Diseases of

Poultry 14th Edition

Editor-in-Chief
David E. Swayne
Associate Editors
Martine Boulianne
Catherine M. Logue
Larry R. McDougald
Venugopal Nair
David L. Suarez

86.9%, 75.9%, and 79.2% resistance, respectively) (104).
The lowest resistance rates were observed for amikacin
(9.5%), cefoperazone (7.2%), imipenem (3.2%), and
neomycin (9.5%). Li et al. (56) studied RA in vitro sus-
­Ornithobacterium rhinotracheale Infection
Hafez M. Hafez and Richard P. Chin
Summary
Agent, Infection, and Disease. Ornithobacterium rhino­
tracheale is a Gram‐negative bacterium which causes
respiratory disease in numerous bird species. Additionally,
it is associated with heavy economic losses caused by
increased mortality and condemnation rates, drop in egg
production, and reduced growth. O. rhinotracheale is
worldwide in distribution.
Diagnosis. The preferred diagnostic test is isolation and
identification of O. rhinotracheale. Additionally, antigen
detection by polymerase chain reaction and detection of
antibodies in the blood is also used.
Intervention. Increased biosecurity practices are
primarily used to prevent the introduction and spread of
O. rhinotracheale. Vaccination using commercial or
autogenous inactivated vaccines reduces mortality and
condemnation rates.
Introduction
Definition and Synonyms
Ornithobacterium rhinotracheale infection is a conta-
gious disease of birds that causes respiratory distress,
mortality, and decreased growth. The severity of clinical
signs, duration of the disease and mortality are extremely
variable and are influenced by several factors such as
concurrent infections, poor management, inadequate
ventilation, high stocking density, poor litter conditions,
and poor hygiene.
Economic Significance
Ornithobacterium rhinotracheale can be associated with
high economic losses in poultry caused by increased
mortality and condemnation rates, drop in egg produc-
tion, or decreased growth.
Public Health Significance
Currently, O. rhinotracheale has not been found to be of
any public health significance.
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Chapter 19 Pasteurellosis and Other Respiratory Bacterial Infections 853
ceptibility to cefquinome, ceftiofur, tilmicosin and flor-
fenicol. They found that cefquinome had the highest
risk of selecting resistant mutants among these 4 anti-
microbial agents.
History
Ornithobacterium rhinotracheale was first character-
ized in 1993 by Charlton et al. (9) and subsequently
named in 1994 by Vandamme et al. (80) the following
year. Since its identification, O. rhinotracheale has been
isolated from birds in numerous countries throughout
the world. For additional earlier references on O. rhinotra­
cheale, see (11).
Etiology
Classification
Name and Synonyms
The genus Ornithobacterium is a member of the
Flavobacteriaceae within the Cytophaga‐Flavobacterium‐
Bacteroides phylum and represents a rather distinct line
of descent within this family. Related bacteria are the
bird pathogens Riemerella anatipestifer and Coenonia
anatina (79, 80). The family includes Flavobacterium, the
type genus, and the genera Bergeyella, Capnocytophaga,
Chryseobacterium, Ornithobacterium, Riemerella and
Weeksella (6).
Morphology and Staining
Ornithobacterium rhinotracheale is a Gram‐negative,
nonmotile, highly pleomorphic, rod‐shaped, nonsporu-
lating bacterium. From agars, it appears as short, plump
rods measuring 0.2–0.9 µm in width and 0.6–5 µm in
length (Figure 19.17). Very long rods measuring up to
15 µm can be observed from fluid media.
Growth Requirements
Ornithobacterium rhinotracheale grows aerobically,
microaerobically, and anaerobically. The optimal growth
temperature is 37 °C; however, growth can occur at
30–42 °C. The bacteria grows best on 5%–10% sheep blood
agar, but readily grows on tryptose soy agar and chocolate
agar. No growth occurs on MacConkey agar, Endo agar,
Gassner agar, Drigalski agar, or Simmons citrate media.
The growth in fluid media can be strain‐dependent, and
854 Section III Bacterial Diseases
Figure 19.17 Ornithobacterium rhinotracheale showing highly
pleomorphic nature. Gram stain of bacteria from a 48‐hour culture.
Gram stain, ×375. (For color detail, please see the color section.)
media such as brain heart infusion broth, Pasteurella broth,
or Todd Hewitt broth are needed.
Colony Morphology
Ornithobacterium rhinotracheale develop very small,
nonhemolytic colonies that are circular, gray to gray‐
white, sometimes with a reddish glow, and convex with
an entire edge. On primary isolation, the colonies of
most O. rhinotracheale cultures show great differences in
size (1–3 mm after 48 hour incubation) but when subcul-
tured, the colony size will become more uniform.
Prolonged incubation can give hemolytic activity on
sheep blood agar. β‐hemolytic activity has also been
found in field isolates (61). Zahra et al. (84) characterized
27 small‐colony variants (SCVs) of O. rhinotracheale iso-
lated from tracheal samples collected from different
avian species. Of the 27 O. rhinotracheale isolates, 21
(77.8%) showed SCVs in their primary cultures. Five of
them showed high levels of stability and were chosen for
further characterization with their wild type isolates.
SCVs were oxidase negative, whereas their wild type iso-
lates were positive. Growth curves for stable O. rhinotra­
cheale SCVs indicated lower growth rates and longer lag
phases than for their wild type isolates. In addition,
Mirzaie et al. (40) isolated 5 O. rhinotracheale from
pigeon and all 4 isolates from turkey, which showed
smaller colony size, whereas other isolates had larger
colonies, when cultured in blood agar. Fifty percent of
the isolates with larger colony but none of the isolates
with small colony size could agglutinate red blood cells.
The relationship between colony morphology and
hemagglutination abilities of O. rhinotracheale and their
virulence is yet to be determined.
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Biochemical Properties
Conventional biochemical tests can be inconsistent.
Phenotypic characteristics include the production of
­oxidase, lack of catalase production, lack of motility, no
reaction on triple sugar iron agar, production of beta‐­
­
galactosidase, the inability to reduce nitrate to nitrite, and
the inability to grow on MacConkey agar. There some
reports of a cytochrome oxidase‐negative strain of
O. rhinotracheale isolated from turkeys in Germany (50, 82).
Susceptibility to Chemical and Physical Agents
Ornithobacterium rhinotracheale strains were completely
inactivated by a 0.5% solution containing formic and
glyoxyl acid, and a 0.5% solution of an aldehyde‐based
(20% glutaraldehyde) product after 15 minutes exposure
time (24). These preparations were able to inactivate
O. rhinotracheale in vitro at concentrations of 0.5%
within 15 minutes.
Antigenic Structure and Toxins
Currently, no special structures or properties such as
pili, fimbriae, plasmids, or specific toxic activities have
been reported.
Strain Classification
Antigenicity
Using boiled extract antigens (BEAs) and monovalent
antisera in the agar gel precipitation (AGP) and enzyme‐
linked immunosorbent assay (ELISA) tests, 18 serotypes
(A to R) of O. rhinotracheale have been determined (71).
Serotype A was the most prevalent serotype among
chicken isolates (97%) and turkey isolates (61%). There
appears to be a correlation between the geographic origin
of the O. rhinotracheale isolates and their serotype.
Serotype C could be isolated only from chickens and
turkeys in South Africa and the United States (71). There
is no indication of host specificity of the serotypes.
Hafez and Sting (25) compared the efficacy of using
different antigen extractions (heat‐stable, proteinase
K‐stable and sodium dodecyl sulfate) for serotyping
O. rhinotracheale in the AGP and ELISA tests. Results
indicate that the AGP test with heat‐stable or proteinase
K‐stable antigen extractions is a suitable method for
serotyping. Numerous cross‐reactions were seen with
the ELISA making it unreliable for serotyping.
Immunogenicity or Protective Characteristics
Using a novel experimental method of combining immune
depletion and passive transfer of immunity within the
same host, Schuijffel et al. (52), found that the antibody‐
mediated immunity in chickens was a key component in
the protection against O. rhinotracheale infection.

Molecular
Amonsin et al. (2) using multilocus enzyme electrophore-
sis, repetitive sequence based‐polymerae chain reacation
(PCR), and 16S rRNA gene sequencing demonstrated
that the majority of 55 O. rhinotracheale isolates recov-
ered from domesticated poultry throughout the world
had limited heterogeneity and were represented by a
small group of closely related clones. They propose that
the bacterium was recently introduced to domesticated
poultry from wild bird populations.
Twenty‐three isolates of O. rhinotracheale from France
were tested using the random amplified polymorphic
DNA (RAPD) analysis (32). Results showed that this
method gave reproducible DNA fingerprints and a good
level of discrimination, thus appearing to be another
method for typing.
Investigation of several O. rhinotracheale isolates from
turkeys and chickens originated from Germany, Hungary,
and Spain by pulsed‐field gel electrophoresis (PFGE) of
genomic macro‐restriction fragments using the enzyme
SalI (27). In general, most isolates showed differences in
DNA fingerprints although the overall profiles were very
similar and a correlation between geographic origin,
serotype and DNA fingerprint pattern was observed.
In contrast, Koga and Zavaleta (31) investigated 25
O. rhinotracheale isolates from broilers, breeders, and layers
from several geographic zones of Peru using PCR and
repetitive extragenic palindromic PCR (rep‐PCR) tech-
niques. All isolates tested had a genetic profile similar to
that of the O. rhinotracheale type strain (American Type
Culture Collection 51463) isolated from a turkey in the
United Kingdom. Molecular typing of O. rhinotracheale
isolates has also been performed using the primers M13
(5′‐TAT GTA AAA CGA CGG CCA GT‐ 3) and ERIC 1R
(5′‐ ATG TAA GCT CCT GGG GAT TCA C ‐3′) and
variations were found between all tested serotypes (29).
Recently, Thieme et al. (63) established an multilocus
sequence typing (MLST) scheme for O. rhinotracheale,
which allows for worldwide comparison of sequence data.
The overall identified low genetic diversity among strains
isolated from turkeys and chickens, independent of host
and geographical origins, suggests that O. rhinotracheale
has only recently been introduced into domestic poultry
and dispersed worldwide. In addition, results clearly
showed that O. rhinotracheale strains from birds of prey
had close genetic relationships to pathogenic strains cir-
culating among turkeys and chickens. On the other hand,
the results further indicate that strains isolated from
pigeons are genetically distant from all other O. rhinotra­
cheale strains and may taxonomically represent their own
O. rhinotracheale‐like species (64).
Pathogenicity
Pathogenicity differences appear to exist between
isolates of O. rhinotracheale. Three South African
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Chapter 19 Pasteurellosis and Other Respiratory Bacterial Infections 855
O. rhinotracheale field isolates inoculated into the caudal
abdominal air sacs of 28‐day‐old broiler chickens showed
significant differences in the production of airsacculitis
and arthritis (66). In addition, van Veen et al. (78) found
that Dutch and South African isolates were more patho-
genic than an American isolate in broiler chickens when
aerosol challenged.
The pathogenicity of 88 O. rhinotracheale isolates,
collected in Germany from turkeys and chickens between
2003 and 2006, was examined using the embryo lethality
test. In total, 54 isolates (61.4%) were mildly pathogenic,
whereas 34 isolates (38.6%) were classified as moderately
pathogenic. There was no correlation between serotype
and pathogenicity. No highly pathogenic isolates were
detected, and no increase in pathogenicity over the years
was observed (82).
Soriano et al. found in vitro adherence of O. rhinotra­
cheale isolates to chicken tracheal epithelial cells (55).
Pathobiology and Epidemiology
Incidence and Distribution
After a first recognition, O. rhinotracheale has been
diagnosed throughout the world (11).
Natural and Experimental Hosts
Ornithobacterium rhinotracheale has been isolated
worldwide from numerous bird species, including chicken,
chukar partridge, duck, falcons, goose, guinea fowl, gull,
ostrich, partridge, pheasant, pigeon, quail, rook and
turkey (11, 83).
In commercial poultry, all ages appear to be susceptible.
Many case reports of O. rhinotracheale infection describe
a concomitant infection with other respiratory pathogens,
such as Escherichia coli (16, 17, 51), Bordetella avium
(17), Newcastle disease virus (65), infectious bronchitis
virus (18), avian metapneumovirus (30, 38), Avian
Influenza H9N2 (5), Streptococcus zooepidemicus (45),
Avibacterium paragallinarum (41), Mycoplasma synoviae
(85), and Chlamydia psittaci (12, 73). Most experimental
studies have concluded that, when experimentally inocu-
lated by itself, O. rhinotracheale causes minimal patho-
logic lesions in chickens and turkeys and that the severity
of lesions are enhanced when there is a concurrent infec-
tion with respiratory viruses or bacteria.
However, some studies report production of pathologic
lesions similar to those seen in field cases in chickens and
turkeys using O. rhinotracheale alone (11, 48, 81).
Transmission, Carriers, and Vectors
Ornithobacterium rhinotracheale infection appears to
have become endemic and can affect every new restocking
856 Section III Bacterial Diseases
even in previously cleaned and disinfected poultry houses,
especially in areas with intensive poultry production as
well as in multiple age farms (26). The infection appears
to spread horizontally by direct and indirect contact
through aerosols or drinking water. O. rhinotracheale
was found to survive 1 day at 37 °C, 6 days at 22 °C, 40
days at 4 °C, and at least 150 days at –12 °C (35). The
survival of O. rhinotracheale at lower temperatures may
be associated with the higher incidence of reported
infections during winter months. It did not survive
24 hours at 42 °C.
Vertical transmission is suspected based on some
reports of the isolation of O. rhinotracheale at a very low
incidence from reproductive organs and hatching eggs,
infertile eggs and dead embryos (15, 62). In addition,
O. rhinotracheale has been isolated from the ovaries,
oviduct, hatching eggs, infertile eggs. However, when
O. rhinotracheale was inoculated into embryonated
chicken eggs, the embryos were killed by the ninth day
and O. rhinotracheale was not isolated from the eggs
suggesting it is not transmitted via eggs during hatching
(81). However, van Veen et al. (77), observed that specific
pathogen‐free broiler chickens placed in a hatcher at a
commercial turkey hatchery during hatch showed res-
piratory tract lesions at postmortem examination that
were positive for O. rhinotracheale by bacteriological
and immunohistological examination.
Incubation Period
Experimental inoculation of 22‐week‐old turkeys with
O. rhinotracheale resulted in depression, coughing, and
decreased feed intake within 24 hours (57). In 48 hours,
turkeys were coughing bloody mucus. Five days post-
inoculation, the coughing had decreased and surviving
turkeys were less depressed.
In experimental infection, broiler chickens were
challenged at 14 days or 21 days with an aerosol and
observed for 2 weeks postinfection. Pathologic lesions
at postmortem investigation in general were mild, with
only significant airsacculitis at first week postinfection
and severe exudate in the trachea at second week
postchallenge (70).
Clinical Signs
The severity of clinical signs, duration of the disease and
mortality of O. rhinotracheale outbreaks are extremely
variable. They can be influenced by many factors such as
poor management, inadequate ventilation, high stocking
density, poor litter conditions, poor hygiene, high ammo-
nia levels, concurrent diseases and the type of secondary
infection.
Clinical signs in broiler chickens generally appear at
3–6 weeks of age with a mortality rate of 2%–10%.
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Affected birds show listlessness, decreased food intake,
reduced weight gains, and transient nasal discharge and
sneezing, followed by facial edema (44, 68). O. rhinotra­
cheale can also cause sudden death (up to 20% in a cou-
ple of days) in young birds with infections of the brains
and skull with or without respiratory symptoms (4).
In broiler breeders the disease affects the birds in the
laying period, primarily at the peak of production or
soon before entering production. There is a slight
increase in mortality, a decrease in feed intake, and
some mild respiratory symptoms. Mortality is variable
and relatively low in uncomplicated cases. There can be
a drop in egg production, decrease in egg size, and poor
eggshell quality. Fertility and hatchability are unaffected
in many cases (21).
In commercial laying‐type chickens, decreased egg
production, increased misshapen eggs, and increased
mortality have been associated with O. rhinotracheale
infection (59).
Roepke (47) found a higher severity of clinical signs
and mortality in older turkeys, and the majority of young
infected flocks appeared clinically normal. In many cases
young poults are affected between 2 and 8 weeks of age.
Mortality ranges between 1% and 15% during the acute
phase (8 days), but infections can be accompanied with
mortality rates of up to 50% (13). Initial symptoms are
coughing, sneezing, and nasal discharge followed, in
some cases, by severe respiratory distress, dyspnea, pros-
tration, and sinusitis. These symptoms are accompanied
with a reduction in feed consumption and water intake.
In turkey breeder flocks, there can also be a decrease in
egg production and an increase in the number of unsuit-
able hatching eggs (13, 68).
Ornithobacterium rhinotracheale has been reported to
cause neurological signs or paralysis through arthritis,
meningitis, osteitis, and osteomyelitis in chickens and
turkeys (17, 60, 68).
Pathology
Gross
In broiler chickens, the common gross lesions include
pneumonia, pleuritis, and airsacculitis. At slaughter or
postmortem examination, foamy, white, yogurt‐like exudate
can be seen in the air sacs (predominantly abdominal)
(Figure 19.18), most of the time accompanied by unilateral
pneumonia (70). Lesions caused by O. rhinotracheale
can lead to condemnation rates of 50% or more (74, 76).
In addition, subcutaneous edema over the cranium with
adjacent osteitis, osteomyelitis and encephalitis has been
reported in chickens.
In turkeys, there is edema and unilateral or bilateral
consolidation of the lungs (26, 27) with fibrinous exudate
on the pleura (Figure 19.19). In addition, there could be
fibrinosuppurative airsacculitis, pericarditis, peritonitis,

Figure 19.18 Thickened, opaque air sacs with white to yellow exudate
(arrows) associated with infection of Ornithobacterium rhinotracheale
in 9‐week‐old turkeys. (For color detail, please see the color section.)
Figure 19.19 Consolidation of the lungs with fibrinous exudate
on the pleura (pleuropneumonia) associated with
Ornithobacterium rhinotracheale infection in a 16‐week‐old turkey.
(For color detail, please see the color section.)
and mild tracheitis. In some cases, swelling of the liver
and spleen, as well as degeneration of heart muscles, has
been observed. Infections of the joints and vertebrae can
be seen in older birds.
Microscopic
Most histologic lesions can be seen in the lungs, pleura,
and air sacs. In field cases, the lungs (Figure 19.20) are
congested, and throughout the parenchyma, there are
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Chapter 19 Pasteurellosis and Other Respiratory Bacterial Infections 857
Figure 19.20 Severe fibrinoheterophilic inflammation of lung
associated with Ornithobacterium rhinotracheale infection in a turkey.
H&E, ×20. (S. Stoute) (For color detail, please see the color section.)
large collections of fibrin admixed with macrophages
and heterophils lying free within the lumen of air capillaries
and parabronchi. There are pronounced and diffuse
interstitial infiltrates of macrophages with smaller
numbers of heterophils. Widespread coalescing foci of
necrosis often centered within the lumen of parabronchi
with extension of the necrosis into the adjacent paren-
chyma are present. These necrotic foci usually are filled
with dense aggregates of necrotic heterophilic infiltrate
or exudate, and there can be scattered small clusters of
bacteria seen within the necrotic foci. Numerous blood
capillaries can be distended and filled with fibrin thrombi.
The pleura and air sacs can be severely thickened and
edematous with interstitial fibrin deposits, diffuse
heterophilic infiltrate, scattered small foci of necrotic
heterophilic infiltrate, and fibrosis.
Immunity
Minimal information is available regarding immunity to
O. rhinotracheale. The active immunity induced by inac-
tivated vaccines was found to be serotype specific, but
live vaccination can induce a degree of cross‐protection
between some serotypes (54). Passive immunity can be
induced for up to 3–4 weeks by maternally derived
antibodies.
Diagnosis
A presumptive diagnosis may be made based on clinical
signs and necropsy findings. However, a definitive diag-
nosis must be based on the isolation and identification
of O. rhinotracheale and/or detection of antibodies
(10, 22).
858 Section III Bacterial Diseases

Isolation and Identification of Causative Agent birds (1, 29). In addition, the immunofluorescence
antibody test and immunohistochemical staining were
Bacterial Isolation and Identification
used to detect O. rhinotracheale in chickens (72).
The trachea, lungs, and air sacs are the best tissues from
Subsequently, van Veen et al. (76) found that the immu-
which to isolate O. rhinotracheale, though it has been
nofluorescence assay and the peroxidase‐antiperoxidase
isolated from numerous tissues, including joint, brain,
test were equally sensitive. Using these tests, they were
and oviduct. The infraorbital sinus and nasal cavity are
able to identify a higher percentage of O. rhinotracheale‐
also suitable sites for culture, but O. rhinotracheale can
infected chicken broiler flocks at slaughter, when
be masked easily by other bacteria overgrowth.
compared with conventional diagnostic methods (i.e.,
Fresh tissues and/or swabs should be collected within
serology and/or bacteriology).
the first week of infection, and shipped cooled in a trans-
port medium, such as Amies gel medium or Stuart gel
medium (43). Serology
Ornithobacterium rhinotracheale can be isolated on
Serology is useful for flock monitoring or as an aid in the
common, nonselective blood or chocolate agar. Colonies
diagnosis of O. rhinotracheale infection.
grow in 24 hours, but it is best to hold inoculated plates
The serum plate agglutination test (SPAT) has been
for 48–72 hours in air enriched with 7.5%–10% CO2.
used as a rapid test for the detection of antibodies against
Colonies will appear pinpoint to small (approximately
O. rhinotracheale (19, 28). One SPAT was developed using
1–2 mm diameter), gray to gray‐white, circular, and con-
a nonserotyped Minnesota isolate of O. rhinotracheale
vex with an entire edge. Gram stain will reveal character-
and was reported to have good sensitivity and specificity
istic pleomorphic Gram‐negative bacteria. Colonies are
(3). However, in another study (36) the SPAT detected
catalase‐negative and oxidase‐positive. Pure O. rhinotra­
only 65% of infected birds during the first 2 weeks of
cheale cultures have a distinct odor, similar to that of
infection and declined significantly thereafter. This sug-
butyric acid.
gests that the SPAT detects IgM antibodies, which are
In contaminated samples with fast growing bacteria,
efficient in agglutination with specific antigens. Erganis
such as E. coli, Proteus sp. or Pseudomonas sp., O. rhinotra­
et al. (19) developed a dot immunobinding assay (DIA)
cheale colonies may be overgrown and are difficult to
which appeared to be less sensitive than other agglutina-
detect in routine investigation. Since most O. rhinotracheale
tion tests.
isolates are resistant to gentamicin the use of 10 µg of
ELISAs have been developed using different serotypes
gentamicin per milliliter of blood agar medium is recom-
and extracted antigens of O. rhinotracheale. Boiled
mended in an effort to isolate O. rhinotracheale from
extract antigens, which are used for serotyping, tend to
contaminated samples. Blood agar containing 5 µg/mL of
give the best results for serotype‐specific tests (68).
gentamicin and polymyxin B was also effective (22).
Conversely, sodium dodecyl sulfate (SDS)‐antigen
The API‐20NE system (bioMérieux, France) was found
extraction (25) and extracted outer membrane proteins
useful for the identification of O. rhinotracheale (71).
of O. rhinotracheale (36) will result in more cross‐reac-
Ninety‐nine percent of isolates were found to have bioco-
tions allowing detection of antibodies against different
des 0‐2‐2‐0‐0‐0‐4 (β‐galactosidase, urease and oxidase
serotypes with 1 test. Field surveys using these ELISAs
positive) (65%) or 0‐0‐2‐0‐0‐0‐4 (β‐galactosidase and oxi-
or commercial ELISA kits have been useful for moni-
dase positive) (34%). For those isolates that were posi-
toring flocks and the diagnosis of O. rhinotracheale
tive for the arginine dihydrolase test, biocodes 0‐3‐2‐0‐0‐0‐4
infections (23, 46, 49, 67). Commercial ELISA kits are
or 0‐1‐2‐0‐0‐0‐4 were found. Also isolates with the code
currently available and able to detect antibodies against
0-0-2-0-0-0-0 (β‐galactosidase positive and urease as well
all tested O. rhinotracheale serotypes.
as oxidase negative) are highly suspected (50).
The effect of amoxicillin treatment on the antibody
The rapid slide agglutination test also has been used
kinetics after experimental infection showed that imme-
for diagnostic purposes. However, auto‐agglutinable
diate treatment did not influence the antibody response,
strains were regularly found (3).
whereas treatment that started 7 days postinoculation
The AGP test, using known positive antisera, is cur-
resulted in a lower antibody response (11).
rently used to identify and serotype O. rhinotracheale
isolates. Conventional and real‐time PCR tests have been
developed and are used for the identification of suspect Differential Diagnosis
isolates (1, 29).
Respiratory lesions associated with O. rhinotracheale are
similar to those caused by numerous bacteria, such as
Antigen Detection E. coli, Pasteurella multocida, Riemerella anatipestifer,
As mentioned above, PCRs was used for the detection of Avibacterium paragallinarum, Coenonia anatine, and
O. rhinotracheale in tracheal swabs of heavily infected Chlamydia psittaci.

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Intervention Strategies
Management Procedures
Ornithobacterium rhinotracheale appears to be highly
contagious and strict biosecurity measures should be fol-
lowed to prevent its introduction into a flock. However,
after a ranch is infected, O. rhinotracheale becomes
endemic, especially in multiple‐age farms and in areas
with intensive poultry production.
Vaccination
Types of Vaccines
Several attempts to combat infection by using several
types of vaccines such as bacterins, live vaccines, and
subunit recombinant vaccines under experimental and
field conditions have been carried out with various results
(11, 20).
Inactivated Vaccines. Vaccination of broiler chickens with
inactivated vaccines was found to be effective (69), but is
probably impractical in most, because the efficacy of the
vaccine is negatively influenced by the presence of
maternal antibodies. On the other hand, vaccination of
broiler breeders with mineral oil adjuvant inactivated
vaccines stimulated the development of high maternal
antibodies (7, 8), which were sufficient to protect progeny
against experimental challenge for up to 4 weeks of age
(69) and produced lower mortality and condemnation
rates in the progeny from vaccinated breeders (8). Using
inactivated vaccines with mineral oil adjuvant, layers
vaccinated at 8 weeks of age with a booster dose at 12
weeks of age, produced an early immune response and
reduced the incidence of airsacculitis and pneumonia (42).
Vaccination of meat turkey flocks using monovalent or
trivalent bacterins in field trials resulted in production of
antibodies for a short duration. Nonetheless, the mortality
and condemnation rates were lower in the vaccinated
group when compared with the unvaccinated group.
Vaccination of young turkeys with autogenous bacterins
successfully reduced the number of outbreaks (11).
Because of the possibility of infection by several sero-
types, it may be necessary to use different serotypes in
the vaccines.
Live Attenuated Vaccines. A temperature‐sensitive mutant
of O. rhinotracheale was developed and used as a live
vaccine in turkeys (33, 34). Turkeys were vaccinated at
5 days of age via the drinking water, and challenged
7 weeks postvaccination. Vaccinated birds had a
significantly lower mean score for gross lesions when
compared with unvaccinated birds, as well as a lower
rate of reisolation and number of colony forming units of
O. rhinotracheale per gram of lung tissue.
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Chapter 19 Pasteurellosis and Other Respiratory Bacterial Infections 859
Sprenger et al. (58) vaccinated 6‐week‐old turkeys
either intranasally with a live vaccine or subcutaneously
with a killed O. rhinotracheale vaccine, and challenged
them intratracheally with live O. rhinotracheale at 14 or
21 weeks of age. Airsacculitis and pneumonia occurred
less frequently in vaccinated birds than in unvaccinated
birds after challenge, and O. rhinotracheale was recov-
ered from unvaccinated, challenged birds, but not from
vaccinated, challenged or unchallenged birds.
Administration of an autogenous live vaccine (oral
route) in 6‐week‐old turkeys resulted in a decrease in
pathologic lesions and mortality when the birds were
older. It is interesting to note that the birds were simultane-
ously spray vaccinated with a live avian paramyxovirus‐1
vaccine without any problems (11).
Recombinant Vaccines. Schuijffel et al. (52) demonstrated
that cross‐protective immunity against different
O. rhinotracheale serotypes can be induced by live
vaccination in chickens. The genes encoding 8 cross‐
reactive antigens (Or01, Or02, Or03, Or04, Or11, Or77,
Or98A, and Or98B) were amplified, cloned in an
expression vector, and expressed in E. coli. Purified
recombinant proteins with a molecular mass ranging
from 35.9 to 62.9 kDa were mixed and tested as a
subunit vaccine for protection against challenge with
homologous and heterologous O. rhinotracheale
serotypes. Subunit vaccination resulted in the
production of antibodies reactive to the recombinant
proteins on Western blot, and this eight‐valent vaccine
provided both homologous and heterologous protection
against O. rhinotracheale challenge in chickens. In a
subsequent study (53), they found that these 8 antigens
are highly conserved among different O. rhinotracheale
serotypes, but the different antigens were not expressed
by all serotypes. In addition, their 4 component subunit
vaccine was able to protect chickens against challenge
with a heterologous O. rhinotracheale serotype.
Treatment
The treatment of O. rhinotracheale infections with
antibiotics is very difficult because of the variable sus-
ceptibility of strains. O. rhinotracheale can acquire
reduced susceptibility or resistance against antibiotics
such as amoxicillin, ampicillin, doxycycline, enrofloxacin,
flumequine, gentamicin, lincomycin, trimethoprim‐
sulfonamide, tetracycline and tylosin (14, 37, 39, 56, 75).
Susceptibility can be dependent on the antibiotic regime
used by the poultry industry in various geographical
locations.
In 1996, Hafez reported that water medication using
amoxicillin at a dose of 250 ppm for 3–7 days gave
­satisfactory results in most cases, and application of
chlortetracycline at a dose of 500 ppm in drinking
860 Section III Bacterial Diseases
water for 4–5 days appeared to be effective (21). How­
ever, further studies have shown that treatment with
amoxicillin is no longer efficacious (39). In some cases,
injections with various tetracyclines and penicillins were
found to be effective.
Sixty‐eight O. rhinotracheale isolates from the United
States were found susceptible to ampicillin, erythromycin,
penicillin, spectinomycin, and tylosin, and 54 of the
68 isolates were susceptible to neomycin, sarafloxacin,
and tetracycline. It was also found that German isolates
­Bordetellosis (Turkey Coryza)
Karen B. Register and Mark W. Jackwood
Summary
Agent, Infection, and Disease.Bordetellosis is an acute,
highly contagious respiratory disease of young turkeys.
Bordetella avium was once considered the sole etiologic
agent but B. hinzii is now also known to be a potential
cause. Mortality in uncomplicated outbreaks is low but
80%–100% morbidity is typical and the economic impact
can be substantial. Mortality may be at least 50% under
poor management conditions or when additional
pathogens are present. Bordetellosis occurs in nearly all
areas of the world where turkeys are intensively raised.
Diagnosis. Diagnosis is based on clinical signs and
lesions and isolation of B. avium or B. hinzii from the
respiratory tract.
Intervention. B. avium vaccines may reduce disease
severity or delay onset but they fail to prevent infection
and are not widely used.
Introduction
Definition and Synonyms
Bordetellosis in poultry is a highly contagious disease
affecting primarily the upper respiratory tract. Once
thought to be caused by only Bordetella avium, it is now
apparent that a closely related bacterium with which it
has frequently been confused, B. hinzii, may also cause
bordetellosis in turkeys (97). The disease is still at times
referred to as turkey coryza. Other synonyms that have
been largely abandoned are alcaligenes rhinotracheitis
(ART), adenovirus‐associated respiratory disease, acute
respiratory disease syndrome, B. avium rhinotracheitis
(BART), and turkey rhinotracheitis. The variety of names
used for this disease reflects the initial confusion that
surrounded its etiology.
www.ajlobby.com
had a significantly lower susceptibility to erythromycin
and sarafloxacin when compared with isolates from the
United States. Furthermore, Zahra et al. (84) found that
antibiotic sensitivity of SCVs O. rhinotracheale isolates
had higher minimum inhibitory concentration (MIC)
values in comparison with their wild type isolates.
They suggested that successful antibiotic treatment of
respiratory diseases associated with O. rhinotracheale
must take into consideration the resistance patterns of
O. rhinotracheale SCVs.
Economic Significance
There are few data available addressing the current
prevalence of bordetellosis in poultry and no detailed
analysis of its economic impact. The number and severity
of outbreaks appears to have lessened in recent years but
the disease remains a major concern for turkey produc-
ers. Impaired growth and high mortality resulting from
secondary colisepticemia probably cause significant
losses to the turkey industry. B. avium or B. hinzii alone
is not known to cause disease in chickens, but related
losses may occur when B. avium infections are complicated
by prior or concurrent infection with other pathogens.
It is not known whether B. hinzii may also contribute to
losses in cases of complicated infections.
Public Health Significance
For many years it was thought that B. avium infected
only avian hosts but it is now apparent that the bacterium
is also a rare, opportunistic human pathogen (41, 121).
B. hinzii is likewise an opportunist in humans, occasion-
ally reported as a cause of respiratory disease, bacteremia
or infections of the digestive system (29, 121). Some
evidence suggests that contaminated poultry or other
avian reservoirs may be among the sources from which
B. hinzii can be transmitted to humans.
History
Turkey rhinotracheitis (coryza) attributable to a bacte-
rium of the genus Bordetella was first reported in Canada
in 1967 (32) and then in Germany, nearly a decade later
(45). Outbreaks with a similar presentation occurring in
the United States and elsewhere were frequently associ-
ated with adenovirus, infectious bursal disease virus
(IBDV) or a variety of other bacterial or viral agents
but none were consistently capable of reproducing the