PMI02-2010 Fungal infections Flashcards

1
Q

What is the difference between yeasts and moulds?

A

Yeast is unicellular, moulds are multicellular
Yeasts reproduce by budding, but moulds reproduce using specialised spore structures
Yeasts may produce hyphae and pseduohyphae, but moulds only produce hyphae

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2
Q

How are pseudohyphae formed?

A

produced by bud elongation

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3
Q

How are true hyphae formed?

A

produced by apical extension

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4
Q

Which fungi are commensal to humans?

A

Yeast

Candida alicans are commensal to the oral cavity and the gut

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5
Q

Are there commensal moulds to humans?

A

no

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6
Q

What factors predispose to candidiasis?

A
Age (infancy and elderly)
Endocrine disorders like diabetes
Cancer
Drug addiction 
Antibiotics, corticosteroids and immunosuppression
Intravenous catheters
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7
Q

How does Candida albicans cause infection?

A
It can adapt to changes in environments 
It can adhere to different surfaces
Produce destructive enzymes 
Change in cellular morphology
Production of biofilm 
Blocks oxygen radical production and degranulation of neutrophils 
Toxin production
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8
Q

What is cryptococcus?

A

A yeast that grows in things like pig droppings

Can cause sub acute to acute pulmonary infections through inhalation of spores

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9
Q

What is a cryptococcus infection?

A

Exists only in the yeast form, no hyphae produced

Their major virulence factor is their ability to produce a capsule which is protective, as it prevents phagocytosis

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10
Q

Why are commensal moulds only exogenously acquired?

A

there are no commensal mould

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11
Q

What factors predispose to mould infections?

A

History of trauma at the site of infections

Other underlying diseases that may influence the persons susceptibility to disease

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12
Q

What are dermatophytes?

A

Dermatophytes are a family of fungi that use keratin as a substrate

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13
Q

What are dermatophytes referred to clinically?

A

tinea

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14
Q

What are risk factors of tinea capitis?

A

scalp infections are common before puberty

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15
Q

What inhibits fungal growth in tinea capitis?

A

sebum production

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16
Q

How is tinea capitis passed on?

A

through inoculation through scratching, hairbrushes or sharing hats/towels

17
Q

What is the pathogenicity mechanisms for tinea?

A

They adhere to the skin through enzymes and fibrillar projections
Can invade skin through serine proteases and phospholipases
They can manipulate the immune response as their cell wall mannan proteins

18
Q

What are the only organisms to break disulphide bridges in keratin?

A

dermatophytes