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Rhodococcus equi
Scientific classification
Kingdom: Bacteria
Phylum: Actinobacteria
Order: Actinomycetales
Suborder: Corynebacterineae
Family: Nocardiaceae
Genus: Rhodococcus
Species: Rhodococcus equi
Magnusson 1923)

Goodfellow & Alderson 1977

Rhodococcus equi is a Gram-positive coccobacillus bacterium. The organism commonly lives in dry and dusty soil and can be important for diseases of domesticated animals (horses and goats). The frequency of infection can reach near 60 percent[1]. R. equi is an important pathogen of pneumonia of foals. Since 2008, it is also known that R. equi can infect wild boars in addition to domestic pigs.[2] In addition, the pathogen can infect humans. The most endangered groups are immunocompromised people and HIV-AIDS-patients. Rhodococcal infection in these groups of patients resemble clinical and pathological signs of pulmonary tuberculosis.

Taxonomically, R. equi can have the synonyms Corynebacterium equi, Bacillus hoagii, Corynebacterium purulentus, Mycobacterium equi, Mycobacterium restrictum, Nocardia restricta and Proactinomyces restrictus.

Contents

Hosts

Virulence

The most common route of infection in horses is probably through inhalation of contaminated dust particles by foals. Inhaled virulent strains of R. equi are phagocytosed by alveolar macrophages, which aim to protect the body from invading micro organisms. Following phagocytosis, bacteria reside inside the phagosome, which fuses with the lysosome releasing nucleases, proteases into the phagosome. In addition, this compartment is acidified, resulting in activation of proteases. The macrophage produces bacteriocidal compounds (e.g., oxygen radicals) following the respiratory burst. However, like its close relative Mycobacterium tuberculosis, R. equi prevents the fusion of the phagosome with the lysosome, and acidification of the phagosome and the respiratory burst do not occur. This allows R. equi to multiply within the phagosome, and is thus shielded from the immune system by the very cell that was supposed to kill it [3]. After about 48 hours the macrophage is killed by necrosis, not apoptosis[4]. Necrosis is pro-inflammatory attracting other phagocytic cells to the site of infection, eventually resulting massive tissue damage.

Virulence plasmid

All strains isolated from foals and the majority of human, cattle and pig isolates harbour a large plasmid. This plasmid has been shown to be essential to infect foals, and presumably plays a similar role for infection of other hosts, although this has not been established yet. Strains that lack the virulence plasmid are unable to proliferate in macrophages. This virulence plasmid has been characterised in detail from equine and porcine strains, although only the former has been functionally characterised [5][6]. These circular plasmids consist of a conserved backbone that is responsible for replication and bacterial conjugation of the plasmid. This part of the plasmid is highly similar to plasmids found in other non-pathogenic rhodococci. In addition to this conserved region, the virulence plasmids contain a highly variable region that has undergone substantial genetic rearrangements including inversion and deletions. This region has a different GC-content than the rest of the plasmid, and is flanked by genes associated with mobile genetic elements. It is therefore assumed to be derived from a different bacterial species than the backbone of the plasmid via lateral gene transfer.

Pathogenicity island

The variable region of the virulence plasmid contain genes that are highly expressed following phagocytosis of R. equi by macrophages [7]. Furthermore, deletion of vapA, a gene within the variable region of the equine plasmid rendered the resulting strain avirulent [8]. It is therefore believed that this variable region is a pathogenicity island that contains genes that are essential for virulence.

A hallmark of the pathogenicity island is that many genes within it do not have homologues in other species. The most notable of these are the vap genes which stands for Virulence Associated Protein. All foals infected with R. equi produce high levels of antibodies directed to VapA, the first vap gene to be characterised. In addition to vapA, the pathogenicity island encodes a further five full lenght vap homologues, one truncated vap gene and two pseudo vap genes. The porcine pathogenicity island contains five full length vap genes including the vapA homologue vapB. In addition to these unique genes the pathogencity island contains genes that have a known function, in particular two regulatory genes encoding the LysR-type regulator VirR and the response regulator Orf8. These two proteins have been shown to control expression of a number of pathogenicity island genes including vapA[9]. Other genes have similarities to transport proteins and enzymes. However, the functionality of these genes has not yet been established, nor how the proteins encoded within pathogenicity island subvert the macrophage.

References

  1. ^ G. Muscatello, D. P. Leadon, M. Klay, A. Ocampo-Sosa, D. A. Lewis, U. Fogarty, T. Buckley, J. R. Gilkerson, W. G. Meijer, and J. A. Vázquez-Boland. (2007) Rhodococcus equi infection in foals: the science of 'rattles'. Equine Vet.J. 39:470-478. In: PMID 17910275
  2. ^ Makrai, L. et al. (2008): Isolation and characterisation of Rhodococcus equi from submaxillary lymph nodes of wild boars (Sus scrofa). In: Vet Microbiol. PMID 18499361 doi:10.1016/j.vetmic.2008.04.009
  3. ^ M. K. Hondalus and D. M. Mosser. Survival and replication of Rhodococcus equi in macrophages. Infect.Immun. 62:4167-4175, 1994. In: PMID 7927672
  4. ^ A. Lührmann, N. Mauder, T. Sydor, E. Fernandez-Mora, J. Schulze-Luehrmann, S. Takai, and A. Haas. Necrotic death of Rhodococcus equi-infected macrophages is regulated by virulence-associated plasmids. Infect.Immun. 72 (2):853-862, 2004. In: PMID 14742529
  5. ^ M. Letek, A. A. Ocampo-Sosa, M. Sanders, U. Fogarty, T. Buckley, D. P. Leadon, P. Gonzalez, M. Scortti, W. G. Meijer, J. Parkhill, S. Bentley, and J. A. Vázquez-Boland. Evolution of the Rhodococcus equi vap pathogenicity island seen through comparison of host-associated vapA and vapB virulence plasmids. J.Bacteriol. 190 (17):5797-5805, 2008. In: PMID 18606735
  6. ^ S. Takai, S. A. Hines, T. Sekizaki, V. M. Nicholson, D. A. Alperin, M. Osaki, D. Osaki, M. Nakamura, K. Suzuki, N. Ogino, T. Kakuka, H. Dan, and J. F. Prescott. DNA sequence and comparison of virulence plasmids from Rhodococcus equi ATCC 33701 and 103. Infect.Immun. 68:6840-6847, 2000. In: PMID 11083803
  7. ^ J. Ren and J. F. Prescott. Analysis of virulence plasmid gene expression of intra-macrophage and in vitro grown Rhodococcus equi ATCC 33701. Vet.Microbiol. 94 (2):167-182, 2003. In: 12781484
  8. ^ S. Jain, B. R. Bloom, and M. K. Hondalus. Deletion of vapA encoding Virulence Associated Protein A attenuates the intracellular actinomycete Rhodococcus equi. Mol.Microbiol 50 (1):115-128, 2003. In: PMID 14507368
  9. ^ D. A. Russell, G. A. Byrne, E. P. O'Connell, C. A. Boland, and W. G. Meijer. The LysR-Type transcriptional regulator VirR is required for expression of the virulence gene vapA of Rhodococcus equi ATCC 33701. J.Bacteriol. 186:5576-5584, 2004. In: PMID 15317761

Literature

  • Monika Venner und Erich Klug: Die Rhodococcus-equi-Pneumonie beim Fohlen: Diagnose, Therapie, Prophylaxe In: Pferde spiegel Nummer 4, 2005. Seiten 155-158 PDF
  • J. Ashour and M. K. Hondalus: Phenotypic mutants of the intracellular actinomycete Rhodococcus equi created by in vivo Himar1 transposon mutagenesis. In: Journal of Bacteriology. Volume 185, Nummer 8, April 2003. Seiten 2644-2652. doi:10.1128/JB.185.8.2644-2652.2003
  • A. Triskatis: Semiquantitative Bestimmung von Antikörpern gegen Rhodococcus equi in Serum und Klolostrum bei Stuten und Fohlen mittels ELISA und der Vergleich mit Befunden der Lungenuntersuchung PDF
  • Letek M et al.: Evolution of the Rhodococcus equi vap Pathogenicity Island Seen through Comparison of Host-Associated vapA and vapB Virulence Plasmids. In: Journal of Bacteriology. Volume 190, Number 17, September 2008. 5797–5805.
  • G. Muscatello, D. P. Leadon, M. Klay, A. Ocampo-Sosa, D. A. Lewis, U. Fogarty, T. Buckley, J. R. Gilkerson, W. G. Meijer, and J. A. Vázquez-Boland. (2007) Rhodococcus equi infection in foals: the science of 'rattles'. Equine Vet.J. 39:470-478.
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