Pneumocystis jirovecii pneumonia

Shmuel Shoham, M.D.
Pneumocystis jirovecii pneumonia is a topic covered in the Johns Hopkins ABX Guide.

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PATHOGENS

  • Causative organism of pneumocystis pneumonia (PCP) is the fungus called Pneumocystis jiroveci.
    • Closest relative is Taphrina deformans, a fungal pathogen of peach trees.
  • There are multiple species within the genus Pneumocystis
    • P. jiroveci (formerly identified as P. carinii and pronounced "yee row vet zee”) cause of disease in humans.
    • P. carinii and P. wakefieldiae infect rats, and P. murina infects mice.
      • Other species infect a range of animals (e.g. rabbits, sheep, monkeys, aquatic mammals).
  • Morphological forms:
    • Trophic form:
      • Predominant forms (>90% in the lungs), multiply through binary fission, heterogeneous in shape, about ∼2 µm at greatest diameter, have a cell membrane and a fragile (not rigid) cell wall.
    • Asci or spore form (also called cyst):
      • Formed by conjugation of two opposite mating type trophic forms (sexual reproduction), more uniform in shape, about 8–10 µm in greatest diameter.
      • Have a rigid cell wall that is important for protecting the organism from environmental conditions when outside of the host (during airborne transmission) and contains beta-glucans.
      • Mature cysts contain 8 intracystic bodies, which can be released to become trophic forms.
  • Important biochemical properties:
    • Cell membrane lacks ergosterol and hence antifungal agents such as azoles and amphotericin B products are not active against Pneumocystis.
    • The fungus must synthesize its own folic acid and hence this is a typical target for treatment (e.g TMP/SMX).
    • Cyst cell wall contains beta-glucans, which can be helpful for diagnosis and perhaps treatment.
  • Ecological niches and transmission
    • Specific environmental reservoirs are not well understood.
    • The organism grows well on epithelial cells within alveoli and fungal burden correlates with the degree of immune dysfunction.
    • P. jiroveci may be present at low levels in healthy humans, who may serve as a source of transmission.
    • Transmission is via airborne asci (cyst) forms passed from person to person.
    • There are constant inhalation and acquisition (transient or long term) of the organism. Clinical disease may be due to new acquisition of the fungus by a susceptible patient or from the transformation of long-term carriage into active disease.

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PATHOGENS

  • Causative organism of pneumocystis pneumonia (PCP) is the fungus called Pneumocystis jiroveci.
    • Closest relative is Taphrina deformans, a fungal pathogen of peach trees.
  • There are multiple species within the genus Pneumocystis
    • P. jiroveci (formerly identified as P. carinii and pronounced "yee row vet zee”) cause of disease in humans.
    • P. carinii and P. wakefieldiae infect rats, and P. murina infects mice.
      • Other species infect a range of animals (e.g. rabbits, sheep, monkeys, aquatic mammals).
  • Morphological forms:
    • Trophic form:
      • Predominant forms (>90% in the lungs), multiply through binary fission, heterogeneous in shape, about ∼2 µm at greatest diameter, have a cell membrane and a fragile (not rigid) cell wall.
    • Asci or spore form (also called cyst):
      • Formed by conjugation of two opposite mating type trophic forms (sexual reproduction), more uniform in shape, about 8–10 µm in greatest diameter.
      • Have a rigid cell wall that is important for protecting the organism from environmental conditions when outside of the host (during airborne transmission) and contains beta-glucans.
      • Mature cysts contain 8 intracystic bodies, which can be released to become trophic forms.
  • Important biochemical properties:
    • Cell membrane lacks ergosterol and hence antifungal agents such as azoles and amphotericin B products are not active against Pneumocystis.
    • The fungus must synthesize its own folic acid and hence this is a typical target for treatment (e.g TMP/SMX).
    • Cyst cell wall contains beta-glucans, which can be helpful for diagnosis and perhaps treatment.
  • Ecological niches and transmission
    • Specific environmental reservoirs are not well understood.
    • The organism grows well on epithelial cells within alveoli and fungal burden correlates with the degree of immune dysfunction.
    • P. jiroveci may be present at low levels in healthy humans, who may serve as a source of transmission.
    • Transmission is via airborne asci (cyst) forms passed from person to person.
    • There are constant inhalation and acquisition (transient or long term) of the organism. Clinical disease may be due to new acquisition of the fungus by a susceptible patient or from the transformation of long-term carriage into active disease.

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Last updated: April 5, 2019