Unit 2 (minus the first three lectures) Flashcards
(344 cards)
1
Q
what are the results of RNA viruses’ high mutation rates?
A
resistance to antivirals, barriers to vaccines, reassortment of genome segments, pandemics
2
Q
“small RNA virus”
A
picornavirus
3
Q
what is the purpose of RNA in an RNA virus
A
genetic material AND template for protein synthesis
4
Q
what is the dual purpose of replication in the RNA virus
A
to copy the genome AND make mRNA
5
Q
what are the characteristics of the rotovirus
A
dsRNA, eurkaryotic virus, icosahedral, enveloped
6
Q
process that makes mRNA from RNA genome of RNA virus
A
transcription
7
Q
process that makes RNA genome in RNA virus
A
replication
8
Q
where do RNA viruses operate in the cell
A
cytoplasm
9
Q
what is (+) RNA used for
A
mRNA sense strand, instructions for protein
10
Q
what is (-) RNA used for
A
template for (+) strand
11
Q
what do RNA viruses use to replicate the RNA genome
A
RNA dependent RNA Polymerase (RDRP)
12
Q
(host/virus) ribosomes translate mRNA into proteins
A
host ribosomes
13
Q
RDRP is highly (efficient/accurate) in replicating RNA virus genomes
A
efficient
14
Q
exception to the rule that RDRP operates in the cytoplasm
A
influenza virus
15
Q
where in the cytoplasm does RNA virus replication specifically occur
A
on cell membranes (endosomes, lysosomes, ER vesicles), this concentrates the components to increase efficiency
16
Q
what contributes to RNA virus genetic diversity
A
low fidelity/no proofreading of RDRP, rapid evolution by recombination, reassortment of genome segments
17
Q
classification of poliovirus
A
picornaviridae, enterovirus, (+)ssRNA genome, linear mRNA, infects human GI cells
18
Q
poliovirus transmission of disease and where it persists
A
fecal-oral, water supply
19
Q
how does poliovirus enter the host cell
A
binds receptor
capsids become hydrophobic > shape change
capsids form pore through membrane
RNA genome enters cell at plasma or endosome membrane
20
Q
3Dpol
A
poliovirus RDRP
21
Q
(the same/a different) enzyme copies (+) and (-) RNA strands in the RNA virus
A
same RDRP
22
Q
when does the virus switch from translating mRNA to packaging it?
A
when there are enough capsid proteins that have accumulated
23
Q
what happens to an RNA virus when RDRP is scarce
A
translation
24
Q
what happens to an RNA virus when RDRP is abundant
A
(-) RNA synthesis
25
which RNA viruses (+/-) must package RDRP in the virion
(-)
26
which RNA viruses (+/-) may or may not package RDRP in the genome
(+)
27
why must RNA viruses code for RDRP in their own genomes
mammalian cells do not have enzymes to transcribe RNA from RNA templates
28
presentation of rotavirus disease
severe gastroenteritis--diarrhea, dehydration, malabsorption
29
key feature of rotavirus genome
segmented
30
accumulation of virus proteins in the cytoplasm that displaces the cytosol
viroplasm
31
how do rotavirus virions enter the rough ER
budding after assembly
32
two ways that rotaviruses exit the host cell
exocytosis/lysis
33
rotavirus prevention
live attenuated vaccines
34
presentation of uncomplicated influenza virus
respiratory tract involvement, fever, headache, myalgia, weakness
35
complicated influenza virus symtpoms
pneumonia, myositis (muscle pain), rhabdomyelitis (muscle break down)
36
where does influenza virus replicate
in the lungs
37
where in the cell does transcription and genome replication take place for influenza virus
the NUCLEUS
38
releases influenza virions from sialic acid on cell surface
N antigen (neuraminidase)
39
how are influenza virions shed
in respiratory droplets
40
characteristic of influenza vaccine
trivalent inactivated vaccine--two strands of A and one strand of B
41
virus binds to CD4 and chemokine receptors on T cells and macrophages
HIV
42
T cell count is (high/low) in HIV infection
low
43
key enzyme involved in converting (+)ssRNA HIV genome to dsDNA
reverse transcriptase (included in the virion)
44
what makes HIV so difficult to treat
dsDNA genome integrates into host chromosome for life
45
which enzyme transcribes mRNA from the integrated HIV genome
RNA Pol II
46
where does HIV virion maturation occur
outside the cell, while the viral protease cleaves the capsid proteins, forming the final trapezoid shape
47
how is the HIV virion released from host cell
budding
48
gold standard for HIV diagnosis
PCR
49
HIV treatment
ART antiretroviral therapy, many drugs must be combined
50
what causes the fever, body aches, and extreme fatigue in influenza virus infection
interferon induction
51
where do DNA viruses carry out transcription and replication (exception: poxvirus)
in the NUCLEUS
52
(host/virus) RNA Pol transcribes mRNA in DNA viruses (exception: poxvirus)
host
53
the viral or host DNA Pol replicates the genome for (DNA/RNA) viruses
DNA viruses
54
cells that have the right transcription factors for a DNA virus to undergo transcription are considered ____
permissive
55
two viruses that use viral DNA polymerase
herpesvirus, adenovirus
56
DNA polymerases for DNA viruses have (high/low) fidelity
high fidelity
57
origin of diversity in DNA viruses
recombination
58
DNA virus with symptoms such as infected conjunctivae, painful sore throat, pneumonia, bad cold with fever
adenovirus
59
particularly susceptible populations to adenovirus infections
military, children at camps or on sports teams
60
(host/viral) RNA Pol II makes adenovirus mRNA
host
61
where does the adenovirus genome replicate
nucleus
62
adenovirus genome is replicated by (host/viral) DNA Pol
viral
63
where does adenovirus capsid assembly take place
in the nucleus
64
how do adenovirus virions egress
lysis
65
there is an adenovirus vaccine but only a select group of people get it--who
military personnel
66
why is HPV hard to replicate in lab
only amplifies when transcription factors in the host cell are just right (different stages of epithelial cells)
67
(host/viral) RNA pol transcribes HPV mRNA
host
68
(host/viral) DNA Pol synthesizes HPV genomes
host
69
viral factors of HPV E6 and E7 are ___
oncogenes
70
how does the HPV vaccine work
no viral DNA, just viral capsid to induce correct antibodies
71
DNA viruses (except poxvirus) use the host RNA Pol II enzyme and what else to synthesize mRNA
viral and cellular transcription factors that bind to viral gene promoters
72
viral DNA polymerase and accessory proteins are required to replicate what type of viral DNA genomes
large DNA genomes
73
DNA virus associated with: gastroenteritis, keratoconjunctivitis, pharyngoconjunctival fever, pneumonia
adenovirus
74
cidofovir is used to treat which DNA virus
adenovirus
75
the initial phase of HPV infection occurs in which cell type
basal epithelium
76
treatments for this DNA virus include: chemical ablation, cryotherapy, colposcopy, VLP vaccine
HPV
77
how many human herpes viruses are there
8
78
most people are infected with __ herpesviruses
three or more
79
major barrier to herpesvirus vaccines
latency
80
classification of herpesvirus
icosahedral, tegument, dsDNA
81
herpesvirus genome replication is by (host/viral) polymerase and (host/viral) accessory factors
viral, viral
82
how is HSV-1 primary infection spread
close contact with active lesions or asymptomatic shedding, usually above waist
83
characteristics of HSV-1 recurrent disease
tingling and itching precede outbreaks, lesions on eyes/genitals/fingers/mouth,
84
what triggers HSV-1 recurrent disease
fever, sunlight, hormones, stress, physical trauma
85
are HSV-1 recurrent disease lesions contagious
yes
86
which herpesviruses cause meningitis
HSV1 and HSV2 primary infections
87
what does HSV recurrent infection cause in the brain
encephalitis
88
how is HSV2 primary infection acquired, and when
adulthood, oral-genital STD
89
HSV2 recurrent disease prodome
itching, tingling at lesion site a day before outbreak
90
can HSV2 recurrent infection spread in the absence of lesions
yes
91
what test is used to distinguish between HSV1 and HSV2
PCR
92
parent drug used to treat HSV2
acyclovir
93
where does chicken pox remain latent in the body after infection
ganglia
94
primary vzv aka
chicken pox
95
how is primary VZV transmitted
aerosol, highly contagious
96
complications possible with primary VZV infection
hepatitis, encephalitis, pneumonitis, bacterial infection of lesions
97
VZV recurrence
herpes Zoster (shingles)
98
complications of VZV recurrence
Bell's palsy, neuralgia, retinitis
99
common sites of shingles
back, shoulder
100
30% of herpes zoster outbreaks affect face, destroying the ____ and leading to _____
retina, blindness
101
when is herpes zoster treatment effective
only during first three days of outbreak
102
vaccines for VZV (exist/do not exist)
exist--live, attenuated virus
103
where does Epstein Barr Virus remain latent
small fraction of B cells
104
what causes EBV recurrences?
immunosuppression
105
EBV recurrences can lead to:
malignancies
106
what are the diagnostic tests for mono
clinical signs, serology for heterophile antibodies, blood smear for elevated WBCs and atypical lymphocytosis
107
does prevention exist for EBV
no
108
CMV
cytomegalovirus
109
presentation of primary CMV infection
usually asymptomatic
110
how is CMV differentiated from EBV
absence of sore throat and presence of rash (not mono!)
111
permanent outcomes of congenital CMV disease
hearing loss, MR, vision loss, seizures, death
112
virus that is a frequent cause of transplant failure
CMV
113
CMV diagnostic methods
serology, culture, PCR
114
does treatment exist for CMV
yes, antiviral drugs
115
does prevention exist for CMV
no--vaccine ineffective
116
what cells does HSV6, 7 infect
CD4+ T cells
117
where does HSV6, 7 remain latent
CD4+ T cells
118
how is HSV6, 7 transmitted
saliva
119
at what age does HSV 6, 7 infection primarily occur
7-13 months of age
120
diagnostic test for Roseola HSV6, 7
clinical manifestations, rule out drug allergy
121
treatment for Roseola HSV6,7
none, treat symptoms, don't give antibiotics
122
prevention for Roseola HSV6, 7
none
123
what is reactivation of HSV 1 characterized by
viral shedding from vesicular or asymptomatic lesions
124
reactivation of VZV is characterized by
painful, unilateral rash
125
risk associated with primary CMV infection
congenital CMV syndrome in neonates
126
EBV infection presentation in children
asymptomatic (teens get mono)
127
acyclovir works for:
HSV 1, HSV 2, VZV
128
how is viral gene expression induced
by binding of cellular transcription factors to promoter regions
129
viral genes are (prokaryotic/eukaryotic)
eukaryotic
130
viral genes in a linear arrangement on one RNA strand, with only a single promoter
simple genome, eg retrovirus
131
viral genes on both strands of DNA, often overlapping, and each with its own promoter
complex genomes, eg adenovirus, herpesvirus, poxvirus
132
how do transcription factors affect cell permissiveness to viruses
only certain cells in certain tissues express the transcription factors needed for the virus to grow (HPV-epithelial, Hep B-liver)
133
viral genomes (have/do not have) non-coding regions
do not have
134
viral genomes (have/do not have) overlapping reading frames
have
135
viral genomes (have/do have) alternative splicing of RNA
have
136
the goal of alternative splicing of RNA is to change the ___ sequence
aa
137
why are viral proteases targets for antivirals
to prevent polyproteins from being divided into appropriate proteins
138
what is the outcome of having only one promoter per viral genome
polyprotein
139
how are polyproteins cleaved into usable proteins
proteases
140
DNA viruses are (stable/unstable)
stable
141
RNA viruses are (stable/unstable)
unstable
142
_____ variants produce new strains of viruses spontaneously over time
antigenic
143
how can mutations lead to drug resistance
if a protease binds to only one site, and the site is mutated, it can't bind and the virus is not disrupted. now antivirals contain several cut sites
144
__________ allow for epidemiological studies and live vaccines (like with polio)
high mutation rates
145
what does epidemiological mean
show where something came from
146
when a gene function of one virus replaces a mutated or missing gene of another, allowing defective viruses to grow
complementation
147
when viruses exchange capsid proteins
phenotypic mixing
148
what does phenotypic mixing achieve
viruses can infect new types of cells
149
the genetic material of one virus in the capsid or envelope of another
pseudotype
150
the exchange of viral genes by crossing over at regions of homology
recombination
151
what does viral recombination produce
a hybrid virus
152
the rearrangement of parts of a segmented genome to form a new set of segments
reassortment
153
reassortment virus example
influenza
154
infection by one virus tends to prevent infection by another
interference
155
how does interference occur (3 ways)
blocking of receptors, competition for resources, production of interferon or other anti-viral agents
156
aims to correct or prevent disease by transfer or appropriate genes to the patient
gene therapy
157
gene therapy (is/is not) approved in the US
is not
158
what are used as vectors in gene therapy
modified viruses
159
diseases that might be treated with gene therapy are those with a congenital lack of:
a single gene
160
examples of diseases that might be treated with gene therapy
CF, combined immune deficiency, hemophilia, liver enzyme disorders
161
viruses used for gene therapy (four)
retroviruses, adenoviruses, herpes simplex, adeno-associated virus
162
two problems with gene therapy
short duration of expression, low efficiency of gene transfer
163
bad side effects of gene therapy (2)
severe inflammation, insertion of virus's genome into a recipient's genome leading to malignant disease (leukemia)
164
virus entry site in resp tract
epithelial, goblet cells
165
__ cells sample the gut contents and present it to underlying immune cells
M cells
166
how do viruses infect the gut
they infect M cells and easily reach the blood stream
167
how is rotavirus transmitted
fecal oral
168
what does rotavirus cause
diarrhea (caused by enterotoxin)
169
prevention for rotavirus
two vaccines
170
exit point for rotavirus
diarrhea
171
"virus in the blood"
viremia
172
(primary/secondary) viremia leads to replication in internal organs, may occur without symptoms
primary
173
(primary/secondary) viremia is when the virus disseminates the virus to organs where it is shed
secondary
174
organs involved in primary viremia
muscle, liver, spleen, blood
175
organs involved in secondary viremia
skin, mucous membrane, lung, kidney, GI, brain
176
how does chicken pox/shingles enter the nervous system
via eyes and mouth (aerosol) to resp tract
177
what causes the host response to infection by virus
interferons and interleukins
178
what causes cell injury in a viral infection
virus replication and host response
179
direct effects on cell by virus
cell lysis when it wants to escape
180
genome of norovirus (cruise ship virus)
ss + RNA
181
direct effect of norovirus
cell inactivation
182
how are hepatitis viruses related
symptoms are similar--all infect hepatocytes
183
transmission of hep A
fecal oral
184
transmission of hep B
blood/sex/birth
185
transmission of hep C
blood/sex/birth
186
how is hep A controlled
vaccine
187
how is hep B controlled
vaccine
188
how is hep C controlled
not well--no vaccine
189
how do you diagnose hepatitis virus infection
serology
190
what IgM test shows for hep A
acute
191
what IgG test shows for hep A
recovered/vaccinated
192
what viral surface antigen test shows for hep B
acute
193
what IgG against viral surface antigen test shows for hep B
recovered/vaccinated
194
what EIA test means for hep C
positive, but lots of false positives
195
how to rule out false positives for hep C
RIBA
196
hep (A/B/C) can cause chronic infection
B and C
197
treatment of chronic hep B or C infection
polymerase inhibitors and interferons
198
side effects of treatment for chronic hep B or C infection
severe
199
use alternative therapy as a ______ to prescribed treatment
complement
200
classification of Hep A
naked icosahedral ssRNA
201
classification of Hep B
enveloped DNA, partly double stranded
202
hepadnavirus
hepatitis DNA virus
203
picornavirus hepatitis (A/B/C)
A
204
flavivirus hepatitis (A/B/C)
C
205
hep C classification
enveloped (+)RNA
206
which hepatitis viruses cause chronic infection
B and C
207
drug used to treat herpes viruses
acyclovir
208
four types of antivirals
nucleoside analogs, non nucleosides, protease inhibitors, entry inhibitors
209
viral entry prohibitor drug active against which virus
HIV
210
protease inhibitors are used against which virus
HIV
211
neuraminidase inhibitors are used against which virus
flu
212
acyclovir mechanism of action
nucleoside analog for thymidine
213
most anti virals are (specific/broad spectrum)
specific
214
off target cytotoxic effects can (harm cells/cause resistance)
harm cells
215
on target cytotoxic effects can (harm cells/cause resistance)
cause resistance
216
most anti viral drug effects are (reversible/irreversible)
reversible
217
when virus replication can resume once anti viral is cleared
rebound
218
four factors that favor emergence of resistant viruses
1- high rate of virus replication
2- high mutation rate (RNA viruses)
3- high selective drug pressure (long term, multiple treatments)
4- immunosuppressed host that cannot clear virus
219
why combine drugs with different targets when fighting viral infection
synergy
| less likely that the virus can select for a strain with resistance to both drugs
220
three ways to counter resistance to anti virals
1- treat immunosuppression in host
2- combine drugs
3- target host functions
221
who should be treated for HSV 1, 2 and VZV
infected neonates, people with frequent recurrences, complicated HSV infections, people with zoster
222
drug used to treat cytomegalovirus
ganciclovir
223
mechanism of action of ganciclovir
nucleoside analog of guanosine--chain terminator
224
who should take ganciclovir
patients in great distress (severe side effects)
225
two broad spectrum anti virals for DNA viruses
Foscarnet and Cidofovir
226
mechanism of action of Foscarnet
inhibits viral DNA polymerase
227
who should take Foscarnet
people with any herpes virus
228
side effects of Foscarnet
toxic to kidneys
229
mechanism of action of Cidofovir
nucleoside analog of cytosine
230
against which viruses is Cidofovir active
herpes, adeno, papilloma, pox
231
why can you use HIV anti virals to treat hep B
because hep B also uses reverse transcriptase
232
what does pegylated interferon alpha do
treats hep B and C with interferon--tells cells to undergo apoptosis or shut down
233
two anti virals for flu
zanamivir and oseltamivir
234
mechanism of action of flu anti virals zanamivir and oseltamivir
sialic acid analogs that inhibit viral neuraminidase
235
mechanism of action of ribavirin
nucleoside analog of guanosine
236
for which viruses is ribavirin specifically approved for use
HCV and RSV
237
for which viruses is ribavirin used
lots and lots
238
treatment for HCV
combo of pegylated interferon alpha with ribavirin
239
(all/not all) HCV genotypes respond to antiviral treatment
not all
240
HCV treatment has (few/many) negative side effects
many
241
mechanism of action of AZT
nucleoside analog for thymidine
242
anti HIV drug that inhibits entry
Maraviroc
243
anti HIV drug that works as a nucleoside RT inhibitor
Tenofovir
244
anti HIV drug that works as a non nucleoside RT inhibitor
Efavirenz
245
anti HIV drug that works as an integrase inhibitor
Raltegravir
246
anti HIV drug that works as a protease inhibitor
Darunavir
247
what is cobicistat
a drug enhancer that inhibits break down of drugs in the liver
248
current HIV treatment and daily dose
Stribild, once a day
249
most fungal pathogens are (environmental/commensal)
environmental
250
most fungal pathogens are (highly/not) contagious
not
251
most fungal pathogens (have/do not have) drug resistance
do not have
252
exception to the rule that fungi are environmental
Candida albicans yeast is normal flora
253
caused by eating fungal toxins (wrong mushroom or spoiled food)
mycotoxicosis
254
mycotoxicosis (is/is not) a fungal infection
is not
255
why are fungal allergies dangerous
asthmatic reaction
256
highly effective and broad spectrum anti fungal, but toxic
polyenes
257
systemic anti fungal, nephrotoxic
Amphotericin B
258
less toxic anti fungal, different ones optimally active against different fungi
azoles
259
major azole used to treat candidaiasis and crytococcosis
Fluconazole
260
low toxicity, highly effective anti fungals active against candida and aspergillus
Echinocandins
261
why are fungi considered eukaryotic
80s ribosomes, nuclei, no peptidoglycan cell wall
262
what is the fungal cell wall made of
chitin
263
anti fungals target which two aspects of the fungus
beta-glucan and ergosterol
264
why are there fewer targets for anti fungals
many of their molecules are too similar to ours
265
fungi (can/cannot) grow in harsher environments than bacteria
can grow--drier, higher osmotic pressure, colder environments
266
what is the implication of fungi growing in harsh environments
more skin infections and food spoilage
267
single celled fungus, reproduce by budding
yeasts
268
grow in hyphae/mycelia and have complex reproduction, multicellular
molds
269
closed mitosis used by (yeasts/molds)
yeasts
270
five types of asexual ____ have distinctive microscopic appearances that may be used for diagnosis
spores
271
several important fungal pathogens grow as mold at 24C and as yeast at 37C
thermal dimorphism
272
(yeast/mold) has more immune-evasive properties
yeast
273
how do you use thermal dimorphism for diagnosis
dual cultures
274
immune response to fungal infection is:
granulomatous
275
what is suppuration
pus--immune response to fungal infection
276
anti fungal agent that disrupts fungal cell membranes at ergosterol insertion sites
polyenes
277
anti fungal agent that inhibits ergosterol synthesis
azoles
278
anti fungal agent that inhibits beta-glucan synthesis
echinocandins
279
gram stain is meaningful for which fungus
candida
280
what will a light microscope show for infection with a virus
cyto-pathic effect (cells dying)
281
how do you perform PCR on an RNA virus
need to use reverse transcriptase
282
spores formed within a sac
sporangiospores
283
how do yeasts reproduce
asexual budding
284
how do molds reproduce
spores (sexual and asexual)
285
(molds/yeasts) are mobile in the body because they are single celled
yeasts
286
asexual spores are known as
conidia
287
mold filaments are (hyphae/mycelium)
hyphae
288
mold mats are (hyphae/mycelium)
mycelium
289
no fungi are (obligate aerobes/obligate anaerobes)
obligate anaerobes
290
nuclear envelope does not disperse during mitosis
close mitosis
291
how are different asexual mold spores used
diagnosis
292
tests for delayed hypersensitivity with fungal antigens can be used to determine exposure to environmental fungi (not normal flora)
PPD skin test
293
toxigenic, non infectious disease from fungi
mycotoxicosis
294
how can mycotoxicosis from aflatoxins cause cancer
mutates p53 tumor suppressor gene
295
Type 1 hypersensitivity response to fungal allergy (same as rxn to mosquito bite)
Wheal and flare
296
when using direct microscopic examination for lab diagnosis of fungal infection, what solution is used to break down tissue
KOH
297
appearance of Cryptococcus neoformans under light microscope
very broad capsule
298
appearance of Coc. immitis under light microscope
spherules
299
how do you limit bacteria growth when culturing fungus
Sabourad's agar--low pH and antibiotics
300
when diagnosing fungal infection, DNA probe tests identify cultured colonies (earlier/later) than microscopy
earlier
301
test for antifungal antibodies in serum or spinal fluid, useful for systemic mycoses
serology
302
caused by fungal growth on the superficial skin layer
superficial mycoses
303
superficial mycoses (requires/does not require) thermal dimorphism
does not require
304
superficial mycoses symptoms are (common and minor/rare and severe)
common and minor
305
treatment for superficial mycoses
topical azoles, oral griseofulvin
306
common example of superficial mycoses
dermatophytosis
307
symptoms of dermatophytosis are called
tinea
308
how is dermatophytosis transmitted
fomites or autoinnoculation
309
diagnosis for dermatophytosis
KOH mount and culture
310
treatment for dermatophytosis
treat all affected areas with topical azole, alternatively oral griseofulvin
311
fungal infection introduced by trauma exposure to soil or vegetation
subcutaneous mycoses
312
subcutaneous mycoses (requires/does not require) thermal dimorphism
requires
313
how is subcutaneous mycoses treated in severe cases
amphotericin B and local surgery
314
how is subcutaneous mycoses treated in less severe cases
oral azoles
315
how is subcutaneous mycoses spread in the body from the trauma site to the trunk
lymph
316
example of subcutaneous mycoses introduced by thorns/splinters
sporotrichosis
317
diagnosis of sporotrichosis
biopsy and culture at room temp from pus
318
subcutaneous mycoses uses the mobile aspects of (yeast/mold)
yeast
319
subcutaneous mycoses uses the antiphagocytic aspects of (yeast/mold)
mold
320
superficial mycoses (is/is not) contagious
is
321
what causes the vesicles on fingers seen in patients with superficial mycoses
immune over reaction
322
what will a Wood's lamp show on a superficial mycoses
fluorescence
323
what are you looking for under the microscope when diagnosing superficial mycoses
hyphae and spores
324
(systemic/subcutaneous) mycoses growth leads to granulomatous lesions
systemic
325
transmission of systemic mycoses
inhaled into lungs via arthrospores
326
systemic mycoses (require/do not require) thermal dimorphism
require
327
range of severity of systemic mycoses
asymptomatic clearance to death
328
systemic mycoses (is/is not) transmissible person-to-person
is not
329
which disease does systemic mycoses mimic
TB
330
what is the source of systemic mycoses
American dirt
331
what are the thermal dimorphic forms of coccidioides
mold/spherule
332
where is coccidioides endemic
American SW
333
what are coccidioides spherules in the lung filled with
endospores
334
when should you treat systemic mycoses
if predisposed to complications
335
diagnosis for systemic mycoses
PPD, serology, biopsy for spherules
336
how should you treat systemic mycoses in pregnant women
amphotericin B
337
optimal treatment for opportunistic mycoses treats:
both the infection and the underlying problem
338
severity of opportunistic mycoses depends on
pre existing conditions
339
example of environmental opportunistic mycoses, enabled by reduced CMI
Cryptococcosis
340
cryptococcosis is (high/low) infammation
very low--suppresses host inflammatory response
341
most important part of exam to diagnose cryptococcosis
history
342
lab work to diagnose cryptococcosis
CSF stain with India ink to observe yeast with wide capsule, serologic test for crag antigen
343
treatment for cryptococcosis
combo of azoles and Amphotericin B
344
the infectious source for most mycoses
environment
