164 • Jane E. Buikstra and Sloan Williams 



1958). We therefore may simply be documenting a flexible 

 host-parasite relationship. An alternative suggestion is the 

 possibility that the prehistoric tuberculosis-like pathology 

 described in Illinois and elsewhere in the Americas was 

 cau.sed by a pathogen other than M. tuberculosis (Buikstra 

 1981; Clark et al. 1987; Eisenberg 1986; Klepinger 1982; 

 McGrath 1986,1988). 



Atypical /en vironmental mycobacteria 



Recently, Clark and co-workers ( 1987) have underscored the 

 importance of considering mycobacteria other than M. tuber- 

 culosis when assessing the impact and origins of the 

 tuberculosis-like lesions of prehistoric tissues in the Amer- 

 icas. 



What is known about the ecology of mycobacterial disease 

 raises the possibilities that pre-Columbian "tuberculosis" 

 was caused ( 1) by M. tuberculosis but in a population im- 

 munized by exposure to environmental ("atypical") my- 

 cobacteria; (2) by M. tuberculosis but a strain of low 

 virulence; (3) by M. bovis transmitted by wild animals 

 (e.g., butchering and tanning skins of infected bison), with 

 infection resulting in self-limiting disease and long-lasting 

 immunity; and/or (4) by one or more of the environmental 

 mycobacterial species. (Clark et al. 1987:51) 



In general , individuals who commented on this manuscript 

 commended the authors for emphasizing the dynamic nature 

 of host-parasite relationships. The possibility that the en- 

 vironmental mycobacteria are heavily implicated in late pre- 

 historic populations from the Americas is, however, ques- 

 tioned. Katzenberg (1987:52) and Klepinger (1987:52), for 

 instance, emphasize that the prevalence of observed 

 tuberculosis-iike pathology reported for late prehistoric pop- 

 ulations in North America is consistent with an infectious 

 disease spread by host-to-host transmission. The environ- 

 mental pathogens are rarely, if ever, transferred between hu- 

 mans (Lincoln and Gilbert 1972; Sommers 1979; Wolinsky 

 1979). 



Steinbock (1987:56) points out that the calcified Ghon 

 complexes reported by Allison and co-workers (1981) for 

 two prehistoric and one colonial period South American re- 

 mains are simply not consistent with disease caused by en- 

 vironmental mycobacteria. Even though the environmental 

 mycobacteria could have produced the acid-fast reaction 

 noted by Allison and co-workers (1973), he considers the 

 calcified Ghon complex specific to tuberculosis. 



Kelley and Eisenberg have suggested that the skeletal le- 

 sions produced by the environmental mycobacteria are "es- 

 sentially identical" to those produced by M. tuberculosis 

 (1987:94). A similar argument is offered by Clark et al. 

 (1987:48-49). This generalization would appear, however, 

 open to debate. In fact, the sources cited by Kelley and Eisen- 

 berg in support of this statement are either silent (Good 1 980) 

 or rather ambiguous concerning the form and distribution of 



skeletal lesions. Wolinsky (1974:645) notes that "several 

 cases of M. kansasii disease of the bones and joints are on 

 record" but does not provide a comparison of the skeletal 

 lesions characteristic of tuberculosis and those caused by the 

 environmental pathogens. In more recent work, Wolinsky 

 (1979) reviews a number of cases of both disseminated and 

 localized infections caused by the atypical mycobacteria. In 

 so doing, he emphasizes occupational trauma as a major 

 factor influencing the distribution of skeletal lesions. Deep 

 hand infection is emphasized, with fewer cases reported for 

 the wrist, hip, knee, spine, and calcaneum. This review indi- 

 cates that while the form taken by specific skeletal lesions 

 may resemble tuberculosis, neither lesion location nor age- 

 specific patterning mirrors that expected for tuberculosis 

 (Wolinsky 1979). 



In fact, when case studies are reviewed, it appears that 

 both age-specific patterning and intraindividual lesion dis- 

 tributions for environmental mycobacterial infection difler 

 from tuberculosis (Ellis 1974; Halla et al. 1979; Halpem and 

 Nagel 1978; Lakhanpal et al. 1980). Vertebrae may be af- 

 fected, but there is no convincing evidence of a tuberculosis- 

 like predilection. Lakhanpal and co-workers, for instance, 

 emphasize that the clinical, radiologic, and histologic ap- 

 pearance of the lesions caused by M. kansasii is distinctive 

 from that of tuberculosis. "It seems as if the basic pathology 

 of lesions caused by these organisms is different from the one 

 caused by Mycobacterium tuberculosis" (Lakhanpal et al. 

 1980:473). 



Lincoln and Gilbert ( 1972:697) point out that "disease of 

 only one area of the skeletal system was reported infre- 

 quently" in their survey of children suffering from disease 

 caused by acid-fast bacilli other than M. tuberculosis and M. 

 bovis. They conclude that the disseminated mycobacterioses 

 attributed to the atypical forms most closely resemble a "ma- 

 lignant type of reticuloendotheliosis" (Lincoln and Gilbert 

 1972:708), not tuberculosis. 



For individual lesions, however, bony involvement in dis- 

 ease caused by environmental mycobacteria could mimic 

 expectations for osseous tuberculosis (e.g., a 14-year-old 

 male with lumbar vertebral and sacroiliac involvement; Ellis 

 1974). Even so, it is difficult to disagree with Steinbock's 

 comment: "It is inconceivable that one of these forms |of 

 environmental mycobacteria] could be the pathogen for pre- 

 Columbian tuberculosis" (1987:56). 



The geographic distribution and balanced gender ratios 

 observed in North American prehistoric samples would also 

 argue against acquisition through butchering or other occu- 

 pations that would place an individual at risk for environmen- 

 tal mycobacteria, as Clark et al. (1987) have argued. Thus, 

 although it certainly is possible that these pathogens may 

 have caused a few of the lesions reported in prehistoric series 

 and they may likewise have influenced the expression of 

 disease in certain individuals, it is unlikely that they can be 

 seriously implicated in the vast majority of prehistoric exam- 

 ples. 



Zagrrb Paleopathology Symp. 1988 



