The Bacteriological Divide: Pellagra in Italy and the United States (The Twentieth Century)

Abstract

At the beginning of the twentieth century, there was still no cure for pellagra. This chapter concludes our look at medical reactions to pellagra over the course of the long nineteenth century, with a study of two vastly different reactions to a new explanatory model of the disease in the period leading up to the First World War. In 1910, a doctor at London’s School of Tropical Medicine concluded that pellagra had a bacterial cause and nothing whatsoever to do with maize consumption. In Italy, this challenged the existing orthodoxy that pellagra was caused by a maize toxin. Meanwhile, in the United States, where the disease was fast becoming epidemic, the bacterial approach seemed to provide a ready solution. This chapter asks whether the bacterial theory effectively side-tracked research on pellagra and diet, in the interests of medical investigators, public officials and maize producers. And it explores what these theoretical shifts and the resulting controversies reveal about the very different medical and public health contexts in Italy and the United States. Paradoxically, and quite tragically, pellagra is an example of a disease for which there were more or less effective preventive measures available (and proposed, but not necessarily practised) long before there was a complete understanding of the disease and its cause.

On 19 December 1910, Bergamo’s main newspaper, L’Eco di Bergamo, reported on a brilliant new idea claiming to explain the causes of pellagra (Anon. 1910). The Bergamo province was one of the areas worst affected. The news thus merited one-and-a-half columns of the four-page newspaper. Signed by ‘un medico condotto’ (a district physician), the article was entitled ‘The Rehabilitation of Polenta’, for the theory asserted that maize and maize consumption had nothing whatsoever to do with pellagra. It meant that local people could eat polenta to their heart’s content and that farmers and producers could cultivate and trade maize unencumbered by the restrictive policies that Italy’s recent anti-pellagra laws had put in place. The new theory identified a small gnat as the culprit, complete with the Latin tag of Simulium, which spread a harmful protozoan from person to person. The originator of the theory, the article reported, was an English doctor named Louis Sambon, lecturer at London’s School of Tropical Medicine; most of the rest of the article was devoted to a Progress Report Sambon had written on the subject, translating its conclusions (Sambon 1910).

Although the newspaper article was signed by a ‘district physician’, there was actually no attempt to evaluate the new theory from a medical point of view. Protecting Bergamo’s pre-eminence as a milling centre, supplying five-eighths of Italy’s maize flour, was the author’s main concern. The medical reaction, when it came a few weeks later, was contemptuous. In a leading article in the Rivista pellagrologica italiana, one of that journal’s co-editors, Giuseppe Antonini, praised L’Eco di Bergamo for bringing Sambon’s theory to the attention of Italians (Antonini 1911). Antonini quoted extensively from the article’s translation of the Progress Report, even as he proceeded to rubbish its conclusions, point by point. Antonini objected most of all to Sambon’s confident assertion that Cesare Lombroso’s spoilt maize theory was wrong, that all the recent measures taken as a result were useless, and that even if every grain of spoiled maize were to disappear from Italy, pellagra would continue to exist as before. ‘I confess, I thought I was dreaming’, was Antonini’s reaction. He went on to point out how the numbers of pellagra sufferers in Italy had declined steadily since 1902, so that in the period 1906–1908 the number of pellagrins was half of what it had been in 1900–1902.

Across the Atlantic Ocean, in the United States, the medical reaction to Sambon could not have been more different. As a professor of medicine in Atlanta, Georgia put it: ‘With the publication of Sambon’s “Progress Report” in 1910, the investigation of pellagra really began. Before that time, men studied a cereal [i.e., maize], and thought they were studying a disease’ (Roberts 1914, p. 291). In a full-page article in the New York Times Sunday magazine section, which announced a privately endowed study of pellagra in the U.S. South, Sambon was credited with having ‘proved almost indubitably that pellagra is an insect-borne disease, and that probably corn or maize does not enter into the problem at all’ (Anon. 1911). The article hailed Sambon’s Progress Report as ‘probably the most important contribution to the literature of pellagra’, and it ended, like the earlier one in L’Eco di Bergamo, by quoting its conclusions verbatim, granting Sambon the final word on the matter.

For all this, and as the historian of nutrition Kenneth Carpenter noted several decades ago in an edited collection of readings dedicated to pellagra, ‘time has not been kind to Sambon’. His ideas, so ‘eloquently expressed’, ‘have proved quite baseless’ (Carpenter 1981, p. 5). There are, however, several reasons why I think studying how yet another ‘wrong’ theory of pellagra (Sambon’s) clashed with another equally wrong theory (Lombroso’s), before what proved to be the ‘right’ theory emerged, can be both revealing and historically important. The first of these concerns the history of work on deficiency diseases. Pellagra would eventually be classified as a deficiency disease, but only after medical investigators were finally forced out of the bacteriological rut into which they had dug themselves. As a theory of disease, the germ concept was ‘vastly more successful than any previous medical concept’; however, its very dominance in medical thought ‘proved a major barrier to the recognition and study of deficiency diseases’ (Ihde and Becker 1971, p. 16). Did bacterial theory effectively side-track research on pellagra and diet for many years, in the interests of medical investigators, public officials and maize producers? The same claim has been made for the investigation of beriberi, that the deficiency concept would have been more readily accepted had there been no bacterial theory (Carpenter 2000; Bay 2012).

The philosopher of science K. Codell Carter has dismissed this contra-factual claim, by stressing ‘the variety of causes contemporary researchers were willing to entertain’ (Codell Carter 2003, pp. 179–180, 193–194). Indeed, the deficiency concept and the bacterial theory belonged to the same scientific research programme, with its general focus on aetiology and the search for causes. This unity is certainly evident when we survey the range of work then being done at an international level, across the different diseases, as Carter does. But when we shift our gaze to the controversies and power structures as they played out at a strictly national level, the picture seems far more divided and confrontational. Sambon’s intervention into the world of Italian pellagrology brought the question of pellagra’s aetiology back on to the table, in a way it had not been for twenty-five years. It is no accident that this decade (1900–1910) saw more pellagra studies published in Italy than any other (Bertolotti 2009). Established interests were challenged—not just in the production of medical knowledge, but in the more materially lucrative production of maize itself—in ways that paralleled the understanding of the role of husked rice in the aetiology of beriberi in Japan.

The second important feature of the reaction to Sambon is the way it can be used to shed light on an emerging international divide. If, as we shall see, the Italian reaction to Sambon’s provocations says much about the continuing dominance of the Lombrosian theory there, its enthusiastic reception in the United States is suggestive of the very different medical context there. It is worth remembering that at the beginning of the twentieth century, there was still no cure for pellagra, and there was still much about it that eluded understanding, regardless of the theory: its seasonal appearance and spontaneous remission, the terrible bouts of insanity it could cause and its varied manifestations, and why it seemed predominantly to affect the poor.

Paradoxically, and quite tragically, pellagra is an example of a disease for which there were more or less effective preventive measures available—and proposed, though not necessarily enacted—long before there was a complete understanding of the disease and a cause pinpointed (from 1924 to 1937, in the United States). From the time of the earliest Italian explorations of pellagra in the mid-eighteenth century, when disease categories were still symptomatic (i.e. based on evident symptoms), through to the rise of aetiology as an explanatory concept in the late nineteenth century and attempts to identify specific causal agents, most theories about pellagra’s causation were at best partial and at worst wrong. What is at issue in this chapter is what these shifts and the resulting controversies reveal about the medical context. The actor-centred approach we adopt here, with reaction to Sambon’s intervention as a kind of test-case, is the key to understanding these controversies and why they mattered.

The Toxicozeist Hegemony

As one of Italy’s leading pellagrologists, Antonini did not take kindly to Sambon’s claim that the spoilt maize theory was ‘the official one, accepted by statisticians who have never seen a pellagra case, laboratory investigators who have studied only damaged maize, and doctors in insane asylums and pathologists who have never visited the places where pellagra is rampant’. And, indeed, Sambon would be one of the few contributors to the pellagra debates who had no asylum experience—an experience we explore in Part II. In any case, Antonini rebutted Sambon’s criticism with reference to Lombroso’s own lifelong efforts to study and eradicate pellagra, before turning to the efforts of local doctors. Antonini argued that no one was better placed to diagnose pellagra than the doctor ‘who has lived in the place where pellagra has been endemic for centuries, who has, because of his profession, to follow the sufferer in all his phases and who knows his family background’. Antonini asked rhetorically what measures had been taken against the Simulium in recent years to account for pellagra’s decline. Sambon may have been justly famous for his work on malaria and sleeping sickness, Antonini admitted; but his view of pellagra had been shaped too much by his work in tropical climes (Antonini 1911).

As we observed in chapter three, by the end of the nineteenth century the ‘Lombrosian hypothesis’ had come to dominate Italian medicine, exercising control over the provincial and national pellagrological conferences and the discipline’s journal, the Rivista pellagrologica italiana. The theory proved to be flexible enough to adapt itself to the latest science, attracting followers from different specialisms, and so survive till the early 1920s in Italy. The spoilt maize or toxicozeist theory came to dominate medical discussions. It was firmly within the still evolving microbiological paradigm, more interested in examining the properties of invading agents under the microscope than actual patients. This was even truer of Lombroso’s followers and successors, who focused on the search for the micro-organism responsible.

The steady decline in the numbers of Italian pellagrins in the years following the enacting of the 1902 law appeared to vindicate the Lombrosian theory. And, with hindsight, there is no doubt that some aspects of the law—especially in the treatment of sufferers and those at risk—had a positive impact. This apparent success bolstered the hegemonic position occupied by toxicozeists in Italy. From 1902 issue after issue of the Rivista pellagrologica italiana charted the successful effects of the law based on the doctrine. There was a regular column devoted to its application, reporting province by province on different initiatives in the implementation of the law, as well as regular articles devoted to studies of the chemical composition of spoilt maize. The journal contained occasional expressions of doubt: that not enough was being done to improve peasants’ living conditions, to track down house-bound pellagrins unknown to the district physicians, to check on the activity of millers or to ensure the sale of spoilt maize was actually prosecuted. However, these were the exceptions to the rule. No voices were raised against the law—not least from the journal’s co-founder and co-editor, Antonini. Antonini (1864–1938) had been a pupil of Lombroso’s and resolutely towed the line of the man he called ‘the great master’, ‘the true father of modern pellagrology’ (Antonini 1902, 1912) throughout this period—and continued to do so well into the 1920s, long after most other Italian pellagrologists had abandoned it.

That said, this is no story of scientific ‘baddies’ versus ‘goodies’. There is no doubting the commitment of someone like Antonini, who worked at the coal-face (as it were) and campaigned tirelessly against pellagra. Director of Pavia’s provincial insane asylum at Voghera, and from 1911 director of the insane asylum at Mombello, outside Milan, where he would have encountered patients driven insane by the disease, Antonini was active in the provincial and national pellagrological conferences and the author of numerous books and pamphlets offering advice on how to understand and combat it.

Antonini must have wondered at the fuss over aetiology that Sambon’s investigations had kicked up, given recent Italian ‘successes’ in pellagra prevention. He must have considered pellagra to be ‘understood’ as a disease—in the way scurvy was ‘understood’ long before the reason why lemons successfully cured it was explained. As Antonini told the delegates at the fifth Pellagrological Congress, meeting in Bergamo in 1912, new ‘doctrines’ like Sambon’s ‘advance threateningly to show the work of the toxicozeists to be, as it were, absurd, and the struggles, sustained victoriously through so many years, to be superfluous’. The risk was that these theories would ‘undermine the foundations of the ancient edifice without presenting reliable elements for the construction of new ones’ (Antonini and Gosio 1912, pp. 180–187). Antonini countered each of the new theories in turn, which if taken together cancelled one another out. From the organisation of his defence down to the very language used, Antonini’s stance was the standard one in scientific controversies. He stressed the uncertainties inherent in the opposing theories, exaggerating their weaknesses and inconsistencies, in order to counter his rivals and ensure the continued predominance of the toxicozeist project.

But was Antonini consciously engaged in producing scientific uncertainty? There are striking parallels with Japanese debates over the aetiology of beriberi and rice consumption, taking place at the same time. In Japan, the dominant bacteriological theory was being challenged by the deficiency theory, and meeting with the same sort of establishment opposition as in Italy (Bay 2012, pp. 106–110). But I think it would be inaccurate to speak of ‘the construction of ignorance’ in Antonini’s response to opponents of the Lombrosian theory in Italy, as Alexander Bay does for the response of Tokyo doctors to the deficiency theory. The reference here is to the tobacco industry’s deliberate and longstanding policy of scientific misinformation regarding the links of cigarette smoking to cancer (Proctor 2008). Antonini was not an ally of maize-producing interests in Italy; indeed the 1902 anti-pellagra law had put curbs on the production and sale of maize. But he did strive to protect his own professional interests and status, marginalising those who questioned the established orthodoxy.

Louis Sambon and His Theory

If the leading Italian toxicozeists were a self-confident lot in 1910, so too was Louis Westenra Sambon. Sambon (1867–1931) had grown up in Italy, mostly in Milan, the son of a Franco-Italian antiquarian father and an English mother. In 1884, he matriculated at the University of Naples, the same year a cholera epidemic struck the city, and the young medical student was called upon to provide assistance. The experience may have sparked Sambon’s interest in epidemiology. In any case, he contributed to the ‘white men in the Tropics’ debate, writing two articles for the British Medical Journal on the acclimatisation of Europeans (Sambon 1897, 1898). His approach mixed geographical analysis and epidemiology and the nascent fields of microbiology and parasitology: an approach that we shall see again in his study of pellagra.

This work brought him to the attention of Patrick Manson, one of the key players in an expanding field grounded in microbiology and parasitology, that of tropical medicine, and who had just founded the School of Tropical Medicine in that same year (1899), in London. By early 1900, Sambon was hired as an occasional lecturer in the London School, lecturing on epidemiology and parasitology. In autumn of 1900, Manson sent Sambon, together with George Low, lecturer at the School, to the Roman Campagna. In the ongoing search for the means of transmission of malaria, Low had just outlined the life cycle of a vector-borne nematode infection. Malaria and its transmission was then medical science’s most engrossing problem. Ronald Ross, working in India, had written about the mosquito transmission of avian malaria, although clear proof of transmission in humans had not yet been found. The ‘Rome school’ of Giovanni Battista Grassi and Angelo Celli were working on similar lines.

Sambon straddled two worlds. For British researchers, malaria was ‘over there’: a colonial problem, a tropical disease. For Italian investigators, it was a disease long endemic to their own country, a tragic reality encountered only seven kilometres from the gates of Rome (Snowden 2006). Sambon evidently cast his lot in with the British, writing exclusively in English and taking part in a British-sponsored expedition. In 1902, two years after intermediating amicably between British and Italian colleagues, Sambon sided with Ross in the priority dispute against the Italian zoologist Grassi and the ‘Rome school’ over the discovery of the role of mosquitoes in the transmission of malaria. Amidst claim and counter-claim, personal ambition and national pride, the Grassi-Ross dispute intensified when Ross was awarded the Nobel prize that same year, 1902 (Capanna 2006). In any case, the discovery of a vector, combined with a national campaign in Italy against mosquito infestation and the free distribution of quinine—a truly effective medicine—helped to reduce malaria deaths in Italy. By 1915, the number of deaths had declined from 600 per million inhabitants to less than 50. It was one of the great success stories of pre-World War I Italian medicine (Snowden 2006). The movement to eradicate both malaria and pellagra would follow similar trajectories, with major learned associations, journals, public health campaigns and national laws launched within a few years of one another at the turn of the century. Pellagra, as we have seen, also declined; but here the role of medicine and public health would be quite different.

As an epidemiologist, Sambon managed to position himself as being just ahead of the other sciences, paving the way for them, as it were. Sambon’s first foray into pellagra came in 1905, hot on the heels of his studies of sleeping sickness and malaria. At the 73rd meeting of the British Medical Association, held in Leicester that year, Sambon voiced his hypothesis on the aetiology and spread of pellagra, using a detailed survey of pellagra’s spread to identify a possible vector or agent. Sambon’s ‘Remarks’ on pellagra came in the section devoted to Tropical medicine and were intended to stamp his name on this theory before anyone else got to it, using his now standard methodology (Sambon 1905). The style is that of an essay: laying out the problem historically and geographically, discussing the dominant ‘zeist’ (maize-related) aetiological theories, then demolishing them in turn, before concluding with what appears to be the only logical solution to the problem—a solution which although glaringly obvious had not occurred to anyone else before. Maize might come into it, but only indirectly, Sambon remarked: ‘Probably, therefore, it is in the maize field that the peasant comes in touch with the specific agent of pellagra, and possibly through the agency of some biting fly’ (Sambon 1905, p. 1275). Sambon seems to toss this suggestion out casually, but this is in fact what he has been leading up to. His conclusion is circumspect and understated, whilst at the same time self-serving. There is no doubt that for Sambon, the ‘Remarks’ marked the start of a project.

Sambon had already gained himself a reputation as an ‘ideas man’. The London School set up a Pellagra Investigation Committee with the aim of raising funds to pay for Sambon’s travel to Italy to study pellagra’s topographical distribution and epidemiology. Sambon could also count on the support of the successful medical entrepreneur and collector Henry Wellcome, who ended up footing most of the bill. Sambon’s proposed visit to Italy was intended to determine whether a small blood-feeding sand-fly (Simulium reptans) was the carrier of pellagra and whether pellagra could be defined as belonging to the group of protozoal diseases.

Sambon’s twelve-week fact-finding trip in the spring and summer of 1910 took him throughout the areas of Italy worst affected, from Bergamo in the north to Perugia in the centre. The resulting Progress Report resembles Sambon’s 1905 ‘Remarks’, albeit on a much grander, and more detailed, scale (Fig. 4.1). Sambon was able to present the work of Lombroso as the ‘old science’ against which he would have to wage his battle. If the label of ‘Lombrosian theory’ was suitable, Sambon argued, it was ‘not that Lombroso suggested the theory, but because he and his school imposed it with a dogmatism and intolerance inconsistent with the spirit of modern science’ (Sambon 1910, p. 290). Pride of place is given to a further issue: the precise geographical spread of pellagra. In Sambon’s mind, this made pellagra similar to malaria, sleeping sickness ‘and other diseases known to be transmitted by mosquito-, fly- or tick-carriers, presenting well-defined habitats’. According to Sambon, it explained: (i) the unchanging boundaries of pellagra’s ‘endemic centres’; (ii) the predominance of farm labourers—and their infants and children—as sufferers, most exposed to the infective agent; (iii) the exemption of towns, since sand-flies had a very limited range; (iv) the increase of cases following flooding; (v) the seasonal eruption of the disease—spring and autumn, when sand-flies were active; and (vi) the areas of the skin particularly affected. In Sambon’s confident words, ‘there is not a single fact which the Simulium theory does not satisfactorily cover’. If the protozoan responsible for the disease had not yet been identified, the role of the Simulium in the transmission of pellagra was ‘almost a certainty’ (Sambon 1910, pp. 271, 321).

Fig. 4.1

Louis Sambon and pellagrous child. From: Edward Jenner Wood, A Treatise on Pellagra for the General Practitioner, 1912

The Italian Reaction

Proud of his findings, Sambon approached the Italian press, including newspapers like L’Eco di Bergamo. The result, according to M. V. Carletti, lecturer in medical pathology at the University of Padua, was that it ‘stirred up lively comments and impassioned discussions in the newspapers and amongst Italian doctors’ (Carletti 1911, p. 5). However, objected local doctors like Cesare Ceresoli from Brescia, Sambon’s press barrage gave the wrong idea to ‘local farmers, administrators, industrialists, and merchants’, who were all hoping for the abolition of the 1902 laws regulating ‘the cultivation, consumption and trade in maize’ (Ceresoli 1911). We have already heard from Antonini, enforcer of the ‘official’ dogma, and many Italian doctors must have shared his reaction, if Carletti’s dismay is anything to go by. At the same time, the fact that so much about pellagra was still up in the air may not necessarily have bothered contemporaries. After all, the German doctor and microbiologist Robert Koch had discovered the tuberculosis bacillus back in 1882 and it was widely accepted as the cause, even if there was still no cure for the terrible scourge—and would not be until the discovery of streptomycin in 1944. We know that other Italian pellagrologists, without necessarily agreeing with Sambon, welcomed his ideas as a breath of fresh air (Pisenti 1912).

That said, Sambon’s theory was a provocation the Italian State could not ignore. In November 1910 the Italian parliament set up the Ministerial commission for the study of pellagra, charged with examining the different aetiological theories then being proposed and how they affected the 1902 law. Commission members, which included Antonini, were asked to undertake a detailed examination of Sambon’s theory and report back. From areas as diverse as Friuli in the far northeast and Umbria in central Italy, the reports came back finding no link between insect bites and pellagra. The Commission concluded that ‘[i]t was clear that in the present state of knowledge the strict enforcement of the current pellagra laws must continue’ (Commissione 1912, p. 162).

This declaration set the tone for the fifth Italian Pellagrological Congress, held in Bergamo in September 1912. Announcing the conference programme, the editors of the Rivista pellagrologica italiana were certain that the discussion of the new aetiological theories would be of ‘very notable importance’. Yet they remained in no doubt that the meeting would have ‘the merit of removing any doubts raised against the Lombrosian theories, which, even for those not expert in pellagrology, have had hitherto the support and justification of practice’ (Anon. 1912). And that is exactly what happened. None of the papers which mentioned Sambon’s theory found any support for it. Even a survey of Italian medici condotti (district physicians)—the very people Sambon had so warmly praised for their openness to his ideas and condemnation of the zeist position—found none who favoured the sand-fly as a cause (Camurri 1912). The 1912 meeting was a monument to Lombroso—almost literally so, since this was the first meeting held after Lombroso’s death (on 19 October 1909) and which announced the imminent completion of a stone monument to him in his native Verona.

Pellagra and the Reaction to Sambon in the United States

If pellagra numbers were dwindling fast in Italy by this time, pellagra seemed to appear from nothing in the United States in the early 1900s. So fast indeed that it was assumed it had to be an infectious disease, for what else could explain its sudden appearance and quick spread (Etheridge 1972; Bollet 1992; Leslie 2002; Marks 2003)? Because pellagra was new to the United States, there was little of the maize-based cultural baggage which weighed so heavily in Italy. Pellagra struck there at a time when a whole range of diseases—anthrax, tuberculosis, diphtheria, typhoid, tetanus, bubonic plague, syphilis—had recently been found to be caused by micro-organisms, so that it seemed self-evident that all epidemic disease would be found to have a microbial cause. If long experience with pellagra had taught the local, family doctor in Italy that maize and poor diets had to be linked in some way, the average US practitioner thought of pellagra as a disease one ‘caught’. The appearance of pellagra in the United States also coincided with the rise of tropical medicine as a discipline. Successes in the field were palpable. For instance, within the space of a few years, by targeting mosquito populations, informed by the latest theories developed by the likes of Koch, Grassi and Ross, the US authorities had managed to make the Panama Canal area relatively safe for human populations. The influence of the ‘infectious paradigm’ thus conditioned early US medical responses to pellagra (Leslie 2002).

The disease was not recognised at first. ‘The authors of English and American textbooks … have told us, if they told us anything at all about it, that pellagra is an Italian disease that does not occur in our country’, the South Carolina doctor James Babcock, superintendent of the State Hospital for the Insane, put it (Babcock 1910, pp. 10–11). As in Italy, American directors of insane asylums witnessed first-hand the worst effects of the disease (Bryan 2014). In 1908, a concerned Babcock travelled to Italy to study pellagra, visiting several pellagra hospitals, the better to diagnose and treat the increasing number of cases back home. Later in the year, the South Carolina State Board of Health held a public conference on the subject, which became something of a scare story in the local press.

In 1909, partly because of his acquired expertise, Babcock was elected president of the newly founded National Association for the Study of Pellagra. In 1910, Babcock and the epidemiologist Claude Lavinder translated a version of Lombroso’s monumental Trattato profilattico e clinico della pellagra (1892), from the heavily abridged French translation by Armand Marie in 1908, to which the two men provided extensive additions and revisions ‘to include the latest opinions regarding the possible parasitic origin of pellagra’ (Marie 1910, pp. 3–4). But Babcock’s warnings about pellagra’s spread in South Carolina and elsewhere; his focus on the relationship between poverty, diet and pellagra; and the threat to the maize business posed by the threat of a maize toxin, made him extremely unpopular. As in northern Italy, vested interests were at stake. The Chicago Post worried that if millers (in the mid-West) or their customers (in the American South) ever ‘get it into their heads that Illinois corn is the cause of pellagra, we shall feel the economic effect of it in this state, worldwide though our markets be’. And when Sambon fortuitously came along, The American Agriculturalist was relieved to relate the news that pellagra might be insect-borne (Etheridge 1972, pp. 21, 26).

With threats to the maize business acting as a push factor and Sambon’s theory as a pull factor, the State of Illinois set up a commission to study pellagra in 1910. The Illinois Commission’s report, issued the following year, adopted Sambon as a constant point of reference. The latest word in pellagrology offered a scientific foundation for discussions of the transmission of pellagra by US doctors, even if evidence in its support was wanting. Maize was let off the hook. It identified Sambon’s own theory as ‘attractive and plausible in many respects’ and it was at one with Sambon in his battle against ‘the maize hypothesis’, arguments in favour of which were deemed ‘extremely slender’ (Singer 1912, pp. 8, 247).

Not everyone was in agreement. Lavinder, now chief investigator for the newly founded US Public Health Service, although impressed by Sambon’s hypothesis, nevertheless followed the investigations originated by Italian toxicozeists. Lavinder took over from Babcock as president of the National Association for the Study of Pellagra in 1912—a year in which South Carolina reported 30,000 cases of the disease and a mortality rate of 40%. Despite this, Sambon’s name crops up in almost every paper presented at the second meeting of the National Association for the Study of Pellagra, which was held in Columbia, South Carolina, in October of 1912. Entomologists, like Kansas’s S. J. Hunter, were in hot pursuit of the sand-fly in their own States (Hunter 1914). Sambon effectively divided opinion, even amongst the undecided (Sandwith 1914). The variety of viewpoints expressed at the Columbia conference is in contrast to the more limited range of opinions voiced at the Italian Pellagrological Congress held in Bergamo the same year.

Meanwhile, the Thompson-McFadden Commission continued its investigations into the source of what it believed to be the pellagra ‘infection’ during the summer of 1913, visiting the home of every mill worker in Spartanburg County, South Carolina. Pellagra had already been pinpointed as a disease of small milling communities. (This was in stark contrast to Italy, where pellagra was most prevalent amongst landless farm labourers.) The highlight of the Commission’s work that summer was Sambon’s visit, the excuse for a special conference in his honour. This was reported in an article in the New York Times bearing the simple headline ‘Prof. Louis Sambon here’. It described Sambon (mistakenly) as the head of the Tropical School of Medicine in London and a recognised authority on pellagra, and related his efforts at ‘exploding’ the maize-based theory (Anon. 1913). The newspaper also reported on Sambon’s triumphal return to New York following the conference, where ‘it was agreed that pellagra was an infectious disease, the germ carried by an insect’. A general interest newsmagazine, The Literary Digest, looked to Sambon and his insect theory to solve a disease now plaguing the United States. It blamed pellagra on the ‘hordes of Italian immigrants who have arrived in the last 30 or 40 years’, bringing their infection with them (Leslie 2002, p. 194)—evidently unaware of Sambon’s own origins.

Notwithstanding Sambon’s inspirational visit and the adulatory media accounts, the Commission actually ruled out the Simulium—locally, the buffalo gnat—as a carrier of pellagra. It agreed with Sambon that maize was probably not a factor but concluded that the real culprit seemed to be poor sanitary conditions and waste disposal, resulting in intestinal infection (Siler et al. 1914). Although Sambon was not aware of it, his gnat-based notoriety had already peaked.

Pellagra as Deficiency Disease

We saw in the previous chapter how as early as 1856, the physiologist Lussana had theorised that a diet poor in ‘albuminoid foods’, or protein, was the cause of endemic pellagra (Lussana and Frua 1856). Although the deficiency theory had substantial support amongst Italian district physicians, the Lombrosian hegemony meant that it was marginalised by pellagrologists for the best part of fifty years—that is, until investigators began to explore what specific nutritional deficiency resulted from a maize diet.

In 1911, a student of Lussana’s, Aristide Stefani, wrote of certain ‘imponderables’ necessary to health but which the body could not manufacture by itself and needed to take on whole. Stefani argued that whilst maize was probably adequate in ‘proteic’ terms, this did not mean it could be considered a complete foodstuff, containing all the dietary ‘principles’ necessary to man, in the way of mother’s milk or wheat (Stefani 1911). That said, his ideas do not appear to have circulated widely. The following year, in June 1912, the Polish biochemist Kasimierz (Casimir) Funk, working in the United States, published his findings on the disease beriberi, linked to a diet of husked rice. This was a process that, Funk suggested, removed a vital substance from the rice which he called a ‘vitamine’ (from ‘vital amine’). He went on to relate beriberi to scurvy and pellagra, calling them all ‘deficiency diseases’ (Funk 1912). If the exact nature of the maize deficiency remained unclear and Funk’s real contribution to an understanding of the aetiology of beriberi, pellagra and scurvy were relatively limited, his coining of the term ‘vitamine’ drew attention to the new and important field of nutritional research.

In the United States, this attention was immediate. The 1912 Columbia conference saw first reference to this new hypothesis in terms of pellagra. Rupert Blue, Surgeon General to the Health Service, identified Funk’s theory as one promising ‘important developments in the future’ (Blue 1914). And F. M. Sandwith—paradoxically, Sambon’s colleague at the London School—asked the question: ‘Is pellagra, too, a deficiency disease, waiting for a “vitamine” to be discovered?’ And he pointed to the benefits of adding tryptophan to a maize-based diet in laboratory mice, a precursor to some ‘substance essential to the processes of the body’ (Sandwith 1914, p. 99).

Sandwith did not know how right he was. Two years later Funk’s hypothesis began to receive serious attention in the United States with the investigations of Joseph Goldberger (1874–1929), a Hungarian-born doctor and epidemiologist in the US Public Health Service. Goldberger’s were the investigations that now seemed to have ‘science’ on their side. In an early paper, Goldberger made an obligatory reference to Sambon, but his sympathies already tended towards diet as a chief factor (Goldberger 1914). There was an urgency and practicality about Goldberger’s work in the United States, with over 100,000 pellagra cases a year during the agricultural depression of the 1920s. Goldberger’s tireless work would eventually pave the way to our modern understanding of pellagra (Etheridge 1972; Kraut 2003). Seventy years after Lussana’s original hypothesis, all of the pieces of the puzzle finally fell into place. The rapid application of the vitamin deficiency model to pellagra, and its general acceptance, ‘suggest that what had been missing until then was the conceptual framework for interpreting otherwise well-established observations’ (Scrob 2018, p. 68).

The medical reaction in Italy could not have differed more. Funk was not even referred to at the 1912 Bergamo congress. The Rivista pellagrologica italiana finally allowed space for the Funk hypothesis in 1914, albeit reluctantly, a breach that with hindsight marked the beginning of the end of the Lombrosian hegemony in Italy (Volpino 1914). By this time, pellagra was clearly on the wane in Italy, making the aetiological question less pressing for Italian medical investigators—or at least less relevant as a scientific issue (Fig. 4.2). As the pellagrologist and historian Luigi Messedaglia summed it up in 1927: ‘The peasant eats better; and pellagra declines’ (Messedaglia 2008, p. 252). World War I, far from increasing pellagra rates, had assisted in its decline, as the Italian government imported massive amounts of wheat and sold it at subsidised prices. By the 1920s, pellagra had all but disappeared.

Fig. 4.2

Table of reported pellagra deaths in Italy, 1887–1930 (Source for data Finzi 1982, p. 412)

Despite this, the Lombrosians hung on to their hegemony till the end. As late as 1921, the disciple Luigi Devoto admitted that the theory might need to be ‘amended’, as he put it (Devoto 1921). But what, then, remained of Lombroso’s original theory to amend? The following year, at the sixth—and, as it turned out, last—Italian Pellagrological Congress, the toxicozeist theory came in for serious criticism, to the dismay of its proponents. In 1924, the Rivista pellagrologica italiana, a Lombrosian stronghold since its inception in 1901, ceased publication, surplus to requirements.

Conclusion

It will be evident by now that medical investigations into the causes of pellagra was an ongoing process at the start of the twentieth century, with as much competition as cooperation, where new knowledge claims did battle with established interests. Did the ‘infectious paradigm’ delay the defeat of pellagra, as has been argued, by getting in the way of the deficiency concept of disease (Leslie 2002)? Or is it more useful to regard all of the investigations as part of the same research programme, united as they were in a quest for causes (Carter 2003, pp. 191–195)?

It is, clearly, a bit of both. On the one hand, there is no doubt that, in Italy, the protection of legitimacy and reputation led to the production of scientific doubt as well as scientific knowledge, similar to what has been suggested for beriberi in Japan (Bay 2012). Neither Sambon nor Antonini had any time for the notion that pellagra might be due to a dietary deficiency. Sambon’s brief foray into Italian pellagrology demonstrated just how entrenched the Lombrosian hegemony was. Sambon may have forced Italian pellagrologists to question their most firmly held and cherished beliefs, but the toxicozeists were strong enough to marginalise not only Sambon but all other alternative aetiologies at the highest levels of medicine and government virtually to the end. On the other hand, in the United States, when it came to investigations into pellagra’s aetiology, there was no prevailing legitimacy to protect. The influence of the infectious paradigm contributed to Sambon’s short-lived notoriety there.

That said, a look at the conferences on pellagra shows just how much open-ended debate and argument was going on throughout this period. This is much more redolent of Carter’s ‘single coherent research programme’—one that would pave the way for Goldberger’s successful investigations into pellagra. Evidence for this view can be found in Italy, too, where research in other areas did go on, sometimes behind the scenes, sometimes quite openly. We have seen how district physicians were less swayed by the Lombrosian hegemony, remaining divided, or undecided, or even combining opposing theories into an original, practical synthesis. Moreover, and despite their mutual antipathy, Sambon and toxicozeists like Antonini had in common a belief that the cause of pellagra was bacterial. What they differed on was the means of transmission, whether the micro-organism was conveyed via an insect or through spoiled maize consumption.

Sambon and Antonini shared something else, too: their concern with a bacterial explanation effectively left society off the hook. There was no need to reform the underlying social conditions that had led to a reliance on maize if the cause was bacterial. In Italy, the gradual disappearance of pellagra took the sting out of the dispute, and may also explain why Italian investigators were not in the forefront of research after World War I, whereas in the United States the worsening of the epidemic made the hunt for a cause all the more pressing throughout the 1920s.