Review 2 Flashcards
(199 cards)
1
Q
What are antivirals used for in influenza?
A
treatment: reduce illness duration
prophylaxis: 70% effective in preventing flu
2
Q
How do adamantanes work?
A
They block uncoating (block M2 channels from allowing pH to drop)
3
Q
What do adamantanes work on
A
just influenza A
4
Q
how do Neuraminidase inhibitors work?
A
They block budding of the influenza virus from the infected cell.
5
Q
What do neuraminidase inhibitors work on
A
Influenza A and B
6
Q
What are the names of adamantanes and Neuraminidase inhibitors
A
adamantanes - amantadine, rimantadine
neuraminidase inhibitors - oseltamivir, zanamavir
7
Q
How is noro spread?
A
Fecal-oral
8
Q
What is an important receptor for noro?
A
The H antigen which is a precursor to A, B, and O blood types on RBC’s
9
Q
Who can resist noro?
A
non-secretors of H antigen (it’s not on their epithelial cells).
10
Q
Where does noro replicate?
A
in the jejunum
11
Q
What are the sx of noro?
A
vomiting
diarrhea
12
Q
noro immunity?
A
none. people can get reinfected over and over again. sometimes within the same month
13
Q
what types of populations is noro associated with?
A
closed populations like cruise ships, nursing homes
14
Q
what makes noro selective for these populations
A
- little host immunity
- efficient transmission by food
- very stable virus (not killes by soap, EtOh, etc.)
15
Q
How is rotavirus spread?
A
fecal oral
16
Q
Who gets rotavirus?
A
6 mos - 2 years
17
Q
what are the sx
A
vomiting and diarrhea
18
Q
immunity to rota?
A
sort of. people usually will become immune and just have subsequent sub-clinical infections where they still shed virus and all.
19
Q
Who is rota a big problem for?
A
developing world?
20
Q
How is it similar to influenza A
A
- segmented genome
2. antigenic variations (antigenic shift and drift) just like flu
21
Q
how does polio spread
A
fecal-oral
22
Q
describe the pathogenesis of polio
A
gets in through the GI lumen -> GI lymphatics ->primary viremia (circulating in the blood) -> replication in viscera (organs) -> secondary viremia -> spreads to the CNS
23
Q
What cells in the CNS does polio infect
A
motor neurons in the ventral horn
24
Q
What does polio do to these cells?
A
causes cell death
25
What is the rate of inapparent and abortive polio?
95%
26
polio leading to aseptic meningitis?
4%
27
rate of paralytic polio?
1%
28
What are the advantages to the inactivated polio vaccine
1. no backmutation
| 2. easy to combine with other vaccines
29
What are the downsides of IPV
1. injection
2. no mucosal immunity
3. expensive
30
What are the advantages to the oral polio vaccine
1. mucosal immunity
2. long lasting immunity
3. ease of administration
4. cheap
31
What are the downsides to OPV?
1. BACK MUTATION, FOOLS!!!
| 2. Need cold chain for transport
32
How does measles spread?
respiratory spread
33
Describe measles pathogenesis
infection of respiratory epithelium -> primary viremia -> replication in reticuloendothelial cells (liver, spleen, monos) -> widespread disseminated replication
34
What are the classic measles sx
1. cough
2. coryza
3. conjunctivitis
4. koplik's spot
THEN rash
35
Immunity to natural measles infection?
life-long
36
complications from measles
respiratory: pneumonia
CNS: encephalitis, subacute sclerosing panencephalitis)
GI: gastroenteritis, hepatitis
37
Describe importance and presentaiton of koplik's spots
1. they precede the rash
| 2. they are blue-shite spots w/ surrounding erythema
38
How does the measles rash spread?
goes from the face downward. rash present on palms and soles. It is a flat rash.
the macules will become confluent with time
39
What are the fecal-oral hepatitides
A and E
40
What are the blood-borne hepatitides
B, D, and C
41
What hepatitides incubate for 2-7 weeks?
A and E
42
What hepatitides incubates for 2-23 weeks
C
43
What hepatitides incubate for 4-25 weeks?
B and D
44
What hepatitides cause chronic hepatitis
B/D, and C
45
Which hepatitides have vaccines?
B, A, E (not in the US)
46
What is it that actually causes hepatic damage in Hepatitis?
The CTL response damages the liver
47
What lab tests do we use for viral hepatitis?
AST and ALT show elevation with hepatic injury
48
What will present after abnormal LFTs?
bilirubin levels will be more elevated later. esp, during acute infection
49
What do we use for Hep A-D for Acute tests
A - IgM anti-HAV
D - IgM anti-HDV
C - Anti-HCV
50
What do we use for for chronic tests?
D IgG and IgM anti-HDV.
| C - anti-HCV+ and the rising and falling of liver enzymes
51
What is the progression of sx of hepatitis after the asymptomatic incubation period?
1-2 weeks of fever, fatigue, nausea, abdominal pain
then later there will be dark urine, clay-coloured stool. Then 1-5 days later there will start to be jaundice, enlarged/tender liver. 1-4 months later there will be recovery OR chronic infection
52
What is the risk of chronic Hep B for adults?
~1% due to the good immune response. Low risk of cancer
53
What is the risk of chronic hep B for kids at birth?
90% due to bad immune response. The risk of cancer is high for these little tikes
54
What is the rate of chronic infection going into a nonreplicative phase?
10%per year of chronic infections will enter a nonreplicative phase which carries a low rate of transmission and little/no liver injury. Mostly asymptomatic
55
what occurs during the replicative phase of chronic infection
there is abundant virus. High rate of transmission and ongoing liver injury
56
What is the first thing that you see in Acute HepB
HB surface Ag. It spill out in larger numbers than needed for viral replication. you will then see a huge
57
What is made after this?
HB e Antigen. This is a protein cleaved from the core cassette
58
What is the first antibody response that you see with HepB?
IgM directed against the HB core antigen
59
What happens after the IgM against core antigen?
you get IgG against Core antigen AND eventually the anti-HB e antigen antibodies
60
When does someone have longstanding HB immunity?
When there is antibody against the HB surface antigen (anti-HBs)
61
What happens during chronic HepB infection?
you get the same HBsAg test positive and then the IgM anti-HBc and class-switch to IgG. BUT you never end up with the nice anti-HBsAg response
62
What tests are positive for acute HBV?
HBsAg, HBeAg, IgM anti-HBc
63
What tests are positive for Recovered HBV?
IgG anti-HBe, IgG anti-HBc, IgG anti-HBs (this is the important one)
64
What tests are positive for chronic infection?
IgG anti-HBc, HBsAg, HBeAg (could be + if ongoing damage or - if in a latent phase), anti-HBeAg (variable)
65
What tests are positive for vaccinated individuals
anti-HBs
66
Why is HDV dependent on HBV?
It uses the HBV capsid protein
67
What does HDV do during acute HBV infection?
This co-infection is pretty bad and will lead to increased risk of fulminant hepatitis. It will clear though if HepB clears
68
What happend if you've got HDV with chronic HBV?
It will lead to fuliminant hepatitis. Increased progression towards hepatocellular cancer.
69
How often does Hep C become chronic in adults?
85% of the time. very few people will actually clear this
70
What makes it unique in it's chronic progression?
intermittent spikes of replication due to the antigenic variation
71
How does the liver get damaged?
Immune response. Can lead to cirrhosis
72
What is the annual risk of hepatocellular cancer with chronic HCV?
1-4%
73
What unites all arboviruses?
the route of transmission through an arthropod vector.
74
What are the 2 main classifications of arboviruses?
1. encephalitic viruses
| 2. hemorrhagic fever viruses
75
What are the 4 encephalitic arboviruses?
1. WNV
2. EEE
3. WEE
4. SLE
76
Humans are usually what type of hosts for the encephalitic arboviruses?
incidental
77
What is the mosquito vector for WNV?
Culex mosquitoes
78
Where do these mosquitoes get WNV?
birds
79
Describe the pathogenesis of WNV
goes to blood -> replicates in lymphatics -> viremia -> infects the brain
80
What percentge are asymptomatic?
75%
81
Describe West Nile Fever
Fever, myalgias, fatigue, headache
82
Describe WNV neuroinvasive disease
meningitis, encephalitis, WNV "poliomyelitis" (infection of anterior horn cells leading to flaccid paralysis)
83
Can humans be reservoirs of WNV?
No
84
What makes dengue and its vector and lifecycle unique among the arboviruses
Humans and Aedes mosquitos are the only reservoirs
85
What is dengue fever also called?
breakbone fever
86
What are the sx of the dengue fever?
musculoskeletal pain, fever
87
What are the sx of dengue hemorrhagiv fever?
bleeding of skin, gums, GI, etc.
88
What are the lab results of DHF
decreased platelets which is a sign of leaky capillaries. Also, this causes hematoconcentration and increased Hematocrit
89
Describe the Dengue Shock Syndrome
DHF plus circulatory failure
90
Describe the pathogenesis of dengue
infection in the blood -> infection of macrophages -> ??something?? -> suppression of hematopoeisis -> widespread replication
91
How many serotypes of Dengue are there?
4
92
What does infection with 1st cause?
Dengue Fever
93
What can infection with the subsequent serotypes cause?
DHF
94
What is the theory for this DHF after multiple serotype infection?
the cross-reactive antibodies against each serotype will actually latch onto the new strain and attract macrophages, BUT this just enhances the infection of these macrophages. antibody-dependent enhancement
95
What is the vector for yellow fever?
Aedes
96
What are the reservoirs for yellow fever?
humans and monkeys
97
Describe the pathogenesis of YF
blood infection -> infection of macrophages -> viremia -> suppression of hematopoiesis
98
What is the first manifestation of yellow fever?
Flu-like sx for 3 days which will resolve and all will be well for 24 hours
99
What can happen after the first initial yellow fever and nice 24 hours period?
high fever, abdominal pain, vomiting
100
What does this high fever sx lead to in yellow fever?
hepatitis -> jaundice -> hemmorrhagic manifestations (renal failure, intravascular pressure fall)
101
What is the ultimate end of this hemorrhagic yellow fever presentation?
coma, death (~50% of cases)
102
What type of a vaccine is there for yellow fever?
a live attenuated vaccine
103
What type of genome do herpes viruses have?
Double stranded DNA
104
Where does the herpes genome replicate?
In the host cell nucleus
105
What is the disease presentation of herpesviruses?
primary infection -> latency -> reactivation
106
What is the most common type of herpes for oral contact?
HSV-1 much more than HSV-2
107
What is the most common type of herpes for sexual contact?
HSV-2 is much more than HSV-1
108
Describe the pathogenesis of HSV
primary infection in epithelial cells -> axonal transport ->latent in sensory neurons -> reactivation and axonal transport ->recurrent infection in epithelial cells -> sx maybe... you can still shed it without being aware
109
What is the classic dermatological presentation of HSV?
painful, clustered vesicle -> ulcerations -> crusting and resolution
110
How is chickenpox spread?
respiratory
111
How is VZV spread when someone has shingles?
contact spread (although this is very uncommon)
112
Describe the pathogenesis of VZV
primary infection in nasopharynx -> (fever) viremia -> infection in other sites (most importantly SKIN and sensory neurons) -> latent in sensory neuron -> reactivation and axonal transport -> replication in skin across a dermatome
113
describe the dermatological presentation of primary VZV (chickenpox)?
Fever with maculopapules, vesicles and crusted lesions together. These start on the trunk. It is often described as a dewdrop on a rose petal because it is a raised lesion
114
What does reactivation VZV look like?
painful vesicular rash in a dermatomal distribution
115
What is the vaccination for VZ
an attenuated viral vaccine
116
What is the difference between the chickenpox vaccine and the zostavax?
same thing just a 4x greater dose
117
How is EBV transmitted?
in saliva (kissing disease)
118
Describe pathogenesis of EBV
primary infection in oropharynx -> viremia -> infection of B-cells -> latent in B-cells -> reactivation
119
Describe severity of primary infection
it is usually mild or even asymptomatic in children
120
Describe the clinical presentation of mononucleosis esp. in adolescent and adults
low-grade fever, pharyngitis, lymphadenopathy. ALSO, you see atypical lymphcytosis (i.e. a giant CD8 response). Serious malaise and fatigue
121
What is the reactivation illnesses associated with EBV?
1. lymphoproliferative diseases
2. burkitt's lymphoma
3. nasoopharyngeal carcinoma
122
What is the diagnostic test for acute EBV?
you test for heterophile antibodies which patients will make when infected
123
How does one test for heterophile antibodies?
you do an agglutination assay with RBC's from sheep, horses, or cows that will show agglutination with the heterophile antibodies of humans. MONOSPOT TEST
124
Are people with latent EBV (also EBV-associated malignancies) going to test positive?
no on the heterophile antibody test
125
How does CMV present?
CMV is exactly like EBV and is another cause of mononucleosis
126
How does one distinguish CMV from EBV?
CMV is NEGATIVE on the monospot test (no heterophile antibodies)
127
When does CMV reactivate?
in transplant patients you see the following: GI inflammation, pneumonia, and disseminated disease
In HIV patients: retinitis (the leading cause)
128
What is HHV-6
6th disease AKA exanthem subitum or roseola
129
How does HHV-6 present?
Fever (maybe seizures) followed by a generalized rash
130
What is HHV-8
Kaposi's sarcoma (but only on reactivation)
131
What is the mechanism of acyclovir?
It is a nucleoside analogue. It is phosphorylated by a viral thymidine kinase where it is then incorporated into the DNA. Then because it has no 3' OH, it STOPS DNA synthesis
132
What is the oral form of acyclovir?
valacyclovir
133
What is a/vala-cyclovir good for?
HSV, VZV
134
How does Ganciclovir work?
Same way as acyclovir (nucleoside analogue), it just targets infected cells a bit better.
135
What is the oral form of ganciclovir?
valganciclovir
136
What is gan/valgan-ciclovir good for?
CMV
137
How does foscarnet/cidofovir work?
It inhibits viral DNA polymerase (not involved with the thymidine kinase)
138
When does one use foscarnet/cidofovir?
After failing acyclovir or ganciclovir
139
How does one acquire HIV?
Sexual contact
140
What 3 things determine the risk of transmission to a partner?
1. type of sex - anal sex>vaginal sex> oral sex
2. level of viruses - higher viral load in source partner increases risk of transmission
3. ulceration - presence of herpes in either partner will increase risk of transmission
141
What is the risk of HIV transmission mother to child without meds?
1 in 3
142
What is the risk of HIV transmission MTC with meds
<1%
143
What are other ways of getting HIV
IDU, medical use of blood products is now very very low
144
what is the first step in HIV life cycle and what are the necessary proteins?
It is entry
gp120 is a docking protein
gp41 is a fusion protein
145
What are the cell proteins that interact with gp120.
CD4 (1st) and CCR5... later in infection there is CXCR4 tropism
146
What does reverse transcriptase do?
It will take the RNA from HIV and convert it to dsDNA getting it ready for it's big proviral debut
147
What does integrase do?
It will take the DNA made from the RT and splice it into the latent provirus
148
What happens when the T cell is activated?
There is more proliferation and the virions will then assemble at the cell membrane.
149
What does the protease do?
It will help to mature the virions
150
Can you remember the natural history of HIV infection withe CD4's and viral load?
YES
151
What happens between 400 and 200 CD4's
TB, zoster, oral candidiasis
152
What happens between 100 and 200 CD4's
PCP, esophageal candidiasis, mucocutaneous herpes
153
What happens between 100 and 50
Toxo, cryptococcosis, MAC, CMV
154
what happens at below 50
cryptosporidiosis, PML
155
What shows up in a test for acute first, p24 or HIV viral load?
viral load
156
What does HIV RNA help with
1. predicts rate of progression
| 2. measures efficacy of ART's
157
How does one do resistance testing?
Sequencing of the HIV RNA for mutation associated with resistance to ARTs
158
What drugs target GP41
fusion inhibitors
159
drugs that targe CCR5?
CCR5 antagonists
160
Drugs that target Reverse Transcriptase?
1. nucleoside RT inhibitors
| 2. non-nucleoside RT inhibitors
161
Drugs that target integrase?
integrase strand transfer inhibitors
162
Drugs that inhibit the protease?
protease inhibitors
163
How do NRTI's work?
incorporate into nascent viral DNA blocking the elongation of that DNA
164
How do NNRTI's work?
Bind outside the active site of the RT and allosterically inhibit RT
165
How do PI's work?
They are structural analogues of the protease substrate and thus block the actual stuff
166
How do integrase strand-transfer inhibitors work?
bind integrase at the catalytic site, blocking the integration of the proviral DNA into the host DNA
167
How do fusion inhibitors work?
Block gp41 from achieving the conformation needed for fusion
168
CCR5 antagonsist
binds the CCR5 stopping the interaction with gp120
169
Who is ART recommended for?
All HIV infected. Even more so with lower CD4's
170
What else is ART advocated for?
PReP
171
What is the formula for starting HIV therapy
2 NRTI's plus your choice of one of the following:
NNRTI
boosted PI
integrase strand transfer inhibitor
172
What is a boosted PI?
It is a PI given with a little bit of ritonivir. The ritonivir will stop the liver from getting rid of the PI and thus make sure there is more in the body.
173
What are things included in the enterovirus group
SO MANY. but among the most important are poliovirus and coxsackieviruses
174
What causes polio
poliovirus 1-3
175
What does Coxsackievirus A cause
hand-foot-mouth disease, herpangina
176
What does coxsackievirus B cause
myocarditis and pericarditis
177
How does mumps spread?
droplet respiratory
178
Where does mumps infect and what are the sx?
parotid glands with swelling and pain with resolution in 7-10 days
179
what are some mumps complications?
complications are orchitis/oophoritis. aseptic meningitis, encephalitis. pancreatitis. Rarely there will be hearing loss in children. Fetal loss in the 1st trimester.
180
Can mumps be prevented?
Yes with a great vaccine
181
How does one get adenoviruses?
respiratory, fecal-oral, and fomite
182
What is the adenovirus fate?
generally self-limited and respiratory manifestations
183
Where else can adenovirus present?
ocular infections
184
Describe the ocular infections of adenovirus infections.
pharyngoconjunctival fever, epidemic keratoconjuncitivits
185
Describe the fecal-oral presentation of adenoviruses
self-limited, acute, watery diarrhea
186
What about adenovirus in the immunocompromised?
there can be reactivation illness or new infection
187
What will happen with adeno in HSCT patient?
usually within 100 days of transplant, you will find:
1. hemorrhagic cystitis
2. enteritis
3. pneumonitis
4. hepatitis with viremia
188
Where does adenovirus play for solid organ transplant?
It will infect the transplant organ
189
How is parvovirus B19 spread?
respiratory AND vertical transmission
190
What is the common name of the Parvo B19 and how does it present
"Slapped cheek disease" or 5th disease. It will present with fever and arthropathy: self-limited symmetric swelling and pain of joints in hands and feet.
191
What is the lab finding with Parvovirus B19 slash where does it replicate?
ANEMIA!!!! It replicates in the erythroblast.
192
What populations do we worry about with parvo and why?
1. people with underlying hemolytic disease
- this can put them into transient aplastic crisis
2. pregnant ladies
- usually ok, BUT small chance for reduced fetal RBC's, fetal death, fetal hydrops
3. immuncompromised
- pur red cell aplasia possible
193
What are the 3 main types of infections in terms of infection control.
1. contact
2. airborne
3. droplet-borne
194
describe contact diseases and give the 6 or 7 examples
Direct person-to-person spread OR contact with a contaminated intermediate object (such as equipment, furniture, etc.
1. MRSA
2. Van-resistant enterococcus
3. C. Diff
4. rotavirus
5. RSV
6. HSV
7. lice/scabies
195
What are the precautions taken for contact?
1. Hand hygiene before gloves
2. Gown
3. gloves
4. Dedicated equipment (e.g. stethoscopes)
5. Single room sometimes
196
describe droplet diseases and give the 5 examples
Large droplets generated during coughing, sneezing, talking.
Propelled a short distance (< 3 feet) and land on eyes, nasal mucosa, or mouth of susceptible individual.
197
What are the droplet precautions?
1. Surgical mask within 3 feet of patient
2. Hand hygiene
3. Single room sometimes
198
describe airborne diseases and give the 5 examples
Small droplet nuclei, skin squames, or dust particles that contain microorganisms are transmitted by air currents over long distances.
Deposited in the lower airways of a susceptible host
1. Tuberculosis
2. Varicella
3. measles
4. smallpox
5. Aspergillus
6. Legionella
199
What are the airborne precautions?
1. Isolation room with negative pressure airflow
2. respirator
3. Visitation Restriction
4. NO VISITATION FOR Non-immune individuals
