Brainscape's Knowledge GenomeTM

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


See full index

MICR 3090 > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

Approximately how many fungal pathogens of humans are there

A

~300

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

Mycosis (pl. mycoses

A

fungal infection of animals

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

Superficial classification

A

infection of hair or skin epidermis

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

Cutaneous classification

A

infection of skin, nails and mucosal surfaces

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

Subcutaneous classification

A

subcutaneous tissues, muscle
-typically initiated by piercing to the skin

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

Systemic classification

A

deep seated infection which affects organs

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

endogenous pathogens

A

come from the microbiome of host and become pathogenic due to a compromised immune system
(ex. Candida species)

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

Exogenous pathogens

A

acquired from the environment via inhalation or penetrating injury
(ex. Aspergillus moulds)

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

Primary pathogens

A

can establish infection in healthy host
(ex. dimorphic fungal pathogens)

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

Opportunistic pathogens

A

can cause disease in individuals within immunocompromised
(Cryptococcus)
-highest mortality rates

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

Why have infections due to opportunistic pathogens been on the rise

A

-can easier find them
-antibiotic resistance
-have adapted to climate change and can better invade the human body

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

Most common opportunistic fungal pathogens of humans

A

-Aspergillus
-Candida
-Cryptococcus

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

tineas

A

superficial cosmetic fungal infections on the outer skin or hair
-no tissue is invaded
-typically innocuous

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

Examples of superficial fungal infections

A

Malassezia species
-Tinea versicolor

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

What does Malassezia use to break down oils on the scalp

A

lipase and phospholipases

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

Where do dermatophytes grow

A

in skin, hair, or nails
-where the protein keratin is deposited

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

What type of fungi are dermatophytes

A

all filamentous ascomycota

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

What symptoms do dermatophytes cause

A

irritation and inflammation of underlying epithelial cells

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

What fungal diseases can dermatophyte species cause

A

common ‘tinea’ diseases like ringworm and athlete’s foot

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

What do dermatophytes secrete

A

proteinases, elastases, and keratinases that break down skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can cutaneous infections cause

A

superficial mucosal infections of the mouth and vaginal yeast infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are subcutaneous mycoses caused by

A

fungi that are normally saprotrophic inhabitants of soil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

symptoms of subcutaneous fungal infections

A

chronic localized infections of the skin and subcutaneous tissue and chronic inflammation and ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is one of the most common pathogens of subcutaneous fungal infections

A

Sporothrix schenckii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Are subcutaneous fungi thermally dimorphic

A

yes
-filamentous fungus in soil/environment, yeast in human host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe primary systemic pathogens

A

rare and can affect healthy people
-often acquired by inhalation of spores from soil and usually begins as a lung infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name 3 important dimorphic fungi pathogens

A

-Blastomyces dermatitidis
-Coccidiodes immitis
-Histoplasma capsulatum
All part of Ascomycota

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What do Histoplama capsulatum form

A

forms microconidia and macroconidia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What can people develop from Histoplasma capsulatum

A

histoplasmosis through inhalation of spores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Where is Histoplasma capsulatum found

A

river valleys and in central/eastern USA, also associated with animal droppings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where is Blastomyces dermatitidis found

A

mould lives in soil and decaying wood, in northern Ontario and Manitoba

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What can people develop from Blastomyces dermatitidis

A

blastomycosis though inhalation of spores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where is Coccidioides immitis

A

lives in dust and soil in southwestern US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are Coccidiodes immitis outbreaks linked with

A

changing climate factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What can people develop from Coccidioides immitis

A

coccidioidomycosis (valley fever)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What spores to Coccidioides immitis form

A

arthroconidia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What do Coccidiodes form during host-associated growth

A

spherules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What do spherules do

A

When it enters the body it expands in size and undergoes cellular division
When it ruptures it releases endospores which can form new spherules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Emergomyces

A

newly emerging group of dimorphic fungal pathogens with global distribution
Primarily affect immunosuppressed patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How do dimorphic fungi sense temperature

A

using histidine kinase signaling cascades

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are histidine kinase signaling pathways

A

well conserved sensory signaling regulators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are histidine kinase signaling cascades made up of

A

a variable N-terminal sensor domain and a conserved C-terminal transmitter domain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does the histidine kinase (HK) act as

A

acts as the environmental sensor of temp change and involves 4 phosphorylation events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the 4 phosphorylation events after HK gets an environmental cue

A
  1. The HK is auto phosphorylated
  2. Intramolecularly HK phosphorylation
  3. Phosphorylation of transferase protein
  4. Phosphorylation of response regulator protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does the MAPK cascade ultimately lead to

A

activation of transcription factors and transcriptional regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What does iprodione do in dimorphic fungi

A

inhibits HK so inhibits yeast growth transtiion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are dimorphic spores ingested by when the are inhaled

A

alveolar macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

When do dimorphic fungi undergo extensive transcriptional re-wiring

A

during morphogenesis from mould to yeast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Name a big cell wall change during morphogenesis

A

there is a reorganization of glucan
beta-glucan declines from~40% in hyphae to ~5% in yeasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does the change in glucan content in cell wall help with

A

helps limit immune cell recognition by Dectin-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Adhesins

A

help yeast adhere to host cell tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Secreted factors

A

induce host macrophage apoptosis and lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What genus is the most common cause of fungal diseases

A

Candida species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Are Candida ascomycota or basidiomycota

A

Ascomycota yeasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the clade called that most Candida species are in

A

CTG clade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What species is the most common cause of candida infections

A

Candida albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Are Candida albicans dimorphic or polymorphic

A

polymorphic yeast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Are Candida albicans infection\s exogenous or endogenous

A

endogenous
- no known environmental reservoir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How do mucosal Candida infections occur

A

result of fungal overgrowth from people taking antibiotics or immunosuppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Describe Candida oral thrush

A

infection of the mucous membranes of the mouth
-occurs when immune system is compromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is a vaginal yeast infections

A

Candida infection of the vaginal mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What host factors could lead to vaginal yeast infections

A

-antibiotics (kills bacteria and yeast take over)
-hormonal changes
-pregnancy
-diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe invasive Candida infections

A

endogenous fungi penetrate through epithelial cells
-Candida enters bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What combination of factors lead to invasive Candida infections

A

-overgrowth
-breach of mucosa/epithelium
-compromised immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Name 3 important immune cells that target Candida

A
  1. macrophages
  2. T helper cells
  3. neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the general host risk factors for invasive Candida

A

-disturbed bacterial community
-immunosuppression
-access to bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Biofilms

A

yeast and hyphal cells, adhering to a surface, enclosed in an extracellular matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Where does C. albicans form robust biofilms

A

medical devices
-catheters, valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How are biofilms removed

A

they are highly resistant to antifungals so typically must be physically removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what are the mortality rates of invasive Candida albicans

A

~50-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the key virulence trait for C. albicans

A

morphogenesis (polymorphic)

72
Q

What are yeast to filament transitions in C. albicans induced by

A

environmental signals
-Peptidoglycan (bacteria), pH, temp, nutrients

73
Q

What triggers yeast growth in C. albicans

A

QSMs (farnesol)

74
Q

What pathways are frequently involved in C. albicans morphogenesis

A

cAMP-PKA and MAPK pathways

75
Q

Are both yeast and filamentous growth needed for virulence

A

Yes

76
Q

Why are yeasts needed to virulence

A

they can more easily disseminate in the bloodstream

77
Q

Why are filamentous forms needed for virulence

A

aid in tissue invasion and adhesion

78
Q

What hyphal-specific genes does yeast>hyphal transition trigger

A

virulence factors like adhesins, proteases and toxins

79
Q

SAPs (secreted aspartyl proteinases)

A

extracellular hydrolytic/proteolytic enzymes that digest and distort host cell membranes

80
Q

What are adhesions

A

larger GPI-modified cell wall proteins

81
Q

What are adhesion made up of

A

N-terminal domain, C-terminal, and a variable domain

82
Q

What is the main role of adhesins

A

interaction and adherence to diverse substrates (human skin, epithelial host tissue, abiotic surfaces (catheters)

83
Q

Describe biofilm formation

A
  1. biofilms adhere to surface as yeast
  2. yeast>pseudohyphal/hyphal growth
  3. extracellular matrix formation
  4. yeast cells disperse to form new biofilms
84
Q

What do Candida cells in biofilms overexpress

A

antifungal drug efflux pumps and have increased membrane sterol content

85
Q

Are biofilms cells active or dormant

A

metabolically dormant (persister cells) which allows them to passively tolerate antifungal drugs

86
Q

What enables interaction between Candida and other speices

A

adhesions

87
Q

What can happen if C. albicans filaments bind with opportunistic bacterial pathogens

A

can enable the formation of interspecies biofilms

88
Q

Flocculation

A

When Candida use adhesins to adhere to each other to form clumps of cells

89
Q

Why do Candida do flocculation

A

because flocs are resilient to environmental stress conditions

90
Q

Impact of ECE1

A

if ECE1 protein is cleaved it releases Ece1 peptides, one of which is a toxin

91
Q

What does Candidalysin do

A

causes rapid permeabilization of mammalian cell membranes via an interaction with cholesterol (its a toxin)
-results in cell content leakage and damage/death

92
Q

Dectin-1

A

host cell receptor that recognizes and binds beta-glucans in the fungal cell wall

93
Q

Why can Dectin-1 recognize beta-glucans and yeast budding

A

beta-glucans become exposed at the bud scar

94
Q

Why can Dectin-1 not be activated during filamentous growth

A

no cell separation or beta-glucan exposure occurs

95
Q

Why are non-albicans Candida pathogens now a bigger problem

A

the use of common antifungal fluconazole (aids and transplant patients)

96
Q

Describe Candida glabrata

A

cant undergo any morphogenetic transitions (just yeast)
-most common non-albicans Candida pathogen to cause disease

97
Q

Describe Candida auris

A

newest Candida pathogen (global)
-highly resistant to antifungal drugs

98
Q

Describe Candida diagnosis

A

visualizing biopsied tissue with microscopy, looking for yeast and hyphae

99
Q

Can Candida be cultured in the lab

A

Yes
-antibiotics may be added to the media to inhibit growth of contaminating bacteria

100
Q

Why phylum are Cryptococcus species in

A

Basidiomycota

101
Q

Describe morphology of Cryptococcus neoformans

A

encapsulated yeast with a large protective, polysaccharide capsule

102
Q

Where is Cryptococcus neoformans found (environment)

A

soil, eucalyptus trees, pigeon poop, human cells

103
Q

What are the 3 life cycle transitions Cryptococcus neoformans undergoes

A
  1. mating
  2. monokaryotic fruiting
  3. titan cell formation
104
Q

How does Cryptococcus neoformans usually exist

A

yeast, almost always haploid

105
Q

How does Cryptococcus neoformans yeasts reproduce

A

asexually by budding

106
Q

Are C. neoformans isolates mostly MAT a or MAT alpha

A

MAT alpha

107
Q

chlamydospore

A

thick-walled hyphal cell that functions as a spore

108
Q

In C. neoformans what can a heterokaryon dikaryon develop into

A

a chlamydospore

109
Q

In C. neoformans what does a dikaryon develop into

A

basidium

110
Q

Describe heterothallic reproduction in C. neoformans (long answer question)

A
  1. cell fusion to form heterokaryon dikaryon which can either develop into a chlamydospore of a dikaryon
    2.dikaryon develops into a basidium
  2. nuclear fusion in basidium to form diploid nucleus
  3. meiosis/sporulation to form strings of haploid basidiospores
  4. spores disperse or germinate into larger yeast cells
111
Q

Describe C. neoformans monokaryotic fruiting

A

unisexual reproduction involving one mating type
cells form a diploid monokaryon hyphae

112
Q

endoreplication

A

replication of the nuclear genome in the absence of mitosis
-leads to it being a diploid

113
Q

What are the 3 mechanisms of monokaryotic fruiting

A
  1. unrelated cell fusion
  2. mother-daughter fusion
  3. endoreplication
114
Q

are alpha cells more likely to be inbreeded or outcrossed? why?

A

inbreeded
- alpha cells mostly reproduce asexually

115
Q

are most life cycle events conserved between heterothallic and homothallic mating? what’s the difference?

A

Yes
-heterothallic = 2 dif cells mating
-homothallic = 2 same cells mating

116
Q

What are advantages to a unisexual/same-sex mating cycle

A

-can lead to recom. if cells aren’t too closely related
-production of diploids and recessive mutations that may be advantageous
-enables production of spores

117
Q

titan cells of C. neoformans

A

during infection C. neoformans enlarge its size to form cells with thick cells walls with increased mannan (polyploid)

118
Q

What buds off of titan cells

A

normal size haploid progeny

119
Q

What triggers heterothallic mating in Cryptococcus

A

nutrient-limiting conditions

120
Q

What triggers monokaryotic fruiting in Cryptococcus

A

-N starvation
-water deprivation
-absence of a mating partner

121
Q

What triggers titanization

A

-mammalian lung environment
-macrophages

122
Q

What pathway is involved in mating and monokaryotic fruiting

A

cAMP-PKA and MAPK (with Ras1)

123
Q

What pathway is involved in titan cell formation

A

PKA

124
Q

Describe 3 steps of C. neoformans infection

A
  1. spores are inhaled into lung alveoli
  2. cells survive intracellularly in alveolar macrophages
  3. cells can disseminate to the central nervous system and cause fungal meningitis
125
Q

What happens to C. neoformans in the lungs

A

-alveolar macrophages engulf it but have limited ability to kill them
-C. neoformans replicate in macrophages

126
Q

Cryptococcus can remain in the lungs and cause a form of __________

A

fungal pneumonia
-in immunosuppressed (AIDs patients)

127
Q

How does C. neoformans pass the blood brain barrier

A

gets engulfed by alveolar macrophages and facilitates dissemination and access to the CNS via a “trojan horse” mechanism

128
Q

Where was Cryptococcus gattii first identified

A

outside a tropical climate on Vancouver island

129
Q

Who does Cryptococcus infect

A

both immunocompromised and immunocompetent people

130
Q

What a way to diagnose Cryptococcus

A

capsule can be seen with India ink which cant enter the capsule and results in a halo around the cell

131
Q

Whats the main polysaccharide in Cryptococcus capsules

A

GXM

132
Q

Are Cryptococcus capsules critical for virulence. Why?

A

Yes
-capsule blocks phagocytosis by immune cells

133
Q

GXM in Cryptococcus capsule masks ____
which helps in evasion from ____

A

beta-glucan, Dectin-1

134
Q

phagosome extrusion (vomocytosis)

A

a way that Cryptococcus can exit a macrophage without host cell lysis

135
Q

Why are melanin producing Cryptococcus strains more virulent

A

melanin can…
-decrease phagocytosis
-scavenger of reactive oxygen species
-fungal cell wall strength

136
Q

What does C. neoformans require the addition of to make melanin

A

exogenous substrate

137
Q

What is the first step of melanin production (conversion of something)

A

DOPA to DOPAQUINONE by Phenol Oxidases

138
Q

Describe toxic black mould and what it secretes

A

found in cellulose-rich environments from water-damaged buildings
secretes mycotoxins

139
Q

mycotoxins

A

toxic secondary metabolites secreted by fungi and harmful to humans

140
Q

Same 3 species that produce mycotoxins

A
  1. Aspergillus
  2. Penicillium
  3. Fusarium
141
Q

Name 2 common toxins

A
  1. Aflatoxin
  2. Fusarium toxins
142
Q

Name 3 common opportunistic moulds

A
  1. Aspergillus
  2. Rhizopus
  3. Mucor
143
Q

Mucormycosis

A

black fungus infection in ppl who are immunocompromised

144
Q

What family are Aspergillus species in

A

Ascomycota

145
Q

Aspergillus oryzae function

A

breaks down rice starches into simple sugars for soy sauce

146
Q

Aspergillus niger function

A

source of citric acid and lactase

147
Q

Aspergillus terreus

A

produces organic acids and enzymes and cholesterol-lowering drug lovastatin

148
Q

Aspergillus fumigatus

A

saprophytic mould that is common in air, soil, water and robust to harsh conditions

149
Q

Cleistothecium

A

type of ascocarp in Aspergillus fumigatus

150
Q

Does Aspergillus fumigatus have sexual or asexual reproduction

A

Was thought to have only asexual but now found out to have both

151
Q

In Aspergillus fumigatus what is disease severity a function of

A

its related to host immune status (hypo or hyper active immune response)

152
Q

neutropenic patients

A

when the are a ICH that has low white blood cells (leukemia, transplant patients)

153
Q

Describe the steps of a Aspergillus fumigatus invasive infection

A
  1. conidia are inhaled
  2. conidia are targeted by macrophages
  3. conidia that evade will undergo germination
  4. hyphae are targeted by neutrophils
  5. If hyphae persist they can enter the vascular system and cause systemic infection
154
Q

What is CPA

A

Chronic Pulmonary Aspergillosis
-long-term infection of the lung

155
Q

What is CNPA

A

Chronic Necrotizing Pulmonary Aspergillosis

156
Q

aspergilloma

A

ball of fungus growing within a cavity occurring when conidia settle in preexisting lung cavities

157
Q

SAFS

A

Severe Asthma with Fungal Sensitization

158
Q

ABPA meaning and cause

A

allergic bronchopulmonary aspergillosis
-caused from improper clearance of A. fumigatus conidia from the lungs and an exaggerated immune response

159
Q

What does A. fumigatus express to improve adhesion to host tissue

A

Sialic acid residues
-present on the surface of conidia

160
Q

Sialic acid mediates adhesion to _____ and ______

A

fibrinogen and fibronectin
(part of mammalian cell extracellular matrix

161
Q

Where are fibrinogen and fibronetin found

A

on wounded surfaces

162
Q

What does A. fumigatus secrete to induce host cell damage

A

proteases and secondary metabolites (gliotoxin)

163
Q

What does the mycotoxin gliotoxin have

A

immunosuppressive properties

164
Q

mucociliary clearance

A

host ability to properly clear pathogens from their airways

165
Q

what reduces mucociliary clearance

A

secreted metabolites and mycotoxins that cause epithelial cell damage

166
Q

What are A. fumigatus conidia phagocytosed by

A

macrophages

167
Q

What are A. fumigatus hyphal cells recognized by

A

neutrophils

168
Q

How can A. fumigatus conidia hide from host cells

A

by masking its cell wall beta-glucan

169
Q

What masks beta-glucan from Dectin-1

A

hydrophobin proteins (rodlet proteins)

170
Q

When is the best time for host cells to attack A. fumigatus conidia

A

When conidia swell prior to germination and reveal beta-glucan

171
Q

What does melanin in A. fumigatus conidia do

A

protect fungus against ROS ( is an ROS scavenger) and inhibits acidification of the phagolysosome

172
Q

Is melanin important for pathogenesis of Aspergillus

A

yes

173
Q

What do catalase and superoxide dismutase enzymes produced by hyphe do

A

help limit the effects of host ROS production

174
Q

What role does GAG when it is secreted from the outer cell wall

A

helps adherence of hyphae to surfaces and host cells
mask immune detection via beta-glucan masking
induces apoptosis of neutrophils

175
Q

How can Aspergillus be diagnosed

A

using silver staining

176
Q
A

MICR 3090 (2 decks)

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