Beating the Odds in a Big Country: The eradication of bovine brucellosis and tuberculosis in Australia

CHAPTER 1

Something to Celebrate

When some 500 cattle producers and people connected with the industry gathered for dinner at Townsville’s Sheraton Breakwater Hotel on 25 November 1992, they were celebrating a remarkable achievement. After a 22-year campaign, Australia was about to be declared ‘impending free’ of one of the worst cattle diseases, bovine tuberculosis; the declaration came on 31 December. Three-and-a-half years earlier; the nation had been declared free of another scourge of beef and dairy herds, bovine brucellosis.

The dinner provided an opportunity to reflect on the campaign’s impact on the lives and fortunes of individuals and on the industry as a whole. Something like 100 million disease tests had been conducted — a massive undertaking that made heavy demands on everybody involved, including property managers and stockmen, government and private vets, stock inspectors, laboratory workers and campaign administrators. The animals that tested positive — totalling in the hundreds of thousands — were sent for slaughter or destroyed on the spot, and in some cases whole herds or properties were ‘destocked’. Spending from campaign funds, mostly derived from an industry levy but with big government contributions as well, reached about 750 million by the end of 1992. When spending by individual producers is added — mainly on the extra mustering and property improvements needed to meet testing requirements — total costs amount to at least 1 billion.

Some producers, unable to meet campaign requirements and remain viable despite the assistance available, left the industry. For many others the outcome was more efficient and profitable enterprises based on improved management procedures and better stock. The nation, as well as producers, gained from the boost to cattle productivity that came with control of TB and brucellosis, and from removal of the human health risks posed by infected animals. And, most important of all, the campaign eliminated a major threat to beef and dairy exports — the prospect of importing nations rejecting Australian produce because of the continuing presence of the diseases.

Keys to the campaign’s success were strong industry support, the commitment of all governments — Commonwealth, State and Territory — to eradication, and the collaborative approach adopted by participants. The Townsville dinner, put on by the national BTEC (Brucellosis and Tuberculosis Eradication Campaign) Committee, reflected this collaboration; as well as producers from all over the country, guests included vets, stock inspectors, laboratory scientists and campaign administrators. They were attending various meetings in Townsville that week on cattle industry matters. One was a workshop on bovine TB called to draw together the collective wisdom of people who had been heavily involved in the TB program — for the benefit, particularly, of those handling the final stages of eradication. The BTEC Committee — the campaign’s main policy-making and coordinating body, with members from the cattle industry and all governments — was in Townsville for a regular 6-monthly meeting as well as to host the dinner.

After the meal (sirloin of beef with black peppercorn sauce), speakers from industry and government looked back over what had been achieved and a specially commissioned video, ‘The Battle for BTEC’, received its first screening. John Holmden, South Australia’s Chief Veterinary Officer, who had been involved in BTEC from the start, recited a 32-verse poem he had written — ‘The Saga of BTEC’. After telling the story of the campaign and its antecedents in rhyming couplets, he ended with this message...

I’m reminded that time’s of the essence tonight,

and so, to avoid a most terrible fight

with the Chairman, I’ll close, with one serious plea

For continuing Freedom from B.R. and T.B.

No-one knows just when and how bovine tuberculosis and brucellosis first found their way to Australia. Unlike diseases such as pleuropneumonia and foot-and-mouth, their impact is often insidious and they can go unrecognised in a herd for a long time. As both were widely distributed around the world, it is reasonable to assume that early cattle importations brought them here and later shipments reinforced the infection.

Australia’s first cattle — four cows and two bulls — came with Captain Arthur Phillip’s first fleet and promptly vanished into the bush south-west of Port Jackson. When rediscovered 7 years later this first herd had already grown to 61 head and, with cattle imported later, it provided meat for the early settlement. After Blaxland, Lawson and Wentworth crossed the Blue Mountains in 1813, opening up the vast pasture lands west of Sydney, cattle numbers grew at a staggering pace. By 1843, New South Wales, with a recorded population of fewer than 190 000, boasted more than one million cattle. Beef was in such plentiful supply that, weight for weight, it was cheaper in the shops than bread.

The gold rushes of the 1850s saw official estimates of Australia’s population grow from 400 000 in 1850 to 1 150 000 in 1860. In response to the rapidly expanding demand for meat, recorded cattle numbers increased in the same period from 1 860 000 to 3 958 000. Over the next two decades, following close on the heels of Stuart, Burke and Wills, Forrest and other explorers, pioneer cattlemen and their herds settled outback pasture lands in western New South Wales and Queensland, northern South Australia, and the Northern Territory and Kimberley. By 1895 cattle numbers exceeded 12 million, about half the current total, and all today’s major cattle-raising regions were occupied. The dairy industry was experiencing rapid growth boosted, like beef production, by the advent in the 1880s of refrigerated shipping to Britain. By 1900 Australia’s dairy herd numbered 1.4 million, and some 90% of the milk output went into butter and cheese production, much of it for export.

Concern about the presence of bovine TB in Australia emerged as early as 1859. Victorian authorities were notified that year of its presence in cattle killed as part of initial efforts to control pleuropneumonia, which had first entered Australia, through Melbourne, the previous year. In 1884 the Victorian Parliament appointed a Board of Inquiry to investigate ‘whether the existence of tuberculosis in cattle was likely to be detrimental to the public health and what preventive measures should be adopted’. It found the disease was widely present and recommended measures, including inspection of dairies and condemnation of cattle seen to be diseased, to reduce the risk of people contracting TB from the milk supply. The first official response to the disease in New South Wales came in 1886 with the passing of the Dairies Supervision Act, which gave an inspector the power to order the destruction of cattle diagnosed as tuberculous.

The bacterium that causes bovine TB is closely related to those responsible for human and avian TB. It is transmitted readily to humans, particularly through cow’s milk, and produces essentially the same disease as that caused by the human TB microbe. Before the widespread introduction of bacteria-killing pasteurisation from the 1930s, infection of children through milk was all too common despite the considerable efforts put into controlling the disease in dairy herds. This is reflected in 1932 figures from Melbourne Children’s Hospital where, at a time when TB was a distressingly common disease in Australia, a study found the bovine form in nearly 26% of cases examined.

Health concerns were, therefore, the main motivation behind early efforts to fight the disease. Other major incentives to action were a reduction in carcase condemnations at abattoirs and the general boost to animal productivity that comes with control of a debilitating disease. The discovery by the German scientist Robert Koch in 1890 of tuberculin, and its value in detecting TB, made an attack on the disease feasible — through a testing campaign and slaughter of any animals that gave a positive response.

Early control efforts in Australia focused on dairy cattle, and the first tuberculin tests were performed within a few years of Koch’s discovery. However, progress up to World War II was hampered by a lack of resources and generally slow. In December 1937, The Australian Veterinary Journal advised in its editorial: ‘The main thing is for our governments to press on courageously with the long-overdue task of eliminating the disease by providing the necessary funds.’

After the war, test-and-slaughter programs in all States, with compensation paid for the animals slaughtered, greatly reduced the prevalence of the disease, particularly in dairy herds. In Queensland, for example, the statistics show a decline in TB prevalence in dairy cattle from 12% in 1945, when the State’s control program began, to 0·025% in 1970. However, little attention was given to TB control in the extensive pastoral regions of the inland and north where, in some areas, high proportions of the stock carried the disease. In the Northern Territory’s Barkly Tableland, for example, up to 30% of cattle were infected in 1970. Despite the success of individual State programs, it had become clear that only a nationally coordinated campaign could eradicate bovine TB.

As a direct cause of economic loss to producers, bovine brucellosis was a more serious disease than bovine TB. However, probably because it posed very little risk to the health of the general population, control efforts were given a lower priority until threats to Australian meat exports, due to the presence of both brucellosis and TB, emerged in the 1960s. A requirement imposed (but soon lifted) by Germany that its meat imports come from herds certified as brucellosis-free dramatised the need for action.

Bovine brucellosis, earlier known as contagious abortion or Bang’s disease (after Dr Bernhard Bang, the Danish discover of the bacterium, Brucella abortus, that causes it), increases the abortion rate in cows and can lead to them becoming permanently or temporarily sterile. It also reduces milk production. People can contract brucellosis from infected animals or contaminated meat or milk, but a large dose of the Brucella organism is needed. As a result, only those in close contact with diseased cattle, notably dairy farmers, vets and meatworkers, have usually been at any risk. In the worst cases, infection produces a range of long-term, debilitating symptoms.

Tasmania was the first State to launch a control campaign, based on systematic testing of herds and the slaughter or isolation of infected animals. Steady progress through the 1930s saw Flinders Island declared free of the disease in 1938 and the north-eastern, midlands and southern regions by 1945. Continued efforts, boosted by the introduction of an effective vaccine, saw eradication finally achieved by 1973.

In the other States, little progress was made against brucellosis until the vaccine, known as ‘Strain 19’, appeared on the scene. Scientists in the United States developed this in the late 1930s from a laboratory strain of Brucella abortus that combined the vital attributes of low virulence and the power to stimulate a high degree of immunity. Production of the vaccine began in Australia, first at the Council for Scientific and Industrial Research (CSIR) and then at the Commonwealth Serum Laboratories, after the Conference of Commonwealth and State Veterinarians in 1943 adopted an Australian Veterinary Association recommendation for its widespread use.

Vaccination programs greatly reduced the prevalence of brucellosis and losses due to it, particularly in dairy herds and in beef cattle in the more accessible parts of the country. As well as protecting cows from infection, Strain 19 reduces the risk of abortion in animals that do become infected. However, as it is only about 70% effective in preventing infection, it does not provide the means on its own to eradicate the disease; all it can do is reduce brucellosis prevalence to a low level — about 2% or below. This had been achieved over much of Australia when the national BTEC campaign started in 1970, although in some remote areas up to 17% of animals were still infected. Only a test-and-slaughter effort could finish the job.

The national campaign was launched with optimism — bolstered by the example of the campaign against bovine pleuropneumonia. This began in 1961; progress was so swift that the last observed lesion associated with the disease was detected just 6 years later. After a further 5 years of monitoring, Australia was declared pleuropneumonia-free in 1973. Bill Gee, who played a key role in the national coordination of BTEC as Director of the Australian Bureau of Animal Health from 1974, suggests the success of the pleuropneumonia campaign may have given the proponents of TB and brucellosis eradication false confidence. He says the nature of pleuropneumonia, and the availability of a good vaccine and a good test, made its eradication relatively quick and easy.

Nevertheless, there was no lack of appreciation of the magnitude of the job ahead — although early emphasis was on the difficulty of eradicating brucellosis rather than TB, which, in the end, proved the tougher adversary. As the third annual BTEC Progress Report, for 1976–77, put it: ‘The brucellosis eradication campaign is the most complex animal health program undertaken in Australia. While the disease itself and the control technology are complex, it is the sheer size and scope of the operation which create the real complexities. The campaign involves eight State and Territory organisations in the screening of 20 million breeding cattle run under a variety of management conditions not matched by any other single country in the world.’

The brucellosis effort combined vaccination to contain the disease with eradication by test and slaughter. Most herds went through two or three routine rounds of testing of all breeding animals. When an infected beast was found, the herd was quarantined and subjected to regular tests and culling until two tests, 6 months or more apart, indicated that all was well. A further check test was performed after another 6 months. As Australia had, in the early 1970s, some 18 million breeding cattle in about 180 000 herds, testing for brucellosis was clearly no small task. Abattoir monitoring and milk testing were also used to check for the disease, with trace-back systems linking any positive samples found to the herds they came from. Complex restrictions on the movement of cattle were imposed to protect clean herds from the disease.

On the face of it, the job required to eradicate bovine TB looked much more straightforward. Thanks to the programs that had already been implemented in all States, the first BTEC Progress Report, covering activities to March 1975, was able to record much lower prevalence figures for TB than for brucellosis — notably 0·007% compared with 2·9% in New South Wales and 0·006% compared with 1·5% in Victoria. Between them, those two States accounted for about 46% of Australia’s cattle in 1975.

The situation was somewhat similar in South Australia’s 6% of the nation’s cattle (TB 0·04% and brucellosis 1·8%) and in Western Australia’s 8% (TB 0·03% and brucellosis 0·13%). However, in Queensland, the State with the biggest cattle population — one-third of the total in 1975 — the TB figure was considerably higher at 0·6%, and the brucellosis prevalence was put at 1·5% in the south and west and only 0·2% in the north-east. This pattern was repeated in the Northern Territory, which at that stage accounted for just over 4% of the nation’s herd. There, the TB figure was 0·4% and the brucellosis prevalence 1·1 % in the southern region and just 0·04% in the north. Tasmania, with 3% of Australia’s cattle, was free of both diseases.

As with brucellosis, eradication of TB required repeated testing of infected herds and the slaughter of animals that tested positive. At least four clean tests were generally required before an initially infected herd achieved the final ‘confirmed free’ status. Detection of infected carcases by abattoir meat inspectors and trace-back to the herds of origin played a vital role in identifying infected properties, and movement restrictions were enforced to prevent infection of clean herds.

For the cattlemen, vets, stock inspectors and others involved in the campaign, the ground to be covered and the sheer number of tests required made it a vast, difficult and often tedious undertaking. Testing had to be timed to fit in as far as possible with farm and station management needs, and the vagaries of climate had to be accommodated. For example, BTEC Progress Report No. 3, covering activities in 1976–77, reported that in northern South Australia ‘testing programs were again interrupted by drought, and in some areas by local flooding’, while in the Northern Territory ‘the highly favourable 1976–77 season and the small increase in cattle prices led to an expansion of tuberculosis testing’. Four years later we read in Progress Report No. 7: ‘Despite the most severe drought that the State has recorded in many years, the brucellosis eradication campaign in New South Wales continued to progress. The drought interfered with testing schedules and led to massive movements of stock throughout the State. Departmental staff enforced movement controls and, to date, very few breakdowns have been attributed to drought movement.’

The difficulties of conducting the campaign were generally much greater on the huge stations of outback central and northern Australia than in more closely settled regions; this is the main reason why, nationally, TB proved harder to eradicate than brucellosis. In what turned out to be the most difficult areas — the Top End of the Northern Territory, far-northern Queensland, and Western Australia’s Kimberley region — TB was firmly established while brucellosis was either absent or rare. Both diseases were present, in some parts at high levels, in the semi-arid pasture lands of western Queensland, the north of South Australia and the Northern Territory.

With a degree of understatement, the first BTEC Progress Report foreshadowed the problems that lay ahead. ‘While confidence can be expressed that tuberculosis will, without great difficulty, be eradicated in areas where cattle husbandry is intensive, there are obviously problems of control in the extensive areas’, it stated. ‘Such problems are not technical as the epidemiology of the disease is understood, but logistics involved in applying an intradermal test and culling reactors present some difficulties in this class of management.’

Over vast areas of the continent, extensive management meant that cattle were, at best, mustered only once a year for branding, culling and disease control. Frequently musters were far from complete, leaving some animals untouched for years. Large numbers of cattle, and buffaloes in the Top End, were not controlled at all; they represented a resource from which beasts were harvested from time to time for sale to meatworks. In the far north, much of the country is extremely rugged, making it close to impossible to locate all the cattle or buffaloes there.

Under these circumstances, mounting a disease eradication campaign was a daunting prospect, and doubts were expressed along the way that the objective could be achieved for TB. Two approaches were available: the normal cycle of repeated testing, with slaughter of infected animals, or the more drastic alternative of destocking whole areas by sending all animals for slaughter or shooting them in the bush. Both methods were difficult and costly, and often traumatic for the producers involved. The test-and-slaughter approach required repeated complete musters, with the cattle having to be held for 3 days as 72 hours have to elapse between the tuberculin injection and feeling for the lump at the injection site that indicates a positive reaction. In most cases new stock-handling facilities had to be built to make testing possible, adding to the additional costs imposed by the vastly increased mustering requirements. Destocking also involved big mustering costs if the animals were sent to meatworks. In addition, large amounts of money had to be spent on replacement stock.

The campaign maintained the support of cattle industry organisations and most producers, and almost certainly could not have succeeded without it. An essential factor was the targeted financial assistance made available and the compensation provided for slaughtered stock. Also vital was the effort put into achieving agreement between station managers and campaign teams on the best way to achieve eradication on individual properties. Then there were the bright ideas; one of these, the ‘Judas cow’ technique, is playing an important role in the campaign’s final stages in the north.

The major problem this addresses is how to find the small groups of possibly infected cattle and buffaloes still roaming free in heavily vegetated or otherwise inaccessible country. The answer that Northern Territory stock inspector Pat Carrick came up with was to fit animals, temporarily grounded by immobilising darts, with radio transmitters housed in special collars. These animals could then be tracked and located by helicopter, and any stock that joined up with them shot. This technique, developed following earlier experiments by Damian Collopy, a member of Western Australia’s BTEC team, with radio-tracking in the Kimberley, has been adopted widely in northern Australia. Initially, large numbers of cattle and buffaloes were located. The steep decline since in the numbers of animals found with the collared ‘Judas cows’ is a sure sign that uncontrolled stock are becoming few and far between.

The declaration at the end of 1992 that the whole of Australia was now ‘impending free’ of bovine TB followed acceptance by the Standing Committee on Agriculture, the principal Commonwealth-State coordinating body for agriculture, that the whole of the Northern Territory and Western Australia had now reached that status. This brought them into line with the rest of the country and signified that no herds were still known to be infected with TB. It was not the end of the story, of course; some herds still required further tests to be confirmed free of the disease and nobody had any doubt that isolated occurrences would continue to be detected from time to time, probably for many years. Nevertheless, it was a very major milestone on the road to complete freedom from the disease and, as the Townsville dinner attested, a clear cause for cattle industry celebration.

CHAPTER 2

Before BTEC

Formby Sutherland, a seaman on the Endeavour, has the distinction of almost certainly being the first victim of tuberculosis buried in Australia. Captain Cook’s diary records that he died of ‘consumption’ and was interred at Botany Bay on 1 May 1770, 2 days after the party’s arrival. His was one of hundreds of thousands of deaths from TB to occur in Australia. Calculations by A.J. Proust, a historian of the disease, put the toll between 1850 and 1990 at roughly 335 000 people, and tens of thousands more must have succumbed between 1788 and 1850. Bovine tuberculosis contracted from infected cattle, their meat and, particularly, their milk was undoubtedly responsible for many of the deaths.

While links between infected animal products and TB in humans had long been suspected — for example, laws were enacted in the Middle Ages in Europe that prohibited the use of tuberculous animals for food — it was not until the 1870s and ’80s that firm scientific evidence of the connection began to emerge. This followed the first demonstration, by the French scientist Jean Antoine Villemin in 1865, that TB is, in fact, transmitted by an infective agent and is not simply a response to cold and damp, or poor nutrition. He showed that the disease could be passed from tuberculous to healthy animals by inoculation.

In 1877, Dr James Law of Cornell University in the United States, lamenting the ‘destruction of infancy and wasting of manhood’ caused by TB, called for action to prevent ‘eating the underdone meat or even drinking the warm milk’ of tuberculous cows. Three years later, an international veterinary meeting at Turin, Italy, urged ‘all governments... to take very severe measures of sanitary police, and to instruct the public of the danger, so as to avoid the transmission [of tuberculosis] from animals to man’.

The Victorian Government was one of the first to act, in 1884 selecting three medical men and two members of the colonial Parliament to form a Board of Inquiry to investigate the public health implications of TB in cattle and recommend preventive measures. After taking evidence from a variety of witnesses, including six veterinarians, the Board found that animals known to be tuberculous should not be used for dairy purposes, and made recommendations on quarantine, the dangers of infected meat and the appointment of dairy inspectors. However, despite this flurry of activity and the declaration in 1887 of bovine TB as a notifiable disease, systematic inspection of dairies did not begin in Victoria until 1906 — 6 years after the introduction of a general system of meat inspection.

In New South Wales, enactment in 1886 of the Dairies Supervision Art brought requirements that all dairymen and milk vendors be registered, dairy premises be kept in a sanitary state, and the milk sold be ‘wholesome’. Importantly, it gave an inspector the power to order the destruction of cattle diagnosed as tuberculous. If a dairyman failed to cooperate, his licence to sell milk could be cancelled. The Diseased Animals and Meat Act, passed into law in 1892, provided for inspection of animals and meat at abattoirs and the condemnation and destruction of diseased animals and carcases.

Statistics from the time suggest that these and other public health measures had a big impact on the death toll from TB, particularly on infant deaths. In 1898 Dr Lane Mullins, in a booklet published in Sydney, noted that between 1857 and 1896 a total of 33 790 TB deaths had been recorded in New South Wales and that ‘in all the Australian colonies, tuberculosis stands at the head of the (medical) causes of death’. The good news was that the TB death rate per 100 000 people in New South Wales had fallen from more than 200 a year between 1875 and 1894 to a considerably lower 158 in 1895–96. He thought the Dairies Supervision Act, by reducing the risk of exposure to bovine TB through the Sydney milk supply, was partly responsible for the improvement.

The New South Wales Government Statistician, J.B. Trivett, provided even more persuasive statistics in a booklet published in 1909. Looking at the figures for 1876 to 1908 he found, among other encouraging signs, that the TB mortality rate for male infants up to the age of four in Sydney fell dramatically after 1890. Having peaked at 618 per 100 000 in 1885 — a figure nearly three times higher than the rate in country New South Wales — it was down to 59 per 100 000 by 1907. He attributed the improvement to government public health measures, principally those involving the milk supply. Regretting that action had not been taken earlier, he wrote that the greatly reduced death rate was ‘melancholy testament to the salvage of life which might have been effected in bygone years’.

Despite evidence such as this, some scientists still doubted that infected animal products were a major cause of tuberculosis in humans. Robert Koch, who first isolated the TB bacterium and in 1890 produced tuberculin and demonstrated its potential in testing for the disease, was an influential sceptic. He advised in 1901 that there was no need to take any measures against human infection by the bovine strain of TB, and continued to maintain as late as 1908 that such infection was of negligible importance.

That the human and bovine strains are distinct had been established in 1896 by an American microbiologist, Theobald Smith, who later published the first full descriptions of them. They are closely related members of a large group of bacteria — known as mycobacteria — characterised by thick cell walls with an unusual, tough structure. Until 1970, they were regarded as separate strains of the one species, Mycobacterium tuberculosis; now that name belongs to the human TB bacterium and the bovine strain has acquired the status of a separate species, Mycobacterium bovis. (A third species, Mycobacterium avis, causes TB in birds.)

The first incontrovertible proof — as opposed to very strong circumstantial evidence — that the bovine TB organism can cause disease and death in humans came in 1902 when it was isolated from a child who had died of tuberculous meningitis in the United States. In the years that followed, many studies — including a number in Australia — set out to discover how much human TB was being produced by the bovine strain, what parts of the body were usually affected, and what role infected milk played in the problem.

An extensive study of specimens from TB victims in the United Kingdom published in 1929 concluded that, in the population at large, only 5% of the deaths could be attributed to the bovine organism. However, in children under 5 years old — those most at risk of milk-borne infection — the figure was 30%. The researchers calculated that in 1918 some 3400 Britons had died as a result of infection with bovine TB, and that in 1927 the toll was nearly 2000.

The first Australian figures came from a 1923 study by Dr W.J. Penfold of Melbourne Children’s Hospital. He found the bovine organism in 20% of his sample of 60 children, and among under-4-year-olds the figure was 26%. The bovine form was much more frequently isolated when the disease affected the digestive system rather than the respiratory tract — infections presumably contracted from infected food or drink. Two other studies from the 1920s provided support for the view that the bovine bacterium was not a major cause of TB of the respiratory system. In one of these, Dr Penfold examined specimens, mainly sputum, from 70 adults and found only the human TB organism. A similar-sized Commonwealth Department of Health study between 1924 and 1928, again mainly using sputum specimens, also detected no bovine tuberculosis.

In 1930 two senior medical men from that Department, M.J. Holmes and W.A.N. Robertson, took on the task of preparing a comprehensive report on ‘bovine tuberculosis in man and animals in Australia’. They came to the view that ‘for all practical purposes the source of infection [of humans] is infected milk from tuberculous cows’ and that the risk of contracting TB of bovine origin occurs mainly in infancy. ‘The intestinal tract is then much more pervious to infecting agents than is the case in later childhood or in adult life’, they wrote.

Statistics published in their report showed that TB was causing much less loss of life then than it had 40 or 50 years earlier. The Australian mortality rate from respiratory forms of the disease fell from 125 to 50 per 100 000 between 1881–90 and 1926–27, and deaths from non-respiratory forms dropped even more dramatically — from 38 to just 6·6 per 100 000. Holmes and Robertson concluded that, as most infections due to the bovine strain were non-respiratory and transmission of the bovine organism occurred almost entirely through milk, ‘it is probable that the improvement in the [non-respiratory] mortality rate has a relationship to improved milk supply’.

They thought a tightening of control measures could, in fact, eliminate bovine TB as a source of infection in humans. ‘The conditions in Australia are very favourable to the attainment of such a result’, they wrote, ‘and the necessary expenditure to attain this end would be fully justified’. Their recommendations included efficient inspection of dairies, expanded tuberculin testing with compensation for diseased animals destroyed, the establishment of laboratories for the bacteriological testing of milk, and pasteurisation of all milk intended for human consumption.

They warned against two common practices of the time — the use of a particular cow in a herd to supply milk for infants and the keeping of privately owned cows. Of the first they wrote: ‘Provided the cow has been subjected to and has passed the tuberculin test, no great harm is done by adopting this method, but without such test the system cannot be too strongly condemned.’ Private cows were condemned without qualification: ‘As they are not subject to any inspection and the milk from them is not subjected to any process of sterilisation, the amount of harm they do cannot be computed.’

The findings of two further Melbourne Children’s Hospital studies on the role of the bovine organism in human TB were published in 1932 and 1941. In the first, involving 81 of the hospital’s young patients, clinical pathologist Dr Reginald Webster found the bovine form was responsible for one-quarter of the cases. In the second — involving some 300 cases from Tasmania, New South Wales, Queensland, the Northern Territory and Canberra as well as Victoria — he found the bovine organism in 9% of under-14-year-olds but in no adults.

Webster’s observations backed the view that the bovine TB bacterium mainly produced non-respiratory forms of the disease in humans. He wrote in his 1941 paper that TB of the neck and abdomen appeared to have become much less prevalent over the previous 20 years, which was consistent with the apparent ‘substantial decline in the activities of the bovine type in tuberculosis of childhood in Victoria’. He linked the change to the fact that 45% of the milk supplied to consumers in Melbourne and its suburbs was now pasteurised compared with 25% 10 years earlier, and to improvements in pasteurisation practice. He also cited the fact that the proportion of tuberculin-tested cows coming up positive had fallen by more than half during the 1930s.

Despite strong evidence from other countries of the effectiveness of milk pasteurisation in protecting children from bovine TB — particularly from New York, which made the practice compulsory in 1914, and Toronto, which took the same step the following year — pasteurisation of all milk produced was a long time coming in Australia. However, Victoria made pasteurisation mandatory in the early 1940s for milk supplied to Melbourne, and by the late 1950s raw milk had become a rare commodity in Australia.

Health concerns were undoubtedly the principal spur to action on bovine TB control up to the middle of this century. But financial losses — mainly due to the destruction of tuberculous dairy cows and the total or partial condemnation by meat inspectors of carcases with TB lesions — were also an important consideration. In their 1930 report, Holmes and Robertson published estimates of annual losses, direct and indirect, from Queensland and New South Wales of, respectively, £400 000 and £221 000 — large amounts in those days. In Victoria, expenditure under the Cattle Compensation Act of 1924, which compensated owners for financial loss resulting from the compulsory destruction of stock, was running at about £30 000 a year. Victoria was the first State to provide such compensation, which proved to be an essential component of eradication campaigns.

There’s no doubting the initial enthusiasm to tackle TB in cattle. One sign was the fact that tuberculin was being used in Australia for TB testing within a few years of its discovery by Koch. Queensland’s Chief Inspector of Stock reported in 1893 that many cattle owners were requesting access to it, and that the newly formed Stock Institute would soon be able to supply all requirements. His 1894 report noted advice that stud cattle be tested before introduction to Australia or to a herd. The following year, veterinarian William Kendall began experiments with tuberculin at the Melbourne Veterinary College, and in 1896 Edward Stanley, the New South Wales Government Veterinarian, reported on his first tuberculin tests. The results he obtained apparently correlated well with the findings of post-slaughter inspection.

Unfortunately, though, the testing procedure used in the early days, and not superseded for 40 years, was cumbersome and not conducive to the rapid screening of large herds. This is one reason why, despite the considerable success achieved in reducing transmission to humans, progress in reducing rates of TB infection in cattle was generally slow up to World War II. The test involved taking the animal’s temperature twice, injecting it behind the shoulder with tuberculin, then taking its temperature again four or more times, at 3-hour intervals, starting 9 hours after the injection. A large temperature rise denoted a positive reaction. Usually the vet injected at 9 pm and started taking temperatures again at 5 or 6 the following morning.

A slightly less awkward test, involving a tuberculin injection into the skin, a second injection (48 hours later) into the swelling caused by the first, and palpation of the swelling after a further 24 hours, found favour in the late 1930s. If the swelling was, as described by veterinarian E.N. Larkin in 1937, ‘soft, hot and tender’, the animal probably had TB. The procedure used during BTEC — a single tuberculin injection into the skin of the ‘caudal fold’ at the base of the tail and then checking, 3 or 4 days later, to see whether a lump has formed at the injection site — came into general use in