Infectious Bronchitis: Update

Introduction

Infectious bronchitis (IB) was first observed in 1930 and has been recognised as a disease of major economic importance in chickens since that time. Infectious bronchitis (IB) is an acute, contagious disease of chickens characterised primarily by respiratory signs. The infection allows secondary invasion of the lungs and air sacs with bacterial infections such as E. coli, which is mostly accompanied with significant losses due to condemnations at slaughter. Weight gain and feed conversion efficiency may be impaired. The Infections may also lead to nephritis and egg production problems. In laying flocks economic losses are due to drop in egg production and egg quality (Cavanagh and Naqi, 2003).

IB virus, a single positive-strand RNA virus, is a member of the genus Coronavirus, of the family Coronaviridae of the order Nidovirales. Coronaviruses were divided into 4 antigenic groups. Infectious bronchitis virus (IBV) was laced in group 3. In recent studies, it was demonstrated that IBV and Turkey coronavirus (TCV) have a lot of antigenic and molecular similarities and both were placed in group 3 (Guy, 2000, Cavanagh et al., 2002).

The virus is enveloped. It is fairly labile, being easily destroyed by disinfectants, sunlight, heat and other environmental factors. Infectious bronchitis virus has the ability to mutate or change its genetic makeup either by mutation or recombination (Cavanagh et al., 1992). As a result, many serotypes have been identified. IB strains vary significantly from country to country as well as from region to region. Three common serotypes in North America are the Massachusetts, Connecticut, and Arkansas 99. In Europe various "Holland variants," usually designated using numbers (D-274, D-212, D-1466), are recognized. Recently, some strains of IB virus particularly the so-called 793/B or 4/91 serogroup, have been isolated from broiler breeder chickens with clinical signs of cyanosis, muscular tremors and hyperventilation, leading to rapid death. At postmortem examination one of the most consistent findings was severe tracheitis and a bilateral pectoral muscle myopathy. This serotype, first reported in the UK in 1992 is now widespread in Europe and other parts of the world (Gough et al., 1992). In addition, several strains of IB virus showing a strong affinity for the kidney (nephropathogenic strains) were isolated (Cumming, 1969) and have become more prevalent in recent years. Although differences in virulence and tropism exist between strains, primary replication in the respiratory tract occurs with most IB viruses.

The virus shedding follows in faeces, respiratory discharges and on contaminated eggshells. The virus is transmitted horizontally by direct contact with infected chickens, indirectly through ingestion of contaminated feed and water or inhalation contaminated particles. Transmission from farm to farm is related to movement of contaminated people, equipment, and vehicles or via airborne transmission and this can occur over considerable distances. Following infection, chickens may remain carriers and shed the virus for several weeks. The virus persists in the intestinal tract and is excreted in the faeces for long periods (Alexander and Gough, 1997). Once the IB virus enters a flock, it spreads quickly among all the birds in the flock. Therefore, the infection rate within an infected flock is close to 100%.

The severity of respiratory infections with IB virus can be greatly enhanced by the presence of other pathogens of the respiratory tract and management factors. The clinical signs of IB include watery discharge from the eyes and nostrils, sneezing, snicking, coughing, tracheal rales and gasping. In many cases, however, the IB virus may spread through the flock without obvious clinical signs of disease except a mild cough. The mortality is usually very low, unless complicated by other factors such as E. coli, Mycoplasma gallisepticum, Mycoplasma synoviae, immunosuppression, poor air quality and high stocking density (McMartin, 1993).

Mortality may occur in young birds due to respiratory or kidney failure. Chickens infected with nephropathogenic IB viruses excrete watery droppings, resulting in wet litter (Cumming, 1969). In recent years, nephropathogenic strains have become more common in laying flocks. These strains may cause a high mortality during the infection or long time after as a result of kidney damage that progress to urolithiasis (Brown et al., 1987). After apparent recovery, chronic nephritis can produce sudden death some time later, especially in brown birds.

In the neonatal, susceptible chick, infection can lead to permanent damage to the developing oviduct resulting in the occurrence in flocks of non-laying hens, the so-called “false layers” (Crinion, et al., 1971). Infection of laying hens with IB virus can result in a drop in egg production and the production of pale, thin-shelled, rough shelled and misshapen eggs, this may occur without respiratory signs. Hatchability may also be reduced. The negative influence of IB on egg quality may persist for many weeks (6 – 8 weeks) or months after production has recovered. A 5 - 10% decrease in egg production may occur in flocks affected with the new IB virus strain 4/91, with some flocks suffering
drops of up to 50%. Pale eggs can appear 2 to 5 days after exposure to the virus. The occurrence of pale eggs can persist for several weeks. In addition, the infection is mostly accompanied with reduced internal egg quality in form of a serous thinning of the thick albumin "watery whites"(McMartin, 1993).

In infected chickens respiratory tract lesions include mucous or thick exudate in the trachea. The mucus tends to accumulate in the lower part of the trachea and a mucus plug is sometimes found near the bronchi. In addition, the air sacs appear cloudy. In case of infection with nephrotropic strain, the kidneys of affected birds are pale, mottled, and can be 2 to 3 times their normal size. Urates are common and can be identified easily in the kidneys and ureters at necropsy. In layers impacted oviducts, ruptured ova, internal layers (egg peritonitis) are constant findings. Infection of very young chicks may result in the development of cystic right oviducts.

Infectious bronchitis is difficult to differentiate from many of the other respiratory diseases. Clinical signs are indicative, but not diagnostic and confirmation requires the direct detection or isolation of IB virus or indirectly by detection of antibodies. Using conventional direct methods many limitations can influence the efficacy of the laboratory diagnosis. In cases of direct detection using electron microscopy, immunofluorescence or immunoperoxidase a sufficient amount of antigen in the samples is necessary and required. For the virus isolation in chicken embryos or in tracheal organ cultures, beside a long time need to isolate the virus also the short shedding duration is a further limited factor (Gelb and Jackwood, 1998) Recently, molecular biological methods have become increasingly applicable to the diagnosis of infectious bronchitis. The availability of these methods can overcome the limitations of traditional approaches in the diagnosis (Jackwood et al., 1992; Handberg et al., 1999). The currently available PCR does not, however, distinguish between vaccine and field strains of this genotype and the vaccinal virus strain could be detected for long time (Zimmermann and Hafez, 2001).

As a result of great heterogeneity of IB virus, serotyping and genotyping using haemagglutination inhibition (HI) or virus neutralization (VN) and PCR of isolates may produce results which are not in agreement. The HI test can be subject to problems with cross reactivity. The VN test is very specific and may result in viruses with very similar amino acid sequences behaving like unrelated strains. With genotyping, using universal oligonucleotides may not bind to “new” variant types, leading to false negatives. It is currently accepted that virus isolation and primary characterisation, followed by serotyping/genotyping, are the recommended procedures for IB diagnosis.

The detection of antibodies can be achieved using haemagglutination inhibition tests (HI), Agar gel precipitation (AGP) or enzyme-linked immunosorbent assays (ELISA) and neutralization tests. The tests differ in their sensitivity and specificity (De Wit et al., 1997). With the widespread use of vaccines for the prevention of diseases in commercial poultry, serology has become of limited value in diagnosing IB infections of chickens. It is essential for routine serological testing to compare two sets of serum samples. One collected at onset of clinical disease and the second at 3 to 4 weeks later. It is also important to mention that none of the available methods can differentiate between the antibody responses to a field challenge from that to vaccination. In addition, a marked increase in antibody using HI with a given IB serotype it cannot be assumed that the field challenge virus was of the same or a closely related serotype. When birds are immunized with one serotype and subsequently challenged with another serotype the antibody response tends to be much higher to the antigen used in the initial vaccination.

Brown and Bracewell (1988) suggested that HI-test may be more strain-than serotypespecific. Prevention of infectious bronchitis is best achieved through an effective biosecurity program. Good management procedures include cleaning and disinfection of the poultry house, proper ventilation, repopulating with day old chicks and strict isolation are very important. The second line of defence is proper vaccination. Vaccines have been used to control the infectious bronchitis infections since the 1950s. Currently, poultry are almost universally vaccinated against IBV. Most vaccines used worldwide are standard Massachusetts strains of the IB virus, e.g., H120, H52, Ma5 and M41.In some European countries, strains D274, D1466, and 4/91, D274, D1466, and 4/91 (793/B) are used. (Cavanagh and Naqi, 2003). Both live and inactivated virus vaccines are used. Infectious bronchitis vaccination programs in broilers involve the use of modified live vaccines.

Vaccination of layers and breeder flocks involve administering a series of live vaccines and progressively increasing the aggressiveness of the route of vaccination (i.e., start with water administration and progress to fine particle spray) and strain of vaccine (highly attenuated, H120) to less attenuated, H52). Evidence that some vaccines increased in virulence after back-passage in chickens was reported by Hopkins and Yoder (1986). Good vaccination practices are especially important when administering live infectious bronchitis vaccines. The virus is relatively fragile and can easily be inactivated if proper vaccination procedures (e.g. protection from sunlight, removal of
sanitizers from water used for mixing/administration, use of skim milk stabilizer, etc.) are not followed. In breeders and some layer flocks an additional vaccination using inactivated oil-emulsion vaccine is used prior to onset of egg production to stimulate the antibody production. Inactivated infectious bronchitis vaccines do not stimulate local (IgA) and cell-mediated (T-cells) immunity as effectively as modified live virus vaccines.

That is why some companies will continue to vaccinate layers and breeder flocks during the production using a live vaccine.

The multiplicity of serotypes identified around the world presents a challenge in choosing appropriate strains for vaccination and designing an effective vaccination program. This means that the efficacy of vaccination program and the economic impact of the disease in an area will vary over the time depending on the nature of the virus strains in circulation and the effectiveness of available vaccines to combat them. Severe outbreaks of IB can occur when a new strain, which is distinct from the vaccine strain, enters a population. A new variant may emerge if just a few amino acids are changed during the emergence of a new virus by mutation. However, in many cases the vast
majority of the viral genome remains unchanged, so that existing vaccines may still control the infection with this new variant. It has also been demonstrated that "classical" strains of infectious bronchitis virus can act at least as partial primers for subsequent administration of an inactivated infectious bronchitis vaccine containing variant and standard strains. In aim to establish an efficient vaccination program against infectious bronchitis, it is essential to identify the prevalent serotypes in the region and to determine the cross-protective potential of available vaccines. Although no reasonable combination of infectious bronchitis vaccine strains provides full protection against all heterologous challenges, it is both undesirable and unnecessary to consider developing a new live vaccine for each new emerging strain, rather than to use a combination of strains, which are able to protect against a wide variety of serotypes “protect types”.

There are combinations, which are able to provide broad protection. Recent studies, showed that for e.g. the use of the two live attenuated IB vaccine strains 4/91 and Ma5, resulted in considerably broaden protection against challenge with a wide variety of antigenically different strains (Cook et al., 1998a).

References

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This paper was presented at the International Seminar Amevea-Peru, 2013. To watch the complete conference, please click here