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avian infectious bronchitis

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avian infectious bronchitis

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • avian infectious bronchitis
  • Overview
  • Avian infectious bronchitis (IB) is an acute, highly contagious respiratory disease of domestic fowl of all types and ages, caused by the coronavirus, infectious bronchitis virus (IBV) (Cavanagh and 

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Identity

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Preferred Scientific Name

  • avian infectious bronchitis

Other Scientific Names

  • infectious bronchitis

International Common Names

  • English: avian infectious bronchitis in chickens and pigeons; avian infectious nephrosis; avian infectious proventriculitis; IB infection; IBV infection; nephritis nephrosis disease

English acronym

  • IB

Overview

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Avian infectious bronchitis (IB) is an acute, highly contagious respiratory disease of domestic fowl of all types and ages, caused by the coronavirus, infectious bronchitis virus (IBV) (Cavanagh and Gelb, 2008). The virus, which can also cause damage to the kidneys and oviducts, is of significant economic importance. In broilers, infection results in reduced weight gain and mortality following secondary bacterial infection. Egg production is adversely affected in layers. Live and killed IB vaccines are widely used. However, a highly significant aspect of IBV is the existence of numerous serotypes; immune responses induced by one serotype often protect poorly against subsequent infection by other serotypes (de Wit et al., 2011a; Worthington et al., 2008; Cook et al., 2012).

The distribution section contains data from OIE's WAHID Interface database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.

Hosts/Species Affected

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The domestic fowl is considered to be the natural host for IBV. However, IBV-like viruses infect other avian species. Coronaviruses with and without serological identity to IBV have been isolated from pheasants, and are associated with respiratory disease and nephritis (Lister et al., 1985; Gough et al., 1996). The gene sequences of the pheasant viruses are distinct from but clearly related to those of IBV from chickens. A pheasant isolate has been propagated in the allantoic cavity of domestic fowl embryos but it did not cause clinical disease when inoculated intranasally into three-week-old chicks (Lister et al., 1985). Some isolates of turkey coronavirus (TCoV) are very closely related to IBV (Guy, 2000) but have an enteric tropism. Therefore, TCoV is considered to be a species distinct from IBV. However, domestic fowl chicks have been experimentally infected with TCoV, the virus growing in the same tissues as in turkey. It is highly likely that other avian species have coronaviral infections.

Probably all breeds of domestic fowl are susceptible to IBV although the severity of the disease may vary. The disease is most severe in chicks, not only in terms of respiratory disease but also with respect to damage of kidneys and oviducts. In intensively reared birds, mortality is highest in broilers, secondary bacterial infection with Escherichia coli, other bacteria and mycoplasmas being the primary cause of mortality. The extent of losses is made worse by poor litter quality and poor ventilation, and nephritis may be exacerbated by food composition and temperature changes (Cumming, 1969; Meulemans and Berg, 1998).

Distribution

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IBV is distributed worldwide (de Wit et al., 2011a).

For current information on disease incidence, see OIE's WAHID Interface.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AfghanistanNo information availableOIE, 2009
ArmeniaDisease not reportedOIE, 2009
AzerbaijanDisease not reportedOIE, 2009
BahrainDisease not reportedOIE, 2009
BangladeshPresentOIE, 2009
BhutanNo information availableOIE, 2009
Brunei DarussalamNo information availableOIE Handistatus, 2005
CambodiaNo information availableOIE, 2009
ChinaRestricted distributionOIE, 2009
-GuangdongPresentWang and Liu, 1998
-HebeiPresentYang and Gan, 1995; Yang et al., 1996; Pan et al., 1998; Zhou et al., 1998; Wang et al., 1999
-HenanPresentXu LanJu, 1995; Cui et al., 1996; Chen et al., 1998
-Hong KongDisease not reportedOIE, 2009
-HunanPresentLiu et al., 1999
-JiangsuPresentChen et al., 1997; Xu et al., 1997
-JilinPresentLiu QingHe et al, 1998
-LiaoningPresentLu et al., 1997
-Nei MengguPresentZhang et al., 1997
-ShaanxiPresentYang et al., 1996
-ShandongPresentQin et al., 1996; Zhang et al., 1997; Wang et al., 1998
-ShanxiPresentNing et al., 1997
-SichuanPresentWu et al., 1996; Zhong et al., 1996; Wang et al., 1997
-ZhejiangPresentZhou et al., 1998
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndiaDisease not reportedOIE, 2009
-Andhra PradeshPresentReddy and Murthy, 1980
-Arunachal PradeshPresentVerma et al., 1987
-Indian PunjabPresentMaiti et al., 1985; Maiti et al., 1985
-Madhya PradeshPresentSingh et al., 1979
-ManipurPresentVerma and Verma, 1983
-Tamil NaduPresentSukumar and Prabhakar, 1993; Rajeswar et al., 1998; Elankumaran et al., 1999
-TripuraPresentVerma et al., 1989
-West BengalPresentMalay et al., 1998
IndonesiaDisease not reportedOIE, 2009
-JavaPresentDarminto, 1988; Darminto, 1992
IranPresentOIE, 2009
IraqDisease never reportedNULLAzab et al., 1989; OIE, 2009
IsraelPresentNULLWeisman et al., 1987; Meir et al., 1997; OIE, 2009
JapanPresentOIE, 2009
-HokkaidoPresentChen et al., 1996
-KyushuPresentYagyu et al., 1985
-ShikokuPresentYagyu et al., 1985
JordanPresentOIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, DPROIE Handistatus, 2005
Korea, Republic ofPresentNULLKim et al., 1987; Kim et al., 1997; Rhee et al., 1998; Song et al., 1998; OIE, 2009
KuwaitDisease not reportedOIE, 2009
KyrgyzstanDisease not reportedOIE, 2009
LaosNo information availableOIE, 2009
LebanonPresentOIE, 2009
MalaysiaPresentNULLOpitz et al., 1979; Anon., 1985; Babjee, 1985; OIE, 2009
-Peninsular MalaysiaDisease not reportedOIE Handistatus, 2005
-SabahLast reported2003OIE Handistatus, 2005
-SarawakReported present or known to be presentOIE Handistatus, 2005
MongoliaNo information availableOIE, 2009
MyanmarPresentOIE, 2009
NepalPresentOIE, 2009
OmanDisease not reportedOIE, 2009
PakistanPresentNULLMuneer et al., 1987a; OIE, 2009
PhilippinesNo information availableOIE, 2009
QatarNo information availableOIE, 2009
Russian Federation
-Russia (Asia)PresentTeryukhanov, 1986; Nonnevitz and Voss, 1993; Teryuhanov et al., 1995
Saudi ArabiaNo information availableOIE, 2009
SingaporeDisease not reported1991Lim, 1977; Chew, 1985; OIE, 2009
Sri LankaDisease not reportedOIE, 2009
SyriaNo information availableOIE, 2009
TaiwanReported present or known to be presentOIE Handistatus, 2005
TajikistanDisease not reportedOIE, 2009
ThailandPresentOIE, 2009
TurkeyNo information availableOIE, 2009
TurkmenistanNo information availableOIE Handistatus, 2005
United Arab EmiratesDisease not reportedOIE, 2009
UzbekistanDisease not reportedOIE Handistatus, 2005
VietnamPresentOIE, 2009
YemenNo information availableOIE, 2009

Africa

AlgeriaDisease not reportedOIE, 2009
AngolaNo information availableOIE, 2009
BeninNo information availableOIE, 2009
BotswanaDisease not reportedOIE, 2009
Burkina FasoPresentOIE, 2009
BurundiNo information availableOIE Handistatus, 2005
CameroonReported present or known to be presentOIE Handistatus, 2005
Cape VerdeNo information availableOIE Handistatus, 2005
Central African RepublicReported present or known to be presentOIE Handistatus, 2005
ChadNo information availableOIE, 2009
CongoAbsent, reported but not confirmedOIE, 2009
Congo Democratic RepublicNo information availableOIE Handistatus, 2005
Côte d'IvoireReported present or known to be presentOIE Handistatus, 2005
DjiboutiDisease not reportedOIE, 2009
EgyptDisease not reported1994Amin and Mostageer, 1977; Amal, 1998; OIE, 2009
EritreaAbsent, reported but not confirmedOIE, 2009
EthiopiaDisease not reportedOIE, 2009
GabonDisease not reportedOIE, 2009
GambiaNo information availableOIE, 2009
GhanaNo information availableOIE, 2009
GuineaNo information availableOIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaNo information availableOIE, 2009
LesothoDisease not reportedOIE, 2009
LibyaDisease not reportedOIE Handistatus, 2005
MadagascarDisease not reportedOIE, 2009
MalawiNo information availableOIE, 2009
MaliNo information availableOIE, 2009
MauritiusPresentOIE, 2009
MoroccoNo information availableNULLEl and Jones, 1985; El et al., 1986; OIE, 2009
MozambiqueDisease not reportedOIE, 2009
NamibiaDisease not reportedOIE, 2009
NigeriaNo information availableNULLKomolafe et al., 1990; OIE, 2009
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE, 2009
Sao Tome and PrincipeSerological evidence and/or isolation of the agentOIE Handistatus, 2005
SenegalNo information availableOIE, 2009
SeychellesDisease not reportedOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaDisease not reportedOIE, 2009
SudanDisease not reportedOIE, 2009
SwazilandDisease not reportedOIE, 2009
TanzaniaNo information availableOIE, 2009
TogoNo information availableOIE, 2009
TunisiaDisease not reportedOIE, 2009
UgandaAbsent, reported but not confirmedNULLMukiibi-Muka and Olaho-Mukani, 1998; OIE, 2009
ZambiaDisease not reportedOIE, 2009
ZimbabwePresentOIE, 2009

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaPresentOIE, 2009
-QuebecPresentMarsolais and Marois, 1982
GreenlandDisease never reportedOIE, 2009
MexicoPresentOIE, 2009
USAPresentOIE, 2009
-ArkansasPresentMuneer et al., 1987a; Gelb and Cloud, 1983; Gelb et al., 1983; King, 1986; Jia et al., 1995
-CaliforniaPresentMoore et al., 1998
-ConnecticutPresentCrinion and Hofstad, 1972; Johnson and Marquardt, 1975; Coria, 1976; King and Hopkins, 1983; Moore et al., 1998
-DelawarePresentKeller and Hoop, 1993
-FloridaPresentJohnson and Marquardt, 1975; King and Hopkins, 1983; Moore et al., 1998
-GeorgiaPresentKing and Hopkins, 1983; Moore et al., 1998
-MainePresentKing, 1988
-MassachusettsPresentKing, 1986; Jia et al., 1995
-New YorkPresentMohammed and Naqi, 1990
-North DakotaPresentSchalk and Hawn, 1931; Beach and Schalm, 1936
-OhioPresentKing, 1988
-PennsylvaniaPresentKing, 1988

Central America and Caribbean

BarbadosOIE Handistatus, 2005
BelizeDisease not reportedOIE, 2009
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease not reportedOIE Handistatus, 2005
Costa RicaPresentOIE, 2009
CubaDisease not reported1990Guilarte et al., 1989; OIE, 2009
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicRestricted distributionOIE, 2009
El SalvadorDisease not reportedOIE, 2009
GuadeloupeNo information availableOIE, 2009
GuatemalaPresentOIE, 2009
HaitiNo information availableOIE, 2009
HondurasDisease not reportedOIE, 2009
JamaicaDisease not reportedOIE, 2009
MartiniqueAbsent, reported but not confirmedOIE, 2009
NicaraguaNo information availableOIE, 2009
PanamaNo information availableOIE, 2009
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease never reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaPresentNULLDelamer, 1974; OIE, 2009
BoliviaRestricted distributionOIE, 2009
BrazilPresentOIE, 2009
-Minas GeraisPresentJorge et al., 1992
-Rio Grande do SulPresentSalle et al., 1988
ChilePresentNULLCeledon and Gomez, 1976; Toro et al., 1989; OIE, 2009
ColombiaDisease not reportedOIE, 2009
EcuadorDisease not reportedOIE, 2009
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease not reportedOIE, 2009
GuyanaDisease not reportedOIE Handistatus, 2005
ParaguayReported present or known to be presentOIE Handistatus, 2005
PeruAbsent, reported but not confirmedOIE, 2009
UruguayPresentNULLCapano et al., 1976; OIE, 2009
VenezuelaDisease not reportedOIE, 2009

Europe

AlbaniaDisease never reportedOIE, 2009
AndorraNo information availableOIE Handistatus, 2005
AustriaNo information availableOIE, 2009
BelarusDisease not reported1996Golod et al., 1990; OIE, 2009
BelgiumDisease not reported2004Meulemans et al., 1976; Meulemans et al., 1981; Meulemans et al., 1987; Meulemans and Berg, 1998; OIE, 2009
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaNo information availableNULLCholakova, 1985; OIE, 2009
CroatiaDisease not reportedOIE, 2009
CyprusDisease not reportedOIE, 2009
Czech RepublicDisease not reported2004Zajac et al., 1992; Snízek, 1993; Krajca and Jiran, 1998; OIE, 2009
Czechoslovakia (former)PresentGdovinova, 1975; Salaj and Cernik, 1979
DenmarkPresentNULLBisgaard et al., 1977; OIE, 2009
EstoniaDisease not reportedOIE, 2009
FinlandDisease not reportedOIE, 2009
FranceNo information availableNULLPicault et al., 1986; Picault et al., 1987; OIE, 2009
GermanyPresentNULLEmele et al., 1985; Philipp et al., 1998; OIE, 2009
GreeceDisease not reported2002Papanikolaou et al., 1985; OIE, 2009
HungaryRestricted distributionNULLNagy and Bozzay, 1991; Pénzes and Mészáros, 1992; OIE, 2009
IcelandDisease not reportedOIE, 2009
IrelandDisease not reportedOIE, 2009
Isle of Man (UK)Disease not reportedOIE Handistatus, 2005
ItalyNo information availableNULLCapua et al., 1994; Capua et al., 1999; OIE, 2009
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE, 2009
LiechtensteinDisease not reportedOIE, 2009
LithuaniaDisease not reportedOIE, 2009
LuxembourgDisease not reportedOIE, 2009
MacedoniaAbsent, reported but not confirmedOIE, 2009
MaltaDisease not reportedOIE, 2009
MoldovaDisease not reportedOIE Handistatus, 2005
MontenegroDisease not reportedOIE, 2009
NetherlandsPresentNULLDavelaar et al., 1983; Wit et al., 1992; Wit et al., 1998; OIE, 2009
NorwayPresentOIE, 2009
PolandNo information availableNULLCapua et al., 1999; Wieliczko et al., 1999; OIE, 2009
PortugalDisease not reported200801Cavanagh et al., 1992a; Cavanagh et al., 1992b; OIE, 2009
RomaniaDisease not reportedNULLBunaciu et al., 1986; OIE, 2009
Russian FederationDisease not reportedOIE, 2009
-Russia (Europe)PresentTeryukhanov, 1986; Nonnevitz and Voss, 1993; Teryuhanov et al., 1995
SerbiaDisease not reportedOIE, 2009
SlovakiaDisease not reported2000Gdovinova, 1975; Salaj and Cernik, 1979; OIE, 2009
SloveniaDisease not reportedNULLMrzel, 1976; Mrzel et al., 1980; OIE, 2009
SpainNo information availableNULLTorrubia and González, 1985; Pagès Manté, 1988; OIE, 2009
SwedenPresentOIE, 2009
SwitzerlandDisease not reportedNULLKeller and Hoop, 1993; Komàromy et al., 1995; OIE, 2009
UKPresentNULLCook, 1983; Cook and Huggins, 1986; Parsons et al., 1992; Adzhar et al., 1997; OIE, 2009
-Northern IrelandReported present or known to be presentOIE Handistatus, 2005
UkraineDisease not reported200303Mamchur and German, 1975; Atamasya, 1986; OIE, 2009
Yugoslavia (former)No information availableGagic et al., 1994; OIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Disease not reportedOIE Handistatus, 2005

Oceania

AustraliaPresentNULLLohr, 1976; Ignjatovic and Ashton, 1996; Sapats et al., 1996; Ignjatovic et al., 1997; OIE, 2009
-Australian Northern TerritoryPresentIgnjatovic et al., 1997
-QueenslandPresentIgnjatovic et al., 1997
-VictoriaPresentIgnjatovic et al., 1997
French PolynesiaPresentOIE, 2009
New CaledoniaPresentOIE, 2009
New ZealandPresentNULLLohr, 1976; Lohr et al., 1991; OIE, 2009
Papua New GuineaPresentKammen A van, 1982; Nunn, 1985
SamoaDisease not reportedOIE Handistatus, 2005
VanuatuDisease not reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathology

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Chickens infected with IBV have serous, catarrhal or caseous exudates in the trachea, nasal passages and sinuses. Air sacs may appear cloudy or contain a yellow caseous exudate. The lower trachea or bronchi of chicks that die may contain a caseous plug and there may be small areas of pneumonia around the large bronchi. Histopathological analysis of the trachea reveals loss of cilia, sloughing off of the epithelial cells and minor infiltration by heterophils and lymphocytes within 18 hours of infection. Regeneration of the epithelium commences within 2 days. There is marked lymphoid infiltration of the lamina propria and a large number of germinal centres (Randall, 1991). Air sacs may exhibit oedema, epithelial cell desqamation and fibrinous exudates within 24 hours.

In those birds with nephritis, kidneys are pale and swollen, the tubules and ureters being clearly visible, distended with urates (Randall, 1991; Cavanagh and Naqi, 1997). Histopathological analysis reveals interstitial nephritis. There is granular degeneration, vacuolation and desqammation of the tubular epithelium and massive infiltration of heterophils in the interstitium in acute stages of the disease. Degenerative changes may persist, resulting in severe atrophy of parts of the kidney. In urolithiasis the ureters associated with atrophied kidneys are distended with urates.

Laying birds may have fluid yolk material in the abdominal cavity.

Diagnosis

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Clinical Diagnosis



The observations described in 'Disease Course' and 'Pathology' are suggestive of IB but are not diagnostic. Laboratory tests are required for definative diagnosis.


Differential Diagnosis



Several respiratory pathogens, including combinations thereof, may produce clinical signs similar to those described for IB. These include mild strains of Newcastle disease virus (Alexander, 1997), infectious laryngotracheitis virus (Bagust and Guy, 1997) and Haemophilus paragallinarum, causing infectious coryza (Blackall et al., 1997). The latter produces facial swelling that is rare in IB, although it is does occur as a consequence of secondary infection with coliform bacteria. Mycoplasma infections can also cause facial swelling. Egg drop syndrome (EDS) adenovirus (McFerran, 1997) produces a drop in egg production and quality similar to that caused by IB, but EDS virus does not affect internal egg quality and does not produce misshapen or ridged eggs. Kidney changes following infection by nephropathogenic strains of IBV may also resemble those caused by infectious bursal disease, mycotoxicosis and drug toxicities (Gelb, 1989).


Laboratory Diagnosis



Laboratory diagnosis is essential for confirmation of IBV infections. Ideally virus isolation (VI) should be performed, followed by tests, firstly to confirm that IBV is present, and secondly to identify the type of IBV. There are numerous ways of achieving all of these stages, each with their own advantages and disadvantages, and it is important to understand the strengths and weaknesses of the various techniques. De Wit (2000) has written a detailed, thoughtful and fully referenced review of all the procedures that have been tried, which have also been reviewed by Cavanagh and Gelb (2008). A brief discussion of the tests, supplemented with recommended protocols (the haemagglutination (HA) and HA inhibition (HI) test) has been produced by the Office Internationale Epizooties; this can also be accessed through the Internet (OIE, 1996).

Fowl can become persistently infected with IBV, which may be detected weeks or months later by virus isolation (Jones and Ambali, 1987). Isolation of IBV from older birds is not in itself, therefore, necessarily proof of the virus being responsible for any clinical disease or production losses that may be occurring at the time of detection. It is necessary to exclude other infections or non-infectious causes (De Wit, 2000).


Detection of IB virus/antigen/RNA


Collection of samples


At the acute stage of the infection (up to 5 days post-infection) live virus isolation is conventionally attempted by swabbing of the trachea or from trachea and lung tissue. Material should be conveyed to a laboratory on ice in transport medium containing penicillin (10,000 IU/ml) and streptomycin (10 mg/ml). Beyond one week after infection IBV is best sought from caecal tonsils or by cloacal swabs (Jones and Ambali, 1987). Kidney or oviduct material might be sampled in cases of nephritis and decreases in egg production, respectively.

If a live IBV isolate is not required and direct detection by reverse transcriptase polymerase chain reaction (RT-PCR) is to be attempted then swabs of the buccal cavity or oropharyngeal region may be made, allowed to dry, and then sent to the laboratory by mail at ambient temperature (Cavanagh et al., 1999). When broiler flocks are naturally infected with IBV in the field, the virus may be detectable in mouth swabs for several weeks by RT-PCR, the infection gradually working through the flock (Cavanagh et al., 1999).


Virus isolation/propagation


Virus isolation (VI) can be performed in embryonating eggs, tracheal organ cultures (TOCs, from 19-day-old embryos; Cook et al., 1976) or cell cultures (chick kidney or chick embryo kidney; Gillette, 1973). Cell cultures are not frequently used because field isolates would have to be adapted to grow successfully in them. Field strains will grow readily in eggs (9 to 11-day-old embryos, inoculation into the allantoic cavity; OIE, 1996) although several passages might be required to observe malformation of the embryo. TOCs have the advantage that field strains produce ciliostasis, easily seen by low power microscope, without adaptation.

Conventional isolation using embryos involves incubation with field material for 5-7 days, followed by several further passages with observation for malformation of the embryo (Cavanagh and Naqi, 1997). On initial infection a field strain would be expected to produce dwarfing of a few embryos, the percentage increasing with passage number, possibly with increasing mortality. Dwarfed embryos have deformed feet over the head with the thickened amnion adhered to it. Allantoic fluid is collected for further analysis. A shorter procedure involves the incubation of inoculated embryos for about 2 days (possibly repeating this once or twice), followed by testing for the presence of IBV by immunofluorescent antibody staining of cells sedimented from the allantoic fluid (Clarke et al., 1972), antigen capture ELISA (Naqi et al., 1993; Ignjatovic and Ashton, 1996) or RT-PCR (Andreasen et al., 1991; Adzhar et al., 1997).


Detection methods


Agar-gel precipitation test (AGPT)


This is simple, quick, inexpensive and more sensitive than is sometimes supposed. Lohr (1981) used the AGPT to detect IBV in tracheal exudates of birds from the field, sensitivity being half that of VI. AGPT is also used to detect IBV after growth in embryos, using allantoic fluid or the chorioallantoic membrane as the source of antigen (Alexander and Gough, 1977; Gelb et al., 1981; MAFF, 1984).


Immunofluorescent antibody (IFA)


This can be used to demonstrate the presence of IBV in whatever medium the virus has been grown. Direct detection by IFA of IBV in tissues from chickens can be complicated by non-specific reactions (De Wit, 2000). Bhattecharjee et al. (1994) used IFA in a very simple way to demonstrate the presence of IBV within 24 hours of inoculation of TOCs; the IF procedure was performed without fixation of the TOCs.

Immunoperoxidase antibody (IPA) staining can also be performed, with sensitivity similar to IFA.


Antigen capture ELISAs


These have not been very successful with tissue from infected birds but have been used successfully following propagation of virus in embryonated eggs (Ignjatovic and Ashton, 1996). These procedures generally require a non-type specific monoclonal antibody.


Haemagglutination (HA)


Treatment of IBV with neuraminidase to produce HA activity is normally done after concentration of the virus from allantoic fluid by ultracentrifugation. Ruano et al. (2000) have recently reported that treatment of unconcentrated infectious allantoic fluid with neuraminidase type V (from Clostridium perfringens, Sigma Chemical Company, Cat. No. N-2876) to produce IBV HA antigen. They mixed allantoic fluid with an equal volume of neuraminidase (at 1 unit/ml) for 30 min at 37°C. The HA test was performed on a ceramic plate by mixing 50 µl of neuraminidase-treated allantoic fluid with 50 µl of a 5% suspension of chicken red blood cells. HA occurred within a minute.


RT-PCR


This has been used either directly on RNA extracted from tracheal/mouth/oropharyngeal swabs (Li et al., 1993; Jackwood et al., 1997; Cavanagh et al., 1999; Worthington et al., 2008) or extracted from infectious allantoic fluid after propagation in the laboratory (Lin et al., 1991; Andreasen et al., 1991; Kwon et al., 1993; Adzhar et al., 1996, 1997). Flinders Technology Associates (FTA) cards have been used successfully for the collection, inactivation and transport of IBV samples (Moscoso et al., 2005).

As there are many types of IBV it is advisable, especially in the early stages of an investigation of infection in a region, to use RT-PCRs designed to detect many types of IBV, using so-called 'universal' oligonucleotides i.e. those corresponding to highly conserved sequences in the IBV genome (Lin et al., 1991; Kwon et al., 1993; Adzhar et al., 1996; Keeler et al., 1998; Handberg et al., 1999; Cavanagh et al., 1999). It is advisable to have more than one set of 'universal' oligonucleotides, corresponding to different genes, in case one set is not appropriate for a given type of virus (Adzhar et al., 1996).

The DNA product of the RT-PCR can be studied further to type an isolate (described below 'Typing IBV isolates').


Detection of antibodies to IBV


Detection of antibodies to IBV is frequently used as part of disease surveillance and for monitoring vaccination. Ideally one should have paired sera, collected before and after a suspected IB infection, especially as birds will probably carry IB antibodies following vaccination.


Agar-gel immunodiffusion test


Several dilutions of antibody may be required to prevent false positives caused by imbalance of the antigen-antiserum ratio (Lohr, 1981). The test is also liable to yield inconsistent results, as the presence and duration of precipitating antibodies may vary with individual birds (Gough and Alexander, 1977; OIE, 1996). This test is perhaps best used for detecting the presence of virus after laboratory propagation, rather than antibody.


ELISA


ELISA is much more sensitive than AGPT and does not suffer from the problems mentioned above. ELISAs can be purchased commercially or prepared (Garcia and Bankowski, 1981; Mockett and Darbyshire, 1981; Snyder and Marquardt, 1989), provided there is access to high-speed centrifugation to concentrate the virus. IB antibody can be detected within one week of infection, so the first set of paired sera must be taken immediately after infection is suspected. As with AGPT, ELISA is a group-specific test, i.e. it may be used for many types of IBV, as different types of IBV will have epitopes in common. Chen et al. (2011) have described a type-specific blocking ELISA for the detection of IBV antibodies.


Virus neutralisation (VN) and haemagglutination-inhibition (HI) tests


VN and HI tests are less suitable than ELISA for the detection of infection by IBV, because both tests are susceptible to serotype differences; antibodies from a fowl may not give VN or HI with a standard reference strain of IBV if they are of different serotypes. These tests are best used when IB has been confirmed or strongly suspected and the typing of the causative strain is required (see 'Typing of IBV isolates'). Notwithstanding, HI antibodies are usually more cross-reactive than VN antibodies, so the HI test, using a standard antigen preparation against one type of IBV, has a reasonable chance of detecting antibodies following a field infection. As most fowl are vaccinated against IB on one or more occasions, cross-reactive antibodies are likely to be encountered following an anamnestic response induced by a field infection.

The HI test with field sera is best used in conjunction with a panel of laboratory strains representing the IBV types most likely to be present in a region.

The procedures for performing the IBV HI test are described in detail by Alexander et al. (1983), King and Hopkins (1984) and OIE (1996). A complicating factor is that IBV does not haemagglutinate spontaneously; pre-treatment with an enzyme preparation is necessary. This can be done with a commercially available phosholipase C type 1 enzyme, from Clostridium welchii. However, results can be erratic, because the active agent for producing HA activity is a contaminant (probably a neuraminidase), whose presence is variable, rather than phosholipase (Schultze et al., 1992). It has been found to be efficient to use crude filtrate from a Clostridium welchii culture as a source of the active enzyme (OIE, 1996).


Typing IBV isolates

There are many types of IBV; dozens have been described and there are probably a greater number still to be discovered (de Wit et al., 2011a; Worthington et al., 2008). New genotypes have been reported in China (Liu and Kong, 2004; Liu et al., 2009; Ma et al., 2012) and in countries where previously data was lacking e.g. Egypt (Abdel-Moneim et al., 2012), and Iraq (Mahmood et al., 2011). The QX serotype, first described in China (Wang et al., 1998), spread to many countries, where it became economically important (Worthington et al., 2008; de Wit et al., 2011a, b; Abro et al., 2012).

Typing can be performed with antibodies (antisera or monoclonal antibodies) in VN or HI tests or, more commonly, by using nucleic acid technology.


Typing with antibodies


Virus neutralization tests


The VN test is expensive and impractical for routine use, as the tester needs to have access to a panel of many IBV types, given the considerable antigenic diversity exhibited by the virus. Furthermore, IBVs that are extremely similar at the sequence level may behave as different serotypes if the changes affect key VN epitopes (Cavanagh et al., 1992a; Cavanagh et al., 1992b). VN tests can be performed on embryonating eggs, tracheal organ cultures (TOCs) or cell cultures. The constant virus (for example, 100 infectious units)-varying serum method is most commonly used (OIE, 1996).


Haemagglutination-inhibition test


The HI test is widely used to type field isolates, and is a valuable tool. However, it is somewhat subject to interpretation by the diagnostician, because of cross-reactions. Conversely, serum raised against a single inoculation of IBV may be strain rather than type-specific (King and Hopkins, 1983; Brown and Bracewell, 1985, 1988). An isolate may be tested against a panel of antisera raised against types of IBV known or suspected to be in an area.

A serum might show HI activity with more than one virus of the panel but show a higher titre with one, tentatively indicating the identity of the field virus. However, it is possible to wrongly assign an isolate to a particular serotype in this way, the serum simply cross-reacting more strongly with one virus type in the panel than the others. If a new type of IBV is suspected, then the virus should be isolated and a type-specific antiserum raised in specific-pathogen free (SPF) birds using a single infection (Gelb, 1989); this should then be used in HI tests with future isolates.


Monoclonal antibodies (Mabs)


Panels of monoclonal antibodies have been used successfully to identify types of IBV but only on a limited scale (Koch et al., 1986; Karaca et al., 1992; Karaca and Naqi, 1993). This is because of the very large number of IBV types and the time and cost of making monoclonal antibodies to new types.


Typing with nucleic acid technology


One approach to the use of RT-PCR is to use universal oligonucleotides designed to bind to the RNA of many, if not all, types of IBV (Lin et al., 1991; Kwon et al., 1993; Adzhar et al., 1996; Keeler et al., 1998; Handberg et al., 1999; Cavanagh et al., 1999; Jones et al., 2005; Worthington et al., 2008). DNA products can be analyzed by nucleic acid sequencing to characterize isolates. Alternatively, when the presence of a particular type of IBV in a region has been established then type-specific RT-PCRs might be used. Sequencing can then be used to put IBVs into epidemiological and phylogenetic contexts.


Nucleic acid sequencing


This is the 'gold standard' amongst nucleic acid approaches to IBV characterization. The S1 gene is generally chosen for typing IBV as it is the S1 protein that is the inducer of protective immunity, and is the major protein in which mutations occur that in turn helps a variant to avoid immunity induced by other types.

 

Type-specific RT-PCRs


When the existence of one or more types of IBV (including vaccinal strains) in a region has been established and they have been characterized by sequencing it should be possible to design oligonucleotide primers specific for each type. The oligonucleotides should be chosen such that the different types of IBV produce DNA products of different sizes, which can be easily differentiated by agarose gel electrophoresis. Subsequently field isolates (or simply RNA isolated from swabs) can be identified by RT-PCR without further routine analysis (Cavanagh et al., 1999). However, occasionally DNA should be analyzed by sequencing. The presence of two or more types of IBV in the same sample can be easily distinguished (Cavanagh et al., 1999).

Any RT-PCR strategy for detecting and differentiating IBV must be flexible. One cannot rely solely on type-specific RT-PCRs. By definition, if a type of IBV new to a region were to be present, it would not be detected. Other approaches should also be used, for example, RT-PCR with universal oligonucleotides followed by sequencing (Capua et al., 1999; Cavanagh et al., 1999; Worthington et al., 2008; de Wit et al., 2011a).

A type-specific RT-PCR might not be sufficiently specific; the oligonucleotides may 'cross-react' with other types of IBV (Capua et al., 1999).


Immunology of the disease


Dhinakar Raj and Jones (1997) have reviewed the immunology of IB. Infection with IB results in the production of antibodies in serum which are detected much earlier by ELISA than by a VN test (Mockett and Darbyshire, 1981). Immunoglobulin IgM reaches a peak concentration about 8 days post-infection and then declines (Mockett and Cook, 1986). IgG can be detected within 4 days of infection, peaks at three weeks and gradually declines. Inactivated vaccines are given to laying birds to induce and maintain a high level of serum antibody which is transmitted to progeny (maternally-derived antibody). Serum antibodies do not correlate with protection, i.e. after vaccination some chicks may have low IBV serum antibody but still be protected against homologous challenge. Local immunity is important (Hawkes et al., 1983) including at the oviduct mucosa (Dhinakar Raj and Jones, 1996). The Harderian gland is the source of antibodies in lachrymal fluid and is believed to play an important role in the development of immunity following vaccination by spray (Davelaar and Kouwenhoven, 1981). Different breeds of chicken may differ in the amounts of serum IgG and lachrymal IgA that they produce (Toro et al., 1996).

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Diarrhoea Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
General Signs / Dehydration Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sign
General Signs / Increased mortality in flocks of birds Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
General Signs / Lack of growth or weight gain, retarded, stunted growth Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
General Signs / Polydipsia, excessive fluid consumption, excessive thirst Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
General Signs / Reluctant to move, refusal to move Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Ophthalmology Signs / Conjunctival, scleral, redness Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Reproductive Signs / Decreased, dropping, egg production Poultry:Mature female Sign
Reproductive Signs / Defective, misshapen, soft, rough, absent egg shell Poultry:Embryo Sign
Reproductive Signs / Flabby egg yolk, thin albumin Poultry:Embryo Sign
Reproductive Signs / Soft, thin egg shell Poultry:Embryo Sign
Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Coughing, coughs Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Ingesta in nasal passage Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Purulent nasal discharge Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Respiratory Signs / Sneezing, sneeze Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male Sign
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel Sign
Urinary Signs / Increased frequency of urination, pollakiuria Sign
Urinary Signs / Polyuria, increased urine output Sign

Disease Course

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Useful reviews are those by Raj and Jones (1997), Jordan (1996) and Cavanagh and Naqi (1997). Morbidity is 100%. Infected birds exhibit a range of respiratory clinical signs, including nasal discharge, tracheal rales, gasping, sneezing and coughing. The infraorbital sinuses may be swollen in some chicks and eyes may be wet. Feed consumption drops, weight gain is slowed and the birds are inactive, tending to huddle together near a heat source in cool environments. In birds over the age of 6 weeks, the spectrum of clinical signs is similar but less marked and may go unnoticed without close inspection. In many parts of the world, intensively raised fowl are vaccinated against IB and, in addition, are often subject to a field infection whilst young, both inducing immune responses which help ameliorate subsequent infections when the birds are mature.

Laying flocks infected by IBV commonly show a drop in egg production and an increase in poor egg quality, even if respiratory signs are not present. Egg production recovers within 8 weeks though usually not to pre-infection levels. Poor egg quality includes eggs that are thin or rough-shelled, misshapen, paler than normal, and possibly with poor internal quality; thin and watery albumen. IBV replicates in the mucosa of the oviduct. In chicks this may result in damage leading to permanently low egg production in the mature bird.

Respiratory infection with IBV per se does not usually result in mortality, although small chicks may die from caseous plugs in the trachea or bronchi, but viral infection predisposes the birds, especially chicks, to secondary bacterial infection that can result in mortality of at least double that of background levels.

IBV may also replicate in the epithelial cells of the kidney, leading to kidney malfunction that may not be manifest until the bird is much older. Some IBV strains are strongly nephropathogenic, resulting in depression, ruffled feathers, wet droppings and increased water uptake. Mortality can be high, especially amongst broilers. Nephritis/nephrosis may also be frequently observed in chicks after infection with IBV strains that are not intrinsically strongly nephrotrophic. Consequences of infection with such strains, and indeed with the nephropathogenic strains, depend on environmental factors e.g. feed containing high levels of animal protein and sharp changes in temperature e.g. between day and night (Cumming, 1969; Meulemans and Berg, 1998).

Epidemiology

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IBV replicates rapidly, new virus being produced within 3-4 hours of infection, and peak titres within a cell are reached by 12 hours. In chickens the incubation period is 18-36 hours, depending on dose and route of inoculation. Maximum release of virus is up to 5 days post-infection, following which there is a rapid decline. Infection spreads rapidly, aerosols probably being mainly responsible for spread within and between flocks. No specific biological vectors are known, but the virus is probably spread on people, their vehicles and (non-specifically) by vermin. Re-infection is common; broiler flocks have been demonstrated to be infected with up to three types of IBV, in addition to vaccinal virus (Cavanagh et al., 1999). Virus can persist in individual chickens for several months and may be re-excreted at times of stress, for example at point of lay.

Impact: Economic

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In countries where Marek’s disease, Newcastle disease and avian influenza are absent or under control, IB is probably the most important viral pathogen in terms of its chronic effect on the intensive domestic fowl industry.

Disease Treatment

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There is no treatment for viral infection. Antibiotics, administered in drinking water, have been successfully used in attempts to minimize losses caused by secondary bacterial infections. Ventilation should be improved and ammonia and dust levels minimized.

Prevention and Control

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Immunization and Vaccines

Vaccination is a key element of control allied with management of the environment (Cavanagh and Gelb, 2008; de Wit et al., 2011a). Both live and killed vaccines are available. However, killed vaccines alone do not induce immunity; a live vaccine is required to prime immunity prior to application of killed vaccine. Broilers are commonly given live vaccine by coarse spray at the hatchery. Depending on the disease situation, they may be vaccinated again at 2-3 weeks of age with vaccine in drinking water. A vaccination programme for breeders and commercial layers might involve live IB vaccination by drinking water at 3 and 8-10 weeks of age, followed by killed vaccine at around 16-18 weeks of age (Pattison and Cook, 1996).

In many countries live vaccines are limited to the 'Massachusetts' type. In the USA, 'Massachusetts' and 'Connecticut' types are used widely, with 'Florida', 'Arkansas' and 'JMK' used regionally, as appropriate. In Europe Massachusetts strains are also widely used, plus vaccines against serotypes not found in North America e.g. D274, D1466, and the ‘4/91’ or ‘793/B’ serotypes. Elsewhere, too, vaccines have been developed against new serotypes e.g. in Korea (Lim et al., 2012). As there are many more serotypes of IBV than there are IB vaccines, it is common to apply combinations of the available IB vaccines, either simultaneously or in sequence (Terregino et al., 2008; de Wit et al., 2011a, b).

Farm-level Control

In addition to vaccination, good biosecurity should be practiced, including attention to temporary storage and disposal of carcasses. Multi-age sites are particularly at risk. As with other viral diseases, good air quality is important to reduce stress on the respiratory mucosa that together with IBV infection can predispose birds to secondary bacterial infections. Control of ventilation, heating, and misting if litter is very dry are important if disease incidence is to be reduced. Overcrowding will exacerbate the effects of infection.

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Coronavirus group, Institute for Animal Healthhttp://www.research.iah.ac.uk/welcome/coronavirus/
infectious-bronchitis.com (Merck Animal Health)http://www.infectious-bronchitis.com/

Distribution Maps

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