Wednesday, September 23, 2015

Infectious bronchitis virus: Range of viral strains makes control complicated

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.


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.


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.


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 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.


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.


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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