Abstract

l h e burst of scientific and public health activity in second half of nineteenth century began before causative organisms of disease had been identified. In 1856, English epidemiologist William Budd wrote: Everywhere along African seaboard, where blacks have come into contact and intimate relations with whites, phthisis causes a large mortality among them. In interior, where intercourse with Europeans has been limited to casual contact . . . there is reason to believe that phthisis does not (1). In France, Villemin infected rabbits with tuberculosis by inoculating them with material from human patients. He also made an observation similar to Budd's that the phthisical soldier is to his messmates what glandered horse is to its yoke fellow (2). And so, even before identification of tubercle bacillus as causative agent of tuberculosis by Robert Koch 100 years ago, there were those who understood many of essential features of transmission of tuberculosis. In 1862, Pasteur published his Memoir on organized corpuscles that exist in atmosphere, in which he demonstrated that organisms appearing next day in a sterile culture medium standing open on a laboratory bench arise not from spontaneous generation, but because medium is inoculated by dust-borne organisms settling into it (3). This scientific experiment, repeated many times with ingenious modifications, sanctified age-old belief that disease is airborne. The physicist, John Tyndall, became an enthusiastic publicizer of Pasteur's work and made wildly exaggerated statements about airborne nature of all kinds of infections (4). But while Tyndall was imagining public health implications of airborne organisms, hard epidemiologic evidence of a contrary nature was accumulating. In 1854, an outbreak of cholera in London was studied by Snow and traced to notorious Broad Street well (5). With increasing awareness of importance of water, food, and milk in transmission of enteric and demonstration of control by sanitary measures, this important group of was removed from airborne category. Then in 1893, Smith and Kilborne showed part played by ticks in transmission of Texas cattle fever (6). In 1895, Ross watched development of malarial parasite in mosquitoes (7). During 1880s and 1890s, Finlay carried on his experimental work on mosquitoes and yellow fever (8). After Yellow Fever Commission and General Gorgas accomplished mosquito control, malaria and yellow fever were wiped out, first in Havana and later in Panama Canal Zone (9). These achievements provided convincing proof that malaria and yellow fever were not airborne in usual sense. Even Tyndall did not claim that venereal were airborne. Thus, with enteric diseases, insectborne diseases, and venereal removed from airborne category, pendulum swung to other extreme, denial that airborne infection was of any importance at all. Tuberculosis was one exception. Toward end of nineteenth century, Cornet demonstrated that guinea pigs could be infected regularly with dust-borne tubercle bacilli (10). Flugge, on other hand, was unable to infect with dust-borne organisms but could infect regularly with respiratory droplets expelled by patients with tuberculosis (11). The confusion was compounded in early twentieth century by demonstration that raw milk was frequently infected with tubercle bacilli and that at least some human cases, particularly among children, were due to bovine bacillus (12). However, infecting animals by gastrointestinal route was not easy. Findel demonstrated in 1907 that millions of organisms were required to infect by gastrointestinal route, whereas only 62 germs were sufficient to infect a dog by inhalation (13). Chapin, in his influential book Sources and Modes of Infection, published in 1910, balanced these factors carefully and brought all available evidence together. He argued strongly against airborne infection and in favor of transmission of contagious by direct contact. But Chapin made an exception of tuberculosis: It is assumed that tuberculosis, as it occurs in human beings, is usually an air-borne disease, and . . . there is more reason for such an assumption concerning this than concerning most diseases (14). In 1930s, William F. Wells, at Harvard School of Public Health, re-explored from beginning physical and physiologic behavior of organisms suspended in air (15). Starting with a study of air of textile mills in Massachusetts, he distinguished, both aerodynamically and bacteriologically, among dust, droplets, and droplet nuclei. He emphasized fact that vast numbers of tiny invisible droplets in addition to a few larger droplets are expelled in coughing and sneezing, and that tiny droplets evaporate almost instantly to still smaller droplet nuclei. These particles are so small that they do not settle out of air of a room, but are wafted about on air currents and are rapidly dispersed. Because of dilution in air, viable droplet nuclei are widely separated by large volumes of uninfected air. The organisms are removed from room air by ventilation or by death, not by procedures used to prevent contact infection. Outdoors, they are eliminated by infinite dilution and by radiation from sun. Thus, droplet nucleus hypothesis

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