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Consumption, the great killer |
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Tuberculosis is an ancient enemy. Human bones from the Near East dating back five millennia show the telltale pitting of TB. Mummies from Egypt ca. 2400 BCE show tubercular decay in their spines. The ancient Greeks described it, too. Around 460 BCE, Hippocrates identified phthisis, or consumption, as the most widespread disease of his age. It was almost always fatal. Because of that, he advised his followers and students against treating late-stage consumption to avoid damage to their reputations. It was called the kings evil in medieval Europe because newly crowned kings (and queens, in England) were alleged to cure scrofula, glandular swellings in the neck associated with TB, with their touch. Moving toward the present, Franciscus dele Bo Sylvius described the progress of the disease in his Opera Medica of 1679. Two decades later, a public-health edict from the Republic of Lucca in Italy recognized the infectious nature of the disease: Henceforth, human health should no longer be endangered by objects remaining after the death of a consumptive. The names of the deceased should be reported to the authorities, and measures taken for disinfection. Benjamin Martin, an English physician and author of A New Theory of Consumption (1720), hypothesized that TB resulted from the actions of wonderfully minute living creatures. Once those creatures established themselves in the body, Martin thought, they would generate the characteristic symptoms of consumption. He further theorized that close contact with a consumptive, including frequent conversation so close as to draw in part of the breath he emits from the Lungs, was enough to transmit the disease. In 1865, a French military doctor, Jean-Antoine Villemin, demonstrated that the disease could be passed from humans to cattle, and from cattle to rabbits. This was a remarkable breakthrough, because despite Martins wondrously small organisms, medical theory still held that each case of consumption arose spontaneously in predisposed people. A few years later, in 1882, Robert Koch demonstrated conclusively that a bacterial infection caused TB. Later investigations proved that air and secretions expelled from consumptive lungs contained live bacteria. Whether it is known as lupus vulgaris (TB of the skin), Potts disease (TB of the bones), or consumption (the classic case of lung disease), TB is one of historys great killers. It is estimated to be responsible for 20% of the deaths in 17th-century London and 30% of those in 19th-century Paris (as recently depicted in the popular film Moulin Rouge). Although not as aggressive as plague, TB has killed more people in history than the black death, leprosy, or HIV. An estimated 1 billion people around the world have been felled by TB in the past two centuries, and the fatalities continue. Romantic and deadly However, after 1000 BCE the strain of TB seems to have changed. After that time, pulmonary TB caused by M. tuberculosis became widespread. M. tuberculosis is most likely an evolved form of M. bovis that developed among milk-drinking Indo-Europeans, who then spread pulmonary TB on their migrations. By the first millennium BCE, pulmonary TB was endemic throughout the world. The earliest recorded symptoms of pulmonary TBcough, expectoration, hemoptysis, and wastingare found in the library of Assurbanipal (668626 BCE), king of Assyria. These same symptoms were well known in Victorias London and the Paris of the Belle Epoque. Pulmonary TB was romanticized in the arts and music of the 19th century. The deaths of Mimi in Puccinis La Boheme and Satine in Moulin Rouge are portrayed as romantic, tragic events, but end-stage pulmonary TB is anything but glamorous, and Mimi and Satine exposed everyone around them to danger with each breath. The dying consumptive faced night sweats and chills, paroxysmal cough, spread of the disease to other organs of the body, and of course, the wasting away that led helpless bystanders to name the disease consumption. The excitement that greeted Robert Kochs eventual demonstration of the bacterial nature of the disease was due to the fact that for the first time the killer of generations had a face. Medicine could finally work toward a cure. The magic mountain The first recorded treatment for pulmonary TB was developed in the early 19th century, when English physician James Carson demonstrated that injecting air into the pleural cavity could collapse a lung and permit it to heal. At the time, the practice went nowhere.
Pneumothorax, the collapsing of the lung, did not become the standard treatment until it was rediscovered in 1882 by C. Forlianini. The affected lung would be collapsed, which allowed it to rest and heal. But as a treatment, pneumothorax was limited. It did not work for late stages of the disease. In the early 20th century, Edward Archibald, a surgeon at the Royal Victoria Hospital in Montreal and himself a recovered consumptive, heard of a new surgical treatment for cases in which artificial pneumothorax was not possible. This method removed portions of the upper ribs on one side of the body to collapse the rib cage. While drastic, this extra-pleural thoracoplasty allowed even certain late-stage tubercular lungs to collapse and heal. Ingenious as this treatment and further refinements were, it was never widely popular. Nonetheless, Archibald was the first surgeon in North America to surgically treat late-stage TB. The procedure offered otherwise doomed patients a chance to recover. In 1895, Wilhelm Conrad Roentgen discovered X-rays. Although this radiation did not cure TB, it allowed physicians to readily monitor the progress of the disease. The magic bullet Streptomycin, isolated from Streptomyces griseus, was the magic bullet that researchers had long sought. It combined low toxicity with high inhibitory effect, and on November 20, 1944, the first critically ill TB patient was treated, and the results were gratifyingly dramatic. Several anti-TB drugs followed; they were important because therapy with a single drug soon sparked resistant TB strains. Multidrug therapy avoided this problem. Out of ammunition? That should have been the end of the story. In the second half of the 20th century, rates of TB infection dropped throughout the developed world. In 1987, the American Medical Associations Advisory Council for the Elimination of TB projected that by 2010 the disease would become extinct worldwide, like one of humanitys other great scourges, smallpox. Yet the warning signs that this would not happen were already there. By 1985, for the first time, the number of new TB cases stagnated and then began to rise. The World Health Organization now calls TB a fire raging out of control in developing nations, among the poor, in prisons, and in people with HIV. Worldwide, someone becomes infected with TB every second. What happened? The multidrug regimen that was developed not long after the discovery of streptomycin is effective if it is taken continually, in regular doses, for 68 months, and therein lies the problem. For various reasons, many patients are noncompliant. Some stop taking the drugs when they feel bettera common problem with antibiotics. Others stop because of the cost or inconvenience or because they distrust the medical establishment. Particularly troubling is the fact that TB and HIV have formed a new and deadly combination. In immunocompromised people, M. tuberculosis is much more likely to cause infection, creating a greater number of active TB cases and more people who spread the disease. WHO estimates that HIV produces 1.4 million cases of TB each year that otherwise would not appear. In addition, the increase in immigration from the developing world to developed countries, combined with the existing poverty in many areas where new immigrants tend to settle, makes a ready pool for TB. For both HIV and TB, misdiagnosis and noncompliance compound the problem. Its a classic story of artificial selection. The initial doses of the antibiotics kill off the susceptible microbes, leaving the resistant ones to reinfect the consumptive. It is estimated that more than half of the isolates from relapsed TB cases are resistant to at least one drug. It takes three years on average to develop a new antibiotic; it takes three months to develop a resistant bug. TB strains seen with HIV are often resistant to many drugs, so the strains being spread are that much harder to treat. To add insult to injury, M. bovis is back and causing TB in humans, particularly those who are HIV-positive. And M. bovis, too, is developing multiple drug resistance. So, despite the prevalence of artistic representations to the contrary, there is no obvious romance to the past or present of this pernicious and once more widespread disease. Suggested reading
Christopher S. W. Koehler holds a Ph.D. in the history of science. He writes and teaches in northern California. Send your comments or questions regarding this article to mdd@acs.org or the Editorial Office by fax at 202-776-8166 or by post at 1155 16th Street, NW; Washington, DC 20036. |