Gumboro Disease in Chickens: Symptoms, Pathogenesis, and Control

Gumboro disease, also known as Infectious Bursal Disease (IBD), is a highly contagious viral infection that primarily affects young chickens from three weeks of age. The disease was first identified by Cosgrove in 1962 in Gumboro, a small town in Delaware, USA. It is caused by a virus belonging to the Birnaviridae family.

In the mid-1980s, a variant strain of the Infectious Bursal Disease Virus (IBDV) emerged in the USA. Subsequently, very virulent forms of the classical IBDV were reported in Europe.

The disease causes significant direct losses due to mortality and indirect losses from reduced production efficiency. These secondary losses often result from immunosuppression, which predisposes the birds to secondary infections. Gumboro primarily targets immature B lymphocytes in the bursa of Fabricius, leading to severe damage to the bird's immune system development.

Two serotypes of the virus have been identified, further complicating control and management efforts.

• Serotype 1 (pathogenic)
• Serotype 2 (non-pathogenic), animals with this serotype have protection against serotype 1

Pathogenesis

The primary route of infection for Gumboro disease is oral ingestion of contaminated feces. Using immunofluorescence techniques, it has been demonstrated that within 4 to 5 hours of oral infection, the virus can be detected in the macrophages and lymphatic cells of the duodenum, jejunum, and cecum. These are the initial sites of viral replication.

Approximately 5 hours post-infection, the virus reaches the liver via the portal venous system. In the liver, some viral particles are phagocytosed by Kupffer cells, while others escape and enter the bloodstream. These circulating viruses are then transported to other organs, including the bursa of Fabricius, where the immature B lymphocytes become the primary targets for viral replication.

By 13 hours post-infection, most follicles in the bursa of Fabricius test positive for the virus. By 16 hours post-infection, pronounced viremia occurs, leading to secondary viral replication in other lymphatic organs. This widespread replication results in clinical disease and, in severe cases, death within 4 to 72 hours post-infection.

Characteristics of the Infectious Bursal Disease Virus (IBDV)

The Infectious Bursal Disease Virus (IBDV) is a small, non-enveloped, double-stranded RNA virus belonging to the Birnaviridae family. It is highly resilient, exhibiting resistance to heat and disinfectants. Studies have shown that environments previously occupied by infected birds can remain infectious for extended periods, with new birds placed in the same houses becoming infected even 54 to 122 days later.

The kinetics of viral replication are consistent across all IBDV pathotypes. However, more virulent strains exhibit significantly higher amplification of viral replication at each stage. This amplified replication leads to earlier onset and more severe clinical signs in affected chickens.

Immunity of the young chicken

Chickens are hatched with passive immunity in the form of circulating antibodies, known as maternally derived antibodies (MDA), which are transferred from the parent hen via the yolk sac. These MDA titers gradually decline over time. In broilers, the MDA virus neutralization titer (log₂) decreases linearly at a rate of approximately 1 log₂ every 3.5 days. In commercial layers, the decline is slower, at a rate of 1 log₂ every 5.5 days, likely due to their slower growth rate.

The virulence of the IBDV strain determines the level of MDA required to prevent bursal damage. For classical IBDV infections, a log₂ titer above 8 is sufficient for protection. However, very virulent IBDV strains require a higher MDA titer, exceeding log₂ 11, to prevent infection.

MDA also neutralizes milder IBDV vaccine strains, meaning that vaccinating chickens in the presence of high MDA levels can result in vaccine failure.

Clinical Signs of Gumboro Disease

Clinical signs of Gumboro disease typically appear 48–72 hours after infection. Early symptoms include depression, ruffled feathers, and whitish or watery diarrhea. As the disease progresses, affected chicks may exhibit anorexia, dehydration, trembling, vent picking, and, in severe cases, death.

In affected flocks, morbidity can reach 100%, while mortality rates vary between 0% and 30%.

The subclinical form of Infectious Bursal Disease (IBD) presents no visible clinical signs but causes immunosuppression, making birds more susceptible to secondary infections such as E. coli, coccidiosis, necrotic dermatitis, and necrotic enteritis. These immunosuppressed birds may also exhibit poor responses to vaccinations.

Necropsy findings include dehydration, hemorrhages in the thigh and pectoral muscles, and a swollen, hemorrhagic, or edematous bursa of Fabricius. By day 8 post-infection, the bursa atrophies to approximately one-third of its original size. Additionally, the kidneys may appear swollen with urine accumulation in the ureters.

Post-Mortem Lesions in Gumboro Disease

Gross Lesions

Birds that succumb to Gumboro disease often display dehydration and darkened discoloration of the pectoral muscles. Hemorrhages are frequently observed in the thigh and pectoral muscles. Intestinal changes, such as increased mucus and prominent renal lesions, may occur in birds that die or are in advanced stages of the disease, likely due to severe dehydration. However, in birds examined during the early stages of infection, the kidneys typically appear normal.

The cloacal bursa is the primary target organ of the virus, with a specific sequence of changes observed over 12 days post-infection (PI):

• Day 3 PI: The bursa begins to enlarge due to edema and hyperemia.
• Day 4 PI: The bursa usually doubles in weight.
• Day 5 PI: The size starts to decrease, returning to normal weight, followed by progressive atrophy.
• Day 8 PI onward: The bursa reduces to approximately one-third of its original weight or less.

By days 2–3 PI, the bursa may have a gelatinous, yellowish transudate covering the serosal surface, longitudinal striations, and a cream-colored appearance. The transudate disappears as the bursa returns to normal size before atrophying further.

Variant strains of IBDV may not induce significant inflammation, although some can cause necrotic foci and petechial or ecchymotic hemorrhages on the mucosal surface of the bursa. In severe cases, extensive hemorrhages may occur, and affected birds may void blood in their droppings.

Other post-mortem findings include:

• Slightly enlarged spleens with small, uniformly dispersed gray foci.
• Hemorrhages in the mucosa at the juncture of the proventriculus and ventriculus (gizzard), occasionally causing melena (black, blood-stained digestive content).
• Severe lesions in lymphoid organs, including the cecal tonsils, thymus, spleen, and bone marrow, particularly with very virulent IBDV (vvIBDV) strains.

Pathogenicity is closely correlated with lesion severity in non-bursal lymphoid organs, suggesting that the distribution of viral antigens in these organs contributes to the disease's virulence.

Diagnosis of Infectious Bursal Disease (IBD)

In cases of acute IBD, a presumptive diagnosis can often be made based on typical clinical signs and characteristic lesions in the bursa of Fabricius. A definitive diagnosis, however, requires histological examination of the bursa or virus isolation. The bursa and spleen are the preferred tissues for isolating the IBD virus.

There is no specific treatment available to prevent the onset of immunosuppression once infection occurs. When secondary infections arise, treatment should target the specific secondary disease.

Given the high stability of the IBD virus in poultry house environments, strict sanitation procedures are critical to minimizing exposure in future flocks.

The most effective method for controlling IBD is vaccination. Chicks are typically vaccinated on the first day of age and receive a booster between 7 and 14 days of age to ensure adequate protection.

Control of Gumboro Disease

The first line of defense against Gumboro disease is strict biosecurity. Effective management practices include limiting and controlling access to poultry houses, using footbaths, and ensuring separate footwear for each house to minimize the risk of pathogen introduction. At the end of a production cycle, especially when birds have been infected with IBDV, thorough cleaning of the site is crucial.

The highest concentration of Gumboro virus is found in chicken manure, so disinfectants such as chlorine-releasing agents, iodophors, or quaternary ammonium compounds are recommended for controlling the virus.

Vaccination is an effective control method and relies on two key aspects:

1. Vaccinating the parent stock to ensure that progeny chickens are hatched with a high and uniform level of maternally derived antibodies (MDA).
2. Administering a suitable live vaccine to the chickens at the correct age.

A high level of MDA in progeny chickens is essential for protecting them from early IBDV infection during the first 10–14 days of life. Studies show that 80–90% protection can be achieved within 4 days of successful vaccination with the D78 strain. Although a serological response following vaccination with a live vaccine typically takes several days to develop, protection is already achieved within the first week, effectively minimizing the window of susceptibility.

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