Rickety monkeys and deformed lions

Tucked away in a corner display of the Royal College of Surgeons Hunterian Museum in London are the limb bones of a monkey. The shafts of the long bones are curved and their ends are thickened and malformed.Footnote ¹⁸ Within the museum store sits another, entire monkey skeleton, exhibiting fractures to its limbs, a distorted sternum and pelvis, and a thickened vertebral column. The accompanying case report suggests that the monkey suffered greatly. Fully grown and kept in captivity, its condition deteriorated gradually. The lower limbs became paralysed, there was urinary and faecal incontinence, and the abdomen became distorted.Footnote ¹⁹ The diagnosis in both cases was the same: rickets.

These bony traces of rickety monkeys were separated from their fleshly bodies and deposited on the historical record by John Bland Sutton, future baronet and president of the Royal College of Surgeons (1923–1925). He obtained them in 1883 from monkeys housed within the London Zoological Gardens.Footnote ²⁰ Monkeys were not the only rickety animals he encountered within the zoo. Traces of many other species feature in the written reports of meetings where he displayed their bodies, in the specimens he deposited within museums, in the copious articles he contributed to the medical and zoological press, and in the discussions his findings provoked within the medical profession. These traces illuminate not only the lives and afterlives of certain inhabitants of Britain's most famous zoo, but also the activities and concerns of the men who studied them, and turned their fates to human advantage.Footnote ²¹

As the impoverished son of a taxidermist, Bland Sutton had paid his way through medical school by working as a demonstrator and private teacher in anatomy.Footnote ²² When newly qualified, he began to perform post-mortems on all the animals that died in the London Zoological Gardens. Although not the first doctor to conduct such examinations, he was far more systematic than his predecessors, incorporating them into a personal research programme that involved the dissection of 12,000 human and animal subjects between 1878 and 1886. For Bland Sutton, the dead animals of London Zoo served as vehicles of professional advancement. His examination of their bodies enabled him to mingle socially with prestigious members of the London Zoological Society. His insights into animal diseases resulted in invitations to address London's many medical societies, whose reports – when published in the medical press – significantly enhanced his professional profile.Footnote ²³ Animals ceased to perform this role only after he won the post of assistant surgeon to the Middlesex Hospital in 1886, and began to focus more intensively upon human patients.Footnote ²⁴

Bland Sutton first entered the zoo at the behest of the Pathological Society of London (PSL). Numbering over six hundred members – mostly private practitioners and London hospital doctors – the PSL was an organization dedicated to ‘the cultivation and promotion of pathology by the exhibition and description of specimens, drawings, microscopic preparations, casts or models of morbid parts’.Footnote ²⁵ While diseases of animals had long featured in its meetings and journals, interest in their relation to human diseases rose up the agenda in the later 1870s. This was due to a series of enthusiastic presidents, as well as wider bacteriological and epidemiological investigations encouraged by new germ theories, which illuminated the animal-to-human transmission of certain infectious diseases.Footnote ²⁶ Rather than embracing the new experimental pathology that employed animals within laboratory settings to investigate infectious disease,Footnote ²⁷ the PSL elected instead to apply older, morbid anatomical methods to all forms of disease. As a scientific institution, where the circumstances of disease and death were closely monitored, and which boasted ample facilities for conducting post-mortems on the many animals that died, the zoo seemed an ideal site of enquiry.Footnote ²⁸

Under the PSL's direction, Bland Sutton approached diseased and dead zoo animals as points of comparison with humans. In contrast with laboratory-based medical scientists, who deliberately created diseased animals that could substitute for humans in experiments, he focused on animals that suffered spontaneously from disease, and sought, by comparison, to determine the similarities and differences between their diseases and those of humans. Whereas experimentalists relied on small rodents and dogs, Bland Sutton was attracted particularly by monkeys, owing to their proximity to humans on the zoological scale. Like experimentalists, he referred to his work as ‘comparative pathology’, but unlike them, his work has passed unnoticed by historians.Footnote ²⁹

In the fourteen months from December 1881, Bland Sutton examined the bodies of a hundred dead monkeys. He discovered that, contrary to popular belief, most had died of bronchitis, not of tuberculosis (which, as in humans, was regarded as the commonest cause of death at the time). Unexpectedly, he found that the second most frequent cause of death was rickets. This, too, was a major health concern in humans. Found especially in poor, urban children, it was characterized by softening and deformity of the bones, stunted growth, a large head, a misshapen chest, twisted long bones and enlarged wrists and ankles. The cause was uncertain, although observers suggested various contributing factors, such as faulty diet, poor hygiene, inheritance, lack of exercise and lack of fresh air and sunlight. The existence of rickets in zoo animals seemed to offer a perfect point of comparison, a ‘side light of no mean power’ to elucidate the disease's manifestations in humans.Footnote ³⁰

To this end, Bland Sutton retained and studied all of the bodies of monkeys that died of rickets in the zoo during 1882. He learned to distinguish different forms of rickets occurring at different ages, and to identify analogous conditions in humans. Moving beyond the comparison of pathological changes, he began to report upon the symptoms that diseased monkeys experienced in life, such as diminished activity and paralysis of the lower limbs. Monkeys responded by using their arms as crutches until these began to bow under the weight. They eventually became paraplegic, and suffered incontinence and priapism. After three to four months, death intervened, usually from bronchitis.Footnote ³¹

Bland Sutton's comparative project grew larger still as he began to identify other animal species that suffered from the disease. In an 1884 paper to the Journal of Anatomy and Physiology which he illustrated with line drawings of affected bones from monkeys, a baboon and a sloth bear, he reported its presence in half of the zoo's dead carnivores, as well as in many rodents, birds and lizards.Footnote ³² Remarking that rickets was ‘as common, or even more frequent, among wild animals in captivity than among children’,Footnote ³³ he began to draw epidemiological analogies between the conditions of animal life within the zoo and those experienced by human sufferers. He identified restricted exercise, exposure to climate and unsuitable diet as common contributing causes, together with the failure of mothers to suckle their human and animal offspring.Footnote ³⁴

Bland Sutton also extended his enquiry to the clinical management and prevention of rickets. Here, he awarded lions the role of patients, and sought to improve and preserve their health, ultimately for the benefit of the London Zoological Society. Lions were costly animals and popular with fee-paying visitors on whom the society depended for the zoo's financial survival. Consequently, their health was a matter of considerable concern. Their offspring had proved virtually impossible to rear within the confines of London zoo. Many were born with cleft palates and did not survive for long. Others developed signs of rickets after keepers removed them from their mothers for fear of harm. Bland Sutton noted that both adults and cubs were typically fed on old horse carcasses, whose bones were generally too tough for lions' teeth. If pregnant lions were fed goat-flesh and soft bones, cleft palates in the offspring did not occur. Moreover, rickety cubs quickly recovered when pounded bones and cod liver oil were added to their diets.Footnote ³⁵

Bland Sutton did not publish a formal account of these findings, perhaps because, from the zoo's perspective, cod liver oil supplements cost as much as replacing a lion.Footnote ³⁶ Dietary changes were not adopted and the disease continued to occur in lions, as shown by the ongoing deposition of their rickety skeletons in the RCS Hunterian Museum.Footnote ³⁷ However, some medical men became very excited by what Bland Sutton's work implied about the causes and management of rickets in humans. Speaking at the Diseases of Children section of the British Medical Association's 1888 Annual Meeting, Dr Cheadle, a senior physician to the Hospital for Sick Children, Great Ormond Street, declared Bland Sutton's dietary experiment ‘a crucial one, and … conclusive as to the chief points in the aetiology of rickets’.Footnote ³⁸ It showed that rickets occurred when diets were deficient in fat and bone salts. This became the accepted view of the disease. Transcending the zoological, anatomical and pathological communities addressed by Bland Sutton, traces of rickety lions began to feature in discussions of human rickets and infant-feeding practices. Their fates also provided the jumping-off point for Edward Mellanby's subsequent discovery that the key anti-rachitic component was a substance found particularly in animal fat, later named fat-soluble vitamin D.Footnote ³⁹ In this way, spontaneously diseased zoo animals became unwitting participants in the advancement of human health, a role analogous to – but distinctively different from – that concurrently performed by the intentionally diseased animal subjects of a quite different, experimental form of ‘comparative pathology’.

Restless marsupials

A North American marsupial, an opossum (Didelphis marsupialis), was stalking an institute of brain anatomy in 1960. Her frantic roaming animated the institute's laboratory at the Waldau, the largest state-run psychiatric hospital in the Swiss canton of Bern. Her pacing left traces in a short paper written by the Waldau's neuropathologist Giorgio Pilleri (born 1925). It reminded him of stereotypical behaviour seen in long-term hospitalized patients, and the ‘quasi-neurotic’ behaviour patterns of mammals held in captivity which German-speaking psychiatrists and zoologists had discussed at length in the 1930s.Footnote ⁴⁰ Pilleri described how the opossum had quieted once she was no longer kept awake during the day contrary to opossums’ nocturnal habits. His account of her movements was a rare, inadvertent portrait of the laboratory's material conditions, otherwise black-boxed in his academic papers. Moreover, in her wandering, the opossum had unintentionally exposed the mid-twentieth-century preoccupation with the effects of long-term hospitalization, behaviourist approaches to mental health and its treatments, and socio-environmental causes of psychiatric disorders.Footnote ⁴¹

The opossum shared the laboratory with a South American paca (Cuniculus paca) who came when called and moved through the building freely, climbing the stairs to the first floor, leaving droppings and marking territory. Within weeks the animal had appropriated part of Pilleri's office and was defending a hallway bookcase by growling.Footnote ⁴² When deprived of her nesting site, the paca ‘lost drive, was listless, seemed somehow different than usual’, Pilleri remarked in a second paper.Footnote ⁴³ Paca and opossum were pets and curiosities, which Pilleri's observations framed as spontaneous analogues to human behaviour. He collected, described and classified observations of living animals as well as of post-mortem specimens, an approach that echoed long-established practices in natural histories.Footnote ⁴⁴ The animals’ provenance reinforced such links. The opossum had been captured in a Mississippi wildlife refuge while still in her mother's pouch, the paca acquired with the help of a Dutch zoo.Footnote ⁴⁵ Pilleri scrutinized the behaviour of other rodents, including aplodontia (North American mountain beaver) during field trips.Footnote ⁴⁶ However brief, the studies were valid according to Pilleri, because they disclosed habits of rare, hitherto under-studied, animals. By embracing species diversity, he sought to reveal the range of healthy behaviour within a taxonomic order. The paca thus was to contribute to understanding the spectrum of rodent behaviour beyond mice and rats which populated behaviourist laboratories and whose behaviour – and brains – were far more familiar to researchers.

While Pilleri acknowledged that his institute was in many ways deeply unsuitable for ethological work, he suggested that his laboratory's ‘utterly unnatural … conditions’ were also a potential asset.Footnote ⁴⁷ They demonstrated the innateness of the paca's marking of territory or the opossum's nocturnal habits. Yet conditions were poor and the laboratory was crowded. Its neuropathological collection threatened to engulf all spaces and surfaces, and the smells from the institute's unrefrigerated autopsy suite were overwhelming.Footnote ⁴⁸ Cantonal financial resources, however, were limited. The institute's director, Ernst Grünthal (1874–1972), therefore appealed for external funding, contacting his collaborators at the Swiss pharmaceutical company JR Geigy AG, in Basel. Grünthal had Pilleri's opossums and beavers in mind when he wrote that systematically observing animals might uncover ‘more advanced[,] spontaneously occurring[,] psychic animal functions’ and therefore previously unknown means to assess drugs.Footnote ⁴⁹ When the institute's new building opened five years later, substantially financed by Geigy, it included in- and outdoor spaces to observe birds and rodents as well as clinical spaces to observe human subjects volunteering in pharmaceutical trials.Footnote ⁵⁰ Tentative and brief in the record, the opossum's traces therefore also substantiated researchers’ career paths and professional identities.

Did the laboratory's furry inhabitants correspond to a more general alignment of psychiatry and animals around 1960? Psychiatric hospitals had long been criss-crossed by animals. They had been considered food and economic resources, feared as disease carriers and public-health nuisances, tolerated as companions; and it had been common to see those afflicted by mental illness as ruled by animal passions. As the opossum paced, Geigy was establishing new research protocols that relied on animal experiments to assay psycho- and neuroactive drugs.Footnote ⁵¹ Yet the traces of the opossum and paca also demonstrated another, non-experimental research direction. Post-mortem the disconcerted opossum might have provided the brain specimen for one of Pilleri's papers in comparative brain anatomy which included photographs of opossum brains and brain tissue.Footnote ⁵² The opossum was known to have a primitive brain, but it had opposable digits and motor skills usually associated with more developed brains.Footnote ⁵³ Did species-specific behaviour correspond to brain or nerve cell composition? Pilleri refuted the link, concluding elsewhere that manual dexterity was indicative of neither an animal's level of brain development nor its ability to shape the environment.Footnote ⁵⁴ In later papers, he stated that brain size did not determine cultural sophistication.Footnote ⁵⁵ Overly specialized brains could indeed be detrimental in evolutionary terms, because they limited avenues of adapting to, and mastering, the environment.Footnote ⁵⁶

The Bernese opossum therefore contributed to a study of instincts that was inspired by the German biologist Konrad Lorenz's mid-twentieth-century ethology, neurologists’ cerebral localization studies, and Darwin's The Expression of the Emotions in Man and Animals (1872). Konrad Lorenz had postulated that instinctual behaviour was innate and fixed in form, and therefore amenable to trans-species comparison. Pilleri argued that this ethological approach systematized clinical observations by grouping symptoms in ‘natural’ orders.Footnote ⁵⁷ Pilleri built on earlier neurological theories that nervous system and behaviour retained archaic roots even as more advanced functions matured. Phylogenetically younger brain components inhibited older structures, but illness or dysfunction could unpick these links.Footnote ⁵⁸ Pilleri's neurological papers thus related automatism seen in patients with severe dementia to infants’ suckling; one patient's ‘climbing motions’ were a return to clinging to a mother's fur.Footnote ⁵⁹ Photographs of patients and primates mid-movement illustrated these connections. Pilleri's papers, moreover, showed that this behaviour, uncalled-for in adult humans but not in infant primates, mapped onto brain lesions identified post-mortem. Scrutinizing animal and human behaviour was therefore diagnostically useful. To closely observe animals was to closely observe humans – and vice versa.

However unusual the marsupial was in the psychiatric hospital, Pilleri was not alone in linking ethology, psychiatry and neurology.Footnote ⁶⁰ A chapter in a 1964 German handbook of psychiatry thus foresaw a brain-based ethology providing psychiatry and psychoanalysis with a much-needed biological foundation.Footnote ⁶¹ Even though ethologists were unable to capture the ‘specifically human’ aspects of human behaviour or its disorder, they could underpin a biological psychiatry equally attuned to soma and psyche.Footnote ⁶² Pilleri's opossum paper also cited interwar authors who had argued that humans and animals alike could be ambivalent, latently neurotic and torn by wants. Some envisaged animal experiments to examine the emergence of neuroses in varying environmental conditions, a research direction subsequently taken up in post-war enquiries.Footnote ⁶³ Pilleri himself pursued few experimental studies in the early 1960s, conceiving of paca and opossum as spontaneous analogues, tools to re-catalogue human behaviour and illness.

The ‘neurotic-like’ opossum and the growling paca inhabited a psychiatry wrestling with demands for patient autonomy, new attempts to localize mental illness in the brain, changing treatment models, and the hope to have finally become a therapeutic discipline. Opossum and paca, moreover, occupied the laboratory at the same time as veterinarians’ attention was turning to animal mental health, therapy animals and symbiotic relationships between companion animals and owners.Footnote ⁶⁴ The animals confronted those who saw psychiatry as exploitative and oppressive. Were psychiatric diagnoses not socially constructed? fumed R.D. Laing, Thomas Szasz and others. For them, ethologists’ projects to found psychiatric knowledge on non-human animals further dehumanized patients and removed their agency. Tracing the opossum and paca was therefore spurious, indeed dangerous. The frantic opossum was thus troubled and troubling as it wandered the hospital.

The opossum's movements intra vitam and post-mortem disclose the growing enmeshment of behaviour, brain and environment – and its challenges – in the second half of the twentieth century. Animals’ habits became framed as a resource to understand, and systematize, human behaviour, a project later extended by sociobiology and evolutionary psychology.Footnote ⁶⁵ Drawing animal and human health together co-constructed new views of mental behaviour and appropriate treatments. First applied to humans, these have been considered for animal health in the last decade. Antidepressants, once appraised with the help of laboratory mice, are being prescribed to companion, farm and zoo animals, and books discussing animal madness are popular.Footnote ⁶⁶ Following the opossum under observation in the psychiatric hospital traverses the assumed disciplinary boundaries of post-war psychiatry and its principles. However, odd, she hints at a wider, densely knit history of psychiatry, its cares and cures which goes beyond patient–doctor dichotomies.

Parasitic tapeworms

In August 1965, surgeons in California carried out an operation on a five-year old boy, known to us only as ‘J.O.’ He had presented with acute abdominal pain that began when he leapt to the ground from the back of a flat-bed truck. Appendicitis was suspected. On opening the abdomen, doctors found that his liver and lungs were strewn with hydatid cysts, ranging in diameter from two to ten centimetres. His leap had ruptured a cyst in his liver and released the contents inside his body.Footnote ⁶⁷ These cysts were the products of a parasitic infection, undoubtedly transmitted to him by one of the many dogs that populated his family's ranch in the San Joaquin valley. Like many sheep ranchers of Basque descent, J.O.’s father, Salvador, differentiated amongst his dogs: while the majority were considered ‘workers’, and kept chained outside at night and treated more firmly, most ranchers also had at least one ‘favourite’, allowed more privileges and closer contact with their masters’ families.Footnote ⁶⁸ A single affectionate lick of the boy's face would have been sufficient to transmit the eggs of the tapeworm, Echinococcus granulosus. Hatching into larvae within J.O.’s intestine, they penetrated the intestinal wall and migrated throughout his body, settling in his lungs and liver, where they grew into cysts, which generated more larvae that spread and anchored to produce cysts in other organs.

The traces that E. granulosus left on J.O.’s body subsequently came to the attention of veterinarian Calvin Schwabe, professor of veterinary epidemiology at the University of California, Davis. For Schwabe, E. granulosus had been a vehicle for professional advancement for at least a decade. Trained also in parasitology and public health, he had built his scientific reputation on investigating the parasite while working as professor of parasitology at the American University in Beirut (AUB) and consultant to the World Health Organization.Footnote ⁶⁹ While rampant in the environs of Beirut, E. granulosus was practically unknown in California when Schwabe arrived there in 1966. Isolated hospital cases like J.O.’s had yet to be situated within a larger epidemiological picture, and parasitologists believed that most American infections had been contracted abroad.Footnote ⁷⁰ In 1967, an unexpected discovery challenged this presumption. While collecting cysts from sheep carcasses at a local abattoir, one of Schwabe's students identified what he believed to be E. granulosus cysts. The news reinvigorated Schwabe's research programme.Footnote ⁷¹ In the Central Valley of California, geographically and culturally removed from Beirut, Schwabe would again observe a network of social and biological links between humans and animals. At the centre of these linkages, articulating existing associations and enabling new ones, was one diminutive but essential animal: the tapeworm E. granulosus. Moving from one animal body to another, it created corporeal connections between bodies – from which many other subsequent connections, both literal and figurative, were generated.

The traces that this diminutive animal left on the historical record enable the historian to reconstruct its social and scientific networks, the roles it played within them, and their implications for scientific understandings of parasites as well as for Schwabe's career. It may seem unusual to award a parasite the status of ‘animal’, yet for a biologist it is self-evident. While the nature of Echinococcus cysts was long ambiguous, tapeworms in general have been recognized as animals since the time of Linnaeus.Footnote ⁷² Their zoological status was further solidified in the late nineteenth century when the study of parasitic helminths and protozoa split off from the study of bacteria – the former considered ‘animal parasites’, the latter ‘plant parasites’. As a member of kingdom Animalia, E. granulosus is known to share characteristics with many free-living animals, including a nervous system and sensory organs. Its key difference lies in its physiological dependence upon the host. On account of this dependence, it has been unusual – in non-scientific discourse – to award parasites the same degree of autonomy and agency as larger, more familiar animals. However, this has not been parasitologists’ perspective. Working at the intersection of medicine, zoology and natural history, they viewed E. granulosus and other parasites as animals in their own right, simultaneously performing the roles of disease threat, predator and symbiont.Footnote ⁷³ E. granulosus functioned also as product and shaper of its environment, an animal that created ecological connections between other animals, and moved opportunistically through the social connections created by humans.

At AUB, Schwabe had used the classic tools and approaches of parasitology to fashion E. granulosus into an object of laboratory experimentation, natural-history study, and public-health disease prevention.Footnote ⁷⁴ He thus sought evidence for the commonly held view that younger humans and animals were more susceptible to infection – although, typically, infections did not become apparent or symptomatic until years later, when cysts that the parasite generated became intolerably large or burst, leading to terrible pain or anaphylactic shock.Footnote ⁷⁵ Schwabe also investigated the physiological mechanisms in the host that allowed the parasite to thrive. As in much laboratory-based infectious-disease research, the researchers’ goals aligned with those of the parasite. Experiments aimed to ensure the parasite's survival and therefore enable it to proliferate and spread between hosts in the lab. While Schwabe's experiments intended to develop defences against the tapeworm and limit infections, he had first to nurture the parasite within his laboratory.

To a parasitologist, different host bodies constitute unique ecological environments for their primary research subjects, the parasites themselves; thus Schwabe sought to understand the tapeworm's ecological requirements and use this knowledge to create conditions in which E. granulosus would flourish.Footnote ⁷⁶ In so doing, he awarded his parasitic animals a form of agency similar to that which featured in the human domestication of animals. E. granulosus succeeded in the laboratory by engaging the cooperation and resources of researchers, and altering their practices and conceptions – a sort of ‘coevolutionary process’ whereby humans moulded animals, and animals moulded humans.Footnote ⁷⁷

After collecting cysts from a human brain, Schwabe gave them new life by injecting them into a laboratory population of mice, thus introducing them into a new ecological environment. The animal traces here may be read in the photographic evidence of the parasite's proliferation. A mouse's abdomen was cut open to reveal enormous clusters of cysts, while micrographs of cyst cross-sections showed the parasitic larvae multiplying on its interior.Footnote ⁷⁸ These traces made visible the extent to which the parasite altered the interior cellular landscape of the host. By making these signs of infection visible, Schwabe also made visible the agency of E. granulosus, evident not only in the way the parasite reshaped its environment, but also in the way it successfully concealed itself from the host animal for long periods so that the cells at the interface of parasite and host became difficult to differentiate.Footnote ⁷⁹

During this period, Schwabe collaborated with colleagues in the AUB chemistry department, measuring the movement of fluid and oxygen between the cyst and the host, to better understand how the parasite adapted to its environment.Footnote ⁸⁰ His published record of the parasite's respiration and how it actively controlled the fluid environment of the cyst brought its fundamental animal nature more clearly into focus. Belying its otherwise passive and inert appearance, the E. granulosus cyst was physiologically responsive to changes in its environment, and capable of altering that environment to suit its requirements.

Yet he was also considering the broader network of biological and social environments, contacts and exchanges that created opportunities for E. granulosus to move between hosts. The insidious nature of the clinical disease caused by E. granulosus made gauging its incidence of infection in the human population a challenge. To make the parasite more visible, he and his colleagues sought evidence of its traces in the surgical records of fifty-four Lebanese hospitals, tabulating the number of hydatid cysts found between 1949 and 1959. Strikingly, they found a high proportion of Christian patients – numbering twice as many as Muslim patients. The study, published in 1961, claimed that ‘religion was a real epidemiological factor’, and posited Muslim cultural prohibitions against close contact with dogs as a possible explanation. Later efforts to gather data further suggested that Christian families were more likely to keep dogs as family pets and encourage children to develop affectionate bonds with them.Footnote ⁸¹ In invoking the importance of these familial, social norms and relationships alongside surgical data, Schwabe turned ephemeral connections between humans and canines into yet another type of animal trace: case studies and personal recollections, which recorded the parasitic animal's movement from one interior host ecosystem to another.

Schwabe's intense awareness of the importance of social relationships and cultural practices proved just as important in California in 1966. Following his student's discovery of hydatid cysts in sheep, he began to seek the parasite actively, discovering ubiquitous traces on hospital surgical records.Footnote ⁸² These led him to the Central Valley sheep ranches and the communities into which ‘J.O.’ was born, which he identified as the main sufferers of echinococcosis in California, thanks to the transhumant sheep-herding practices that Basque ranchers had brought to the United States.Footnote ⁸³ Just as in Beirut, E. granulosus traversed a unique network influenced by the local peculiarities of human sociocultural practice. In California this network connected families and ranch hands to their sheepdogs and sheep, as well as to the deer and coyotes that roamed far beyond the domestic sphere.Footnote ⁸⁴ As both product and shaper of its environment, the tapeworm created bodily connections between other animals that already shared an ecological and social space, and simultaneously built relationships between them, which would leave bodily traces upon the victims, and literal traces in the work of their investigator, Calvin Schwabe.

Tuberculous badgers

In April 1971, a farmer in the Gloucestershire Cotswolds brought the dead body of a wild badger he had found on his farm into his local government animal health office. Roger Muirhead, one of the veterinary officers there, conducted a post-mortem examination of the animal. He reported pathological lesions caused by tuberculosis, and identified its causal bacterium, Mycobacterium bovis, in fluids taken from the badger's lymph gland. The diagnosis was subsequently confirmed by scientists at the government's Central Veterinary Laboratory, and was immediately communicated to other officials and scientific experts within the Ministry of Agriculture, Fisheries and Food (MAFF).Footnote ⁸⁵

Within four years this badger had stimulated a major programme of laboratory, clinical, experimental and field investigations into ‘TB in cattle and badgers’ conducted by the ministry. It had also precipitated a series of laws on the protection and management of wild badgers, which in adapted form still remain in force. Given that in 1971 relatively little was known about the pathology, microbiology and epidemiology of bovine tuberculosis (bTB) in wildlife, or about the ecology and behaviour of badgers, how did one sick animal end up performing such significant roles in such a short space of time? What can the history of this animal and its tuberculous compatriots tell us about human–animal relations, environmental politics and animal health policy in the early 1970s, and what light can its traces shed on the repeating cycles of public controversy over bTB which have unfolded between scientists, veterinarians, conservationists, farming interests and politicians over the last five decades?

By the 1970s, MAFF had been attempting to control bTB in cattle for several decades, initially for the purposes of public health – because the meat and milk of affected cattle were a major source of tuberculosis in humans – and latterly to boost cattle health and productivity. The chronic nature of bTB meant that affected cows showed few overt symptoms until the disease was well advanced, by which time they were significant spreaders of infection. In the 1950s, the government had rolled out compulsory testing of cattle herds at regular intervals, with enforced culling of those affected.Footnote ⁸⁶ Together with the compulsory pasteurization of milk, this spelt an end to bTB as a major public-health threat. By the 1960s, bTB rates in cows had fallen substantially. MAFF declared a number of regions in the UK to be free of the disease, and its eradication was confidently predicted.Footnote ⁸⁷

However, pockets of infection persisted, particularly in Gloucestershire and Cornwall, where some farms experienced repeated outbreaks. Unable to explain this, MAFF dispatched a veterinary team to the West Penwith area of Cornwall to conduct a full epidemiological investigation of the area.Footnote ⁸⁸ This investigation was inconclusive, but shortly afterwards the fate of the Gloucestershire badger came to light. It seemed to prove what some vets and farmers had long suspected: that badgers could spread tuberculosis to cattle. Further evidence emerged the following year, when Muirhead and his colleagues examined fifty-five badger carcasses from the surrounding area and found eleven suffering from bTB.Footnote ⁸⁹ News about these unpredictably infected animals almost immediately generated public calls for badger extermination.Footnote ⁹⁰ Ministers of agriculture appeared sympathetic to these calls. The parliamentary secretary commented, ‘Fond as I am of badgers, I am quite clear that we could not permit a situation to continue in which they were proved carriers of TB’.Footnote ⁹¹

However, other parties were less certain what the discovery of diseased badgers meant and what action should be taken. Members of the Nature Conservancy Council (NCC), the government body responsible for scientific advice on conservation issues, were concerned about a potential ‘widespread purge of badgers’.Footnote ⁹² Discussions of badger extermination had been ongoing since the late nineteenth century and generated conflicts around the role of the badger: was it sport animal, vermin or victim of human cruelty?Footnote ⁹³ Public campaigns for further badger protection had been gathering pace since the mid-1960s, and several attempts had already been made to pass private member's bills to effect this.Footnote ⁹⁴ Given the localized nature of the bTB problem and the small number of animals involved, NCC officers were also sceptical of the badger's posited role as disease transmitter, claiming, ‘The evidence for the badger as a source of infection is therefore somewhat flyblown. If anything, badgers are more likely to have been infected from the cattle in the first place’.Footnote ⁹⁵ Unlike government veterinarians, who employed epidemiological methods of tracing disease outbreaks through geographical association,Footnote ⁹⁶ the zoologists and ecologists of the NCC saw only the coincidental colocation of sick badgers and cows, which proved nothing about the ultimate source of infection.Footnote ⁹⁷

The evidence was also treated as tentative by MAFF's in-house experts on wildlife, albeit for more pragmatic reasons. Its Pest Control Division (PCD) and associated Pest Investigation Control Laboratory (PICL) were primarily concerned with the badger's potential role as a pest animal that damaged human crops and food supplies. Since at least 1946 PCD had received regular correspondence implicating badgers in digging up gardens, spoiling and raiding crops, destabilizing riverbanks and stealing poultry. Field officers and scientists had followed up these complaints and generally concluded that culprits were most likely other wildlife species, or sometimes aberrant old or sick individuals described as ‘old rogue badger[s]’.Footnote ⁹⁸ Yet the occasional need to remove badgers meant that scientists at the PICL had investigated ways of controlling them. As badgers were not a legally designated ‘vermin’ species, it was illegal to kill them with cyanide gas or powder, which was standard practice with burrowing pests such as rabbits and moles. PICL officers instead recommended capturing ‘rogue badgers’ with snare traps, or, if all else failed, using expert marksmen to shoot them.Footnote ⁹⁹ Occasionally a whole group caused problems, for example when human housing developments brought humans and badgers into uncomfortably close proximity. In such cases the entire sett could be excavated and destroyed. However, this was often ineffective, as badgers persisted in returning to a cleared area.Footnote ¹⁰⁰ PICL scientists therefore recommended first trying to drive the animals away using strong-smelling materials such as creosote.Footnote ¹⁰¹

The scientific uncertainty surrounding the badger's role as transmitter of bTB to cattle, combined with a keen awareness of the political implications of the news, led MAFF to commission further scientific investigations. These involved not only MAFF's veterinary and pest-control experts, but also ‘wildlife interests’ external to MAFF: scientists, amateur natural-history groups and badger protection campaigners. They were invited to head off public controversy, an approach which initially had some success.Footnote ¹⁰² These new interlocutors awarded very different roles to badgers than did MAFF officials – as a species to be conserved, as repositories of rural values, and as victims of human cruelty in need of protection. Drawing upon their expertise, PCD and veterinary officers began to survey the immediate area in which the sick badgers had been found. Constructing badgers as both disease victims and transmitters, they sought evidence of their infection with bTB through sampling and testing their faeces, and collecting and examining their dead bodies (which were increasingly presented by members of the public).Footnote ¹⁰³ Maps and data sheets recorded the locations of diseased and healthy badgers, badger setts and cattle herds with varying incidences of TB. They also incorporated features of the terrain and notes on the presence of other wild animals, which were also investigated as potential bTB transmitters.Footnote ¹⁰⁴

These field investigations were far from straightforward. Badgers were a poorly understood, nocturnal species that lived underground in inaccessible rural areas. Investigators therefore ‘had the arduous and painstaking task of finding as many setts as possible’ in a 150-square-kilometre area of Gloucestershire ‘which is well populated by badgers and where steep wooded hillsides make searching quite tiring’.Footnote ¹⁰⁵ Nevertheless, researchers continued to follow traces of badger bodies, bodily fluids, tracks and behaviour, and to document these traces using maps, photographs, post-mortem and microbiological reports, and numerical data. In so doing, their understanding of the problem changed: not only were other wildlife samples testing negative for TB, but increasing numbers of TB-positive badgers were identified. Officials had initially regarded the occurrence of bTB in badgers as a relatively isolated incident amenable to sett-by-sett solutions, but as the traces mounted, they identified a rapidly escalating disease outbreak affecting multiple parts of the country.Footnote ¹⁰⁶

These shifting understandings brought the problem of badger control to the fore and created another new role for the animals, as subjects of government legislation. In 1973, the government passed the Badgers Act. On the one hand the Act responded to the lobbying of naturalists and badger advocates granting the animals specific protections against killing or cruelty. At the same time, it introduced a framework for licensing ‘to kill or take’ the animals for research or conservation purposes, as well as ‘for purposes of preventing the spread of disease’.Footnote ¹⁰⁷ While farming and wildlife interests publicly welcomed the Act, it proved unable to achieve these very different purposes at the same time, as shown when badger campaigner Ruth Murray attempted to use it to prosecute a PCD officer and the minister of agriculture on grounds of animal cruelty after a MAFF demonstration of methods for killing badgers.Footnote ¹⁰⁸ This incident precipitated further legislative changes that strengthened the licensing framework and made it legal for MAFF officers to kill badgers with cyanide powder blown into setts, which was a standard pest-control method at the time. Early acknowledgements of the circumstantial nature of the evidence linking bTB transmission to badgers faded into the background, to be replaced by reports discussing the ‘important role’ played by badgers ‘in perpetuating the disease’, and public plans for ‘action to eliminate this reservoir of infection’.Footnote ¹⁰⁹ By late 1975 a formal badger-culling policy was in place, and the former, rather ad hoc collaborative investigations had been transformed into a formal MAFF research programme into ‘TB in cattle and badgers’, which continued until 1997.Footnote ¹¹⁰ All of these activities generated additional badger traces and made them visible to new sets of human actors, including veterinarians, policymakers, politicians and journalists, while generating further concern among farmers, scientists and campaigners.

Although legislative changes and the commencement of culling operations in 1975 reinforced the badger's role as a threatening vector of disease, MAFF's expanded research effort tacitly acknowledged that its role in propagating bTB was not yet settled. In the years that followed, the circumstantial nature of the evidence was one important source of scientific and policy controversy, but the multiple and contradictory roles assigned to badgers in the early 1970s and publicized via policy documents and in national and local media also drove ethical, political and emotional responses, which fuelled debates over tuberculous badgers that are still ongoing today.