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micro exam 3 > FUNgi > Flashcards

FUNgi Flashcards

1
Q

WHat niche does FUngi fill

A

Principle decomposers (Saprophytic)

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2
Q

how does Fungi decompose

A

Secrete digestive enzymes

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3
Q

What kingdom are fungi

A

Their own kingdom

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4
Q

what type of cell are Fungi

A

Eukaryotes

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5
Q

where does Fungi live

A

Most are free living in nature

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6
Q

how does one get fungi

A

acquired from the environment, and some are part of the normal human flora

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7
Q

are fungi anaerobes or aerobes

A

Most are strict aerobes ( few are facultative anearobes)

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8
Q

how does Fungi cause disease

A

Induce an inflammatory response
through direct invasion
Destruction of tissues (some produce toxins)

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9
Q

Nucleus of Fungus as eukaryotic organisms

A

defined nucleus

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10
Q

chromosomes of Fungus as eukaryotic organisms

A

Linear Chromosomes

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11
Q

ploidy of Fungus as eukaryotic organisms

A

Diploid (mostly

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12
Q

can Fungus reproduce sexually as eukaryotic organisms

A

possibly

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13
Q

sexual reproduction of fungi leads to

A

Polyploidy leads to creating genetic diversity

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14
Q

What separates Fungi from plants

A

No chloroplasts or photosynthetic energy-producing mechanisms
Obtain nutrients from exogenous sources ( In nature, decaying organic matter)

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15
Q

what does Fungus cell membrane consist of that is different from mammalian cells

A

Contains Ergosterol (mammalian cells contain cholesterol)

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16
Q

how are Fungus cell walls diff from plants and bacteria

A

No peptidoglycan, LPS, glycerol or teichoic acid

Fungal walls contain chitin, mannan, and Glucan

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17
Q

The 3 categories of Fungi

A

Yeast
Molds
Dimorphic Fungi

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18
Q

Unicellular fungi

A

Yeast

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19
Q

Multicellular fungi

A

Molds

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20
Q

fungi that can exist as both mold and yeast

A

Dimorphic fungi

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21
Q

how does yeast reproduce

A

Asexual reproduction by budding

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22
Q

What kind of fungi is Candida albicans

A

Yeast

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23
Q

Types of Molds

A

Mycelium (Vegatative)

Hyphae (filamentous, tube-like)

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24
Q

how does Mold reproduce

A

sexual and asexual reproduction

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25
Q

How does Mold reproduce asexually

A

By conidia that form on the tips of growing Hyphae

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26
Q

how does mold reproduce by sexual reproduction

A

Through the development of spores

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27
Q

Septated Fungus

A

Hyphae that are separated protoplasm by cell walls

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28
Q

diagnostic factors for modlds

A

Are Hyphae present, and are they septated

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29
Q

What type of mold reproduction involved rearrangement

A

Asexual

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30
Q

are all hyphae the same for molds

A

Vary depending on species

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31
Q

what may be contained on the septa of molds

A

Pores and incomplete walls

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32
Q

why would septa of molds be incomplete or contain pores

A

Allow movement of Nutrients, organelles, and nuclei between adjacent cells

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33
Q

where does Mycelium Conidia form on mold

A

On hyphae

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34
Q

where does Arthroconidia develop

A

within the hyphae and eventually break off

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35
Q

Size of chlamydoconidia compared to hyphae

A

Chlamydoconidia are larger

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36
Q

how does Chlamydoconidia develop

A

with the cell or terminally

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37
Q

where are sporangioconidia borne

A

Terminally in sporangium sac

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38
Q

Where does Simple Conidia arise

A

Directly from a conidiophore

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39
Q

Types of Mycelium conidia

A

Arthroconidia
Chlamydoconidia
Sporangioconidia
Simple Conidia

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40
Q

asexual form of Fungus

A

Anamorph

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41
Q

what does an anamorph form to do asexual reproduction

A

Conidia

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42
Q

how does Asexual reproduction of fungus occure

A

Mitotic division of haploid nucleus with not genetic recombination

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43
Q

sexual form of fungus

A

Teleomorph

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44
Q

what is formed in sexual reproduction by fungus

A

spores (also called ascospores, sygospores, basidiospores, depending on strucutre)

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45
Q

how is a diploid nucleus created in sexual fungal reproduction

A

Haploid nuclei of donor and recipient cells fuse (Allowing for genetic recombination) then devides by classic meiosis

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46
Q

When temperature determines whether a fungi is mold or yeast

A

Thermally dimorphic

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47
Q

what does the temperature shift from soil to host in Histoplasma Capsulatum lead to

A

over 500 differently expressed genes

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48
Q

Is Dimporphism perminant

A

No it is reversable

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49
Q

what pathogenic part of fungi dimorphism linked to

A

Linked to virulence (if Dimorphic removed, loses it Pathogenicity)

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50
Q

How are Fungi encountered

A

Incidental contact In envirnoment
Normal Human Flora
Contact with infected individual

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51
Q

what does incidental contact with fungi do to healthy people

A

Develop no symptoms

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52
Q

what is needed to create an infection due to incidental contact with fungi

A

High inoculum exposure

Immunosuppression

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53
Q

what types of fungi are the normal human flora

A

Yeasts

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54
Q

What kind of infection can the normal human flora of yeast create

A

Disseminated infection in immunocompromised hosts

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55
Q

what are Dermatophytes

A

Fungi from contact with infected individuals

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56
Q

how good is the immune system at fighting fungi

A

Provides great protections (most infections are mild and self-limiting)

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57
Q

what is the primary barrier for fungal entry

A

Intact skin and mucosal surfaces

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58
Q

what all in the skin and mucosa provides a barrier to fungus

A

Desiccation
Epithelial Cell turnover
Fatty acids and low pH of skin

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59
Q

what on the skin prevents fungi growth

A

Bacterial normal flora

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60
Q

what may allow Fungus to enter the body

A

Alterations in normal flora (antibiotics)

Compromised Skin/mucosal surfaces (trama..) allow for entry and infections

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61
Q

what is needed to Eliminate fungal infections

A

T Cell-mediated immunity

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62
Q

what is the immune repsonse to fungal infections

A

CD4+ TH1/TH17

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63
Q

what patients are susceptible to fungal infections

A

AIDS patients

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64
Q

How are Fungal infections controlled and killed

A

Phagocytosis and killing by Neutrophils

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65
Q

What does the immune sytem do if fungal infectiosn are too large to be phagocytized

A

Phagocytic cells secrete enzymes and reactive oxygen species that can digest or kill large fungi

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66
Q

antibodies effect on fungi

A

can kill some fungi, as a minor component to protection (but may also be detrimental)

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67
Q

what cells are used to meidate immunity to fungal infections

A

T cells

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68
Q

How does the body respond to infection by fungus

A

CD4+ cells recognize presented antigens in MHC complex on APC (dendritic Cell) through interaction with their TCR
Stimulates release of Cytokines, which activate neutrophils and macrophages

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69
Q

Problem with Anti-fungals

A

unstable, toxic to humans, have undesirable side-effects

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70
Q

what type of therapy is preferred if possible to treat fungal infections

A

Topical Therapy

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71
Q

Types of antifungals

A

Azoles

Polyenes

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72
Q

Types of Azoles

A

Itraconazole
Ketoconazole
Clotrimazole
Micronazole

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73
Q

action of azoles

A

Interfere with ergosterol synthesis

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74
Q

What type of antifungal is an azoles

A

Fungistatic

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75
Q

Action of Polyenes

A

Lipophilic - bind to cell envelope ergosterols and form channels

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76
Q

Types of Polyenes

A

Amphotericin B
Nystatin
Hamycin

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77
Q

Amphotericin B action

A

Forms a pore in the membrane allowing for stuff to leak out

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78
Q

Itraconazole action

A

target enzyme for synthesis of Ergosterol

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79
Q

what do other anti-fungals target

A

DNA synthesis
PAthways downstream of ergosterol
Cell wall synthesis

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80
Q

What drug targets ergosterol in fungal cell membranes by forming channeling leading to the leakage of essential small molecules and cell death

A

Polyenes (amphotericin B)

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81
Q

Effectiveness of Polyenes (Amphotericin B)

A

Effective against most fungus ( can cross react with mammalian sterols too )

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82
Q

Problems with Polyenes (Amphotericin B)

A

Can cross reaction with mammalian sterols
Not Abosbed in GI tract
Not soluble at physiologic pH, must be administered intravenously at coloidal suspension
Side Effects: Chills, fever, headache, dyspnea
Can cause renal dysfunction leading to nephrotoxicity

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83
Q

when would you use Polyenes (Amphotericin B)

A

Life threatening Fungal infections

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84
Q

Resistance to Polyenes (Amphotericin B)

A

Rare as the fungi much change sterol composition of membrane

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85
Q

what can Systemic Azoles target

A

Either Yeast or mold forms of fungi

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86
Q

Body tolerance to azoles over Amphotericin B

A

Better Tolerated

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87
Q

Action of Azoles

A

Target enzymes that convert lanosterol to ergosterol resulting in defective membranes

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88
Q

Problems with Azoles

A

Toxic to liver

Cause cardiac myocyte repolarization increasing risk of cardiac arrhythmias

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89
Q

Resistance to Azoles

A

Can occure due to efflux pumps that transport drug out of cell

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90
Q

Types of Medically important fungi

A

Superficial cutaneous mycoses
Subcutaneous Mycoses
Opportunistic mycoses
Endemic (aka systemic) mycoses

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91
Q

the common fungal infection limited to the skin and skin strucutres

A

Superficial cutaneous mycoses

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92
Q

the fungal disease of the skin, subcutaneous tissue and lymphatics

A

Subcutaneous mycoses

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93
Q

Cause life-threatening system disease in immunosuppressed patients

A

Opportunistic mycoses

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94
Q

Infections caused by geographically restricted fungi (true pathogens) - cause serieous systemic infections in healthy individuals

A

Endemic (a.k.a systemic) mycoses

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95
Q

who usually gets cutaneous and superficial Mycoses

A

humans

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96
Q

Types of Cutaneous and Superficial Mycoses

A

Dermatophytes (tinea)

Malassezia (yeast or normal flora)

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97
Q

The most common fungal infection in humans

A

Dermatophyte

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98
Q

what is the source of Dermatophytes

A

Soil, animals, or humans

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99
Q

What do Dermatophytes infect

A

Keratinized Tissues (nails, hair, and skin) - the keratinase enzyme

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100
Q

what type of skin are dermatophytes restricted to

A

Non-viable skin (can’t grow at body temps of 37 degrees)

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101
Q

what type of Dermatophyte infections are hard to treat

A

Nail infections

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102
Q

Clincal diseases by Dermatophytes

A

Tineas (ringworm, athletes foot , Jock itch

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103
Q

Types of Dermatophyte skin infections

A

acute or chronic

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104
Q

What etiological genera are Dermatophytes

A

Molds :
Microsporum
Trichophyton
Epidermophyton

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105
Q

How to name Dermatophyte infections

A 
Based on latin word
Capitis: head
Corporis: body
Pedis: foot
Unguium: toenail
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106
Q

Niches for Dermatophytes

A

GEophilic: soil
Zoophili: domestic and wild aniamls
Anthropophilic: live in humans

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107
Q

how does Anthropophilic Dermatophytes establish infection in humans

A

Chronic

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108
Q

Dermatophytes as part of Normal flora

A

NO

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109
Q

how does Dermatophytes tend to spread with humans

A

Crowding facilitates spread, due to contagious nature

Survives on locker room floors

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110
Q

what does the most body do to fight pathogenic immunity of Dermatophytes

A

Innate immunity high for most people

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111
Q

how does Innate immunity stop dermatophytes

A

Skin and mucosa a good barrier (dry, cell sloughing, fatty acid, low pH)
Bacterial Flora hostile to fungus

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112
Q

what is required for Dermatophytes to infect

A

Skin trama

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113
Q

what helps Dermatophytes to establish and maintain infection

A

Moisture

skin occluded with nonporous materials (shoes)

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114
Q

how does Hydration and temp effect Dermatophytes

A

Increase due to interference with stratum corneum function

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115
Q

how can chronic infection with Dermatophytes occure

A

When fungal growth rate and skin dequamation are balanced

Poor Inflammatory response

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116
Q

why do dermatophytes grow in a circle

A

Hyphae grow outward in centrifugal pattern

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117
Q

what is found at the Inflammed margin of the Dermatophyte damage

A

Viable fungal elements

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118
Q

what is found at the center of the Dermatophytes

A

few/no viable fungi

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119
Q

What does healing tissue do to the Dermatophyte infection

A

Healing tissue is refactory (resistant to infection)

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120
Q

Commonality of systemic infection of Dermatophytes

A

extremely rare

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121
Q

why are systemic infections of Dermatophytes so rare

A

Inability to grow at human body temp

Hard to get iron

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122
Q

what binds to iron, harming the Dermatophytes ability to grow

A

Transferrin

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123
Q

were can Dermatophytes spread

A

From skin to other keratinized strucutres

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124
Q

when Hyphae invade the ahir shaft, causing the hair to break

A

Tinea Capitis

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125
Q

what Can Tinea Capitis do if hair breaks at the root

A

Fungus can plug hair follicle, cuasing bald pathces

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126
Q

Nail plate fungal invasion

A

Tinea Unguium

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127
Q

nail plate invasion by fungus leads to

A

Hyperkeratosis and discoloration

Dislodges and distorts nail (onychomycosis)

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128
Q

What is Dermatophytes often diagnosed incorrectly as

A

Non-infectious disorder that cause similar skin inflammation

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129
Q

What disease may have similar feats and are treated with steroids (bad for fungi) incorrectly instead of Dermatophytes

A

Psoriasis and contact dermatitis

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130
Q

how to diagnose Dermatophytes

A

FLuoresce in UV (somtimes)

Microscopic examination of material from lessions

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131
Q

How Can septate Hyphae be visualized

A

Using potassium hydroxide or cacofluor white preparations of scales scraped from advancing edge of lesions

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132
Q

Superficial Mycoses causing Patches with greasy Scales in facial hiar and scalp

A

Dandruff

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133
Q

Superficial Mycoses that causes Hypopigmented or Hyperpigmented pathces on chest or neck with Scaling

A

Tinea Versicolor

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134
Q

what can cause Tinea Versicolor

A

Malassezia Furfur

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135
Q

where does Malassezia Furfur grow

A

On skin lipids - common to normal flora

136
Q

How can Malassezia( cause superficial mycoses

A

Part of normal flora, but may colonize the stratum corneum

137
Q

what kind of fungus is Malassezia

A

Yeast

138
Q

how does Dermatophytosis and Superficial mycoses usually resolve

A

spontaneously

139
Q

how to treat Dermatophytosis and superficial mycoses

A

Topical anti-fungal (terbinafine or azoles)

140
Q

time it tkaes for topical antifungals to work

A

Takes several weeks

141
Q

when would systemic antifungals be indicated

A

In some wide-spread infections (miconazole or ketoconazole)

142
Q

why are nail infections hard to treat

A

Slow turnover of infected nail and poor penetration of antifungals

143
Q

Mycoses of Implantation

A

Subcutaneous Mycoses

144
Q

how does Subcutaneous Mycoses organisms enter skin

A

Via thorns or splinters

145
Q

how do subcutaneous mycoses infections evolve

A

over several weeks

146
Q

Spread of Subcutaneous Mycoses

A

Generally localized

147
Q

who does Subcutaneous Mycoses effect the worst

A

Immunocompromised patients (lesions usually heal following antifungal treatment)

148
Q

What happens when Subcutaneous Mycoses infects Immunocompromised patients

A

Widespread cutaneous and visceral infections

149
Q

Types of Subcutaneous Mycoses

A

Sporothrix Schenckii
Chromoblastomycosis
mycetoma (madura foot)

150
Q

what type of Fungus is Sporothrix Schenckii

A

Thermally dimorphic fungus (environment - mold, tissue - yeast)

151
Q

where is Sporothrix schenckii found

A

soil, moss, decaying wood, and veggies

152
Q

what does Sporothrix schenckii cuase

A

Sporotrichosis

Disseminated disease

153
Q

Other name for Sporotrichosis

A

Rose picker’s disease

154
Q

how is fungus introduced for sporotrichosis

A

By trauma (thorn prick)

155
Q

What does sportrichosis once infection begins and spreads

A

Starts as a small lesions (ulceration and/or erythema)

spreads through lymphatic vessels

156
Q

when Sporothrix schenckii gets in to the lymph

A

Lymphocutaneous sporotrichosis

157
Q

who gets disseminated disease

A

only in immunocompromised patients

158
Q

what does Disseminated disease affect

A

Afflicts joings, brain, spine (serious)

159
Q

How is Disseminated disease treated

A

Antifungals (itraconazole for 3-6 months)

160
Q

Infection progression by Sporothrix Schenckii

A

Painless papules developing a few weeks to a few months after inoculation
Papules enlarge and eventually ulcerate, leaving open sores
Infection follows lymphatic’s

161
Q

Why is Microscopic examination of Sporothrix Schenckii not very helpful in diagnosis

A

Very few organisms can be detected with KOH preparations

162
Q

How definitively diagnose Sporothrix Schenckii

A

depends on Culture of infected pus or tissue, grow 205 days on standard medical mycology media

163
Q

treating Cutaneous Sporotrichosis

A

Oral anti-fungals (itraconazole)

164
Q

treating Pulmonary systemic infections

A

Itraconazole, but may require additional drugs like amphotericin B

165
Q

What does CHromoblastomycosis cause

A

Dematiaceous Fungi (pigmented black fungus)

166
Q

What does Chromoblastomycosis result in

A

Scaly, wart like lesions on feet or leg

167
Q

what causes Chromoblastomycosis

A

Soil mold (working barefoot in endemic areas is a risk factors

168
Q

How to treat chromoblastomycosis

A

Surgery or amputation

169
Q

what can Chromoblastomycosis infect

A

Also infect bone and muscle

170
Q

where in the world does Chromoblastomycosis occur

A

In rural tropical areas of the world (Madagascar and brazil)

171
Q

what causes Mycetoma

A 
Different species of environmental fungi)
also actionomycetes (Nocardia)
172
Q

what does cronic infection by mycetoma lead to

A

sinus tract nodule

discharge of visible grains (colonies of fungus)

173
Q

what happens to the draining sinuses in Mycetoma

A

Massive induration (loss of elasticity and pliability) with draining sinuses

174
Q

what is a risk factor for Mycetoma

A

Walking barefoot in tropical environments

175
Q

Opportunistic Fungal Pathogens

A

Candida (albicans, glabrata, Parapsilosis)
Aspergillus (fumigatus, Flavus)
Mucormycetes (Rhizopus, Mucor)
Pneumocystis jiroveci

176
Q

What causes Candidiasis

A

Candida

177
Q

What causes Aspergillosis

A

Aspergillus

178
Q

what causes Mucomycosis

A

Mucormycetes

179
Q

what causes Pneumocytosis

A

Penumocystis jiroveci

180
Q

source of Candida

A

Normal flora - yeast

181
Q

Source of Aspergillus

A

Common environmental mold

182
Q

Source of Mucomycetes

A

Environmental mold

183
Q

source of Pneumocystis jiroveci

A

Fungus

184
Q

why are opportunistic fungal pathogens not considered true pathogens

A

only cause disease when host defenses are decreased

185
Q

What type of patients would be immunocompromised

A

Immunosuppressive therapy - organ and stem cell transplant
Hematologic malignancies
HIV infection
Corticosteroid and other immunosuppressive drugs (Humara)

186
Q

Risk factors aside from immunocompromised for opportunistic fungal pathogens

A 
Major burns wounds or trauma
Central Venous Catheters
Broad-spectrum antibiotics
Intensive care unit
Real failure requiring dialysis
Premature babies
187
Q

Most frewuent oppotrunistic fungal pathogen

A

Candida Albicans

188
Q

where do candida albicans grow

A

Rapid growth on standard rich media

189
Q

what does Candida albicans look like on standard rich media

A

Staphlococci

190
Q

how does Candida albicans reproduce

A

Form buds or blastoconidia

191
Q

formation of Hyphae by candida albicans

A

some form hyphae or pseudohyphae in vivo

192
Q

what type of Fungus is Candidia Albicans

A

Polymeorphic (not true dimorphism)

193
Q

what typ eof hyphae are associated with invasive candidiasis

A

Mycelial (hyphae)

194
Q

What does Candida Shift from and to with pathogenesis

A

Shift from yeast to hyphae

195
Q

what does hyphae of Candida do with Epithelial cells

A

Form strong attachment

196
Q

what does the Hyphae of Candida secrete

A

Proteinases and phospholipases that digest epithelial cells

197
Q

what is the roll of the proteinases and phospholipases secreted by Hyphae of Candida do

A

Facilitate invasion by digesting keratin and collagen

198
Q

Problem with Candida and Prosthetics

A

Biofilm

199
Q

what type of infection is most Candidiasis

A

Endogenous

200
Q

where is Candidiasis found as a colony

A

GI tract
Vagina
Skin

201
Q

who all is colonized by Candidiasis

A

30-50% of people

202
Q

when does Candidiasis infect

A

Only when normal flora is disrupted or patient is immunocompromised

203
Q

what is the biggest Culprit of normal flora disruption leading to Candidiasis

A

Bread spectrum antibiotics ( then skin macerations, moist hot conditions)

204
Q

what increses mucosal infections of CAndidiasis

A

Decreased T-cell function (aids patients)

205
Q

What Candidiasis yeast infection is in the Mucosa

A

Trush

206
Q

Appeaenceof thrush

A

Thick, white plaques on oropharyngeal and vaginal mucosa

207
Q

when Candidiasis yeast infections is Cutaneous

A

Intertriginous Candidiasis

208
Q

where does one find Intertriginous candidiasis

A

warm and moist areas of skin (groin, under boobs, Diaper rash)

209
Q

what does Candidiasis yeast infections do to the Urinary tract

A

Produce Cystis, pyelonephritis, renal abscenss

210
Q

what would casue of UTI by Cndidiasis yest infections

A

Urinary catheters, Kidnery transplants

211
Q

a systemic Candidiasis infection

A

Disseminated candidiasis

212
Q

hoe does a systemic infection of Candidiasis occur

A

Follows superficial infections when candida gains access to the bloodstream

213
Q

When Candida gains access to bloodstream

A

Disseminated Candidiasis

214
Q

Seriousness of Disseminated Candidiasis

A

Life threatening

215
Q

How does CAndida enter the blood stream

A 
Through Skin lesions
Disruption of GI tract
Prosthetic Devices colonized by Candida biofilms
Intravenous catheters
Urinary tract
216
Q

Where does Candida form Micro-abscesses once in the blood stream

A 
Kidneys
Meningitis
Eyes
liver and spleen
Spine
Heart on prosthetic valves
217
Q

What are the symptoms of Disseminated CAndidiasis

A

Similar to bacterial infections

often involve eyes though to lead to blindness (endopthalmitis)

218
Q

Diagnosis of Mucosal or cutaneous candidiasis

A

Microscopic examination of scrapping - budding yeast and pseudohyphae
Culture on blood agar plates to grow within 24 hours

219
Q

Diagnosis of Invasive (Disseminated) Candidiasis

A

Hard to document:
culture from blood (not sesnitive) requires biopsy of involved tissue
Germ-test tube - elongated buds from yeast when exposed to calf serum

220
Q

treatment of Mucosal Candidiasis

A

Topical antifungal creams

Systemic therapy for severe cases

221
Q

TReatment for Systemic Candidiasis infection

A

systemic antifungal (min of 2 weeks)

  • Fluconazole and Echinocandin most common
  • AMphotericin B - used in some cases
222
Q

Immunity to Candidiasis

A

Humoral and cell mediated immunity are involved in defence

223
Q

activity of Antibodies against CAndidiasis

A

Oposonizing IgG antibodies fight against yeast carbs mannan

- this activates the classical complement pathway

224
Q

What keeps CAndidiasis in check on mucosal surfaces

A

T cell mediated Immunity via Neutrophils

225
Q

The main host defence against invasion through mucosa

A

Neutrophils (T-cell mediated immunity)

226
Q

What immuno-deficiency leads to high spread of candida

A

Neutropenia (low neutrophils)

227
Q

What balance is needed to clear Candidiasis infection

A

Balance between Th1 and Th2 mediated Cytokine response

228
Q

what cytokine is correlated with enhance resistance to Candida Infection

A

Th1 - mediated immunity (IL-2, IFN-gamma, TNF-alpha)

229
Q

what Cytokine response is associated with Chronic disease of Candida

A

Th2 response (IL-4, IL_6, and IL-10)

230
Q

What does Aspergillosis look like?

A

Filamentous fungi

231
Q

how does Aspergillosis reproduce

A

Forming conidia and aerial conidiophores (sexual reproduction)

232
Q

where is Aspergillosis found

A

Uniquitous in soil, manuure, decomposing vegitation

233
Q

how would someone get pneumonia from apsergillosis

A

Inhalation of spores by immunocompromised people

234
Q

How does Aspergillosis enter

A

Conidia are inhaled into the upper and lower respiratory tracts where they can germinate into hyphae

235
Q

What happens to inhaled Aspergillosis (Conidia) in healthy individuals

A

Macrophages kill conidia that reach aveoli (but can’t kill hyphal form)
Neutrophils line up along hyphae and secrete reactive oxygen intermediates that kill the fungus

236
Q

Where does Conidia aspergilosis infection occur

A

in immunocompromised host

237
Q

WHere hyphae invade through blood vessel walls causing tissue infarction, hemorrhages, and necrosis)

A

Agioinvasiv fungus

238
Q

Aspergillosis infection manifestations

A

Aspergillus pneumonia
Disseminated aspergillosis
Allergic respiratory disease
Aspergilloma (fungus Balls)

239
Q

most common ASpergillosis infection

A

Aspergillus pneumonia

240
Q

who is at increased risk of aspergillus pneumonia

A

Patients with emphysema and bronchiectasis

241
Q

how does Disseminated aspergillosis occure

A

Through the bloodstream and affects any organ system

242
Q

what type of disseminated aspergillosis is the worst

A

CNS

243
Q

How does Allergic respiratory diease from aspergillosis occure

A

People with allergies build up mucus allowing fungus to grow, cuasing more allergies and more mucas in inflammation

244
Q

how gets Aspergilloma

A

REsults in patients with prior lung infections with scarring and cavities (TB) and fungal spores germinate in cavities and fungal hyphae grow into balls

245
Q

where do people with emphysema and bronchiectasis get more aspergillus pneumonia

A

Walls of airways thicken from chronic inflammation and resident macrophages and neutrophils are less effective at clearing infections from areas

246
Q

result of ASpergillus pneumonia in people with severe defects in immunity

A

fungal hyphae penetrate intact lung tissue leading to necrosis

247
Q

when does DIsseminated aspergillosis occure

A

Follows primary aspergillosis when fungus enters blood stream and then spreads to organs

248
Q

CNS involvement of DIsseminated aspergillosis leads to

A

Mental status changes

249
Q

how to increase survival rate of disseminated aspergillosis patients

A

Surgical debridement

250
Q

Diagnosis of ASpergillosis

A

Grow on Sabouraud

Tissue biopsy to confirm hyphae in tissue, but not specific for Aspergillus

251
Q

why is it hard to grow Aspergillosis

A

Contamination

252
Q

Treating Aspergillosis

A

Voriconazole - choice

Amphotericin B or echinocandin also used

253
Q

Why was there an outbreak of fungal meningitis

A

Steroids contaminated with aspergillus

254
Q

Most common species of Zygomycosis

A

Absidia, Rhizopus and Mucor

255
Q

where are Zygomycetes found

A

Ubiquitous saprophytes in soil, food, bread

256
Q

Where can Zygomycetes colonize

A

Oral mucosa, Paranasal sinuses, and pharyngeal mucosa

257
Q

Who does Zygonmcetes cause disease in

A

People with diabetes(Diabetic Ketoacidosis) and immunosuppressed people

258
Q

How my Zygomycetes manifest

A

Pulmonary disease (fungal pneumonia) or rhinocerebral disease (invasive necrotic lesions)

259
Q

where does Pneumocystis colonize

A

Ubiquitous colonizer of human airway

260
Q

who gets a disease from Pneumocystis

A

Immunovompromised persons with aids

261
Q

Virulence of Pneumocystis

A

Low Virulences

262
Q

How does Pneumocystis Pneumonia present itself

A

Diffuse Pneumonitis (lung inflammation) leading to diffiult labored and rapid breathing , mild fever

263
Q

Progressive Dyspnea and Tachypnea

A

Difficult labored and rapid breathing

264
Q

what type of fungus is Crytococcosis

A

Environmental yeast

265
Q

what does Cryptococcosis express in the host

A

Huge Polysaccharide Capsule

266
Q

Where is Crytococcosis found

A

Soil and brid exceta

267
Q

can Crytococcosis infect normal people

A

Yes, about 20%

268
Q

VIrulence factors of Cryptococcus neoformans

A

Capsule
Laccase enzyme
Phospholipases
Urease

269
Q

What is Cryptococcus Neoformans Capsule made of

A

Glucuronoxylomannan and glucuronoxylomannogalactan

270
Q

roll of Capsule

A

Immunosuppresssive function (repressed under environmental conditions)

271
Q

what does the LAccase enzyme do

A

Produces antioxidant melanin pigments

272
Q

does Fungi have virulence factors like bacteria

A

Yes

273
Q

How does Cryptococcois infect

A

yeast are inhaled into alveoli producing an asymptomatic lung infections

274
Q

what controls the Cryptococcosis infections

A

T cell mediated immunity

275
Q

where does Cryptococcosis spread

A

HematogenousSpread from the lung to meningitis

276
Q

Severity of Meningitis from Cryptococcis

A

Acute to Chronic

277
Q

If you have aids and Cryptococcosis, what happens

A

Diffuse pulmonary infiltrates
Skin lesions
Widespread visceral infection in internal organs

278
Q

Culturing Cryptococcosis

A

Easily cultured on agar for identification

279
Q

How to Diagnose Cryptoccosis

A

Culture, oberseve Encapsulated uding yeast in CSF using latex agglutination

280
Q

Treating Meningitis via Cryptococcosis

A

Amphotericin B and Flucytosin followed by fluconazole

281
Q

Treating Pulmonary infection from Cryptococcosis

A

Fluconazole

282
Q

Endemic Mycoses

A

Geographically restricted
Dimorphic
infect healthy

283
Q

where is Histoplasmosis found

A

Bird and bat poop in the Mississippi and Ohio river valleys

284
Q

where is Blastomycosis found

A

Soil mold in the Mississippi river valley and southereastern and North central steates

285
Q

where is Coccidioidomycosis found

A

Desert soils in Southwestern U.S.

286
Q

Symptoms of Endemic Mycoses

A

Mostly asymptomatic and mild self- limiting

287
Q

Clearing Endemic Mycosis

A

Cell mediated (CD4- T cells)

288
Q

Primary site of entry for Endemic Mycoses

A

Lung

289
Q

What type of Fungus is Histoplasmosis

A

Dimorphic soil fungus

290
Q

where is Histoplasmosis a mold and yeast

A

Environment with macroconidia and microcondidia ( mold)

yeast in body

291
Q

The infectious form of Histoplasmosis

A

Microcondidia

292
Q

Who all has been infected by Histoplasmosis

A

90% of people in endemic areas

293
Q

Where is Histoplasmosis found

A

Soil with High nitrogen (poop)

294
Q

Why would there be an outbreak of Histoplasmosis

A

Disrupt soil due to demolition of old buildings

295
Q

where does Histoplasma tun into yeast

A

in the lungs

296
Q

What does Histoplasma infect

A

inside Macrophages and neutrophils by modulating phagolsomsomal pH

297
Q

why does Histoplasmosis disease manifestation change

A

Based on number of Conidia inhaled and host response

298
Q

most Infected people with Histoplasmosis symptoms

A

None or mild

299
Q

If large amounts of Histoplasmosis is inhaled

A

Even healthy people get bad pneumonia

300
Q

How to get rid of Histoplasmosis in healthy people

A

Will clear on its own without antifungals

301
Q

Who has difficulty clearing Histoplasmosis

A

Patients with COPD- eventually becomes fatal

302
Q

How common is Hisseminated Histoplasmosis

A

Nearly everyone that is infected

303
Q

Symtpotms of Disseminated Histoplasmosis

A

usually asymptomatic

Symptoms in people with AIDs ro Immunosuppressive therapy

304
Q

Symptoms of Acute Disseminated Histoplasmosis

A

Fever, chils, fatigue, mucous membrane ulcer, Hepatosplenomegaly, pancytopenia, sepsis syndrome

305
Q

who gets chronic progressive disseminated histoplasmosis

A

Old people

306
Q

What happens if Chronic Progressive Disseinated Histoplasmosis is untreated

A

Patients dies

307
Q

Diagnoisi if Histoplasmosis

A

Grow from sputum, blood, tissues, or body fluids

Histopathological analysis of intracellular yeast in bone marrow, liver, lungs, lymph nodes- faster

308
Q

treating Histoplasmosis for healthy, moderate and sever infrections

A

healthy- none
moderate: itraconzaole
Severe> amphotericin B to contain than itraconzole

309
Q

Whereis Blastomycosis a fungus and yeast

A

Fungus in envirnoment and yeast in body

310
Q

Cell wel of Blastomycosis

A

Thicccc with broad based budding

311
Q

Commonness oF blastomycosis outbreaks

A

Mostly sporadic cases with maybe a small outbreak

312
Q

Who does Blastomycosis disease occure

A

INhaled into lungs leading to pneumonia

313
Q

What does Blastomycosis do when out of lungs

A

Disseminated
Skin lesions occur
GRanulomas develop

314
Q

Who to clear Blastomycosis

A

Cell-mediated immunity to clear yeast by phagocytosis by macrophages and neutrophils

315
Q

Why does Coccidioidomycosis/ valley fever form blooms

A

Proper envirnomental conditions

316
Q

How many people are infected by Coccidioidomycosis/ valley fever in endemic areas

A

80% of the pop

317
Q

How is Coccidioidomycosis spread preson to person

A

It is not

318
Q

What causes the Dimoprhic change in Coccidioidomycosis.valley fever

A

Not temp

319
Q

Treatment and diagnosis of Blastomycosis

A

Similar to Histoplasmois

320
Q

the mold form of Coccidioidomycosis

A

Arthroconidia

321
Q

what happens to Arthroconidia of Coccidioidomycosis when in tissue

A

transform into Spherules filled with Endospores

322
Q

is Arthroconidia or Spherules(yeast) of Coccidioidomycosis resistant to phagocytosis

A

Spherules

323
Q

is Arthroconidia or Spherules(yeast) of Coccidioidomycosis infections

A

Arthroconidia (inhaled by lungs)

324
Q

Life cycle of COccidioides

A 
Hyphae differentiate into arthroconidia 
These break loose and suspend into air
spread in soil and air
in human differentiation produces cleavage and spherules
spherules rupture and release endospores
325
Q

Coccidiomycosis infections symptoms in healthy people

A

None or mild

326
Q

What is a symptomatic Coccidiomycosis infection

A

Desert rheumatism or valley fever

327
Q

Stages of Acute Pulmonary Coccidiomycosis infection

A 
Chest pain, cough, fever, and chills
Joint pain, stiff neck, muscle ache
Erythema nodosum (rash and painful lumps in lower legs
328
Q

What happens to Acute pulmonary infection

A

Usually self limiintg,
may become disseminated
Also may lead to A chronic Pulmonary infections

329
Q

Control of Coccidiomycosis

A

Cell-mediated immunity (CD4 T cells)

330
Q

Commonnes of Disseminated and Chronic Coccidiomycosis

A

less than 1%

331
Q

Who is most likely to get Disseminated and CHronic Coccidiomycosis

A

Dark people
Pregnant women
Immunocompromises

332
Q

Disseminated an Chronic Coccidiomycosis can lead to

A

Cutaneous, subcutaneous, and osteoarticular infections that spread to other organs

333
Q

Result of Chronic Meningitis of Coccidiomycosis

A

Complication can be fetal

334
Q

Treating Chronic Meningitis of Coccidiomycosis

A

Life time antifungal

335
Q

Diagnosis of Coccidiomycosis

A

Cultured

Histopathological analyis to seee if presence of spherules in tissues

336
Q

Problem with Culturing Coccidiomycosis

A

Mold is highly infectious and may infect lab workers

337
Q

treatment of Coccidiomycosis if chronic pulmonary infections

A

Itraconazole or fluconazole for 12-24 months

Amphotericin B - if severe

micro exam 3 (15 decks)

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