Infectious Fear

Politics, Disease, and the Health Effects of Segregation

Samuel Kelton Roberts Jr.

• Publisher: The University of North Carolina Press
• Year: 2009
• ISBN:
  9780807894071
• Topic: Medicine
• Subtopic: Public Health, Administration & Care

For most of the first half of the twentieth century, tuberculosis ranked among the top three causes of mortality among urban African Americans. Often afflicting an entire family or large segments of a neighborhood, the plague of TB was as mysterious as it was fatal. Samuel Kelton Roberts Jr. examines how individuals and institutions--black and white, public and private--responded to the challenges of tuberculosis in a segregated society. Reactionary white politicians and health officials promoted "racial hygiene" and sought to control TB through Jim Crow quarantines, Roberts explains. African Americans, in turn, protested the segregated, overcrowded housing that was the true root of the tuberculosis problem. Moderate white and black political leadership reconfigured definitions of health and citizenship, extending some rights while constraining others. Meanwhile, those who suffered with the disease--as its victims or as family and neighbors--made the daily adjustments required by the devastating effects of the "white plague." Exploring the politics of race, reform, and public health, Infectious Fear uses the tuberculosis crisis to illuminate the limits of racialized medicine and the roots of modern health disparities. Ultimately, it reveals a disturbing picture of the United States' health history while offering a vision of a more democratic future.

1
TOWARD A HISTORICAL EPIDEMIOLOGY OF AFRICAN AMERICAN TUBERCULOSIS

Baltimore’s Negro death rate is nearly twice that which obtains among the white population. . . . In this simple statement is seen the result of conditions against which serious protest has been and will continue to be lodged by all who appreciate their significance. Poorly constructed houses of bad design, and in need of repair, streets and alleys with defective drainage, congested living conditions . . . are some of the factors which prevent the Negro from attaining the standards of health which the white race reaches without difficulty. In large measure they are beyond the power of the Negro to remedy. He must usually wait for the landlord to build his houses. He certainly must wait for the city to drain the streets in the districts where he lives and to open up highways through the dense settlements where he is now crowded.

—Baltimore Sun, 4 February 1925

This book is primarily concerned with two overlapping and mutually informative periods in U.S. urban history: the era of infectious fear all but vanquished by the discovery of antimicrobial therapies, and a period, before the Second World War, when health policy and social policy were, comparatively speaking, overwhelmingly dominated by politics derived from local rather than federal mandates. Key to understanding the first half of this equation—the politics of race and tuberculosis in the early twentieth century—is an understanding of the transmission of the disease and the state of medical knowledge during this period. While chapter 2 examines the historical frame of tuberculosis—its popular and medical understandings as “disease of civilization” and the shifting terrain of national racial politics—this chapter explains that elevated rates of mortality and morbidity among African Americans derived largely from conditions of living and from certain populations’ time of infection, themselves the products of shifting ecological imbalances between rural and village hinterlands (sending societies) and emerging urban industrial spatial orders (receiving societies).

Although five types of tuberculosis afflict animals, only two, human and bovine, may actually cause the disease in the human body. Humans may contract the bovine form through the ingestion of bovine tissue or cow’s milk in which the bacillus is present. After the turn of the century, however, and particularly after the implementation of milk-purification regulation, most human tuberculosis was caused by the human form of the bacillus, the mycobacterium bacillus, or M. tuberculosis. Most often, M. tuberculosis originated with inhalation, producing pulmonary tuberculosis.

Once the bacillus is introduced into the human body and allowed to reproduce, it may attack any organ and spread to others, causing tuberculosis to develop into one or more forms. Particularly when the bacillus is ingested, the disease may manifest itself in the abdominal lymph nodes and the small intestine. It then becomes the clinical condition tabes mesenterica, recognizable by the symptoms of abdominal pain, nausea and vomiting, and diarrhea (probably the condition to which young Archer Barnes succumbed).¹ Tuberculosis of the joints and bones most often affects children, particularly those who are unable to fight off their first, or “childhood,” infection. This form may be less debilitating than pulmonary tuberculosis or the associated disease of kidney and bladder tuberculosis and today is more easily treated. If not treated, however, the disease will literally gnaw away at bone tissue, causing osteomyelitis.

From internal organs, infection may spread to the skin (tuberculosis is not communicable by epidermal contact), causing lupus vulgaris (Latin for “common wolf”), in which discolored nodules appear across the victim’s body and especially the face. These nodules grow slowly but eventually will cause the ulceration and destruction of the skin itself, leading to other infections. Much worse is tuberculosis of the spine (known as Pott’s disease after surgeon Percival Pott [1714–88]). Before the urbanization and industrialization of the nineteenth century and the subsequent rise of the pulmonary form, Pott’s disease was one of the more common manifestations of tuberculosis. It left its victims with hunched backs resulting from abscesses in one or more vertebrae, the softening of which eventually could cause paralysis or death. If the disease spreads from the organs to the bloodstream (producing miliary, or galloping, tuberculosis), it rapidly becomes fatal as it gains easy access to other parts of the body.

Since the late nineteenth century, the most common form of tuberculosis has been pulmonary tuberculosis, caused by bacilli contained in droplets orally expelled from an infected host. The bacillus may travel in dust particles (dried sputa), in moist droplets, or in droplet nuclei, left in the air when airborne sputa evaporate quickly. Exposure to the bacillus technically may occur at any place and time when the bacillus is present in its vector state. Common encounters during which an infected person’s exhaled or discharged sputa become present technically constitute exposure, although such encounters are mediated by environmental and biological circumstances. By the late nineteenth century, for example, researchers had recognized the tubercle bacillus’s sensitivity to natural light and the necessity of sufficient quantities of bacteria to cause infection (the public health impetus of the tenement reform movement).

A distinction may be made between two types of tuberculosis infection, the initial, or primary, infection (also called “childhood” infection because it typically occurred among the young) and the postprimary, or secondary, infection. This distinction generally was not made before 1915. In primary infection, bacilli entering the lungs will reproduce and cause dispersed and miniscule lesions until an immunological response is created. (Because the M. bacillus reproduces at one-thirtieth the rate of average bacteria, it may reside within a host for days or weeks before the immune system is signaled to produce antibodies.)² Initial symptoms include fever, lethargy, and swelling of the tracheobronchial and other lymphatic glands (producing a condition that, before its recognition as a tubercular manifestation in the late nineteenth century, was called scrofula, a disease to which physicians believed Negroes particularly prone). Primary infection is more likely to be fatal in very early infancy (before six months) or in adults (risk increasing with age). Children over the age of two stand a very high chance of surviving primary infection, and those between two and five (and even as late as ten) may experience these symptoms as nothing more than a very bad cold. However, massive exposure or a state of immunological compromise will cause further disease in children, often meningeal tuberculosis or tuberculosis of the bones or stomach. In adults, disease resulting from a primary infection often will spread rapidly through the lymphatic system and the bloodstream, causing multiple organ failure and death. Barring the kind of medical interventions developed after the late 1940s, encounters between uninoculated adult populations and the bacillus often result in epidemic tuberculosis, with first a sharp rise in incidence and then a high ratio of disease incidence to exposure (and generally a higher ratio of mortality to disease incidence).

In postprimary infections, bacilli entering the lungs will encounter a more immediate immune response, and the infected area will be enveloped in fibrous tissue, forming on the lung a cheesy nodule resembling a tuber. All remaining bacteria will be destroyed by white blood cells. In this stage, known as latent tuberculosis, the body will not exhibit symptoms. With the right nutrition, rest, and the absence of further exposure (reinfection or exogenous infection), dormancy will continue, and the lesion may heal entirely, leaving only a small calcified mass or a fibrous scar. The victim may live life normally and oblivious of infection, and little or no danger of contagion will exist. Massive exposure or a weakening of the body (by age, other diseases, mental or physical stress, malnutrition, or continual overexertion), however, may prevent the nodule from fully healing. A rupture in the nodule will cause endogenous reinfection, the migration of bacilli to other parts of the infected organ. Those, too, will be walled off. Each cycle of tubercle formation, reinfection, and more tubercle formation increases the probability that the immune system will be overpowered by the infection and that tuberculosis will develop. Initial symptoms of pulmonary tuberculosis include dyspnea (difficulty breathing), a persistent cough, prolonged fever, and weight loss. As lung tissue is necrotized, caseation (the general liquefying of affected tissue) is initiated, and pus will begin to fill the affected area of the lung. Coughing will continue in varying degrees of frequency and severity. After time, violent coughing eventually will cause hemorrhage, producing the telltale hemoptysis, the coughing up of arterial blood. At the same time, the infection may spread from the lungs to the surrounding outside tissue or to the intestines via swallowed sputum. Organ failure and death become imminent.³

First interactions between the bacillus and a given population may produce the violent waves of primary infections typical of epidemic tuberculosis. Tuberculosis becomes endemic when subsequent interactions eventually ensure that most children within a population have been exposed and have survived primary infection. In conditions of endemicity, therefore, the bulk of adult tubercular deaths result from postprimary infections. Tuberculosis resulting from postprimary infection typically runs a longer course than tuberculosis from primary infection (turn-of-the-century physicians commonly referred to the disease caused by postprimary infection as chronic), making recovery more likely but also ensuring that persons with the active disease will have more time to spread the bacillus. A sort of ecological stasis has been reached. Because the bacillus is fairly ubiquitous in conditions of endemicity and a majority of persons therefore may expect to be exposed, the rise or fall of incidence and mortality will be mediated largely by the combined effects of frequency and intensity of encounters (environment), the proportion of the population having experienced primary infection in childhood, and individuals’ immunocompetence (influenced by diet and other health factors). Although a better understanding of immunology and childhood infection did not begin to make clear the processes of tubercular endemicity until around the early 1920s, the development of the von Pirquet tuberculin skin test in 1907 (followed by the Mantoux test, a version of which—the purified protein derivative [PPD]—remains in use today in the United States) allowed the detection of infection by testing for an antibody reaction, revealing high rates of exposure in urban populations. Because conditions of living and composition of population vary over space and time, it is entirely possible to have epidemic tuberculosis within endemically tuberculous societies. Unexposed rural-to-urban migrant populations are the classic example, but so, too, are populations living in such extremely intense and frequent exposure or in deteriorated immunocompetence (conditions commonly occurring in poverty) that very young infants do not survive primary infection and/or adults who have survived primary infection nonetheless succumb to postprimary infections.

Various groups of A...

Table of contents

• Cover Page
• infectious fear
• Copyright Page
• Dedication
• CONTENTS
• ILLUSTRATIONS, FIGURES, AND TABLES
• ACKNOWLEDGMENTS
• INTRODUCTION
• 1 TOWARD A HISTORICAL EPIDEMIOLOGY OF AFRICAN AMERICAN TUBERCULOSIS
• 2 THE RISE OF THE CITY AND THE DECLINE OF THE NEGRO
• 3 URBAN UNDERDEVELOPMENT, POLITICS, AND THE LANDSCAPE OF HEALTH
• 4 ESTABLISHING BOUNDARIES
• 5 LOCATING AFRICAN AMERICANS AND FINDING THE “LUNG BLOCK”
• 6 THE WEB OF SURVEILLANCE AND THE EMERGING POLITICS OF PUBLIC HEALTH IN BALTIMORE
• 7 THE ROAD TO HENRYTON AND THE ENDS OF PROGRESSIVISM
• CONCLUSION
• NOTES
• INDEX
• STUDIES IN SOCIAL MEDICINE