Introduction and Historical Perspektive

Introduction and Historical Perspektive - Considering the centuries during which TB has been afflicting humanity, awareness that the disease is the result of a transmissible airborne infection is surprisingly recent. Although scientists such as Aristotle and his contemporaries believed that TB was contagious, they had no understanding of what caused it or exactly how it was spread. During the Middle Ages through to the seventeenth century, clinical practice and societal laws in Europe attested to the fact that the contagiousness of TB was suspected, if imperfectly understood.

Tuberculosis

M. Tuberculosis

In Italy and Spain, cases of TB had to be reported to city authorities, and, when a patient with TB died, his personal belongings were burned in order to eradicate any traces of the disease that might spread to others. Moreover, physicians of the time, such as Valsalva and Morgagni, refused to perform autopsies on victims of TB, concerned that the procedure would spread the disease, as indeed

it does.1 In the seventeenth century, however, a contrary view began to emerge. Eminent scientists and clinicians in Europe started to question whether TB was really transmissible. As proof, they offered observations that many healthcare workers who came into contact with TB patients did not themselves acquire the disease. Under situations ideal for transmission, they reasoned, how could TB possibly be considered a transmissible disease? Instead, noting the clustering of cases within families, they concluded that infection with TB was probably a hereditary phenomenon.1 Given the long latency periods that routinely occur between exposure and disease development, firm conclusions about transmissibility were understandably elusive. By 1910, decades after Koch discovered the tubercle bacillus, Chapin, in his influential book The Sources and Modes of Infection argued against the airborne mode of transmission of any organism:

Bacteriology teaches that former ideas in regard to the manner in which diseases may be airborne are entirely erroneous; that most diseases are not likely to be dust-borne, and they are spray-borne for only 2 or 3 feet, a phenomenon which after all resembles contact infection more than it does aerial infection as ordinarily understood Chapin did concede that, if any infection was airborne, it would likely be TB. But, in Thomas Mann’s 1927 novel The Magic Mountain, visitors to the fictitious alpine sanatorium lived with patients for weeks at a time with no apparent fear of contagion.3 As recently as 1932, Fishberg wrote that it was not risky for ‘healthy adults to be coughed at by patients suffering from pulmonary or laryngeal tuberculosis’.4 The partial immunity acquired by infection early in life undoubtedly contributed to the misleading observation thatmany of those exposed did not develop disease. By 1947, the American Public Health Association (APHA) stated that ‘conclusive evidence is not available at present that the airborne mode of transmission is predominant for any particular disease’.5 Instead, it was postulated that TB might be spread by direct contact with infected sputum. Public health campaigns to discourage spitting were a logical consequence. 

The prevailing perception through the early 1900s, therefore, was that the airborne spread of TB beyond the immediate proximity of the source was unlikely. Yet even as many in the medical, public health, and scientific communities accepted Chapin’s view on airborne transmission, other researchers were working to better understand the propagation of infections, including TB. It was not until the late 1950s, however, a full decade after the APHA’s conclusion, cited above, that the tide of

scientific opinion once again turned on this matter. Among the landmark investigations in this areawere those ofWilliam FirthWells,who while working as a sanitary engineer at Harvard University first conceptualized how certain infectious agents such as measles and TB might become airborne and travel from person to person.

In his seminal 1934 paper entitled ‘On air-borne infections. II. Droplets and droplet nuclei’, Wells introduced the notion that transmissible infections fell into two major categories: those spread by local, direct, person-to-person contact and those spread more widely without direct contact by the airborne route.6 In 1931 Wells had developed an air centrifuge, a device that allowed him to concentrate airborne microorganisms from air samples. He had been commissioned by the Massachusetts Department of Health to investigate the aetiology of respiratory infections among textile mill workers. He speculated that the source of these infections was bacteria from contaminated standing water that had been aerosolized to keep dust down in the mill. Using his air sampler, he identified the same organisms in the air and in the standing water.7

The next intellectual leap was to theorize that aerosols produced by coughing and sneezing could also be responsible for person-to-person airborne transmission. He was assisted in this investigation by then Harvard medical student Richard Riley, with whom he shared credit for making the distinction between ordinary large respiratory droplets and so-called droplet nuclei – the dried residua of larger respiratory droplets. He ultimately published a comprehensive exposition of his theories and observations in his now classic 1955 text ‘Airborne contagion and air hygiene’, much of which remains valid to this day.8 Riley later updated and summarized this work in his 1961 monograph Airborne Infection and Control.