Tuberculosis and leprosy: Evidence for interaction of disease • 33 



mode of transmission is common to both infections, although 

 the additional mode of gastrointestinal tuberculosis is distinct 

 to the tubercle bacillus. Pulmonary tuberculosis and leprosy 

 are, therefore, diseases dependent for their transference upon 

 {wpulation density and intimacy of contact. Both diseases are 

 more common in socially and economically disadvantaged 

 groups: they are. in the main, disea.ses of the poor. 



Thus it is expected that those factors, significant in the 

 epidemiology of the two diseases, would influence infection 

 by M. tuberculosis and M. leprae in the same direction. For 

 example, in the absence of other influences, a deterioration 

 or improvement in the socioeconomic status of the popula- 

 tion would be expected to produce, respectively, an increase 

 or a decrease in the incidence rates of both tuberculosis and 

 leprosy. Increasing population density would be expected to 

 favor increasing incidence rates of both diseases. 



But, in spite of these common influential factors, the two 

 diseases did not move in parallel in British antiquity. The 

 increasing prevalence of both diseases during the late Anglo- 

 Saxon and early post-Norman Conquest periods has been 

 outlined, but the continued increase of tuberculous preva- 

 lence and the simultaneous and rapid decline of leprosy in the 

 later Middle Ages is a major fact. 



Ikwueke has proposed ( 1984: 1357) that in the concept of 

 aging disease, there is a gradual decline in severity, and that 

 disease eventually declines and dies. This phenomenon is 

 proposed in the absence of effective therapy. From the cen- 

 turies of coexistence in antiquity, osteoarcheological and 

 documentary evidence does not support the tenet of declining 

 severity in tuberculosis and leprosy. Within the constraints of 

 archeological stratigraphy already considered, there is no 

 paleopathological evidence to suggest that leprosy, during its 

 period of epidemiological decline, declined in severity. But 

 in this context it is acknowledged that a decline in severity, 

 that is, a "population upgrade in immunity" from lep- 

 romatous to tuberculoid leprosy, may be accompanied by a 

 gradual disappearance of pathognomonic bone change. 

 Thus, an absence of osteological evidence of severity decline 

 may not be truly evidence of absence. This problem remains 

 unresolved. The corollary of the decline in severity proposed 

 by Ikwueke is the decline and disappearance of the disease. It 

 is true, of course, that both diseases have declined in Britain, 

 and that leprosy has disappeared as an endemic disease. The 

 decline of tuberculosis was, however, a phenomenon of the 

 post-Industrial Revolution era, even before the advent of 

 antituberculous chemotherapy, whereas leprosy decline was 

 some 500 years or so previous and was a much more rapid 

 phenomenon. Was, perhaps, segregation a factor influencing 

 this medieval decline of leprosy? It has been noted that the 

 incubation period of leprosy is long, during which time there 

 are no clinical manifestations to warrant segregation, and 

 during which time the infected individual was, himself, in- 

 fectious. As a preventative of transmission, segregation was 

 clearly of limited value because the practice was akin to 

 "shutting the stable door when the bacterial horse has 



Zagrrb Pahopaihotogy Symp. 1988 



bolted." Also, as noted (v.s.). segregation of infected indi- 

 viduals in the medieval community was not absolute. 



Genetic immunity is of unknown, but probably little, sig- 

 niflcance in tuberculosis and leprosy. Ikwueke comments 

 (1984:1357) that there is growing evidence which makes 

 transmission of acquired features a feasible proposition. 

 How far this is applicable to immunity is unknown. 



An equally vexed problem is that of genetic susceptibility 

 to the two diseases. Fine (1981:452) remarked that there is 

 evidence, albeit contentious, for some role of genetic factors 

 in determining responses in leprosy and tuberculosis, al- 

 though a "major role of genetic polymorphisms in determin- 

 ing epidemiological patterns" is unconvincing. Thus, al- 

 though there may be some genetic influence in the initial 

 setting of an individual on the immune spectrum in leprosy, it 

 is doubtful if genetic factors are an influence, ah Initio, in the 

 susceptibility of individuals to infection by M. tuberculosis 

 or M. leprae. 



INTERACTION 



As already discussed, immunity in both leprosy and tuber- 

 culosis is cell mediated, and antibodies have been considered 

 unimportant, although in leprosy this matter is under review 

 (Harboe 1981:5-6). The cell mediated immunity is not abso- 

 lutely pathogen specific, as indicated in the varying response 

 to infection by M. leprae following prior inoculation with 

 BCG. 



The concept of cross immunity between leprosy and tuber- 

 culosis was examined in depth by Chaussinand ( 1 948 . 1 950), 

 and by Lowe and McNulty (1953). Chaussinand's proposals 

 are based on epidemiological observations of the two dis- 

 eases in Africa. India. Indochina, and Japan. Immunological 

 evidence in support of cross immunity is outlined earlier in 

 this paperfv.i. j. Consideration of cross immunity in relation 

 to the history of the two diseases in mankind has also been 

 made by Steinbock (1976:197-198), Grmek (1983:291- 

 306), Manchester (1984), and Clark et al. (1987:50-51). 



What support then does paleocpidemiology afford to the 

 concept of cross immunity and interaction of disease? 



It is suggested that, within the village-orientated and rela- 

 tively isolated communities of the sub-Roman and Anglo- 

 -Saxon periods, tuberculosis was of primary gastrointestinal 

 focus due to M. bovis. Infection was sporadic and overall 

 population immunity was insignificant. Both leprosy and 

 tuberculosis smoldered unabated. Toward the end of the 

 Anglo-Saxon period, townships and markets developed. 

 These aspects developed particularly with the Norman and 

 later towns and cities. Population density, consequent upon 

 this development, prompted respiratory transmission of A/. 

 tuberculosis. The introduction of Touching for King's Evil, 

 an indication of droplet transmission, is in support. Crowd- 

 ing of peoples facilitated the widespread urban, and to a 

 lesser extent rural, exposure to the tubercle bacillus. Then, as 

 in more modem context, the primary infection was probably 



