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Artefacts & Environmental Evidence: The Human Bone

Malin Holst HND BA MSc

introduction | osteological analysis | palaeopathological analysis | dental pathology | discussion & summary

introduction | conjenital disease | metabolic conditions | infectious disease | joint disease | trauma | neoplastic disease | miscellaneous pathology | cremated | disarticulated | conclusion

3.4 Infectious Disease

Before the advent of antibiotics, infectious disease was one of the greatest causes of fatalities. 'In the past, mortality, morbidity and misery wrought by micro-organisms far exceeded that of warfare and famine.' (Roberts and Manchester 1995, 124). Indeed '...our first recordings of human history tell of plagues and pestilences playing havoc among armies and populations from the earliest times onwards, and infectious disease has probably been the major cause of death in all periods and all ages in our history.' (Birkett 1983, 99).

Infectious diseases encompass respiratory and gastrointestinal infections, influenza, tonsillitis and bronchitis, and epidemics such as plague or smallpox. They also include diseases which are still common today, such as measles, pneumonia, appendicitis or meningitis. However, evidence for infectious disease is relatively rare in skeletons as compared with the actual numbers of individuals who have suffered from infections, in particular because transmission and death can be rapid, and frequently occurs before the skeleton becomes affected (Grauer 1993, 204). Skeletal evidence only develops when the disease is chronic and affects the actual bone; example of such diseases include syphilis and leprosy, as well as dental abscesses and sinusitis.

Infections can be sub-divided into specific and non-specific infections. Specific infections include leprosy, syphilis and tuberculosis and can be diagnosed if the disease's characteristic distribution and expression of lesions can be observed in the skeleton. Non-specific infections are those which cannot be attributed to a specific disease. They might represent a minor inflammation following trauma, or the early stages or single expression of a specific infection. Non-specific infection is commonly observed in archaeological populations, particularly in those from the medieval period. The lesions can affect the bone surface (periosteal inflammatory lesions), the bone cortex (osteitis) or the medullary cavity of the bone, which contained the marrow (osteomyelitis), or all three bone elements (Roberts 2000 a, 1 46).

3.4.1 Periosteal inflammatory lesions

Periosteal inflammatory lesions are the most common type of non-specific infection found in archaeological skeletons (Birkett 1983, 102). The lesions may manifest in the form of proliferative grey woven bone which adheres to the outer bone surface while the inflammation is active (Plate 4, right). Alternatively, if the inflammation is subsiding, it is characterised by remodelling lamellar lesions, in the form of integrated longitudinal striae on the bone surface. Other expressions of periosteal inflammation include porosity and hypervascularity.

The cause of periosteal inflammatory lesions is currently not fully understood, although it is known that they can manifest as a result of leg ulcers, varicose veins or haematomas (blood clots) (Roberts and Manchester 1995, 130). The lesions may also be the extension of a soft tissue infection, or can be manifestations of a generalised infectious disease, such as leprosy or syphilis (Aufderheide and Rodríguez-Martín 1998, 179). Periosteal inflammatory lesions have also been attributed to direct and minor trauma. Detailed analyses of periosteal inflammatory lesions has been carried out in modern child abuse cases, where the lesions could be attributed to forceful handling of a child, hitting with hands or objects, and instances in which the child was beaten against an object. The periosteal reaction in these cases is due to compressive forces which cause tissue damage and internal bleeding ibid, and tend to form a few days after the injury was sustained. However, in adults such reactions may only begin to form after two weeks ibid, 205).

All children's age groups, with the exception of the adolescents, displayed a considerable number of periosteal lesions (Table 24). However, in children, these lesions may not simply be inflammatory in origin, but may represent normal bone growth, which proceeds in the same way - through bone formation on the bone surface and at the fusion centres. Bone formation in children , which was bilateral or symmetrical, and therefore possibly indicative of normal bone formation, was excluded from the analysis of inflammatory lesions.

Table 24: Summary of periosteal inflammatory lesions
Sex Age No. % of individuals No. of bones affected % of total Type of infection % of infection type Bone element affected % unsided bones affected % of right bones affected % of left bones affected
N Foetus - - - - - - - - - -
Neonate 3 75% 3 1% 3 woven 5% 3 crania 50% - -
Infant 2 11% 5 1.50% 4 woven 7% 2 crania 33% - -
1 porosity 6% 1 radius - 17% (1) -
2 ribs - 12.5% (1) 12.5% (1)
Juvenile 19 24% 38 12.50% 8 lamellar 4.50% 12 crania 21% - -
23 woven 38% 2 humeri - 2% (1) 2% (1)
2 porosity 12% 9 ribs - 7% (5) 6% (4)
1 hypervascularity 14% 1 spine 1.50% - -
2 lamellar/ woven 33% 3 femora - 2% (1) 4% (2)
2 woven/ lesion 50% 7 tibiae - 5.5% (3) 8% (4)
2 fibulae - 4% (1) 4% (1)
2 metatarsals - 3% (1) 2.5% (1)
Adolesc 6 40% 29 9.50% 7 lamellar 4% 2 crania 25% - -
9 woven 15% 1 mandible 11% - -
1 porosity 6% 1 sternum 11% - -
1 hypervascularity 14% 1 rib - 12.5% (1) -
4 lamellar/ woven 20% 3 spines 33% - -
4 woven/ hypervascularity 80% 4 pelvises - 22% (2) 22% (2)
2 woven/ lesion 33% 1 sacrum 11% - -
3 femora - 18% (2) 10% (1)
8 tibiae - 33 % (4) 33 % (4)
4 fibulae - 17 % (2) 17 % (2)
2 calcanei - 10% (1) 11% (1)
All 30 26.5% of non-adults 76 25% of all cases 15 lamellar 8% 19 crania 24% - -
39 woven 65% 1 mandible 1% - -
4 porosity 23.50% 1 sternum 2% - -
2 hypervascularity 28.50% 12 ribs - 8% (7) 5% (5)
6 lamellar/ woven 30% 4 spines 4% - -
4 woven/ lesion 67% 4 pelvises - 2% (2) 2.5% (2)
4 woven/ hypervascularity 80% 1 sacrum 1.50% - -
1 radius - 1% (1) -
6 femora - 3% (3) 4% (3)
15 tibiae - 9% (7) 10.5% (8)
6 fibulae - 4% (3) 4% (3)
2 calcanei - 1.5% (1) 1.5% (1)
2 metatarsals - 2% (1) 2% (1)
F 18-25 5 100% 17 65.50% 14 lamellar 8% 2 crania 67% - -
2 woven 3% 1 mandible - 33% (1) -
1 porosity 6% 2 femora - 20% (1) 25% (1)
10 tibiae - 100% (5) 100% (5)
2 fibulae - 20% (1) 20% (1)
26-35 4 40% 10 3% 4 lamellar 2% 2 ribs - 11% (1) 11% (1)
2 lamellar/woven 10% 1 femur - 17% (1) -
4 lamellar/woven/ 80% 5 tibiae - 40% (2) 60% (3)
spicules   2 fibulae - 20% (1) 20% (1)
26-35 9 60% 23 8% 17 lamellar 9.50% 1 cranium 11% - -
1 porosity 6% 1 pelvis - 10% (1) -
1 lamellar/woven 5% 3 femora - 22% (2) -
2 woven/ spicules 33% 10 tibiae - 55% (5) -
2 woven/ lesion 33% 7 fibulae - 30% (3) -
1 metatarsal - 10% (1) -
46+ 14 61% 39 13% 30 lamellar 17% 4 crania 29% - -
3 woven 5% 1 mandible - 7% (1) -
2 porosity 12% 2 clavicles - 9% (1) 6% (1)
2 hypervascularity 28.50% 2 sterni 15% - -
1 lamellar/ woven 5% 2 spines 11% - -
1 lamellar/woven/ 20% 1 humerus - 5.5% (1) -
spicules   2 ulnae - 6% (1) 5.5% (1)
17 tibiae - 56% (9) 50% (8)
7 fibulae - 23.5% (4) 20% (3)
1 metatarsal - 8% (1) -
All 32 60% of females 89 29% of all cases 65 lamellar 36.50% 8 crania 24% - -
5 woven 8% 2 mandibles - 6% (2) -
4 porosity 23.50% 2 clavicles - 3% (1) 3% (1)
2 hypervascularity 28.50% 2 sterni 6% - -
6 lamellar/woven 30% 2 spines 4% - -
2 woven/ spicules 33% 2 ribs - 2% (1) 2% (1)
2 woven/ lesion 33% 1 pelvis - 2% (1) -
5 lamellar/woven/ spicules 100% 1 humerus - 3% (1) -
2 ulnae - 2.5% (1) 3% (1)
6 femora - 11% (4) 5.5% (2)
42 tibiae - 60% (21) 58% (21)
18 fibulae - 24% (9) 25% (9)
2 metatarsals - 6% (2) -
M 18-25 3 43% 9 3% 8 lamellar 4.50% 1 cranium 25% - -
1 porosity 6% 2 femora - 17% (1) 17% (1)
6 tibiae - 50% (3) 60% (3)
26-35 6 43% 17 5.50% 12 lamellar 7% 1 cranium 14% - -
1 porosity 6% 10 tibiae - 50% (5) 55% (5)
4 lamellar/woven 20% 6 fibulae - 30% (3) 33% (3)
26-35 9 64% 29 9.50% 15 lamellar 8% 1 cranium 8% - -
8 woven 13% 3 ribs - 14% (2) 7% (1)
1 hypervascularity 14% 1 spine 7% - -
6 lamellar/ woven 30% 1 ulna - - 8% (1)
2 woven/ spicules 33% 2 femora - - 15% (2)
11 tibiae - 38% (5) 50% (6)
7 fibulae - 36% (4) 25% (3)
1 calcaneus - - 8% (1)
2 metatarsals - 12% (1) 12% (1)
46+ 12 75% 49 16% 35 lamellar 20% 8 crania 53% - -
7 porosity 41% 1 mandible 7% - -
5 woven 8% 2 ribs - - 17% (1)
2 hypervascularity 28.50% 1 femur - - 8% (1)
22 tibiae - - 100% (11)
14 fibulae - - 64% (7)
1 f phalanx - - 10% (1)
Adult 4 66% 12 4% 10 lamellar 6% 8 tibiae - 100% (3) 100% (5)
2 woven 3% 4 fibulae - 67% (2) 50% (2)
All 34 60% of males 119 39% of all cases 80 lamellar 45% 11 crania 29% - -
15 woven 25% 1 mandible 3% - -
9 porosity 53% 5 ribs - 8% (3) 5% (2)
3 hypervascularity 43% 1 spine 2% - -
10 lamellar/ woven 50% 1 ulnae - - 1
2 woven/ spicules 33% 5 femora - 2% (1) 7% (4)
57 tibiae - 60% (27) 71% (30)
31 fibulae - 37% (16) 37% (15)
1 calcaneus - - 3% (1)
2 metatarsals - 3% (1) 3% (1)
1 f phalanx - - 3% (1)
U 18-25 1 33% 4 1% 1 woven 1.50% 1 cranium 100% - -
26-35 1 14% 2 0.50% 2 lamellar 1% 2 tibiae - 100% (1) 100% (1)
Adult 8 50% 20 6% 18 lamellar 9% 14 tibiae - 55.5% (5) 70% (7)
2 woven/ spicules 33% 4 fibulae - 27% (3) 10% (1)
1 calcaneus - - 8% (1)
1 metatarsal - 9% (1) -
All 10 48% undetermined adults 26 8% of all cases 20 lamellar 10% 1 cranium 25% - -
1 woven 2% 14 tibiae - 54.5% (6) 67% (8)
2 woven/ spicules 33% 4 fibulae - 25% (3) 8% (1)
1 calcaneus - - 7% (1)
1 metatarsal - 8% (1) -
All Total 102 42% of population 306 100% of cases 180 lamellar 58.50% 39 crania 26% - -
60 woven 20% 4 mandibles 3% - -
17 porosity 5.50% 1 sternum 1.50% - -
7 hypervascularity 2% 19 ribs - 6% (11) 4% (8)
20 lamellar/woven 7% 7 spines 4% - -
6 woven/lesion 2% 5 pelvises - 2% (3) 1% (2)
6 woven/spicules 2% 1 sacrum 1% - -
5 woven/ hypervascularity 1.50% 2 clavicles - 0.5% (1) 1% (1)
5 lamellar/woven/ spicules 1.50% 1 humerus - 0.5% (1) -
3 ulnae - 0.5% (1) 1% (2)
1 radius - 0.50% -
17 femora - 5% (8) 5.5% (9)
130 tibiae - 36% (61) 40% (67)
59 fibulae - 18% (31) 17% (28)
4 calcanei - 1% (1) 2% (3)
7 metatarsals - 4% (5) 1.5% (2)
1 f phalanx - - 1% (1)

In total, 42% of individuals from Fishergate House were affected by periosteal inflammatory bone formation, with lesions on 304 bone elements (if more than one vertebra, rib or toe was affected, it was classed as one skeletal element). Female and male adults were affected equally (60%) and were more likely to suffer from periosteal inflammations than adults of undetermined sex (48%) or children (26.5%). The risk of inflammation generally rose with increasing age in both children and adults, although there were exceptions.

The majority of periosteal lesions (58.5%) were expressed as lamellar bone, suggesting that they had either healed or were healing. In 20% of cases, inflammation was still active at the time of death, and was characterised by grey woven bone formation. In a small number of cases (7%), both woven and lamellar bone formation was noted on the same bone, implying different stages of healing. Microporosity on the bone surface, indicative of inflammation, was noted in 5.5% of cases, with most of these lesions being concentrated on the outer (ectocranial) surface of the skull. Hypervascularity, which was most frequent on the lower limbs, was observed in 2% of cases; 1.5% of cases included both woven bone formation and hypervascularity.

Woven bone formation was observed together with small oval destructive lesions in 2% of cases, all of which concentrated on the inner surfaces of the ribs, adjacent to the lungs. Lesions of the same type were also observed in a small number of skeletons from St Andrews and were interpreted as indicative of tuberculosis (see below).

A small number of bones (2%) exhibited periosteal lesions in the form of thick deposits of woven bone and outcrops of irregular spicular bone formation (Plate 5, right), and in some cases, lamellar bone (1.5%). This severe form of lesion affected solely the tibiae and fibulae, often with irregular thickening and complete distortion of the bone surface. One individual, who exhibited the woven and spicular inflammatory lesions together with resorption of the toe bones, is thought to have suffered from leprosy (C1251). A further individual, an old middle adult male (C1117) with equally severe tibial lesions, is thought to have suffered a direct injury to his shin, which penetrated the skin and allowed bacteria to enter the wound. The original injury could still be detected as an oval lesion on the anterior surface of the tibia, surrounded by spicular bone formation.

The nature of lesions varied considerably with age, with a considerably higher percentage of woven (active) bone formation in the children (65% of all children's lesions), and more healed or healing (lamellar) lesions in the adults. Spicular bone formation was not observed in any of the children. Hypervascularity was observed in only the older age groups, including adolescents and older adults; similarly, porosity was most likely to develop in older adults, particularly mature adult males.

The bones most commonly involved in periosteal inflammatory lesions were tibiae, especially on the left side (40%). In most cases, the medial or lateral surfaces of the central or distal tibial shafts were affected. Fibulae were also frequently affected (17% of left and 18% of right fibulae), which was expected due to their close proximity to the tibiae. Tibiae have been found to be the most common sites of periosteal inflammatory lesions in other populations, which has been attributed to the close proximity of the bone under the skin surface. Thus, the shins are more prone to damage from falls, knocks and kicks than most other parts of the body. In addition, tibiae are also prone to inflammatory lesions as a result of chronic infectious diseases, particularly syphilis and leprosy. At Hull Magistrates Court, a monastic population with several cases of severe syphilis, 59% of all tibiae showed periosteal inflammatory lesions (64% of the population was affected), many of which were attributed to treponemal disease (Holst et al, forthcoming). It is possible that some of the lesions noted at Fishergate House may also have been caused by infectious disease, although without the presence of other indicative lesions, it is not possible to make a diagnosis.

Prevalence rates of periosteal inflammation at Fishergate House (42%) were considerably higher than those observed in other populations in York, with 22.4% of individuals affected at St Helen's-in-the-Walls (Grauer 1993, 208) and 17% of individuals at St Andrew's, Fishergate. At St Helen's-in-the-Walls, periosteal inflammation usually affected children over six, and the age of onset was linked to the age at which children normally began apprenticeships (Lewis 2002a). At St Andrew's, the under-fives suffered most from the lesions, but 17% of female and 18% of male adult tibiae were also affected (Stroud 1993, 219). At Blackfriars, Wiggins et al (1993) found that only 11% of the population suffered from periosteal inflammation, with 19.6% of right and 22.2% of left tibiae affected. The high prevalence of periosteal reactions in the tibiae of this population has been attributed to chronic infection.

Femora were also prone to periosteal inflammation, with 5% of femora exhibiting the lesions. The prevalence at Fishergate House is only slightly lower than that observed at Hull Magistrate's Court (7%). Femoral periosteal lesions were most commonly observed in adolescents and young adult males and females at Fishergate House. The presence of femoral involvement is indicative of infectious disease, rather than bumps or varicose veins, as the bone is protected by a thick layer of muscle and fat.

Cranial inflammation is usually relatively rare in populations from archaeological contexts. At Hull Magistrate's Court, for example, only 1% of individuals suffered from cranial lesions. However, a high prevalence of cranial cases of periosteal new bone formation and porosity (26%) were observed in this population (affecting 16% of the total). Both adults and children, as well as individuals of both sexes were affected to the same extent, although the expression and location of lesions varied according to age group. Endocranial (inner skull table) periosteal new bone formation affected young infants between birth and two years of age almost exclusively, with the exception of a young adult C1322, and may have been caused by infections such as meningitis (see Plate 4). The parietals were most commonly affected by ectocranial (outer skull table) lesions, and usually displayed periosteal reactions in the form of porosity, whereas inflammation of the temporal, occipital, orbit and maxilla took the form of woven bone formation.

The cranial inflammatory lesions can be attributed to a number of causes, including two cases of possible scurvy (C1143 and C1328) and one juvenile with hydrocephalus (discussed above) (C1480; Plate 2). In two individuals, cranial periosteal reactions were probably secondary to weapon trauma. A mature adult male with a well-healed depression fracture on the left parietal also showed evidence for cranial porosity on the superior part of the frontal and parietals. It is possible that he suffered from slight scalp inflammation as a result of the fracture. A further mature adult male had sustained a blade injury to the left part of the frontal, superior to the eye orbit. Woven bone formation on the inner and outer part of the frontal bone indicates that this individual survived the injury for some time. However, he must have succumbed eventually to the effects of the injury or infection, as little evidence for healing could be observed around the wound. One possible case of meningitis was noted in a young adult of undetermined sex (C1322), who not only suffered from cribra orbitalia and sinusitis, but also exhibited thick deposits of woven bone on the endocranial (inner) surface of the frontal and parietals.

Cranial periosteal reactions were associated with a high prevalence of cribra orbitalia (45%) and sinusitis (57%), as well as five possible cases of rickets, two cases of DISH (discussed below) and two individuals with arachnoid granulations (discussed below). Thirty percent of individuals with cranial inflammation suffered from periosteal reactions in another part of the skeleton, usually in the tibiae or ribs. The range of cranial lesions and associated pathological conditions suggests that these reactions had a number of causes.

Thirteen individuals were found to suffer from periosteal reactions to the ribs, which were mostly on the neck or angle of the inner (pulmonary) rib surface, in the form of woven bone. In all but two cases, more than one rib was affected, and in several cases, all but the first rib from one side of the body was affected. Two mature adult males (C1163 and C1185) with rib inflammation also suffered from rib fractures. It is possible that their periosteal reaction can be attributed as secondary infections to these fractures; this can cause death in infirm patients (Dandy and Edwards 1998, 161). Ten of the thirteen individuals with rib inflammation also suffered from additional inflammatory reactions on different parts of the skeleton, including the lower limb tarsals or metatarsals, spine and skulls. Further areas affected included the sternum, pelvis, sacrum and humerus. The nature and distribution of periosteal lesions in three individuals from Fishergate House could be indicative of tuberculosis (discussed below).

Inflammatory lesions were noted in the spines of six individuals. These were concentrated on the lower thoracic vertebrae and lumbar vertebrae, usually on the vertebral bodies. Vertebral inflammatory reactions were most likely to affect the adolescents and older adults. Other parts of the axial skeleton affected included five hips (iliae) and two sternums, although in the case of a mature adult female, the periosteal reaction is thought to have been secondary to direct trauma to the sternum.

Inflammatory lesions were also noted on a small number of upper and lower limb bones, including two clavicles, a right humerus, three ulnae and a radius, as well as on four calcanei, seven metatarsals and one foot phalanx. According to Aufderheide and Rodríguez-Martín (1998, 124), the metatarsals and phalanges, as well as the sternum, pelvis, ribs and cranium, can be involved in primary tuberculous infection and this may have been the cause for some of the lesions observed.

The relatively high rate of periosteal inflammatory lesions can be attributed to a number of causes, including trauma, teething, rickets, scurvy, hydrocephalus, varicose veins and ulcers, but the greater majority of lesions are probably due to the presence of specific infections, such as meningitis, tuberculosis and leprosy.

3.4.2 Osteitis

Osteitis is an inflammation of the compact bone and can be observed in the form of swelling on the outer and inner surface of the bone (Plate 6, right). Ten individuals (4%) suffered from osteitis, all of whom were adults. In all but one case, osteitis was identified by an abnormal enlargement of the bone, which could be considerable. The only exception was the right ulna of a young middle adult female (C1095) who had additional osteitis of the left femur. While the ulna was not enlarged, the medullary cavity (void inside the bone) was filled entirely with bone, suggesting osteitis as a possible cause.

Tibiae were most commonly affected by osteitis, followed by two femora, a fibula, radius and ulna (Table 25). All ten individuals with osteitis also suffered from periosteal new bone formation in one or several long bones. In most cases, both inflammatory conditions affected the same bone, which was severe in three cases, with woven and irregular spicular bone formation on top of the bone swelling.

Table 25: Summary of individuals with osteitis
Context No. Age Sex Site of osteitis Periosteal new bone formation Healed fracture Metabolic condition Other
1095 26-35 f r ulna l tibia - - osteochondritis dissecans
1117 26-35 m r tibia r tibia and r fibula (severe), l tibia, l fibula l radius and ulna, r fibula, r tarsals, r metatarsals rickets? sinusitis
1163 46+ m l tibia tibiae, l femur, r ribs, r 4th metatarsal ribs Harris line sinusitis
1251 26-35 f l radius tibiae and fibulae (severe), r femur 5th proximal hand phalanx - leprosy
1312 36-45 f r tibia tibiae, fibulae, femora, right 5th metatarsal - - sinusitis
1313 46+ m r tibia cranium, tibiae, fibulae - - rheumatoid arthritis, sinusitis
1320 18+ u l tibia and l fibula l tibia and l fibula (severe), r fibula, l tarsals r 1st distal foot phalanx - rheumatoid arthritis?
1385 46+ m r tibia, foot phalanx? cranium, tibiae, fibulae, l rib r ribs - sinusitis
1391 46+ f tibiae ulnae, tibiae, fibulae - - -
1525 46+ f r tibia r tibia and r humerus (severe), manubrium, clavicles, fibulae, l tibia - - sinusitis

In three cases, the bone affected by osteitis was adjacent to a skeletal element which had fractured and healed. An old middle adult male (C1117) had suffered an avulsion fracture of the right fibula malleolus, which was well-healed. The shafts of the fibula and adjacent tibia were covered in active periosteal new bone formation and the proximal tibia was enlarged as a result of osteitis. Additionally, a compression fracture had affected the right fourth and fifth metatarsals, cuneiforms and navicular (foot bones). It is probable that the injury of the foot and ankle and the infection below the knee had the same origin. An accident may have forced adduction or external (twisting) rotation of the ankle and crushing of the foot, probably causing an open wound at the upper shin. Bacteria entered the open wound and while the foot and ankle were healing, an infection, possibly septicaemia developed, which affected the soft tissues, bone surface and bone cortex of the upper tibia and fibula.

Two further individuals had less dramatic injuries. A young middle adult female suffered from osteitis of the left radius and severe periosteal new bone formation of the lower limbs. It is possible that the infection of the radius was related to the fracture of her fifth proximal hand phalanx. A similar disease spread was observed in an adult of undetermined sex (C1320), who had suffered from a fractured right first distal foot phalanx and acute periosteal inflammatory bone formation and osteitis of the left tibia and fibula. An accident may have caused the fractures and contributed to the secondary infection.

The causes of osteitis infection could not be identified in the remaining six individuals. While it may have been caused by soft tissue injuries, with bacteria entering the skin, or by haematomas forming beneath the skin, thus providing a breeding ground for bacteria (Dandy and Edwards 1998, 305), it could also have represented the early stages of osteomyelitis, without cavity involvement (discussed below).

3.4.3. Osteomyelitis

Osteomyelitis is an infection within the bone cavity. The most common cause for osteomyelitis is a secondary infection, which spreads to the bone via the bloodstream from a primary infectious focus, such as the throat (tonsillitis) or the chest (bronchitis) (Roberts and Manchester 1995, 127). However, osteomyelitis can often result from direct infection of a bone-penetrating injury, or from surgery, allowing bacteria to enter the bone from the skin surface (Ortner and Putschar 1985, 105). In such cases, evidence for surgery or injury should be apparent in the skeleton.

Osteomyelitis can have a dramatic effect on the skeleton through bone destruction and formation, with irregular enlargement of the bone, either in part or in its entirety. Pus within the bone cavity can penetrate the bone cortex, creating a cavity through which it is discharged into the soft tissues or through the skin. Bone within the medullary cavity can die and be discharged with the pus from skin sores (Roberts and Manchester 1995, 126). Osteomyelitis can be rapidly fatal, with mortality rates of 20% documented for the 19th and early 20th centuries (Ortner and Putschar 1985, 115). However, the infection can also be long-standing, can heal and recur, or can heal completely ibid. Symptoms include fever, pain and immobility, with a serious risk of septicaemia.

Osteomyelitis affects juveniles most commonly, particularly children under the age of twelve. However, diagnosis of osteomyelitis in young infants is still problematic today, because there a few clinical signs of the infection, causing delay in diagnosis and identification of the sceptic focus (Staalman et al 1984, 10). The infection tends to develop in the growing ends (metaphyses) of the long bones. Usually, only a single bone is subject to the infection, with knee involvement being most common. Lesions in adults are usually the result of recurrent juvenile osteomyelitis (Ortner and Putschar 1985, 116). When adults with no previous history of osteomyelitis are affected, they tend to be over fifty years of age (Aufderheide and Rodríguez-Martín 1998, 173).

Osteomyelitis could be observed in two individuals from Fishergate House; one of these was a three year old juvenile, whose left third metacarpal was greatly enlarged. The whole bone shaft was covered in porous new bone formation, with a small circular cavity on the bone surface which did not penetrate into the medullary cavity. It is probable that this cloaca represents a pus-containing abscess on the bone surface. In children, osteomyelitis tends to be relatively common in hand and foot bones, with rapid destruction of the thin cortex of these bones (Ortner and Putschar 1985, 116). This juvenile may have succumbed to septicaemia; however, the child also suffered from erosive rib lesions and periosteal new bone formation on the left humerus and both tibiae. These inflammatory lesions may have been the expression of another, fatal, infection.

An old middle adult male (C1184) had an abscess at the anterior part of the maxillary palate (incisive canal), which penetrated the palate to the sinuses, causing severe sinusitis (discussed below). The dental health of this male was very poor, with severe dental wear, considerable periodontitis and ante-mortem tooth loss. It is probable that the poor oral health had contributed to the development of osteomyelitis at such an unusual site. The infection must have been long-standing to cause the severity of the sinus lesions. Nevertheless, it is possible that this individual eventually died as a result of the infection.

Further cases of osteomyelitis may not have been identified because pus from within the medullary cavity had not penetrated the bone cortex and discharged, and thus the lesions were not visible on the bone surface. Such cases could only be identified if the whole assemblage was subjected to radiography.

3.4.4 Sinusitis

One of the most common non-specific infections in past and modern populations is maxillary sinusitis. Sinusitis is characterised by the inflammation of the mucous membrane of the sinuses (cavities in the cheek bones). Acute sinusitis lasts between seven days and one month, but the condition is classed as chronic if it persists for more than three months (Merrett and Pfeiffer 2000, 304). Symptoms include pain in the forehead, cheeks and eyes, together with fever and a general feeling of illness (Youngson 1992, 551), and the sufferer's quality of life and productivity can be greatly reduced. Modern treatment of sinusitis can include courses of antibiotic and surgical drainage of the sinuses (Merrett and Pfeiffer 2000, 304). If untreated, chronic sinusitis can persist for years.

Sinusitis is a good indicator of endemic chronic respiratory stress, as it is the body's first defence against airborne particles and pathogens (Merrett and Pfeiffer 2000). The causes of sinusitis can be primary, through nasal infection, or secondary, through dental abscesses or cavities with a subsequent spread of the dental infection to the sinus (Wells 1977, 175). A large number of predisposing factors can make an individual susceptible to sinusitis; these can be divided into three basic categories, including congenital predisposition, systemic susceptibility and environmental conditions. Congenital predispositions for sinusitis include conditions such as cleft palate, which allows bacteria easier access to the sinuses, or blocks the sinuses and causes a build-up of bacteria. Systemic susceptibility for sinusitis is thought to include conditions such as hay fever and asthma (Lewis et al 1995 a, 499), although the relationship between these conditions and sinusitis is not yet fully understood. However, it has been found that if sinusitis is treated successfully, asthma also tends to improve (Rachelefsky et al 1988, 1095). Additionally, pregnancy, menopause, leprosy, tuberculosis, syphilis, bronchitis, trauma, acute periodontitis, poor dental hygiene, malnutrition and poor general health can predispose a person to sinusitis (Boocock et al 1995a and 1995b; Lewis et al1995 a. A wide variety of environmental factors can make individuals susceptible, including air pollution from fire, industry, tobacco, pollen, dust and animal hair, effects of the climate (particularly cold and damp conditions), crowded living conditions, poor hygiene, under-ventilation and overheating. Significantly, in a study of three populations from medieval Maastricht in Holland, social status was found to have no effect on the prevalence of sinusitis (Panhuysen et al1997).

Skeletal changes resulting from this condition begin to occur after a number of weeks (Lewis et al 1995 a, 498). In modern groups, around 60% of patients with chronic sinusitis develop bone changes that are radiographically visible (Boocock et al 1995b:484). Most commonly, the skeletal manifestations take the form of pitting or spicular bone formation on the floors of the sinuses (Plate 7, right).

For the Fishergate House population, all accessible maxillary sinuses were examined for sinusitis. The sinuses of three individuals (1%) were intact and could not be examined without creating a cavity and introducing an endoscope into the sinus, and this method was not applied. Additionally, the sinuses of 126 (52%) individuals were missing. The remaining 115 (47%) sinuses were examined for the presence or absence of characteristic pitting and spicule formation. Fifty-seven (49.5%) individuals showed no evidence for sinusitis (Table 26). However, fifty-eight (50.5%) individuals had sinusitis in one or both sinuses. This implies that at least half of the population from Fishergate House suffered from chronic sinusitis. Additionally, it is probable that a much greater number of individuals suffered from acute sinusitis, which had not produced skeletal lesions.

Table 26: Summary of prevalence and expression of sinusitis in preserved sinuses
Age Group Male Female Undetermined Spicules Porosity Total
No. % No. % No. % No. % No. % No. %
Foetus - - - - 0 0 0 0 0 0 0 0
Neonate - - - - 0 0 0 0 0 0 0 0
Infant - - - - 0 0 0 0 0 0 0 0
Juvenile - - - - 16 40 3 19 13 81 16 28
Adolescent - - - - 2 25 0 0 2 100 2 3
18-25 1 33 3 100 1 100 3 60 2 40 5 9
26-35 2 33 5 83 0 0 5 71 2 29 7 12
26-35 7 64 3 50 1 100 7 64 4 36 11 19
46+ 10 83 7 54 0 0 12 70 5 30 17 29
Adult 0 0 0 0 0 0 0 0 0 0 0 0
Total 20 34.5 18 31 20 34.5 30 52 28 48 58 100

Only a small number of cases of sinusitis could be attributed to dental infections. A total of twenty individuals (17% of individuals with sinuses or 34.4% of individuals with sinusitis) also had maxillary dental abscesses. Of these, only the abscess of one old middle adult male (C1184) had created a cavity which penetrated into the sinuses. This man suffered additionally from severe periodontitis and considerable dental wear. The remaining individuals' dental abscesses did not penetrate the sinuses, but may have contributed to the infection of the maxillary sinuses. It is noteworthy that eleven of these individuals had more than one dental abscess.

It is possible that factors causing ante-mortem tooth loss also contributed to the prevalence of sinusitis in this population. However, as the jaw bones had healed over the cavity left by the tooth roots, it was not possible to identify whether the ante-mortem tooth loss had been caused by dental abscesses, and whether these had been responsible for sinus infections.

The prevalence rate of sinusitis from Fishergate House (50.5%) compared well with that from other medieval sites. The prevalence of sinusitis at the rural site of Wharram Percy in North Yorkshire was similar to that from Fishergate House, with 50.9% of individuals showing sinusitis lesions (Roberts and Cox 2003). Lewis et al(1995a) suggest that the inhabitants of Wharram Percy were less likely to suffer from sinusitis because they lived in less dense conditions, and were not subject to the same amount of pollution as their urban counterparts ibid. However, the prevalence of sinusitis at Wharram Percy was still relatively high; this suggests that even this rural environment was not free of predisposing factors. At the medieval leprosy hospital of St James and St Mary Magdalene in Chichester, Sussex (Boocock et al1995a) and at St-Helen's-on-the-Walls (Lewis et al1995 a, 55% of individuals were affected. Both of these, like Fishergate House, were urban cemeteries, and exposure to pathogen load and effects from pollution must have been considerable.

At Fishergate House, the young adult age group was most severely affected by sinusitis (71%), although the frequency of lesions was similar in all adult groups. Twenty-five percent of adolescents with extant sinuses suffered from sinusitis, and 40% of juveniles, with a total of 35.7% of children's sinuses affected. All juveniles affected were between the ages of two and nine years. It is possible that a much larger number of children were affected by acute sinusitis and did not display skeletal lesions because the condition had improved, or because their immune system was weakened and they had succumbed to other diseases. At St Helen's-on-the-Walls, only 17% of children had sinusitis, and children were even less commonly affected at Wharram Percy (9%) (Lewis 2002b). This suggests that the children at Fishergate House experienced worse environmental factors or greater pathogen loads than those from the two other cemeteries.

The prevalence rates of sinusitis for the different sexes were markedly different (Figure 14). All of the young adult females and the majority of the young middle adult females had sinusitis, whereas only one third of the young adult and young middle adult males suffered from the disease. Interestingly, female prevalence rates decreased with advancing age, but in contrast, the occurrence increased with age in males. This considerable sexual dimorphism suggests that sinusitis was caused by different factors in females and males. At both Wharram Percy and St Helen's-in-the-Walls, females had a higher frequency of the lesions, which was attributed to smoke exposure from their daily work within the proximity of the hearth. However, urban men were more likely to suffer from sinusitis than their rural counterparts (Lewis et al1995a, 502), which may have been due to work-related industrial pollution in foundries, tanneries and apothecaries ibid, 503-504).

Figure 14

At Fishergate House, the high prevalence rate of sinusitis in the younger females may be attributed to greater susceptibility to infection during pregnancy, or to poor general health. This, together with sinusitis, may have contributed to the mortality of the females. Similarly, the children who suffered from sinusitis may have been less healthy generally than their surviving counterparts, accounting for the high frequency of sinusitis.

In contrast, the males probably suffered from accumulated pollution exposure from their working environment, which affected them increasingly in old age. It is clear from documentary evidence that pollution was a considerable problem in medieval cities. Brimblecombe (1976) describes how complaints were made about the perceptibly poor air quality in medieval towns in the 13th century, and its effect on human health. Of particular concern was the contemporary shift from charcoal and wood burning to coal burning. The changes in fuel were initially implemented in industry, such as in smithing and lime burning, and later spread to the domestic sector ibid, 942). Inhabitants of cities felt that the smoke, smell and dirt generated from coal burning had an adverse effect on their health, and visitors to cities were shocked by the distinctly poor air quality in urban areas ibid, 945). Documentary evidence from York details the presence of foundries and tanneries in the city, and this must have released considerable toxins into the air, aggravating sinusitis and lung infection (Lewis et al1995a, 503). Additionally, a lime kiln was established at York Minster in the 13th century to provide cement for the Minster's construction, and this would have contributed further to the pollution problem ibid.

Infectious disease is a contributing factor in the incidence of sinusitis, since its presence may reduce the immune competence of a population, resulting in greater susceptibility to other infections, including sinusitis. Conversely, sinusitis may also contribute to greater susceptibility to infectious disease (Merrett and Pfeiffer 2000, 316), particularly lepromatous leprosy (Boocock et al1995a, 266). However, only one individual with possible leprosy was identified (C1251), and her sinuses did not survive, so this relationship could not be tested. Merrett and Pfeiffer (2000) also found a possible association between sinusitis and tuberculosis. Thirteen individuals from Fishergate had lesions indicative of tuberculosis and of those individuals with sinuses, 57% suffered from sinusitis, supporting a possible link between the two diseases.

In common with skeletons from other medieval cemeteries, more individuals suffered from spicular bone formation in the sinuses than from porosity. However, unlike at St Helen's-in-the-Walls and Wharram Percy, where 61% of lesions were spicular, only 52% of individuals at Fishergate suffered from spicular bone formation. The characteristics of lesions changed with age: the majority of children suffered from porosity of the sinus floor, whereas two thirds of adults had spicular bone formation in the sinuses. The greater frequency of porosity in the children's sinuses may be due to pitting which occurs as part of the normal bone development (Lewis et al 1995a, 501), and it is possible, therefore, that sinusitis was slightly overestimated in this age group.

The spatial distribution of skeletons with all types of non-specific infection demonstrates certain patterns, but these reflect largely the predominance of particular age groups within certain interventions. Individuals with periosteal inflammation were most likely to be found in Intervention 2, particularly in the eastern end of this excavation area, whereas only one case of sinusitis could be observed in that intervention; this may be a reflection of the young age of the majority of individuals buried there, as children were not as susceptible to sinusitis as adults. Cases of sinusitis and periosteal inflammation were found throughout Interventions 1 and 4. Osteomyelitis, on the other hand, was limited to Intervention 1, and all except the individuals with osteitis were found in Intervention 1.

3.4.5 Tuberculosis

The first archaeological cases of tuberculosis from Britain date to the Roman period (Anderson 2001). Even today, following treatment with drug therapies and vaccines, an estimated 1.7 billion people are infected with tuberculosis worldwide, with 3.3 million deaths per year (Bannister et al 2000). In the pre-antibiotic era, between 35-40% of individuals with major pulmonary tuberculosis could have expected to die within five years (Aufderheide and Rodríguez-Martín 1998, 132). Younger age groups were more likely to become infected, with the highest mortality rate being amongst infants ibid. Pulmonary tuberculosis in a mother was rapidly passed to her baby, with fatal consequences (Rhodes 1995, 124). Until the introduction of antibiotics in the mid-20th century, the only treatment for neonates was separation of the mother and baby to prevent cross-infection ibid. A large part of the infected population could survive with chronic tuberculosis for one or more decades, but with reduced work capacity and fertility ibid. Those suffering from tuberculosis would no longer have been active members of the community and would also have required care.

Overcrowded conditions, poor hygiene, unclean surroundings, sharing of accommodation with animals, poor diet and psycho-social stress can increase the virulence of tuberculosis (Santos and Roberts 2001, 39; Pfeiffer 1991, 196). The most effective control of tuberculosis is, therefore, improvement of living conditions, nutrition and social deprivation (Bannister et al 2000).

Because tuberculosis is distributed via the blood stream, it can affect any part of the human body (Bannister et al2000, 337). The commonest sites of infection are the lungs and lymph nodes, although it can also affect the bowel, meninges, kidneys, skin, bones and joints (Bannister et al 2000). Clinical reports found skeletal involvement in around 1% of individuals suffering from tuberculosis; however, in the pre-antibiotic era, this was probably much higher, with skeletal involvement at perhaps 5-7% (Aufderheide and Rodríguez-Martín 1998, 133). It usually takes between one and six years from the initial infection for bone and joints to become involved (Mishra and Nigam 1984, 175).

Skeletal elements containing a large proportion of spongy (trabecular) bone, such as the vertebrae, have a good blood supply and are therefore most likely to be affected by tuberculosis. Lesions in the spine or weight-bearing joints tend to be destructive, causing spongy bone cavitation and spinal collapse. Diagnosis of tuberculosis in historic populations, therefore, relies on the presence of lesions in the spine and joints. However, recent research on three skeletal collections from the late 19th and early 20th centuries, containing individuals who died of known causes, has demonstrated that new bone formation can be related to tuberculosis, particularly rib lesions.

Kelley and Micozzi (1984) found that 8.8% of those with pulmonary tuberculosis suffered from rib manifestations in the form of periosteal inflammatory lesions, or to a lesser extent from localised abscesses. Research on living individuals and cadavers from the Terry Collection in the United States (Roberts et al 1994) and skeletons from the University of Coimbra, Portugal (Santos and Roberts 2001), has shown a much higher correlation between tuberculosis and new bone formation on the ribs. In the Terry Collection, 61.6% of those who had died of tuberculosis had rib lesions, whereas only 22.2% of those who died of a non-tuberculous cause had such new bone formation (Roberts et al 1994). In the Portuguese collection, 90.9% of individuals with pulmonary tuberculosis had rib lesions. Fourteen percent of those with other forms of tuberculosis, and 14.3% of those suffering from other pulmonary conditions, had new bone formation on the ribs (Santos and Roberts 2001, 41). Only one individual had the vertebral lesions, and this was an adolescent with enteric, rather than pulmonary, tuberculosis ibid, 42).

Eyler et al (1996) also noted a positive correlation between lung disease and new bone formation in modern patients, with pulmonary tuberculosis being the most common cause. Other diseases known to produce rib lesions, but to a much lesser extent than tuberculosis, are non-tubercular empyemas (a collection of pus between the lungs and the chest wall), thoracic surgery, blunt trauma, chronic bronchitis, pneumonia, metastatic tumours, and actinomycosis (bacterial infection) (Santos and Roberts 2001). Aufderheide and Rodríguez-Martín (1998, 124) also suggest that rib lesions are more likely to be the result of empyema caused by tuberculosis than by acute pneumonia, as individuals would rarely have survived pneumonia for long enough to develop rib manifestations. Clinical diagnoses of tuberculosis do not mention the subtle bone lesions which are expressed as bone formation, rather than destruction. This is probably because they are not visible on x-rays in and are, therefore, not used as diagnostic criteria, nor are they examined in modern autopsies (Santos and Roberts 2001, 46).

Thirteen individuals from Fishergate House had new bone formation on one or several ribs, but no spinal or joint involvement (Table 27). In one case of a six to eighteen month old infant (C1017), the bone formation was on the outer side of all the central and lower ribs, unlike the lesions found in the skeletal collections discussed above, all of which were on the internal (visceral) surfaces of the ribs. It is suggested that in this case, the lesions may be the result of normal growth, blunt force trauma, or another undefined condition, rather than tuberculosis. A further infant (C1575) had porous sternal rib ends, suggesting a possible inflammatory response, with additional woven bone on the skull, particularly along the sutures. The cause of these lesions was not identified, but it is unlikely to be tuberculosis.

Table 27: Individuals with rib lesions and possible associated conditions
Context Age Sex Pathology Expression Bone Side Element Part
1163 45+ m periostitis lamellar metatarsals right 4th shaft
periostitis lamellar tibia right shaft medial
periostitis lamellar tibia left shaft all
osteitis thickened tibia left shaft central
periostitis lamellar femur left shaft medial, proximal
periostitis woven ribs right 2nd to 12th angle, neck
fracture transverse ribs bilateral l 7, 10th, r 5th neck, angle
1178 5.5-6.5 s periostitis woven tibia bilateral shaft lateral, medial
periostitis woven fibula bilateral distal posterior
periostitis lamellar tarsals bilateral calcaneus lateral, medial
periostitis lamellar metatarsals bilateral 1st shaft
periostitis lamellar, woven ribs bilateral l 2nd-10th; r 8th neck
1188 35-45 m anomaly fusion pelvis left auricular surface to sacrum
periostitis lamellar, woven thoracics bilateral 6th-10th anterior bodies
periostitis woven ribs bilateral l 5th-11th; r 5th-12th neck, angle
1205 12-14 s periostitis lamellar tibia bilateral shaft medial
periostitis woven femur bilateral proximal neck
periostitis hyper-vascularity femur right proximal neck
periostitis lamellar pelvis right ilium inf. gluteal line
periostitis woven pelvis left ilium all
periostitis woven sacrum bilateral 1st, 2ns, 3rd anterior bodies
periostitis woven sternum bilateral posterior all
periostitis woven lumbars left 2nd body
periostitis destructive lesion, woven lumbars right 1st body
periostitis woven thoracics right 7th, 12th body
periostitis destructive lesion, woven thoracics right 9th-11th body
periostitis destructive lesion, woven ribs right 2nd-12th angle, neck
1259 25-35 f periostitis lamellar, woven ribs bilateral l 2-12th; r 5th, 10-12th; ? 3 angle, neck, shaft
1271 6-10 s periostitis woven tibia right shaft medial
periostitis woven ribs ? 4 frags shaft
1382 4-5 s periostitis hypervascularity humerus right distal coronoid fossa
periostitis woven ribs left 2nd-10th neck, angle, shaft
1385 45+ m periostitis porosity cranium bilateral parietals, occipital ectocranial
periostitis lamellar tibia bilateral shaft lateral, medial
osteitis thickened tibia right shaft central
periostitis lamellar fibula bilateral shaft lateral, medial
periostitis woven ribs left 6th rib & 2 frags angle
fracture transverse ribs right 7-9th, 12th shaft
1400 6-7 s periostitis hypervascularity humerus bilateral distal coronoid fossa
periostitis woven femur bilateral proximal posterior
periostitis woven tibia left shaft medial
periostitis woven fibula bilateral distal shaft lateral, medial
periostitis woven vertebrae bilateral 6 thoracics, 1 lumbar spinous canal
periostitis woven ribs bilateral l 2nd, 4-9th; r 5-9th, 6 ? neck, angle, shaft
1427 1-2 s periostitis destructive lesion, woven ribs right 4th, 2? angle
1560 35-45 m periostitis woven ulna left proximal medial
periostitis woven ribs right 6th neck
anomaly non-fusion sternum bilateral segment superior
periostitis lamellar tarsals left calcaneus all
periostitis woven tibia left distal shaft posterior
periostitis woven fibula left distal shaft posterior
unknown erosive lesion foot phalanges right 1st proximal distal joint

The remaining eleven individuals (4.5% of individuals or 5.7% of individuals with extant ribs) had new bone formation on the ribs (Plate 8, right), which corresponded with that observed in the known cause of death collections discussed above. All age groups and both sexes were represented, with a predominance of male adults, a trend observed in most archaeological groups (Roberts et al 1998). The inflammatory response was invariably located on the internal surface of the ribs, and usually at the vertebral end (at the head and neck of the rib) and the rib angle (side of the chest). However, new bone formation was also noted on the rib shafts (the anterior rib end) in four cases. As in the modern skeletal collections, the lesions were usually located on more than one rib, and often on adjacent ribs, particularly those of the central rib cage (the greatest concentrations are in ribs five to ten), although all ribs with the exception of the first were affected (Figure 15).

Figure 15

Both sides of the rib cage were affected to the same extent, although the lesions frequently affected only one side of the body (eight cases), while both sides were equally affected in two individuals. In one case (C1271), the ribs were so fragmented that it was not possible to determine w h ether the fragment derived from the left or right side. The populations with a known cause of death appear to show a side preferences, but this varied between collections (Kelley and Micozzi 1984; Roberts et al 1994; Santos and Roberts 2001). The inflammatory response usually took the form of woven bone, which was well-defined and raised, but relatively dense. In two cases (C1163 and C1259), lamellar (remodelled) bone was also present. A twelve to fourteen year old adolescent who suffered most severely from inflammatory lesions also had oval, well-defined 'scooped out' lesions on the necks, angles or shafts of the right ribs, which may represent localised abscesses (Kelley and Micozzi 1984, 383). These types of lesions were also observed at St Andrew's Fishergate, where eight individuals had new bone formation on the ribs, two of which were associated with focal oval lesions (Stroud 1993, 221). Six of the eight individuals with rib manifestations from St Andrew's also had destructive lesions in the spine, all of which were thought to be tuberculous ibid. Seven of the individuals (63.6%) also had periosteal new bone formation on the long bones.

Three individuals from Fishergate with ribs also had new bone formation on the vertebral bodies, particularly on the anterior surface of the thoracic vertebrae (C1188, C1205) and on the spinous canal (C1400). Other sites of new bone formation include calcanei, metatarsals, a pelvis, sacrum and sternum (Figure 16).

Figure 16

A twelve to fourteen year old adolescent (C1205) suffered from destructive and proliferative lesions on the ninth to eleventh thoracic vertebrae and first lumbar vertebrae, as well as on the second to twelfth right ribs. Additionally, this individual displayed lamellar and woven bone inflammatory lesions on all lower limb bones, as well as the pelvis, sternum, sacrum, eighth and twelfth thoracic and second lumbar vertebrae. The distribution and nature of lesions in this individual were indicative of tuberculosis.

Inflammatory lesions on the ribs of eleven individuals from Fishergate corresponded with those identified in recent research on skeletons of known cause of death, as well as on archaeological assemblages, suggesting that the most likely cause for these lesions is pulmonary tuberculosis. It is probable that an infection of the lung tissues would have spread directly to the ribs and caused an inflammatory response on the internal rib surfaces (Roberts et al 1998, 58). The similarity of the inflammatory response on the ribs from Fishergate House and on those from the adjacent site of St Andrew's suggests that the lesions had the same tuberculous origin. Because tuberculosis only affects the skeleton in 5% to 7% of cases (Aufderheide and Rodríguez-Martín 1998, 133), the presence of any skeletal tuberculous lesions implies that a much greater proportion of both populations suffered from the disease, but had succumbed to the disease before skeletal manifestations developed.

Significantly, cases of possible tuberculosis are restricted to Intervention 1 and Intervention 2, and only in the southern part of both areas, suggesting that these may have been used during periods in which tuberculosis was endemic. The burials of individuals suffering from possible tuberculosis were close to each other in Intervention 2, but were widely dispersed in Intervention 1.

3.4.6 Leprosy

Leprosy is a chronic infectious disease affecting the skin, nasal tissues, nerves, muscles and bones and is spread by droplet transmission from saliva or nasal discharge. Although it is highly infectious, it affects only those with a low immune system. Symptoms include progressive crippling loss of hand and foot function, with deformities of the extremities, socially ostracising facial disfigurement, blindness and male infertility. Leprosy may take two forms, both of which are caused by Mycobacterium leprae. The form of disease depends on the immunological status of the patient - the high resistance form is termed tuberculoid leprosy, while the low resistance form is lepromatous leprosy. The effects of the disease are less obvious in tuberculoid leprosy, with a lack of facial lesions, and fewer skin lesions, but earlier and more intense bone involvement (Aufderheide and Rodríguez-Martín 1998, 146).

Leprosy was very common in Britain from the 12th to the 16th century, although the earliest cases date to the 4th century AD (Roberts 2002, 213). Leprosy is rarely seen in Britain today, with the last indigenous case recorded in Shetland in 1758 ibid. However, in Norway, leprosy was endemic until the 1920s, and has been attributed to poor nutrition (probably caused by high taxation imposed first by the Danes and later the Swedes), and the presence and recurring infection of leprosy in isolated rural communities (Irgens 1981). Today, the disease is most commonly observed in Africa, South America and Asia, and the small number of cases registered in Britain are in immigrant populations, usually from the subcontinent (Roberts 2002).

During the medieval period, infection was thought to be the result of divine punishment for sin, particularly that of a sexual nature. It is probable that the symptoms and mode of transmission were confused with those of syphilis, both of which have venereal associations (Lewis 2002b, 165). Diagnosis was carried out by village elders, clerics and occasionally physicians, and was eccentric, including placing a raven's egg into the suspect's blood which, if it hardened, confirmed leprosy (Roberts 1987, 168). Treatments for the disease included prayers, incantations, herbal concoctions, blood letting and specific diets (Roberts 1987), and cures ranged from the sensible to the bizarre, including eating dead infant's flesh or anthill earth, or the belief that cure would follow the touch of a monarch ibid, 169-170).

Diagnoses of leprosy, frequently incorrect, led to social segregation and confinement in leper hospitals, termed leprosaria, most of which were founded between the 12th and 16th centuries (Roberts 2002, 213). However, such segregation is unlikely to have halted transmission on the disease, as the more specific symptoms only became obvious with the progression of the disease (Lee and Magilton 1989, 280), and many individuals would have remained undetected in the community during the early stages, thereby spreading the infection. According to Irgens (1981, 161), 'As long as infectious patients remain in the community, susceptible individuals may be infected and contract the disease, even if the dose is low and duration of exposure is short.'

Two hundred leprosaria are known to have been established in Britain, and these were mostly located on the periphery of urban settlement, in extramural or suburban locations (Gilchrist 1992, 115). As leprous individuals were seen as both symbolically and legally dead, some had metaphoric funerals before their segregation from society (Gilchrist 1995, 39). In York, four leprosaria are thought to have been established, one near each of the City's gates. These include St Loy's (to the east, at Monk Bridge), St Katherine's (to the west, at the Mount), Our Lady's (to the north, at Horsefair) and St Nicholas' (to the south, at Lawrence Street). Many leprosaria were run by monks, probably on account of the close association between religion and medicine during the medieval period (Roberts 1987), as well as the aim of providing holistic cures for both the body and the soul.

The steep decline of the disease in the late 13th century, while the population of Britain was increasing dramatically, is not yet understood. Furthermore, the persistence of the disease in Scandinavia despite the sparsely settled nature of this part of Europe remains to be explained. As the prevalence of leprosy decreased, leprosaria often became poor houses or hospitals; this shift in function is illustrated by the large number of non-leprous skeletons in cemeteries associated with these institutions.

Diagnosis of leprosy in skeletons relies on the presence and distribution of lesions, and therefore, on the immune status of the person suffering from the disease, the severity of the disease at death, and the quality of bone preservation (Lewis 2002b, 165). Roberts (2002) carried out a study of reports from forty-one sites in Britain which were known to contain leprous skeletons, dating from the 4th to the 19th century, and found that 1.55% of individuals (128 skeletons) showed evidence for the bone lesions. However, if all of the skeletons studied in Britain were taken into account, the prevalence would be around 0.26% ibid. Nevertheless, it must be kept in mind that leprosy manifests in the skeleton in only 15% to 50% of cases (although a rate of around 70% can be observed in leprosaria ibid. Roberts (2002) found an increase in prevalence rates from the Roman period (0.14%) to the later medieval and post-medieval periods (2.28%), which she attributed to denser living conditions, promoting the rate of transmission. At the leprosarium at Chichester, 14% of skeletons had leprous lesions (Lewis et al 1995b), while 70% of skeletons at the Danish leprosarium at Næstved had leprous bone changes (Roberts 2002).

It is possible that the lower number of leprous skeletons in Britain compared with those from other European countries is due to the disease being less endemic in this country. Most sites containing individuals with leprous lesions were located in southern and eastern England, and contained only one individual with the lesions each, although thirteen cemeteries contained more than one victim, five which were associated with hospitals. The inclusion of leprous individuals in parish and monastic cemeteries suggests perhaps less regimented segregation than is reported by historical sources, at least after death.

Leprosy can be passed on in utero, but such children probably rarely survived infancy, often suffering from low birth weight and foetal distress, slower growth and a susceptibility to disease (Lewis 2002b, 163 i. However, leprosy is often acquired during childhood (Ortner 2002, 74), particularly in areas where leprosy is hyperendemic (Lewis 2002b). mptoms could develop during childhood, but the disease can be very subtle in children and can hSyeal spontaneously ibid. Bony lesions do not develop until an older age, and as a result, very few children have been found with leprous manifestations, particularly in Britain ibid. The small number of children with leprosy may also be explained by the high susceptibility of these children to other infections, with death often occurring before leprous lesions could develop. Furthermore, children are more likely to develop tuberculoid, rather than lepromatous leprosy, without the nasal changes, therefore adding to the difficulties of diagnosis ibid.

The disease can shift between relative quiescence and acute activity, with recurrent ulceration, inflammation and remodelling (Ortner 2002, 74). This was illustrated at Chichester, where most individuals had lesions which were indicative of a slow and chronic disease process that had developed over years ibid.

A single young middle adult female (C1251) from Fishergate House suffered from irregular, thickened active and remodelled new bone formation on the tibiae and fibulae and remodelled inflammatory lesions on the bones of the feet (Plate 9, right). Most of the foot bones present, including the calcanei, tali, cuneiforms, naviculars, cuboids and second to fourth metatarsals, were fused together and also fused to the tibiae. The distal ends of the metatarsals had the classic leprous 'pencil-shaped' appearance, with the shaft of the bone ending in a sharp point, rather than the original rounded joint. The sharp joints were smooth (common in leprosy), suggesting recurrent short destructive phases followed by bone repair (Ortner 2002, 74). Only two foot phalanges were present, one of which was of normal appearance, while the second phalanx was eroded at the distal end. Unfortunately, the skeleton was poorly preserved, with particularly severe foot erosion, which hindered diagnosis.

No leprous changes were noted in any of the hand bones. However, further evidence for infection, which was probably unrelated, was noted in the left radius in the form of osteitis, with external thickening of the bone and reduction of the medullary cavity (which holds the bone marrow).

It is suggested that this woman suffered from typical leprous symptoms, including loss of function of the nerves, leading to muscle paralysis, with collapse of the central part of the foot (plantar arch) and loss of sensation and anaesthesia in the feet (Andersen etal 1994, 22). This loss of feeling can lead to minor superficial injury with subsequent infection. This often becomes progressively worse, with ulceration affecting the skin, causing tissue death (avascular necrosis) and allowing bacteria to enter the wound. The infection can then spread to the deeper tissues and eventually the bones and joints ibid, 24). This may lead to a progressive loss of the bone at the toes (phalanges and metatarsals), new bone formation and fusion of the joints, all of which were noted in this female. The infected skin lesions can also cause inflammation of the tibia and fibula, even before the bones of the feet become infected (Andersen et al1994, 29) and is almost always seen in individuals with leprous skeletal lesions (Manchester 2002, 70).

This individual's facial bones were not preserved, so the facial changes, with collapse of the nose leading to bone resorption of the nasal and maxillary bones (rhinomaxillary syndrome), could not be observed. Thus, it was not possible to determine whether this woman suffered from tuberculoid or lepromatous leprosy.

If more than one individual from this population had suffered from leprosy, which is likely considering that between 15% to 70% of victims of the disease develop skeletal lesions, then the rate of infant may be attributed partly to this disease. Today, females with lepromatous leprosy often suffer miscarriages as a result of bacteraemia (when bacteria enter the blood stream) or transplacental infection (Lewis 2002b, 163).

3.4.7 Bacterial infection

One individual, an eleven to fourteen year old adolescent (C1132) was thought have suffered from a bacterial or fungal infection. The dental development and long bone fusion suggested a much younger age than that estimated from the length of the long bones. The adolescent showed evidence for flaring of the rib shafts, smooth pitting (hypervascularity) on the anterior surface of the thoracic and lumbar vertebrae, and on the posterior surface of the manubrium. Because bacterial and fungal infection are rarely observed in skeletal examples it is difficult to accurately diagnose the type of infection this child had suffered from. An alternative diagnosis of the condition may be a developmental defect, which caused growth spurts and therefore hypervascularity on some of the bones.

3.4.8 Conclusion

The presence of tuberculosis, which is higher than at other sites in York, implies that this population was the subject of considerable psycho-social stress, such as poor housing, poor nutrition and social deprivation. It is probable that the Fishergate population had a low immune system as a result of hard physical work, poor nutrition and a high pathogen load, thus making it susceptible to infection with leprosy and tuberculosis. Ironically, infection with leprosy is thought to have provided cross-immunity to plague, preventing sufferers from succumbing to the great epidemic of 1347 to 1350 and subsequent outbreaks (Ell 1987). Equally, infection with tuberculosis may have provided some cross-immunity to leprosy, as the bacteria causing the two infectious diseases are related (Lee and Magilton 1989, 281). It is possible, therefore, that the suggested presence of tuberculosis in the Fishergate population may have protected parts of the community from infection with leprosy.

The population's pathogen load may have contributed to the high prevalence of sinusitis, which affected more than half of the skeletons with extant sinuses. In reality, the figure was probably higher. However, the prevalence rate of sinusitis is lower than at St Helen's-in-the-Walls, perhaps indicating a lower exposure to pollution at this extra-mural site.

Evidence for non-specific inflammatory lesions in 42% of the population further illustrates the susceptibility of this population to infection. It is probable that such inflammation was caused by a variety of factors, including minor trauma, varicose veins, ulcers, and also infections such as leprosy and meningitis. As the prevalence rate of inflammatory lesions in most comparative medieval cemeteries was lower, this reinforces the suggestion that this population was exposed to a high pathogen load.

apc > monographs > blue bridge lane & fishergate house > artefacts & environmental > human bone: palaeopathological analysis

Spall, C. A. and Toop, N. J. (eds.). 2005. Blue Bridge Lane & Fishergate House, York. Report on Excavations: July 2000 to July 2002
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