polio and small pox Flashcards
(160 cards)
1
Q
polio is considered
A
enterovirus
-attack the intestinal area
-readily passed in the stool
2
Q
polio main route od transmission
A
stool
-can shed for long periods of time after someone is asymptomatic
fecal -oral transmission
3
Q
3 subtypes of polio
A
1,2,3
immunity to one of them does not mean you have immunity to all 3
4
Q
who did polio use to mainly infect
A
children
-affect the legs
5
Q
children saw polio first time during
A
infancy when still had mothers antibodies to it
-continuously exposed throughout life
-build up immune response to polio
6
Q
paralytic polio was rare due to
A
herd immunity
7
Q
what changed in the 20th century with paralytic polio
A
indoor plumbing – no exposure to polio in infancy anymore
-this was the few time in history better sanitation lead to epidemic
8
Q
how does polio enter the body
A
mouth
primary site of multiplication is oral region and then GI tract
9
Q
even before symptomatic polio is found in
A
stool and throat
-still transmit when asymptomatic
-in a week will no longer be found in throat but in bloodstream and stool
10
Q
once polio is in the blood stream can travel to
A
nervous system and attach anterior horn and brain stem – now we see symptoms
11
Q
reservoir of polio
A
humans
12
Q
how long will people remain asymptomatic/ incubation period
A
20 days
95% people who come in contact will be asymptomatic
13
Q
5% will manifest flu like symptoms called
A
abortive polio myelitis
14
Q
in 2% of people
A
non paralytic aseptic meningitis (viral meningitis)
-abnormal sensations, stiff back, resolve in a few weeks
15
Q
in 1% of people with polio
A
symptoms of paralyzing polio
paralysis can stop and never progress OR weeks to months later can start up and get more paralyzed
16
Q
spinal polio
A
most common of paralytic polio
-involved just legs and asymmetric paralysis
17
Q
bulbar polio
A
weakness of muscles that could include breathing muscles
-from this came iron lung - first attempt of artificial ventilation
18
Q
bulbospinal polio
A
-all different muscles in body could affected
-death rate is highest
19
Q
post polio syndrome
A
happened 30-40 years after original contracted the disease
-start with new muscle pain and new paralysis
-more weakness than previous
-not considered to be infectious, it was damaged
20
Q
why was polio vaccine so difficult to make
A
no one knew so only made one type of polio
21
Q
first one to come up with vaccine that looked like it had promise
A
sauk
-could grow the virus in cell cultures (essential)
-realized the subtypes of polio and found a way to combine all into one vaccine
22
Q
sauk created
A
IPV- killed vaccine
- in early testing wasn’t completely inactivated so some people got polio
-given in 3 doses and required a booster
23
Q
came up with live attenuated vaccine
A
sabin
oral vaccine - OPV
given in 1 dose; cheaper and prove to confer longer immunity than original Sauk vaccine
droplet form
24
Q
big disadvantage to OPV
A
live vaccine and you still can shed it in your stool
-could not be around immunocompromised people after vaccine
-immunocompromised people could not receive this vaccine
25
VAPP
vaccine associated paralytic poliomyelitis
-rare adverse reaction following live oral vaccine
-this did not happen after killed vaccine
-now we do shots- killed vaccine
26
OPV
still used in world today
-vaccine of choice in underdeveloped countries
27
small pox belongs
poxviridae family
DNA virus
no animal reservoir; easier to make a vaccine
28
2 forms of small pox
major: main form
minor: can cause pox like illness, don't die and no disfiguring scarring
29
ordinary type - major small pox spread
person to person by respiratory droplets
30
ordinary type incubation time
2 weeks
asymptomatic - not contagious until symptoms appear
higher fevers, muscle pain
31
as fever subsides you get
the rash (on the tongue) and blisters are filled with the virus
-when break open contagious
will start on the face and spread downwards
32
when first start out spreading downwards called
macules
-had indentation
-will fill with pus like material ( live virus)
33
after macules turn into
pustules
-falls off and leaves a scab
-when scab falls off you will have no scarring
-some people will have BAD scarring
contagious until last scab falls off
34
small pox is declared to be
wiped off planet due to vaccine
-decided no vaccines for small pox
35
who still gets vaccine for chicken pox
military
36
vaccine for small pox
vaccinia polio virus family
-not from small virus itself
-too dangerous to make from small pox virus itself
-when vaccinated keep it covered until scab falls off
37
multipuncture vaccine
dipped into solution that contains live virus
-tap into you-- prongs
38
stockpile of virus for
incase need to make vaccine
US and Russia
1990 both were supposed to destroyed the pile but Russia never did and abandoned lab (who has it)
threat of biological warfare
39
one of most deadly virus we known of
rabies
40
contract rabies through
a bite of animal
-coming in contact with saliva is main way to transmit rabies
-can be aerosolized
41
where does rabies replicate
striated muscles
42
Rabies will remain at site of inoculation for
several days
-this is time you want to treat
-asymptomatic
43
after at site of inoculation will affect
peripheral nerves
44
after peripheral nerves moves to
central nervous system, get into brain and spinal cord
-can cause encephalitis, degeneration of the nerves including paralysis and then death
45
once display symptoms almost always
fatal
-start with double vision, gait in affected
46
remains localized for a period of time--
you can get vaccine after been bitten or exposure to virus
47
Post exposure prophylaxis
If had bat in your house you can get rabies from being bitten in middle of night -- get vaccine
48
if not previously vaccinated for rabies
○ Day 0 - day of exposure
○ Day 3, 7, 14
?????
49
if previously vaccinated to rabies
Booster day 0,3
50
how to get passive immunity for rabies
Can get vaccine and immunoglobulin
51
Only true way to diagnose rabies is
autopsy and look for inclusion negri bodies that brain cell and tissues will have when infected
52
known as german measles or 3 day measles
rubella
MMR
53
host of rubella
humans
54
how is rubella spread
respiratory secretions
55
diagnosis rubella by
rash pattern
-starts on face, travels downward and would clear
56
Most significant sequel or complication of rubella
congenital rubella
57
If a mother contracted rubella during pregnancy
could easily cross placenta and infect the fetus
58
percent of baby contracting rubella in utero
85%
-highest rate during 1st trimester
59
signs of congenital rubella
cataract formation or pearly cataract
60
what does congenital rubella cause
○ Cause mental retardation
○ Deafness
○ Cardiac anomalies
○ Still born
○ Severe anemia
61
what caused the start of making the vaccine for rubella
congenital rubella
62
diagnosis of rubella
○ Typically via serology
-Look for IgM -- acute infection; IgG seen in vaccine
63
back in day vaccine was recommended for
women of childbearing age -- state mandated
-could not get marriage license unless tested for rubella
64
why was screening for rubella done
○ Screening was done to give that piece of advice cause if negative could get congenital rubella and get vaccine
65
If get MMR as an adult it is recommended you don’t get pregnant for 3 months after receiving the vaccine
Why?
Virus may mutate to wild type and if you get it could pass congenital rubella to baby
66
when screening for rubella look for
immune versus non immune status
67
immune =
IgG antibodies
68
If fall below certain titer you are said to be
non immune
69
measles also called
rubeola
-childhood disease
70
measles sero type
1
-humans are natural host
71
how to catch measles
spread respiratory droplets or fomites
72
symptoms for measles appear
10-14 days after exposure
2 week incubation period
73
symptoms for measles
high fever
3 C's
Rash- congregate and looks like blotch
74
what are the 3 C's
Cough- dry
Conjunctivitis
Coryza - runny nose
75
classic thing seen in measles that set apart from german measles
Koplik spots
-small white bumps occur in mouth area
76
specific about rash seen in measles
starts behind the ear and on face and progresses downward
last 7 days
slowly disappears the way it appeared
77
when measles rash appears
fever gets the highest
78
when are you contagious for measles
4 days before the rash begins to 4 days after the rash begins
79
most common cause of death in young children
measles
80
complications of the measles
pneumonia - caused by virus or secondary invader
encephalitis-swelling of brain
81
2 kinds of encephalitis caused by measles
-acute post infection encephalitis
-Subacute sclerosing panencephalitis (SSPE)
82
Acute post infection encephalitis
-most common of the 2
-start to show symptoms a week after other symptoms begin
83
Subacute sclerosing panencephalitis (SSPE
-occur years after having the measles
-ability to move cell to cell without immune system seeing so won't have complete immunity
-mutated form of virus -- lead to mental decline
84
what to look for in SSPE
abnormal amount of antibody in spinal fluid
-this is odd because measles typically doesn't get into spinal fluid
85
how to avoid measles
only way is the vaccine - complete series
live attenuated vaccine
USED to be killed vaccine- but wouldn't get full immunity and get atypical measles
86
mumps attack what
parotid glands in cheek area
-one or both gland affected
87
symptoms of mumps
no rash
low grade fever
swollen lymphs
sore throat
trouble swallowing
88
incubation for mumps
7-10 days
89
mumps spread
respiratory droplets
-so contagious a few days before disease state
90
complications of mumps
deafness
infertility - esp. men (inflammation of testicles)
-women inflammation of vulvar area- no infertility
-cardiac anomalies
91
how to detect mumps
enzyme: amylase
increase in enzyme and look for IgM
- is resolving if enzymes =low
92
MMR
mumps
measles
rubella
93
considered 4th most common cause of death in world
HIV
men having sex with men
94
#1 cause of death in africa
HIV
-believed to originate here
95
what was HIV used to be
HTLV virus
96
HIV stands for
human immunodeficiency virus
97
HIV considered what kind of virus
retrovirus
-RNA genome and transcription and turns into DNA
98
end stage of HIV infection
AIDs
99
HIV1
what we normally associate infections with, more global form, more predominantly moves into AIDs stage
100
HIV2
seen more commonly in Africa, create a milder form of infection, lower rate of transmission, but can still progress to AIDs
101
transmission of HIV
-sexual -oral or genital
-infected blood and body fluid (NOT found in saliva)
-mother to baby
102
If baby is born HIV - to HIV + mom
baby has 25% contracting through breast milk
103
what kind of virus is HIV
retrovirus
-2 identical pieces of RNA in the center
-has glycoprotein that contains various genomes
104
glycoprotein in HIV is used for
attachment of HIV to cell of choice
105
3 main structural genes in HIV
gag
env
pol
106
gag gene
-found in capsid
-gag 17 and 24
107
env gene
env gp120
gp 41
108
main gene look for in identification of HIV
GP120
-allows the virus to attach to whatever cell its going to invade
109
pol gene
mainly used for HIV replication
-code for enzyme needed for replication
110
main cell that serves as target for HIV
CD4
120 likes to attach to this
111
what other cells can attach to (mini amounts of CD4)
-macrophages
-dendritic cells
-b cells
all APC
112
once HIV inside host cell
becomes integrated into host genome and replicates along with the host cell
-HIV has ability to become latent-- may not start replication immediately
113
what does immune response look like in normal person with HIV
increased amount of antigen
MAIN response: cell mediated response - increase in b cell response
114
what antigen do we see increased in for HIV
p24 and HIV RNA
115
as we have an immune response we will have decrease in
viral load
116
why is HIV never completely cleared by our immune response
HIV has high mutation rate
-undergo antigenic shift
-latency of virus: reactivate over many years
-HIV immune complex trapped by dendritic cells in lymph nodes
117
where does HIV remain latent
CD4 cells, macrophages, dendritic cells and some privileged sites
-these are sites not seen by immune system; not a lot of blood flow
118
how is HIV trapped in lymph nodes
trapped and continually activated T helper cells to produce more CD4
-more t helper and more CD4 -- continues to invade cells
119
why so much CD4 destruction in HIV
-produce in such large numbers that we have so many virus particles budding out of cell at once will have destruction of CD4 cell
120
CD4 once a virus particle becomes apart of it become
altered self
121
these look at altered CD4 cells and will attack and kill it off
CD8
122
When CD4 cells become destroyed
nothing in immune system will work properly
-when immune system depleted viral load will increase
123
primary stage
first after initial infection
-classifed by increase in p24 antigen and normal immune response
-move to other organs
-flu like symptoms
124
when does primary stage occur
3-6 months after contact with HIV
125
latency
-virus kept at bay
-immune system is actively fighting
-virus particles going down
126
when is latency stage
couple of years to 10
127
AIDs
defined clinically by symptoms or lab testing
128
opportunistic infections seen with AIDs
- Cryptococcus neo forms-- form of meningitides
- Herpes 8
-Pneumocystis
-Cryptosporidium
-Hep C
-Histoplasmosis
129
CDC tries to track number of
HIV + patients and those who go to AIDs
130
HIV testing starts with
ELISA
131
draw back of ELISA
There can be a window period where there is not a large enough amount of antigen or antibody to be detected
132
When ELISA testing first started and you were negative and started to display flu like symptoms it is recommended you
get tested again because such a large window period
133
if you were + with ELISA have to
retest the sample and then confirm with western blot
134
after ELISA next gen could detect
antibodies to HIV1 or HIV2
-could not determine which one exactly
-need to be retested and confirm with western blot
135
Gen 4 testing
-HIV1, HIV2 and now look for p24 antigen
-eliminated a lot of false negatives
-but now so sensitive has false +
136
in gen 4 if positive it was recommended
to have nucleic acid testing done to look for presence of a virus
-western blot not used because not as sensitive
137
with gen 5 we can now
differentiate between HIV1 and HIV2 antibodies and detect p24 antigen
138
in gen 5 if screen positive, do
NAT testing to confirm RNA particles
-also provides baseline
139
home testing for HIV
ELISA based and lateral flow
140
pro of HIV at home testing
Afraid to go to doctor and be tested, can do test at home
141
cons of HIV at home test
○ At first would send out after get specimen
○ Now can read at home
○ If negative, won't want to see a physician
○ May not follow the directions exactly so they get the result they want
-Trick yourself into seeing a particular end result
142
when is western blot done on HIV
when positive on 2 specimens
143
what bands are you looking for on western blot
p24, gp 41, gp120/160
144
if 2/3 bands present
+ HIV
145
if 1/3 bands present
indeterminate; will be asked to come back in a few weeks to be retested
146
in molecular/ NAT testing for HIV what are you looking for
RNA levels
-can rise 11 days after initial infection
-set point
147
When put on therapy, goal is to have less then (HIV)
50 copies of RNA per mL
-should be retested every 4 months
148
If increased after baseline has been established,
you are becoming resistant to the treatment or not responding
149
when is CD4 counts done
is there progression of the disease aka CD4 cells decreasing
150
normal ratio of CD4 count
2:1
151
as person enters AIDs CD4 ratio is flipped to
1:1 or 0.5:1
-means CD4 cells are being destroyed
152
calculation for absolute CD4 count
WBC count x %lymphs x %CD4 t cells = #CD4
-if below 200, said to be in AIDs
153
calculation for % of CD4 cells
#CD4 cells X 100
-----------------------
Total # lymphs
-if % less than 14 said to be in AIDs
154
treatment for HIV
cocktail of drugs because major antigenic drift
155
Nucleoside analog RT inhibitors
-first class developed
-delay person from going into AIDs
-help reverse transcriptase enzyme once into host cell
156
Nonnucleoside RT inhibitors
same as nucleoside analog, inhibit reverse transcriptase but did in different manor
157
protease inhibitors
Stop virus being reassembled and released
158
HAART
highly active anti retro viral therapy
-on a combo of classes of drugs
159
now seeing resistance with HIV drugs which means
-need to switch drugs
-once resistance becomes harder for them to respond to anything
160
pre-prophylactic drugs
taken by people who are NOT HIV +, but in higher risk category for contracting HIV
-truvada and descovy
-no protection against STD
-once HIV+ can not be on drugs anymore
