Bacteriology - Rhodococcus

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Bacteriology - Rhodococcus
2013-02-15 00:58:15

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  1. Rhodococcus equi
    • Gram-positive coccobacillus
    • Slightly larger than Streptococcus
    • Suppurative bronchopneumonia with abscesses in lungs and hilar lymph nodes of foals
  2. Rhodococcus equi (ecology)
    • Occurs in soil and manure (secondarily - the intestine of mammals and birds)
    • -High prevalence on "problem farms"
    • -Robust soil organism, optimal growth in presence of horse manure and 10-41C
    • -Foal intestine (up to 3 months) serves as incubator (105 organisms per gram of feces)

    • Acquired by inhalation of dust, ingestion, umbilicus(?)
    • -Possibly contagious disease by aerosolization from infected foals

    No difference in number of organisms in soil of endemic versus "no-disease" farms
  3. Rhodococcus equi (Clinical Signs)
    • Chronic pyogranulomatous inflammation
    • -Lesions are abscesses, granulomas, caseopurulent

    Suppurative bronchopneumonia with abscesses in lungs and hilar lymph nodes of foals

    Occasional localization in joints, skin, spleen, ulcerative enteritis with abscessed mesenteric lymph nodes

    • Rarely associated with abscesses, cervical lymphadenitis, or pneumonia in numerous species
    • -emerging as an important pathogen in several immunocompromised humans
  4. Rhodococcus equi (Pathogenesis)
    Foals become at-risk for infections as maternal antibody declines with the peak incidence at 6-12 weeks of age

    Sporadic, opportunistic infections (including wound entry) have been reported in older horses and many other diverse animals (cattle, goats, pigs, sheep, dogs, cats, buffalo, koala, seals, crocodiles, alligators, etc.)

    Neutrophils are fully competent bactericidal defense

    • Infection is largely, or exclusively, within macrophages/monocytes
    • -Entry by non-Fc receptors (CRs) allows evasion of antibody-mediated killing in macrophages and intracellular survival
    • -Presence of vapA plasmid is necessary to arrest phagosome maturation
  5. Rhodococcus equi (virulence factors)
    • Virulent, pneumonic isolates produce virulence associated proteins encoded on one of at least 12 large virulence plasmids (85-90 kb); arranged in a pathogenicity island
    • -VapA is a highly immunogenic, lipid-modified protein anchored on the bacterial surface. Restoration of vap region deletion by only vapA is sufficient to restore virulence

    • Contribution of the antiphagocytic capsule and other exoenzymes to virulence is poorly defined
    • -Greater than 25 capsular serotypes with no known epidemiological or clinical significance
  6. Rhodococcus equi (Immunoprophylaxis)
    Commercially available vaccines have not been approved in the USA due to lack of efficacy

    • Passive immunization with hyperimmune plasma has yielded variable results. The passively transferred antibodies are not fully characterized but presumed to be specific for the Vaps.
    • -Passive transfer via colostrum does not protect
    • -IgGa - dominant response seems to be beneficial
    • -IgGT (and possibly IgGb) - dominant responses seem to be associated with disease
    •      -IgGT does not fix complement and may   inhibit activity of IgGa and IgGb

    Hyperimmune plasma is commercially available
  7. Rhodococcus equi (Diagnosis)
    Most cases today are subclinical infections or a clinical diagnosis

    Serological diagnosis is unreliable because the widespread exposure of foals to either avirulent or virulent strains at a young age leads to antibody production w/o necessarily producing clinical disease

    Cytology and culture often unrewarding

    Molecular detection: vapAchoE (cholesterol oxidase gene)
  8. Rhodococcus equi (Antimicrobial selections)
    • Predictable susceptibility
    • -Erythromycin + Rifampin or Gentamicin + Rifampin
    • -Clarithromycin, azithromycin, chloramphenicol, trimethroprim/sulfas, quinolones, vancomycin, or other synergistic combinations

    • Resistance Issues
    • -Intracellular and abscess penetration pharmacokinetics
    • -High frequency emergence of resistant mutants: rifampin, aminoglycosides, quinolones, except when used in combinations