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Veterinary research2004; 35(4); 383-396; doi: 10.1051/vetres:2004024

Rhodococcus equi.

Abstract: Rhodococcus equi is an important cause of subacute or chronic abscessating bronchopneumonia of foals up to 3-5 months of age. It shares the lipid-rich cell wall envelope characteristic of the mycolata, including Mycobacterium tuberculosis, as well as the ability of pathogenic members of this group to survive within macrophages. The possession of a large virulence plasmid in isolates recovered from pneumonic foals is crucial for virulence. The plasmid contains an 27 kb pathogenicity island (PI) that encodes seven related virulence-associated proteins (Vaps), including the immunodominant surface-expressed protein, VapA. Only PI genes are differentially expressed when the organism is grown in macrophages in vitro. Ten of the PI genes, including six Vap genes, have signal sequences, suggesting that they are exported from the cell to interact with the macrophage. Different PI genes are regulated by temperature, pH, iron, oxidative stress and probably also by magnesium, all environmental changes encountered after environmental R. equi are inhaled in dust and are ingested into macrophages in the lung. The basis of pathogenicity of R. equi is its ability to multiply in and eventually to destroy alveolar macrophages. Infectivity is largely or exclusively limited to cells of the monocyte-macrophage lineage. Current evidence suggests that infection of foals with virulent R. equi results in some foals in subversion of cell-mediated immunity and development of an ineffective and sometimes lethal Th2-based immune response. Significant progress has been made recently in the development of R. equi-E. coli shuttle vectors, transformation and random and site specific mutagenesis procedures, all of which will be important in molecular dissection of the mechanisms by which R. equi subverts normal macrophage killing mechanisms and cell-mediated immunity.
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Publication Date: 2004-07-09 PubMed ID: 15236672DOI: 10.1051/vetres:2004024Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The researchers in this study have explored how Rhodococcus equi, a bacteria that frequently causes bronchopneumonia in young foals, multiplies within and eventually destroys alveolar macrophages, which are immune cells in the lungs. They’ve found that the bacteria’s pathogenicity is primarily limited to cells from the monocyte-macrophage lineage, and that a significant virulence factor is a large plasmid in the bacteria that contains a pathogenicity island (PI) encoding for several virulence-associated proteins (Vaps).

Importance of Rhodococcus equi

  • Rhodococcus equi is significantly detrimental to the health of young foals, causing severe bronchopneumonia that is hard to control and treat.
  • This bacterium belongs to the mycolata group and shares key characteristics with pathogenic members, such as Mycobacterium tuberculosis. They can survive within macrophages, which is an unusual feature and makes them particularly harmful.

Role of the Plasmid and Pathogenicity Island

  • R. equi has a large virulence plasmic crucial for its pathogenicity.
  • This plasmid contains a 27 kb pathogenicity island that encodes seven related virulence-associated proteins (Vaps), including the immunodominant surface-expressed protein, VapA.
  • Only genes on the PI are differently expressed when the bacterium grows in macrophages in vitro, signifying the importance of these genes in the survival and multiplication of the bacteria within these immune cells.
  • Among the PI genes, six of them are Vap genes with signal sequences, suggesting they are likely exported from within the bacterium to carry out interactions with the macrophage.

Environmental Regulation and Pathogenesis

  • Various environmental changes including temperature, pH, iron, oxidative stress, and potentially magnesium regulate the expression of different PI genes.
  • The main pathogenicity of R. equi lies in its ability to multiply within and eventually destroy alveolar macrophages. The vulnerability seems to be particularly high for cells from the monocyte-macrophage lineage.
  • The research suggests that infection with virulent R. equi can circumvent normal cell-mediated immunity in some foals, leading to an ineffective and sometimes lethal Th2-based immune response.

Progress in Research

  • The study concludes that significant strides have been taken in the development of R. equi-E. coli shuttle vectors, transformation procedures, and random and specific mutagenesis.
  • These advancements will aid in further molecular dissection of how exactly this bacterium circumvents normal macrophage killing mechanisms and cell-mediated immunity.

Cite This Article

APA
Meijer WG, Prescott JF. (2004). Rhodococcus equi. Vet Res, 35(4), 383-396. https://doi.org/10.1051/vetres:2004024

Publication

Veterinary research
ISSN: 0928-4249
NlmUniqueID: 9309551
Country: England
Language: English
Volume: 35
Issue: 4
Pages: 383-396

Researcher Affiliations

Meijer, Wim G
  • Department of Industrial Microbiology, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin 4, Ireland.
Prescott, John F

    MeSH Terms

    • Actinomycetales Infections / microbiology
    • Actinomycetales Infections / veterinary
    • Animals
    • Animals, Newborn
    • Bronchopneumonia / microbiology
    • Bronchopneumonia / veterinary
    • Horse Diseases / immunology
    • Horse Diseases / microbiology
    • Horses
    • Rhodococcus equi / pathogenicity

    Citations

    This article has been cited 45 times.
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