Avian Infectious Bronchitis: Coronavirus Of Birds

Infectious bronchitis virus (IBV) is one of the most lethal viruses in the birds, it causes huge economic losses in terms of productivity of the flock.

By: Dr. Muhammad Ali Tahir Rana, Dr. Asghar Abbas, Dr. Muhammad Asif Raza, and Dr. Kashif Hussain

  1. Introduction

Infectious bronchitis is a disease that is caused by the infectious bronchitis virus (IBV). The disease was first identified in North Dakota, USA when Schalk and Hawn reported a new respiratory disease in young chickens Since then, IBV has been recognized widely, especially in countries with large commercial poultry populations. Apart from respiratory infections, IB affects the kidney and reproductive tract, causing renal dysfunction and decreased egg production, respectively. Although the disease first was believed to occur primarily in young chickens, however, chickens of all age are also susceptible

  1. Etiology and Microbiology

IBV is a single-stranded positive-sense, enveloped RNA virus of 27–32 kb length. The virus has been classified under the Gammacoronavirus genus in the family Coronaviridae, order Nidovirales. Like other members of the coronavirus family, the IBV genome is composed of structural and nonstructural proteins. Structural proteins include the spike [S] glycoprotein, envelope [E], matrix [M], and nucleocapsid [N]. These proteins together play different roles in viral attachment, replication, and inducing clinical disease. The M protein is the most abundant transmembrane protein, which plays a vital role in coronavirus assembly through interaction with viral ribonucleocapsid and spike glycoprotein. IBV E protein is, however, scant and contains highly hydrophobic transmembrane N- terminal and cytoplasmic C-terminal domains. Studies have shown that the E protein is localized to the Golgi complex in IBV infected cells and is integrally associated with viral envelope formation, assembly, budding, ion channel activity, and apoptosis

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Figure 1 Infectious bronchitis virus structure

  1. Transmission

The virus tends to spread via respiratory secretions and fecal droplets.  Airborne transmission occurs between the birds from a distance of 1.5m. The prevailing winds also cause the infection spread between farms that are separated by a distance of 1,200 meters. The virus can survive in the fecal droplets at a longer period and thus causing re-infection during the recovery phase of the disease. Contaminated utensils, litter, footwear, clothing, and equipment are the potential sources of virus for indirect transmission and have been implicated in IBV spread over large distances. After the aerosol transmission virus remains active in the Bursa of Fabricius, trachea, and kidney. Detection of the virus in the cecal tonsils up to 14 weeks and from faeces 20 weeks after infection might suggest a role of fecal shedding in viral transmission and persistence. Generally, the short incubation period for IBV varies with the infective dose and route of infection. For example, while infection via the tracheal route may take a course as short as 18 hours, ocular inoculation leads to an incubation period of 36 hours.

  1. Pathogenesis

IBV virus has a wide range of tropism including the respiratory, reproductive urogenital, and digestive systems. IBV initially infects the upper respiratory tract, the virus attaches itself to the glycoprotein receptors that contain sialic acid, where it is restricted to the ciliated and mucus-secreting cells. Replication of the virus starts in nasal turbinates, nose, trachea, lungs, air sacs, and the harderian gland. This will lead to the mucus accumulation in the nose and trachea which will further cause hemorrhagic tracheitis. Furthermore, viremia occurs and the virus will be disseminated to other tissues through a hematogenous route. The neuropathogenic strain of the virus replicates in the segments of tubules and ducts, but more frequently in the epithelial cells of collecting ducts collecting tubules, distal convoluted tubules, and Henle’s loops lead to kidney failure  IBV virus also grows in the oviduct, the virus can cause permanent damage to the respiratory, urinary organs, digestive tracts and generative organs at less than 2 weeks of age. It can also grow in testes, and many parts of the alimentary tract –esophagus, proventriculus, duodenum, jejunum, bursa of Fabricius, caecal tonsils (near the distal end of the tract), rectum and cloaca (the common opening for release of eggs and faeces). Some Asian strains may cause lesions in the proventriculus. Infection of enteric tissues usually does not manifest itself clinically

  1. Clinical Signs

Clinical signs will vary based on the age of chicks, pathogenicity, and strain of the virus. infectious virus may be asymptomatic or may relate to their tissue namely respiratory, reproductive, and nephritic disorders. Following are the signs that are most common in baby and adult chickens

  • Baby chicks

Signs include coughing, sneezing, gasping rales, and nasal and ocular discharge (Fig. 1). Morbidity is virtually 100%, although the severity of signs varies. Signs can develop within 48 hours postinfection. There is weakness, depression, and huddling near heat sources. Mortality in young chicks is usually negligible unless the disease is complicated by other infectious agents. Nephrogenic strains may cause high mortality.

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Figure 2 Baby chick doing gasping accompanied by nasal and ocular discharge

5.2. Broilers and Laying chickens

Coughing, sneezing, and rales are common. Seldom is there nasal or ocular discharge. . Egg production drops markedly (up to 50%). Effects on production can last 6-8 weeks or longer. Eggs are often soft-shelled or misshapen Egg albumin may be watery. Low egg quality and shell irregularities may persist long after an outbreak of IB. Chickens that had IB or a severe reaction to the IB vaccine when less than 2 weeks of age may suffer permanent damage to the oviduct resulting in poor-to-no egg-laying capacity.  Chickens infectious virus that have IB or a severe reaction to IB vaccination may develop airsacculitis, due to an increased susceptibility to secondary infectious agents (especially Escherichia coli or Mycoplasma gallisepticum). This complication can be very severe and may accentuate respiratory signs, especially in young chickens. Mortality associated with swollen pale kidneys and urolithiasis is induced by nephrotropic IBV strains in pullets and even in mature birds.

Figure 3 Misshaped and soft-shelled eggs from IB positive broiler breeder hens.

  1. Lesions

Lesions associated with IB include a mild to moderate inflammation of the respiratory tract. On necropsy infected chickens have serous, catarrhal, or caseous exudates in the trachea, nasal passages, and sinuses are congested with excessive amounts of mucus, and where the infection has been complicated with E.coli, airsacculitis, pericarditis, and perihepatitis may also be observed  Airsacs may be foamy during the acute infection, then become cloudy and contain yellow caseous exudates. A caseous plug may be found in the lower trachea (at the point of bifurcation) or bronchi of chicks that die. Small areas of pneumonia may also be seen around the large bronchi [The lesions associated with the infection of pheasants by coronaviruses in the field are visceral urates deposition (“visceral gout”) and urolithiasis with swollen pale kidneys.

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Figure 4 Mild and acute airsacculitis in a broiler chicken. Note the foamy exudate in the abdominal air sac.

Figure 5 Mild to moderate inflammation of the upper respiratory tract (Left)  and swollen pale kidneys (Right)

  1. Diagnosis

7.1 Demonstration of Virus

  1. Isolation of virus in embryonated eggs
  2. Cultivation of virus in trachea rings
  3. Detection of viral nucleic acid

7.2 Detection of Antibody (Serological Tests)

  1. Virus neutralization (VN)
  2. Agar gel immunodiffusion (AGID)
  3. Haemagglutination inhibiting (HI)
  4. Enzyme-Linked Immunosorbent Assay (ELISA)

 Prevention and Control

Prevention and control measures mainly include follow up of strict biosecurity, good hygiene, and sanitation practices, along with a judicious vaccination program.

  1. A one –age system (all-in /all-out) of rearing, cleaning and disinfection between batches will reduce the level of infection.
  2. Good management practices comprise strict isolation/quarantine, repopulation with disease-free day-old chicks, and adapting appropriate cleaning, disinfection, and hygienic measures in the poultry farm.
  3. Disinfectants can be very helpful for preventing virus infections in a farm
Authors: Dr. Muhammad Ali Tahir Rana, Dr. Asghar Abbas, Dr. Muhammad Asif Raza, and Dr. Kashif Hussain
Faculty of Veterinary and Animal Sciences MNS- Agriculture University Multan, Pakistan

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