Infectious bronchitis virus (IBV), the coronavirus of the chicken (Gallus gallus), is one of the foremost causes of economic loss within the poultry industry, affecting the performance of both meat-type and egg-laying birds. The virus replicates not only in the epithelium of upper and lower respiratory tract tissues, but also in many tissues along the alimentary tract and elsewhere e.g. kidney, oviduct and testes. It can be detected in both respiratory and faecal material. There is increasing evidence that IBV can infect species of bird other than the chicken. Interestingly breeds of chicken vary with respect to the severity of infection with IBV, which may be related to the immune response. Probably the major reason for the high profile of IBV is the existence of a very large number of serotypes. Both live and inactivated IB vaccines are used extensively, the latter requiring priming by the former. Their effectiveness is diminished by poor cross-protection. The nature of the protective immune response to IBV is poorly understood. What is known is that the surface spike protein, indeed the amino-terminal S1 half, is sufficient to induce good protective immunity. There is increasing evidence that only a few amino acid differences amongst S proteins are sufficient to have a detrimental impact on cross-protection. Experimental vector IB vaccines and genetically manipulated IBVs - with heterologous spike protein genes - have produced promising results, including in the context of in ovo vaccination.

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Coronavirus avian infectious bronchitis virus.

Avian pathogenic Escherichia coli (APEC) cause aerosacculitis, polyserositis, septicemia and other mainly extraintestinal diseases in chickens, turkeys and other avian species. APEC are found in the intestinal microflora of healthy birds and most of the diseases associated with them are secondary to environmental and host predisposing factors. APEC isolates commonly belong to certain serogroups, O1, O2 and O78, and to a restricted number of clones. Several experimental models have been developed, permitting a more reliable evaluation of the pathogenicity of E. coli for chickens and turkeys. Hence, virulence factors identified on APEC are adhesins such as the F1 and P fimbriae, and curli, the aerobactin iron sequestering system, K1 capsule, temperature-sensitive hemagglutinin (Tsh), resistance to the bactericidal effects of serum and cytotoxic effects. Experimental infection studies have shown that the air-exchange regions of the lung and the airsacs are important sites of entry of E. coli into the bloodstream of birds during the initial stages of infection and that resistance to phagocytosis may be an important mechanism in the development of the disease. They have also demonstrated that F1 fimbriae are expressed in the respiratory tract, whereas P fimbriae are expressed in the internal organs of infected chickens. The role of these fimbrial adhesins in the development of disease is not yet, however, fully understood. The more recent use of genetic approaches for the identification of new virulence factors will greatly enhance our knowledge of APEC pathogenic mechanisms. Diagnosis of APEC infections is based on the clinical picture, lesions and isolation of E. coli. This may be strengthened by serotyping and identification of virulence factors using immunological or molecular methods such as DNA probes and PCR. Approaches for the prevention and control of APEC infections include the control of environmental contamination and environmental parameters such as humidity and ventilation. Antibiotherapy is widely used, although APEC are frequently resistant to a wide range of antibiotics. Vaccines containing killed or attenuated virulent bacteria protect against infection with the homologous strain but are less efficient against heterologous strains. Hence, vaccination for colibacillosis is not widely practised because of the large variety of serogroups involved in field outbreaks.

https://hal.archives-ouvertes.fr/hal-00902571/document

Avian pathogenic escherichia coli (apec)

This review is focused on the acute form of infectious bursal disease (IBD) caused by very virulent IBD virus (vvIBDV). First described in Europe about 10 years ago, this new form of the disease has rapidly spread all over the world, causing dramatic losses; after a decade, it still represents a considerable threat to the poultry industry. Emergence of the acute forms of the disease has drastically changed the epidemiology of IBD. Although their origin is still under investigation, vvIBDVs have spread all over the world in a very explosive but conserved manner. This raises the question of the origin of vvIBDVs, of the possible existence of reservoirs and of the possible emergence of new, distinct lineages in the future. While it has become clear that amino acids within the variable region of virus protein VP2 account for the molecular basis of antigenic variation, no definite hot spot that determines pathogenicity has been identified. Fingerprints of VP2 on vvIBDVs have to be considered more as common evo...

https://www.tandfonline.com/doi/pdf/10.1080/03079450050045431

Acute infectious bursal disease in poultry: A review

Infectious bursal disease (IBD), caused by an avibirnavirus, has been an economically significant, widely distributed condition affecting immature chickens since 1960. The classical type 1 conventi...

Infectious bursal disease.

Factors Affecting Intestinal Health in Poultry

Specific-pathogen-free (SPF) chickens were inoculated with several different concentrations of chicken anemia agent (CAA) by the intra-abdominal, intratracheal, or oral routes. Based on lowered hematocrit values, the birds were most susceptible to CAA introduced by the intra-abdominal route. When SPF chickens were infected with infectious bursal disease virus (IBDV) at 1 day of age, they remained susceptible to CAA up to at least 21 days, whereas birds inoculated with CAA alone were susceptible only at 1 day of age. Infectious bursal disease virus introduced at 1 day of age also increased the susceptibility of birds to contact infection with CAA and resulted in increased mortality rates in CAA inoculates. The response of SPF birds to CAA infection varied following exposure at 1 day of age to two different strains of IBDV (STC and Variant-E). Chicken anemia agent contacts and inoculates infected with the Variant-E strain were affected 1 week earlier by CAA than by STC inoculates, as evidenced by depressed hematocrits. However, the total number of birds affected was similar for both the Variant-E and STC-inoculated chickens. Commercial broiler chickens inoculated at 1, 7, 10, and 14 days of age by non-parenteral routes with CAA or a combination of CAA and IBDV had mean hematocrits that were lower than controls. Several CAA-inoculated birds were considered anemic, with hematocrit values of 25 or less, while uninoculated birds remained within normal ranges.

The effects of age, route of exposure, and coinfection with infectious bursal disease virus on the pathogenicity and transmissibility of chicken anemia agent (CAA).

Over a 2 1/2-year period (January 1981 to June 1983), 177 Escherichia coli isolates were obtained from 145 field-reared broiler flocks in the Delmarva peninsula, and 20 were obtained from clinically normal day-old hatchery chickens representing an additional 17 flocks in Delmarva. Ninety-one isolates obtained from the field-reared birds between 2 and 8 weeks of age were associated with complicated air-sac disease. Serotyping efforts demonstrated a predominance of O2, O35, and O78 serogroups and a large number of untypable isolates. More than 50% of the isolates in each of the three dominant serogroups were collected from broilers with colibacillosis, but they were never detected in the yolk-sac samples of clinically normal day-old hatchery chickens. In vitro biochemical characterization of the E. coli isolates revealed variable rates of carbohydrate fermentation and amino acid decarboxylation. No common characteristics appeared to be shared by the predominant serogroups isolated from clinically affected birds, although several serogroup-specific reactions were noted. The majority of the isolates were sensitive to chloramphenicol, gentamicin, nalidixic acid, ormethoprim-sulfadimethoxine, spectinomycin, neomycin, and ampicillin. About half of the isolates were sensitive to nitrofurantoin and the sulfa compounds. Less than 25% of the isolates were sensitive to streptomycin, erythromycin, tetracyclines, novobiocin, penicillin, bacitracin, and lincomycin.

https://www.jstor.org/stable/info/1590463

In vitro and in vivo characterization of avian Escherichia coli. I. Serotypes, metabolic activity, and antibiotic sensitivity

A previously unrecognized infectious bronchitis virus (IBV) serotype, referred to hereafter as the Delaware variant (DE var), was isolated from commercial broiler chickens during a severe, widespread respiratory disease epornitic in the Delmarva peninsula region of the United States in January-March 1992. The DE var serotype was found to be antigenically unrelated by virus-neutralization (VN) test to nine reference IBV serotypes from North America. Additional VN tests indicated that the DE var isolates (DE/072/92, DE/121/ 92, DE/152/92, and DE/174/92) from broilers were fully or partially neutralized by monospecific antisera prepared against themselves and against two IBV field isolates (DE/492/90 and DE/903/90) recovered from a Delmarva commercial layer flock experiencing egg production losses in 1990. Antigenic relatedness values determined by VN indicated layer isolate DE/492/90 was more closely related to the broiler DE var isolates than was layer isolate DE/903/90. Cross-challenge tests performed in specific-pathogen-free chickens also demonstrated the antigenic similarity of the broiler (DE/072/92 and DE/174/92) and the layer isolates (DE/492/90 and DE/903/90), with heterologous strain protection values ranging from 55% to 100%. Protection values of DE var isolates vs. Massachusetts 41 and Arkansas DPI were considerably lower (0-60%). The S-1 gene of the US/DE/072/92 isolate of the DE var serotype was amplified by reverse transcription polymerase chain reaction, cloned, and sequenced. The DE var S-1 gene sequence was compared with the S-1 gene sequences of IBV serotypes from North America, Europe, and Australia. A dendrogram based on this analysis supported the conclusion that the DE var serotype is highly novel among IBV. A high degree of similarity (> 88%) was observed between the S-1 genes of the DE var broiler isolates (DE/072/92 and DE/174/92) and layer isolates (DE/492/90 and DE/903/90). These data, taken with the VN and cross-challenge results, establish a genetic as well as an antigenic link between the isolates from layers and broilers and indicate the DE var serotype was responsible for both infectious bronchitis outbreaks.

https://www.jstor.org/stable/pdfplus/1592158.pdf

Antigenic and S-1 Genomic Characterization of the Delaware Variant Serotype of Infectious Bronchitis Virus

The pathogenicity of 197 Escherichia coli isolates obtained from clinically affected commercially grown broiler chickens and normal hatchery chicks was assessed by inoculating day-old broilers intratracheally. The degree of pathogenicity (high, intermediate, low) was judged according to mortality and lesions occurring within 7 days following inoculation. Serotype, metabolic activity, motility, and in vitro antibiotic sensitivity of each isolate were evaluated and related to pathogenicity. Seventy-five of the isolates of high to intermediate pathogenicity belonged to serogroup O2, O78, or O35. In addition, 51 pathogenic E. coli isolates could not be serotyped, and several had multiple serotypes. Most isolates had similar metabolic activity, as determined by amino acid decarboxylation and carbohydrate fermentation, regardless of pathogenicity. An exception was the fermentation of adonitol, which occurred more frequently with the highly pathogenic strains. Motility and in vitro antibiotic sensitivity were not related to pathogenicity. An age-associated resistance to intratracheal E. coli administration occurred by 15 days of age in uncompromised birds. Relative susceptibility of birds older than 2 weeks to intratracheal and/or intravenous E. coli inoculation could be increased by prior exposure to pathogenic reovirus 1733, adenovirus 3167, or infectious bursal disease virus (IBDV). Birds infected with IBDV at 3 weeks failed to clear apathogenic and pathogenic E. coli from circulating blood.

In vitro and in vivo characterization of avian Escherichia coli. II. Factors associated with pathogenicity.

A chicken anemia agent (CAA) isolated from commercial broilers in the United States was characterized in vivo and in vitro. When inoculated into susceptible 1-day-old chickens, the agent induced a severe bone marrow aplasia, thymic atrophy, multiple subcutaneous and intramuscular hemorrhages, and anemia, as evidenced by reduced hematocrits. Chickens derived from different breeder flocks and inoculated in ovo or at 1 day of age varied in their susceptibility to the CAA, with some flocks being highly susceptible, while others were almost totally resistant. This was true for both specific-pathogen-free and commercial chickens. The isolate was able to pass through a 50-nm-pore-size filter and was resistant to inactivation at 56 C for 30 minutes. It failed to agglutinate avian and mammalian erythrocytes and could not be propagated in conventional cell cultures. The physical and biological characteristics of the agent and the disease it induces indicate that it is similar to the CAA found in Japan and Europe.

S. S. Cloud

Papers

The effects of age, route of exposure, and coinfection with infectious bursal disease virus on the pathogenicity and transmissibility of chicken anemia agent (CAA).

In vitro and in vivo characterization of avian Escherichia coli. I. Serotypes, metabolic activity, and antibiotic sensitivity

Antigenic and S-1 Genomic Characterization of the Delaware Variant Serotype of Infectious Bronchitis Virus

In vitro and in vivo characterization of avian Escherichia coli. II. Factors associated with pathogenicity.

The isolation and characterization of chicken anemia agent (CAA) from broilers in the United States.