Category Archives: Palaeopathology

Yersinia pestis, ancient DNA and the Black Death


The Black Death is the name given to a pandemic which killed up to a third of the European population between 1347 and 1352. Over the next three hundred years this pandemic was followed by further plagues of lesser mortality. These are historically ascribed to bubonic plague whose aetiological agent is the bacterium Yersinia pestis.

Recently, DNA specific for Y. pestis was amplified from 16th and 18th century human teeth believed to be French plague victims (Drancourt et al., 1998) and 14th century French Black Death victims (Raoul et al, 2000). The lead authors of these reports now believe that the consideration of any cause for the Black Death other than Y. pestis is now speculative.

Ancient DNA analysis:

The study of aDNA involves the extraction and analysis of DNA from the remains of organisms preserved as fossils, skeletons or mummified tissues. Studies are hampered by extremely low levels of preservation, often coupled by the presence of much greater levels of modern contaminants. Characteristically only short aDNA fragments can be amplified and easy amplification of longer fragments is an indication that contamination has occurred.

In the case of Y. pestis, fatal infection would not be expected to leave any specific bony changes, so no osteological confirmation is available and any retrospective diagnosis is completely DNA-based. Two studies from the same research group reported the successful extraction and sequencing of Y. pestis-specific DNA retrieved from the dental pulp cavities of plague victims. Findings that pathogen-specific DNA can be recovered from this source in systemically infected animals have led Drancourt et al (1998) to hypothesise that teeth provide a lasting, contamination-free refuge where pathogen aDNA may survive.


  • Previous extraction techniques are unsuited to preventing bacterial contamination of the DNA extract. Dental enamel is extremely resistant to diagenesis, but may be permeable to contaminating DNA using both the ‘ground’ and the ‘scraped’ methodologies. Encasing teeth in silicone appears to act as a barrier to movement of DNA between the tooth and the gloved hand and this may explain the reduction in contamination with this method.
  • No evidence of surviving Y. pestis DNA was found in this study, despite the examination of a large number of samples from five mass graves, including two well-documented plague pits and several other probable plague-victim burial sites.
  • Previous studies reported successful direct sequencing from ancient teeth. This implies a low-level of contaminating non-Y. pestis bacterial DNA, despite using a dentine extraction method demonstrated to be contamination prone. This raises two questions:
    1. why such levels of contaminating DNA from other bacteria were found in this study, and
    2. why it was not possible to amplify Y. pestis-specific DNA from samples of plague victims that yield what appears to be authentic human DNA.
  • It is possible that diagenetic conditions in the relatively drier and warmer Southern French locations were more conducive to ancient DNA survival than those of north-western Europe. However, aDNA studies have repeatedly demonstrated an inverse correlation between average temperature, humidity and aDNA retrieval. It is, therefore, surprising that warmer locations would be more successful.
  • An alternative environmental variable is groundwater. An inverse correlation has been noted between sample survival and exposure to water. However the ability to amplify host DNA suggests survival is not an issue.
  • A further explanation is that the individuals from whom the samples derive were either infected by a Y. pestis strain lacking the plasmid-located sites for amplification or not infected with Y. pestis (because they were not victims of the Black Death, or because the infection did not seed the pulp cavity, or because the Black Death and subsequent plagues were not caused by Y. pestis). The first hypothesis is unlikely as the plasmid containing the pla gene is a consistent feature of contemporary isolates. The second hypothesis is plausible. There is no guarantee that bacteria causing a systemic infection entered the teeth. It is, therefore, possible that Y. pestis may not have been present in the teeth specimens but that infection by this bacteria caused death. The third hypothesis is controversial, but cannot immediately be discounted.


Gilbert, M.T.P, Cuccui, J. White, W, Lynnerup, N, Titball, R.W, Cooper, A and Prentice, M.B. 2004. Absence of Yersinia pestis-specific DNA in human teeth from five European excavations of putative plague victims. Microbiology 150: 341-354.

Know Your Pathology: Calculus

In this edition of ‘Know Your Pathology’, we shall examine the subject of calculus, also known as calcified plaque. This consists of micro-organisms, which accumulate in the mouth, embedded in a matrix partly composed of the organisms themselves and partly derived from proteins in the saliva (Roberts and Manchester, 2005: 71). It accumulates faster when there is a high protein and/or carbohydrate diet favouring an alkaline oral environment (Roberts and Manchester, 2005: 71).

Where crystallites of mineral are deposited in the plaque, the plaque can be mineralised and form calculus (Roberts and Manchester, 2005: 71-71). Two types are commonly seen:

  1. Supragingival calculus (above the gum) is more common and is usually thicker and grey or brown in colour;
  2. Subgingival calculus (below the gum) is often seen on exposed tooth roots and is harder and green or black in colour.

Calculus varies widely in mineralisation, but subgingival calculus is more heavily mineralised (46-83% by colume) than supergingival (16-80% by volume). The minerals include apatite, whitlockite, octacalcium phosphate and brushite, all of which have been found in archaeological specimens (Hillson, 1996: 257). Brushite is prominent during the earlier part of calculus deposition, whilst mature supergingival calculus has more apatite and brushite, and subgingival calculus has abundant whitlockite (Hillson, 1996: 257).

Beneath a Scanning Electron Microscope, it is possible to see that calculus is more heavily mineralised than dentine or cement, but less so than enamel, and that it presents an irregular appearance with layerings, voids and clefts (Hillson, 1996: 257). Outlines of bacteria are presented as voids with mineralised shells – the filamentous forms as 2um diameter tubules, and shorter rods or cocci as globular outlines – and similar outlines have been demonstrated in calculus from English medieval human remains (Dobney and Brothwell, 1986).

Dental reports from some archaeological human populations indicate that calculus was common in all periods (Roberts and Manchester, 2005: 72).


Dobney, K and Brothwell, D. 1986. Dental calculus: its relevance to ancient diet and oral ecology, pp 55-82. In Cuwys, E and Foley, R.A. Teeth and Anthropology. BAR International Series 291. British Archaeological Reports: Oxford

Hillson, S. 1996. Dental Anthropology. Cambridge University Press: Cambridge.

Roberts, C. and Manchester, K. 2005. The Archaeology of Disease. 3rd Edition. Stroud: Alan Sutton Publishing Ltd.

NB: For those looking for past editions of ‘Know Your Pathology’, and so that I can keep track of which topics I’ve covered and which I’ve not, there is now an index.

The Origins of Syphilis

The origin of syphilis has been hotly debated in recent years. Was it already in the Americas by the time of Columbus’ landing, or were he and his men somehow fundamentally linked to its arrival in the New World, are some of the questions typically asked. John Hawks looks at a new paper on just this topic in ‘Syphilis origin pinpointed?‘.

Know Your Pathology: Dental Caries

What is dental caries?

Dental caries is a destruction of enamel, dentine and cement, ultimately leading to the formation of a cavity in the crown or root surface (Hillson, 1996: 269). It is caused by the fermentation of food sugars, especially sucrose in the diet, by bacteria that occur on the teeth in plaque, such as Lactobacillus acidophilus and Streptococcus mutans (Roberts and Manchester, 2005: 65). Carious cavities usually develop in three regions of the tooth (Brothwell, 1981: 153):

  1. on the occlusal (biting) surface, generally in the region of natural fissures;
  2. in the region of the neck (cervical area) of the tooth, either on the lingual (tongue) or labial (lip) side;
  3. in the region of the neck of the tooth, but between the teeth (mesial and distal).

Caries in modern human populations

In living human populations, caries has a characteristic pattern. For all types of carious lesions, molars are most commonly affected, followed by premolars and then anterior teeth. Coronal caries is a disease of children, rising steadily to fifteen years or so of age, and then falling away in early adulthood. It is more common in girls than boys, but earlier dental eruption in girls exposes their teeth to risk for longer (Hillson, 1996: 281-282). Root surface caries also particularly affects the approximal surfaces of cheek teeth, but is a disease of adults (Hillson, 1996: 282). The pattern of caries is similar in members of the same family over several generations, perhaps due to inherited factors, but environmental factors such as dental treatment and diet also have a large role (Hillson, 1996: 282). The clearest single factor in caries is sugar, as shown by the decrease in caries rates during sugar rationing in Japan, Norway and Jersey during the 1939-45 war, which was followed by a rise when normal supplies resumed (Hillson, 1996: 282).

Caries in archaeological populations

Caries was very uncommon amongst fossil hominids, into Palaeolithic and Mesolithic contexts. Nevertheless, there are celebrated examples such as the rampant caries in the Middle Pleistocene skull from Broken Hill, Zambia, and coronal caries has also been noted in Australopithecus and Paranthropus (Hillson, 1996: 282). In European material, there is a an apparent gradual rise from very low caries rates in Palaeolithic to Iron Age contexts, to a rapid rise through medieval and post-medieval times (Hillson, 1996: 282). In parallel, the number of carious teeth per mouth increased, with more pit and fissure caries, less cervical caries, and more children affected. Similar trends have been demonstrated for Egypt and Nubia (Hillson, 1996: 282).

In North America, increased reliance upon maize agriculture is a clear cultural horizon (Hillson, 1996: 283). Several studies have show an increase in caries rate associated with the change from a hunter-gatherer diet to a diet heavy with starch-rich cereal (Hillson, 1996: 283). Similar rises in caries rate have been associated with increased reliance on arable agriculture in South America, South Asia, Egypt and Nubia (Hillson, 1996: 283). Meanwhile, a recent innovative survey of a Mayan population dated to the Classic period in Mexico (AD 250-900) demonstrated that the lowest rate of caries, and the highest rate of ante-mortem tooth loss, occurred in elite males; this correlated with poor oral hygiene and a softer and more refined diet (Roberts and Manchester, 2005: 67).

Caries in animal populations

Caries is an ancient phenomenon in non-human populations. Carious lesions have been reported in Permian fish, as well as mastodon and cave bear teeth. Caries with possible actinomycosis infection has also been noted in the three-toed horse, Merychippus campestris (Rothschild and Martin, 1993: 211-212). They are moderately common amongst wild great apes, particularly chimpanzees, whose diet includes a lot of fruit and, therefore, sugar. Gorillas, which eat considerably less fruit, have much lower caries rates, whereas orangutans seem to occupy an intermediate position (Hillson, 1996: 282).


Brothwell, D. 1981. Digging up Bones. Third Edition. New York: Cornell University Press.

Hillson, S. 1996. Dental Anthropology. Cambridge University Press: Cambridge.

Roberts, C. and Manchester, K. 2005. The Archaeology of Disease. 3rd Edition. Stroud: Alan Sutton Publishing Ltd.

Rothschild, B.M. and Martin, L.D. 1993. Paleopathology: Disease in the Fossil Record. CRC Press: London.

Know Your Pathology: Diffuse Idiopathic Skeletal Hyperostosis

Diffuse idiopathic skeletal hyperostosis (DISH), also known as Forestier’s disease, is primarily a disease of the spine, but individuals suffering from this condition exhibit characteristic bony abormalities elsewhere in the body that distinguish it from ankylosing spondylitis. DISH is not a true arthropathy because it does not affect cartilage or synovium (Roberts and Manchester, 2005: 159). Instead, there is gradual and complete fusion of the spine, particularly in the thoracic region, with retention of the integtrity of vertebral articular surfaces and joint spaces (Roberts and Manchester, 2005: 159). The anterior longitudinal ligament of the spine and paraspinal tissues ossify, the osteophytes that are produced being large and flowing like ‘candlewax’ (Roberts and Manchester, 2005: 159-160). In addition, there are enthesopathies at tendon and ligament insertions and cartilage, especially in the neck and ribs, ossifies (Roberts and Manchester, 2005: 160).

Its specific cause is unknown, but it appears to be associated with obesity and Type 2 diabetes (Roberts and Manchester, 2005: 159). Males are slightly more affected than females and the age of onset is usually over 50 years of age (Roberts and Manchester, 2005: 159). DISH is found more in Northern European people (Roberts and Manchester, 2005: 160).

A disease of some antiquity, the earliest known case is that of a Neanderthal skeleton from Iraq, dated between 40,000 and 73,000 years BP (Roberts and Manchester, 2005: 159). It is also increasingly being seen in both monastic and non-monastic cemetery groups in the archaeological record (Roberts and Manchester, 2005: 160). It has been suggested that a rich diet and lack of exercise predisposed medieval monks to obesity and late onset diabetes. Such high status people may also have lived longer to develop the condition (Roberts and Manchester, 2005: 160).

DISH has also been reported in an Alaskan bear, as well as in extinct Mammut, Teleoceras, Menoceras, Equus, Bison bison, Canis diris, Ovibos, Smilodon, megatheridae, Thinocetus arthritis and Pelocetus, and in contemporary Papio, Cercopithecus, Macaca, Erythrocebus, and Gorilla gorilla gorilla (Rothschild and Martin, 1993: 236). Ossified tendons are also present in most dinosaurs (including ceratopsians, hadrosaurs, iguanodonts, and pachycephalosaurs). This includes a juvenile Pinacosaurus grangeri and Pachyrhinosaurus and has even been observed in an embryonic duckbill (Hypacrosaurus ?) (Rothschild and Martin, 1993: 235-236). Whilst these non-pathologic phenomenon are considered simply as extensions of presygophases by some researchers, they are considered by others to be indistinguishable from the tendon ossification seen in DISH (Rothschild and Martin, 1993: 236). Analogous tendon ossification has also been noted in c. 50% of sauropods, resulting in the fusion of two to four cervical vertebrae, something considered non-traumatic in origin as CT scans reveal the zygoapophyseal facets are unaffected (Rothschild and Martin, 1993: 236).


Roberts, C. and Manchester, K. 2005. The Archaeology of Disease. 3rd Edition. Stroud: Alan Sutton Publishing Ltd.

Rothschild, B.M. and Martin, L.D. 1993. Paleopathology: Disease in the Fossil Record. CRC Press: London.

More about tuberculosis in Homo erectus

Following up the other day’s blog about tuberculosis in Homo erectus, John Hawks, having seen a pre-print of the report, writes more about ‘A new Middle Pleistocene hominid from Turkey‘.

Tuberculosis in Homo erectus?

Does a Homo erectus fossil recently discovered in Turkey show evidence of tuberculosis?

Well, the paper isn’t published yet, so we’ll have to wait and see. Human tuberculosis is “an acute or chronic infection of soft or skeletal tissues by Mycobacterium tuberculosis or M. bovis” (Aufderheide and Rodríguez-Martín, 1998: 118). The first of these is conducted via droplet infection from human to human, the second through ingesting meat and milk from animals, particularly cattle, or via droplet infection (Roberts, 2000: 151).

Whilst nobody disputes that it is a disease of some antiquity, some of the earliest cases I know about (if there are any older, please do leave a comment with the reference) come from Neolithic Italy (Canci et al., 1996; Formicola et al., 1987). If the news of this new fossil is true, it is a massive leap back in time as far as the known history of the disease goes.

In the meantime, the following blogs raise some interesting points that we need to consider whilst we’re thinking about this topic:

Tuberculosis in an archaic human‘ – John Hawks

Dark-skinned H. erectus had tuberculosis?‘ – Gene Expression

500,000 year old Homo erectus from Turkey, and with Tuberculosis‘ –


Aufderheide, A. C. and Rodríguez-Martín, C. 1998. The Cambridge Encyclopedia of Human Paleopathology. Cambridge: Cambridge University Press.

Canci, A., Minozzi, S., and Borgognini, S. M. 1996. New evidence of tuberculous spondylitis from Neolithic Liguria (Italy). International Journal of Osteoarchaeology 6: 497-501.

Formicola, V., Milanesi, Q., and Scarsini, C. 1987. Evidence of spinal tuberculosis at the beginning of the Fourth Millennium BC from Arene Candide Cave (Liguria, Italy). American Journal of Physical Anthropology 72: 1-6.

Roberts, C. 2000. Infectious Disease in Biocultural Perspective: Past, Present and Future Work in Britain, pp 145 – 162. In Cox, M and Mays, S (eds.) Human Osteology in Archaeology and Forensic Science. London: Greenwich Medical Media Ltd.

Know Your Pathology: Avian Osteopetrosis

Avian osteopetrosis is an infection that can reach epidemic proportions. Caused by the action of the avian leucosis virus group, which belongs to the family Retroviridae, that stimulates the proliferation of osteoblasts in chickens, this leaves characteristic evidence on the skeleton (Brothwell, 1993: 41) that is visible macroscopically to the archaeozoologist, such as thickening of the metatarsals, symmetrical thickening of the long bones, and changes in other parts of the skeleton which are similar but not as pronounced (Biltz and Pellegrino, 1965: 1365). This proliferative growth of immature bone fails to become fully mineralised even after the growth of new bone subsides and a new phase of osteogenesis becomes evident (Biltz and Pellegrino, 1965: 1376).

Chemical and histological analysis of avian osteopetrotic bone from modern chickens has shown the disease to be characterised by (Biltz and Pellegrino, 1965: 1374-1375):

  1. An increase in total bone mass caused by overproduction of bone and resulting in hypermineralisation;
  2. Decreased hydrated-bone density reflecting an increase in water content and an increase in vascularity or porosity;
  3. A decrease in the apparent densities of dry bone, mineral, and organic fractions;
  4. A decrease in the degree of mineralisation or dry-bone density

Avian osteopetrosis has many similarities with human osteopetrosis and infantile cortical hyperostosis, all manifesting distinctive histological features and presenting similar appearances in x-rays. Chemical evidence of disturbance of maturation in avian osteopetrotic bone also accords well with histological evidence of a similar defect in humans with the condition (Biltz and Pellegrino, 1965: 1375). The study of avian osteopetrosis, therefore, presents an opportunity to not only study such a condition in chickens, but may also be helpful in understanding the disorder in other species (Biltz and Pellegrino, 1965: 1375). Besides humans and birds, the condition has been described in an inbred herd of rabbits, where the condition was caused by an inherited lethal factor that was present at birth (Marks et al., 1986), as well as cattle and rodents (Smith and Ivanyi, 1980: 523), and dinosaurs (Campbell, 1966).

However, whilst human osteopetrosis (Albers-Schonberg disease) and avian osteopetrosis appear to have some common characteristics, it has been argued by some authors (Simpson and Sanger, 1968: 278-279) that the two are fundamentally different. In humans, the disease is hereditary, whilst the avian disease is caused by a virus. In humans, the problem is a failure to remove the primary spongiosa underneath the epiphyseal plate and there is no excess proliferation of periosteal bone. It has therefore been suggested that the disease in humans results from an imbalance between the formative and resorptive mechanisms.

A crude attempt to construct the historical geography of avian osteopetrosis (Brothwell, 2002: Fig. 2) demonstrates, albeit tentatively, that the leucosis virus was established in some chicken flocks in South East England by Roman times, and there is growing evidence for osteopetrosis by the post-Roman period, possibly over a wider area. There are potential sources of the infection in other parts of the Roman Empire as the condition has been identified at the Roman castellum at Velsen in the Netherlands (Prummel, 1987) and in the Lower City at Troia (Fabis, 1997).

Whilst currently infrequently reported in archaeological material, this may be due to either small sample size or a failure to recognise the early stages of the condition. The variable incidence of whole or complete chicken bones in the archaeological record also makes it difficult to determine the prevalence in Gallus populations. However, as the virus causes bone changes in only a small proportion of infected birds, even one incidence of pathology may indicate a notable infection within the flock (Brothwell, 2002: 318). It can, therefore, provide evidence for the conditions in which the stock were kept.


Biltz, R. M. and Pellegrino, E. D. 1965. Avian osteoporotic bone: A correlation of its chemical composition with its roentgenographic and histological appearance. Journal of Bone and Joint Surgery 47-A (7): 1365-1377.

Brothwell, D. 1993. Avian osteopathology and its evaluation. Archaeofauna 2: 33-43.

Brothwell, D. 2002. Ancient avian osteopetrosis: the current state of knowledge. Proceedings of the 4th Meeting of the ICAZ Bird Working Group Kraków, Poland, 11-15 September 2001. Acta zoologica cracoviensia 45 (special issue): 315-318.

Campbell, J. G. A dinosaur bone lesion resembling avian osteopetrosis and some remarks on the mode of development of the lesions. Journal of the Royal Microscopical Society 85 (2): 163-174

Fabis, M. 1997. A case of infectious disease among domestic fowls of Troia IX. Sonderdruck aus Studia Troia Band 7. Verlag Philipp von Zabern: Mainz an Rhein.

Marks, S. C., Seifert, M. M. F., and Fox, R. R. 1986. The osteopetrotic rabbit: general and skeletal features of a new outbred stock. Bone 7: 359-364

Prummel, W. 1987. Poultry and fowling at the Roman castellum Velsen. Palaeohistoria 29: 183-201

Simpson, C. F. and Sanger, V. L. 1968. A review of avian osteopetrosis: comparisons with other bone diseases. Clinical Orthopaedics 58: 271-281

Smith, R. E. and Ivanyi, J. 1980. Pathogenesis of virus-induced osteopetrosis in the chicken. Journal of Immunology 125 (2): 523-530.

Know Your Pathology: Osteomalacia and Rickets

Osteomalacia, literally softening of the bones, is a metabolic disorder of the adult skeleton that is usually defined in terms of its major causes: deficiency of phophorus or vitamin D. Osteomalacia is characterised by accumulation of excess, unmineralised and presumably unmineralisable osteoid on trabecular surfaces. Osteomalacic bones have a diminished resistance to pressures and tensions, and increased susceptibility to the stresses and strains of ordinary activity. As a result, there is excess deposition of matrix where mechanical stimuli are strongest, such as at insertions of tendons and fascia, places of angulation and curvature, and on stress-oriented epiphyseal trabeculae. When the disease is advanced, bones break easily, the marrow cavity is enlarged and the cortex is thin, spongy and soft. Deformities are often present.

Osteomalacia due to deficiency of phosphorus is uncommon in animals except in areas of the world, such as South Africa, northern Australia and the North Island of New Zealand, where the pasture is low in phosphorus and supplemental feeding is rare. Cattle are more susceptible than sheep, and horses seem to be remarkably resistant to phosphorus deficiency. Osteomalacia due to vitamin D deficiency occurs in grazing animals where the combination of relatively high latitudes and relatively mild climates allow them to be pastured for much of the year. Critical factors are probably the unavailability of sun-cured hay, the demands of pregnancy and lactation, and inadequate exposure to ultraviolet light.

Whereas osteomalacia is a disease of mature bones, rickets is a disease of growing bones. The causes and pathogenesis are the same, but the vitality of youthful tissue and the transformations and vulnerability of growing bone introduce greater complexity into the morphogenesis of rickets. Since bones mature at different times, the two diseases may co-exist in a skeleton.

There is still controversy about the respective role of vitamin D, calcium and phophorus in the aetiology of rickets. The basic question is where vitamin D prevents rickets solely by increasing blood calcium or whether it also changes the matrix (osteoid or cartilage) so it can accept mineral. The fact that uncomplicated calcium deficiency does not produce rickets is inconclusive because only in the terminal stages of this deficiency does severe hypocalcaemia occur, at which time growth slows, obviating the development of rickets.

Enlargement of joints is a typical sign of rickets. It involves long bones and is usually accompanied by lateral or medial deviation. The enlargement is partly due to the flaring of the metaphysis and partly to retarded longitudinal growth of the epiphysis and its flattening by weight bearing. Normally, the growth of bone at the physis is followed by subperiosteal resorption at the metaphysis. In rickets, osteoid (and unmineralised cartilage) persists in the metaphysis and modelling of the shaft fails because the osteoid is resistant to resorption. This results in the club-like thickening in the metaphyseal region known as rachitic metaphysis; it is most prominent at the costochondral junctions where the row of beaded metaphyses is called the rachitic rosary.

In humans, the squat bow-legged figure is not so familiar in European countries as they were 100 years ago. Evidence has been found in Neolithic skeletons from Denmark and Norway, and more plentiful evidence comes from Hungary in the Roman period. However, rhe rarity of this disease in the past is attested by the few cases described even in exhaustive studies of human remains prior to the Medieval period. Urbanisation and the later industrial revolution in cities with their crowded housing and industrial smoke created this ‘disease of civilisation’. Rickets was a common disease in England in the 17th and 18th centuries (’The English Disease’) and Madonna and Child paintings produced in the Netherlands in the 15th and 16th centuries show characteristic deformities in the form of bowed legs and deformed chests. It was described in 17th century England as a new disease, which does support the lack of evidence before that time in the British archaeological record. Today it may be seen in Asian women in western countries where clothing covers most of their skin (and they may not consume enough vitamin D), but anybody who is housebound and not exposing their skin to the sun is susceptible.


Jubb, K. V. F., Kennedy, P. C., and Palmer, N. 1993. Pathology of Domestic Animals. 4th Edition. Volumes 1, 2 and 3. London: Academic Press.

Roberts, C. and Manchester, K. 2005. The Archaeology of Disease. 3rd Edition. Stroud: Alan Sutton Publishing Ltd.

Early Cat Taming in Egypt


Domestication of the cat

The wild ancestor of our domestic cat is Felis silvestris, and more precisely its Levantino-African subspecies, F. s. lybica. The exact place and date of its domestication is unknown, but domestic status seems to have been reached by the Middle Kingdom (c. 2040 – 1782 BC) in Egypt, at the latest during the 12th dynasty (c. 1976 – 1793 BC) when the animal begins to appear frequently in Egyptian art. However, a tomb painting from Saqqarah dated to the 5th dynasty (c. 2500 – 2350) depicts a cat with what seems to be a collar around its neck and three hieroglyphs representing seated cats have been found on a limestone building block probably dating to the end of the Old Kingdom and perhaps to the 6th dynasty (Pepy II c. 2278 – 2184 BC).


Hierakonpolis is located between Esna and Edfu in Upper Egypt, and is the largest pre- and protodynastic site known to date, occupied from at least 4000 BC onwards. The so-called elite cemetery (KH 6) is one of the areas that have yielded unique results. Excavations have been on-going since 1979. Thus far, two phases have been recognised:

  1.  Naqada IC – IBB period (c. 3800 – 3650 BC)
  2. Naqada IIIA2 – IIIC1 period (c. 3200 – 3000 BC) and continuing into the 1st dynasty (c. 3050 – 2890 BC)

HK6 is unparalleled in the Predynastic period for the number and variety of animal taxa discovered buried within the graves. These included both domestic animals and wild species such as baboon, elephant, wild donkey, hartebeest, hippopotamus and aurochs.

A small felid

Recent re-examination of the contents of Tomb 12 at HK6 revealed the remains of a small, young felid together with the bones of at least 7 baboons and a hippoptamus of only a few days old. The felid appears to be too small for the swamp cat (Felis chaus) and too large for sand cat (Felis margarita). Although not conclusive, the evidence is in favour of the small felid being the wild cat (Felis silvestris) and, considering the geographical area, this would most likely be the subspecies Felis silvestris lybica. Fusion data indicates that the animal was probably about 6 to 8 months old at death, and was most probably a male. The left humerus shows a healed fracture with a smooth callus in the upper third part of the diaphysis. This fracture is consolidated in an oblique angle of about 30 degrees, as a result of which the bone is about 7% shorter than the right humerus. The right femur also shows evidence of a healed fracture which lead to shortening of the bone.

Whilst wild cat remains from settlement contexts merely prove that the species was hunted, the buried individual from HK6 indicates that it was also caught to be kept in captivity. The bone fractures probably healed without direct intervention, but without human protection against predators and without nursing, the cat would probably not have survived. Taking the length of the healing period into account, the animal most probably was held in captivity for at least 4 – 6 weeks. This, therefore, suggests attempts to tame cats. The process of cat domestication was probably very gradual, leading to full domestic status only during the Middle and New Kingdom. The felid from HK6 provides us with evidence for an early stage in that process.

Reference: Linseele, V., Van Neer, W., and Hendrickx, S. 2007. Evidence for early cat taming in Egypt. Journal of Archaeological Science 34: 2081-2090