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Micro unit 2 > L8 > Flashcards

L8 Flashcards

1
Q

Fungi fill an important niche in nature:

A

Principle decomposers (saprophytic) - secrete digestive enzymes

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2
Q

Make up their own

A

Kingdom - Fungi are Eukaryotes

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3
Q

Most fungi are

A

free living in nature and are acquired from the environment - a few are part of normal human flora.

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4
Q

Most fungi are

A

• Mostly strict aerobes (a few are facultative anaerobes)

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5
Q

Fungi cause disease by

A

• Cause disease by inducing an inflammatory response or through direct invasion or destruction of tissues (some produce toxins)

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6
Q

Fungus have

A

defined nucleus

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7
Q

Fungal Cell membrane consists of

A

ergosterol

• Mammaliancellscontaincholesterol

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8
Q

Fungal Cell walls are unique

A
  • With chitin, mannan and glucan

* Different from cell wall of plants and bacteria

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9
Q

Fungi of medical importance - 3 major categories

A

Yeast- unicellular fungi • Example: Candida albicans
• Molds- multicellular fungi • Mycelium (vegetative)
• Dimorphic fungi- exits as both mold and yeast

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10
Q

Fungal – Molds (multicellular)

A

Filamentous fungi- (mycelial - vegetative form)

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11
Q

molds - reproduction

A

asexuallybyconidiathatformonthetips
of growing hyphae
• Sexual reproduction through the development of spores

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12
Q

Dimorphic fungi determined by

A

Thermally dimorphic- Temperature determines whether mold or yeast

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13
Q

Fungi are encountered by three ways

A

Incidental contact in the environment
• Most healthy people develop no symptoms
• High inoculum exposures and/or immunosuppression can result in infection

Normal human flora (commensal organisms)
• Usually yeasts
• Disseminated infections in immunocompromised hosts

Contact with infected individual – (dermatophyte)

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14
Q

Innate immunity provides

A

great protection against fungi

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15
Q

• Most fungal infections are

A

mild and self-limiting

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16
Q

• Intact skin and mucosal surfaces are

A

primary barriers

-Desiccation, epithelial cell turnover, fatty acids and/or low pH of skin- important in limiting fungi

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17
Q

• Bacterial normal flora compete with

A

fungi and inhibit growth

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18
Q

Alterations in normal flora (antibiotics) or compromised skin/mucosal surfaces (trauma, etc.) allow for

A

entry and infection

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19
Q

T cell-mediated immunity is required to eliminate

A

fungal infections.

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20
Q

Phagocytosis and killing by Neutrophils is primary mechanisms for containing

A

fungal infections

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21
Q

Some fungi are too large to be

A

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

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22
Q

Antibodies participate in

A

killing some fungi

• minor component to protection, can even be detrimental

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23
Q

Fungal Diseases examples

A

thrush, Oral histoplasmosis

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24
Q

Endemic mycoses-

A

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

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25
Q

Opportunistic mycoses-

A

cause life-threatening systemic disease in immunosuppressed patients.

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26
Q

Subcutaneous mycoses-

A

fungal disease of the skin, subcutaneous tissue, and lymphatics.

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27
Q

Superficial cutaneous mycoses-

A

common fungal infections limited to the skin and skin structures.

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28
Q

Histoplasmosis- endemic mycoses

A

Histoplasma capsulatum (Mississippi and Ohio River Valleys) Bird and bat poop

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29
Q

Endemic mycoses - Blastomycosis-

A

Blastomyces dermatitidis (Mississippi river valley and southeastern and North Central States) Soil mold

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30
Q

Coccidioidomycosis- endemic mycoses

A

Coccidioides (Southwestern United States) Dessert soils

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31
Q

Endemic mycoses description

A

Common infections restricted to geographical areas
• Mostly asymptomatic- or mild self- limited symptoms
• Cell-mediated immunity (CD4- T- Cells) required for clearance
• Lung is primary site of entry

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32
Q

Histoplasmosis-

Histoplasma capsulatum description

A

Dimorphic soil fungus- mold in environment with macroconidia (tuberculate) and microcondidia (infectious form). At 37 °C (body temp.) assumes a yeast like form
• 90% of people have been infected in USA
• Grows in soil with high nitrogen content fertilized by birds and in caves where bat guano (poop) is present
• Clusters of infection (outbreak)- demolition of old buildings that disrupts soil

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33
Q

Histoplasma capsulatum In lungs, transforms into

A

yeast phase

-poorly understood process but essential for disease process.

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34
Q

Histoplasma capsulatum Reticuloendothelial (macrophage) system infection

A

Remains viable in macrophages-

modulates phagolysosomal pH

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35
Q

Histoplasmosis - Disease manifestation depends on

A

number of conidia inhaled and the host response (cell-mediated immune response)

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36
Q

Histoplasmosis - • Most infected people have no or only

A

mild symptoms

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37
Q

Histoplasmosis - • Ifalargeamountisinhaledevenhealthypeopleget

A

severe pneumonia

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38
Q

Histoplasmosis - • Somepatientsdevelop

A

fever,chills,anorexia,fatigueanddry cough:

• If healthy- infection can clear on its own without antifungal treatment

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39
Q

Histoplasmosis - • PatientswithCOPDareat

A

higherriskofcomplications- • Chronic cavitary pulmonary histoplasmosis, which is eventually fatal

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40
Q

Disseminated Histoplasmosis - Occurs in nearly everyone infected with

A

H. capsulatum- usually asymptomatic

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41
Q

Disseminated Histoplasmosis - Symptomatic disease more likely in people with

A

AIDS (cell-mediated immune deficiencies) or with immunosuppressive therapy

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42
Q

Disseminated Histoplasmosis - Acute disseminated histoplasmosis-

A

fever, chills, fatigue, mucous membrane ulcers, hepatosplenomegaly, pancytopenia, sepsis syndrome.

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43
Q

Disseminated Histoplasmosis - Chronic progressive disseminated histoplasmosis-

A

happens in older adults- patients die if not treated

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44
Q

Diagnosis of Histoplasmosis - Growth of organism (definitive) -

A

from sputum, blood, tissues, or body fluids. Can take up to 6 weeks

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45
Q

Diagnosis of Histoplasmosis - Histopathological analysis (with a special stain) of

A

small intracellular yeasts in bone marrow, liver, lung, or lymph nodes is quicker.

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46
Q

Treatment of Histoplasmosis - In healthy patient- self limited no

A

treatment needed

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47
Q

Treatment of Histoplasmosis - Mild-to-moderate infections-

A

Itraconazole for 3 to 12 months

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48
Q

Treatment of Histoplasmosis - Severe infections-

A

amphotericin B to contain, then switch to itraconazole

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49
Q

Blastomycosis - Dimorphic (fungus in environment, yeast at 37∘C)

A

yeast have a thick cell wall and broad- based budding

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50
Q

Blastomycosis - Endemic to

A

Mississippi River Valley and Southeastern states

Soil and decaying wood a likely source

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51
Q

Blastomycosis - Mostly

A

sporadic cases- sometimes small outbreaks

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52
Q

Blastomycosis infection - Disease occurs when

A

inhaled into the lungs- multiplies leading to pneumonia

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53
Q

Blastomycosis- infection - Skin lesions also

A

commonly occur- dissemination - spread by blood

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54
Q

Blastomycosis- infection - Granulomas can develop

A

• Yeast remains viable and reactivate later

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55
Q

Blastomycosis- infection - Cell-mediated immunity is necessary for

A

clearance-yeast are phagocytosed by macrophages and neutrophils

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56
Q

Blastomycosis- infection - Diagnosis and treatment

A

similar to histoplasmosis

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57
Q

Coccidioidomycosis - Valley fever - Found in

A

dessert soil and burrows

of desert animals

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58
Q

Coccidioidomycosis - Valley fever - Proper environmental conditions allow

A

“blooms” to form (perfect storm of rainfall, heat, and wind)

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59
Q

Coccidioidomycosis - Valley fever- In endemic areas-

A

80% of population have been infected

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60
Q

Coccidioidomycosis - Valley fever- San Jaquin Valley Fever-

A

real problem for prison population- efforts to keep dust levels down

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61
Q

Coccidioidomycosis - Valley fever - Dimorphic - not

A

temperature dependent

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62
Q

Coccidioidomycosis - Valley fever - Arthroconidia (mold form) are highly

A

infectious; inhaled into alveoli (lungs)

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63
Q

Coccidioidomycosis - Valley fever - In tissues- transform into large

A

spherules (50-

100 𝝻m) filled endospores (100’s)

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64
Q

Coccidioidomycosis - Valley fever - Arthroconidia are

A

phagocytosed and killed, but spherules (yeast) resist phagocytosis

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65
Q

Coccidiomycosis infections - Most healthy people have

A

no or only mild symptoms

66
Q

Coccidiomycosis infections - When symptomatic-

A

Desert rheumatism or Valley Fever

67
Q

Coccidiomycosis infections - Acute pulmonary infection-

A

self-limiting (no treatment required)

68
Q

Coccidiomycosis infections - symptoms

A

Chest pain, cough, fever and chills
• Joint pain (arthralgias), stiff neck, muscle aches
• Erythema nodosum (rash and painful lumps-lower legs)
• Can become disseminated disease
• Chronic pulmonary infection can occur months or years later

69
Q

Coccidiomycosis infections - Cell-mediated immunity

A

(CD4 T-cells) is needed to control (AIDS patients are more susceptible)

70
Q

Disseminated Coccidiomycosis - Increased risk in:

A

dark-skinned individuals, pregnant women, and immunocompromised

71
Q

Disseminated Coccidiomycosis - Can result in

A

cutaneous, subcutaneous, and osteoarticular infections that spread to other organs (CNS)

72
Q

Disseminated Coccidiomycosis - Chronic meningitis can be a

A 
complication
• Fatal if not treated
• Requires life-time antifungal therapy
• Antifungals have severe side effects- light sensitivity
• Skin cancers results
73
Q

Coccidiomycosis- diagnosis - Can be cultured-

A

growth within several days

74
Q

Coccidiomycosis- diagnosis - Mold on plates can be highly infectious-

A

laboratory workers should

be warned coccidomycosis is suspected

75
Q

Coccidiomycosis- diagnosis - Histopathological analysis possible-

A

presence of spherules in tissues is diagnostic.

76
Q

Coccidiomycosis- treatment - Itraconazole or fluconazole for

A

12-24 months depending on extent of

disease.

77
Q

coccidiomycosis - treatment - Amphotericin B-

A

if infection is severe

78
Q

Opportunistic fungal pathogens-Not considered true

A

pathogens - only cause disease when host defenses are decreased

79
Q

• Patients at high risk for fungal infections:

A

Immunocompromised patients

Otherriskfactors

80
Q

Immunocompromised patients

A

Immunosuppressive therapy- organ and stem cell transplant
• Hematological malignancies
• HIV infection
• Corticosteroids and other immunosuppressive drugs (Humara)

81
Q

Candidiasis - Reproduce by forming

A

buds or blastoconidia

82
Q

Candidiasis - Some form

A

hyphae in vivo (non temp- dependent dimorphism)

83
Q

Candidiasis - Dimorphism exception –

A

mycelial (hyphae) not yeast form found in tissues

84
Q

Candida albicans- Most frequent

A

opportunistic fungal pathogen

85
Q

Candida albicans- Most infections are

A

endogenous (derived from host’s normal flora)

• Colonized: gastrointestinal tract (mouth to rectum), vagina, and skin

86
Q

Candida albicans-Do not cause infection unless

A

normal flora is disrupted or
patient is immunocomprimised:
• Broad spectrum antibiotics biggest culprit, followed by skin macerations
• Decreased T-cell function increases mucosal infections (AIDS patients)

87
Q

Candida albicans- T-Cell-mediated immunity keeps

A

Candida in check on mucosal surfaces (Neutrophils) main host defense against invasion through mucosa

88
Q

Candida albicans- Neutropenia (low neutrophils) -

A

candida can spread to many organs (eyes, kidneys, heart, brain, liver, and spleen) - disseminated infections

89
Q

Candidiasis- yeast infections - Mucosal (Thrush)-

A

Thick, white plaques on oropharyngeal and vaginal
mucosa
• Sometimes ophthalmic

90
Q

Candidiasis- yeast infections - Cutaneous (Intertriginous candidiasis)- Proliferation of

A

candida in warm moist areas of skin (groin, under breasts)

• Babies – Diaper Rash

91
Q

Candidiasis- yeast infections - Systemic infection (Disseminated candidiasis)

A
  • Can follow superficial infections and central intravenous catheters, renal failure requiring dialysis
  • Microabscesses in multiple organs - meningitis, eyes, liver and spleen abscesses, spine, heart on prosthetic valves
  • All systemic infections of candida are life-threating and require therapy
92
Q

Candidiasis- diagnosis - Mucosal candidiasis-

A

thrush
• Microscopic examination of scrapping- budding yeasts and pseudohyphae • Culture on blood agar plates- growth within 24 hrs.

93
Q

Candidiasis- diagnosis - Invasive (disseminated) candidiasis -

A

hard to document
• Culture from blood (not very sensitive)- may require biopsy of involved tissue • Germ-tube test- elongated buds from yeast when exposed to calf serum

94
Q

Candidiasis- treatment - Mucosal infections-

A

topical antifungal creams

• Systemic therapy for severe cases

95
Q

Cadidiasis - treatment - Systemic infections-

A

always require systemic antifungal (min. of 2 wks)
• Fluconazole and Echinocandin - most common
• Amphotericin B- used for some invasive candidiasis

96
Q

Cryptococcosis – Cryptococcus neoformans

A

Environmental yeast

97
Q

Cryptococcosis – Cryptococcus neoformans - Expresses a huge

A

polysaccharide capsule in host

98
Q

Cryptococcosis – Cryptococcus neoformans - Found worldwide in

A

soil contaminated with bird excreta

99
Q

Cryptococcosis - cryptococcus neoformans - Approximately 20% of cases are

A

in seemingly immunocompetent patients.

100
Q

Cryptococcosis - Yeast are inhaled into

A

alveoli- producing asymptomatic lung

infection

101
Q

Cryptococcosis- In lungs, yeast produce

A

polysaccharide capsule- major virulence factor- prevents phagocytosis by macrophages

102
Q

Cryptococcosis - T-Cell mediated immunity is

A

crucial for control of infection- capsule can prevent appropriate response

103
Q

Cryptococcosis - Most often presents as Meningitis-

A

resulting from hematogenous spread from asymptomatic lung infection.

104
Q

Cryptococcosis- Meningitis is subacute to

A

chronic (worsening headache, fever, cranial nerve palsies, mental status changes)

105
Q

Cryptococcosis - AIDS patients with meningitis also present with

A

diffuse pulmonary infiltrates, skin lesions, and widespread visceral infection (internal organs).

106
Q

Cryptococcosis- diagnosis - • Can easily be cultured on

A

agar media within a few days- easily identifed

107
Q

Cryptococcosis- diagnosis - Observation of

A

encapsulated budding yeast in cerebrospinal fluid (India ink

on slide).

108
Q

Cryptococcosis- diagnosis - • Latex agglutination test for

A

capsular polysaccharide- sensitive and specific

109
Q

Cryptococcosis- treatment - Meningitis -

A

Amphotericin B and flucytosine (several weeks) followed by fluconazole for several months

110
Q

Cryptococcosis- treatment - Since the advent of

A

antiretroviral drugs to treat HIV infections-

cryptococcosis meningitis is rare

111
Q

Cryptococcosis- treatment - • Pulmonary infections –

A

fluconazole

112
Q

Aspergillosis- Aspergillus fumigatus or flavus - Filamentous fungi-

A

mycelium of septate
hyphae
• Fluffy mold

113
Q

Aspergillosis- Aspergillus fumigatus or flavus - Reproduce by forming

A

conidia and aerial conidiophores (sexual reproduction)

114
Q

Aspergillosis- Aspergillus fumigatus or flavus - • Ubiquitous in

A

soil, manure, decomposing vegetation

115
Q

Aspergillosis - Entry - Conidia are inhaled into

A

upper and lower respiratory tracts -

germinate into hyphae

116
Q

Aspergillosis - Entry - • Macrophage can kill conidia that reach

A

aveoli- unable to kill hyphal form

117
Q

Aspergillosis - Entry - Neutrophils line up along

A

hyphae and secrete reactive oxygen intermediates that kill the fungus

118
Q

Aspergillosis - Invasive infection only occurs in

A

immunocompromised host

119
Q

Aspergillosis - infection - Angioinvasive fungus-

A

hyphae invade through blood vessel walls

Tissue infarction, hemorrhage, and necrosis

120
Q

Aspergillosis - infection - Invasive pulmonary aspergillosis-

A

Fever, pleuritic chest pain, cough with blood, and difficulty breathing

121
Q

Aspergillosis - infection - Sinus invasion-

A

acute facial pain

122
Q

Aspergillosis - infection - Dissemination is common-

A

necrotic skin lesions and brain abscess (rarely found in blood)

123
Q

Aspergillosis - diagnosis - Growth on Sabouraud agar in

A

a few days (issue with contamination- common in laboratory)

124
Q

Aspergillosis - diagnosis - Tissue biopsy- to confirm

A

tissue invasion (identify septate hyphae in tissue)- not specific for Aspergillus

125
Q

Aspergillosis - treatment - • Voriconazole-

A

drug of choice

126
Q

Aspergillosis - treatment - • Amphotericin B or echinocandin are also

A

used

127
Q

Superficial and cutaneous mycoses - limited to

A 
limited to (epidermis) skin and skin structures
• Dermatophytes (tinea)
128
Q

• Subcutaneous mycoses- involve the

A

skin, subcutaneous tissue and lymphatics
• Sporotrichosis
• Myocytomas
• Chromoblastomycosis

129
Q

Superficial Mycoses - Colonization of

A

stratum corneum by Malassezia (yeast)- normal flora

130
Q

Superficial Mycoses - • Usually

A

asymptomatic

131
Q

Superficial Mycoses - Seborrheic dermatitis

A

• Patches with greasy scales

in facial hair and scalp (dandruff)

132
Q

Superficial Mycoses - Tinea versicolor (misnomer)

•

A

Hypopigmented or hyperpigmented patches on chest or neck with scaling

133
Q

Dermatophyte Skin Infections - • Most common

A

fungal infections in humans

134
Q

Dermatophyte Skin Infections - • Infect

A

keratinized tissues (nails, hair and skin)- Keratinase enzyme • Restricted to non-viable skin- can’t grow at body temperature (37∘C)

135
Q

Dermatophyte Skin Infections - Clinical diseases called

A

tineas- (ringworm, athletes foot, jock itch) • Latin for “worm”

136
Q

Dermatophyte Skin Infections - • May be

A

acute or chronic

137
Q

Dermatophyte Skin Infections - Three etiological genera- (molds)

A

Microsporum
• Trichophyton
• Epidermophyton

138
Q

Dermatophytes - Encounter - Different ecological niches

A

Geophilic – found in soil
• Zoophilic – domestic and wild animals
• Anthropophilic – exclusively in humans and their habitat • Often cause chronic infections
• May be difficult to treat

139
Q

Dermatophytes - Encounter - • Not members of the

A

normal flora

140
Q

Dermatophytes - Encounter - • Crowding facilitates

A

spread- contagious

141
Q

Dermatophytes - Encounter - • Survives on

A

locker room floors

142
Q

Dermatophytes -Entry - Innate immunity to

A

pathogenic fungi is high for most people

143
Q

Dermatophytes -Entry - Skin and mucosa are excellent

A

barriers to fungi • Dry, cell sloughing, fatty acids, low pH

• Bacterial flora hostile to fungal colonization

144
Q

Dermatophytes -Entry - • Skin trauma required

A

Continuous moist conditions important
• Infections more common when skin is occluded with nonporous materials
• Increases hydration and temperature of skin interferes with stratum corneum function

145
Q

Dermatophytes-Damage - • Hyphae grows

A

outward in centrifugal pattern

146
Q

Dermatophytes-Damage - Viable fungal elements

A

at inflamed margin
• Central area has few/no viable fungi
• Healing tissue refractory to infection

147
Q

Dermatophytes-Damage - • Systemic infections extremely

A

rare

Inability of dermatophytes to grow at human body temperature • Presence of non-specific serum factors
• Transferrin binds iron needed for organism to grow

148
Q

Subcutaneous Mycoses - • “Mycoses of implantation”

A

Organisms usually enter skin via thorns or splinters • Infections evolve over several weeks

149
Q

Subcutaneous Mycoses - • Generally localized with

A

few systemic symptoms • Lesions usually heal following antifungal treatment

150
Q

Subcutaneous Mycoses - Immunocompromised patients

•

A

Widespread cutaneous and visceral infections

151
Q

Subcutaneous Mycoses - • Thermally dimorphic

A

fungus (environment - mold, tissues - yeast)

152
Q

Subcutaneous Mycoses - • Found in

A

soil, moss, decaying wood and vegetation

153
Q

Subcutaneous Mycoses - Sporotrichosis-

A

“rose picker’s disease” • Fungus is introduced by trauma (thorn prick)
• Starts as small lesion (ulceration and/or erythema)
• Can spreads through lymphatic vessels- Lymphocutaneous sporotrichosis

154
Q

Subcutaneous Mycoses - Disseminated disease

A

only in immunocompromised patients • Afflicts joints, brain, and spine (very serious)

155
Q

Subcutaneous Mycoses - Successfully treated with

A

antifungals- Itraconazole for 3-6 months

156
Q

Other Subcutaneous Mycoses - Mostly occur in

A

rural tropical areas of the world (Madagascar and Brazil)

157
Q

Other Subcutaneous Mycoses - • Caused by

A

soil mold

158
Q

Other Subcutaneous Mycoses - Mycetoma (Madura foot)

A

Chronic infection with sinus tract nodules and
discharge of visible grains (colonies of fungus)
• Can infect the bone or muscle

159
Q

Other Subcutaneous Mycoses - Chromoblastomycosis

A

Caused by “dematiaceous fungi” (black fungus) • Scaly, wart-like lesions usually on feet
• Usually require surgical intervention or amputation

160
Q

Treatment of Fungal infections - Azoles

A
  • Itraconazole, ketoconazole, clotrimazole, miconazole

• Interfere with ergosterol synthesis • Fungistatic

161
Q

Treatment of Fungal infections - Polyenes-

A
  • Lipophilic – bind to cell wall ergosterol and forms channels
  • Amphotericin B • Nystatin
  • Hamycin

Micro unit 2 (12 decks)

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