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PH-IM09

Fungal infection

How barriers and phagocytes keep fungi in check, why most fungal disease follows a failure of one of them, how moulds invade blood vessels, and how the same fungus can cause allergy, a fungus ball or invasive disease.

By the end, you can

  • Describe the barriers and immune cells that normally keep fungi in check.
  • Distinguish yeasts, moulds and dimorphic fungi, and relate their forms to what is seen in tissue.
  • Explain why mucosal candidiasis follows changes in the microbiota or in T-cell immunity.
  • Explain how invasive moulds invade blood vessels and cause infarction when neutrophils fail.
  • Relate the state of the host’s immunity to allergic, colonising, granulomatous and invasive fungal disease.
  • Recognise the classic tissue forms, stains, classifications and tests of fungal infection, and explain how each antifungal class acts on the fungal membrane, wall or nucleic acids.

What it is

A fungal infection (mycosis) is disease caused by fungi: eukaryotic organisms with a rigid wall of chitin and glucans and a membrane containing ergosterol. Most fungi that infect people are opportunists that cause serious disease only when barriers or immunity fail; a few primary pathogens, such as the dimorphic fungi of particular regions, can infect healthy people. Infections range from superficial (skin, hair, nails and mucosa) to invasive (blood and deep organs).

4 types to tell apart
Superficial and mucosal
Dermatophytes in the keratin of skin, hair and nails; Candida on the mucosa of the mouth, oesophagus and vagina.
Invasive
Candida in the blood, and moulds such as Aspergillus and the Mucorales invading the lungs, sinuses and blood vessels, mostly when immunity is weakened.
Allergic and colonising
Allergic bronchopulmonary aspergillosis in asthma or cystic fibrosis; a fungus ball (aspergilloma) in an old lung cavity.
Endemic (dimorphic) mycoses
Histoplasma, Coccidioides, Blastomyces and others, inhaled in particular regions, causing granulomatous lung disease that resembles tuberculosis.

Normal function

Barriers and phagocytes keep fungi out

Fungal spores are everywhere: everyone inhales Aspergillus spores (conidia) every day, and Candida lives harmlessly on the skin and in the mouth, gut and vagina of many healthy people. Intact skin and mucosa, and the bacteria of the normal microbiota, which compete for space and nutrients, keep Candida in small numbers and in its harmless yeast form.

Conidia are small enough (2–3 micrometres) to reach the , where engulf and kill them. Any that germinate into hyphae, too large to be engulfed, are attacked by neutrophils, which gather round them and release reactive oxygen species and enzymes.

T cells shape the response. Th17 cells release IL-17, which recruits neutrophils and boosts antimicrobial peptides at the skin and mucosa: the main defence against mucosal Candida. Th1 cells activate macrophages to kill fungi living inside them, as in histoplasmosis, and organise granulomas.

Point to it on the model