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 cellmediated 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.

Neumonía cavitada por Rhodococcus equi en paciente inmunocomprometido no infectado por virus de inmunodeficiencia humana: Caso clínico y revisión

“…El mecanismo de transmisión sería a través de su inhalación desde la tierra, inoculación en heridas o membranas mucosas, o ingestión de alimentos contaminados 4,20,21, . Gracias a los ácidos micólicos presentes en su pared logra sobrevivir en el medio intracelular y puede persistir dentro de macrófagos generando así granulomas 22,23 . Dicha característica sumada a plásmidos intra-celulares que codifican para factores de virulencia, constituyen su principal mecanismo de patogenicidad 22,24 .…”

Molecular Epidemiology of Rhodococcus equi Based on traA, vapA, and vapB Virulence Plasmid Markers

“…In nonhorse hosts, a variant plasmid encoding VapB, a VapA-related surface antigen of larger size (18)(19)(20), has been identified [19][20][21]. Lack of detection of VapA/B proteins (or vapA/B DNA sequences) is relatively common in nonhorse isolates [22] and is assumed to be due to an absence of virulence plasmids. However, these strains may carry other types of uncharacterized R. equi virulence-associated extrachromosomal replicons.…”

Rhodococcus equi Parte 2: imunologia e profilaxia

“…A grande maioria das tentativas de imunização ativa de éguas e a subsequente transferência de imunidade passiva para o potro via Ciência Rural, v.41, n.12, dez, 2011. colostro não promoveu proteção contra o desenvolvimento da rodococose (CAUCHARD et al, 2004) e, segundo MEIJER & PRESCOTT (2004), essa falha pode estar relacionada à qualidade da vacina ou a classe de anticorpo cuja produção foi suscitada pelas vacinas utilizadas experimentalmente, já que estudos têm demonstrado não haver uma diminuição significativa na incidência da pneumonia causada por R. equi quando a bactéria morta ou inativada é usada como imunógeno (MADIGAN et al, 1991;VARGA et al, 1997). Já CAUCHARD et al (2004), utilizando VapA como imunógeno em éguas prenhas, demonstraram um aumento sérico de IgG e da atividade opsonizante, que foi transferida para seus potros.…”