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Eight and Poverty

In the nineteenth century more people in the Western world died of tuberculosis than of any other epidemic disease. The "White Plague" generated enormous fears, for good reason. Yet for all its importance, and all the attention lavished on it, tuberculosis presented a tangled picture to nineteenth- century thinkers, who could not agree on its causes. Of great antiquity, tuberculosis appeared in different symptomatic guises, inspiring a great variety of etiological theories and an even greater variety of therapies, while different social and political beliefs became associated with those theories and treatments.

Twentieth-century microbiologists may have a firmer grip on the causes of tuberculosis, which (we now believe) has a number of manifestations and may be caused by two different organisms: Mycobacterium tuberculosis or Mycobacterium bovis. The first of these (although it may infect other animals as well as humans) passes from person to person, most often via the respiratory system. The second infects most domestic animals and reaches humans when they consume the products of such diseased creatures. The bacteria lodge in many possible places in the human frame. Mycobacterium bovis often finds its way into glands and joints, and one group of symptoms that results is called scrofula, the medieval "King's Evil" (see Chapter Two). Although Mycobacterium tuberculosis may also infect different parts of the body, when it settles into the lungs it may produce pulmonary tuberculosis, known earlier as "consumption" or "phthisis." Many people infected with M. tuberculosis do not develop "consumption" at all, however, and many others only show consumptive symptoms after a long period of infection. A large number of others do develop such symptoms, and it was that pulmonary form of the disease"consumption'' or "phthisis"which attracted particular nineteenth- century attention. But for all that apparent simplicity and certainty, the history of

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tuberculosis remains unusually complex even in the context of past epidemics. The rhythm of its past severity has not yet been convincingly explained, so that even with a surer grasp of its "cause," we cannot be certain why it savaged the early nineteenth century and abated in the late nineteenth and early twentieth.

Early History

Tuberculosis in humans has an ancient history, revealed by paleopathology. The Hippocratic writings of the ancient Greeks discuss consumption at length. Some evidencescanty to be suresuggests that its ancient and medieval incidence varied more or less directly with population density. Thus classical Roman civilization, relatively urban, may have suffered high rates of tuberculosis, while the medieval West, rural and thinly settled especially in its early centuries, offered fewer opportunities for contagious respiratory infections. The resurgence of tuberculosis in the West, accompanying the urban growth of the twelfth and thirteenth centuries, may have affected the incidence of that other great mycobacterial killer, leprosy (see Chapter Two). Certainly by the early modern period of European history tuberculosis had resumed a place among the major epidemics, and in that period (coinciding with the scientific revolution) a diverse collection of explanations of phthisis arose.

Those explanations rested, first of all, on an understanding of the sensible symptoms of the disease: shortness of breath, coughing, blood-flecked phlegm, progressive weakness and debility, and loss of skin color, all of which only became characteristic of the disease in its later stages. The persistence of such complaints in the same family encouraged notions about the hereditary character of consumption, notions that had found expression as early as Hippocrates and that the chronic nature of the disease perhaps strengthened. The prolonged presence of a victim of a chronic disease may burn images into the memories of onlookers, and these may be recalled when others in the same family recapitulate the symptoms. But not all early modern theorists accepted the hereditarian explanation. Others, attracted to the general notion of contagion that gained credence in the sixteenth and seventeenth centuries (see Chapter Three), applied that to consumption as well as to plague. The consumptive, like the leprous the victim of a chronic complaint, posed a long-standing threat by her simple existence; that sense of danger, perhaps intuitively felt by neighbors, was given theoretical justification by the doctrine of contagion. Both these hypothesesheredity and contagionremained popular into and through the nineteenth century and affected responses to the tubercular.

With the improvement of anatomical knowledge between 1500 and 1700 came an awareness of consumption's pathological signs, especially the lesions or "tubercles" formed in the lungs. That knowledge led to other etiological ideas, especially those that saw such lesions as the product of some form of irritation, perhaps

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caused by physical agents such as improper food or ingested matter, perhaps the product of muscular (or even nervous) exhaustion. Such beliefs led in turn to therapeutic suggestions: change diet, change environment, rest, avoid stress. Whether tubercular lesions represented one disease or a panoply of them formed part of the larger pattern of nosological uncertainty discussed in Chapter Six.

Tuberculosis and

These general etiological viewsheredity, contagion, and irritation of tissue whether physical or psychologicalinformed Western responses to tuberculosis in the age of "romanticism," when the disease seemed to threaten the well-born and the gifted. Between the late eighteenth century and the mid-nineteenth, a variety of cultural circumstances led literate observers to associate pulmonary tuberculosis with the upper and middle reaches of society, and the disease acquired an air of fashion. In reality, of course, most of its victims belonged to the lower orders, but its associations with misery and poverty only became more widely acknowledged later in the nineteenth century.

Romanticism remains an elusive historical construct, but I will assume here that it may represent a net of cultural practices and beliefs that had particular importance between the late eighteenth and mid- nineteenth centuries. Those practices and beliefs included an emphasis on emotions, mystery, and spontaneity as opposed to the Enlightenment's practice of reason, an interest in the remote (whether in time or space), and a glorification of the beauties of nature; politically, "romantics" could be either radically revolutionary (glorying in bold breaks with tradition and in the virtues of the common man) or very conservative (viewing aspects of especially the medieval past with favor). Such tendencies, perhaps "endemic" (in Lilian Furst's words) at all times in some thinkers and artists, became "epidemic" for many between roughly 1775 and 1850. 1 Some of those tendencies (certainly not all) related to the themes of health, disease, and death. Romantics, H. G. Schenk argues, suffered a "malady of soul," a Weltschmerz, as a consequence of religious frustration; for them the "bonds of allegiance and belief' to and in religion had been weakened by rationalism, leaving a nihilistic preoccupation with the ''dark side of life," a fascination with sleep, death, "utter extinction." Schenk holds that this weariness of life was deepenedthough not primarily causedby the physical suffering and early death that came to many of the leaders of romanticism.2

Tubercular experience may also have reinforced a more specific "romantic" view of disease and its causes. As Hermione de Almeida puts it, "rivalling theories of disease and its treatment could and did flourish [see Chapter Six], and the Romantic fascination with the 'energizing' ambiguity of illness found ample domain."3 Romantic thinkers, de Almeida argues, believed disease to be always present, part of a continuum of energy that included life itself. An inexorable chronic condition

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such as consumption confirmed such a belief, especially for a as well informed as , who had studied medicine, observed consumption in his family, and then suffered (and died) from it himself.

Certainly a remarkable collection of cultural figures, many of them "romantics," succumbed in relative youth between 1775 and 1850 (see Table 8.1). Little wonder that death was a favorite romantic theme, especially the death of the young, or that romantic writers and artists focused on tombs, sorrowful weeping willows, and the heart-wrenching ruins of decayed monasteries. Autumn, as René and Jean Dubos noted in their classic study of tuberculosis, came to rival spring as the poet's favorite season: the autumn of melancholy and falling leaves, not autumn the season of jolly harvest. 4

As many as twenty-three of that formidable list (of forty-four) in Table 8.1 suffered from tuberculosis, even ifas was true for instance of Pëtofi, who was presumed killed in a battlethey did not succumb to the disease. Some of their livesnotably those of , Keats, Chopin, and the Brontë sistersbecame paradigms of romantic tubercular suffering. Consumption's victims slowly and chronically declined, gradually wasting away, becoming fragile and pale. Seeking relief they traveled to warmer climes or undertook sea voyages. Such travels often took them to the Mediterranean, where notions of the contagiousness of disease in general and tuberculosis in particular remained more influential than they did in northern Europe. The tubercular travelers thus met hostility that added to the pathos of their stories: Keats, feared by his Italian landlady; Nicolò Paganini (1782-1840), the violin virtuoso, thrown out of a house in Naples; Chopin shunned on Majorca; François René de Chateaubriand, the French author, unable to sell his carriage in Rome because he had allowed a consumptive to ride in it. Consumptive northern European artists who stayed home may have thus contravened medical advice, but their compatriots, apparently less terrified of contagious disease, may have spared them such ostracism. The composer , in the last stages of consumption, was lionized by concertgoers in London and literally embraced by his musical admirers, one of whom lent a shoulder to help Weber to his carriage.5

Such experiences contributed to a romantic view of the effects of tuberculosis. A wasted pallor acquired a fashionable beauty; whitening powders replaced rouge; the Pre-Raphaelite artists of England, in the mid-nineteenth century, exaggerated the thinness and paleness of their female subjects.6 Keats saw love and consumption as closely related products of similar causes; his "La belle dame sans merci," de Almeida maintains, serves as an "emblem of the destructive aspect of love, of frustrated creative endeavor, and of death by consumption," at one and the same time.7 Romantic, pathetic literary sufferers abounded: David Copperfield's Dora, Dombey and Son's Little Paul, La Dame aux Camélias's Marguerite Gauthier, Scènes de la Vie de Bohème's Mimi. The last two entered the operatic

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Table 8. 1

Deaths at an Early Age, 1776-1849

*Ludwig Christoph Hölty, German poet 1748-1776

*Johannes Ewald, Danish poet 1744-1781

Wolfgang Mozart, Austrian composer 1756-1791

*Joseph Michael Kraus, German-Swedish composer 1756-1792

*Karl Philipp Moritz, German author 1757-1793

Wilhelm Wackenroder, German author 1773-1798

*Novalis (Friedrich von Hardenberg), German poet 1772-1801

Thomas Girtin, English painter 1775-1802

*, German painter 1777-1810

*Cecilia Tychsen, bride of Ernst Schulze 1794-1812

Franz Pforr, German painter 1788-1812

*Ernst Schulze, German poet 1789-1817

*Karl Solger, German philosopher 1780-1819

*Friedrich Gotlob Wetzel, German author 1779-1819

*John Keats, English poet 1796-1821

*, English poet 1792-1822

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Erik Johan Stagnelius, Swedish poet 1793-1823

J.L.AT. Géricault, French painter 1791-1824

George Gordon, , English poet 1788-1824

*Franz Horny, German painter 1797-1824

*Carl Maria von Weber, German composer 1786-1826

Wilhelm Hauff, German author 1802-1827

Wilhelm Müller, German poet 1794-1827

Richard Bonington, English painter 1801-1828

Franz Schubert, Austrian composer 1797-1828

*Wilhelm Waiblinger, German poet 1804-1830

*Victor Meyer, German sculptor 1807-1831

*"Napoleon II" ("King of Rome"), son of Napoleon I 1811-1832

Vincenzo Bellini, Italian composer 1801-1835

Karel Mácha, Czech poet 1810-1836

Mariano Josá de Larra, Spanish author 1809-1837

Aleksander Pushkin, Russian poet 1799-1837

Giacomo Leopardi, Italian poet 1798-1837

Mikhail Lermontov, Russian author 1814-1841

José de Espronceda, Spanish poet 1808-1842

Henrik Wergeland, Norwegian author 1808-1845

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*Nicholaus Becker, German poet 1809-1845

*Alphonsine Plessis, French actress 1824-1847

Felix Mendelssohn, German composer 1809-1847

*Emily Brontë, English author 1818-1848

Edgar Allan Poe, American author 1809-1849

*Anne Brontë, English author 1820-1849

*Frédéric Chopin, Polish composer 1809-1849

*Sándor Pëtofi, Hungarian poet 1823-1849

Source: The major source for this table is Erich Ebstein, Tuberkulose als Schicksal (: Ferdinand Enke Verlag, 1932).

*Suffered from tuberculosis

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repertoire in Verdi's La Traviata and Puccini's La Bohème. Perhaps the memory of Paganini, playing as one possessed while in the throes of consumption, lent credence to the sopranos who filled an opera house with their voices despite their characters' tubercular lungs.

Tuberculosis conferred therefore a kind of beauty; men, according to René and Jean Dubos, strove for a fashionable emaciated look, a fashion to which even the corpulent père aspired. 8 In addition, some in the early nineteenth-century also associated consumption with genius. Sensitive souls seemed prone to consumption. Did consumption impart a nervous force to the mind? Did it lead to a frantic urge to accomplish something great before the shadow fell? Modern authors recognize that some connections (hardly necessary or sufficient to explain genius) might exist. Henry Sigerist notes that suffering from tuberculosis was "a profound experience which must reflect itself in the work of a creative artist."9 René and Jean Dubos grant that consumptives may be drawn to mental activity by default, since much physical activity may be denied them (a point that may extend to many chronic ailments). The empirical evidence for such causal connections was not very convincing, however, and here as in other respects tuberculosis defied nineteenth-century attempts to generalize about its causes or effects. As the Duboses point out, four of the six children of Thomas and Frances Trollope died of tuberculosis between the ages of twelve and twenty-three, showing no sign of literary gifts. The two other childrenThomas (1810-1892) and Anthony (1815-1882)were prolific authors, as was their mother. The Trollope authors never manifested consumptive symptoms.10

The Decline of the Nineteenth-Century Epidemic

Romantic views of tuberculosis may obscure the real demographic importance of the disease, the greatest epidemic killer in the nineteenth-century West, and one that affected far more of the poor than the romantically creative. In the first half of the nineteenth century mortality rates from tuberculosis probably ranged between 300 and 500 per 100,000 population in most Western countries. When England and Wales had about eighteen million people (in 1851), over 50,000 people died there of tuberculosis annually, compared with the 40,000 cholera victims in the worst single cholera year, 1849. Cholera epidemics appeared as spikes on a graph, but those spikes rarely (if ever) rose above the high annual level of tuberculosis deaths.

In the second half of the nineteenth century the mortality of tuberculosis began declining in most of western Europe and North America. This decline occurred in different places at different times and rates. The industrial pioneers, England and Belgium, whose mortality rates had risen above 300 (per 100,000), were the first countries whose rates then fell below that appalling figure: Belgium in the mid- 1860s, England about 1870. (Some placesbucolic Ireland and Switzerland,

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thinly settled Australia and New Zealandmay never have been that high.) Between about 1890 and World War I rates fell below 200, again chiefly in the most advanced industrial states: Italy in 1891, Belgium in 1892, England in 1894, the and the United States in 1901, Denmark in 1902, in 1906, Scotland in 1909, Switzerland in 1914. In 1921 the mortality rate from tuberculosis dropped below 100 in the United States and Denmark; the Netherlands followed in 1925, Belgium, England, and Germany in 1926, Scotland in 1928, Italy in 1933, Switzerland in 1935. 11

Exceptions to the pattern existed, however. In Ireland the tuberculosis mortality rate did not peak until the late 1890s, declined only slowly until about 1908, and thenwhile it fell more rapidlyremained above 100 until after World War II. 's experience mirrored Ireland's, although its mortality fell below 100 by 1937. In east-central EuropeAustria, Hungary, Czechoslovakiatuberculosis mortality remained very high (and perhaps even peaked) in the first decade of the twentieth century, fell below 300 by 1914, surged upward again in World War I, and then dropped rapidly after the war. But like Ireland they all remained over 100 until after World War II. In France, something of an anomaly in western Europe, rates remained well over 200 during World War I and fell below that number only in 1920.

The decline in the tubercular death rate, accomplished before the dramatic reductions that followed antibiotic treatments after World War II, poses some of the thorniest problems in the disease's history. Those problems are ultimately those of explanation: did deliberate human measures contribute in some way to loosening the hold of tuberculosis? If so, how decisive were those interventions? Or were all such human responses overshadowed by more general changes in the social and economic condition of the poor? Or did tuberculosis decline for reasons entirely exogenous to any human actions, whether deliberate or inadvertent?

Because etiological views about tuberculosis remained in conflict for much of the nineteenth century, disagreement persisted about what possible measures could have a beneficial effect. As the century went on (and the disease's mortality started to fall) many thinkers came to view consumption more clearly as a social problem, or as the product of social problems, and to tie it less clearly to romantic sensibilities. Associations of tuberculosis and romantic suffering did not disappear; the consumptive images of Thérèse de Lisieux (in real life) and Sarah Bernhardt (on the stage) remained a part of late nineteenth- and early twentieth-century French conceptions of tuberculosis.12 The romantic view of the creative, artistic tubercular sufferer persisted outside France as well; Puccini's La Bohème was, after all, first performed in 1896. But that opera may also illustrate the point that more often slums, not literary salons, yielded the prototypical consumptive. Mimi may have a beautiful voice, and the characters may live in a creative Latin Quarter, but they are also poor and cannot afford medical treatment. Tuberculo-

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sis might accordingly confer shame, not cachet. The new perspective almost certainly reflected a more accurate demographic understanding than the old, for tuberculosis had always been a disease that ravaged the poor. But with it came a further burden of stigma, which associated poverty and tuberculosis in a symbiotic relationship of individual failure.

Nineteenth-century etiological arguments about tuberculosis, centering on either contagion or heredity, remained uncertain in part because neither explanation seemed entirely satisfactory. Too many members of "consumptive" families remained free of disease; descent from a tubercular parent did not inevitably lead to consumption, and sharing a house with one apparently did not either. Those circumstances lednaturally enoughto an emphasis on "predisposing" causes that might explain why the basic cause (be it heredity or contagion) could overcome the resistance of some and not others.

It might be well at this point to consider modern explanations of tuberculosis. The causative "germ," whether M. tuberculosis or M. bovis, lodges in the human body. Immunological reactions shortly begin, and a walled-off "tubercle" results that contains the bacillus and prevents its further spread through the body. The person so infected may now be said to "have" tuberculosis, if by that word is meant a positive reaction to a tuberculin test; but in many cases no clinical symptoms ever develop, so that if the tuberculin test were not administered no assumption of tuberculosis would ever be made. In some individuals, howeverand here the etiological puzzles arisethe body's immune systems fail to contain the spread of the bacillus, and different clinical manifestations of tuberculosis result, sometimes rapidly, more often much more gradually.

Some people apparently enjoy more resistance to tuberculosis than others. Their resistance is not to the initial infection, for bacilli make their way into the body (through either respiration or ingestion) without much interference. Resistance rather arises when the body's immunological defenses respond to the invasion. Many possible variables have been suggested to explain different powers of resistance. In the nineteenth century "predisposing" causes included diet, stress, dirt, general bad habits, andfor those who denied the primacy of one or the otherheredity and contagious contact. In some form modern discussions still debate some of those causes as possible explanations of varying tuberculosis mortality and morbidity.

Pulmonary tuberculosis undoubtedly found favorable conditions for spread in the nineteenth century, in both Europe and North America, if only because of the rapid increase of population and its dramatic urbanization. Cities grew explosively; more than that, they experienced remarkable congestion, especially in the earlier decades of urban growth, before the cities began their expansion into the suburban hinterland. Dwellings crowded together; within dwellings lived more people per room. Urban and industrial life also meant more crowded workplaces, whether

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