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Microbiology > Mechanisms of Fungal Pathogenesis > Flashcards

Mechanisms of Fungal Pathogenesis Flashcards

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1
Q

PATHOGENESIS OF FUNGAL DISEASE

Capable of initiating infection in a normal, immunocompetent host

A

Primary pathogens

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2
Q

Able to colonize the host, find a suitable microenvironmental niche withsufficient nutritional substrates, avoid or subvert the normal host defense mechanisms, and then multiply within the microenvironmental niche

A

Primary pathogens

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3
Q

what pathogen is this?

  • Growth at 37C
  • Thermal dimorphism
  • modulation of yeast-host
  • generation of th2 response
  • shedding of Bad-1
A

BLASTOMYCES
DERMATITIDIS

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4
Q

saprobic phase

BLASTOMYCES
DERMATITIDIS

A

septate mycelium and conidia

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5
Q

parasitic phase

BLASTOMYCES
DERMATITIDIS

A

large, broad-based, budding yeast

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6
Q

Habitat/Infection of BLASTOMYCES
DERMATITIDIS

A

soil, organic debris,
endemic area: southeastern US & Ohio-Mississippi river valley
- infection through inhalation of conidia

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7
Q

BAD-1 is

A

a cell surface glycoprotein

BLASTOMYCES
DERMATITIDIS

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8
Q

clinical syndromes of BLASTOMYCES
DERMATITIDIS

A
  • pulmonary blastomycsis (pneumonia)
  • ulcerative/verrucous skin lesions
  • osteomyelitis
  • prostatitis
  • meningitis
  • intracranial abscess
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9
Q

Pathogenesis of what fungi?

inhaled conidia convert to yeast; localized yeast invasion of host invokes inflammatory reaction; yeast escapes recognition by macrophages and disseminates via bloodstream

A

Blastomyces dermatitidis

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10
Q

Promotes adhesion of the yeast cell to macrophages and elicits a potent response of both the humoral and cellular immune systems. BAD1 for what fungi?

A

Blastomyces dermatitidis

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11
Q

what fungi?

Resistance of conidia to phagocytic killing:

A

Coccidioides

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12
Q

Saprobic phase of C. immitis consists of septate filamentous hyphae that when mature produce

Coccidioides

A

barrel-shaped arthroconidia separated form one another by empty disjunctor cells

chinchin

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13
Q

Arthroconidia are very hydrophobic and easily aerosolized. Small enough that when inhaled, ___

Coccidioides

A

they can be carried deep into respiratory tract to level of alveoli

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14
Q

Saprobic phase:

Coccidioides

A

septate hyphae and arthroconidia

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15
Q

Parasitic phase:

Coccidioides

A

spherules with endospores

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16
Q
  • Pathogenesis: inhaled arthroconidia reach alveoli; convert to spherule that gives rise to endospores; endospores phagocytosed but survive; large spherules escape phagocytosis; alkaline environment allows survival within phagosome

what fungi?

A

Coccidioides

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17
Q

what fungi?

urease production

A

Urease make the alkaline environment especially suitable to survive in the stomach and to grow out in the wild desert

Coccidioides

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18
Q

○ Mimics a estrogen binding protein (progesterone and 17-beta-estradiol)

A

molecular mimcry

Coccidioides

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19
Q
  • Saprobic phase:

HISTOPLASMOSIS

A

septate hyphae, microconidia, and tubercule macroconidia

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20
Q

Parasitic phase:

HISTOPLASMOSIS

A

small, intracellular, budding yeast

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20
Q

what fungi?

Pathogenesis:inhaled conidia convert to yeast,
1. yet ingested by macrophages, survive and proliferate within phagosome,
2. some yeast forms remain dormant within macrophage,
3. others proliferate and kill macrophages, releasing daughter cells

A

HISTOPLASMOSIS

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21
Q

What fungi?

Virulence factors:
* alteration of cell wall composition (1,3-alpha glucans and sphingolipids for antiphagocytic property and oxidative response)
* * growth at 37 degrees C
* thermal dimorphism
* survival in macrophages
* modulate pH of phagosome
* iron and calcium uptake (siderophores and calcium binding protein, CBP1)

A

HISTOPLASMOSIS

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22
Q

mode of infection

HISTOPLASMOSIS

A

inhalation of conidia

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23
Q

Clinical diseases:
* clinically asymptomatic pulmonary
* “cryptic dissemination”
* acute pulmonary ____
* mediastinitis and pericarditis,
* chronic pulmonary ____,
* mucocutaneous, disseminated

A

HISTOPLASMOSIS

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24
Q

what fungi?

  • Conversion of inhaled conidia to yeast cells is critical for survival of the pathogen within the host and occurs within hours
    ○ Would also need a large amount of conidium for infection of immunocompetent person
A

HISTOPLASMOSIS

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25
Q

what fungi?

Macrophages are the primary host cells in which the yeast phase is important strategy for survival and dissemination of the pathogen

A

HISTOPLASMOSIS

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26
Q

Dermatophytes:

PATHOGENESIS OF DERMATOPHYTIC FUNGI

A

Trichophyton, Epidermophyton, and Microsporum

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27
Q

Dermatophytes cause disease in

PATHOGENESIS OF DERMATOPHYTIC FUNGI

A

humans and/or animals

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28
Q

what kind of fungi?

Invade the skin, hair, or nails

A

Dermatophytes

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29
Q

Keratinophilic and keratinolytic, Utilizes

PATHOGENESIS OF DERMATOPHYTIC FUNGI

A

keratinases

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30
Q

DERMATOPHYTIC FUNGI Invade only the upper, outermost layer of the

A

epidermis (the stratum corneum)

31
Q

With hair and nails (being part of the skin), only the

DERMATOPHYTIC FUNGI

A

keratinized layers are invaded

32
Q

The various forms of dermatophytosis are referred to as

DERMATOPHYTIC FUNGI

A

“tineas” or “ringworm” infections

33
Q

tinea capitis of the

A

scalp, eyebrows, and eyelashes

34
Q

tinea barbae

A

of the beard

35
Q

tinea corporis of the

A

smooth or glabrous skin

36
Q

tinea cruris of the

A

groin

37
Q

tinea pedis of the

A

foot

38
Q

Microsporum produces large

A

multicellular, thick-and rough-walled macroconidia (most common infection A)

39
Q

what fungi?

produces microconidia that are teardrop or peg shaped and borne along the sides of hyphae

A

T rubrum

Trichophyton

40
Q

what fungi?

produces both single, cigar-shaped macroconidia and grapelike clusters of spherical microconidia D

A

T mentagrophytes

Trichophyton

41
Q

what fungi?

produces variably sized and shaped microconidia with relatively large spherical conidia often located right alongside small, parallel-walled conidia and other microconidia of various sizes and shapes [C]

A

○ T tonsurans

Trichophyton

42
Q

does not produce microconidia but its smooth-walled macroconidia borne in clusters of two or three are quite distinctive

A

Epidermophyton

43
Q
  • In hair infections pattern can be and septate hyphae may be seen within the hair shaft in all three patterns:
A

Ectothrix, endothrix, favic

44
Q

what dermatophytes does not infect hair?

A

Epidermophyton

45
Q

what fungi is associated with this pattern?

Ectothrix: arthroconidia are formed on the outside of the hair

A

MICROSPORUM

46
Q

what fungi is associated with this pattern?

Endothrix: arthroconidia are formed inside the hair

A

TRICHOPHYTON

47
Q

what is the name of this pattern?

hyphae, arthroconidia, and empty spaces resembling air bubbles (honeycomb patter) are formed inside the hair

A

Favic:

48
Q
  • Hair infected with M. canis, M. audouinii, and T. schoenleinii often fluoresce yellow-green when exposed to a
A

Wood light

49
Q

topical azoles that treat dermatophytic

A

(azoles): Miconazole, clotrimazole, econazole, tioconazole, and itraconazole

50
Q

topicals that treats dermatophytic

A

Terbinafine

51
Q

Oral antifungals that treat dermatophytic

A

Griseofulvin, itraconazole, fluconazole, terbinafine

52
Q

Saprobic phase and parastic:

ASPERGILLOSIS

A

septate mycelium, conidial heads and conidia

53
Q

what fungi?

Pathogenesis: inhaled conidia bind to fibrinogen and laminin in alveolus;
* conidia germinate
* hyphal forms secrete proteases and invade epithelium
* vascular invasion results in thrombosis
* infarction of tissue
* hematogenous dissemination

A

ASPERGILLOSIS

54
Q

what fungi?

  • VF: growth at 37 degrees C, binding to fibrinogen and laminin, secretion of elastase and proteases, catalase, gliotoxin, and other mycotoxins
    ○ Creates an IgE response which creates those allergy symptoms/diseases
    ○ Gliotoxin: allow it to evade phagocytosis and inhibits host immune response
A

ASPERGILLOSIS

55
Q

mode of infection

ASPERGILLOSIS

A

inhalation of conidia and transfer to wounds via contaminated tape/bandages

56
Q

Replication of cryptococcosis is by

CRYPTOCOCCOSIS

A

budding from a relatively narrow base

57
Q

what fungi?

Germ tubes, hyphae, and pseudohyphae are usually absent in clinical material

A

CRYPTOCOCCOSIS

58
Q

what fungi?

  • VF: growth at 37 degrees C, polysaccharide capsule, melanin, alpha-mating type, urease (from pigeon droppings)
    ○ Alpha-mating type (gender) which produces melanin in capsule
A

CRYPTOCOCCOSIS

59
Q

what fungi?

  • Pathogenesis: inhaled yeast cells ingested by macrophages; survive intracellularly; capsule inhibits phagocytosis; capsule and melanin protect from oxidative injury; hematogenous and lymphatic dissemination to brain
A

CRYPTOCOCCOSIS

60
Q

what fungi?

  • Clinical diseases: primary ____ pneumonia, meningitis/meningeal encephalitis, hematogenous dissemination, genitourinary (prostatic) ____, primary cutaneous ____
A

CRYPTOCOCCOSIS

61
Q

Most common diagnosis of cryptococcal meningitis is made by

A
  • direct detection of the capsular polysaccharide antigen in serum or CSF (India ink)

Accomplished by using one of several commercially available latex agglutination or enzyme immunoassay kits

62
Q

what fungi?

Found in environmental niches, food and water, and normal human microbial flora

A

CRYPTOCOCCOSIS

63
Q

95% of all candida blood stream infections come from

A

C. albicans, C. Glabrata, C. parapsilosis, C. tropicalis

64
Q

CANDIDIASIS

Microscopically

A

All species exist as oval yeastlike forms that produce buds or blastoconidia
○ Also produce pseudohyphae and true hyphae (no glabrata)
○ Albicans: forms germ tubes and terminal, thick-walled chlamydoconidia (yeast)

65
Q

may undergo phenotypic switching - where a single strain of candida may change reversibly among several different morphotypes

what fungi?

A

Candidasis Albicans

Frequency of the switching phenomenon is too high to result from gene mutations and too low to be attributable to mass conversion (all cells in the population change their phenotype in response to signals from the environment

66
Q

what fungi?

VF: growth at 37 degress C, bud-hyphae transition, adherence, cell-surface hydrophobicity, cell wall mannans, proteases and phospholipases, phenotypic switching

A

Candidasis

67
Q

what fungi?

Pathogenesis: mucosal overgrowth with subsequent invasion; usually impaired mucosal barrier; hematogenous dissemination; transfer from hands of health care worker to catheter hub; catheter colonization and hematogenous dissemination

A

Candidasis

68
Q

what fungi?

Mode of infection: gastrointestinal translocation, intravascular catheters

A

Candidasis

69
Q

Most types of candidiasis represent endogenous infection in which the

A

normally commensal host flora take advantage of the host’s anti-candida barrier

Candidasis

70
Q

Clinical diseases: simple mucosa colonization, mucocutaneous ___, oral/vaginal thrush, hematogenous dissemination, hepatosplenic ___, endophthalmitis

A

Candidasis

71
Q

what fungi?

Primary site of colonization is the GI tract from mouth to rectum (saprobic habitat)
○ Found as commensals: vagina, urethra, skin, under nails

A

Candidasis

Albicans can be found in air, water, and soil

72
Q

what fungi and description

Oropharyngeal infection

A

○ Mucosal infections = thrush
○ Pseudomembranous type: raw bleeding when scraped
○ Erythematous type: flat, red, and sore areas
○ Leukoplakia: nonremovable white thickening of epithelium caused by candida spp
○ Angular cheilitis: sore fissures at the corners of the mouth

Candidasis

73
Q

what fungi?

Bronchopulmonary form: asthma, pulmonary infiltrates, peripheral eosinophilia, elevated serum IgE, and evidence of hypersensitivity to ____ antigens (skin test) may be seen

A

ASPERGILLOSIS

74
Q

___ can form either in the paranasal sinuses or in a preformed pulmonary cavity secondary to old tuberculosis or other chronic cavitary lung disease
§ May be seen on radiographic examination but are usually asymptomatic

A

Aspergilloma

ASPERGILLOSIS

75
Q

form of fungi in the human body?

A

yeast bc of 37c

76
Q

risk factor of candida infection

A

diabetes melitus

Microbiology (21 decks)

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