Infectious Bronchitis in the USA

An update for 2009, provided by Dr. Mark Jackwood.

Avian infectious bronchitis costs the U.S. poultry industry millions of dollars annually and it remains one of the top research priorities for commercial poultry worldwide. Avian infectious bronchitis is a highly contagious upper‐respiratory disease in chickens that is extremely difficult to control because different types of the virus that cause the disease do not cross-protect. Different types of infectious bronchitis virus (IBV) include multiple serotypes and variants of the virus, which emerge due to selection pressure working on genetic mutations and recombination events between different strains of the virus during replication in the host.

The best strategy for control of this disease is the use of attenuated (non‐pathogenic) IB viruses. Typically attenuated viruses are developed by passage of the virus in embryonating eggs. As the virus adapts to grow in eggs, it looses its ability to cause disease in chickens and thus can be developed into safe and effective vaccines. But, because different types of the virus do not cross-protect vaccines must be produced to the many different types of the virus.

Picking the correct vaccine type is extremely important for sound protection against IBV. Vaccine type viruses commonly used in the United States are Ark‐DPI, Conn, DE072, GA98, and Mass41. Making informed decisions regarding vaccine type to be used in a particular flock of chickens depends on information obtained from constantly monitoring the different types of IBV circulating in the field. We previously published data from 11 years of IBV isolation and identification, collected in the USA from July 1994 to December 2004 (Avian Dis. 49: 614‐618, 2005). In that study, we examined a total of 1,511 IBV isolates and not surprisingly, we found that the virus continues to evolve and cause disease outbreaks.

Genetic diversity in Infectious Bronchitis Virus

Infectious bronchitis virus like most RNA viruses has an extremely high mutation rate because the RNA‐dependent RNA‐polymerase, the enzyme that copies the viral genome during replication, has limited or very little proofreading capability. Consequently, many of the mistakes made during replication of the genome go uncorrected. This high mutation rate creates a diverse population of virus particles that allows IBV to quickly adapt to selection pressures such as the innate immune response and the adaptive host immune responses (IBV specific antibodies and T‐cells). We observe this adaptation as the emergence of variant viruses or emerging new serotypes of the virus.

The most common serotypes of IBV in the USA are Arkansas, Connecticut, Delaware, GA98, and Massachusetts. However, when those IBV types undergo genetic changes or genetic drift, it can result in considerable variation away from the original serotype. The Arkansas type viruses appear to be quite prone to genetic drift resulting in viruses designated Arkansas‐like viruses. If the amount of genetic change, which can accumulate over time, reaches a critical point, the Arkansas vaccine strain (Ark‐DPI) may no longer provide sound protection against the Arkansas‐like viruses.

In addition to genetic drift, genetic shift can lead to a dramatic genetic change that results in a unique variant virus. These variant viruses are defined as previously unrecognized IBV types that are clearly different from the known IBV serotypes. Genetic shift usually results from recombination between two different parent viruses (that infected the same cell) to produce a distinct progeny virus. Recombination events occur by a template switching mechanism between two different viruses during replication of the viral genome. Recombination sites tend to favor conserved regions of the genome (called “hot‐spots”) but have been shown to occur across the entire viral genome. The resulting chimera is a hybrid of the two parent viruses that, under the right conditions, can break through immunity induced by the common vaccine types.

Making informed decisions regarding vaccine type depends on information obtained from constantly monitoring the different types of IBV circulating in the field.

Infectious bronchitis virus Arkansas variants

The most recent data in the USA, shows that Arkansas type viruses continue to evolve to produce Ark‐like variants, which are commonly isolated in both broilers and layer type birds. But, it appears that sound immunization with Arkansas type vaccines (See Mildvac Ark) continues to protect against them. We also found that the Ark‐DPI strain was and still is the most frequently identified type of IBV in the field. Studies on field isolates (Jackwood et al. Avian Dis. 53:175‐183, 2009) indicate that the Ark‐DPI isolates are indeed vaccine viruses persisting in the vaccinated flock. Whether the persisting vaccine is connected to the emergence of Ark‐like viruses remains to be determined, but persistence of Ark‐DPI in the flock obviously provides an opportunity for that virus to mutate and evolve. Following spray application of the Ark‐DPI vaccine in the field, the vaccine was found in a significant number of birds, which varied depending on the sampling time post‐vaccination but the virus continued to be found in the birds for the length of the grow out period.

It is not clear why only the Arkansas vaccine viruses are persisting in broiler flocks and other IBV vaccine types given to the birds at the same time do not. Studies examining reisolated IBV vaccine viruses showed that selection of vaccine subpopulations as well as mutations in the spike glycoprotein can be detected after only one infectious cycle (McKinley et al. Vaccine 26:1274‐1284, 2008). Additional studies specifically examining the Ark‐DPI vaccine identified 5 subpopulations positively selected for in the chicken whereas the predominant population in the vaccine was negatively selected (van Santen et al. Avian Pathol. 37:293‐306. 2008). Preliminary data indicates that spray vaccination of the Ark‐DPI vaccine in the hatchery may not be providing adequate priming of the immune response, which may play a role in persistance. Further research is being conducted to answer that question, and to provide a possible mechanism for the persistence of Ark‐DPI vaccines in broilers in the USA. This work is extremely important because the longer IBV persists in the field the more opportunity it has to undergo genetic drift and shift resulting in new variant viruses.

Infectious bronchitis virus variant GA98

In 1998, a variant of IBV was identified as the cause of a severe and widespread outbreak of the disease and was designated GA98. Molecular and serotypic characterization of the virus showed that it was related to the Delaware strain of IBV. However, currently available vaccines were not providing adequate protection against this new variant virus so a new vaccine, MILDVAC‐GA‐98 was developed. The new vaccine provided sound protection against the GA98 strain of IBV and as an added advantage, MILDVAC‐GA‐98 was also found to provide very good protection against Delaware type strains. Use of this vaccine has lead to the control of this damaging strain of IBV.

Infectious bronchitis virus California variants

Geographically restricted variant viruses have been reported in California since 1975. Studies examining the nature of these viruses (Jackwood et al. Avian Dis. 51:527‐533, 2007 and Francia et al. Avian Dis. 55:422‐428, 2011) found that unique variant strains continue to emerge and cause disease in California chickens. In the 1990’s the California variant (CAV) virus was isolated and identified. That virus was significantly different from the available vaccine strains and caused widespread disease in broilers and breeder type birds. The CAL99 variant viruses were isolated in 1999, and emerged as a distinct genetic and serotypic group from the CAV isolates. In addition, 3 new variant viruses (CA557/03, CA706/03, and CA1737/04) isolated in 2003 and 2004, appear to fall into different and unique molecular and serotypic groups. Unfortunately none of the currently available vaccines are effective against any of the California variant viruses. Until recently, the 2003‐2004 California variant viruses appeared to be geographically restricted like the other California variant viruses; however, a recently identified variant virus in Georgia and elsewhere has genetic ties to the California viruses.

Infectious bronchitis virus variant GA08

In 2007‐2008, an outbreak of bronchitis in North‐Georgia, USA broilers lead to the identification of two new IBV strains designated GA07 and GA08. The GA07 virus is genetically similar to the California variant virus CA/1737/04 whereas the GA08 virus is genetically similar to the California variant virus CA557/03 virus. These viruses quickly spread throughout Georgia and to surrounding states in the Southeast but the GA07 virus eventually disappeared and the GA08 persisted. None of the commercially available vaccines in the USA either alone or in combination were found to be effective against the GA08 virus. One commercial company produced an attenuated live autogenous vaccine and used it for a little over a year to control this new IBV type. The vaccine program was successful and the company ceased use of the vaccine. The most recent data (spring 2012) indicates that the GA07 virus is again causing disease in the Southeast. The significance of that virus re‐emerging remains to be determined and leads to important questions including; where was the virus sequestered prior to its re‐emergence, is there a reservoir for IBV in wild birds or small mammals commonly found around commercial poultry houses, and does a carrier state exist in chickens or other animals?


Variant IBV types are constantly emerging and circulating in the field, and disease outbreaks associated with variant types continue to occur. Constantly monitoring IBV types is extremely important because it allows us to follow changes in their incidence and distribution and to identify and control new problematic variant viruses as they arise.

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