader all his life.
He was elected to membership of the Wallaby Club of Victoria, which is a select club for men distinguished in science, the law and letters. He is also recorded as being a member of the Graduates' Union, Melbourne University.
In his acceptance speech following the award of the Gilruth Prize for 1958, Turner was moved to reveal the debt he perceived he owed to others for his success. We can do no better than to quote from this. He said, inter alia:
...luck and good fortune have been kind to me; for I had the foresight to choose the right period to be born in, the right parents to stint themselves in order to educate me, the right wife to endure patiently and willingly what I now realize was my own selfish pursuit of happiness through study and research, the right teachers to inspire and guide me, and the right colleagues to help me. I have been fortunate in having been presented with problems which had been brought almost to solution by my predecessors. Sir Isaac Newton, once said "If I have seen further, it is because I stood on the shoulders of giants" Gentlemen, I too have stood on the shoulders of giants - men like Sydney Dodd, Grahame Edgar and Harold Albiston in Australia, and innumerable others here and abroad, from whose shoulders I was able to gain that revealing glimpse ahead which brought some problems a little nearer to solution. I have been able to follow my bent in a way impossible for less fortunate colleagues and have been able to make of my research life a joyous adventure.
Like many Australian scientists who went through the stringent financial times of 1929-1939, Turner worked long hours in his laboratory and then went home to several more hours of reading and writing each night. He was probably partly driven by the need to succeed in his work in order to make a secure life for his family, as well as by the natural curiosity he alluded to. One suspects however, that even though he had the support of his wife, Grace, family life for her and the children may have been a little lonely at times.
In April 1982, Grace Turner died and Arthur lived alone in Ringwood near Melbourne until he married, in June 1988, Kathleen Nora Trevillian, the widow of William Keith Trevillian who had died in 1964. Arthur and his second wife, Nora, eventually went to live in the Highvale Retirement Village in Glen Waverley, Melbourne. They spent the next period happily and quietly together until, early in 1989, failing health caused Arthur's admission to a nursing home. He died peacefully of a heart attack on 20 December 1989, and is survived by his wife Nora, his son, Dr A.M. Turner, his daughter Mrs Dyson, and five grandchildren.
He was cremated and his ashes deposited in the rose gardens at
the Springvale Crematorium near those of his first wife, Grace.
Arthur Turner was a distinguished research scientist. He was fluent in French, German and English and he had a good reading knowledge of Russian and Dutch as well as a love, and understanding, of classical Greek and Latin. He worked for nearly all his professional life in Melbourne, either in the University or in the C.S.I.R.O. Division of Animal Health. He was loyal to his colleagues and quick to encourage the young men who came to work with him, either as graduate research assistants or as laboratory technicians fresh from secondary school. He was a highly respected member of the veterinary profession, an inspiration to many younger members who have followed him into research, and a benefactor of the livestock industries through his work on black disease of sheep and cattle and contagious bovine pleuropneumonia .
With his passing, the Academy lost one of its very distinguished members and Australia, a productive and worthy citizen.
The writers gratefully acknowledge the assistance of the present Chief of the C.S.I.R.O. Division of Animal Health, Professor M.D. Rickard, and his staff at the Parkville Laboratory, Melbourne for access to files. Mrs Heather Matthews, the Librarian of the Parkville Laboratory, and her staff provided considerable library assistance. Ms Patricia Zimmer efficiently and uncomplainingly typed the various drafts. Dr A.W. Rodwell supplied information on some of his early work with Turner. Mrs Nora Turner, Dr A.M. Turner and Arthur Turner's sister, Mrs Ellen Bradshaw, supplied some family details.
Our thanks are extended to all the above for their assistance
in preparing this memoir.
- Bosworth, T.J. and Glover, R.E., (1934-35) Rep. Dir. Inst. Anim. Path. Cambridge, 4:79-93.
- Brünnich, J.C., (1909) Rep. Aust. Ass. Adv. Sci., 12:129-133.
- Bull, L.B., (1921) J. Dept. Agric. S. Aust., 25:403-412.
- Bull, L.B., (1972) Rec. Aust. Acad. Sci., 2:7-22.
- Campbell, A.D., (1938a) J. Counc. Sci. & Ind. Res. Aust., 11:112-118.
- Campbell, A.D., (1938b) J. Counc. Sci. & Ind. Res. Aust., 11:119-126.
- Dale, H.H., (1920) Proc. Roy. Soc. London, Series B, 41:126-146.
- Dodd, Sydney, (1921) J. Comp. Path. Therap., 34:1-26.
- Edgar, Grahame, (1929) Aust. Vet. J., 29:55-59.
- Fairley, N.H., (1925) J. Path. Bact., 28:591-606.
- French, E.L. and Stewart, D.F., (1983) Hist. Rec. Aust. Sci., 5:91-110.
- Gay, C.C., Blood, D.C. and Wilkinson, J.S., (1975) Aust. Vet. J., 51:266-269.
- Gilruth Prize Citation, (1958) Aust. Vet. J., 34:262-264.
- Heslop, G.G., (1921) Proc. Roy. Soc. Vic., 38(NS):160-211.
- Oxer, D.T., (1937) Aust. Vet. J., 13:3-15.
- Shulman, A., Shaw, F.H., Cass, N.M. and Whyte, H.M., (1955) Brit. Med. J., No. 4924, 1238-1344.
A.K. Sutherland was formerly Director of Veterinary Research of the Nicholas Institute for Medical and Veterinary Research in Victoria.