What Is Rhodococcus Equi Biology Essay


Rhodococcus equi is a gram positive cocco-bacillus soil-borne microorganism. It is a bacteria which causes chronic bronchopneumonia in foals under 5 months old with immature immune systems and waning maternal immunity and has recently been found to also affect wild and domestic pigs, cattle and immunocomprimised humans. It is an opportunistic pathogen which is an emerging human infectious disease that is potentially life threatening.

Route of infection is respiratory and alimentary. Primary route of infection is through inhalation of dust. Exposure to domestic horses and pigs may play a role in the transmission of the pathogen to humans, although many cases of infection have denied any animal contact (Manosuthi et al 2009). Horses almost exclusively carry a virulent strain, the virulent factor is yet to be explained but believed to be plasmids that encode VapA antigen, presence of a polysaccharide capsule which may prevent phagocytosis by innate immune system and cell wall mycolic acids (Dawson et al 2009). Humans, goats and occasionally foals can have strains that lack the virulent factor but still cause disease. Symptoms include chronic and severe pyogranulomatous pneumonia, ulcerative colitis, lymphadenitis and polyarthritis. Incidents occur mainly in the summer months which are peak foaling period and optimum conditions for the bacterium.

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The bacteria behave as facultative intracellular pathogens. It resists the innate immune system by inhibiting phagolysosome fusion within alveolar macrophages. Virulent strains are able to replicate within approximately 6-8hrs inside macrophages (Hondalus 1997) Infection can cause pyogranulamatous pneumonia characterized by granuloma, a mass of immune cells formed when immune system is unable to destroy the bacteria. Advancement of disease causes necrosis and destruction of lung cells, although this appears to be present only in virulent plasmid-positive strains. The disease has also been found to disseminate to other areas causing infections of the intestinal tract, due to ingestion of infected sputum.

Dissemination from lungs to other sites (humans and foals)

With increased human cases in severely immunocomprimised individuals R. equi has proven difficult to treat with reports of over 60% fatality rate. This may be due to compromised immune systems and bacterial resistance to antibiotics (Meusse et al 2007)

The characteristic pathological findings associated with infection with previous termRhodococcusnext term spp, collectively termed malakoplakia, were seen in biopsy specimens from our case ([Figure 1], [Figure 3] and [Figure 4]). Although features of malakoplakia are preserved across affected tissue types, they are most commonly seen in settings of R previous termequinext term-induced pulmonary disease. Malakoplakia is generally characterised by a dense infiltration of foamy histiocytes with intracellular coccobacilli and scattered concentric basophilic inclusions termed Michaelis-Gutmann bodies,19 which likely represent an artifact of impaired degradation of ingested bacteria in infected macrophages.20 G Yuoh, MG Hove, J Wen and AK Haque, Pulmonary malakoplakia in acquired immunodeficiency syndrome: an ultrastructural study of morphogenesis of Michaelis-Gutmann bodies, Mod Pathol 9 (1996), pp. 476â€"483. View Record in Scopus | Cited By in Scopus (20)20 Although malakoplakia is not specific to infection with R previous termequinext term, because Mycobacterium tuberculosis, Pasteurella multocida, and Escherichia coli can cause similar pathological changes, it is often associated with R previous termequinext term disease in immunocompromised patients.2

R previous termequinext term is thought to possess several virulence factors that likely contribute to the pathological changes associated with this disease process. The most important virulence determinant for infection of animals with R previous termequinext term is its ability to survive in macrophages. Cultured foal alveolar macrophages show effective uptake of opsonised R previous termequinext term, but Zink and colleagues22 MC Zink, JA Yager, JF Prescott and BN Wilkie, In vitro phagocytosis and killing of Corynebacterium previous termequinext term by alveolar macrophages of foals, Am J Vet Res 46 (1985), pp. 2171â€"2174. View Record in Scopus | Cited By in Scopus (10)22 describe that 75% of phagocytosed organisms remain viable after incubation within macrophages for 4 h. Electron microscopy studies of macrophages infected with R previous termequinext term show inhibition of phagosome-lysosome fusion, leading to intracellular proliferation of organisms and subsequent destruction of infected cells.23 The exact mechanism underlying the survival of R previous termequinext term in macrophages is unknown, although inadequate acidification of phagolysosomes seems to lead to ineffective degradation of phagocytosed bacilli.24

Additional virulence factors that might allow R previous termequinext term to proliferate as an intracellular pathogen have been identified in veterinary settings, but little is known about the correlation of these findings with the pathogenesis of R previous termequinext term infection in human beings. For instance, the vapA gene belongs to a large ubiquitous R previous termequinext term plasmid that encodes a pathogenicity island consisting of multiple expressed genes.25 R previous termequinext term strains missing the virulence plasmid fail to survive in macrophages, and are avirulent in mice and foals.26 However, a human study of 39 R previous termequinext term isolates from immunocompromised patients showed that only 21% contained the full 85 kb virulence plasmid including vapA.27 Although all isolates were deemed causative of overt clinical disease in the original human host, only isolates containing the full plasmid were virulent when inoculated into mice.27 These findings suggest that pathogenesis of disease in human beings, especially in the populations of immunocompromised patients, likely differs substantially from that seen in animal species.

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Similarly, little is known about the human immune response to R previous termequinext term, because most available information are immunological studies of mouse models and infected foals. Nonetheless, important information regarding cellular immunity to R previous termequinext term infection has been generated from studies of immune-depleted mice. Poor outcomes in CD4 and CD8 deficient mice show the importance of these T-cell subsets in the immune response to R previous termequinext term infection.[28] and [29] These data, especially in context of other mouse studies showing that an interferon-γ driven T-helper-1 response is more protective than a response skewed towards T-helper-2 cells,30 suggest that cell-mediated immunity is essential for control of R previous termequinext term infection. This seems consistent with our understanding of immune responses to other intracellular pathogens, and confirms our clinical observations that have historically placed patients with defects of cell-mediated immunity due to transplant-related immunosuppression or HIV at higher risk of acquisition of this organism.