Gumboro Disease in poultry

Introduction

Gumboro Disease, also known as Infectious Bursal Disease (IBD), is a highly contagious viral infection affecting young chickens. The infectious bursal disease in poultry was first found in Gumboro, Delaware, in 1962. It ranks second most important poultry disease after Newcastle disease (Ranikhet). The virus primarily targets the bursa of Fabricius, a crucial organ for immune system development in young birds, leading to severe immunosuppression. This makes affected birds more susceptible to secondary infections such as Escherichia coli infections and gangrenous dermatitis. Moreover, immunosuppression can result in vaccination failures, further exacerbating disease outbreaks.

This disease affects chickens worldwide and is responsible for high morbidity and variable mortality rates, depending on the strain of the virus. It typically affects birds between 18 to 40 days of age, but in some cases, it can be seen in layers up to 14 weeks of age.

Cause of Gumboro Disease

The disease is caused by a birnavirus, specifically the Infectious Bursal Disease Virus (IBDV).

Virus Characteristics

• Serotypes: Two serotypes exist—Serotype 1 and Serotype 2. Only Serotype 1 of the Infectious bursal disease virus is pathogenic to chickens.

• Strain Variation:

  • Some strains cause mild disease with low mortality.

  • Others are highly virulent, leading to 50% or higher mortality rates.

• Tropism: The virus primarily targets the bursa of Fabricius, leading to its destruction and immunosuppression.

• Stability: IBDV is highly resistant to heat, disinfectants, and environmental conditions, making it difficult to eradicate from infected farms.

• Shedding: Infected birds excrete the virus in feces for 10–14 days, contaminating their environment.

Transmission and Spread

• The virus spreads mainly orally through contaminated feed, water, litter, and droppings.

• It is highly resistant in poultry farms and can persist in poultry houses for up to 122 days after an outbreak.

• Water, feed, and droppings in infected farms remain contagious for over 52 days.

Clinical Signs of Gumboro Disease

The severity of symptoms depends on the virulence of the virus strain, the bird’s age, and its maternal antibody levels.

Severe Form (3 to 6 weeks of age)

• Vent pecking (early symptom).

• Depression, ruffled feathers, and closed eyes.

• White watery diarrhea and soiled vents.

• Loss of appetite and trembling.

• Lying down in exhaustion and unwillingness to move.

• Mortality: Ranges from 0% to 50% (severe strains cause 90–100% mortality).

Mild Form

• No noticeable clinical signs except poor growth.

The course of the Disease

• The disease progresses rapidly, with infected birds either recovering or dying within 5–7 days.

Postmortem Findings

Lesions in affected birds are characteristic and help in diagnosing the disease.

Diagnosis of Gumboro Disease

• Postmortem Examination: Characteristic bursal lesions confirm the disease.

• Laboratory Tests:

  • Enzyme-linked immunosorbent Assay (ELISA) for IB virus detection.

  • Virus Isolation from infected tissue.

Differential diagnoses of Gumboro disease:

• Marek’s disease

• Aflatoxicosis

• Inclusion body hepatitis

• IBDV vaccination

• stress

Treatment

• No specific treatment is available for Gumboro disease.

• Supportive care (electrolytes, vitamins) can help reduce mortality.

Prevention and Control

1. Vaccination

• Breeder Vaccination: Ensures maternal antibodies are passed to chicks.

• Live Attenuated Vaccines: Used in young chicks by way of eye drops, in drinking water, and subcut at the age of 1-21 days old.

• Killed Vaccines: Boost immunity in breeders.

2. Biosecurity Measures

• Strict farm hygiene and sanitary precautions to prevent virus spread.

• Regular disinfection of poultry houses with effective virucidal agents.

About the outbreak of IBD

Infectious Bursal Disease (IBD) outbreaks continue to affect poultry worldwide, particularly young chickens. The disease is caused by the IBD virus, which targets the bursa of Fabricius, a critical immune organ, leading to immunosuppression. Recent outbreaks have been reported in various countries, with novel strains of the virus emerging in regions like China, causing more severe impacts. Despite widespread vaccination efforts, IBD remains a challenge due to its ability to cause subclinical infections, which makes it difficult to monitor. These outbreaks emphasize the need for improved biosecurity measures and ongoing research to better control and prevent IBD in poultry.

Modern Research on Infectious Bursal Disease in Poultry

Infectious Bursal Disease (IBD), also known as Gumboro disease, is a highly contagious viral infection caused by the Infectious Bursal Disease Virus (IBDV), a member of the Birnaviridae family. Primarily affecting young chickens, IBD targets the bursa of Fabricius, a key immune organ, leading to immunosuppression and increased susceptibility to secondary infections. In the context of splenomegaly, IBD is significant because it can cause initial spleen enlargement followed by atrophy, reflecting its complex impact on the immune system. Recent research has advanced our understanding of IBD’s viral evolution, pathogenesis, diagnostics, and control strategies, offering new tools to manage this global poultry health challenge.

Viral Evolution and Strain Diversity

 A 2023 study in China identified novel variant IBDV strains in vaccinated flocks, characterized by unique antigenic profiles and severe bursal damage without significant mortality. These strains showed less than 98% amino acid similarity to classic strains in the VP2 protein, critical for antigenicity. Similarly, a 2021 Latvian study reported a reassortant IBDV with a very virulent (vvIBDV) segment A and a classic-like segment B, causing splenomegaly and bursal atrophy. These findings highlight the virus’s adaptability, which challenges vaccine efficacy and contributes to subclinical infections that exacerbate splenic changes.

Phylogenetic studies reveal regional strain variations. In Argentina, a 2023 analysis noted a shift to genogroup 2 IBDV strains, with an evolutionary rate of 1.7 × 10⁻³ substitutions/site/year, replacing older genogroups. In Malaysia, diverse vvIBDV strains were detected in 2021, emphasizing the need for region-specific vaccines. Whole-genome sequencing is now a cornerstone of IBD research, enabling precise tracking of viral evolution and informing targeted control measures.

Pathogenesis and Splenic Involvement

IBDV infects B-lymphocytes in the bursa of Fabricius, peaking in 3–6-week-old chickens when bursal tissue is most developed. This leads to lymphoid depletion, bursal atrophy, and immunosuppression, increasing risks of secondary infections like Escherichia coli, which can further contribute to splenomegaly. A 2022 study in Argentina found that chicken genetic background influences bursal inflammation and splenic responses, with susceptible breeds showing pronounced splenomegaly early in infection. Transcriptomic research in 2023 revealed that vvIBDV triggers intense proinflammatory responses, correlating with initial spleen enlargement followed by atrophy as lymphoid tissue is depleted.

Subclinical IBD, common in chicks under three weeks, causes significant B-cell loss without overt clinical signs, complicating detection. A 2020 study noted that variant strains induce rapid bursal and splenic changes, with splenomegaly as an early marker of infection. These insights underscore IBD’s role in splenic pathology and the need for early monitoring to mitigate immunosuppression.

Diagnostic Innovations

Accurate diagnosis is critical for managing IBD and its splenic effects. Real-time reverse transcription-polymerase chain reaction (RT-PCR) is the gold standard, detecting IBDV RNA in bursal or splenic tissue with high sensitivity. A 2023 Indonesian study used RT-PCR to identify variant strains, noting macroscopic lesions like splenic mottling and bursal hemorrhages. High-throughput sequencing, as applied in Latvia, provides full-genome data, enabling strain classification and outbreak tracing.

Serological tools, such as enzyme-linked immunosorbent assay (ELISA), measure maternally derived antibodies (MDA) and vaccine responses. A 2020 Nigerian study detected IBDV antibodies in wild birds, suggesting their role as reservoirs, with seroprevalence of 3–7%. Histopathology remains essential, revealing lymphoid depletion and splenic changes. These diagnostic advances facilitate early detection, crucial for controlling IBD’s impact on spleen health and overall immunity.

Vaccine Development and Challenges

Vaccination is the primary defense against IBD, but evolving strains pose challenges. Traditional live-attenuated vaccines, effective against classic IBDV, often fail against vvIBDV or variant strains. A 2016 South Korean study showed that herpesvirus of turkey (HVT)-IBD vector vaccines provide robust protection against vvIBDV, even in the presence of high MDA. A 2023 trial of oil-emulsion vaccines demonstrated complete protection against homologous variant strains, inducing strong VP2-specific antibodies.

Maternally derived antibodies, protective above an ELISA titer of 400, can interfere with live vaccines, reducing efficacy in young chicks. Recombinant VP2-based vaccines, explored in 2017, show promise for broad-spectrum protection. However, vaccine-induced bursal damage remains a concern, prompting research into low-attenuated strains. These advancements are critical for preventing IBD-related splenomegaly and immunosuppression.

Wild Birds and Biosecurity

Wild birds may serve as IBDV reservoirs, complicating control efforts. A 2020 global review reported low sero-viroprevalence in species like pigeons, but studies in Nigeria confirmed antibodies, indicating natural exposure. Enhanced biosecurity, including restricted farm access and vector control, is essential to prevent viral spillover between poultry and wild populations, reducing risks of splenic and bursal pathology.

Future Directions

Current research aims to develop universal vaccines targeting conserved IBDV epitopes, minimizing strain-specific limitations. CRISPR-based gene editing is being explored to enhance chicken resistance by modifying immune genes. Portable RT-PCR kits are under development to improve diagnostics in resource-limited settings. Integrating genomic surveillance, biosecurity, and advanced vaccines will be key to managing IBD’s evolving threat and its impact on splenic health.

Frequently Asked Questions (FAQs)

Q1: At what age does Gumboro disease affect poultry?

A1: It commonly affects birds between 18 to 40 days of age but can occasionally be seen in layers up to 14 weeks of age.

Q2: Is Gumboro disease fatal?

A2: Yes, depending on the virus strain. Some strains cause mild symptoms, while highly virulent strains can lead to 90–100% mortality.

Q3: Can antibiotics treat Gumboro disease?

A3: No, antibiotics do not work against viruses. However, supportive therapy can help reduce secondary bacterial infections.

Q4: How long does the virus persist in the environment?

A4: The virus can survive in poultry houses for up to 122 days and in infected litter, feed, and water for over 52 days.

Q5: What is the best method to control Gumboro disease?

A5: Vaccination is the most effective control measure, along with strict biosecurity and sanitation.

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References

• Kahn, C. M., & Line, S. (Eds.). (2010). The Merck Veterinary Manual (10th ed.). Merck & Co., Inc.

• Vegad, J. L. (2004).  Atlas of Poultry Diseases