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PH-RS21

Fungal and parasitic lung disease

How the lung, which filters both the air and all the venous blood, meets fungi and parasites: why the host decides the Aspergillus disease, how Pneumocystis fills the alveoli, and how cysts, migrating larvae and trapped eggs injure the lung.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Explain why the lung meets fungi through the air and parasites through the blood, and which defence controls each.
  • Relate allergic, cavity-colonising and invasive aspergillosis to the host’s immunity and the structure of the lung.
  • Explain how Pneumocystis, the endemic dimorphic fungi and Cryptococcus damage the lung, and why weak T-cell immunity favours them.
  • Explain how a hydatid cyst, migrating worm larvae and schistosome eggs cause a lung cyst, fleeting eosinophilic shadows and pulmonary hypertension.
  • Recognise the classic appearances and tests of each, and explain how antifungal, antiparasitic and other treatments act on the mechanism.

What it is

Fungal and parasitic lung disease is injury to the lung by fungi, which mostly arrive as inhaled spores, or by parasites, which mostly arrive in the blood as larvae, cysts or eggs. The disease depends on the organism, the route and above all the host: the same fungus can cause allergy, a ball in a cavity or a fatal invasive pneumonia.

5 types to tell apart
Allergic
The host’s response is the disease: allergic bronchopulmonary aspergillosis in asthma or cystic fibrosis, and Löffler syndrome as worm larvae cross the lung.
Colonising a damaged lung
Aspergillus grows in an old cavity as a fungus ball (aspergilloma), or slowly destroys lung as chronic pulmonary aspergillosis.
Opportunistic and invasive
Invasive aspergillosis with very few neutrophils; Pneumocystis pneumonia and spreading cryptococcal or histoplasma infection with weak T-cell immunity.
Granulomatous (endemic mycoses)
Histoplasma, Coccidioides and Blastomyces, inhaled in particular regions, cause granulomas that can mimic tuberculosis even in healthy people.
Blood-borne parasites
A hydatid cyst grows where an Echinococcus larva lodged; schistosome eggs block and inflame the small pulmonary arteries.

Normal function

Two doors into the lung: the air and the blood

The lung meets the outside world through the air. Particles about 1–5 micrometres across, including the conidia (spores) of Aspergillus and the yeasts of Histoplasma and Cryptococcus, travel past the airways and settle on the . There engulf and kill most of them. Neutrophils deal with any spore that germinates into hyphae, which are too large to swallow.

Organisms that survive inside macrophages, such as the dimorphic fungi and Pneumocystis, are controlled by CD4 T cells: Th1 cells release interferon-gamma, which arms macrophages to kill what they hold and builds granulomas round what they cannot. Worms, far too large for any phagocyte, provoke the type 2 response of IgE and eosinophils.

The lung is also the body’s filter for venous blood. All the blood returning from the tissues passes through the in the , which are narrower than many objects the blood carries. Larvae of worms, tapeworm embryos that escape the liver and parasite eggs are caught here, which is why parasites reach the lung by the blood rather than the air.

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