International Journal of Osteoarchaeology

Int. J. Osteoarchaeol. 21: 1931 (2011)

Published online 15 October 2009 in Wiley Online Library
(wileyonlinelibrary.com) DOI: 10.1002/oa.1103

A Case of Treponematosis from

Pre-Columbian Chaco Canyon,
New Mexico
K. MARDEN a,b* AND D. J. ORTNER b,y
a
b

ABSTRACT

Department of Anthropology, Tulane University, New Orleans, LA, USA

Department of Anthropology, National Museum of Natural History, Washington, DC, USA

Although numerous cases of treponemal infection have been identied in prehispanic New World skeletal
remains, none has been reported from Chaco Canyon, New Mexico. Chaco Canyon was the epicentre of a
broad culture system that spanned the Four Corners region of the pre-Columbian Southwestern United States.
A burial recovered from the central Great House of Chaco Canyon, Pueblo Bonito, exhibits lesions indicative of
treponematosis. However, the pathological condition of this individual has heretofore been only tentatively
diagnosed because the skeleton was collected from a commingled context and distributed across four
separate catalogue numbers. Now reassociated, these remains exhibit a pattern of pathological changes
strongly indicative of treponemal disease. This case not only adds to the growing body of literature on the
clinical expression and geographic distribution of pre-Columbian treponematosis, but also demonstrates the
utility of painstaking reassociation of commingled human remains. Copyright 2009 John Wiley & Sons, Ltd.
Key words: Chaco Canyon; paleopathology; southwest; syphilis; treponematosis

Introduction
The presence of treponemal infection in the preColumbian New World is now well established
(Steinbock, 1976; Baker & Armelagos, 1988; Bogdan
& Weaver, 1992; Ortner, 1992, 2003; Verano, 1997;
Brothwell, 2005; Cook & Powell, 2005; Stodder, 2005)
and there is mounting evidence of treponematosis in
the prehispanic Southwest (Baker & Armelagos, 1988;
Lahr & Bowman, 1992; Stodder, 1996, 2005). However, no case of treponemal disease has yet been
reported among the ancestral Puebloan populations of
Chaco Canyon.
Located in the San Juan River basin in northwest
present-day New Mexico (Figure 1), Chaco Canyon
boasts some of the earliest and most impressive
architectural accomplishments in the Southwestern
United States. Cluttered with monumental Great
Houses comprised of hundreds of rooms and encompassing multiple ritual kivas, Chaco Canyon is widely
believed to have been a major centre of social, political,
* Correspondence to: c/o 23 Flicker Drive, Topsham, ME 04086, USA.
E-mail: kmarden@tulane.edu
y
The contribution of D. J. Ortner to this article was prepared as part of his
ofcial duties as a United States Federal Government employee.

Copyright # 2009 John Wiley & Sons, Ltd.

economic and/or ritual activity (Vivian, 1990; Mills,

2002; Neitzel, 2003). Construction of these immense
stone structures is estimated to have begun in Chaco
Canyon at approximately AD 850, and they served as
the archetype for an architectural form that was soon
echoed throughout the San Juan Basin, linked by a
unique system of roads (Lekson, 2006: 11). The
systematic spread of Great House architecture and
roads indicates that during the period of its occupation
(approximately AD 8501150), Chaco Canyon was the
origin and focal point of a broad culture system
(Neitzel, 2003). The present study describes the rst
case of treponematosis found in this cultural epicentre.
The National Museum of Natural History (NMNH)
houses a collection of partially commingled human
remains recovered from burial rooms within Pueblo
Bonito (29SJ387), the largest and most geographically
central Great House of Chaco Canyon. The rst step in
researching the multiple, commingled individuals represented by this assemblage involved painstaking
reassociation of as many of the skeletal elements as
possible into discrete individuals. This task was
accomplished on the basis of skeletal morphology,
size, articular t, cortical characteristics, taphonomic
condition and careful analysis of eld records and
photographs taken at the time of excavation. Once
Received 11 February 2009
Revised 12 May 2009
Accepted 15 May 2009

K. Marden and D. J. Ortner

20

Figure 1. Location of Chaco Canyon, New Mexico relative to other modern geographic landmarks (adapted from Vivian & Matthews,
1965: 2, Figure 1).

reassociated, one of these nearly-complete individuals

(catalogue number 327066) was found to exhibit a
combination of cranial and postcranial lesions that is
pathognomonic for treponematosis in morphology and
distribution. Most notably, these include ectocranial
cavitations and stellate lesions on the frontal and
parietals, an unremodeled cavitation perforating the
naso-palatine region, a gummatous lesion on the tibia,
and focal cavitations on the radius and clavicle.
Documentation of this case amongst the wellprovenienced, carefully excavated NMNH collection
of prehispanic human remains from Pueblo Bonito
provides further support that treponemal disease was
present in North America many centuries prior to
Columbus arrival on the continent. These ndings also
contribute to the understanding of the scope,
distribution and expression of the disease in the preColumbian New World, and respond to assertions that
treponemal infection could not survive at high altitudes
(Stodder, 2005). Further, this case highlights the
Copyright # 2009 John Wiley & Sons, Ltd.

critical importance of careful reassociation of commingled human remains in order to reach an accurate
diagnosis of skeletal lesions.

Previous reports
The cranium associated with NMNH catalogue
number 327066 has been mentioned as a possible
case of treponemal disease in previous publications
(Hrdlicka, n.d.; Stewart & Quade, 1969; Mulhern et al.,
2006). However, these reports were restricted to vault
lesions and were generally equivocal about their
etiology, primarily due to the lack of corresponding
postcrania to support this diagnosis. The earliest
published mention of this individual as a pathological
specimen stated, the upper two-thirds of the frontal
and the anterior halves of the parietals show
pathological irregular depressions, with two deeper
Int. J. Osteoarchaeol. 21: 1931 (2011)

Treponematosis from Pre-Columbian Chaco Canyon

scar-like lesions, that remind one of syphilitic lesions,
without however permitting a denite conclusion. . .the
few bones that came with this skull (no long bones) are
normal (Hrdlicka, n.d.). The cranium of 327066 was
later included in a study of frontal bone lesions, in
which the pathological changes were classied nonspecically as large scars probably caused by
inammatory lesions (Stewart & Quade, 1969: 104)
in contrast to traumatic etiology. Despite noting
diagnostic features in the morphology of the lesions
and the extent of cranial involvement, the authors
did not classify this individual as syphilitic, arguing
that the tendency to regard a combination of
lesions involving the skull and long bones as evidence
for syphilis has been prevalent for a long time. . .
Unfortunately, the Pueblo Bonito female (?) with
extensive frontal lesions has no postcranial skeleton
(ibid: 97). The same cranial specimen was also
mentioned more recently in a brief communication
regarding incidence of hyperostosis frontalis interna, in
which the authors note ectocranial lesions on the
frontal and parietals, consistent with treponemal
disease and the presence of a possible hemorrhagic
response with associated vascular channels on the
endocranial surface (Mulhern et al., 2006: 482).
However, none of these previous reports described
lesions other than the skeletal vault scarring, thus omitting changes to the anterior nasal oor of the associated
facial skeleton and to the shaft of the left clavicle of
catalogue number 327066. Moreover, the affected long
bones housed under other catalogue numbers that have
now been reassociated to this individual (the right
tibia, right humerus, right ulna and possibly the right
third metacarpal) have not been described as evidence
of treponematosis in any previous publication. The
present analysis is the rst to involve reassociation of
commingled remains from Chaco Canyon in order to
reconstruct a complete diagnostic picture of the
pathological conditions observed.

Provenience and provenance

The skeletal remains described in this study were
recovered from Room 326 in the western cluster of
burial rooms of Pueblo Bonito, the central Great House
of Chaco Canyon. Pueblo Bonito was inhabited
between approximately AD 850 and AD 1150, with
the western block of rooms believed to have been built
at the earlier end of this range, around AD 890
(Windes, 2003). Room 326, from which this individual
was collected, was excavated under the supervision of
Neil Judd in July of 1924 as part of the Smithsonian
Copyright # 2009 John Wiley & Sons, Ltd.

21
Institution/National Geographic Society joint archaeological expedition to Chaco Canyon. The skeleton is
well provenienced with careful eld notes and
photographs (Judd, 19211927a,b), and was found
under a layer of fallen roof beams, precluding the
possibility that the burial was a later intrusion. Judds
eld note cards for Room 326 describe the remains as
disturbed and signicantly commingled in situ:
Decayed ceiling poles & adobe from upper oors lay
on the 1500 accumulation in middle of room. On,
between and beneath these poles & adobe spalls were
several disturbed burials; above them, an 1800 layer
debris of occupations; above latter, about 20 blown sand
& oor sweepings with a 2nd layer of ceiling poles
about 5 ft. above oor level. Above this 2nd pole layer,
fallen masonry & blown sand to height of walls...Burials:
Nos 14, disarticulated, lay under & among decayed
ceiling poles 152000 above oor in middle of room
(Judd, 19211927a).
More than 10 adults are represented in the Room
326 assemblage. The remains were found in various
states of anatomical disarray and distributed across
several catalogue numbers, each consisting of the
bones of multiple individuals. However, it was possible
to reassociate the affected skull and clavicle identied
as catalogue number 327066 with postcrania from
three other catalogue numbers, thus restoring many of
the skeletal remains of a 3545 year old female from
four separate original catalogue numbers (Figure 2).
The determination of the sex of this individual was
based primarily on pelvic morphology, supported by
cranial morphology and population-relevant skeletal
size and robusticity. Age was determined on the basis
of pelvic changes (auricular surface, retroauricular
surface, pubic symphysis), degenerative joint changes
and dental wear.
Sorting and reassociation of the commingled
remains required careful comparison of the size,
morphology, robusticity, rugosity, cortical quality,
taphonomic condition and articular t of the elements
in relation to each other. This process was enhanced by
the use of scanned photographs taken of the bones
in situ during the excavation process more than 70 years
ago. These historical photographs are of such high
quality and clarity that, by using a zoom function to
scrutinise the scanned images, it was possible in some
cases to identify specic bone specimens in the
photographs, as described below.
The cranium and mandible, both clavicles and both
scapulae were originally designated catalogue number
327066, with which elements from other individuals
were commingled. The vertebrae (cervical 14,
thoracic 612, lumbar 15) were originally numbered
Int. J. Osteoarchaeol. 21: 1931 (2011)

22

K. Marden and D. J. Ortner

Figure 2. Original catalogue numbers for skeletal elements reassociated to comprise the nearly complete individual associated with the
affected skull in catalogue number 327066.

327067, but were at some later point renumbered and

rehoused with 327066 by unidentied museum staff,
along with right ribs 1 and 710, left ribs 1 and 711,
the manubrium, the sacrum, both ossa coxae, the left
fth metacarpal and four hand phalanges (the left fth
proximal phalanx and the right fth proximal, middle
and distal phalanges). Catalogue number 327078 contained this individuals right radius and ulna, the right
third and fourth metacarpals and two hand phalanges.
This catalogue number also contained much of this individuals lower limbs, including both tibiae, bulae, tali,
calcanei and naviculars, as well as the left rst cuneiform,
the left femur and the distal end of the right femur.
The remainder of the tarsals and foot bones were
reassociated from catalogue number 327068, including
both cuboids, second and third cuneiforms, the right
rst cuneiform, all 10 metatarsals and the rst proximal
and distal pedal phalanges from both sides. The right
rst cuneiform is clearly the antimere to the left rst
cuneiform from catalogue number 327078, which
articulates perfectly with the navicular and second
cuneiform from this catalogue number, supporting the
Copyright # 2009 John Wiley & Sons, Ltd.

contention that these bones represent the same

individual. Furthermore, photographs depicting the
excavation of this room offer enough detail to permit
identication of the diseased tibia in situ, and adjacent
to it, the tarsals, metatarsals and pedal phalanges, all in
anatomical position (Figure 3). Therefore, the fact that
the ankle and foot bones received a different catalogue
number than the tibiae and bulae is most likely due to
an error in bagging or labelling in the eld.
The humeri and left lower arm bones for this
individual have not been identied, and the shaft of the
right femur is presumed to have been destroyed, as it is
visibly crushed in the excavation photograph (foreground of Figure 3). Despite these missing elements,
however, reassociation of the extant skeletal remains
reveals a pattern of lesions that is highly diagnostic of
treponematosis.

Observed pathological changes

The morphology and distribution of lesions observed
in this case present a pattern that is highly diagnostic of
Int. J. Osteoarchaeol. 21: 1931 (2011)

Treponematosis from Pre-Columbian Chaco Canyon

Figure 3. Right tibia with lesion (arrow) depicted in situ. Note

that the tarsals and rst metatarsal are clearly in anatomical
position, although these bones were later labelled with three
separate catalogue numbers, as was the left leg shown in midground. Reproduced by permission of National Anthropological
Archives, Smithsonian Institution (Neil Judd Papers Neg
#28471).

treponematosis (Figure 4). More than one bone is

affected and skeletal lesions are widely distributed
throughout the skeleton. Although the postcranial
lesions in this individual are concentrated on the right
side of the skeleton, only the left clavicle is involved
and the cranial lesions are bilateral, consistent with

Figure 4. Skeletal elements exhibiting lesions consistent with

treponemal infection in individual 327066 after reassociation.

Copyright # 2009 John Wiley & Sons, Ltd.

23
treponemal infection (Aufderheide & Rodrguez-Martn,
1998). The skeletal elements most affected in this
casethe tibia, the nasal region and the cranial
vaultare those most commonly involved in tertiary
treponematosis (Hackett, 1976; Steinbock, 1976;
Rogers & Waldron, 1989; Meyer et al., 2002; Ortner,
2003). These three anatomical regions together
comprise roughly 70% of all skeletal lesions caused
by treponematosis (Ortner, 2003).
Pathological changes observed in the cranial vault
include several focal cavitations that penetrate into the
diploe but do not affect the inner table. There are also
compact bone depressions with radial grooves that
create a stellate pattern (Figures 5 and 6) consistent
with caries sicca. These stellate lesions have been
indentied as the only reliable and pathognomonic
lesion of syphilis (Virchow, 1896, in Hackett, 1976:
44). The cranial lesions in this case are focused on the
frontal bone and extend bilaterally to the parietals. The
anterior endocranium contains regions of hypervascularity and thickened diploe of the vault that are
nonspecic, but in conjunction with the ectocranial
lesions are suggestive of treponematosis. The frontal
bone also exhibits irregular, endocranial exostoses that
are consistent with the benign, idiopathic condition
hyperostosis frontalis interna and unrelated to treponemal infection (Hackett, 1976; Mulhern et al., 2006).
There is also mild endocranial pitting consistent with
the thickened vault and the age of the individual. A
gummatous lesion also perforates the anterior nasal
aperture oor on the left side, exhibiting a rough,

Figure 5. Cranial vault lesions. Black arrow points to depressed

lesions with stellate scarring. White arrows point to a supercial
focal cavitation perforating into the diploe.

Int. J. Osteoarchaeol. 21: 1931 (2011)

24

K. Marden and D. J. Ortner

Figure 7. Superior view of active lesion in left anterior nasal oor.

Figure 6. Detailed view of ectocranial lesions. (a) Supercial

cavitation perforating into the diploe. The lesion exhibits stellate
grooves and a sclerotic margin, although some postmortem
breakage is observed. (b) Stellate grooves around a healed,
depressed lesion.

porous margin and a granular interior surface (Figure 7).

No sclerotic response is noted in this lesion, the palate
has not been perforated and the margins of the piriform
aperture are intact, indicating that this lesion was of
relatively recent development and was active at the
time of death. Oronasal lesions are highly characteristic of treponemal infections in general (Engelkens
et al., 1999; Parish, 2000; Antal et al., 2002), and of
treponarid in particular (Aufderheide & RodrguezMartn, 1998).
The most notable postcranial change in this
individual is a lesion on the right distal tibia
(Figure 8), the bone 10 times more likely to exhibit
treponemal infection than any other appendicular
skeletal element (Bogdon & Weaver, 1992; Ortner,
2003). This granulomatous lesion is characteristic of
Copyright # 2009 John Wiley & Sons, Ltd.

tertiary treponematosis in both morphology and

location, formed as a striated nodule located on the
anteromedial aspect of the tibial shaft with a central
gummatous cavitation (Hackett, 1976: 7680). No
bowing deformity or expansion is observed in either
tibia, and the edges of the gummatous cavity are not
markedly sclerotic, suggesting relatively late involvement of this bone in the disease process.
A few other long bones show lesions indicative of
systemic infection. The right radius exhibits a small
cluster of focal pitting with a lateral border of blastic
activity. The adjacent ulna shows a thin, barely
adherent plaque of woven bone on the proximal
surface, consistent with inammation and supportive of
a diagnosis of treponematosis when considered in
tandem with the radial lesion. The left clavicle likewise
exhibits a small region of supercial pitting, with a thin
layer of periosteal reaction but no striations (Figure 9).
Clavicular involvement is a hallmark of treponemal
infection. There is also a slightly raised, sclerotic
region with healing porosity on the medial shaft of the
left femur along the linea aspera, which is nonspecic
Int. J. Osteoarchaeol. 21: 1931 (2011)

Treponematosis from Pre-Columbian Chaco Canyon

Figure 8. Striated node on medial aspect of right distal tibial

shaft.

but supports the interpretation of a cycle of active and

healing systemic inammation suggested by the various
stages of cranial lesions.
Other slight skeletal changes observed in this
individual are not diagnostic of treponemal infection

Figure 9. Small destructive lesion on midshaft of left clavicle.

Copyright # 2009 John Wiley & Sons, Ltd.

25
and are more likely to result from separate causes. Most
interesting among these is fusion of the distal head of
the right third metacarpal to the third proximal hand
phalanx. While destruction and fusion of the interphalangeal joints, or destructive dactylitis can be
characteristic of yaws (Ortner, 2003: 276), the
metacarpal-phalangeal joint is not commonly involved,
and yaws would not be expected to occur either in an
older adult or in such an arid climate (Hackett, 1976;
Steinbock, 1976). Therefore, this lesion is more likely
to be the result of traumatic insult than of infectious
disease process.
The axial skeleton exhibits no clear involvement in
the disease process, although there is a sclerotic
buttressing on the visceral aspect of two lower left ribs,
which suggests nonspecic inammation. This skeletal
response is seen in several individuals from Pueblo
Bonito and has been explained as a result of mechanical
stressors (Lambert, 2002). Other skeletal changes
noted include mild blastic changes to the subchondral
bone of the patella, porosity and lipping on the
superior-most point of dens of the second cervical
vertebra and asymmetrical development of the bodies
of several adjacent thoracic vertebrae accompanied by
signicant lipping. All of these changes are more
consistent with generalised age-related osteoarthritis
rather than with treponemal infection. The cortical
bone of the left navicular and both tali exhibit porosity
and proliferative bony excretions, but this is most likely
related to age and general degenerative processes
common to the lower leg and ankle bones of the Chaco
skeletal assemblage.

Differential diagnosis
Pathological changes in this case are consistent with
the characteristic traits of treponematosis, which
usually affects multiple bones, is bilateral, and
preferentially manifests in the ectocranial vault, the
tibia and the nasal region (Hackett, 1976; Steinbock,
1976; Bogdan & Weaver, 1992; Aufderheide &
Rodrguez-Martn, 1998; Ortner, 1992, 2003). Treponematosis also commonly affects other long bones, and
clavicular involvement is particularly suggestive of
treponemal infection (Bogdan & Weaver, 1992; Ortner,
2003).
However, in weighing the likelihood of treponemal
disease, one must consider several alternative etiologies, including other disease processes or trauma.
Although the healed, sclerotic depressions on the vault
might be confused for remodelled traumatic insult, the
overall pattern of healed, stellate depressions between
Int. J. Osteoarchaeol. 21: 1931 (2011)

26
perforating, unhealed gummatous nodules observed in
this cranium is inconsistent with trauma but is strongly
diagnostic of treponematosis. Likewise, the striated
nodules and destructive lesions of the long bones in
this case are inconsistent with a traumatic etiology in
both morphology and distribution.
Tuberculosis is known to affect the cranium, although
it is more likely to be expressed as erosion of the
endocranium than the outer table (Hackett, 1976;
Steinbock, 1976), unlike the ectocranial lesions and
naso-palatine destruction observed in this case (Ortner,
2003). In the long bones, tuberculosis characteristically
attacks the joints and cancellous tissue at the metaphyses
rather than cortical lesions in the diaphyses as seen in this
case (Hackett, 1976). Tuberculosis also commonly
causes destruction of the vertebrae, which are not
affected in this case, and rarely involves the formation
of new bone as observed on the margins of the lesions
in this case (Buckley & Tayles, 2003).
Damage caused by leprosy is almost exclusive to the
nasal region, metacarpals and hand and foot phalanges,
although reactive bone formation from a secondary
infection of the foot can involve the distal tibia and
bula (Steinbock, 1976; Buckley & Tayles, 2003). In
contrast, the most pronounced skeletal changes in this
case are those of the cranial vault and tibial midshaft.
Although the nasal region of 327066 exhibits pathological changes, this relatively small, granulomatous
lesion perforating the nasal oor is not consistent with
the extensive destruction of the piriform margin and
atrophy of the anterior nasal spine characteristic of
leprosy (Mller-Christensen, 1961, in Hackett, 1976:
65). Rather, this type of nasal lesion is highly
characteristic of the clinical expression of tertiary
treponemal infection, wherein soft tissue destruction of
the nasopharynx progresses into the facial skeleton
(Engelkens et al., 1999; Parish, 2000; Antal et al., 2002).
This is particularly true in endemic syphilis (Aufderheide
& Rodrguez-Martn, 1998; Parish, 2000), although
oronasal involvement is also observed clinically in
benign tertiary syphilis (Pletcher & Cheung, 2003).
Similarly, the involvement of a hand bone in this case is
restricted to a single ankylosed metacarpophalangeal
joint, rather than the extensive joint resorption and
deformation associated with leprosy (Steinbock, 1976;
Aufderheide & Rodrguez-Martn, 1998; Ortner, 2003).
The typical pathological signature of chronic,
pyogenic osteomyelitis involves enlargement of the
long bone shafts accompanied by sequestrated bone,
involucra and cloaca formation (Hackett, 1976;
Steinbock, 1976; Ortner, 2003), none of which occur
in this case. Neoplasms can generate lesions in the
outer surface of the cranial vault, but cancer is usually
Copyright # 2009 John Wiley & Sons, Ltd.

K. Marden and D. J. Ortner

destructive and tends to affect the diploe (Hackett,
1976: 68). Both osteomyelitis and neoplasm are
possible, although the morphology of the lesions
makes the latter unlikely. Sarcoidosis produces similar
lesions but is a very rare disorder (Bogdon & Weaver,
1992; Aufderheide & Rodrguez-Martn, 1998; Ortner,
2003). Overall, the pattern of supercial cavitations
and stellate scars on the external cranial vault, a
destructive lesion perforating the naso-palatine region,
a striated node on the medial tibial shaft and
involvement of multiple long bone shafts with blastic
lesions create a diagnostic portrait best attributed to
treponematosis.

Differentiation between treponemal

infections
Although the pattern of radial cranial scarring, striated
nodules and gummatous lesions observed in this case is
indicative of treponemal disease, these changes are not
specic to a single form of treponematosis. Infection
caused by the Treponema bacterium manifests in four
forms that are very similarpinta, yaws, endemic
syphilis and venereal syphilis. Pinta, caused by
T. carateum, is primarily a skin condition with no
known skeletal involvement. The remaining three
treponemal infections are each caused by subspecies of
the Treponema pallidum bacterium and each can cause
skeletal lesions (Centurion-Lara et al., 1998; Kolman
et al., 1999; Meyer et al., 2002; Powell & Cook, 2005;
Harper et al., 2008). Some authors (e.g. Baker &
Armelagos, 1988; Aufderheide & Rodrguez-Martn,
1998) refer to the causative bacterium for yaws as a
separate species, T. pertenue. However, we have chosen
to follow the interpretation of recent molecular studies
and treat all three forms as subspecies of T. pallidum.
Each of these three forms of infection can affect the
skeleton, although there are some discernable differences in the epidemiology and clinical expression of
the disease (Morand et al., 2006). Yaws, caused by
T. pallidum subsp. pertenue, most commonly has a
childhood age of onset, with tertiary development
starting 510 years after the initial infection stage. The
tertiary lesions of yaws are identical to those of
acquired syphilis, the difference being a matter of
degree (Aufderheide & Rodrguez-Martn, 1998),
except that yaws can produce erosive joint involvement
that may be unique among the treponematoses (Ortner
et al., 1992). This form of the disease is believed to be
transmitted primarily through direct contact via skin
lesions, although the possibility of an insect vector has
been raised (Aufderheide & Rodrguez-Martn, 1998;
Int. J. Osteoarchaeol. 21: 1931 (2011)

Treponematosis from Pre-Columbian Chaco Canyon

Powell & Cook, 2005: 13). Yaws is generally restricted
to humid climates (Hackett, 1983; Aufderheide &
Rodrguez-Martn, 1998; Ortner, 2003; Powell &
Cook, 2005). However, there are cases in which the
clinical expression of yaws and endemic syphilis is
observed well outside of the expected geographic
parameters (Brothwell, 2005).
Endemic syphilis, also referred to as bejel or
treponarid, is caused by T. pallidum subsp. endemicum,
and occurs in arid, temperate and subtropical
nonhumid environments. Like yaws, endemic syphilis
usually begins in childhood, with a peak incidence
between 2 and 10 years of age (Bogdon & Weaver,
1992; Aufderheide & Rodrguez-Martn, 1998). Endemic syphilis is transmitted through direct or indirect
contact with lesions of the skin or mucous membrane,
and can therefore be passed through the shared use of
eating and drinking vessels or other household and
personal items which come into contact with infected
mucosae (Parish, 2000; Powell & Cook, 2005). In
contrast, acquired or venereal syphilis (also referred to
simply as syphilis) is caused by T. pallidum subsp.
pallidum. This treponeme has no geographic limits and
climate does not inuence development of disease
(Baker & Armelagos, 1988; Aufderheide & RodrguezMartn, 1998; Bogdon & Weaver, 1998). Acquired
syphilis is transmitted through sexual contact, resulting
in an age of onset that is normally later than the other
forms, at approximately 1530 years with peak age of
onset around 2024 (Aufderheide & Rodrguez-Martn,
1998). The tertiary stage can develop many years after
initial infection.
Although it is widely held that acquired syphilis is
the only form known to have a congenital transmission
(Aufderheide & Rodrguez-Martn, 1998; Powell &
Cook, 2005), there is evidence of that yaws can also
pass transplacentally from mother to foetus (Hoeprich,
1989, in Ortner, 2003: 277). Transplacental transmission of treponematosis is most likely in the early
stages of infection, so that a woman who acquires the
disease during pregnancy is apt to transmit the disease
to her developing foetus (Rein, 1983, in Resnick, 2002:
2552). Therefore, although yaws is most commonly
acquired in childhood, congenital transmission is
possible if a woman contracts the disease during
pregnancy (Ortner, 2003).
The source of this variation in the expression of the
treponemal infections is debated. While some researchers assert that each form is caused by a distinct
pathogen (Hackett, 1976; Rothschild & Rothschild,
1995, 1996), others support a unitarian theory, which
interprets the four forms as temporally, environmentally or culturally dependent variants of the same
Copyright # 2009 John Wiley & Sons, Ltd.

27
disease (Hudson, 1965; Steinbock, 1976; Baker &
Armelagos, 1988; Heathcote et al., 1998) or rapid
adaptations to new environmental conditions (Livingstone, 1991). Evidence exists to support both sides of
the argument. There appears to be some degree of
cross-immunity between the forms (Baker & Armelagos, 1988; Aufderheide & Rodrguez-Martn, 1998;
Ortner, 2003). Infection with bejel or yaws in
childhood serves as a partial protectant against adult
infection with syphilis, and venereal syphilis generally
occurs where the other forms are not prevalent
(Steinbock, 1976; Garruto, 1981). Although this
relationship is not fully understood (Brothwell, 2005;
Powell & Cook, 2005), it supports an interpretation of a
single pathogen causing all three forms, since a
population which is mostly immune to infection by
the age of sexual maturity would be unlikely to sustain a
venereal mutation (Meyer et al., 2002). Early immunological and DNA studies of the bacterium indicated
that the spirochetes causing yaws, bejel and syphilis
were identical (Baker & Armelagos, 1988; Ortner et al.,
1992). Conversely, more recent molecular research has
identied distinctions in treponemal DNA (e.g.
Centurion-Lara et al., 1998). This led to the identication of a single-base polymorphism in a centuries-old
skeletal specimen from Easter Island that distinguished
T. pallidum subsp. pallidumthe causative agent for
venereal syphilisfrom the other three human
treponemes (Kolman et al., 1999). However, these
genetic differences were found only in a non-coding
portion of the DNA and therefore do not explain the
variations in the expression of disease (Morand et al.,
2006). Subsequent molecular researchers have been
unable to replicate these results and therefore question
their validity (Bouwman & Brown, 2005; Barnes &
Thomas, 2006; von Hunnius et al., 2007). The debate
regarding the nature of the difference between the
forms of treponemal infection continues.
Irrespective of the origins and epidemiology of the
causative pathogen(s), however, the lesions resulting
from the tertiary stage of any of the three skeletal forms
of treponematosis are generally accepted as indistinguishable (Hackett, 1976; Aufderheide & RodrguezMartn, 1998; Ortner, 2003; Powell & Cook, 2005).
Rothschild and Rothschild (1995, 1996) claim to have
developed a set of diagnostic criteria to distinguish
between the causative pathogens in dry bone samples,
asserting that syphilis alters the appearance of bones in
a highly specic manner, which one can nd if one
knows how to look (Rothschild, 2005: 1459).
However, the validity of these criteria has been
vigorously challenged (Heathcote et al., 1998; Cook &
Powell, 2005). Until valid and reliable diagnostic
Int. J. Osteoarchaeol. 21: 1931 (2011)

28
criteria between the treponematoses are rmly
established, the distinction between the skeletal
manifestations of these infections can be best understood as a matter of degree, geographic distribution
and demographic expression (Rogers & Waldron, 1989;
Aufderheide & Rodrguez-Martn, 1998; Ortner, 2003).
Of the four known forms of treponematosis, the
present case is most consistent with acquired syphilis.
Although yaws can cause skeletal lesions in the tertiary
stage that are almost identical to those of syphilis, this
form is restricted to humid climates and is most
commonly acquired by young children, making it an
unlikely cause of disease in this older adult from the dry
climate of Chaco Canyon (Hackett, 1983; Ortner,
2003). Endemic syphilis is common in arid, temperate
and subtropical climates like that of Chaco Canyon,
but is also a disease with a childhood age of onset, with
a peak prevalence in the rst decade of life (Hackett,
1983; Aufderheide & Rodrguez-Martn, 1998; Meyer
et al., 2002), and tertiary lesions usually develop
between 2 and 10 years from the initial stage of
infection (Bogdon & Weaver, 1992; Farnsworth &
Rosen, 2006). This period may vary somewhat, and
both yaws and endemic syphilis exhibit cycles of
remission and activity in which an initial infection in
childhood can reappear later in life. However, the
characteristic latency period of 210 years reduces
the likelihood that this pathogen is responsible for the
active tertiary lesions observed in this 3545 year old
female skeleton if she was infected during childhood.
Alternatively, if this individual had not contracted
endemic syphilis as a child, she may have been
susceptible to an initial treponarid infection as an adult.
There is some evidence that yaws and bejel elicit a
natural immunity against subsequent infection, whereas
venereal syphilis confers no such immunity (Garruto,
1981; Aufderheide & Rodrguez-Martn, 1998).
Although this individual could certainly have contracted the infection as a young adult through sexual
contact, this would not be the only possible manner of
infection. If treponarid was not endemic to preColumbian Chaco Canyon, it is just as likely that,
lacking immunity to bejel conferred by childhood
infection, she contracted the disease through use of
shared food vessels or utensils while passing through an
endemic areaor during a visit to the canyon by
someone from an endemic area. Exotic goods found in
Chaco Canyon that originate as far away as Mexico and
California indicate that Chaco was part of an extensive
trade network, providing opportunity for infection by
outsiders from endemic regions.
However, yaws has been clinically identied in such
varied environments as Scotland and Bosnia, challenCopyright # 2009 John Wiley & Sons, Ltd.

K. Marden and D. J. Ortner

ging the widely-accepted geographic restriction of the
different forms of treponemal infection (Brothwell,
2005). Therefore, the possibility remains that Chaco
Canyon was indeed endemic for treponarid, and that
this individual simply avoided childhood infection and
was subsequently vulnerable to treponarid as an adult.
Alternately, it is possible that the expression of the
disease has changed over time, with a more protracted
latency period between initial treponarid infection and
the tertiary symptoms than recognised in a modern
clinical context. Therefore, while the geographic and
demographic details of this case are most consistent
with our current understanding of acquired syphilis, it
is possible that 327066 could represent any of the three
skeletal forms of treponematosis.
Aufderheide and Rodrguez-Martn (1998) assert
(contra Baker & Armelagos, 1988) that it is possible to
reliably discern between the treponemal infections,
given an entire skeletal series and taking into
consideration climatic and social factors. However,
these authors concede that a paleopathological
diagnosis based on a single bone exhibiting nonspecic periostitis or osteoperisostitis, is very difcult
and vulnerable to error (1998: 171). The specimen
represented by catalogue number 327066 falls somewhere between these two extremes. This individual
exhibits a pattern of distinctive lesions affecting those
skeletal elements characteristic of treponemal infection, and ts the geographic and age distribution most
consistent with acquired syphilis. Nonetheless, the
accurate determination of the causative pathogen of
lesions observed in a single skeleton remains problematic, and the possibility of an atypical infection by
treponemal subspecies endemicum or pertenue cannot be
discounted. It is also possible that an extinct form of
infection, treponemal or otherwise, could have
produced these lesions (Ortner, 1992; Meyer et al.,
2002). Until molecular methods are enhanced, it is not
possible to offer a denitive diagnosis of treponematosis in generalor of venereal syphilis in particular
in an isolated specimen. However, given the current
state of knowledge, syphilis remains the most likely
cause for the lesions exhibited in this individual.

Discussion and conclusions

This case presents strong skeletal evidence for
treponemal infection in a burial from Pueblo Bonito,
Chaco Canyon, dated to between AD 950 and AD
1150. Whereas previous studies have accepted nonspecic periostitis of the long bones as evidence of
treponemal infection (Rothschild & Rothschild, 1996;
Int. J. Osteoarchaeol. 21: 1931 (2011)

Treponematosis from Pre-Columbian Chaco Canyon

Rothschild et al., 2000; Stodder, 2005), this specimen
exhibits lesions which are pathognomonic of treponematosis in both morphology and distribution. The
pattern and appearance of these lesions, combined with
the established prehispanic abandonment of Chaco
Canyon, the stratigraphic location of the burial
underneath fallen roof beams, and the associated
ceramic and tree-ring dates make strides towards
meeting the fundamental requirements for establishing
pre-Columbian treponematosis in Chaco: unambiguous identication of treponemal disease and. . .unambiguous determination of pre-Columbian age (Ortner,
2003: 297).
The morphology and distribution of skeletal lesions
in this individual exhibit a pattern that is highly
diagnostic of treponemal infection. Although a single
diagnostic case does nothing to establish prevalence
rates for the disease in Chaco (Hackett, 1983; Ortner,
1992), it does indeed help to establish the presence of
the disease at the very centre of the Chacoan world.
This is of particular value since Chaco Canyon has
been specically noted for its absence of archaeological evidence of treponematosis (Stodder, 2005),
despite burgeoning evidence of treponematosis elsewhere in the prehispanic Southwest. If treponarid was
not endemic to Chaco Canyon, then the fact that an
individual buried in Chaco Canyon exhibits characteristic skeletal signs of treponemal infection indicates
either that the treponemal disease was acquired
through contact with an infected outsider, or that this
individual had grown up in an area where treponarid
was endemic, where she was infected before moving to
Chaco later in life. However, the fact that this middleaged woman exhibited active lesions indicates a longer
latency period than is normally expected between a
childhood infection and the tertiary stage of the
disease. Therefore, unless the expression of the disease
has changed over time, it is more likely that this
individual was infected as a young adult, either by the
venereal or the endemic form.
It should also be noted that the absence of other
recognised cases of treponematosis among the burials
in Chaco Canyon does not preclude the possibility that
more individuals were infected. Lack of treponemal
infection in the few hundred skeletons found in the
canyon is not, in itself, sufcient evidence for the absence
of the disease in Chaco. Since treponemal disease affects
the skeleton in less than 10% of all infections, a single
case of skeletal treponematosis implies the presence of
many more cases in the population. As the rst report
of treponematosis in Chaco Canyon, this case
enhances understanding of health status in Chaco
Canyon during its occupation and augments mounting
Copyright # 2009 John Wiley & Sons, Ltd.

29
evidence of treponemal infection in the prehispanic
Southwest. Although this case improves our understanding of the geographic and temporal scope of the
disease, it does little to help discern between the
different forms of treponematosis.
Whereas the massive architecture of Chaco Canyon
was initially interpreted as dwellings for tens of
thousands of canyon residents, these Great Houses
have been more recently interpreted as sociopolitical,
economic or ritual centres and the population of the
canyon is now widely accepted to have been as low as
fewer than 2000 (Judge, 2004). This estimate is
supported by the fact that only a few hundred skeletons
have been found buried in Chaco (Akins, 1986).
Although such a small population size is generally
considered to be too low to support acute infectious
disease (Aufderheide & Rodrguez-Martn, 1998; Meyer
et al., 2002), it must be remembered that Chaco was the
social, political, economic and ritual core of the broad
pre-Columbian Chacoan culture system, and therefore
was likely subject to a regular inux of visitors, allowing
the introduction and/or local support of syphilis.
Furthermore, the abundance of exotic goods excavated
from Chaco Canyon Great Houses indicates longdistance trade systems extending beyond the San Juan
River Basin as far as Mesoamerica, coastal California
and elsewhere (Mathien, 2003), suggesting consistent
interaction with outside populations.
This research also demonstrates the importance of
careful reassociation of commingled skeletal elements
in establishing an accurate diagnosis. The timeconsuming process of reassociation not only claried
the total minimum number of individuals present in
the assemblage, but also reduced the minimum
number of pathological specimens from four individuals with somewhat ambiguous, isolated lesions to a
single case of skeletal disorder. Reassociation of
commingled remains is crucial in order to develop a
clear understanding of the distribution pattern of the
pathological changes in a skeleton or skeletal sample.
Although the cranial vault of this individual has been
previously mentioned as a possible case of treponematosis, the reassociation of the affected cranium with
postcranial elements reveals a pattern of lesions that
allows a more certain diagnosis.

References
Akins NJ. 1986. A Biocultural Approach to Human Burials from
Chaco Canyon, New Mexico. Reports of the Chaco Center,
No. 9. U.S. Department of the Interior, National Park
Service, Santa Fe, New Mexico.
Int. J. Osteoarchaeol. 21: 1931 (2011)

30
Antal GM, Lukehart SA, Meheus AZ. 2002. The endemic
treponematosis. Microbes and Infection 4(1): 8394. DOI:
10.1016/j.clindermatol.2005.11.004
Aufderheide AC, Rodrguez-Martn C. 1998. The Cambridge
Encyclopedia of Human Paleopathology. Cambridge University
Press: Cambridge, U.K; 154171. DOI: 10.2277/
0521552036
Baker BJ, Armelagos GJ. 1988. The origin and antiquity of
syphilis: paleopathological diagnosis and interpretation.
Current Anthropology 29(5): 703738. DOI: 10.1086/203691
Barnes I, Thomas MG. 2006. Evaluating bacterial pathogen
DNA preservation in museum osteological collections.
Proceedings of the Royal Society of Biological Sciences 273: 645
653.
Bogdan G, Weaver DS. 1992. Pre-Columbian treponematosis in coastal North Carolina. In Disease and Demography in
the Americas, Verano JW, Ubelaker DH (eds). Smithsonian
Institution Press: Washington; 155163. DOI:
10;1;.1002/ajpa.1330940214
Bouwman AS, Brown TA. 2005. The limits of biomolecular
palaeopathology: ancient DNA cannot be used to study
venereal syphilis. Journal of Archaeological Science 32: 703
713.
Brothwell DR. 2005. North American treponematosis
against the bigger world picture. In The Myth of Syphilis:
The Natural History of Treponematosis in North America, Powell
ML, Cook DC (eds). University Press of Florida: Gainsville; 480496.
Buckley HR, Tayles NG. 2003. The functional cost of
tertiary yaws (Treponema pertenue) in a prehistoric Pacic
Island skeletal sample. Journal of Archaeological Science
30(2003): 13011314.
Centurion-Lara A, Castro C, Castillo R, Shaffer JM, Van
Voorhis WC, Lukehart SA. 1998. The anking region
sequences of the 15-kDa lipoprotein gene differentiate
pathogenic treponemes. Journal of Infectious Diseases 177:
10361040.
Cook DC, Powell ML. 2005. Piecing the puzzle together:
North American treponematosis in overview. In The Myth
of Syphilis: The Natural History of Treponematosis in North
America, Powell ML, Cook DC (eds). University Press
of Florida: Gainsville; 442479.
Engelkens HJH, Vuzevski VD, Stolz E. 1999. Nonvenereal
treponematoses in tropical countries. Clinics in Dermatology.
17(2): 143152. DOI: 10.1016/S0738-081X(99)00007-3
Farnsworth N, Rosen T. 2006. Endemic treponematosis:
review and update. Clinics in Dermatology. 24(3): 181
190. DOI: 10.1016/j.clindermatol.2005.11.004
Garruto RM. 1981. Disease patterns of isolated groups. In
Biocultural Aspects of Disease, Rothschild H (ed.). Academic
Press: New York; 557597.
Hackett CJ. 1976. Diagnostic Criteria of Syphilis, Yaws, and
Treponarid (Treponematoses) and of Some Other Diseases in Dry
Bones. Springer-Verlag: Berlin.
Hackett CJ. 1983. Problems in the paleopathology of the
human treponematoses. In Disease in Ancient Man, Hart GD
(ed.). Clarke Irwin: Toronto; 106128.
Copyright # 2009 John Wiley & Sons, Ltd.

K. Marden and D. J. Ortner

Harper KN, Ocampo PS, Steiner BM, George RW, Silverman MS, Bolotin S, Pillay A, Saunders NJ, Armelagos GJ.
2008. On the origin of the treponematoses: a phylogenetic approach. PLoS Neglected Tropical Diseases 2(1): e148.
DOI: 10.1371/journal.pntd.0000148
Heathcote GM, Stodder AL, Buckley HR, Hanson DB,
Douglas MT, Underwood JH, Taisipic TF, Diego VP.
1998. On treponemal disease in the Western Pacic:
corrections and critique. Current Anthropology 39(3): 359
368.
Hrdlicka A. n.d. Brief report on skeletal material from Pueblo
Bonito and nearby ruins, New Mexico, Collected by Neil
M. Judd, by Ales Hrdlicka. In Papers of Neil M. Judd, Box
6, Chaco Canyon Notes, Notebooks and Note Cards.
NotesNotebooks, folder Notes on Burials at Pueblo
Bonito, on le, National Anthropological Archives,
National Museum of Natural History, Washington, DC.
Hudson EH. 1965. Treponematosis and mans social evolution. American Antiquity 67: 885901.
Judd NM. 1921-1927a. Field notes of the National Geographic
Society Expedition. Box 8, Chaco Canyon Notes, Notebooks
and Note Cards. Note cards, Pueblo Bonito, Notes on
excavations. On le, National Anthropological Archives,
National Museum of Natural History, Washington, DC.
Judd NM. 19211927b. Field notes of the National
Geographic Society Expedition. Box 10, Chaco Canyon
Notes, Notebooks and Note Cards. Note cards, Pueblo
Bonito, Specimen eld notes, numbers 11822368, on
le, National Anthropological Archives, National
Museum of Natural History, Washington, DC.
Judge WJ. 2004. Chacos Golden Century. In In Search of
Chaco: New Approaches to an Archaeological Enigma. School of
American Research Press: Santa Fe; 16.
Kolman CJ, Centurion-Lara A, Lukehart SA, Owsley DW,
Tuross N. 1999. Identication of Treponema pallidum subspecies pallidum in a 200-year-old skeletal specimen. The
Journal of Infectious Diseases 180(6): 20602063. DOI:
10.1086/315151
Lahr MM, Bowman JE. 1992. Paleopathology of the Kechipawan site: health and disease in a southwestern Pueblo.
Journal of Archaeological Science 19: 639654.
Lambert PM. 2002. Rib lesions in a prehistoric Puebloan
sample from southwestern Colorado. American Journal of
Physical Anthropology 117: 281292.
Lekson SH. 2006. Chaco matters: an introduction. In The
Archaeology of Chaco Canyon, Lekson SH (ed.). School of
American Research: Sante Fe; 344.
Livingstone FB. 1991. On the origin of syphilis: an alternative hypothesis. Current Anthropology 32(5): 587590. DOI:
10.1086/204004
Mathien FJ. 2003. Artifacts from Pueblo Bonito: one hundred
years of interpretation. In Pueblo Bonito: Center of the Chacoan
World, Neitzel JE (ed.). Smithsonian Institution Press:
Washington, DC; 127142.
Meyer C, Jung C, Kohl T, Poenicke A, Poppe A, Alt KW.
2002. Syphilis 2001a paleopathological reappraisal.
Homo 53(1): 3958.
Int. J. Osteoarchaeol. 21: 1931 (2011)

Treponematosis from Pre-Columbian Chaco Canyon

Mills BJ. 2002. Recent research on Chaco: changing views
on economy, ritual, and society. Journal of Archaeological
Research V 10 I (1): 65117.
Morand JJ, Simon F, Garnotel E, Mahe A, Clity E, Morlain B.
2006. Overview of endemic treponematosis. Medecine tropicale: revue du Corps de sante colonial. 66(1): 1520.
Mulhern DM, Wilczak CA, Dudar JC. 2006. Brief communication: unusual nding at Pueblo Bonito: multiple
cases of hyperostosis frontalis interna. American Journal of
Physical Anthropology 130: 480484.
Neitzel JE. 2003. Three questions about Pueblo Bonito. In
Pueblo Bonito: Center of the Chacoan World, Neitzel JE (ed.).
Smithsonian Institution Press: Washington, DC; 19.
Ortner DJ. 1992. Skeletal paleopathology: probabilities,
possibilities and impossibilities. In Disease and Demography
in the Americas, Verano JW, Ubelaker DH (eds). Smithsonian Institution Press: Washington; 513. DOI:
10.1002/ajpa.1330940214
Ortner DJ. 2003. Identication of Pathological Conditions in Human
Skeletal Remains. Smithsonian Institution Press: Washington, DC.
Ortner DJ, Tuross N, Stix AI. 1992. New approaches to the
study of disease in archaeological New World populations. Human Biology 64: 337360.
Parish JL. 2000. Treponemal infections in the pediatric
population. Clinics in Dermatology 18(6): 687700. DOI:
10.1016/S0738-081X(00)00152-8
Pletcher SD, Cheung SW. 2003. Syphilis and otolaryngology. Otolaryngologic Clinics of North America. 36(4): 595605.
DOI:10.1016/S0030-6665(03)00025-2
Powell ML, Cook DC. 2005. Treponematosis: inquiries
into the nature of a protean disease. In The Myth of
Syphilis: The Natural History of Treponematosis in North America,
Powell ML, Cook DC (eds). University Press of Florida:
Gainsville; 962.
Resnick D. 2002. Diagnosis of Bone and Joint Disorders, 4th ed.,
Vol. 3. W.B. Saunders Co: Philadelphia.
Rogers J, Waldron T. 1989. Infections in palaeopathology:
the basis of classication according to most probable
cause. Journal of Archaeological Science 16(6): 611625.
Rothschild BM. 2005. History of syphilis. Clinical Infectious
Diseases 40: 14541463. DOI: 10.1086/429626

Copyright # 2009 John Wiley & Sons, Ltd.

31
Rothschild BM, Rothschild C. 1995. Treponemal disease
revisited: skeletal discriminators for yaws, bejel, and
venereal syphilis. Clinical Infectious Diseases 20: 1402
1408.
Rothschild BM, Rothschild C. 1996. Treponemal disease in
the New World. Current Anthropology 37(3): 555561.
Rothschild BM, Calderon FL, Coppa A, Rothschild C. 2000.
First exposure to syphilis: the Dominican Republic at the
time of Columbian contact. Clinical Infectious Diseases 31:
396441.
Steinbock RT. 1976. Paleopathological Diagnosis and Interpretation. Charles C. Thomas: Springeld, IL.
Stewart TD, Quade LG. 1969. Lesions of the frontal bone in
American Indians. American Journal of Physical Anthropology
30: 80110.
Stodder ALW. 1996. Paleoepidemiology of eastern and
western Pueblo communities in protohistoric and early
contact period New Mexico. In Disease and Biocultural
Frontiers: Native American Adaptation in the Spanish Borderlands,
Baker BJ, Kealhofer L (eds). University of Florida Press:
Gainesville; 148176.
Stodder ALW. 2005. Treponemal infection in the prehistoric Southwest. In The Myth of Syphilis: The Natural History
of Treponematosis in North America, Powell ML, Cook DC
(eds). University Press of Florida: Gainsville; 227280.
Verano JW. 1997. Advances in the paleopathology of
Andean South America. Journal of World Prehistory 11(2):
237268.
Vivian RG. 1990. The Chacoan Prehistory of the San Juan Basin.
Academic Press: San Diego.
Vivian RG, Mathews TW. 1965. Kin Kletso: A Pueblo III
Community in Chaco Canyon, New Mexico. Technical Series
6(1), Southwest Parks and Monuments Association:
Globe, AZ.
Von Hunnius TE, Yang D, Eng B, Waye JS, Saunders SR.
2007. Digging deeper into the limits of ancient DNA
research on syphilis. Journal of Archaeological Science 34:
20912100.
Windes TC. 2003. This old house: Construction and abandonment at Pueblo Bonito. In Pueblo Bonito: Center of the
Chacoan World, Neitzel JE (ed.). Smithsonian Books:
Washington, DC; 1432.

Int. J. Osteoarchaeol. 21: 1931 (2011)