Infectious bronchitis (IB) has
been reported as a disease only in chicken. All ages of chickens are
susceptible to infection but the severity of the clinical disease varies.
Infectious bronchitis is considered to be worldwide in distribution. The
incidence is not constant trough the year,
being reported more of during the cooler months.
History
The disease was first described
in 1931 in a flock of young chickens in the USA. Since that time, the disease
has been identified in broilers, layers and breeders chickens throughout in the
world. Vaccines to help reduce losses in chickens were first used in the 1950s.
Aetiology
Infectious bronchitis is caused
by a coronavirus. It is an enveloped, single stranded RNA virus. Three virus
specific proteins have identified; the spike (S) glycoprotein, the membrane or
matrix (M) glycoprotein, and
nucleocapsid (N) protein (Figure 1). The crucial spike glycoprotein is
comprised of two glycopolypeptides (S1 and S2). These spikes or peplomers can
be seen projecting through the envelope on electron micrographs giving the
virus its characteristic ‘corona’ (Figure 2). H1 and mos SN antibodies are
directed against the S1 glycopolypeptide. The unique amino acid sequences,
epitopes, on this glycoprotein determine serotype. The virus is fairly labile
(fragile), being easily destroyed by disinfectants, sunlight, heat and other
environmental factors. Infectious bronchitis virus has the ability to mutate or
change its genetic make-up readily. As a result, numerous serotypes have been
identified and have complicated efforts at control thorugh vaccination. Three
common serotypes in North America are the Massachusetts, Connecticut, and
Arkansas 99 IB viruses. In Europe, various ‘Holland variants’, usually
designated using numbers (D-274, D-212), are recognised.
Several strains of infectious
bronchitis have a strong affinity for the kidney (nephropathogenic strains).
These strains may cause severe renal damage. This affinity for kidney tissue
may have resulted from mutation as a result of selection pressure following
widespread use of the modified live IB vaccines. That is, after prolonged use
of live IB vaccines, which initially provided protection against IB virus
infection in respiratory tissues, viral mutation allowed new tissues to be
infected, where there was little protection. These viruses have become less
prevalent in recent years.
Transmission
The IB virus is spread by the
respiratory route in droplets expelled during coughing or sneexing by infected
chickens. The spread of the disease trough a flock is very rapid. Transmission
from farm to farm is related to movement of contaminated people, equipment, and
vehicles. Following infection, chickens may remain carriers and shed the virus
for several weeks. Egg transmission of the virus does not occur.
Clinical signs in young chicks
Clinical signs include coughing,
sneezing, rales, nasal discharge and frothy exudate in the eyes. Affected
chicks appear depressed and will tend to huddle near a heat source. In an
affected flock, all birds will typically develop clinical signs within 36 to 48
hours. Clinical disease will normally last for 7 days. Mortality is usually
low, unless complicated by other factors such as Mycoplasma gallisepticum, immunosuppression, poor air quality, etc.
Clinical signs in older chickens
Clinical signs of coughing,
snezing and rales may be observe in older birds. A drop in egg production of
5-10% lasting for 10-14 days is commonly reported. However, if complicating
factors are present, production drop may be as high as 50%. Egg produced
following infection may have thin or irregular shells, and thin, watery
albumen. Loss of pigment in brown-shelled eggs is common. In severe complicated
cases, chickens may develop airsacculitis. Chickens that experienced a severe
vaccination reaction following chick vaccination or field infection during the
first two weeks of life may have permanent damage in the oviduct, resulting in
hens with poor production.
Nephropathogenic stains have been
recognised in laying flocks. These strains may cause an elevated mortality
during the infection or long after as a result of kidney damage that progresses
to urolithiasis. However, there are numerous causes of urolithiasis and it
cannot be assumed that IB is the cause of this condition without supporting
laboratory data.
Lesions
Lesions associated with IB
include a mild to moderate inflammation of the upper respiratory tract. If
complicating factors are present, arisacculitis and increased mortality may be
noted, especially in younger chickens. Kidney damage may be significant
following infection with nephropathogenic strains. Kidney of affected chickens
will be pale and swollen. Urate deposits may be observed in the kidney tissue
and the ureters, which may be occluded. Laying chickens may have yolk in the
ovary may be flaccid. Infection of very young chicks may result in the
development of cystic oviducts.
Diagnosis
Serologic testing to determine if
a response to IB virus has occurred in a suspect flock is performed by
comparing two sets of serum samples; one is collected at the onset of clinical
disease and the second sample 3 ½ -4 weeks later. Serological procedures
commonly used include ELISA, virus neutralisation, and Hl. Confirmation of IB
requires isolation and identification of the virus. Typically, this is done in
specific pathogen-free (SPF) chicken embryos at 9-11 days of incubation by the
allcantoic sac route of inoculation. Tissues collected for virus isolation
attempts from diseased chickens include trachea, lungs, air sacs, kidney, and
caecal tonsils. If samples are collected
more than one week after infection, cecal tonsils and kidney are the preferred
sites for recovery of IB virus. Virus typing has traditionally been performed
by neutralisation using selected IB antisera. More recently, polymerase chain
reaction (PCR) and restriction fragment length polymorphism (RFLP) have been
used to differentiate IBV serotypes. Lesions in embryo are helpful in
diagnosing IB, Affected embryos examined at 7 days after inoculation are
stunted, have clubbed down, an excess of urates in the kidneys, and the amnion
and allantois membranes are thickened and closely invest the embryo. These
embryo will not hatch. IB field virus may have to be serally passed in embryos
to adapt the field virus to the embryos before typical lesions are recognised.
Control
Prevention of infectious
bronchitis is best achieved through an effective biosecurity programme. As a second
line of defence, chickens in IB problem areas should be vaccinated with
modified live vaccines to provide protection. The multiplicity of serotypes
identified in the field presents a chalennge in designing an effective
vaccination programme. To be successful in protecting chickens against
challenge, it is essential to identify the prevalent serotypes in the region
and to determine the cross-protective potential of available vaccines. In North
America, the common sertypes used in most vaccinating programmes are the
Massachusetts, Connecticut and Arkansas serotypes. These serotypes are
available in both modified live vaccines and inactivated water-in-oil
emulsions. Regionally important serotypes (e.g. California strains) may be
included in inactivated vaccines. In Europe, various ‘Holland variants’ usually
designated by number (e.g. D-274, D-1466) are recognised. Polyvalent vaccines,
which contain multiple strains, are also available. Control of other
respiratory disease, e.g. Newcastle disease, Mycoplasma gallisepticum, and strongly immunosuppressive disease,
e.g. infectious bursal disease or Marek’s disease, must not be forgotten.
Vaccines selection
IB vaccination programme is
broilers involve the use of modified live vaccines. Vaccination of layers hgas
historically involved administering a series of live vaccines and progressively
increasing the aggresiveness of the route of vaccination, i.e. start with water
administration and progress to fine particle spray, and strain of vacccine
(highly attenuated to less attenuated). In breeders, a similar programme is
often followed. However, prior to onset of production, an inactivated vaccine
is also administered to stimulate antibody production. Inactivated vaccines
stimulate higher levels if circulating antibodies than live vaccines and would
be of value in a breeder programme where maternal antibody protection is neede.
Modified live vaccines provide better stimulation of cell mediated (T cell
system) and elicit a superior local antibody (immunoglobulin A, IgA) response
as a result of local mucosal infection and thus would be of more value in
protecting commercial layers.
With dozens of IBV strains having
been identified around the world, choosing approriate strains for vaccination
may seem a daunting task. The immue response produced to one strain, however,
often shows a significant degree of cross-protection to heterologous challenge.
Cross-protection has been demonstrated especially for the live type of
vaccines. If the prevalent strains for a region have been identified, it is
often possible to design a programme using commercially available vaccine
strains Although no reasonable combination of IB vaccine strains provides full
protection against all heterologous challenges, there are combination that
offer broad coverage. Once the prevalent serotypes in an area have been
identified, the use of modified live vaccines containing carefully chosen
trains can be used to immunise broilers, layers and breeders. Additionally,
polyvalent inactivated vaccines can be administered to breeders at
point-og-lay. It has been demonstrated that ‘classical’ strains of IBV can act
at least as partial primes for susequent administration of an inactivated
infectious bronchitis vaccine containing variant dan standard strains. Inactivated
IB vaccines do not stimulate local and cell=mediated immunity as effectively as
modified live virus IB vaccines. However, they can provide a degree of immunity
against variant strains without the risk of introducing new strain of IB into a
poultry operation. Imprudent over-use of live IB vacines results in the
vaccines becoming the problem rather than part of the solution.
While deciding which strains to
utilise in an IB vaccination programme, the basic must not be ignored. Good vaccination practise are especially
important when administering live IB vaccines. It is relatively fragile virus
and can easily be inactivated if proper vaccination procedures are not
followed. Good practise include protection of the vacine from sunlight, removal
of sanitiser from water used for mixing/administration and the use of a skim
milk stabiliser.
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