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Colonisation of Pathogens01:25

Colonisation of Pathogens

Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...
Infection01:20

Infection

When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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Microbial Interactions: Parasitism01:22

Microbial Interactions: Parasitism

Parasitism is a form of microbial interaction in which parasitic microbes exploit a host organism for nutrients and shelter, often at the host's expense. Unlike mutualistic relationships, where both organisms benefit, parasitism benefits only the parasite and harms the host.Classification of ParasitesMicrobial parasites are broadly classified based on their location relative to the host.Ectoparasites remain on the host’s surface, such as the skin or outer tissues, drawing nutrients...
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Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
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Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
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Related Experiment Video

Updated: May 12, 2026

An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis
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An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis

Published on: October 4, 2018

Infectious Bursal Disease: a complex host-pathogen interaction.

Fiona Ingrao1, Fabienne Rauw, Bénédicte Lambrecht

  • 1Avian Virology & Immunology Unit, Veterinary and Agrochemical Research Centre, Brussels, Belgium.

Developmental and Comparative Immunology
|April 10, 2013
PubMed
Summary

Infectious Bursal Disease Virus (IBDV) severely impacts chickens by damaging their immune system, leading to immunosuppression and increased susceptibility to other infections. Understanding IBDV

Keywords:
Avian cytokinesBursa of fabriciusIBDImmunosuppressionInnate immunityVaccination

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Area of Science:

  • Avian immunology
  • Virology
  • Immunopathology

Background:

  • Infectious Bursal Disease (IBD) is caused by a highly resistant virus (IBDV) that targets the chicken immune system.
  • IBDV infection leads to B lymphocyte destruction, T cell attraction, and macrophage activation, causing complex immunosuppression.
  • The exact molecular basis of IBDV pathogenicity and clinical outcomes, including death, remain poorly understood despite extensive research.

Purpose of the Study:

  • To elucidate the immunological mechanisms underlying Infectious Bursal Disease (IBD) in chickens.
  • To investigate the role of innate immune responses and cytokine storms in IBDV pathogenesis.
  • To explore the impact of IBDV-induced immunosuppression on cell-mediated immunity and vaccine efficacy.

Main Methods:

  • Analysis of immune cell interactions (B lymphocytes, T cells, macrophages) following IBDV infection.
  • Investigation of promediator production and cytokine storm induction during early infection stages.
  • Assessment of immunosuppression effects on cell-mediated immunity (CMI) and subsequent vaccination responses.

Main Results:

  • IBDV infection causes direct and indirect immunosuppression by targeting immune cells and disrupting immune network interactions.
  • An exacerbated innate immune response, characterized by a cytokine storm, plays a significant role in early IBDV infection.
  • IBDV impacts both humoral and cell-mediated immunity, increasing disease severity and affecting vaccine effectiveness.
  • Parental antibody interference is a major challenge for IBDV vaccination programs.

Conclusions:

  • IBDV infection results in significant immunosuppression, compromising the chicken's overall immunocompetence and increasing susceptibility to secondary infections.
  • Recent advancements in avian immunology provide better tools for understanding and measuring IBDV-induced immunosuppression.
  • Novel vaccine strategies, including recombinant HVT and immune complex vaccines, show promise for controlling IBDV, despite challenges like parental antibody interference.