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PRODUCTION ANIMALS

Is Mycoplasma bovis a missing component of the bovine

respiratory disease complex in Australia?
PF Horwood,a ML Schibrowski,b,c EV Fowler,a JS Gibson,b TS Barnes,c and TJ Mahonyc*

Background Bovine respiratory disease complex (BRDC) is a

multi-factorial disease in which numerous factors, such as animal
management, pathogen exposure and environmental conditions,
contribute to the development of acute respiratory illness in feedlot
cattle. The role of specic pathogens in the development of BRDC
has been dicult to dene because of the complex nature of the
disease and the presence of implicated bacterial pathogens in the
upper respiratory tract of healthy animals. Mycoplasma bovis is an
important pathogen of cattle and recognised as a major contributor to cases of mastitis, caseonecrotic bronchopneumonia, arthritis
and otitis media. To date, the role of M. bovis in the development of
BRDC of Australian feeder cattle has not been investigated.
Methods In this review, the current literature pertaining to the
role of M. bovis in BRDC is evaluated. In addition, preliminary data
are presented that identify M. bovis as a potential contributor
to BRDC in Australian feedlots, which has not been considered
previously.
Results and Conclusion The preliminary results demonstrate
detection of M. bovis in samples from all feedlots studied. When
considered in the context of the reviewed literature, they support
the inclusion of M. bovis on the list of pathogens to be considered
during investigations into BRDC in Australia.
Keywords bovine respiratory disease complex; cattle; feedlots;
Mycoplasma bovis
Abbreviations BoHV-1, bovine herpesvirus 1; BPIV-3, bovine
parainuenza virus 3; BRDC, bovine respiratory disease complex;
BRSV, bovine respiratory syncytial virus; BVDV-1, bovine viral diarrhoea virus 1; URT, upper respiratory tract; VSP, variable surface
lipoproteins
Aust Vet J 2014;92:185191

doi: 10.1111/avj.12184

ovine respiratory disease complex (BRDC) is the most signicant health problem aecting intensively nished cattle.1 It is
a multifactorial disease, with many factors contributing to its
aetiology and pathogenesis. In feedlot cattle, management and environmental factors such as pathogen exposure, stocking density, cattle
mixing, dust, transport time, nutritional changes and other stressors
*Corresponding author.
a
Animal Science, Queensland Department of Agriculture, Fisheries & Forestry, St
Lucia, Queensland, Australia
b
The University of Queensland, School of Veterinary Science, Gatton, Queensland,
Australia
c
The University of Queensland, Queensland Alliance for Agriculture and Food
Innovation, Centre for Animal Science, St Lucia, Queensland 4072, Australia;
t.mahony@uq.edu.au

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REVIEW

can predispose susceptible cattle to the development of BRDC.2 The

rst 45 days within a feedlot environment is generally accepted as the
most critical time period for disease development3 and this time
period is crucial for the application of eective management strategies
to reduce its impact. Although the various factors contributing to
BRDC have been well documented, it remains one of the greatest
challenges facing the feedlot industry.4
Many viral and bacterial agents have been implicated in BRDC. The
most commonly accepted model of the pathogenesis involves an
initial viral infection that causes the primary lung damage and/or
immune dysfunction. Consequently, bacteria that are often commensals of the upper respiratory tract (URT) are able to opportunistically
colonise the compromised lung tissue, resulting in clinical disease.
The viral agents most commonly implicated include: bovine herpesvirus 1 (BoHV-1), bovine viral diarrhoea virus 1 (BVDV-1), bovine
respiratory syncytial virus (BRSV) and bovine parainuenza virus 3
(BPIV-3).4,5 The bacteria that are most commonly isolated in BRDC
cases include: Mannheimia haemolytica, Histophilus somni (formerly
Haemophilus somnus), Pasteurella multocida and Mycoplasma
bovis.1,4,5 There is also evidence for the bacterial pathogens, such as
Mann. haemolytica, acting as a primary pathogen during the development of BRDC. Currently, all of these pathogens are considered in
investigations of BRDC in Australian feedlot cattle, with the exception
of M. bovis.
Here, the role of M. bovis in BRDC in literature from North America
and Europe is reviewed, which reveals a surprising decit in the evaluation of the role of this pathogen with respect to BRDC in Australian
beef cattle. In support of this notion, we present preliminary evidence
from BRDC outbreaks that support the addition of M. bovis to the list
of pathogens that should be considered when investigating BRDC in
Australian feedlot cattle.
Impact of BRDC
In the USA, BRDC is the most signicant disease of feedlot cattle,
where the total losses attributed to BRDC have been estimated to be
between US$500 million and US$1 billion per year.6 In Australia,
BRDC has been estimated to account for >70% and >50% of all feedlot
morbidity and mortality, respectively, based on industry survey data.7
Using these data, the annual losses to the Australian feedlot sector
have been estimated to be at least A$40 million in 2001.7 Costs associated with the disease include animal deaths, reduced animal performance and carcase quality, increased animal morbidity and the costs
associated with treatment, including drugs, labour and additional
animal handling.6

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Mycoplasma bovis
Mycoplasma bovis belongs to the genus Mycoplasma within the Class
Mollicute. All mycoplasma species are pathogens or commensals of
vertebrate hosts.8 They are the smallest prokaryotic cells known to be
capable of self-replication and are characterised by the absence of a
cell wall, dependence on cholesterol for growth, structural simplicity,
small genome (0.61.3 megabases) and limited metabolic
capability.911 The absence of a cell wall results in pleomorphic cell
shapes, prevents Gram-stain analysis and makes treatment with many
of the common antimicrobials, such as penicillin and other -lactams,
ineective.10
Mycoplasma bovis was rst isolated in the USA in 1961, following an
outbreak of severe mastitis in a diary cattle herd.12 Subsequently,
strains have been isolated from cattle worldwide,13 with only Norway
and New Zealand being free of infection.14 It was initially assigned the
name Mycoplasma agalactiae var. bovis because of clinical similarities
to contagious agalactia of small ruminants caused by M. agalactiae.12
It was not until 1976, following total DNADNA hybridisation experiments,15 that M. bovis was elevated to species rank and given its
current name. Today, little is known about the prevalence of this
organism in Australian cattle, despite M. bovis having a worldwide
distribution and being recognised as the most frequently occurring
pathogenic bovine mycoplasma in Europe and the USA.16
In Australia, the rst reported isolation of M. bovis in 1970 was from
a case of mastitis in a dairy cow.17 Since then, research on M. bovis in
Australia has been limited to its association with mastitis in dairy
cattle.18 The involvement of M. bovis in BRDC in Australian beef
cattle, including the feedlot sector, has not been addressed in the
scientic literature.
Epidemiology
In enzootically infected areas, M. bovis has been isolated from the
lungs of a high percentage of calves in the absence of clinical signs,
especially within the rst 34 months of age.19 Mycoplasma bovis can
also be isolated from the URT of cattle in the absence of disease,
allowing it to persist within herds without detection.20 Consequently,
the movement of infected animals between properties and countries is
thought to be the most important method of dissemination of
M. bovis.16
Animals subclinically infected with M. bovis can act as reservoirs,
shedding the organism sporadically for many months to years via
mucosal secretions from the URT or genital tract, or in milk.9,21 Shedding is thought to increase considerably at the beginning of clinical
disease among infected animals21 When exposed to mucosal secretions, the URT mucosa is the primary site of M. bovis colonisation.13
Once established where there are cattle of multiple ages, M. bovis is
dicult to eradicate.16
Historically, environmental persistence by M. bovis was not considered a major source of infection compared with animal to animal
transmission.22 The absence of a protective cell wall can render
mycoplasma species susceptible to inactivation by environmental
conditions such as temperature uctuations, ultraviolet light and desiccation.23,24 However, it has been demonstrated that M. bovis produces a biolm that provides it with a degree of protection from these

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factors25 and it is capable of surviving on fomites for more than 2 days,

in milk at 4C for nearly 2 months and for more than 2 weeks in
water.23 Therefore, the possibility of environmental persistence
playing a role in the transmission of M. bovis to susceptible animals
cannot be excluded.
The most common clinical disease associated with M. bovis infection
in cattle is mastitis; however, infectious bronchopneumonia in calves,
arthritis, keratoconjunctivitis and otitis media have been widely
reported.22,24,2628
In relation to BRDC, M. bovis is an accepted cause of acute respiratory
disease in calves, typically those under 6 months of age,16,24 and a cause
of the chronic bronchopneumonia that is characteristic of persistent
or chronic infections that are poorly responsive to antimicrobial
therapy.24,29 Questions remain as to whether M. bovis can act both as a
primary pathogen of BRDC in Australian feeder-age cattle and as an
opportunistic secondary pathogen following a predisposing primary
infection.
Mycoplasma bovis and BRDC
Because of the complicated, multifactorial nature of BRDC, it is difcult to determine the associated factors, with the isolation and detection of M. bovis further complicating attempts to link this pathogen
with BRDC development.
Firstly, mycoplasma species are fastidious microorganisms that
require specialised media and expertise for their isolation and culture
compared with the other pathogens associated with BRDC.30 The
relative ease of culture and isolation of BRDC co-pathogens such as
Mann. haemolytica, P. multocida, BVDV-1 and BoHV-1 may have
contributed to the presence of M. bovis being under reported in cases
of BRDC in Europe.22 Awareness of the organism, its associated
pathology and the availability of diagnostic tests may have also led to
under reporting in some situations. A Canadian retrospective study
that looked at archival lung specimens from pneumonia cases
between 1979 and 1982 found that 20% had been previously diagnosed as abscesses or mistaken for the focal necrosis seen in lesions of
Mann. haemolytica pneumonia, but were actually lesions associated
with M. bovis.31
Secondly, M. bovis is a common inhabitant of the both the upper and
lower respiratory tract of healthy and pneumonic cattle32,33 so its presence cannot be easily linked directly with a particular clinical syndrome. There is a wide variation in the clinical signs expressed by
animals following natural and experimental M. bovis infections,20 and
because these signs are non-specic to M. bovis infections, it is dicult
clinically to distinguish M. bovis-associated respiratory disease from
that associated with other BRDC pathogens. Studies of BRDC outbreaks in feedlot cattle have reported that M. bovis was the predominant pathogen detected in the lungs of diseased animals.3437 One
study reported an increase in the severity of respiratory morbidity and
mortality, which was linked to a corresponding increase in the isolation of M. bovis from lung tissue, suggesting that M. bovis enhanced
the severity of disease.38 That nding was also supported by others
who found an association between M. bovis seroconversion and an
increase in the rate of respiratory disease.39

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Thirdly, there is a lack of correlation between antibody titres and

resistance to re-infection with M. bovis, making it problematic to apply
classical pathogen/disease association models. The lack of an eective
vaccine and/or specic treatment for M. bovis prevents accurate estimation of the proportion of BRDC cases that might be directly attributable to this pathogen.24
Finally, co-infections of M. bovis and other BRDC pathogens are
common, which confuses the issue of whether M. bovis is a primary
cause of BRDC or a secondary opportunistic pathogen. A possible
synergism between BVDV-1 and M. bovis has been suggested. One
study detected BVDV-1 antigen in 4 of 16 lung tissue sections from
lesions suggestive of M. bovis pneumonia,40 although another did not
nd that BVDV-1 infection preferentially predisposed to M. bovis
pneumonia, but was more common in calves that died as a result of
bacterial pneumonia in general.31 Others have shown that previous
exposure to BoHV-1, but not BVDV, caused M. bovis-related respiratory disease in 68-month-old beef calves,41 whereas others suggested
exacerbation of disease from M. bovis and Mann. haemolytica
co-infection, which appears to result in more severe clinical disease
and lesions than either infection alone.42
It remains to be determined if M. bovis can act as a primary initiator
of BRDC in feedlot cattle. Experimental infection studies have provided evidence that inoculation of M. bovis alone can result in clinical
cases of pneumonia in calves.4345 However, M. bovis alone failed to
cause respiratory disease in a challenge mode experiment by Pyrsliak
et al. and previous exposure to BHV-1 was required for disease to
develop.41 Those authors speculate this was related to using older,
more immunocompetent calves, which were more resistant to
M. bovis.41 Research conducted in Europe suggests that M. bovis infection is a critical predisposing factor in the development of BRDC.22,45
Those studies suggested that the presence of M. bovis and predisposing conditions can result in diminished immune function, thereby
increasing the likelihood of other bacteria invading the lower respiratory tract.45 This was illustrated by large outbreaks of pneumonia,
arthritis and mastitis in Ireland, Greece and Israel following the introduction of M. bovis into nave herds in the early 1990s.22
Pathology and clinical disease

infected calves compared with uninfected 3-month-old calves46 and

identied properties that enabled the dierentiation of M. bovisinfected lung tissue from uninfected lung tissue. Once validated in the
eld, this approach should be very useful in improving the identication of M. bovis infections associated with deaths from BRDC.
The clinical signs associated with M. bovis pneumonia are indistinguishable from other causes of BRDC in feedlot cattle.24 Non-specic
clinical signs include fever, anorexia, nasal discharge, hyperpnoea,
depression, intermittent coughing and lethargy.24,26,44 In addition,
animals infected with M. bovis have been described as chronically ill,
failing to thrive, lacking weight gain and failing to respond to treatment, highlighting the potentially chronic nature of the infection.40
Studies examining feedlot cattle with chronic, non-responsive respiratory disease corroborate this description, although other organisms
have been identied, alone or in combination with M. bovis.40,47 Others
have also suggested that M. bovis infection is responsible for a high
proportion of the chronic disease occurring in feedlots in the USA,48
but no data are available to evaluate the role of M. bovis in similar cases
in Australian feedlots.
Bacteraemia commonly results from respiratory infections involving
M. bovis.24 Challenge trials in the USA have shown that M. bovis can be
recovered by blood culture for up to 9 days following intranasal and
intratracheal challenge.43 Dissemination of M. bovis throughout the
body often results in septic arthritis and, less frequently, meningitis,
tenosynovitis, decubital abscesses and abortion.26 The clinical signs of
M. bovis arthritis are typical of septic arthritis, with aected joints
being swollen and tender. Aected animals display a varying degree of
lameness and multiple joints may be involved.26,31 Indeed, many of the
losses that have been directly attributed to M. bovis infection are
humane euthanasia of cattle because of chronic disease.24
Diagnosis
Conventional PCR49,50 and quantitative real-time PCR51,52 have been
used to study infections involving M. bovis. Because of the close
genetic relationship between M. bovis and M. agalactiae, speciesspecic PCR tests must be used to distinguish between the two
species.50 Although M. agalactiae is primarily associated with contagious agalactia of small ruminants (sheep and goats), it has been
detected in cattle49 and thus must be excluded in clinical investigations
using molecular technologies.

The gross pathological lung lesions associated with M. bovis pneumonia have been described as a caseonecrotic bronchopneumonia.40,31
Multifocal nodules of caseous necrosis within the lesions of
cranioventral bronchopneumonia have been described as unique to
the lung lesions associated with M. bovis infection.31 The circular,
raised white-yellow nodules containing dry, friable foci of caseous
material that is often seen with M. bovis-associated lung lesions diers
to the non-raised, red or pink, irregularly shaped, non-friable foci of
coagulative necrosis typical of Mann. haemolytica or H. somni.31
Experimental and clinical studies have conrmed an association
between these lesions and M. bovis infection.31,40 Lung lesions associated with M. bovis also lack the liquid purulent material seen in lung
abscesses and within lesions of chronic undierentiated bacterial
bronchopneumonia.31

Serological methods continue to play an important role in elucidating

the role of M. bovis infection in disease development. Although
M. bovis can be commonly isolated from the nasal passages of healthy
animals, the detection of specic antibodies in serum indicates a previous invasive infection of the lower respiratory tract.22 Because of
the high seroprevalence of M. bovis antibodies in some cattle populations, the usefulness of serological methods for routine diagnosis in
disease investigations is somewhat limited.24 As a method to indicate
exposure within herds, however, serology has proven to be reliable
and eective.22

An experimental infection trial quantied the morphological and

histochemical dierences in the bronchial epithelium of M. bovis-

The absence of a cell wall makes treatment of M. bovis infections with

antimicrobials from the -lactam class ineective. Only limited

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Treatment and prevention

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success in the control of M. bovis-associated disease has been achieved
using other antimicrobial therapies, because of the incomplete clearance of M. bovis from the respiratory tract of treated animals. The
alleviation of clinical signs without eradication of the organism is a
common result from antimicrobial studies involving commonly used
antimicrobials for the treatment of BRDC, including spectinomycin,45
tilmicosin,38 tulathromycin,53 enrooxacin and valnemulin.44

second Australian study, Fell et al.64 reported the experimental preparation of cattle (n = 209) for feedlot placement with matched industry
cattle. Again, age was not specied, but based on the information
provided it is estimated the age range of these cattle was between 390
and 450 days of age. As M. bovis has historically been considered most
important in younger cattle, this may be one reason why it has not
been considered as a contributor to cases of BRDC in Australia.

Vaccination is an attractive alternative strategy for improved M. bovis

control, because of the ineectiveness of many antimicrobials, but the
development of an eective vaccine targeting M. bovis has proven
problematic.24 Mycoplasma bovis has both lipid and protein antigens
that elicit host antibody responses.48 The immunodominant components of M. bovis are a family of related variable surface lipoproteins
(VSP).54,55 The vsp genes exhibit high variation in random phase (on/
o) expression and size switching of the VSP components, which gives
M. bovis enormous antigenic variability.56 Consequently, the VSP
expression patterns can be highly divergent in clonal lineages of
M. bovis isolates and are thought be a response to host antibody and
other factors.57,58 The VSP system is believed to be one of the most
important factors allowing M. bovis to establish long-term chronic
infections by preventing immune clearance by the host.24 This capacity to evade specic immunological responses has made the development of an eective vaccine dicult. Vaccination studies with
inactivated M. bovis have reported reductions in lung lesions, arthritis
and the severity and incidence of clinical disease.13,26,59,60 However, in
common with antimicrobial treatments for this organism, the prototype vaccines have failed to completely protect cattle from M. bovis
respiratory tract colonisation.

There are no studies that have been conducted to estimate the prevalence or genotypic diversity of M. bovis in Australian feedlot cattle, or
beef cattle in general. Ghadersohi et al. estimated M. bovis exposure
and subsequent mastitis among dairy cattle populations in Victoria
and northern Queensland.18,65,66 Using a conventional PCR assay it
was determined that M. bovis was present in 43% and 62% of Victorian and north Queensland dairy herds, respectively. Although that
conrms M. bovis is present and circulating in Australian dairy cattle
herds, it does not provide any insight into the situation for the Australian beef cattle population.

Recent studies using recombinant M. bovis glyceraldehyde-3phosphate dehydrogenase protein61 and M. bovis extracts, including
membrane fractions,62 as experimental vaccines reported that both
were able to elicit strong humoral and weak cell-mediated responses.
However, neither study reported protection from M. bovis infection.
The immunogen composed of the membrane fractions alone was not
as eective as the total cell extract in inducing antibody titres.62 Future
research is required to identify the type of immune response required
to protect cattle against M. bovis infection and which antigens are
required to stimulate it.
Mycoplasma bovis in Australia
There are no studies to date that have investigated the role of M. bovis
in the development of BRDC in Australian feedlot cattle, which is
surprising, given the importance placed on this pathogen in other
countries. One contributing factor could be perceived dierences in
the cattle populations arriving at feedlots in Australia and in the US.
One anecdotal example of this is the generally held view that cattle
arriving at Australian feedlots are older than those entering feedlots in
the USA. This industry view is supported by a 15-year study of 18,112
calves placed in US feedlots, where the average age of the study population was 176 days and the average placement weight was 205 kg.2
Although no comparable study has been completed in Australia to
date, Cusack et al.63 reported a study of 2,468 cattle with an average
placement weight of 340 kg. Although age was not reported in their
study, the higher placement weight is indicative of older cattle. In a

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The experimental infection study of calves by Wawegama et al.46 is

important in the context of BRDC in Australia, as it is the rst
reported experimental infection trial with an Australian strain of
M. bovis. Although the study used calves that were atypical of the
Australia feedlot population, the study did demonstrate the Australian
isolate of M. bovis could induce pneumonia and lung lesions in an
experimental setting.
Of the pathogens most commonly associated with the BRDC in the
USA and Europe, the viral agents have been subjected to the most
research in Australia. Those studies indicate a specic spectrum of
viral subtypes associated with BRDC in Australia compared with other
countries. Horwood et al. identied a novel genotype of BPIV-3 in the
Australian cattle population67 and Mahony et al. also reported that the
Australian BVDV-1 strains lack the genotypic diversity of both the US
and Europe strains, with only 2 of the 16 characterised genotypes of
BVDV-1a and 1c identied, with the latter being most commonly
detected.68 In comparison, the BVDV-1a and 1b genotypes have been
most commonly associated with BRDC in the USA. Similarly, only
one of the three known subtypes of BoHV-1 has been reported in
Australia.69 Collectively these studies suggest that the isolation, both
geographic and regulatory, of the Australian cattle population may
have resulted in specic genetic lineages of the various BRDC viral
pathogens. It remains to be determined which genetic lineages of
M. bovis and other bacterial pathogens are associated with BRDC in
Australia.
During investigations into BRDC outbreaks in Australian feedlot
cattle, the presence of M. bovis in nasal swabs collected from clinical
cases and tissue samples collected from fatal cases was determined.
Samples were provided by seven Australian feedlots between April
2008 and November 2010 and tested for M. bovis using an in-house
real-time PCR assay targeting the 16S rRNA as part of clinical investigations into BRDC outbreaks. To dierentiate between M. bovis and
M. agalactiae, the PCR amplicons from positive samples were subjected to nucleotide sequence analyses to conrm the presence of
M. bovis in positive samples (data not shown). The samples tested
included 315 nasal swabs, as well as 2 lung samples and 12 tracheal
samples from BRDC deaths. Samples were also tested for the presence

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Date

April 2008
July 2008
February 2009
June 2009
June 2009
September 2009
July 2010
November 2010

Feedlot

1
1
2
3
4
5
3
3

49
64
7
46
47
2
67
33

Pathogen
BVDV-1

BoHV-1

BPI3

BRSV

Mycoplasma bovis

Co-infectiona

1 (2%)
0
1 (14%)
2 (4%)
0
1 (50%)
6 (9%)
10 (10%)

5 (10%)
10 (15%)
1 (14%)
11 (24%)
24 (51%)
0
11 (16%)
8 (24%)

0
0
0
0
3 (6%)
0
0
0

0
0
0
4 (9%)
6 (13%)
1 (50%)
13 (19%)
0

42 (86%)
51 (78%)
3 (43%)
45 (98%)
40 (85%)
2 (100%)
7 (10%)
19 (58%)

6 (12%)
9 (14%)
1 (14%)
16 (35%)
29 (62%)
2 (100%)
8 (8%)
7 (21%)

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Table 1. Summary of results from the nasal swab samples collected from cattle diagnosed with bovine respiratory disease complex in Australian
feedlots

Extracts from nasal swabs were tested for the presence of bovine herpesvirus 1 (BoHV-1), bovine viral diarrhoea virus (BVDV-1), bovine respiratory
syncytial virus (BRSV), bovine parainuenza virus 3 (BPIV-3) and Mycoplasma bovis using real-time PCR. The number of positive samples is shown
for the respective pathogen with the percentage of positives shown in parentheses.
a
The number of samples testing positive for M. bovis in combination with one or more viruses, with the percentage in parentheses.

Table 2. Summary of results from the tissue samples collected from cattle diagnosed with bovine respiratory disease complex in Australian feedlots

Date

February 2009
February 2009
March 2009
September 2009

Feedlot

2
6
7
5

2
2
7
3

Tissue

Lung
Trachea
Trachea
Trachea

Pathogen
BVDV-1

BoHV-1

BPI3

BRSV

Mycoplasma bovis

Co-infection

0
0
1
0

1
2
2
3

0
0
0
0

0
0
0
0

2
2
5
3

1
2
3
3

Extracts from tissue samples were tested for the presence of bovine herpesvirus 1 (BoHV-1), bovine viral diarrhoea virus (BVDV-1), bovine
respiratory syncytial virus (BRSV), bovine parainuenza virus 3 (BPIV-3) and Mycoplasma bovis using real-time PCR. The number of positive samples
is shown for the respective pathogen with the percentage of positives shown in parentheses.

of BoHV-1, BVDV-1 and BPIV-3, using a multiplex real-time PCR70

and BRSV using a published real-time PCR assay.71 The results of the
analyses for the nasal swabs and tissue samples are shown in Table 1
and Table 2, respectively.
Mycoplasma bovis was the most frequently detected and most widely
distributed pathogen in nasal swab extracts (Table 1). With respect to
the viruses, BVDV-1 and BoHV-1 were more common than BPIV-3
and BRSV. Interestingly, in each group of animals, M. bovis was
detected in association with one or more of the viruses. Although M.
bovis and BoHV-1 was the combination most frequently detected, the
bacterium was also detected in combination with each virus in one or
more samples.
Mycoplasma bovis was also the most frequently detected pathogen in
the tissue samples (Table 2). Similar to nasal swabs, M. bovis was
detected in combination with BoHV-1 in the majority of samples.
Neither BPIV-3 nor BRSV was detected in the limited number of
tissue samples examined.
Though preliminary in nature, these results demonstrate the presence
of M. bovis in both clinical and fatal cases attributed to BRDC in

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Australian feedlots. Clearly, more comprehensive research is required

to determine the nature of this indicative association between M. bovis
and BRDC in Australian feedlots. Future studies should include
attempts to isolate M. bovis from diseased animals and histological
examination of lungs to identify the characteristic lesions of this infection. As in overseas research, a key component will be elucidating the
relationship between M. bovis and other pathogens.
Conclusions
Mycoplasma bovis is accepted as a key pathogen involved in the development of BRDC in intensively nished cattle in North America and
Europe. Further research is required to determine if M. bovis is solely
a secondary infectious agent or also has the capacity to be a primary
cause of pneumonia in feeder-age cattle. Similar to the situation in
North America, BRDC is consistently identied as a major health
issue in Australian feedlots; however, despite this neither the presence
nor the role of M. bovis in the disease complex has been investigated
in this country. The results of preliminary investigations presented
here, in combination with the existing literature from overseas,

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support the addition of M. bovis to the list of pathogens to be considered in BRDC investigations in Australia.
Acknowledgments
The authors acknowledge the provision of clinical samples and tissues
from Drs Tony Batterham, David Frith, Kev Sullivan and Matt George.
This study was supported by grant B.FLT.0224 from Meat and
Livestock Australia, with matching funds provided by the Australian
Government.
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