Rhodococcus equi
| Rhodococcus equi | |
|---|---|
 |
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| Scientific classification | |
| Kingdom: | Bacteria |
| Phylum: | Actinobacteria |
| Class: | Actinobacteria |
| Order: | Actinomycetales |
| Suborder: | Corynebacterineae |
| Family: | Nocardiaceae |
| Genus: | Rhodococcus |
| Species: |
Rhodococcus equi Magnusson 1923) Goodfellow & Alderson 1977 |
Goodfellow & Alderson 1977
Rhodococcus equi is a Gram-positive coccobacillus bacterium. The organism is commonly found 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%.R. equi is an important pathogen causing pneumonia in foals. Since 2008, R. equi has been known to infect wild boar and domestic pigs. In addition, R. equi can infect humans. At-risk groups are immunocompromised people, such as HIV-AIDS patients or transplant recipients. Rhodococcus infection in these patients resemble clinical and pathological signs of pulmonary tuberculosis. It is facultative intracellular.
Taxonomically, R. equi has been categorized as Prescottia equi,Corynebacterium equi, Bacillus hoagii, Corynebacterium purulentus, Mycobacterium equi, Mycobacterium restrictum, Nocardia restricta, and Proactinomyces restrictus.
The most common route of infection in horses is likely via inhalation of contaminated dust particles. Inhaled virulent strains of R. equi are phagocytosed by alveolar macrophages. During normal phagocytosis, bacteria are enclosed by the phagosome, which fuses with the lysosome to become a phagolysosome. The internal environment of the phagolysosome contains nucleases and proteases, which are activated by the low pH of the compartment. 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. Additionally, the respiratory burst is inhibited. This allows R. equi to multiply within the phagosome where it is shielded from the immune system by the very cell that was supposed to kill it. After about 48 hours, the macrophage is killed by necrosis, not apoptosis. Necrosis is pro-inflammatory, attracting additional phagocytic cells to the site of infection, eventually resulting in massive tissue damage.
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