Читать книгу Tuberculosis and War - Группа авторов - Страница 18

During the 16th century, most of Europe was just beginning to recover from the devastating population losses that occurred during the 14th century pandemics of bubonic plague, which were exacerbated by local famines and wars. England’s population was 2.1 million inhabitants in 1400, half the number estimated in 1348 [53]. During the next 100 years, population growth in England had resulted in 4.1 million people by 1570, and a further increase to 4.8 million in 1600. The majority of the English in the early Middle Ages were subsistence workers, farmers, and laborers, eking out life despite wretched harvests, dreadful climates, and prevalent sickness. Local magistrates took care of business on behalf of wealthy nobles and landed gentry. Workers were widely dispersed throughout the countryside; towns were small and scarce: obviously unfavorable conditions for the spread of TB. Feudal society declined, however, in the 13th and 14th centuries due in part to the rise of a thriving merchant population that established sophisticated trading networks throughout England and Europe and weekly markets and fairs that promoted greater access to commercial goods, the expansion of towns, and the development of an urban artisan population that catered to local needs. Expanded trade and communication probably hastened the spread of TB at the time.

Consequently, during the next century, agricultural practices became more efficient, requiring fewer laborers and less physical input. Food became cheaper, wages rose a trifle; industrialization advanced and towns began to increase in size and number. Meanwhile, from 60,000 to 70,000 inhabitants in 1500, London, already by far the largest city in England, kept making room for ever-increasing numbers of people, causing the population to grow to 250,000 at the end of the 17th century [54]. And to make matters worse, these indigents, often desperately poor and undernourished, had to survive packed into abysmal living conditions: London became a model of crowd diseases. So, by the year 1631, as shown in Figure 2, 15% of all deaths in the city of London that year were attributed to TB [55]; and for the next nearly 200 years, the death rate from TB in the city of London remained enormous, peaking at around 25%, and finally beginning to decline around 1830.

A schematic model showing the trend of mortality from TB in Western Europe from 1740 to 1985 is illustrated in Figure 3 [56]. Death rates from TB peaked at the astronomic value of 1,000/100,000 population in 1800, and then declined at a fairly constant rate for more than 100 years, until the abrupt upsurge that occurred during and immediately after WWI, which was in part lengthened by the Spanish influenza pandemic that lasted until around 1920. Finally, the model illustrates the arrival in 1952 of “triple therapy,” which heralded the steep decline of TB mortality resulting from effective chemotherapy [56].

No one is quite sure what triggered the initial reduction in TB mortality that began around 1800. (Note that both the year and country of the decrease in death rates from TB varied from location to location, but from whatever peak was finally identified, mortality began to go down, with a few wrinkles but fairly consistently and for well over the succeeding 100 years.) In 1800 in Germany, there was no obvious cause for the decline, and it took place at least 82 years before Robert Koch discovered M. tuberculosis. One of the most frequently cited reasons for the reduction remains a rising standard of living, which includes better housing, improved nutrition, higher wages, and lower costs, when and if these actually occurred; public health efforts were meager at the time but may have helped somewhat; and there was the dawning realization that TB was a contagious disease that warranted isolation of sick patients.

The ups and downs of TB mortality varied considerably from one country to another during the 19th century: in Great Britain, it declined; in Ireland and Norway, it increased first; but in France mortality stayed “extremely high” the entire century [54]. During the 17th, 18th, and 19th centuries in Western Europe and then in the 18th and 19th centuries in the Eastern US, TB was by far the most important cause of death, and it remained the highest or one of the highest causes of mortality in several countries, including the US until around 1900. But once TB death rates started going down, they kept steadily decreasing until interrupted by WWI and then again by WWII.

The Industrial Revolution began in England in the mid-18th century and then spread to the rest of Western Europe. While the first and more famous phase is often dated 1760–1810, a second phase of the industrialization process based on developments in physics and chemistry and advancements in the steel and petroleum industries continued up to WWI, with Germany eventually surpassing England in industrial output. Living conditions in neighboring English mills and factories during the first phase of the broadening industrialization period were deplorable and deteriorated even further to an unprecedented extent. Five-year-old boys and girls worked dangerous 10–12 h shifts. Sanitation and personal hygiene for practical purposes vanished. Overflowing cesspools required emptying into local rivers and streams, and on a regular basis night porters emptied human excrement into the Thames River, a chief source of drinking water for London. Similar conditions existed on the continent in industrial centers, especially in the Ruhr Valley in Germany, a country that unified in 1871 and rose in power during the period of the second Industrial Revolution. Cholera was rampant and both typhus and typhoid were endemic, but as usual, TB remained the chief scourge.

Around midway, or even a little earlier during the Industrial Revolution, historically high death rates from TB began to go down even while the number of deaths continued to rise. Redeker [58] reported that TB death rates in London peaked at 950/100,000 as early as 1755. Kraus [59], however, states that mortality from “consumption,” also in London, was cataloged at 1,121/100,000 during 1771–1780, after which it declined to 716/100,000 during 1801–1810. The explanation – for the decrease in death rates while the number of deaths rose – was the ongoing, striking increase in the size of the English population during that period, which included more and more new professionals, doctors, lawyers, bankers, business-men, and entrepreneurs of all sorts. “Thus was born the English middle class” [57], an increasingly important group that was much less vulnerable compared to their TB-stricken predecessors.

Two related scientific articles tackle the important question of whether there were individuals or families that stood out as being protected from TB-induced disease and death during the 17th to 19th centuries, when practically everyone was infected by tubercle bacilli and mortality from active disease hovered around 50% or even higher. Lipsitch and Sousa [60] ask whether the presence and magnitude of natural selection contributed to the development of resistance to TB, which had been proposed as a factor affecting the historical decline in TB, before chemotherapy was introduced. The authors concluded that natural selection by deaths from pulmonary TB cannot account for the 150-year-long ongoing reduction in TB detected in Europeans and their descendants, except during both WWI and WWII, the latter of which was recorded just before the arrival of anti-TB treatment.

Thanks to the exceptional reduction in death rates from TB chemotherapy after the mid-20th century and onwards, Stead [61] showed a significant difference in the percentage of persons who developed positive tuberculin skin test reactions following exposure to severe outbreaks of TB in white communities compared with those in African-American communities. Stead hypothesized that everyone infected by M. tuberculosis should develop a positive tuberculin reaction, and if an individual remained negative, it implied the presence of genetically determined innate resistance to TB in both them and their ancestors.

Both of these investigations are of interest, but fail to completely explain what actually caused the historically conspicuous and lengthy decline in TB deaths rates.