Tuberculosis and leprosy: Evidence for interaction of disease • 27 



examined from the prechemolherapeutic era, it is noted (Fine 

 1984: 14 1 ) that the highest mortality occurs before the age of 

 five years, failing dramatically thereafter and rising again 

 markedly in the third decade (Figure 2). This may be inter- 

 preted as a high infant mortality associated with primary 

 infection and a further high and sustained mortality with 

 fwst-primary infection, if these late 19th century data can be 

 assumed representative of medieval populations, then initial 

 exposure to M. nihcnulosis and the development of primary 

 infection and consequent immunity occurred during infancy. 

 Because the ELISA test for leprosy infection is a relatively 

 recent introduction which has not. as yet, had a wide applica- 

 tion in epidemiology, age patterns in leprosy can be deter- 

 mined only in relation to clinical disease. The age of in- 

 fection and, in consequence, the age of development of 

 immunity, are unknown. However, the age of infection is, 

 post hoc propter hoc, dependent upon the age of contact of an 

 individual with an infective case. It is also dependent upon 

 the intimacy of contact (v.i.). In infected families young 

 children are likely to have more intimate contact than older 

 individuals, and therefore the young are more likely to be- 

 come infected (Badger 1964:84). Clinical disease is rarely 

 encountered below the age of five years. The incidence then 

 rises to a plateau in the fourth decade. With acceptance of the 

 long and variable incubation period, it seems likely that the 

 age of infection in leprosy may be somewhat later than that 

 for tuberculosis. Thus the age of development of acquired 

 immunity may, likewise, be somewhat later. 



700- 



600- 



500- 



o 

 o 



o 



cr 



LlJ 

 Q- 



a: 



I 

 < 



200 



100- 



20 



30 40 50 60 70 



AGE AT DEATH 

 (IN YEARS) 



Figure 2. Tuberculosis death rates by year 

 of death, late 19th century, Massachusetts. 

 (After Fine 1984:141) 



SEX 



Although variations according to age and sex in incidence 

 rates of both tuberculosis and leprosy as clinical diseases are 

 known, it is considered that the sex variation has little bear- 

 ing on the proposed immunological interrelationship. Further 

 analysis is, therefore, not relevant within this paper. 



POPULATION DENSITY 



Leprosy has been described as a "disease of the villages" 

 (Hunter 1986:5). But against this generalization, there is 

 considerable evidence that household contacts of patients 

 with lepromatous disease are at a high risk of infection. 

 Epidemiological studies in Burma, South India, and the Phil- 

 ippines has indicated a familial clustering of infection (World 

 Health Organization 1985:23-24). It is noted (Badger 

 1964:72) that the more intimate the contact the greater the 

 risk of infection, and the risk of infection is greater with 

 intrafamilial than with cxtrafamilial contact. In keeping with 

 this, the rate of infection is also influenced by the number of 

 contacts to whom an individual is exposed. Such interpreta- 

 tion of familial susceptibility is also complicated by the influ- 

 ence of socioeconomic status, hygiene, nutrition, and a "ge- 

 netically determined susceptibility" of blood relatives. 

 Studies suggest that there is an association between crowding 



Zagreb Paleopalhology Symp. 1988 



and leprosy, but the problems of poverty and mobility of 

 peoples further complicate the picture. The inhalation mode 

 of transmission of A/, leprae suggests that crowding of peo- 

 ples and intimacy of contact are important epidemiological 

 factors. Therefore, it is expected that leprosy is a disea.se of 

 village and urban communities alike. 



Buikstra and Cook ( 1 98 1 : 1 1 8) described tuberculosis as a 

 population density-dependent disease, and Cockbum ( 1963:88) 

 also considered the disease to be a crowd disease of urban 

 society. However, with regard to the different modes of trans- 

 mission of M. bovis and M. tuberculosis and, in conse- 

 quence, to the diHerent primary manifestations and immu- 

 nity therefrom, the relation, in immunological perspective, 

 of infection to pt)pulation density may be twofold. Primary 

 gastrointestinal disease caused by M. bovis is dependent 

 upon human contact with an animal reservoir of tuberculous 

 beast. Herd size, not human population size, is the critical 

 factor for cndemicity of human primary gastrointestinal tu- 

 berculosis (Manchester 1986). Thus, this disease is likely to 

 atTect urban and rural peoples alike, assuming the general 

 availability of milk and flesh. The growth of markets in 

 medieval towns and cities in Britain is likely to favor urban 

 exposure. Pulmonary tuberculosis is, in contrast, entirely 



