Download L13 Classical and variant infectious bronchitis viruses: epidemiology

L13 Classical and variant infectious bronchitis viruses: epidemiology, diagnosis
and control strategies
K. Ganapathy
University of Liverpool, Institute of Infection and Global Health & School of Veterinary Science, Leahurst Campus, Neston, Cheshire, CH64 7TE, UK
E-mail：[email protected]
Keywords: infectious bronchitis virus, classical, variant, epidemiology, diagnosis and control strategies
Summary
Avian infectious bronchitis virus (IBV) causes respiratory, renal and reproductive diseases in chickens, leading to economic losses for producers and increased welfare concerns. With the use of traditional
and molecular techniques, numerous variant strains have been identified globally, in addition to classical
strains. In general, these strains can be divided into 3 main categories; i) classical strains, mainly the
Massachusetts (Mass) and related, ii) variant strains of global importance, iii) variant strains of regional
importance. Though the reason for the emergence of variant genotypes is unclear, it has been suggested
that the RNA virus undergoes point mutation or recombination events which may allow emergence of
new genotypes. Other than the Mass, currently 793B, QX and Q1 IBVs are considered to have significant global impact. Almost every country has their own population of IBVs, some examples being Arkansas, Delaware (GA 07, GA 08) and California in the USA. In addition, IS/885/00 and IS/1494/06
(variant 2) are commonly found in the Middle East, BR1 and BR2 in Brazil, It-02, D1466, B1648 in Europe, genotype I, II or III in Korea, and LDL, BJ, LHLJ and LDT3 in China. With regards to control of
production losses due to IBV, live and inactivated vaccines are available. Though developments of new
live vaccines are ideal for emerging variant IBVs, it is not possible to manufacture one for every variant
IBV. Live vaccines of Mass, 793B, D274, QX, few regional vaccines, and inactivated vaccines of M41,
D274, 793B and QX, are used worldwide. It has been reported that a combination of classical and variant live vaccines could increase and broaden the protection conferred against classical and variant IBVs.
Whilst waiting for an innovative biotechnology-based vaccine, at present, it appears that strategic vaccinations using heterologous live classical and variant vaccines, alongside appropriate inactivated vaccines, is the best option available for many chicken producers.
Introduction
After avian influenza and Newcastle disease viruses, infectious bronchitis virus appears to be the
most important cause of respiratory diseases in chickens. In addition, this virus also causes reproductive
and renal infections and pathology. Co-infection with other pathogens tend to cause more severe disease
outcomes. Damages to the respiratory, reproductive and renal systems lead to huge economic losses due
to poor health, production and welfare concerns (Jackwood and de Wit, 2013, Ganapathy, 2009). The
losses due to IBV are controlled with the use of live and inactivated vaccines. However, the virus continues to pose a great danger to the chicken industry worldwide, especially with the emergence of variant strains. This paper highlights some importance aspects of IBV epidemiology, variations in the disease caused by different IBVs, advances in the diagnosis, and current strategies in the control and prevention of IBV globally.
Global Epidemiology
In 1936, the causative agent of respiratory infections (Schalk and Hawn, 1931) affecting flocks of
chicks was named infectious bronchitis virus (IBV), belonging to the Massachusetts (Mass) serotype.
Thereafter a number of IBV strains divergent from the Mass were reported and classed as new serotypes
(eg. Connecticut, Arkansas, D388) through serum neutralisation. By the 1990’s, wider availability of
molecular techniques advanced strain typing onto genotyping. Ease of use, speed, and high sensitivity
and specificity resulted in IBV genotyping being widely used worldwide. IBV is a single stranded RNA
enveloped virus with four structural proteins: the spike (S), membrane glycoproteins (M), a small mem69
brane envelope protein (E) and an internal nucleocapsid protein (N) (Lai and Cavanagh, 1997). The S
protein consists of two subunits, S1 and S2. The S1 subunit plays an important role in inducing the release of neutralizing and haemagglutination inhibiting (HI) antibodies against IBV (Koch et al., 1990,
Cavanagh et al., 1988). To date, rather than full S1 or whole genome sequencing, the majority of research laboratories only undertake amplification and sequencing of part-S1 gene for genotyping.
Though epidemiology has a wide application, this write up concentrates on the distribution of IBV
strains globally. Based on serotyping and genotyping, the current population of IBVs can be grouped into three main segments; i) the classical strains, basically Massachusetts or related viruses that present
worldwide, ii) the variant IBVs that are of global importance (eg. 793B, QX, Q1), and iii) regional variant IBVs that are of importance in a specific region or country (eg. Arkansas, Delaware (GA 07, GA 08)
and California in the USA, IS/885/00 and IS/1494/06 (variant 2) in the Middle East, BR1 and BR2 in
Brazil, It-02, D1466, B1648 in Europe, genotype I, II or III in Korea, LDL, BJ, LHLJ and LDT3 in China) (Jackwood, 2012). The main reason for the appearance of variant strains seem to be point mutations
or recombination events when more than one genotype infects the same cell (Cavanagh et al., 1992, Lai
and Cavanagh, 1997, Wang et al., 1994).
Changing disease manifestation (or severity)
The first description of the disease caused by IBV was reported by Schalk and Hawn in 1913, where
primarily respiratory signs and pathology were described (Schalk and Hawn, 1931). In the 1960’s, evidence of IBV causing renal disease emerged (Cumming, 1963, Winterfield and Hitchner, 1962). In laying birds, certain IBV strains can cause a drop in egg production and quality (Muneer et al., 1986, Cook
and Huggins, 1986). Subsequently, a number of studies using different IBV isolates around the world
demonstrated very similar pathogenesis. The only differences highlighted were the tropism of the new
isolates, where some caused more severe respiratory, renal or reproductive diseases than others. There
were few exceptions to this observation, wherein certain isolates tended to cause signs and/or pathology
away from the traditionally affected tissues. For example, IBV 793B causes deep pectoral myopathy
(Gough et al., 1992, Raj and Jones, 1996), QX is associated with proventriculitis (Wang et al., 1998, Ganapathy et al., 2012), and other reports have associated IBV with swollen head syndrome (Awad et al.,
2016, Droual and Woolcock, 1994, Morley and Thomson, 1984) and enteritis (Villarreal et al., 2007). In
general, the disease severity varies depending on the virulence and dosage of the strain, secondary
agents, flock age, host immune status, management and environmental factors (Cavanagh and Naqi,
2003, Ganapathy, 2009).
Traditional to molecular diagnosis
Clinical diagnosis of IBV is difficult as the resulting signs and pathology are similar to those produced by many other diseases. History taking, clinical and pathological assessments must be followed
with appropriate sample collection for demonstration of the antigen or antibodies against it (Ganapathy,
2009).
For antigen detection, an attempt is made for the virus to be traditionally grown in the SPF embryonated eggs and/or in tracheal organ cultures (Cook et al., 1976). In recent decades, the most frequently
used tool for IBV detection is either the conventional or real-time reverse transcription polymerase chain
reaction (RT-PCR). Subsequently, the PCR product is sequenced and analyzed to determine the genotype (Adzhar et al., 1996, Worthington et al., 2008, Awad et al., 2014) In most instances, this would allow genotype identification and to some extent, differentiation of the vaccine against virulent strains. Evidence of immune responses are mostly confined to detection of humoral antibodies by the enzyme
linked immunosorbent assay (ELISA) and hemagglutination inhibition (HI) (Awad et al., 2014, Ganapathy, 2009, de Wit, 2000), and occasionally virus neutralization. In monitoring protection against virulent
IBVs, it appears that IgA in tear and CD8+ populations in the trachea could be an important immune indicator (Chhabra et al., 2015). For an efficient diagnosis and surveillance of IBV in endemic regions/
farms, it is best to use a combination of serology and virus detection by PCR, isolation and genotyping.
Evidence-based preventive measures
There are three main elements for control and prevention of losses caused by IBV. These are generally
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management, biosecurity and vaccination, the first two forming the foundations for an environment that
is minimal or free from virulent IBVs, and more importantly sustaining healthy and immunocompetent
flocks. With these strongly established, an‘immunological shield’is formed in the flock(s) through the
use of appropriate live and inactivated vaccines in the breeder, layer and broiler flocks. For a successful
and effective IBV vaccination program, it should link the immunological shield in the breeders to the
shield in the layer and broiler flocks. It is essential to remember that what provides the protection
against losses caused by IBV is the immunological package developed in the flock(s). In inducing such
immunological development, two important factors need to be considered, i) protection against which
strain of IBVs, ii) what sort of live and inactivated vaccines could possibly induce a protective immunological shield.
In regards to evaluating vaccination against IBV, following vaccination and challenge, most studies
concentrate on demonstrating freedom of disease (eg; clinical signs, macro and microscopic lesions),
production losses and reduction in antigen concentration (de Wit and Cook, 2014). Studies to date have
shown that strategic heterologous vaccination leads to higher and broader protection against classical
and variant viruses (Cook et al., 1999, Awad et al., 2015, Chhabra et al., 2015). Chhabra and others demonstrated that the increased protection provided was mainly associated with IgA in the tears and CD8+
cells in the tracheal sections (Chhabra et al., 2015).
Conclusions
Historically, the main body systems affected by classical and variant IBVs remain the same -respiratory, reproductive and urinary systems. However, the disease severity varies according to the genotype,
with some having a more severe impact on certain systems. It appears that the emergence of variant IBVs are unavoidable, as IBV is a RNA virus which tends to go through point mutations and possible recombination events. This is encouraged by complex chicken production systems and often inappropriate use of vaccines and vaccination programs that leads to partial flock immunization. Overall improvement in the chicken management and biosecurity is essential, and this needs to be supplemented with an
appropriate strategic vaccination. Inclusion of more than one genotype of live and/or inactivated antigens is often preferred. A vaccine strain(s) that is closely-related to the circulating IBV should be included in the vaccination program for optimal protection. Control of IBV by vaccination needs to be coordinated, as programs in the breeders will most likely have some influence on the choice of vaccine and
vaccination strategies in the layer and broiler flocks. To date, IBV vaccination is still relying on the use
of conventional live and inactivated vaccines, and this would continue until an innovative biotechnologically based vaccine is found.
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