Mycoplasma iowae associated with chondrodystrophy in commercial turkeys.

Abstract

Opportunistic observations of and necropsies from selected commercial (meat) turkey flocks revealed skeletal lesions consistent with chondrodystrophy, characterized by leg and vertebral deformities, occurring at very low incidences in turkeys from two primary breeds and various multiplier breeder flocks. Mycoplasma organisms were cultured and identified as Mycoplasma iowae by immunofluorescence and polymerase chain reaction from some of the vertebral lesions but not from leg joints. This is the first detailed description of the gross and microscopic lesions of vertebral chondrodystrophy associated with M. iowae, which should now be considered in the differential diagnosis of turkeys with these lesions.

Full text

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Mycoplasma iowae associated with chondrodystrophy in
commercial turkeys
David H. Ley*, Rosemary A. Marusak, Eduardo J. Vivas$, H. John Barnes and
Oscar J. Fletcher
Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University,
4700 Hillsborough Street, Raleigh, NC 27606, USA
Opportunistic observations of and necropsies from selected commercial (meat) turkey flocks revealed
skeletal lesions consistent with chondrodystrophy, characterized by leg and vertebral deformities, occurring
at very low incidences in turkeys from two primary breeds and various multiplier breeder flocks.
Mycoplasma organisms were cultured and identified as Mycoplasma iowae by immunofluorescence and
polymerase chain reaction from some of the vertebral lesions but not from leg joints. This is the first detailed
description of the gross and microscopic lesions of vertebral chondrodystrophy associated with M. iowae,
which should now be considered in the differential diagnosis of turkeys with these lesions.
Introduction
Husbandry practices, metabolic and infectious diseases,
and rapid growth may all play a role in the development
of skeletal diseases in poultry (Morrow et al., 1997).
Bone abnormalities occur in all ages of growing poultry
with incidences ranging from 0.5 to 25% (Morrow et al.,
1997). An estimated annual cost due to skeletal problems
in the US turkey industry was $32 million to $40 million
(Sullivan, 1994). Skeletal problems described in poultry
include: dyschondroplasia, spondylolisthesis, chondro-
dystrophy, osteomyelitis and synovitis, Mycoplasma
synoviae infection, and others (Sullivan, 1994; Crespo
& Shivaprasad, 2008).
Mycoplasma iowae infection in turkey breeder hens
causes late embryo mortality, reduced hatchability (2
to 5%), and leg abnormalities in progeny (Bradbury
et al., 1988; Trampel & Goll, 1994; Bradbury & Kleven,
2008). In experimentally infected chickens and turkeys,
M. iowae also induced airsacculitis, tenosynovitis and
arthritis, rupture of digital flexor tendons, rotated tibia,
and cartilage erosion (Trampel & Goll, 1994; Bradbury
& Kleven, 2008). Following experimental infections
of 1-day-old poults (Bradbury et al., 1988), M. iowae
caused stunting, poor feathering, and leg abnormalities
including chondrodystrophy. Infection in ovo caused
severe generalized disease in hatched poults with high
mortality, and the only two birds that survived into the
third week developed chondrodystrophy (Bradbury
et al., 1988). M. iowae was most widely disseminated in
tissues following in ovo infection, and least disseminated
after oral infection. Isolations became less frequent with
age and no organisms were recovered in birds sampled
at 12 weeks (Bradbury et al., 1988).
Trampel & Goll (1994) described 17-day-old turkey
poultswithleg weakness,dehydration,chondrodystrophy
of the hock joints, clear fluid in hock joint spaces, valgus
deformities, shortening of the tarsometatarsal bones, and
curled toes associated with M. iowae. M. iowae was
recovered from hock joints of 1-day-old poults and older
turkeys (up to 8 weeks of age) with leg deformities, and
from intervertebral spaces of older turkeys with wry neck
and back deformities (H. J. Barnes & D. H. Ley, personal
communication reported in Al-Ankari & Bradbury,
1996). More recently, Dunn et al. (2005) reported several
cases of commercial turkeys from 3 days to 3 weeks of age
with leg problems, uneven growth, increased culls, and
histories suggesting that infection originated from certain
multiplier breeder flocks. Leg lesions were suggestive
of chondrodystrophy, and M. iowae was identified from
joint swabs. The presence of vertebral lesions was not
noted.
Control of M. iowae by eradication from some
primary turkey breeder flocks has been accomplished
(Al-Ankari & Bradbury, 1996; Bradbury & Kleven,
2008), but M. iowae is not currently included in the US
National Poultry Improvement Plan.
Herein, we report the association of M. iowae with a
range of skeletal lesions consistent with chondrodystro-
phy in commercial turkeys of two primary breeds from
various multiplier breeder flocks. We describe in detail
the gross and microscopic lesions, and include a discus-
sion of the relevant terminology and description of
lesions.
Materials and Methods
2006 turkey flocks. In 2006, a North Carolina commercial turkey
company obtained breeding stock (eggs) of the same primary breed
(Nicholas 700; Aviagen Turkeys Inc., East Lewisburg, West Virginia,
*To whom correspondence should be addressed. Tel: ?1 919 513 6269. Fax: ?1 919 513 6464. E-mail: david_ley@ncsu.edu
$Current address: Western Institute for Food Safety and Security, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA.
Received 7 October 2009
ISSN 0307-9457 (print)/ISSN 1465-3338 (online)/10/020087-07 # 2010 Houghton Trust Ltd
DOI: 10.1080/03079451003599276
Avian Pathology (April 2010) 39(2), 87?93
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Page 2

USA) from two different multiplier breeder sources (A and B).
Company A multiplier hens were 43 weeks of age, and company B
multiplier hens were 48 weeks of age. Poults from each multiplier
breeder company were separated according to sex at the hatchery
and females were placed at production facilities in two locations. One
production facility was a typical commercial (COM1) farm that
received 8000 turkeys from each multiplier breeder source (16,000 in
total). The other production facility was the Teaching Animal Unit
(TAU) at the North Carolina State University, College of Veterinary
Medicine (NCSU CVM), which received 1000 turkeys from each
breeder source (2000 in total). Thus, each location/production facility
had female poults from both breeder sources A and B.
At the COM1 farm, poults A and B were brooded in rings on
different sides of the same house, separated (according to breeder flock
source) by a heavy wire fence. This was a typical commercial turkey
production house for the southeastern US, with curtain side-walls,
cross-ventilation, end doors, and automatic watering and feeding
systems. After they were released from the brooder rings, poults
A and B remained separated in the house by the wire fence, which
allowed them to be distinguished in the brooder house. The house
contained 8000 A poults and 8000 B poults. At 6 weeks of age, poults
from each breeder source (A and B) were moved to two separate grow-
out houses, each containing approximately 8000 turkeys. These turkeys
were to be processed as ‘‘heavy hens’’ with a target weight of 23 lbs
(10.43 kg) at an approximate age of 18.5 weeks. The COM1 flock was
examined at weeks 1, 2, 4, 6, 8, 10, and 12 of production.
The TAU production facility is a commercial-style house constructed
on a smaller scale (40?140 sq ft; 12.19?42.67 m2) with curtain side-
walls, cross-ventilation, end doors, automatic watering and feeding
systems, and is used for both brooding and growing. This facility
produces one flock of meat turkeys and one flock of broiler chickens
each year. Poults from each breeder source intended for the TAU were
distinguished by different trimming of the first toe at the hatchery. At
1 day post-hatch, poults from breeder sources A and B were transported
to the TAU. On arrival, 1000 A and B poults (2000 in total) were
commingled and placed in brooder rings for 2 weeks. Poults placed in
the TAU were to be raised as ‘‘light hens’’ with a target weight of 15 lbs
(6.8 kg) at approximate age of 13.5 weeks.
2008 turkey flocks. In 2008, Hybrid Converter turkeys (Hybrid;
Hendrix Genetics, Kitchener, Ontario, Canada) from a single multiplier
breeder source were grown at the same TAU facility but a different
commercial turkey farm (COM2) from that described above. Otherwise,
the production facilities and management were similar to those
described above. Two thousand female poults were placed at the TAU
and 7000 poults at COM2. Various production and sampling data were
collected at the same intervals from TAU and COM2 flocks. Necropsies
and sampling were done on all TAU and selected COM2 culls and
mortalities.
Necropsy and histopathology. Among the reasons for culling were
musculoskeletal disorders that prevented turkeys from accessing feed
or water and/or if they were severely stunted. Turkeys were killed by
cervical dislocation. Carcasses (culls and daily mortalities) from the
commercial turkey farms were transported on ice to the NCSU CVM
for necropsy and sample collection. TAU turkeys were observed two or
more times each day throughout production. Each turkey that was
found dead or culled was necropsied. TAU turkeys were individually
identified by numbered wing bands and necropsies were performed,
usually on the day of death, but occasionally after overnight refrigera-
tion at 48C. A record of each necropsy was kept and any samples taken
were labelled to match the wing band number. Samples of tissues taken
at necropsy were placed into 10% neutral buffered formalin. Fixed
tissues were trimmed, and spinal columns decalcified, processed by
standard paraffin embedding procedures, sectioned, and stained with
haematoxylin and eosin (HE) for histopathologic examination.
At the TAU, daily observations were made and recorded from
placement to processing. Turkeys were culled based primarily on
stunting and lameness. Culled birds were killed by cervical dislocation,
individually identified with a numbered wing band, and taken to the
necropsy room for a complete external and internal examination and
sample collection.
Routine bacteriology, mycoplasma culture and identification. At ne-
cropsy, enlarged hock joints and vertebral lesions were sampled after
surface disinfection with 70% alcohol and incision of the affected area
with a sterile blade. Joint fluid and exudate from the lesions were
sampled using two sterile swabs, one of which was used immediately to
inoculate blood and MacConkey’s agar plates and the other to inoculate
2 ml Frey’s mycoplasma broth with 15% swine serum (FMS) (Kleven,
2008). From each inoculated FMS broth, 1 ml was used for myco-
plasma culture and 1 ml was removed and used for molecular
identification of M. iowae by polymerase chain reaction (PCR) as
described by Boyle et al. (1995) and Lauerman (1998), or Laigret et al.
(1996). Inoculated FMS broths were incubated aerobically at 378C with
periodic transfer of aliquots to FMS agar. Mycoplasmal colonies on
agar were identified as M. iowae by direct immunofluorescence (Kleven,
2008) using fluorescein-conjugated rabbit antiserum (Leiting & Kleven,
2000) provided by S. H. Kleven (College of Veterinary Medicine,
University of Georgia, Athens, Georgia, USA), and some isolates in
FMS broth cultures were identified as M. iowae by PCR.
Results
2006 turkey flocks. Eight turkeys (four TAU and four
COM1) were identified at necropsy with swollen hocks
or vertebral lesions. Swollen hocks were noted at 12 and
15 days of age in three turkeys: two TAU breeder source
A, and one COM1 breeder source B. M. iowae was not
identified by culture or PCR of joint swabs from any of
these three turkeys. However isolations of Escherichia
coli plus Enterobacter spp., and of Staphylococcus spp.
were made from two of these turkeys. Vertebral lesions
were noted in five turkeys necropsied between 5 and 10
weeks of age: two TAU breeder source A, two COM1
breeder source A, and one COM1 breeder source B.
M. iowae was identified by culture or PCR from spinal
lesions of three turkeys (two TAU breeder source A, and
one COM1 breeder source B). In two of three M. iowae-
positive cases, the initial PCR tests from spinal lesion
swabs were negative, although the organism was isolated
in culture and identified by immunofluorescence and
repeat PCR. In another case, initial PCR from the lesion
was not done, but the organism was isolated in culture
and the follow-up PCRwas positive for M. iowae. In one
case the initial M. iowae PCR was negative and the
mycoplasma culture was contaminated, thus not permit-
ting isolation or follow-up PCR. Therefore, the M. iowae
status of this case is considered uncertain. In the final
vertebral lesion case, M. iowae PCR and mycoplasma
culture were both negative.
2008 turkey flocks. A variety of skeletal lesions occurred
at a low estimated rate in the TAU (0.25 to 0.5%) and
COM2 turkey flocks. The most common gross lesion
was chondrodystrophy characterized by short, thick,
deformed legs and enlarged joints. Other gross lesions
consisted of vertebral malformations involving the free
thoracic vertebra and adjacent ribs, with wry neck an
uncommon finding. Splenomegaly was common, but
arthritis and tenosynovitis (swollen joints, feet, or
tendon sheaths) was not a finding in chondrodystrophic
turkeys. The diagnosis of chondrodystrophy was based
on gross lesions, not histopathology, as discussed below.
Chondrodystrophy was found in turkeys at 3 to
7 weeks of age, and accounted for 17.3% of the
mortalities and culls in the TAU flock. Of 21 samples
from chondrodystrophic leg joints (foot, hock, or stifle),
none were positive for M. iowae by culture or PCR.
M. iowae was detected in only five (from one neck and
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four back lesions) of 33 samples (15.2% positive rate)
submitted from chondrodystrophic TAU and COM2
turkeys. Four of 11 samples from backs with vertebral
lesions were positive for M. iowae, and five samples
submitted from normal backs were negative. Several
turkeys were noted with wry neck, but only one was
sampled from the cervical spine and it was positive
for M. iowae. Mycoplasmas were not detected in two
samples from air sacs or two samples from spleens.
Pathology. Clinical signs and gross lesions compatible
with chondrodystrophy were characterized by lameness,
stunting, and legs that were short, bowed and thickened,
with enlarged hock joints (Figure 1). Cut sections of
affected tibiotarsi showed enlargement of the ends with
thickening of the bone and growth plate, hypertrophy of
cartilage, and curvature of the bone (Figure 2). Typical
examples of spinal lesions noted at necropsy were
vertebral columns markedly shorter in length than
normal (Figure 3) with severely deformed caudal thor-
acic vertebrae because of lesions in the caudal notarium
and free thoracic vertebra, with resulting deformity of
adjacent ribs (Figure 4). Wry neck (Figure 5) was the
least common skeletal change seen in the turkeys. The
neck was permanently deviated laterally and actually
rotated, not simply held to the side.
Representative microscopic lesions in the vertebral
column are shown in Figures 6 to 9. Figure 6 shows a
distorted free thoracic vertebra that compressed the
spinal cord causing mild demyelination. Longitudinal
bands of cartilage represented persisting lateral growth
plates. Joint surfaces were irregular due to degeneration
and necrosis. There was excess cartilage matrix and
disorganization of chondrocytes, features of osteochon-
drosis, also shown at higher magnification in Figure 7.
Chondrocytes were haphazardly arranged in a matrix
with irregular, acellular areas of degeneration. Larger
areas of acellular matrix were in some regions of
persisting cartilage. Degeneration of cartilage was char-
acterized by accumulation of eosinophilic material with
loss of chondrocytes, and there were focal areas of
chondrocyte necrosis. Articular cartilage of the free
thoracic vertebra was necrotic (Figure 8). Cartilage
persisted in the ventral portions of the vertebra adjacent
to the articular surface, which showed degeneration and
necrosis of cartilage with an irregular surface. Osteo-
myelitis was in the bone beneath the cartilage. Figure
9a, b present a higher magnification of Figure 8d,
showing a tag of degenerated and necrotic cartilage in
the expanded articular space of the thoracic vertebra.
Necrotic cartilage was also on the left side of this space.
Chondrocytes were disorganized and necrotic, and
osteomyelitis was in bone beneath the articular surface
of the vertebra. Higher magnification of Figure 8a
(Figure 9c, d) showed the distorted articular surface
and prominent persisting cartilage. An area of degenera-
tion of cartilage was characterized by loss of cells and
accumulation of eosinophilic material. Chondrocytes
were variable in size and arranged in an irregular
pattern.
Discussion
The TAU at NCSU CVM includes an on-site poultry
house that is used to provide our veterinary students and
Poultry Health Management residents with production
experience. For the 2006 and 2008 TAU turkey flocks,
plans were in place to compare TAU flocks and
commercial turkey flocks for breeder source effects and
time-of-placement effects, respectively. However, in the
course of observing these flocks for clinical signs and
Figure 1.
legs of a 42-day-old turkey showing bilateral chondrodystrophy;
although weights were comparable, the chondrodystrophic turkey
has short, thick shanks and toes compared with the unaffected
turkey. The affected legs also have enlarged hocks, and there is
marked medial bowing of both, which has resulted in bilateral
varus deformity. The unaffected turkey died of round heart
disease while the chondrodystrophic turkey was a cull.
(1a) Normal legs of a 28-day-old turkey and (1b)
Figure 2.
chondrodystrophic turkey (right) from the birds in Figure 1.
Thickening of the bone and physis, and curvature of the
tibiotarsus are evident in the bones from the affected bird.
Proximal tibiotarsi of unaffected turkey (left) and
Figure 3.
old turkeys. Spines are from two similarly sized birds. The upper
chondrodystrophic spine is much shorter than that of the bird with
the normal back; the vertebral column is distorted and thickened,
and the ribs are unevenly spaced.
Normal and chondrodystrophic spines from 43-day-
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conducting necropsies on cull and dead turkeys, we
identified an association between chondrodystrophy and
M. iowae.
In 2006 we found M. iowae variably associated with
low incidences of stunting, lameness, swollen hocks/
arthritis, and vertebral lesions in turkeys of the same
primary breed from two multiplier breeder companies in
two production locations/systems. Possible sources of M.
iowae infections could have originated with the primary
breeder, or both multiplier breeder flocks could have
been infected without regard to the primary breeder.
Swollen hocks and arthritis were noted in a few turkeys
between 12 and 15 days of age, with no evidence of
M. iowae but with other bacteria present. This does not
completely rule out the possibility that M. iowae was
involved in the development of these leg lesions, but does
show that other bacteria may be involved as primary or
possibly secondary aetiologies. Dunn et al. (2005) found
that M. iowae was associated with swollen joints in
turkeys from 3 days to 3 weeks of age, and that PCRwas
more sensitive than culture with pooled joint swabs. The
evidence from experimental and natural infections with
M. iowae suggests that the organism may be associated
with lesions in low numbers and relatively early in the
development of pathology, properties that add to the
challenges of determining aetiology and making a
definitive diagnosis.
In our study, vertebral lesions commonly described as
chondrodystrophy were noted in turkeys between 39 and
65 days of age, and M. iowae was identified in samples of
these lesions. The incidence of vertebral lesions was
apparently very low and their occurrence could easily
be missed without a careful examination of the spine.
This was a small dataset, but the results suggested that
mycoplasma culture of spinal lesions was a more
sensitive diagnostic method than M. iowae PCR. We
found instances where viable M. iowae was present in
lesions but below the detection threshold of PCR on
initial testing, but was detected by PCR following
enrichment in culture. Recently we compared the sensi-
tivities of M. iowae PCR using two different primer sets
for conventional PCR (Boyle et al., 1995; Laigret et al.,
1996) and real-time PCR (Raviv & Kleven, 2009), and
found real-time PCR the most sensitive and superior to
culture that relies on the presence of viable organisms
(data not shown).
In 2008 similar clinical signs and pathology were
found in turkeys from another primary breeder. Gross
lesions were consistent with chondrodystrophy, and
microscopic lesions consisted of osteochondrosis, with
dyschondroplasia and osteomyelitis also present. Based
on these findings, M. iowae should be considered in the
differential diagnosis of turkeys with chondrodystrophy.
There is no universal acceptance of the terminology
describing skeletal lesions. One problem is that terms are
sometimes used to name a disease condition or to
describe gross changes, while in other instances the
terms are used to describe microscopic lesions (morpho-
logic diagnosis). Words with the root ‘‘chondro’’ or
‘‘osteo’’ refer to cartilage or bone, respectively. When
both cartilage and bone are involved, then the term
should include both roots (e.g. osteochondrosis). The
root ‘‘osis’’ indicates a degenerative change while ‘‘itis’’
indicates an inflammatory change in otherwise normal
tissue. The roots ‘‘plasia’’ and ‘‘trophy’’ refer to growth,
and ‘‘dys’’ to abnormal. This means that chondrody-
strophy and dyschondroplasia are synonymous with
respect to morphologic changes, both meaning some
abnormality in the growth and development of cartilage.
However, both also have disease connotations that are
quite different from each other*chondrodystrophy is
the basis for a type of dwarfism (more commonly called
‘‘achondroplasia’’ medically) that is characterized by
normal appositional growth of bones coupled with
impaired linear growth, which makes the bones short
and thick. Affected individuals are short but more or less
normal in width. A number of different types of animals
are affected. Affected turkeys have short, thick legs,
which is why the term ‘‘chondrodystrophy’’ has been
used to describe them. Other causes include nutrient
deficiencies (biotin, zinc, others) and genetics as in other
species, although this may not have been thoroughly
investigated.
Dyschondroplasia has been used to describe a specific
disease characterized by the retention of cartilage in
the growth plate of the proximal tibiotarsus. So, using
the term ‘‘chondrodystrophy’’ for these turkeys is
describing their clinical appearance and not any micro-
scopic changes. For chondrodystrophy to be used to
describe the microscopic changes there would need to be
evidence that the cartilage was growing in an abnormal
Figure 5.
after (5b) removal of the skin. The neck is permanently deviated
to the right and is actually rotated, not simply held to the side.
Inflammation of cervical air sacs that spreads to the inter-
vertebral joints is believed to cause the lesion. M. iowae was
detected in a sample from the intervertebral space of this turkey.
Wry neck in a 30-day-old turkey before (5a) and
Figure 4.
due to stunting and lameness with vertebral chondrodystrophy.
The caudal thoracic vertebrae are severely deformed because of
lesions in the caudal notarium (N) and free thoracic vertebra
(FTV). Mycoplasma iowae was isolated from the intervertebral
space within the lesion.
Spine of a 39-day-old female turkey that was culled
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way. If the cartilage appears normal but shows degen-
eration, or if there is involvement of the underlying
bone (subchondralbone),
would be osteochondrosis. As a further complication,
chondrodystrophy and osteochondrosis could occur
together, because the chondrodystrophy could produce
the microscopic lesion
abnormalities that would predispose to osteochondrosis.
The gross description may not match the morphologic
description and still be correct because terms are being
used for both disease or gross changes, and morphologic
descriptions. Microscopically, the questions to be asked
are ‘‘Is only cartilage involved, or only bone, or both?’’
Figure 7.
are haphazardly arranged in a matrix with irregular, acellular areas of degeneration. Bar?50 mm. HE. 7b: Larger areas of acellular
matrix are in some regions of persisting cartilage. Bar?50 mm. HE. 7c: Degeneration of cartilage is characterized by accumulation of
eosinophilic material with loss of chondrocytes. Bar?50 mm. HE. 7d: A focal area of chondrocyte necrosis. Bar?50 mm. HE.
Cartilage lesions in osteochondrosis. This series of images are higher magnification of areas * in Figure 6b. 7a: Chondrocytes
Figure 6.
cartilage (*) represent persisting longitudinal growth plates. Joint surfaces are irregular due to degeneration and necrosis. Bar?20 mm.
HE. 6b: A longitudinal band of cartilage (*) is prominent and the free thoracic vertebra (arrow) is distorted on the ventral surface.
Compression of the spinal cord is mild, but some demyelination is present. Bar?20 mm. HE. 6c: Excess cartilage matrix and
disorganization of chondrocytes, features of osteochondrosis, are shown. This is a higher magnification of area * in 6b. Bar?20 mm. HE.
6d: Higher magnification of 6c shows the disorganization of chondrocytes within an expanded matrix. Bar?20 mm. HE.
Vertebral lesions. 6a: The free thoracic vertebra (arrow) is distorted and compressing the spinal cord. Longitudinal bands of
Mycoplasma iowae chondrodystrophy in turkeys91
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Figure 9.
cartilage in the expanded articular space of the thoracic vertebra. Necrotic cartilage also is on the left side of this space. Bar?100 mm.
HE. 9b: Chondrocytes are disorganized and necrotic. Osteomyelitis is in bone beneath the articular surface of the vertebra. Bar?100 mm.
HE. 9c: A higher magnification of Figure 8a (* below the box) and shows the distorted articular surface and prominent persisting
cartilage. The area within the box is shown at higher magnification in 8d. Bar?200 mm. HE. 9d: An area of degeneration of cartilage is
characterized by loss of cells and accumulation of eosinophilic material. Chondrocytes are variable in size and arranged in an irregular
pattern. Bar?100 mm. HE.
Osteochondrosis in vertebral cartilage. 9a: A higher magnification of Figure 8d shows a tag of degenerated and necrotic
Figure 8.
(*) in the ventral portions of the vertebra adjacent to the articular surface. Note the compression of the spinal cord. Bar?20 mm. HE. 8b:
A higher magnification of 8a from the region at the bottom and just below the box. The articular surface is irregular and a large mass of
cartilage persists in this ventral portion of the free thoracic vertebra. Bar?20 mm. HE. 8c: A higher magnification of the region within the
box in 8a shows degeneration and necrosis of cartilage with an irregular surface. Osteomyelitis is in the bone beneath the cartilage on the
right. Bar?20 mm. HE. 8d: A higher magnification of 8c shows irregularity of the articular surface and streaks in the articular cartilage
indicative of degeneration and necrosis. Bar?200 mm. HE.
Lesions in vertebral articular cartilage. 8a: Articular cartilage of the free thoracic vertebra is necrotic (box). Cartilage persists
92 D. H. Ley et al.
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and ‘‘Has the lesion resulted from abnormal growth, or
was normal tissue subsequently affected with either
degeneration or inflammation?’’
Evidence from experimental infections, and recent
clinical cases in commercial turkeys, suggests that
M. iowae may be associated with the development of
chondrodystrophy in all of its manifestations even
though it may be difficult to demonstrate the organism
at affected sites. However, the origin (primary and/or
multiplier breeder flocks) and the precise role (primary,
secondary, predisposing, synergistic, other) of M. iowae
in the pathophysiology of the disease, and its prevalence,
extent and economic importance, are presently undeter-
mined. This information is necessary if M. iowae is to be
considered for inclusion in monitoring and control
programmes such as the US National Poultry Improve-
ment Plan. Key epidemiologic and economic data,
especially disease prevalence correlated with presence
or absence of the organism, need to be developed using
the most sensitive and specific tests available.
Acknowledgements
This work was supported, in part, by the NCSU College
of Veterinary Medicine and the State of North Carolina.
The authors thank Paula Jay, Sile Huyan and Judith
McLaren for valuable technical assistance.
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Mycoplasma iowae chondrodystrophy in turkeys 93
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ERRATUM
Mycoplasma iowae associated with chondrodystrophy in
commercial turkeys
David H. Ley, Rosemary A. Marusak, Eduardo J. Vivas, H. John Barnes and Oscar J. Fletcher
(April 2010) 39(2), 87?93
On page 89, the caption for Figure 1
Figure 1. (1a) Normal legs of a 28-day-old turkey and (1b) legs of a 42-day-old turkey showing bilateral
chondrodystrophy; although weights were comparable, the chondrodystrophic turkey has short, thick shanks and toes
compared with the unaffected turkey. The affected legs also have enlarged hocks, and there is marked medial bowing of both,
which has resulted in bilateral varus deformity. The unaffected turkey died of round heart disease while the
chondrodystrophic turkey was a cull.
should have read
Figure 1. (1a) Normal vs. chondrodystrophic legs of 28-day-old turkeys. Although weights were comparable, the
chondrodystrophic turkey (left) has short thick shanks and toes compared to the unaffected turkey (right). The unaffected
turkey died of round heart disease while the chondrodystrophic turkey was a cull. (1b) Legs of a 42-day-old turkey showing
bilateral chondrodystrophy. The affected legs are short, thick, with enlarged hocks, and there is marked medial bowing of
both legs, which has resulted in bilateral varus deformity.
Taylor & Francis wish to apologise for any inconvenience caused.
Avian Pathology (August 2010) 39(4), 307
ISSN 0307-9457 (print)/ISSN 1465-3338 (online)/10/040307-01 # 2010 Houghton Trust Ltd
DOI: 10.1080/03079457.2010.507400
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