174 • Mary Lucas Powell 



Table 1. Tuberculosis and endemic treponematosis: comparison of morbid and mortal effects 



Pathogen 



Mode of infection 

 Modal age at exposure 

 Modal age at onset 



of disease 

 Duration of infectious 



state of patient 



Initial lesions 

 Subsequent lesions 

 Prevalence of disease 



in endemic contexts 

 Prevalence of skeletal 



involvement 

 Predominant skeletal 



response 

 Skeletal regions 



typically affected 



Potential for mortal 

 effect 



Tuberculosis 



Treponematosis 



EPIDEMIOLOGY 



Mycobacterium 



tuberculosis 

 Respiration, ingestion 

 Childhood 

 Late adolescence, 



early adulthood 

 Decades (with 



latent periods) 



Treponema pallidum, 

 T. pertenue 

 Skin lesions 

 Childhood 

 Childhood 



5-10 years 



PATHOLOGY 



Lungs, hilar lymph nodes 

 Any organ system 

 10-50% of exposed 

 individuals 

 3 - 15% of cases 



Major: osteolytic 

 Minor: osteoblastic 

 Spinal column, 



hip and knee joints, 



ribs, sternum 



Moderate to high 



Mucocutaneous tissues 

 Mucocutaneous tissue, bone 

 Virtually 100% of exposed 

 individuals 

 50-75% of cases 



Major: osteoblastic 

 Minor: osteolytic 

 Tibia, fibula, humerus, 



radius, ulna, clavicle, 



cranial vault, 



nasopalatal region 

 Low 



Sources: Hackett 1951, Hoeprich 1977, Hudson 1958, Kelley and Micozzi 1984, Myers 1951, 

 Ortner and Putschar 1981, Robbins and Cotran 1980 



teolytic lesions of the external cranial vault and nasopalatal 

 region), many more exhibited minor nonspecific bone reac- 

 tions (periostitis of long bone shafts, particularly the tibia, 

 fibula, ulna, radius and clavicle). Subsequent radiographic 

 examination of these patients indicated long-term persistence 

 of bone changes after the disappearance of the clinical symp- 

 toms. 



Commenting upon the high level of moderate skeletal mor- 

 bidity without associated mortality, Hackett concluded that 

 "it is improbable that septic infection of the bones is responsi- 

 ble for the changes seen. Untreated septic infection of the 

 extent necessary to produce the wide spread changes seen in 

 some cases would be accompanied by grave general symp- 

 toms and high mortality; whereas the patients showing these 

 bone lesions were not severely ill. although they suffered 

 considerable discomfort" ( 1 95 1 : 1 3). Studies of yaws in other 

 populations (Grin 1956) and of endemic syphilis in Bosnia 

 (Grin 1953) and in southern Africa (Murray et al. 1956) 

 present similar pictures of the biological costs of these dis- 

 eases. 



Zagreb Paleopathology Symp. 1988 



Tuberculosis is a chronic infectious disease caused by the 

 gram-negative Mycobacterium tuberculosis. Clinical studies 

 indicate that in endemic contexts, most people are infected in 

 infancy or childhood, but more than half of the exposed but 

 otherwise healthy individuals may never develop clinical dis- 

 ease (Myers 195 1 ). Individuals with poor immune response 

 may develop primary lesions within the lungs and hilar 

 lymph nodes. If death does not ensue during the primary 

 infection, the invading pathogens may be encapsulated by 

 calcified tissue. This response halts immediate progression 

 of the disease, but the organisms remain viable for decades 

 (Robbins and Cotran 1980). Localized foci may rupture and 

 spread mycobactena via direct or hematogenous dissemina- 

 tion throughout the body, affecting all types of tissue includ- 

 ing bone. Reinfection from active cases or reactivation of 

 latent foci because of severe systemic stress may produce 

 acute symptoms later in life (Hoeprich 1977). 



In chronic tuberculosis overstimulation of immune re- 

 sponses in sensitized tissues may result in such proliferation 

 of granulomatous tissue within the lungs that pulmonary 



