Gram-positiveBacilliBranching filaments

Nocardia asteroides

Partially acid-fast, branching filamentous Gram-positive aerobic bacterium causing pulmonary nocardiosis and disseminated infections, particularly in immunocompromised hosts.

Organism Card

DomainMust know
Identity
  • Aerobic actinomycete; filamentous Gram-positive bacterium
  • Branching, beaded, filamentous rods — resembles fungi morphologically
  • Weakly acid-fast (modified Ziehl-Neelsen / Kinyoun positive) — key distinguishing feature
  • Belongs to order Actinomycetales; NOT a true fungus despite filamentous growth
Lab discriminator
  • Modified (weak) acid-fast stain positive — distinguishes from Actinomyces (acid-fast negative)
  • Gram stain: branching filamentous G+ve rods
  • Aerobic growth on Sabouraud or Lowenstein-Jensen media; slow grower (2–14 days)
  • Actinomyces = anaerobic, NOT acid-fast; Nocardia = aerobic, weakly acid-fast
  • Urease positive; may partially resist decolorisation by 1% H₂SO₄
Reservoir / transmission
  • Ubiquitous soil saprophyte; found worldwide including Hong Kong
  • Inhalation of contaminated soil/dust is primary route
  • NOT person-to-person transmission
  • Percutaneous inoculation (traumatic wound, thorn prick) — causes mycetoma
  • Construction site / gardening / soil exposure = classic vignette clue [1]
Key virulence
  • Catalase and superoxide dismutase → resist oxidative killing within macrophages/neutrophils
  • Cord factor (trehalose dimycolate analogue) → impairs phagosome–lysosome fusion
  • Cell wall mycolic acids → resist intracellular killing; basis for partial acid-fastness
  • Obligate aerobe; thrives in lung tissue with high O₂ tension
Clinical syndromes
  • Pulmonary nocardiosis (most common, ~70%) — subacute/chronic pneumonia in immunocompromised; cavitary lesions on CXR [1][2]
  • CNS dissemination → brain abscess (second most common site; ~30% of disseminated cases)
  • Cutaneous/subcutaneous: mycetoma (Madura foot), lymphocutaneous sporotrichoid spread
  • Classic host: immunosuppressed — transplant recipients, chronic corticosteroids, HIV/AIDS, haematological malignancy post-chemotherapy [1][2]
  • Triad to remember: Lung + Brain + Skin in an immunocompromised patient
Diagnosis
  • Specimen: sputum, BAL, brain abscess aspirate, skin biopsy
  • Modified acid-fast stain (1% H₂SO₄) showing branching filamentous rods = key finding
  • Culture on blood agar / Sabouraud agar — hold for ≥2 weeks (slow grower)
  • Pitfall: may be dismissed as contaminant; lab must be alerted to hold cultures longer
  • MALDI-TOF MS or 16S rRNA sequencing for species-level identification [3]
Treatment
  • First-line: TMP-SMX (co-trimoxazole / Septrin) — drug of choice for all forms [1][2]
  • Alternatives / combination for severe/CNS disease: imipenem, amikacin, linezolid
  • Prolonged course required: 6–12 months (at least 6 months for pulmonary; 12 months if CNS)
  • Brain abscess may require neurosurgical drainage + prolonged antibiotics
  • Key caveat: sulfonamide resistance emerging; susceptibility testing recommended
Prevention
  • TMP-SMX prophylaxis in transplant / immunocompromised patients also covers Nocardia (as well as PJP) [1][2]
  • No vaccine available
  • Not a notifiable disease in Hong Kong
  • No isolation required (no person-to-person spread)
Classic traps
  • Nocardia vs Actinomyces: Nocardia = aerobic + weakly acid-fast + no sulfur granules; Actinomyces = anaerobic + NOT acid-fast + sulfur granules + associated with IUD/dental/jaw
  • Nocardia vs TB: both acid-fast; Nocardia is weakly/partially acid-fast (modified ZN), TB is strongly acid-fast (standard ZN with 20% H₂SO₄)
  • Nocardia vs fungal infection: filamentous morphology mimics fungi but is a bacterium — responds to antibacterials, NOT antifungals
  • Vignette discriminator: immunocompromised + cavitary lung lesion + brain abscess + weakly acid-fast branching rods = Nocardia

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