G. Donald RITTER
DVM, ACPV
Director of Health Services
Mountaire Farms Inc.
Millsboro, DE, U.S.A.
Inclusion body hepatitis (IBH) reemerged to be a disease of clinical significance in two broiler companies on the Delmarva peninsula. In addition, much of the commercial broiler industry in Canada has had similar clinically significant issues with IBH during the past few years. The field presentation of inclusion body hepatitis and laboratory findings from diagnostic case submissions will be discussed.
Causative agent
Avian adenoviruses (AAVs) are the causative agents of IBH. AAVs are ubiquitous in commercial poultry production flocks and have been isolated from both healthy and sick birds. In the past it was thought that clinically significant disease from AAV infection could only occur in severely stressed or immunosuppressed poultry, usually caused by infectious bursal disease and/or chicken anemia virus. More other reports, however, indicate that more virulent strains of AAV alone can and do produce inclusion body hepatitis.
Avian adenoviruses are divided into three Groups. Group 1, or conventional adenoviruses, causes IBH, hydropericardium syndrome (HP), and quail bronchitis. Using cross- neutralization and genetic sequencing testing, Group 1 AAV is further divided into five species that include 12 serotypes. To complicate matters even more, the nomenclature used to identify AAV serotypes is inconsistent due to at least three different typing systems used in Europe and the United States to identify AAVs. Historically, IBH in North America has been most commonly associated with serotype 8a. The various serotypes do not induce cross-protection to each other.
Clinical disease description
The disease usually occurs in broilers that are 3 to 4 weeks of age, although clinical signs can be detected in affected flocks as early as 7 days of age. The first sign of IBH is severe stunting and unevenness in the flock. As the disease progresses, affected birds look and act very sick, although overall morbidity is usually low.
Mortality increases in the third week and ranges from severe (20+ birds/1000/day) to moderate (3 birds/1000/day). Mortality usually peaks and abates in the span of 7 to 10 days, but the subsequent unevenness in the flock persists until the birds are moved to the processing plant. Subsequent culling of small birds by the grower adds to the mortality total, which averages 10%, with severely affected flocks approaching 20% mortality.
The disease usually begins with observance of stunted birds followed by a sudden and sharp increase in mortality. Birds that have inclusion body hepatitis exhibit signs of extreme depression and refuse to eat or move. Abnormal wing feathering (“helicopter wings”) can also be seen in affected birds. Winter and spring are the most common seasons for the disease to occur, and recurring infections occurred in 2 or 3 successive flocks on the same farm.
Gross necropsy lesions
Typical gross liver lesions of IBH are transient in nature. However, when observed, gross liver changes associated with AAV infection are virtually diagnostic. The primary liver lesion is an enlarged, pale or yellow and friable liver with hemorrhagic patches forming a “soccer ball” pattern in sections of the liver or uniformly throughout the entire organ.
In some birds hydropericardium, consisting of clear, yellow fluid around a slightly enlarged heart, can also be observed. Although not described in the literature reviewed, severe swelling and edema of the proventriculus is commonly observed in affected birds and flocks. Birds with deeply yellow skin and body fat can be found. Kidneys may be pale and enlarged, and rarely hemorrhagic lesions may be observed in the pancreas.
Breeder flock influence
IBH is primarily a vertical disease, passing from hen to chick via hatching eggs. Chicks from young breeder flocks are most commonly associated with infection. This bias is most likely due to infection with AAV early in the laying cycle, allowing for the vertical transmission of the virus to occur. The most severe clinical cases observed were commonly from “first” hatches of eggs from 26-27 week old breeder flocks. Both companies on Delmarva with IBH problems do not reuse litter in breeder pullet houses, and presumably some of their breeders may not have been exposed any type of adenovirus infection during the pullet rearing stage of production.
Although not researched for this report, IBH cases in chicks from older breeder flocks may be caused by the mixing of young “spiking” males into a breeder flock where the introduction of a pathogenic adenovirus could then occur, again resulting in vertical shed of virus from infected hens.
Once adequate seroconversion in the breeder flock occurs, vertical shed of AAV ends and broiler field problems associated with the flock in question cease.
Therapeutic treatments
Although no specific treatment for AAV is available, many IBH flocks were treated with sulfa drugs for treatment and prevention of secondary infections due to E. coli.
Disinfection of built-up litter with Virkon-S to prevent recurrence in subsequent flocks was also used with mixed results. Heating of affected houses to 110+F between flocks was ineffective in preventing recurrence of IBH.
Laboratory findings
Histopathology of affected livers showed areas of necrosis in which liver cells contained numerous enlarged nuclei filled with basophilic intranuclear inclusion bodies. Basophilic inclusion bodies were also observed in sections of pancreas. Similar inclusion bodies were not seen in the proventriculus.
Virus isolation of affected tissues in embryonated eggs resulted in isolation of AAV. Agar gel immunodiffusion tests using Group 1 AAV antigen were positive on livers from infected embryos. Serotyping was carried out on several isolates.
Discussion
Why only two of four broiler companies on Delmarva experienced clinical problems with IBH is somewhat puzzling. However, both companies affected reared all breeder pullet flocks in cleaned and disinfected houses bedded with new litter between each flock. The two unaffected Delmarva companies normally reuse pullet house litter for two subsequent flocks. Although raising breeder pullets on fresh litter is considered to be best for food safety concerns, increased sanitation of pullet houses may delay natural infection and seroconversion to AAV until later in the production cycle in some pullets, triggering vertical shed of AAV to and subsequent clinical IBH problems in some progeny from young breeder flocks.
Company A: Approximately 40 cases (houses) of confirmed IBH were diagnosed in broilers during winter. IBH problems ended during the summer, with only one case confirmed during the month of September.
The control plans include assessing AAV serologic status of pullets and breeders, and consideration of administration of inactivated autogenous AAV vaccines to pullets to ensure consistent seroconversion to AAVs of clinical significance prior to the onset of lay.
Company B: Approximately 50 cases (houses) of confirmed IBH were diagnosed in broilers during winter. IBH problems virtually ended during the summer, with only a few cases confirmed.
The control plans include: 1) assessment of IBDV protection from different breeder vaccination programs, 2) assessment of AAV serologic status of pullets and breeders and 3) priming of pullet flocks with autogenous live AAV vaccine is being tried to ensure consistent seroconversion to AAVs of clinical significance prior to the onset of lay.
From Proceedings of the 40th National Meeting on Poultry Health and Processing, Ocean City, Maryland.
