26 • Keith Manchester 



the respiratory tract from inhalation of droplets infected by 

 M. tuberculosis and exhaled by a person with open, infec- 

 tious, pulrnonary tuberculosis. The primary lesion is there- 

 fore in the respiratory tract, either tonsillar bed or, more 

 commonly, lung. Because of this mode of transmission, pul- 

 monary tuberculosis may be considered to be a population 

 density-dependent disease (v.i.). 



The incubation period, that is the latent interval between 

 implantation of bacillus and the development of clinical dis- 

 ease, in tuberculosis is long. Dependent upon the course of 

 development of tuberculous infection, the incubation period 

 may vary from two years to several decades. In terms of 

 immunity, these figures are largely meaningless and depend 

 upon interpretation of clinical disease. The first manifesta- 

 tion of infection, termed primary tuberculosis, consists of an 

 infected lesion at the site of entry of bacilli, and associated 

 infective change in regional lymph nodes. This state, which 

 may be without clinical symptoms, is associated with the 

 development of immunity to further infection. Thereafter, 

 and dependent upon such other factors as general health sta- 

 tus, there may be complete resolution of the primary complex 

 but with maintenance of immunity. Survival of the individual 

 and restoration of total health ensues. The end result is a 

 healthy person immune to tuberculosis and, in some mea- 

 sure, to other mycobacterial diseases. Alternatively, the pri- 

 mary infection may progress as a disseminated, fulminating, 

 and fatal disease with distant organ involvement or miliary 

 lesions. Whatever the mortal presentation, these individuals 

 are removed from the scene of population immunity and are, 

 therefore, irrelevant to the present discussion. Those individ- 

 uals surviving the primary lesion and restored to health may, 

 at some future date, subject to a deterioration of general 

 health status or to the development of intercurrent infection. 

 develop progressive tuberculous disease. This post-primary 

 or secondary infection may be the result of reactivation of 

 quiescent primary lesions, or the result of reinfection by the 

 pathogenic organism. The difficult differentiation in the 

 etiology of post-primary tuberculosis between reactivation or 

 reinfection is of significance epidemiologically and may be 

 of significance in the history of the disease. The endogenous 

 or exogenous .source of bacilli is of no significance in the 

 clinical course of the disease or in immunological status. 

 Post-primary infection is the familiar disease of adulthood, 

 characterized pathologically by progressive granulomatous 

 and caseating lesions, and clinically by progressive emacia- 

 tion, cough, dyspnea, and hemoptysis in pulmonary disease 

 and abdominal pain, distension, and pyrexia in gastrointesti- 

 nal disease. Subsequently, other organ involvement may en- 

 sue, and bone and joint infection are of major importance in 

 osteoarcheology. 



To repeat and stress however, it is the primary infection in 

 tuberculosis, with tuberculin conversion indicating immu- 

 nity, which is of significance in the immune profile of the 

 surviving individual and, through his place therein, of the 

 population as a whole. 



After many years of uncertainty, it has now been demon- 

 strated that the clinically important mode of transmission of 

 M. leprae is by inhalation of infected droplets from a leprous 

 individual harboring bacilli in his nasal mucosa (Jopling 

 1982:295). Transmission of leprosy is, therefore, largely 

 from individuals with multibacillary disease, that is, those 

 from the low-resistant end of the immune spectrum. The 

 criteria for such infectivity is the presence of a "highly 

 bacilliferous nasal discharge" (Pedley and Geater 1976:97). 

 The infectivity of paucibacillary. tuberculoid leprosy is 

 slight. In contrast to earlier thought, it is now considered that 

 leprosy, from Icpromatous cases, is a highly infective dis- 

 ease, but that, because of the immune status, only a small 

 proportion of people infected with the bacillus actually de- 

 velop clinical disease. 



The incubation period of leprosy is. like tuberculosis, of 

 uncertain and long duration, probably between two and sev- 

 en years (Jopling 1982:296). 



Unlike tuberculosis, the pathogenesis of leprosy is not 

 biphasic. There is no primary and secondary complex in 

 leprosy. As previously noted, M. leprae is an intracellular 

 pathogen, and has an affinity for Schwann cells of peripheral 

 nerves and for cells of the reticuloendothelial system. After 

 infection, tissue change and consequent clinical disease is 

 progressive, modified only by the immune status, and 

 change therein, of the host. Although, as yet. the stage of 

 development of acquired immunity in leprosy is incom- 

 pletely understood, it has been demonstrated by immunolog- 

 ical testing in Micronesia and Sri Lanka that an immunity has 

 developed from three months to two years before the onset of 

 clinical disease (World Health Organization 1985:23). 



Leprosy, unlike tuberculosis, is generally not a fatal dis- 

 ease. It is a relentlessly progressive and mutilating disease, 

 but further discussion of the clinical symptoms and signs of 

 the disease is beyond the scope of this paper. 



AGE 



In tuberculosis, the development of CMI is coincident with 

 the pathological changes of primary infection. Tuberculin 

 sensitivity is a codevelopment of CMI. albeit associated with 

 antibody production, itself of little significance in the tuber- 

 culous defensive mechanism. Tuberculin sensitivity conver- 

 sion can however be taken as a guide to the acquisition of 

 immunity and, as a corollary, to the period of primary infec- 

 tion. Unfortunately, the age of conversion is incompletely 

 known for modem developed nations and is almost com- 

 pletely unknown for undeveloped nations. It follows, by na- 

 ture of the evidence, that the age of conversion can never be 

 known for archaic peoples. Neither, of course, can it be 

 known for more recent peoples before the advent of tuber- 

 culin sensitivity testing. Some other guide to primary infec- 

 tion, appropriate, by extrapolation, to archaic peoples must 

 be used. 



If the death rate from tuberculosis, by year of death, is 



Ztij^reb Paleopathology Symp. I98H 



