Infectious bronchitis is primarily a disease of chickens. The pathogenicity of IBV can vary widely between strains. The clinical outcome of infection in chickens depends on many variables such as the virus strain and type; sex and age of the chicken; immune status (vaccination, immune suppression and maternally derived antibodies); co-infections; and environmental circumstances such as climate, dust, ammonia, and cold stress.
Important points
- Initiation of Infection: Infection is initiated via the respiratory tract regardless of the tissue tropism of the strain (respiratory, kidney, reproductive organs).
- Pathogenicity of IBV is higher in 3 target organs: The virus replicates and produces lesions in many types of epithelial cells, including those of the respiratory tract (nasal turbinates, Harderian gland, trachea, lungs, and air sacs), kidney, and reproductive organs (oviduct, testes).
- Pathogenicity is low in other organs: The the virus also grows in many cells of the alimentary tract (esophagus, proventriculus, duodenum, jejunum, cloacal bursa [bursa of Fabricius], cecal tonsils, rectum, and cloaca) often with little pathobiological clinical effect.
Chronic Epiphora: Other clinical outcomes associated with IB infection include frothy conjunctivitis, profuse lacrimation, oedema, and cellulitis of periorbital tissues. - Lesions of IBV: All IBV strains produce lesions of varying severity in the respiratory tract depending on their virulence, chicken age at infection, genetic susceptibility of the chicken line, climate, and maternal or active immunity of the chicken. Therefore,
- Synergistic pathogenicity of IBV: IBV infections often increase the susceptibility to secondary respiratory infections or increase the damage of infections with primary respiratory pathogens*. IBV synergize with Escherichia coli, Mycoplasma gallisepticum, Mycoplasma synoviae, Mycoplasma imitans, and Haemophilus paragallinarum. The damage caused by these secondary infections can be substantial, especially in broilers, resulting in a higher mortality, growth depression, increase of feed conversion, use of antibiotics.
- *Note: Proper vaccination against IBV also can be useful to prevent the chickens developing clinical IB and subsequent E. coli airsacculitis.
- Involvement of Kidneys: Some strains of IBV are highly nephropathogenic that may be associated with nephritis to some degree in the field; environmental factors are probably important as to whether kidney complications are significant. Greater mortality was seen in males, with cold stress, in certain breeds, or when animal byproducts were the major component of high-protein diets.
- Calcium in diet: Chickens infected with nephropathogenic strain of IBV when fed with increased levels of calcium in diet may frequently developed urolithiasis and kidney lesions.
- Effect of age on kidney lesions: The virulence of the strains for the kidney also depends on the age of infection. Young birds (less than 2 weeks of age) typically show more severe nephritis and higher mortality than older birds. Significant effects of maternal antibodies have been seen in protecting the young birds from kidney lesion induced mortality. Chicks from breeders having high titers of antibodies against IBV shows greater resistance against nephropathogenic strains of IBV.
- Damage to oviducts in young birds: Virulence for the reproductive tract also may differ among IBV strains. Presence of maternal antibody could prevent damage to the oviduct during an early-age IBV infection.
- Susceptibility to layers: In susceptible layers, different IBV strains produced a range of effects varying from shell pigment changes with no production drop to production drops of up to 70%
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