Fungal Infections Flashcards

1
Q

What are fungi?

A

Eukaryotic
Obtain nutrients from environment
Can be environmental, commensal or pathogenic

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2
Q

What are the 2 types of fungi?

A

Yeast

Moulds

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3
Q

What are the main characteristics of yeasts? (3)

A

Unicellular
Budding (reproduction; copy themselves)
Some may produce hyphae and psuedohyphae

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4
Q

What are the main characteristics of moulds? (3)

A

Multicellular
Reproduce using specialised spore structures
Produce hyphae

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5
Q

What is pseudohyphae?

A

Elongated bud until it gets to a point where it can’t extend anymore, so it buds off again and it continues. Can look like string of sausages

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6
Q

What is ‘true’ hyphae?

A

Produced by apical extension from protrusion out of cell. Have even and parallel sides

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7
Q

What would mould look like if grown on a culture plate?

A

Round, sub-surface growth and special spore structures may be on the surface.
Hyphae in culture and on surface

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8
Q

When using a microscope, how could you differentiate between mould and yeast?

A

With mould it would look more regular due to presence of only true hyphae.
In yeast, you could see buds, pseudohyphae and true hyphae, so would much less regular

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9
Q

What are examples of commensal yeasts found in human?

A

Candida albicans (GI tract, oral)
Other candida species in GI
Malassezia (skin)

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10
Q

What are examples of commensal moulds found in the human body?

A

TRICK QUESTION

There are no commensal moulds found in humans

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11
Q

Name 5 factors that may predispose someone to candidiasis (8)

A
Age (infancy, elderly) 
Endocrine disorder
Defects in cell mediated immunity
Cancer
Drug addiction 
Drug therapy - ABs, corticosteroids, immunosuppression
Surgery 
IV catheters
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12
Q

Which yeast infection is most common in hospital outbreaks?

A

Candida albicans

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13
Q

Which type of candida is highly resistant to antifungals?

A

Candida auris

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14
Q

Outline the 3 oral manifestations of candidiasis

A
  1. Acute pseudomembranous detachable plaques
  2. Chronic pseudomembranous, AIDS persistent
  3. Chronic mucocutaneous candidiasis
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15
Q

Which viral infection greatly increases the chance of a candida infection?

A

HIV

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16
Q

In what parts of the body could you get superficial candida albicans infection?

A

Interdigital (finger web, finger nail)
Paronychia and onychomycosis
Intertrigo (e.g. breasts or groin area or obesity)

Usually due to occlusion and wetness

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17
Q

Which candidiasis affect babies?

A

Nappy dermatitis

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18
Q

What sites are mainly affected by systemic candidiasis?

A

Blood, lungs, skin, internal organs

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19
Q

Outline the 7 ways candida albicans causes infection

A
  1. Ability to adapt to changes in environment
  2. Ability to adhere to different surfaces
  3. Production of destructive enzymes (e.g. phospholipases)
  4. Changes in cellular morphology
  5. Production of biofilms (protects from environment, antifungals etc)
  6. Evasion of host defence mechanisms
  7. Toxin production (candidalysin damages tissue and activates the immune response)
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20
Q

Which destructive enzyme is produced by candida that have roles in adherence, invasion and development of disease?

A

Secretory aspartyl protease

21
Q

What is cryptococcosis?

A

It is a chronic, subacute pulmonary infection resulting from inhalation of cryptococcus yeasts.

22
Q

What is the causative organism of cryptococcosis?

A

Cryptococcus neoformans

23
Q

What happens when cryptococcosis disseminates?

A

Often travels to the CNS and cryptococcal meningitis occurs

In blood - it can result in skin lesions and infection of bone and internal organs may occur

24
Q

What are cryptococcal infections most associated with?

A

Bird droppings

25
Q

Which type of cryptococcuscan cause infection of mostly immune competent hosts?

What is this most associated with?

A

Cryptococcus gattii

Associated with trees and soil - is endemic to certain regions (e.g Vancouver Island)

26
Q

Does cryptococcus produce hyphae?

A

No - it only exists in yeast form

27
Q

What major virulence factor does cryptococcus have?

A

It is able to form a capsule - this is protective and prevents phagocytosis.

28
Q

What characterises a dermatophyte mould infection?

A

Common
Superficial infection
Healthy host
Sources include human, animal and soil

29
Q

What characterises an Aspergillus mould infection?

A

Uncommon
Systemic infection
Environmental source
Immune compromised host or predisposing factors underlie disease

30
Q

What factors predispose to mould infection? (5)

A
  • History of trauma to site (cutaneous and subcutaneous)
  • Host immune status: can determine extent of disease, duration, outcome
  • Underlying disease: may influence susceptibility to certain types of infection
  • exposure to a source
  • Portal of entry
31
Q

Ring worm is an example of what?

A

Dermatophyte mould

32
Q

What do dermatophytes use as their main source of nutrients?

A

Keratin

33
Q

What parts of the body can dermatophytes infect? (3)

A

Skin, nail, hair

34
Q

Which mould family are the commonest cause of human mould infections?

A

Dermatophytes

35
Q

Which dermatophyte is the commonest cause of skin and nail infections?

A

Trichophyton rubrum

36
Q

What is the clinical name for dermatophyteinfection?

A

Tinea

37
Q

How can you contract a dermatophyte infection?

A

Results from contact with a source (source can be from humans, animals or soils)

38
Q

Do dermatophyte infections affect healthy people, immunocompromised people or both?

A

Both

39
Q

What is the highest risk factor for Tinea capitis?

A

AGE

Most infections occur before puberty.
Uncommon in adults. This is because post-puberty scalps and skin tends to be greasier which is less favourable for fungal infections

40
Q

The production of what is inhibitory to fungal growth?

A

Sebum production

41
Q

How do you contract tinea capitis?

A

Exposed to a source - source can be human, animal or soil (most common is human to human).
Also require a minor trauma in order to inoculate (e.g. scratching, hair dressing, barbers, sharing hats etc)

42
Q

Does tinea capitis affect healthy hosts, immune compromised or both?

A

Both - not more common in one than the other.

Although infection does tend to be more widespread in immune-compromised people

43
Q

What is a kerion?

A

It is an inflammatory type of tinea capitis characterised by swelling and alopecia of the scalp

44
Q

Outline the 5 pathogenicity mechanisms for tinea

A
  1. ADHERENCE: adhesins, enzymes, fibrillar projections on cell surface
  2. INVASION: phospholipases etc complex process regulated by protein content and pH
  3. UTILISE KERATIN: proteins in cornified layers of skin are rich in disulphide bridges. Dermatophytes use a sulphite pump to reduce disulphide bond in proteins that are then cleaved.
  4. MANIPULATION OF IMMUNE SYSTEM: cell wall mannans suppress lymphoproliferative activity
  5. HOST ADAPTATION: zoophilic species produce more protease than anthropophilic species

(Also tends to get passed around as people tend to get minor infections that they ignore or don’t realise as they are asymptomatic)

45
Q

How does a person get an aspergillus infection?

A

They inhale spores and cause systemic disease

46
Q

Which 2 aspergillus species are the most common causes for infection?

A

A. Fumigatus

A. Flavus

47
Q

The type of disease caused by Aspergillus is determined by what?

A

Host status

48
Q

Where might you find aspergillus?

A

In agriculture - like compost, soil, hay etc

49
Q

Outline the 4 types of aspergillus infection

A
  1. Allergic aspergillus: temporary presence of aspergillus in respiratory tract, healthy host. Agricultural link, or exposure to large numbers of spores.
  2. Aspergilloma: colonisation of pre-existing cavities, fungal ball in lung, predisposing factors for lung cavitation but may otherwise be healthy
  3. Invasive aspergillosis: pulmonary focus, dissemination possible, immune compromised host
  4. Systemic aspergillosis: lungs, brain, other organs, immune compromised host.