Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HUMAN HEALTH AND DISEASE > Fungal Infections > Flashcards

Fungal Infections Flashcards

1
Q

What are fungi?

A

They are eukaryote heterotrophs (obtain nutrition from their environment) that have cell walls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between yeasts and moulds?

A

Yeast:
-unicellular
-reproduce by budding
-some may produce hyphae and pseudohyphae

Moulds:
-multicellular
-reproduce using specialized spore structures
-produce hyphae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how do yeast reproduce by?

A

Budding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are structures produced by yeast?

A

pseudohyphae
budding yeast
hyphae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are pseudohyphae produced by and what do they look like?

A

Budding and elongation, and can resemble a string of sausages.

look at slide 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are hyphae produced by and what do they look like?

A

Apical extension from the protrusion out of a cell and these tend to have even and parallel sides at all times

look at slide 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What kind of colonies does yeast produce?

A

Moist looking ones
slide 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What kind of colonies do mould hyphae produce?

A

They’d form a colony on solid media that is round.

Sub-surface growth occurs & special spore structures may be on the surface

slide 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How can you distinguish mould and yeast infections in tissue by microscopy

A

Compare the hyphae

Mould infection in skin. Hyphae are parallel sided and regularly septate (true hyphae)

Candida infected skin. Budding yeasts, pseudo hyphae and true hyphae present.

slide 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Are any fungi commensal to humans?

A

Yeast:
Candida albicans- GI tract/oral
Other Candida species may be found in the GI
Malasezzia- skin

Moulds: No commensal moulds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What factors can predispose to candidiasis (risk factors)?

A

Age- infancy, elderly
Endocrine disorders
Defects in cell mediated immunity
Cancer
Drug addiction/Drug therapy- antibiotics, corticosteroids, immunosuppression
Surgery/IV catheters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the commonest Candida species?

A

Candida albicans, C. glabrata, C. tropicalis, C. parapsilosis, C. krusei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do most Candida infections arise?

A

The species is commensal to GI tract, so usually infections arise from the endogenous flora but occasionally exogenous sources are implicated

e.g. hospital outbreaks and the commonest cause of these are C. albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the latest nosocomial (hospital acquired)problem?

A

Candida auris

Colonises readily, persists in environment, highly resistant to antifungals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give some examples of oral manifestations of candidiasis.

A

slide 11

Acute pseudomembranous, detachable plaques

Chronic pseudomembranous, AIDS persistent

Chronic mucocutaneous candidiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does oral candidiasis look like in children?

A

slide 12

Angular cheilitis may be present - an inflammatory skin process of variable etiology occurring at the labial commissure, the angle of the mouth

Oral candidiasis occurs in 4-8% infants, but if HIV+ 72-99%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are predisposing factors for intertrigo?

A

slide 13

intertrigo is the inflammation caused by the rubbing of one area of skin on another. caused by candida albicans

Obesity

Diabetes

Anything that increases your risk of skin folds because it’s brought on by occlusion, so the increase in moistness and colonisation of the skin eventually leads to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what Superficial infections are caused by Candida albicans?

A

interdigital
intertrigo
onychomycosis and paronychia -an infection of the skin around a fingernail or toenail.

Fingerweb / finger nail - occlusion and wetness, carriage of candida.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is Candidiasis - nappy dermatitis?

A

Buttocks, perianal, groin.

Erythema, scaling, satellite lesions

1o or 2o invader? Association with faecal carriage of C. albicans

slide 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is chronic mucocutaneous candidiasis?

A

CMC may be inherited, associated with hypoparathyroidism or hypoadrenalism, hypothyroidism, or idiopathic.

Recurrent oral, skin, nail infection

Skin lesions on the face and scalp = candida Granuloma

slide 15

21
Q

Can Candida cause systemic infection?

A

yes
Systemic means affecting the entire body, rather than a single organ or body part.

22
Q

What do we mean by systemic infections?

A

Infection you find in the blood, lungs & internal organs, skin.

Endogenous source– resulting from predisposing factors

Exogenous source – outbreaks can occur in wards with severely debilitated hosts, uncommon

23
Q

How does Candida albicans cause infection (1)?

A
  1. Ability to adapt to changes in environment- eg. pH. Sites include mouth, GI, vagina, skin
  2. Ability it adhere to different surfaces - Surface molecules bind to: iC3b, fibrinogen, fibronectin, laminin, epithelial cells , bacterial coaggregation with Streptococci and Fusobacterium species
  3. Production of destructive enzyme - Secreted aspartyl proteinases, phospholipases, hyaluronidase, degrade extracellular matrix proteins, etc enabling invasion
  4. Changes in cellular morphology -
    Yeast, hyphae, pseudohyphae
  5. Production of biofilms - Offers protection from environment, phagocytosis, and antifungals
  6. Evasion of host defence -
    Block oxygen radical production and degranulation of PMN, kill monocytes. Cell wall components may have immunomodulatory effects, may stimulate cytokine release, may activate complement cascade
  7. Toxin production - Candidalysin is a cytolytic peptide toxin secreted by C. albicans during hyphal invasion. Damages tissue and activates the immune response
24
Q

What is the Candida pathogenicity?

A

Secretory aspartyl proteses (SAPs) have roles in adherence, invasion and development of disease

25
Q

What is cryptococcosis?

A

A chronic, subacute to acute pulmonary infection resulting from inhalation of cryptococcus yeasts

On dissemination the yeast shows a predilection for the CNS & cryptococcal meningitis occurs.

26
Q

What can systemic spread of cryptococcosis result in?

A

Skin lesions
Infection of bone and internal organs may also occur

27
Q

how can Cryptococcosis be distributed?

A

Distribution - worldwide especially associated with bird droppings (eg. pidgeon)

28
Q

what is the cause of Cryptococcosis

A

causative organism Cryptococcus neoformans

29
Q

Is cryptococcosis particularly dangerous?

A

Only if you have HIV/AIDS or anything that makes your immune system extremely weak

30
Q

How does cryptococcus exist?

A

Only in the yeast form, no hyphae produced

31
Q

What is the major virulence factor of cryptococcus?

A

Capsule is protective, prevents phagocytosis
can synthesise Melanin which is immunomodulatory

32
Q

how are moulds acquired by humans?

A

No commensal mould to the human body. Infections always exogenously acquired.

33
Q

what are the two types of moulds

A

dermatophytes and aspergillus

34
Q

What kind of infections do dermatophytes cause and what is the source?

A

Ringworm fungi

Common, superficial infection (affetcs outer layers)

Sources include human, animal & soil

35
Q

What kind of infections do aspergillus cause and what is the source?

A

Uncommon, systemic (affect the blood) infection
Environmental source
Can often infect immunocompromised hosts

36
Q

What factors predispose to mould infections?

A
  1. History of trauma to site of infection (cutaneous and subcutaneous)

2.Host immune status - can determine the extent of disease, duration, outcome

3.Underlying disease - may influence susceptibility to certain types of infection

4.Exposure to a source

5.Portal of entry

37
Q

What do dermatophytes use as substrates?

A

Dermatophytes are a family of fungi that use keratin as a substrate
(so species infect hair, skin, nails).

Infections result from contact with a source

Affect healthy and immune compromise people

38
Q

What is the commonest cause of skin & nail dermatophyte infection?

A

Trichophyton rubrum

39
Q

What is tinea?

A

Medical term for ringworm (a clinical dermatophyte infection)

40
Q

What is tinea capitis?

A

A fungal infection of the scalp characterised by red papules or spots at the opening of the hair follicle

41
Q

What are the risk factors for tinea capitis?

A

Risk factors
age – most infections before puberty (mid teens). Uncommon in adults. Sebum production is inhibitory to fungal growth.

contact with infection - relevant history of exposure to source (human, animal, soil)

minor trauma to inoculate - scratching, hair dressing, barbers, sharing hats / towels etc

affects healthy hosts. Not more common in immune compromised hosts, but infections may be more florid.

42
Q

What do clinical presentations of tinea capitis look like?

A

Often fine scaling, mild erythema, patchy alopecia
Hairs break at skin level: black-dot alopecia

slide 30

43
Q

who is most likely to have
Dermatophyte scalp infection- tinea capitis?

A

Highly contagious among pre-pubescent children. Practice good hygiene and disinfect chairs and headrests.

44
Q

What are the pathogenicity mechanisms for tinea?

A
  1. Adhesion (e.g by adhesins, enzymes)
  2. Invasion ( produce hyphae, complex process regulated by protein content and pH)
  3. Utilise keratin (breaking disulphide bridges)
  4. Manipulation of the immune response - cell wall mannans suppress lymphoproliferative activity
  5. Host adaptation (species associated with humans cause low grade chronic infections compared to animals)

look at slide 32 and 33

45
Q

what is aspergillosis?

A

Causes systemic disease following inhalation of spores. Type of disease is determined by host status

46
Q

what is the common form of aspergillosis?

A

Aspergillus fumigatus, A. flavus, A. nidulans, A. niger, A.terreus.

All are referred to as species complex as each comprises closely related organisms that are only distinguished genetically

47
Q

What can aspergillosis cause?

A
  • environmental moulds (decay in leaves + compost)
48
Q

What are the different types of aspergillosis?

A

Allergic aspergillosis - temporary presence of aspergillus in respiratory tract, healthy host. Agricultural link, or exposure to large nos. spores

Aspergilloma - colonisation of pre-existing cavities, fungal ball in lung, predisposing factors for lung cavitation but may otherwise be healthy

Invasive aspergillosis - pulmonary focus, dissemination possible, immune compromised host

Systemic aspergillosis - lungs, brain, other organs, immune compromised host

Cutaneous aspergillosis – primary infection due to skin damage (healthy or immune compromised).

49
Q

what does A. flavus cause?

A

A. flavus causes aflatoxicosis due to ingestion of toxin produced in contaminated foods (peanuts), healthy host

HUMAN HEALTH AND DISEASE (58 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions