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BOD MVST 1b > Fungi > Flashcards

Fungi Flashcards

1
Q

What do fungi feed on?

A

Dead plant or animal material in soil and compost heaps

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2
Q

Name some similarities between the genomes of fungi and humans

A

Eukaryotes
Membrane-bound nucleus with several chromosomes
DNA contains introns
Plasma membrane and cytoplasmic organelles

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3
Q

Name some differences between the genomes of fungi and humans

A

6000 genes

Normally haploid, only briefly diploid

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4
Q

What is the structure of a fungal cell wall?

A

Cell wall of polysaccharides
Inner layer of chitin microfibrils (beta-1,4-NAG)
Outer layer of glucans (beta-1,3-linked glucose) and glycoproteins (asp-N-mannose or galactose, ser/thr-O-mannose or galactose)

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5
Q

What are the three categories of fungal morphology?

A

Yeasts
Filamentous moulds
Dimorphic fungi

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6
Q

Discuss yeasts: shape, growth

A

Oval or round
Unicellular
Mitotically divide by symmetrical binary fission or asymmetrical budding
Others grow as short cylinders called pseudohyphae

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7
Q

How does Schizosaccharomyces pombe divide?

A

Symmetrical binary fission

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8
Q

Discuss filamentous moulds: shape, growth

A

Hyphae - thin branching multicellular cylinder

Apical growth - mitosis at tip or t side branches behind the tip

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9
Q

What are the different structures hyphae can make up, and give examples of fungi of each of these categories?

A
  1. Septate: interconnected compartments (Aspergillus)
  2. Aseptate: many nuclei in common cytoplasm (Mucor)
  3. Mycelium: many hyphae forming an interwoven mass when compacted together. Can form macroscopic structures (mushrooms)
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10
Q

Dicuss dimorphic fungi

A

Fungi that are a different shape based on temperature
e.g. Histoplasma
Filamentous mould at 22 degrees in the environment
Yeast at 37 degrees in the body of a mammal

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11
Q

What are spores?

A

Small, tough, light fungal cells adapted for dispersal to new habitats and/or survival in hostile environments

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12
Q

What are the two states of differentiation of spores?

A
  1. Asexual/anamorph/mitotic/imperfect - yeasts produce internal endospores, moulds produce external endospores called conidia or internal spores inside a special hypha called a sporangium
  2. Sexual/telomorph/meiotic/perfect - motile gametes or specialised sexual hyphae. Means undergoes recombination and chromosome reassortment
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13
Q

What are conidia?

A

Mould external endospores - asexual spores

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14
Q

What is a sporangium?

A

A special hypha that some moulds form internal asexual spores in

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15
Q

How do Deuteromycota replicate?

A

Asexually - incapable of sexual reproduction

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16
Q

Where are sexual spores formed?

A
  1. Internally within tubular structure called an ascus
  2. Externally on specialised club-like structure called basidum
  3. Externally following fusion of specialised sexual hyphae
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17
Q

Discuss Ascomycota - where are the spores formed, give examples of yeasts and moulds

A

Sexual spores in an ascus
Asexual spores in a conida
Yeast = schizosaccharomyes, saccharomyces, pneumocystis, candida
Moulds = asperfillus, fusarium, microsporum, trichophyton, epidermophyton
Dimorphic = histoplasma

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18
Q

Discuss Basidomycota - where are the spores formed, give examples

A

Sexual spores on a basidum

Yeasts = Cryptococcus, malassezia

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19
Q

Discuss Zygomycota - where are the spores formed, give examples

A

Sexual spores = external fusion of hyphae
Aseuxal = sporangium
Moulds = mucor, rhizopus

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20
Q

Discuss Deuteromycota (imperfect fungi)

A

Only asexual - conidia

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21
Q

Which 3 lifestyles do fungi use to get nutrition?

A
  1. Saprotrophs - feed on dead plant or animal material. Infect by accidental inhalation or implantation
  2. Parasites of living plants - diseases of crops mainly
  3. Parasites of humans - can cause disease
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22
Q

How does an intact epithelium inhibit fungal entry?

A
  1. Physical barrier
  2. Secrete anti-microbial peptide
  3. Commensals inhibit multiplication of fungi on the surface
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23
Q

Which PRRs recognise fungi?

A
  1. MBL mannose-rich structures
  2. Dectin-1 beta1,3glucan
  3. Dectin-2 mannan
  4. DC-SIGN mannose-rich structures
  5. Mincle Mannose-rich structures
  6. TLR2 - Phospholipomannan
  7. TLR4- O-linked mannose
  8. Mannose receptor N-linked mannose
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24
Q

What does MBL recognise?

A

Mannose-rich structures

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25
Q

What does dectin1 recognise?

A

Beta1,3glucan

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26
Q

What does dectin2 recognise?

A

Mannan

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27
Q

What does DC-SIGN recognise?

A

mannose-rich structures

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28
Q

What does mincle recognise?

A

mannose-rich structures

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29
Q

What does TLR2 recognise?

A

Phospholipomannan

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30
Q

What does TLR4 recognise?

A

O-linked mannose (linked to a ser/thr)

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31
Q

What does the mannose receptor recognise?

A

N-linked mannose (linked to an asp)

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32
Q

Which PRRs activate the Syk pathway?

A

Dectin1

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33
Q

Which PRRs activate the Myd88 pathway?

A

TLR4

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34
Q

What are the key effector cytokines in response to fungi?

A

IL-17, IL-22

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35
Q

What is the pathway to activate proIL-1beta?

A
  1. Dectin1 –> Syk –> Inflammasome NLRP3/ASC/Casp1 –> proIL-1beta to IL1beta
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36
Q

What are the pathways to activate NFkappaB?

A
  1. Beta1,3-glucan –> Dectin2 –> Syk –> CARD9 –> MALT –> NFkappaB –> pro-IL1B + secrete IL6, IL23, IL12, TNFalpha
  2. O-linked mannose –>TLR4 –> Myd88 –> NF-kappaB –> pro-IL1b, secrete IL6, IL23, IL12, TNFalpha
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37
Q

Which cytokines, secreted in response to NFkappaB, stimulate a Th17 response?

A

IL6, IL23

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38
Q

Which cytokines, secreted in response to NFkappaB, stimulate a Th1 response?

A

IL12 TNFalpha

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39
Q

Which conditions can cause impaired fungal sensing? What does this make you susceptible to?

A

Susceptible to superficial fungal infections

  1. Dectin1 deficiency
  2. CARD9 caspase recruitment domain-containing protein 9 mutation
40
Q

What does impaired IL-17 receptor sensing do?

A

Susceptibility to chronic superficial Candida infection, or where auto-antibodies against IL-17 (or 22) inactivate the cytokines

41
Q

What does impaired neutrophil number predispose to? When does this occur?

A

Deep fungal infections
Opportunistic filamentous moulds esp Aspergillus
Cytotoxic chemotherapy, chronic granulomatous disease where there is a mutation in one of the genes of the neutrophil NADPH oxidase system that normally generates superoxide needed to kill fungi after phagocytosis

42
Q

What does impaired T cells and macrophage number or function predispose to? Why do people get this?

A 
Yeast infection (superficial and deep) (candida, pneumocystitis, cryptococcus) and dimorphic fungi that can invade the body as yeasts (histoplasma)
Primary immunodeficiency syndromes, immunosuppressant drug reatment, haematological malignancies, AIDS
43
Q

How do you diagnose a fungal infection?

A
  1. Culture of fungus from clinical sample e.g blood, urine, skin scraping, lung biopsy
  2. Detection of fungal polysaccharide or fungal DNA in a sample e.g Cryptococcal polysaccharide in blood or CSF, pneumocystitis DNA in lung fluid
  3. Tissue biopsy for microscopy and culture - morphology to ID moulds
44
Q

Amphotericin, nystatin

A

Polyene

Inhibit ergosterol function

45
Q

Clotrimazole, fluconazole, voriconazole

A

Azoles

Inhibit ergosterol synthesis

46
Q

Terbinafine

A

Allylamine

Inhibit ergosterol synthesis

47
Q

Grisofulvin

A

Inhibit fungal microtubule synthesis

48
Q

Caspofungin

A

Echinocandin

Inhibits beta-1,3-glucan synthesis of the fungal cell wall

49
Q

What is ergotamine?

A

A fungal toxin in rye crops

Potent vasoconstrictor that causes painful ischaemia/gangrene of fingers and toes

50
Q

Where are filamentous moulds commensal?

A

NOWHERE

51
Q

What is ringworm?

A

Superficial fungal infection of dead keratinised tissues (skin, nails, hair)

52
Q

What are dermatophyte moulds?

A

Microsporum, trichophyton, epidermophyton (all cause athlete’s foot)
Very common in humans, wild and domestic animals
Acquired by spores: direct person-to-person contact, indirect sharing contaminated clothing or environment
Not life threatening, don’t invade into deeper tissues
Chronic
Induce local type IV sensitivity (host CD4+ T) so increased skin proliferation –> flaky, scaly skin + itching, leading to scratching and secondary bacterial infection
Hard to eradicate, may recur

53
Q

What does candida albicans cause superficially?

A

Disfiguring chronic fingernail condition

54
Q

What does Malassezia furfur cause?

A

Pityriasis versicolor (blothy skin rash that doesn’t tan)

55
Q

What is rose picker’s disease?

A

Subcutaneous fungal infection
Invades as a yeast at 37 degrees
Forms chronic skin nodules that may spread up the arm

56
Q

What are the different levels of fungal infection?

A
  1. Toxins
  2. Commensals overgrowing
  3. Superficial
  4. Subcutaneous
  5. Systemic
57
Q

What are the two main types of systemic fungal infections?

A

Systemic pathogens and systemic opportunists

58
Q

How do histoplasma change morphology?

A

Temperature-sensitive dimorphism regulating kinases DRK1 and RYP1 induce a pattern of gene expression:

  • Expression of alpha-1,3-glucan not recognised by host PRRs
  • Fungal hsp60 which binds to CD11/CD18 on the surface of human mphages
  • Secreted protease-resistant calcium binding protein that facilitates fungal growth within macrophage vacuoles
59
Q

What are the temperature-sensitive dimorphism regulating kinases called?

A

DRK1 and RYP1

60
Q

How are fungal infections controlled?

A

T cell response –> mphages –> granulomas

61
Q

How do you identify if people have a memory T cell response against Histoplasma?

A

Skin test- inject dead histoplasma antigen into the skin

62
Q

How does histoplasma enter the body?

A

Lung (accidentally breathed in)
Soil and bat droppings in Mississippi and Ohio valleys
Inhaled by bats

63
Q

Name the forms of histoplasmosis, the clinical features, and the final outcome

A

Asymptomatic: positive skin test only, resolution
Acute pulmonary (influenza-like): lung infiltrates, enlarged hilar lymph nodes, resolution
Chronic pulmonary: chronic lung inflammation, fibrosis, cavitation, progressive incapacity
Disseminated (spread through blood): focal spread outside lung or widespread disease (skin, larynx, adrenal), often fatal

64
Q

Which host defects can predispose to systemic opportunist fungal infection?

A

Defect in skin barrier (IV, burns)
Neuropenia (leukaemia or its treatment)
Reduced function of neutrophils (chronic granulomatous disease)
Reduced number/function of T cells - lymphoma, AIDS, immunosuppressive drug treatment
NOT LACK OF AB

65
Q

What is the receptor on dendritic cells used to recognise histoplasma?

A

VLA-5 fibronectin and fibrinogen receptor

66
Q

What type of response is the histoplasma response?

A

Th1

67
Q

How does candida divide?

A

Divide by asymmetrical budding

68
Q

What is the structure of candida?

A

Commensal yeast on moist mucosal surfaces
Some strains have increased capacity for adhesion and invasion through the epithelial surface by forming pseudohyphae
Forms a biofilm: large communities of organisms embedded in a sticky extracellular matrix at the interface between a liquid medium and a sticky extracellular matrix

69
Q

Where do you find candida?

A

Throat, gut, vagina

70
Q

What is candidalysin?

A

A secreted 31 aa peptide toxin that damages epithelial cells

71
Q

When does oral candidiasis occur?

A

Newborn babies, following inhaled steroid treatment for asthma, following antibiotics

72
Q

When does vulvo-vaginitis candidiasis occur?

A

Pregnancy, following antibiotic treatment, nappy rash

73
Q

When does UTI candidiasis occur?

A

Following urethral catheter and/or previous antibiotic treatment

74
Q

When does oesophageal candidiasis occur?

A

Advanced HIV, organ transplant

75
Q

When does candidaemia occur?

A

Bloodstream infection

IV cannula in hospital, IV drug users, endotracheal tube

76
Q

When does disseminated infection of candida occur?

A

Spreads through blood to eyes, liver and spleen, heart valves
Mainly in immunosuppressed people

77
Q

How do you treat candida?

A

Fluconazole or caspofungin

78
Q

Name a species of candida resistant to fluconazole

A

Candida krusei

79
Q

How is pneumocystitis jirovecci transmitted?

A

Human-to-human by inhalation, obligate intracellular parasite

80
Q

Are recurrences of pneumocystitis jirovecci due to re-activation or re-acquisition when individuals have impaired T cell immunity?

A

Re-acquisition.

81
Q

What does pneumocystitis jirovecii cause? e.g. pathophysiology, signs, symptoms

A

Diffuse inflammation of lung alveoli
Clusters of oval fungal organisms in the alveolar airspaces, injury to alveolar epithelial cells, alveoli filled with protein-rich foamy exudate
Impairs gas exchange so arterial hypoxaemia worst during exercise
Dry cough, progressive breathlessless, fever, weight loss
X-ray widespread hazy opacification

82
Q

Treament of pneumocystitis jirovecii?

A

Co-trimoxazole - inhibits fungal folic acid synthesis +

Prednisolone = inhibit innate inflammatory response to fungal polysaccharides released by dying organisms

83
Q

How does pneumocystitis jirovecii replicate?

A

Trophic form = binary fission

Sexual form = sexual spore/cyst, after maturation the collapsed spore releases trophic forms

84
Q

How do you prevent pneumocystis pneumonia in high-risk immunocompromised patients?

A

Regular low dose treatment with co-trimoxazole or inhaled pentamide

85
Q

Pentamide

A

Used to prevent pneumocystis pneumonia in high-risk immunocompromised patients
Inhibits topoisomerase enzymes in mitochondria

86
Q

How do humans acquire Cryptococcus neoformans?

A

Inhalation of bird droppings, then spreads through lung to CNS

87
Q

What is a key virulence factor of Cryptococcus neoformans?

A

Thick polysaccharide caspule

88
Q

Are the types of infection of Cryptococcus neoformans?

A

Pneumonia rarely, meningo-encephalitis when T cell immunodeficiency

89
Q

What does Cryptococcus infection cause?

A 
Slowly worsening meningo-encephalitis
Progressively worsening headache
Fever
Confusion
Hydrocephalus
Coma
20% fatality
Survivors may have persistent neurological disability including blindness
90
Q

How do you treat Cryptococcus?

A

Amphotericin + flucytosine, then high dose fluconazole long term

91
Q

Amphotericin

A

Polyene antifungal and antiparasitic, forms pores in the membrane by an ergosterol-dependent mechanism. Drug of choice for most systemic mycoses: Cryptococcus, candida, aspergillus. Also antiprotozoal

92
Q

How is aspergillus fumigatus acquired?

A

Air-borne spores
Inhaled
Mouldy hay, compost heaps, hospital re-building work

93
Q

What types of infection does aspergillus cause and under which conditions?

A

Airway colonisation - asthma
Aspergilloma (localised mass of hyphae) - pre-existing lung cavity e.g. after prev TB
Invasive infection of lung or paranasal sinuses - severe neutropenia e.g. after chemotherapy for leukaemia
V high fatality

94
Q

Treatment for aspergillus?

A

Amphotericin or voriconazole, surgery if poss

95
Q

How do you get mucormycosis?

A

Inhalation of spores
Direct contamination of wounds (tornado or tsunami)
Invades aggressively through paranasal sinuses or lungs

96
Q

How do you treat mucormycosis?

A

Urgent surgery to remove dead tissue + IV amphotericin

BOD MVST 1b (9 decks)

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