First, a quick note about the disease itself. Leprosy is a chronic infectious disease, and is caused by a parasite known as Mycobacterium leprae (Roberts and Manchester 2005:194). Leprosy is not highly infectious, and most who acquire the disease have had a history of long-term contact with infected individuals (Larsen 1997:104). Studies by Job et al. (2007) indicate that the M. leprae can be contracted from human contact with the infected skin or due to nasal mucosa and skin cells of the infected being released into the environment. Once an individual has been infected, and the bacteria have had time to develop, the skin and nerve cells are the first to be affected by the disease. The bacteria proliferate within the nerves, which damages them and causes a loss of sensation. Due to the anesthetized nerves, victims are prone to repeated accidents on their fingers and toes which leads to infection and deformation (Eichman 1999:494). Swelling, lesions, tissue destruction, loss of hair and teeth cause the faces of many infected individuals to become severely deformed (Roberts and Cox 2003:267). After the disease infects the bone marrow the skeleton weakens, leaving the individual prone to fractures and deformation (Rawcliffe 2006:3).
While leprosy can be easily identified by the lesion prone flesh and discoloration of the skin cells, these indicators are not useful for identifying the disease in historical populations. The primary evidence for leprosy within the archaeological record is the skeletal remains of those who were infected. Due to its slow pace, the longevity of infected individuals and proclivity to deformation of the body, leprosy can be readily identified in skeletal remains (Stanford and Stanford 2002:26). Damage to the bone can be found in the face, hands, feet, tibia and fibula (Roberts and Manchester 2005:195). The bone can be found within a wide range of healing and destruction depending on when death within the individual occurred. As a result, it is important to recognize that the skeletal indicators can be severe or minor, and some may even be absent depending on the victim’s immunity, nutrition and overall social environment (Ortner 2002:73-74).
In order to best interpret data from the past, the skeletal markers of leprosy have been derived primarily from studies which have used medieval cemeteries and skeletal collections as the source of their information. Known as facies leprosa, the changes in the cranium consist of “the progressive erosion of the alveolar process of the maxilla with the loosening and ultimate loss of the central and lateral maxillary incisor teeth” (Manchester 1984:167). The bone within the jaw is reabsorbed, which often causes the front teeth to fall out. Infection and inflammation around the mouth can also lead to pitting of the maxilla, mandible and palatine bones (Cook 2002:82). Due to the infection of the nasal tissue, the nasal aperture also becomes swollen, leading to bone remodeling and inflammation the conchae and septum (Roberts and Manchester 2005:198). Severe infection can lead to bone atrophy in both the nasal and maxillary regions of the face (Larsen 1997:105).
Overall, post-cranial bone may show a variety of irregular bone formations due to healing of bone lesions, or small pitting when unhealed (Manchester 2002:69). This is due to infection of the skin progressing into the underlying bone. Post-cranial damage to the skeleton occurs mainly in the hands and feet due to the proliferation of bacterium in these areas. Re-absorption of the bone and the proclivity to trauma and infection cause the loss of the phalanges and the distal heads of the metacarpels or metatarsels (Roberts and Cox 2003:268). Infection in the feet can spread to the lower leg, the tibia and fibula through the nerves, causing periostitis (Roberts and Manchester 2005:196). Periostitis is a non-specific infection of the periosteum of bone occurring as new bone buildup on the surface of the bone. There is also a tendency for bone to become irregular and inflamed as infection worsens. (Manchester 2002:70). It is the overall pattern of infection, in addition to temporal and spatial location, that lead to diagnosis since a number of these pathologies can be due to other infections and the full range only occurs in the most severe cases.
Studies of leprous skeletal collections continue to define and increase understanding of the extent of leprosy. One of the first to conduct archaeological excavation of leper cemeteries was Vilhelm Møller-Christensen in the 1930’s, when information on leprosy was still veiled in religious superstition and social stigma (Bennike 2002:136). He argued that the pathognomonic, or diagnostic, indicator of leprosy was the presence of facies leprosa. He concluded this from four Danish leper hospital excavations, and a variety of cases throughout the United Kingdom and France. His excavations at Naestved, Denmark alone led to the recovery of 650 skeletons (Larsen 1997:104). It is Møller-Christensen’s studies that most paleopathologists use as the base reference when ascertaining whether their skeletal findings are considered leprous.
Other excavations of leper cemeteries, specifically those in the United Kingdom, that have added to this data include: South Acre cemetery in Norfolk (Wells 1967), burials in Orkney (Taylor et al. 2000), St. James and St. Mary Magdalene in Chichester (Lee and Magilton 1989), St. Margaret in High Wyncombe (Farley and Manchester 1989), St. Leonard in Newark (Bishop 1983), St. Patrick in Armory (Murphy and Manchester 1998), and many more. Excavations of more cemeteries and their corresponding hospitals and churches continue to add to the paleopathological evidence of leprosy. As we will see in the next section, it is important to understand the real impact of leprosy on individuals in comparison to the medieval construction of the leper (Roberts and Cox 2003:269).
Works Cited will be posted at the end of this series