Common Avian Infection Plagued the Tyrant Dinosaurs
Ewan D. S. Wolff1*, Steven W. Salisbury2,3*, John R. Horner4, David J. Varricchio5
1Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin, United States of America, 2School of Biological
Sciences, The University of Queensland, Brisbane, Queensland, Australia, 3Vertebrate Paleontology, Carnegie Museum of Natural History, Pittsburgh, Pennsylvania, United
States of America, 4Museum of the Rockies, Montana State University, Bozeman, Montana, United States of America, 5Department of Earth Sciences, Montana State
University, Bozeman, Montana, United States of America
Background: Tyrannosaurus rex and other tyrannosaurid fossils often display multiple, smooth-edged full-thickness erosive
lesions on the mandible, either unilaterally or bilaterally. The cause of these lesions in the Tyrannosaurus rex specimen FMNH
PR2081 (known informally by the name ‘Sue’) has previously been attributed to actinomycosis, a bacterial bone infection, or
bite wounds from other tyrannosaurids.
Methodology/Principal Findings: We conducted an extensive survey of tyrannosaurid specimens and identified ten
individuals with full-thickness erosive lesions. These lesions were described, measured and photographed for comparison
with one another. We also conducted an extensive survey of related archosaurs for similar lesions. We show here that these
lesions are consistent with those caused by an avian parasitic infection called trichomonosis, which causes similar
abnormalities on the mandible of modern birds, in particular raptors.
Conclusions/Significance: This finding represents the first evidence for the ancient evolutionary origin of an avian
transmissible disease in non-avian theropod dinosaurs. It also provides a valuable insight into the palaeobiology of these
now extinct animals. Based on the frequency with which these lesions occur, we hypothesize that tyrannosaurids were
commonly infected by a Trichomonas gallinae-like protozoan. For tyrannosaurid populations, the only non-avian dinosaur
group that show trichomonosis-type lesions, it is likely that the disease became endemic and spread as a result of
antagonistic intraspecific behavior, consumption of prey infected by a Trichomonas gallinae-like protozoan and possibly
even cannibalism. The severity of trichomonosis-related lesions in specimens such as Tyrannosaurus rex FMNH PR2081 and
Tyrannosaurus rex MOR 980, strongly suggests that these animals died as a direct result of this disease, mostly likely through
Citation: Wolff EDS, Salisbury SW, Horner JR, Varricchio DJ (2009) Common Avian Infection Plagued the Tyrant Dinosaurs. PLoS ONE 4(9): e7288. doi:10.1371/
Editor: Dennis Marinus Hansen, Stanford University, United States of America
Received March 13, 2009; Accepted August 28, 2009; Published September 30, 2009
Copyright: ? 2009 Wolff et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: Gerry Ohrstrom, the Geological Society of America, Montana State University’s College of Letters and Sciences (to EDSW); Carnegie Museum of Natural
History and The University of Queensland (to SWS). A. Wolff and H. Wolff covered publication charges for this manuscript. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: firstname.lastname@example.org (EDSW); email@example.com (SWS)
Dinosaur fossils often display evidence of injuries that can be
attributed to accidents, old age or metabolic disorders. Among
predatory dinosaurs, the most commonly encountered abnormal-
ities are bite-marks and related bone traumas on the head [1,2].
Tooth strike trauma in theropods occurs on or around the face,
particularly on the maxillary rostrum and dentary bones, and the
injuries are often undergoing active healing at the time of death.
The associated lesions include solitary or multiple round or oval-
shaped puncture marks, and elongate gouges and scores caused by
tooth tips being dragged across the surface of the bone. Depending
on the extent to which they have healed, puncture marks typically
have centrally infolded margins, whereas gouges have ragged
margins . Comparisons with unhealed tooth marks on prey
suggests that wounds of this type were inflicted by other large
theropods, most likely conspecifics, as a result of territorial
disputes, mating and possibly cannibalism [1,2]. Although the
possibility remains that theropods within the same geographic
range [e.g. Daspletosaurus and Albertosaurus] could have made similar
bite marks on each other’s skulls, such interaction amongst
relatively few individuals is unlikely. Furthermore, bite marks
made by Tyrannosaurus rex are unmistakable and no similarly sized
predator is known from the latest Maastrichtian of North America.
Many tyrannosaurids display a second category of cranial
abnormalities distinct from the traumas associated with head-
biting. These abnormalities are smooth-edged fully erosive lesions
that are most commonly present in the mandible. They occur
either singly or in multiples and vary in size from millimeters to
several centimeters in diameter. The edges of the bone in these
lesions varies from tapered to sub-rounded, but all exhibit
extensive surrounding remodelling of the bone surface texture,
occasionally accompanied by mild rugosity of the bone surface, as
is seen in FMNH PR2081 [3, Supporting Information S1]. These
smooth-edged lesions have had only anecdotal mention previously,
and their origin is poorly understood. For example, cylindrical
erosive lesions on the surangular and dentary of ‘Sue’ (FMNH
PR2081; Fig. 1) were attributed to an Actinomyces bovis infection .
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While actinomycosis leads to extensive osteomyelitis in hominids
and other mammals , bone-penetrating mandibular lesions
from Actinomyces bovis infections in extant archosaurs remain
unknown [6,7], making this diagnosis unlikely.
To investigate the significance of these unusual smooth-edged
abnormalities in tyrannosaurids, a detailed oral pathology survey
of fossil and extant archosaurs was undertaken. Herein we
demonstrate that these abnormalities have a strong resemblance
to those lesions resulting from an infectious disease known to occur
in modern birds called trichomonosis. This finding not only
establishes that some non-avian theropods had a similar infectious
disease to that found in living birds, but also suggests a similar or
common immune response to the disease.
Nearly 15% of the 61 tyrannosaurid individuals examined
during this study exhibited trichomonosis-type lesions on the
mandible (Figure 1, Figure 2, and Supporting Information S1). In
seven out of nine cases, the trichomonosis-type lesions showed a
unilateral distribution (Figure 2, A, D, E, F and G, and Supporting
Information S1). In the remaining cases, they occurred on both
sides of the mandible (Figure 1, Figure 2, B and C, and Supporting
Information S1). These abnormalities comprise multiple chronic
smooth-edged erosive lesions with a focal distribution in the caudal
part of the mandible, usually on the surangular and less commonly
on the dentary (Figure 1, Figure 2, and Supporting Information
S1). The abnormalities typically have a circular or slit-like shape,
with moderate surrounding thickening of the bone. In the majority
of cases, these lesions exhibit neither alteration to the bone fabric,
deformation of the periosteal bone nor exposure of the endosteal
bone. Instead, the outward appearance often consists of a
developmental change in the bone with no indication of any
obvious mechanism of formation.
The position and morphology of these lesions does not
correspond with any fenestrae or foramina typically seen in non-
avian dinosaurs, birds or other archosaurs, so individual variation
in morphology can be ruled out . The known pathology of
modern archosaurs, on the other hand, provides useful insights
into the nature of these abnormalities.
Superficial injuries in extant crocodylians usually heal, leaving
scars on the skin [9–13]. Depending on the degree to which they
heal, superficial wounds may form a point of entry for infectious
agents such as ‘crocodile/caiman pox’ (Parapoxvirus) . Croco-
dylian poxvirus is similar to a poxviral disease of modern birds of
prey known as ‘raptor pox’, where crusty nodular lesions form
within the skin . However, lesions from these diseases are
proportionately very small, and their morphology does not
compare well with the trichomonosis-type lesions seen on
Deeper facial wounds in extant crocodylians, particularly those
that penetrate bone, often become infected by a variety of
bacterial agents. Bacterial infection of such wounds may result in
the formation of abscesses . Such abscesses may eventually
form large, localized caseous masses through the accumulation of
heterophil-induced fibrin deposition. Fungal infections of deep bite
wounds in captive crocodylians can result in heterophilic
granulomatous inflammation [14,16] and gingivitis . Despite
the superficial resemblance of the tyrannosaurid mandibular
lesions to abnormalities that may stem from crocodylian poxvirus,
abscesses, granuloma, bite-wound gingivitis, and bite trauma, the
trichomonosis-type lesions in tyrannosaurids differ in their location
and distribution at the caudal end of the mandible (Figure 1 and
The only known disease among extant crocodylians affecting
similar areas on the mandible is a skin infection caused by
Fusarium, a filamentous fungus that is normally part of the
crocodylian oral flora [14,17]. Manifestation of this type of
dermatomycosis, however, is strictly necrotic, not erosive; the
infection does not lyse the underlying bone. The bone remains
present but dead rather than being lysed by the infection. Also, the
disease occurs only in hatchlings and relates principally to nesting
The modern avian differential diagnostic possibilities for these
tyrannosaurid mandibular lesions include vitamin C or D
deficiency, aspergillosis, avian (raptor) pox, capillariasis and
trichomonosis. Vitamin C or D deficiencies in extant birds and
crocodylians can lead to a general decrease in bone density and
integrity [14,18] and regionalized thinning of bone . This
diffuse bone loss differs from the focal trichomonosis-type lesions
in tyrannosaurids. The opportunistic fungal infection, aspergillosis,
can lead to ‘space occupying masses in the skin’ of raptors [18,19].
Figure 1. Tyrannosaurus rex (FMNH PR2081). Left mandibular
ramus exhibiting multiple trichomonosis-type lesions (indicated by
arrows); (A and D), lateral view (photo; schematic interpretation). (B
and E) medial view (photo; schematic interpretation). (C), schematic
interpretation of the reconstructed skull of FMNH PR2081 in left lateral
view with the mandibular ramus shown in red. Anatomical abbrevia-
tions: ang, angular; art, articular; corn, coronoid; d, dentary; fen mand
ext, external mandibular fenestra; for my, mylohyal foramen; for sa
caud, caudal surangular foramen; for sa rost, rostral surangular foramen;
preart, prearticular; sa, surangular; sd, supradentary; sp, splenial. a and b
modified from ?1999 The Field Museum, GEO86260_7c and
GEO86262_4c, respectively. Photographer John Weinstein.
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Erosive lesions form by pressure erosion from the overlying
dermis, as might occur with a fibriscess. However, there are no
reported occurrences of osteological lesions from aspergillosis on
avian mandibles. Avian pox represents a viral disease in the
Poxviridae clade known to lead to large papules in the skin and
adjacent layers [18,19]. These lesions typically occur ventral to the
orbit and caudal to the jaw articulation . No specific
presentation is reported in the mandible. Capillaria is a nematode
parasite that commonly forms granulomatous plaques on the
palate of raptors [18,19]. If the infestation progresses, the infection
of oral mucosa can lead to ‘localized’ mandibular abscesses
[18,19]. However, these abscesses are rare, and if present, they are
Avian trichomonosis is a strongly erosive parasitic infection
caused by the flagellate protozoan Trichomonas gallinae . There
are numerous strains of T. gallinae, some of which cause no clinical
signs and possibly provide immunity against other, highly
pathogenic strains [20,21]. In a non-immune bird, infection can
cause necrotic ulceration in the upper digestive tract, principally in
the mouth, oesophagus, crop and protoventriculus . Columbi-
forms are the most common host for avian trichomonosis ,
with most wild and almost all domestic pigeons being infecting
with T. gallinae . The parasite also occurs commonly in
galliforms (turkeys and chickens)  and avivorous falconiforms
(raptors) [21–26]. Galliforms acquire T. gallinae through drinking
contaminated water [7,27], while falconiforms acquire it through
foraging on infected columbiform prey [21–26]. Vertical trans-
mission from parents to offspring has also been demonstrated
among falconiforms, either through nestlings being fed meat with
adherent flagellates in it or by direct bill-to-bill contact with
infected parents [21,22,23,26]. The disease can have the most
serious effects in young birds, often causing rapid weight loss and
eventually death [21,26].
In severe cases, trichomonosis in falconiforms leads to the
formation of large oropharyngeal lesions , including erosive
deformations of the craniomandibular apparatus  (Figure 3).
In osteological specimens that we have observed, these erosive
deformations are typically cylindrical or oblate in shape, and may
Figure 2. Tyrannosaurid mandibular pathology (arrows indicate trichomonosis-type lesions; the position of each specimen is shown in red on
the accompanying schematic interpretation of the reconstructed skull of Tyrannosaurus rex, FMNH PR2081); (A), Tyrannosaurus rex (holotype; CMNH
9380) right caudal mandibular ramus in lateral view, displaying a large circumscribed erosive lesion on the caudal part of the dentary. (B)
Daspletosaurus torosus (RTMP 2001.36.01) left caudal mandibular ramus in lateral view, displaying a single erosive lesion. (C), Daspletosaurus torosus
(RTMP 2001.36.01) multiple erosive lesions are visible on the right surangular in medial view. (D), Albertosaurus sarcophagus (RTMP 1981.10.01), left
caudal mandibular ramus in lateral view, showing a slit-shaped trichomonosis-type lesion in the middle of the angular, (enlarged area, inset). (E)
Tyrannosaurus rex (MOR 1125), caudal part of left dentary in lateral view, showing a cylindrical-shaped lesion, with smooth edges and almost no
surrounding bony alteration. (F), Daspletosaurus torosus (RTMP 94.143.1), surangular in ventral view, with one slit-shaped lesion and one intermediate
lesion. The close-up shows the smooth edges and limited surrounding bony alteration characteristic of a trichomonosis-type lesion. (G),
Tyrannosaurus rex (MOR 980), left surangular in lateral view, exhibiting multiple oval- to sub-oval-shaped lesions.
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occur on one or both of the mandibular rami, either fully
penetrating the bone, or just the lateral surface. They are
randomly positioned and not symmetrical in their distribution
between the rami. Significantly, they tend to concentrate in the
caudal portion of the mandibular ramus, usually on the dentary,
the surangular, the angular and the articular (the sutures between
these bones in many falconiforms often fuse early in ontogeny
, so that only a single mandibular element may be present).
Such osteological deformations are large relative to the size of the
mandible, covering much of the bone surface in certain areas
(Figure 3). The margins of the lesions appear smooth, with no
apparent alteration to the surrounding bone texture. In some
instances, the deformations demonstrate multiple stages of
development, with internal trabecular struts eroded at their centre
(Figure 3, A and B).
The distribution, size, shape and nature of trichomonosis-type
lesions in tyrannosaurid specimens are similar in nature to those
manifested in modern falconiforms infected with the protozoan
Trichomonas gallinae. Our differential diagnosis of possible diseases
within the phylogenetic bracket of tyrannosaurids and modern
falconiforms supports the diagnosis of a trichomonosis-type disease
in these non-avian theropod dinosaurs. Thus, there is a good
possibility that the disease we have identified in tyrannosaurids is
homologous with modern avian trichomonosis. Indeed, the
diagnosis of a disease with strong similarities to a modern
transmissible avian infectious disease in tyrannosaurids suggests
not only that they may have been susceptible to a similar or even
the same parasite, but also that the innate immune response of
some basal coelurosaurian theropods to chronic infection was
similar to that which now occurs in their living descendents.
Comparable lesions in modern birds are prevented from spreading
throughout the medullary cavity due to the focalization of
granulomatous inflammation by profound fibrin secretion elicited
by the innate immune response of heterophils . Therefore, it
can be hypothesized that the lesions present in the tyrannosaurid
specimens examined in this study are discrete, and do not invade
substantially into surrounding parts of the mandible as a result of a
similar innate immune mechanism. This differs from the
neutrophil-induced development of extensive purulent osteomye-
litis that is seen in mammals .
Given the ways in which Trichomonas infection is spread among
extant birds, the occurrence of a similar disease in tyrannosaurids
suggests five possible scenarios for transmission: water-borne
transmission, feeding of tainted prey to nestlings, consumption of
infected prey, cannibalism, and snout to snout contact during face
biting between adults or between infected adults and nestlings.
Water-borne transmission, although possible, cannot be demon-
strated from available evidence. A causal link of individuals to one
particular area with a contaminated water supply cannot be
demonstrated with tyrannosaurids, although taphonomic evidence
can demonstrate such a phenomenon with multiple coincident
individuals . The second scenario – feeding of tainted prey to
nestlings [21,22,23,26] – is hard to evaluate for tyrannosaurids due
to a lack of available material. If infection of a Trichomonas-type
protozoan could be acquired during the tyrannosaurid nestling
stage we would expect to find occasional nestlings that had died of
an acute disease course due to a naı ¨ve immune system as is seen in
modern birds. It remains to be seen whether these individuals
would have had the time to develop lesions before death or not
because we lack tyrannosaurid nests or nestlings, so this hypothesis
is hard to evaluate.
Consumption of infected prey is an important mode of
Trichomonas transmission among modern birds of prey [21–26].
From traces left on bones, tyrannosaurids can be shown to have
consumed a wide variety of dinosaur prey as is evidenced by bite
marks on hadrosaurs, ceratopsians, other ornithischians and
tyrannosaurids [33,34]. Despite extensive records, no ornithischi-
ans of the Late Cretaceous have been reported to bear
trichomonosis-like lesions. Resorptive lesions are found in the frill
of some ceratopsians, as reported recently , but the
distribution and character of these lesions are different enough
to remove them from any suspicion of relationship to those found
Figure 3. The mandible of a modern falconiform, Pandion
haliaetus, the osprey (USNM 561853), exhibiting multiple
trichomonosis lesions (indicated by arrows); the animal most
likely acquired the disease by feeding on an infected pigeon . (A)
(photo) and (B) (radiograph), mandible in left ventrolateral view,
exhibiting multiple oblate to cylindrical erosive lesions. (C), schematic
interpretation of the normal skull of Pandion haliaetus (Queensland
Museum O31935) in left lateral view with the mandible shown in red.
Anatomical abbreviations: d, dentary; ram mand, mandibular ramus;
rost mand, mandibular rostrum. (D) (photo) and (E) (X-ray), mandible in
right lateral view, exhibiting multiple oblate to cylindrical erosive
lesions. The X-rays show that the lesions are largely resolved, except for
a slight radiodensity indicative of thickening along the lesion edges.
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in tyrannosaurids. For one, the resorptive lesions on ceratopsian
frills are very substantial in nature . Secondly, the location of
these lesions bear no relationship to those found in tyrannosaurids
or modern birds known to have trichomonosis. Therefore, we
believe that one of the ways that tyrannosaurids may have
acquired the parasite was through feeding on sympatric or
conspecific tyrannosaurids, in addition to other undocumented
prey that may have acted as a host.
Although known to occur in basal allosauroids such as Sinraptor
dongi , bite marks (deep gouges, conical, depressed fractures etc)
thought to be associated with head-biting behavior are most
commonly found in large-bodied tyrannosaurids. Of well-sampled
collections, the relative frequency of these bite wounds is as high as
44% for mature individuals and 60% for sub-adults , with the
implication being that head-biting behavior was characteristic of
the clade. The coupling of pathological evidence for both head-
biting behavior and a Trichomonas-type infection in tyrannosaurids
may be more than just coincidental as is shown by the co-
occurence of these features in the specimens that we examined
[Supporting Information S1]. Head or face-biting behavior
relating to intraspecific territoriality, social dominance, courtship,
feeding or some other unknown aspect of tyrannosaurid behavior
would have provided the ideal mechanism for the transmission of
this trichomonosis-like disease.
Importantly, we do not claim that these erosive lesions are bite
wounds, but instead that the evidence supports the possibility of
transmission via snout-to-snout contact in a modification of the
[21,22,23,26]. Sporadic acquisition via cannibalism and feeding
on unknown infected sources should not be ruled out as part of the
complex ecology of this disease.
Disease development of a triomononosis-type disease in
tyrannosaurids likely followed the same trajectory as in modern
birds. Regardless of the scenario of initial infection with a
can occurin livingbirds
T. gallinae-type protozoan, an infection within the oropharynx
would then have seeded protozoa into surrounding tissues by
invading through the mucosal surface, as is seen in modern birds
[18,19]. Lesions represent focal sites of chronic infection within the
mandible that can be reconstructed to give a general sense of the
appearance of the lesions in life (Figure 4). The size and
distribution of these lesions in the different individuals we observed
suggest the severity of disease course in these animals.
For a trichomonosis-like disease in tyrannosaurids to progress to
the point where it resulted in erosive deformation of the
mandibular bones, multiple distributed oropharyngeal lesions
must have been present, in addition to necrotic ulceration in the
upper digestive tract, principally in the mouth and oesophagus
(Figure 4). As with modern birds with trichomonosis [24,26],
feeding may have become difficult once the disease progressed to
this stage, and it is very probable that Tyrannosaurus rex FMNH
PR2081 (‘Sue’) and other more seriously affected individuals
succumbed to starvation. In a current poignant example,
Sarcophilus harrisi, the Tasmanian devil, is undergoing a similar
fate today. Face-biting in devils transmits a type of malignant
debilitating oral cancer, and infected individuals find themselves
ultimately unable to eat . Through the vehicle of disease, this
head-biting behavior is bringing about a population bottleneck. In
the late Maastrichtian, a disease like modern-day avian tricho-
monosis may have been the scourge of tyrannosaurids, thanks in
part to their antagonistic behavior.
Whether or not the lesions in tyrannosaurids were caused by
Trichomonas gallinae or a similar organism may be impossible to
discover at this time, but we have provided evidence of homology
of disease transmission, lesional morphology and immune
response. These multiple lines of evidence within archosaur
phylogeny indicate that this trichomonosis-type disease may
represent the origins of modern avian trichomonosis. The record
of infectious diseases of non-avian dinosaurs may yet provide us
Figure 4. Hypothesized reconstruction of the Trichomonas-like infection of the oropharynx and mandible of MOR 980, commonly
known as ‘Peck’s Rex’ (Figure 2G). Note the yellowing of the oropharyngeal area at the back of the mouth and developed lesions within the
mandible that penetrate the full thickness of the bone. This reconstruction is based on photographs of living birds and bird necropsies of individuals
with trichomonosis. Illustration by Chris Glen, The University of Queensland.
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with an understanding of the development of modern avian
disease and avian immunity.
Materials and Methods
A: Morphological examinations
Morphological measurements of mandibular skeletal elements
were taken for each specimen to give general dimensional
information. This was followed by measurement of observed
lesion dimensions, and the location of the lesion in reference to
anatomical landmarks such as the surangular foramen and
articulations between elements. The subsequent description of
oral lesions was conducted using descriptive terminology that took
into account alterations, texture, and deformation of the
surrounding bone. Radiographs of USNM 561853 (Pandion
haliaetus) were taken on a digital radiography system at the
National Museum of Natural History, Ichthyology Department at
55 kVp and 70 seconds exposure time. The subsequent differential
diagnosis was undertaken with comparison to veterinary literature,
texts and consultation on similar veterinary cases.
B: Tyrannosaurid specimens examined
Sixty one tyrannosaurid specimens were examined for this
study: Albertosaurus sp. MOR 657, Albertosaurus sp. RTMP
1999.50.10, Albertosaurus sp. RTMP 1998.68.35, Albertosaurus sp.
RTMP 1983.29.01, Albertosaurus sp. 1985.98.01, Albertosaurus sp.
RTMP 1967.9.164, Albertosaurus sp. RTMP 2003.45.84, Alberto-
saurus sp. RTMP 1997.50.02, Albertosaurus sp. RTMP 1998.63.82,
Albertosaurus sp. RTMP 1981.3.6, Albertosaurus sp. NMNH 16475,
sp. RTMP 1999.50.170,
1981.10.1, Albertosaurus libratus AMNH 5458, Albertosaurus libratus
AMNH 5336, Albertosaurus sp. RTMP 1981.10.1, Albertosaurus sp.
RTMP 1986.49.29, Albertosaurus sp. RTMP 1992.36.749, Alberto-
1994.12.602, Albertosaurus sp. RTMP 1995.05.01, Albertosaurus sp.
RTMP 1982.28.01, Albertosaurus sp. RTMP 2002.12.11, Alberto-
saurus sp. NMNH 12814, Albertosaurus sp. RTMP 1994.12.155,
Albertosaurus sp. RTMP 2001.12.12, Albertosaurus sp. RTMP
1990.56.6, Albertosaurus sp. RTMP 1996.12.142 Albertosaurus sp.
RTMP 1992.36.390, Tyrannosaurus (labelled Aublysodon) sp. RTMP
1985.62.01, Daspletosaurus sp. RTMP 1975.11.03, Daspletosaurus sp.
RTMP 1994.143.1, Daspletosaurus sp. MOR 590, Tyrannosaurus rex
(labelled Nanotyrannus) RTMP 1995.06.07, Tyrannosaurid sp.
RTMP 1986.03.02, Tyrannosaurid sp. RTMP 1987.46.01,
Tyrannosaurid sp. (Proprietary RTMP), Tyrannosaurid sp.
RTMP 1983.29.02, Tyrannosaurid sp. 1998.93.12, Tyranno-
saurid sp. RTMP 2002.12.101, Tyrannosaurid sp. RTMP
1996.03.13, Tyrannosaurid sp. RTMP 1994.12.155, Tyranno-
saurid sp. RTMP 2001.12.02, Tyrannosaurid sp. MOR 1130,
Tyrannosaurus sp. NMC 8540- cast, Tyrannosaurus rex CM 9380
(holotype), Tyrannosaurus rex, FMNH PR2081 ‘Sue’ (from original
and casts on exhibit, and literature ), Tyrannosaurus rex RTMP
1992.15.1- cast, Tyrannosaurus rex RTMP 2001.12.147, Tyrannosau-
rus rex RTMP 81.6.1 ‘Black Beauty’, Tyrannosaurus rex BHI 3033
(seen as cast - ‘Stan’ at NMNH), Tyrannosaurus rex MOR 980
(‘Peck’s Rex’), Tyrannosaurus rex MOR 555, Tyrannosaurus rex MOR
1128, Tyrannosaurus rex MOR 1126 Tyrannosaurus rex MOR 1628,
Tyrannosaurus rex MOR 008, Tyrannosaurus rex MOR 1125,
Tyrannosaurus rex AMNH 5027.
Supporting Information S1
co-occurrence of face-biting evidence and the trichomonosis-type
disease (Table S1), a description of archosaur mandibular
morphology (Text S1), and descriptions of pathology in tyranno-
saurid specimens (Text S2)
Found at: doi:10.1371/journal.pone.0007288.s001 (0.07 MB
This section includes a table with
We thank M. C. Lamanna, M. Brett-Surmann, J. Boardman, P. Currie, D.
Tanke, P. J. Makovicky, C. Mehling and H. Jenetzki for access to
specimens, and Z.-X. Luo, M.C. Lamanna and D. Naish and two
anonymous reviewers for comments on earlier drafts of our manuscript.
We also thank P. J. Makovicky and J. Barrios for images of ‘Sue’, M. Wolff
for assistance with figures, and C. Glen for doing Figure 4.
Conceived and designed the experiments: EDSW SWS. Performed the
experiments: EDSW SWS. Analyzed the data: EDSW SWS JH DJV.
Contributed reagents/materials/analysis tools: EDSW SWS JH. Wrote the
paper: EDSW SWS JH DJV.
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