24 • Keith Manchester 



isolated from clinical material are tubercle bacilli. Such bac- 

 teria may be regarded as opportunist pathogens. 



At present, there is not total agreement on the taxonomy of 

 the bacilli causing tuberculosis in man and in cattle. One 

 taxonomic opinion regards the responsible mycobacteria as 

 separate species, M. tuberculosis, M. bovis, and M. afri- 

 canum. Alternatively, these are considered to be variants of 

 the single species M. lubenulosis. and there are noted to be 

 five recognizable variants of this species (Collins and Grange 

 1983:19). Differentiation, regardless of taxonomic debate, is 

 based on in vitro growth characteristics, aerobic status, and 

 enzymatic properties (Grange 1980:22; Collins and Grange 

 1983: 17), but differentiation into these separate strains has no 

 clinical value. 



However, while the dialectic of taxonomy may be relevant 

 to the evolution of tuberculosis as a human disease, the im- 

 munity induced by infection by the various bacilli is common 

 to them all. 



Immunology 



The basis of host defense against infection is twofold: innate 

 nonspecific immunity, and acquired specific immunity. 



Natural or innate immunity is not directed at any specific 

 invading organism. It is of multifactorial component and 

 consists of biological host factors such as secretory and me- 

 chanical barriers to invasion by pathogens, bactericidal prop- 

 erties of body fluids, phagocytic cellular activity, and deter- 

 minants such as general health and nutritional status, age, 

 and hormonal balance (Weir 1986:42-44). It is thus depen- 

 dent upon the milieu inteheur. In socioeconomically unsta- 

 ble archaic communities this innate immunity must surely 

 have played an important role in the epidemic and endemic 

 infections of antiquity. This is mirrored today, perhaps, in the 

 famine and war-torn peoples of the Third World, and the 

 attendant endemic and fulminating epidemic infections. 



But it is the second immune mechanism which is of partic- 

 ular interest in M. leprae and M. tuberculosis interrelation- 

 ship. This is the acquired mechanism of adaptive immunity, 

 characterized by memory, specificity, and the recognition of 

 "non self" (Roitt 1980:1). The recognition of non self is 

 axiomatic and refers to the specific antigens, in the present 

 case M. leprae and M. tuberculosis. Memory too is implicit; 

 exposure to the specific pathogen (antigen) induces long- 

 term host protection to future infection and development of 

 clinical disease. Specificity in the immune response depends 

 principally upon the host synthesis of antibody (immu- 

 noglobulin) to a specific antigen and its release into the blood 

 and other body fluids. This is the very basis of humoral 

 immunity. There is no evidence that humoral immunity plays 

 any significant role in the defense mechanisms against my- 

 cobacterial infection. It is another distinct acquired immune 

 mechanism which is active in mycobacterial infection: cell 

 mediated immunity (CMI). M. leprae and M. tuberculosis 

 are intracellular facultative parasites inducing, ipso facto. 



LEPROMATOUS 



TUBERCULOID 



Figure 1 . The spectrum of immunity and clinical disease in 

 leprosy. (After Jopling 1982:296) 



pathological change and clinical disease. Upon invasion of 

 the body, the mycobacteria are ingested by phagocytic cells 

 (macrophages), and the bacterial intracellular faculty stimu- 

 lates action by T lymphocytes. The stimulated T lympho- 

 cytes produce and release a biologically active molecule 

 called lymphokine. Within this group of substances are fac- 

 tors which influence the activity and movement of mac- 

 rophages. The macrophage so influenced produces a greater 

 intracellular content within itself of lysosomal enzyme. This 

 increased enzyme content heightens the ability of the mac- 

 rophage to kill intracellular parasites contained within it. 

 This, the basis of CMI, and considered very superficially 

 here, is complex when applied to A^. /cprac infection with the 

 broad immune, and consequent clinical spectrum. In tuber- 

 culosis, host immunity is absolute; clinical response to infec- 

 tion is not dependent upon and modified by a gradation of 

 immunity, either innate or acquired. By contrast, it has been 

 demonstrated (Ridley and Jopling 1966; Jopling 1982:296) 

 that there is a spectrum of host immunity to M. leprae infec- 

 tions, and it is the status of the individual within this spec- 

 trum which determines the severity and type of clinical dis- 

 ease, and its infectivity, within the individual (Figure 1 ). The 

 concept has also been applied in paleopathology (Andersen 

 1982:223). At one end of the spectrum is the state of absence 

 of immunity, that is, low resistance to the pathogenic effects 

 of invasion by M. leprae. The resultant clinical disease is 

 lepromatous leprosy, a multibacillary condition charac- 

 terized by high infectivity. At the other end of the spectrum is 

 the state of high immunity, or high resistance to the pathogen. 

 In this state the clinical disease is tuberculoid leprosy, 

 paucibacillary and of low infectivity. There is gradation of 

 clinical presentation and infectivity between these extremes. 

 Indeed, beyond the high-resistant tuberculoid end of the 

 spectrum lies the concept of subclinical infection, a state of 

 noninfective bacterial presence within the host, but without 

 pathological manifestation. Paleopathologically, the low- 

 resistant, lepromatous or near lepromatous state is uniquely 

 differentiated by its development of rhinomaxillary change 

 (Andersen 1982:223). It is a reality, dependent upon such 



Zugrel) Paleopalhology Symp I'iHS 



