Abstract: Inhalation of the soil-borne organism, Rhodococcus equi, can lead to a chronic and severe pyogranulomatous pneumonia in young horses and immunocompromised people. In addition, ulcerative colitis is a common sequela to infection in foals, and dissemination from the lung to other body sites is not uncommon in either the horse or man. Although the facultative intracellular bacterium is susceptible to neutrophil-mediated killing, it is able to resist innate macrophage defenses and establish residence within the intracellular environment of that phagocyte. Definitive virulence factors of R. equi have not yet been determined, but potential candidates include capsular polysaccharide, the exoenzyme cholesterol oxidase, cell wall mycolic acids, and the products encoded by a virulence-associated plasmid. The ability to replicate within the macrophage is associated with virulence, and correlates in animals with the possession of a large plasmid and expression of the plasmid-encoded, surface-expressed lipoprotein, VapA. All strains of R. equi isolated from horses with clinical disease possess a large plasmid and express VapA antigens. In addition, bacterial clearance and granuloma development in mice is linked to plasmid possession and VapA expression. Plasmid containing strains replicate within the tissues of the mouse. whereas plasmid-cured strains are rapidly cleared. At present, the function of the VapA protein is unknown. In contrast to what is observed in the foal, only a small percentage of R. equi strains isolated from humans with rhodococcal disease express VapA antigens, although a high proportion of others express a related protein which is associated with reduced virulence and is also plasmid-encoded. In a limited number of plasmid-negative human isolates, virulence has been linked to beta-lactam resistance, and preliminary evidence suggests that the phenotype may be phage encoded. It is likely that the immune status of the patient can influence whether a particular strain of R. equi is able to produce clinical disease, and certainly experimental infection in mice has confirmed that an intact cellular immune response is necessary for clearance of the organism.
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The research investigates the behavior of the bacterium Rhodococcus equi, which can cause severe pneumonia in young horses and immunocompromised individuals, detailing how it resists immune defenses and its potential virulent factors.
Understanding Rhodococcus equi’s Pathogenesis and Virulence
When the soil-borne organism Rhodococcus equi is inhaled, it can result in chronic and severe pyogranulomatous pneumonia, a type of severe lung infection primarily seen in young horses and immunocompromised individuals. This bacteria also has the capacity to cause ulcerative colitis, a type of inflammatory bowel disease, particularly noticeable in foals, or young horses.
Rhodococcus equi can also spread from the lungs to other parts of the body in both human and equine hosts. Although susceptible to killing by neutrophils, a type of white blood cell, Rhodococcus equi can resist the innate defenses of macrophages, another type of immune cell, and take up residence within them.
Virulence Factors of Rhodococcus equi
The research has not definitively identified the bacterium’s virulence factors but suggested potential elements include capsular polysaccharide, the exoenzyme cholesterol oxidase, cell wall mycolic acids, and products encoded by a virulence-associated plasmid.
The bacteria’s ability to replicate within a macrophage appears to be linked with virulence. This ability has been observed in animals to be associated with possession of a large plasmid and expression of lipoprotein, known as VapA.
All strains of R. equi identified from clinically ill horses possess a large plasmid and express VapA antigens.
Role of VapA and Plasmids
In studies using mice, the progression of bacterial clearance and granuloma development, a form of inflammation, is linked to both the possession of a plasmid and expression of VapA. Plasmid-containing strains of R. equi are able to replicate within mouse tissue. Conversely, strains without a plasmid are rapidly cleared from the system.
The exact function of the VapA protein, however, is currently unknown.
Similar virulence patterns have not been observed in humans, where only a small percentage of R. equi strains produce VapA antigens. A more significant number of human strains express a related protein, also encoded by the plasmid, but associated with reduced virulence.
Influence of Immune Status and Potential Resistance Factors
In a small number of human cases without plasmid, virulence has been linked to beta-lactam resistance, suggesting the phenotype might be phage encoded. However, this is based on preliminary evidence and needs further corroboration.
The research notes that an individual’s immune status may influence whether a strain of R. equi can cause clinical disease. This idea has been confirmed in mice, where an intact cellular immune response has been found necessary for the clearance of the bacteria from the body.
Cite This Article
APA
Hondalus MK.
(1997).
Pathogenesis and virulence of Rhodococcus equi.
Vet Microbiol, 56(3-4), 257-268.
https://doi.org/10.1016/s0378-1135(97)00094-1
Howard Hughes Medical Research Institute, Albert Einstein College of Medicine, Bronx, NY 10461, USA. hondalus@aecom.yu
MeSH Terms
Actinomycetales Infections / epidemiology
Actinomycetales Infections / physiopathology
Actinomycetales Infections / veterinary
Animals
Antigens, Bacterial / biosynthesis
Bacterial Proteins / biosynthesis
Horse Diseases
Horses
Humans
Immunocompromised Host
Lipoproteins / biosynthesis
Macrophages / microbiology
Mice
Phagocytes / microbiology
Phagocytosis
Rhodococcus equi / pathogenicity
Rhodococcus equi / physiology
Virulence
Virulence Factors
References
This article includes 77 references
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This article has been cited 42 times.
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