Inclusion Body Hepatitis (IBH)/ Hydropericardium Syndrome (HPS)

🔊 Listen to Post

Etiology:

The disease is caused by a virus belonging to fowl adenovirus, a member of the family Adeno-viridae. FAdV is non-enveloped, double-stranded DNA with a genome of 43-45 kb in size. FAdVs are grouped into 5 species (A-E) based on their molecular structure i.e. based on their restriction site patterns. Based on the cross-neutralization tests, they are further divided into 12 serotypes (FAdV-1 to 8a and 8b to 11). Based on epidemiological findings, serotypes 2, 8a, 8b, and 11 causes IBH.

Fowl adenovirus (FAdV) serotype-4 is highly pathogenic for chickens, especially for broilers aged 3 to 5 wk, and it has emerged as one of the foremost causes of economic losses to the poultry industry in the last 30 years. FAdV 4 serotype, is the causative agent of hydropericardium syndrome (HPS), a severe disease in broiler chickens that is characterized by the accumulation of a clear, straw-colored fluid in the pericardial sac, as well as nephritis and hepatitis.

Adenoviruses are resistant to lipid solvents such as ether and chloroform, sodium deoxycholate, trypsin, 2% phenol, and 50% alcohol. They are inactivated by a 1:1,000 concentration of formaldehyde. FAdV is distributed widely throughout the world, and domestic avian species of all ages are susceptible.

Classification of Adenovirus affecting Poultry:

IBH: Inclusion Body Hepatitis HHS: Hepatitis Hydropericardium Syndrome HE: Hemorrhagic enteritis MSD: Marble spleen disease EDS: Egg drop syndrome

Epidemiology

The disease was first described in the USA in 1963. The firstincidence of FAdV-4 in Asia was recorded in Pakistan in 1987, then after the virus had propagated to vast regions of Asia, Central and South America, and some European countries. In India, the first outbreak of FAdV-4 was documented in the poultry farms of Jammu and Kashmir, Punjab, and Delhi in 1994. Months later, HPS caused by FAdV-4 spread to other parts of India, including Terai of Uttarakhand, Uttar Pradesh, Maharashtra, Andhra Pradesh, Karnataka, Tamil Nadu, and Kerala. The disease is commonly called “leechi disease”.

Transmission:

Transmission of FAdVs occurs both vertically (from infected breeders to progeny) and horizontally (direct contact, contaminated feed/water). Infections with FAdVs are widespread and endemic worldwide. In many cases, they are present without any signs of clinical disease. Many layer and breeder flocks in the field are serological positive for FAdV antibodies. Birds of all age groups are susceptible to FAdV. The severity of lesions depends on the age of the birds infected and the levels of maternal antibodies.

Clinical Signs and Lesions:

IBH has been documented in chickens as young as 7 and 10 days old, even though it typically affects poultry between the ages of 3–5 weeks. IBH can impact breeders, broilers, and layer hens. Flocks affected with IBH often have abrupt onset of mortality, and individual chickens may show nonspecific clinical signs such as lethargy huddling, ruffled feathers, and yellow, mucoid droppings due to excess bile acids.IBH is characterized by sudden onset of mortality peaking after 3–4 days and usually stopping on day 5 but occasionally continuing for 2–3 weeks.

Pathology: Gross and microscopic lesions

The major liver abnormalities in IBH are pale, friable, enlarged livers, and has yellowish discoloration, and multiple palehaemorhagic foci. Lymphocytic infiltration, cellular necrosis, and degeneration of infected organs have also been observed within three to nine days post infection, and atrophy of bursa and swelling in the kidney have been reported in some cases Broilers are more vulnerable to greater mortality because of the severe metabolic imbalance and the substantial damage of the pancreas in addition to the liver. Concerning microscopic lesions Intranuclear inclusion bodies in the liver is a hallmark of FAdV infection.

Metabolic effects in birds

IBH-HPS in general influences the bird metabolism. Especially, during the peak of infection broilers will suffer from hypoglycaemia, in which there will be severe lesions in the liver and pancreas. It can be concluded that FAdV infections in broiler chickens can lead to metabolic disorders which mainly affects glucose metabolism in the affected flock.

Diagnosis of Inclusion Body Hepatitis:

A tentative diagnosis is usually based on a pattern of spiking mortality and typical gross lesions on the post-mortem. The diagnosis is confirmed by histopathology, microscopic examination of the affected tissues and detection of typical lesions, especially intranuclear inclusion bodies. Molecular diagnosis can be done by using PCR and Real-time PCR using the specific primer sequences. Primers are designed mostly based on the hexon gene, and the sequencing of its variable sections is used to classify viruses into species.

(Gross Lesions In IBH-HPS)

Intervention strategies to control IBH

Management procedures to prevent or minimize IBH disease

Preventing aviadenovirus infection is primarily based on strict biosecurity practices. Strict managemental practices, such as cleaning and disinfection of farm premises and equipment; restriction of entry and usage personal protection of visitors and vaccination crews into poultry houses, play an important role in IBH prevention. The resistance of aviadenoviruses for heat inactivation (up to 70◦C) and common disinfectants (particularly lipid solvents such as ether, chloroform, and phenol) causes a significant challenge, particularly in poultry houses with impervious floors and walls.

Therefore, effective FAdV control begins at the primary breeder level with optimum disinfection and vaccination as two parallel lines that could prevent infection and, as a result, protect against vertical transmission. However, the horizontal spread is a significant issue that should not be overlooked, and it takes some effort to keep a commercial flock free of FAdV infection.

Additionally, affected flocks may exhibit metabolic disease as a result of damage to the liver & pancreas which results in hypoglycemic conditions. Corrective actions include restoring liver and pancreatic functions to normal levels which in turn improves glucose metabolism and limits the mortality in the IBH affected flocks.

Vaccination

In recent years, outbreaks of IBH have resulted in higher bird mortality compared to early milder outbreaks, resulting in severe economic losses to the poultry sector. As a result, effective vaccination is required to control the infection. Both live and inactivated vaccines are available to combat IBH. Breeders to be administered with inactivated vaccines at 12, 18 and 45 weeks and commercial chicks should be vaccinated at 0^th day during vulnerable period (June to October).The FAdV serotypes 4 and 8 are most commonly used in commercial vaccine preparation. However, for disease prevention and control in endemic areas, it is recommended that autogenous inactivated vaccines prepared from the prevalent serotype of FAdV be administered. Primarily breeders with strict biosecurity practices used autogenous inactivated vaccines to prevent vertical transmission and ensure the transfer of maternal immunity from breeding flocks to their progeny.

References available on request

by Dr Ashok Reddy & Dr Mounika, Immeureka Animal Health Pvt Ltd