Mycoplasma Gallisepticum Pathogenesis in Poultry Systems

Mycoplasma gallisepticum is a cell wall–deficient bacterium that colonises the mucosal surfaces of the avian respiratory tract, causing chronic respiratory disease in chickens and other poultry species. Pathogenesis begins with adhesion to tracheal epithelial cells, mediated by specialized surface proteins and lipid‐associated membrane proteins, which trigger a cascade of host responses. Antigenic variation of surface antigens enables the pathogen to evade humoral immunity and persist within the host. Upon colonisation, M. gallisepticum activates innate immune receptors, notably Toll‐like receptor 2, leading to nuclear factor κB (NF-κB)–driven production of pro‐inflammatory cytokines. This inflammatory milieu, together with oxidative stress and apoptosis induced in lymphoid organs such as the thymus and bursa of Fabricius, results in tissue damage, impaired mucociliary clearance and immune dysregulation. Chronic infection predisposes to secondary bacterial or viral co-infections, exacerbating pathology through pathways such as IL-17 signalling. The pathogen’s ability to manipulate host microRNAs and suppress key inflammatory mediators further contributes to persistent infection. These mechanisms lead to airsacculitis, tracheitis and pneumonia, causing reduced productivity and substantial economic losses in global poultry production. Control measures combine stringent biosecurity, antimicrobial therapies and vaccination, yet antigenic variation and incomplete vaccine efficacy remain significant challenges.

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Mycoplasma Gallisepticum Pathogenesis in Poultry Systems publication trend

The graph below shows the total number of articles in mycoplasma gallisepticum pathogenesis in poultry systems across all publications each year (not limited to Nature Index journals).

Technical terms

Antigenic variation: The process by which pathogens alter surface proteins to evade host immunity.

Lipid-associated membrane proteins (LAMPs): Surface lipoproteins that interact with host receptors to initiate inflammation.

Toll-like receptor 2 (TLR-2): An innate immune receptor that recognises bacterial lipoproteins and triggers NF-κB activation.

NF-κB: A transcription factor central to the induction of pro-inflammatory genes in response to infection.

JAK/STAT pathway: A key signalling cascade in cytokine receptor signalling that regulates gene expression during immune responses.

MicroRNA (miRNA): Small non-coding RNAs that modulate gene expression post-transcriptionally, influencing host–pathogen interactions.

Oxidative stress: An imbalance between reactive oxygen species production and antioxidant defences, leading to cellular damage.

References

1. Immune Evasion of Mycoplasma gallisepticum: An Overview. International Journal of Molecular Sciences (2024).
2. Research Progress in the Development of Vaccines against Mycoplasma gallisepticum and Mycoplasma synoviae. Microorganisms (2024).
3. Co-infection of Mycoplasma gallisepticum and Escherichia coli Triggers Inflammatory Injury Involving the IL-17 Signaling Pathway. Frontiers in Microbiology (2019).
4. Mycoplasma gallisepticum Lipid Associated Membrane Proteins Up-regulate Inflammatory Genes in Chicken Tracheal Epithelial Cells via TLR-2 Ligation through an NF-κB Dependent Pathway. PLOS ONE (2014).
5. Baicalin mitigated Mycoplasma gallisepticum-induced structural damage and attenuated oxidative stress and apoptosis in chicken thymus through the Nrf2/HO-1 defence pathway. Veterinary Research (2019).
6. Mycoplasma gallisepticum Infection Impaired the Structural Integrity and Immune Function of Bursa of Fabricius in Chicken: Implication of Oxidative Stress and Apoptosis. Frontiers in Veterinary Science (2020).
7. Infection, Transmission, Pathogenesis and Vaccine Development against Mycoplasma gallisepticum. Vaccines (2023).
8. Mycoplasma gallisepticum escapes the host immune response via gga-miR-365-3p/SOCS5/STATs axis. Veterinary Research (2022).