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Microbiology > Exam 2.1 > Flashcards

Exam 2.1 Flashcards

1
Q

What are 5 possible responses a cell can have to a virus

A
  1. abortive
  2. lytic
  3. non-lytic
  4. latent
  5. transformation
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2
Q

What is more hardy, enveloped or non-enveloped virus

A

non-enveloped because the envelope is sensitive to desiccation

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3
Q

How does a virus get into a cell

A

Its spike proteins bind to cell receptors

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4
Q

What is a capsid

A

Protein coat or bottle around the viral genome

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5
Q

What types of capsids can a virus have

A

helical or icosahedral

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6
Q

What type of genome can a virus have

A

Either double or single stranded RNA or DNA

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7
Q

What are the 4 viral morphologies

A

Capsid, envelop, Genetic material including genetic sense, spike proteins

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8
Q

How does the body deal with a virally infected cell

A

a CD8 killer cell or Natural Killer cell will kill the cell

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9
Q

What is a viral envelop formed from

A

Normally formed when the virus buds out of a cell, and so is composed of that cell’s membrane and viral spike proteins

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10
Q

What are the 2 requirements for viral replication

A
  1. virus must cause the replication of their genetic material
  2. Virus must produce (+) RNA to replicate protein components
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11
Q

What 2 things happen to a (+)ssRNA virus when it enters a cell

A
  1. It can be translated immediately into proteins, 1 of which must be RNA-d, RNA-p
  2. It must be copied to (-)RNA for synthesis of many (+)RNA strands
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12
Q

What 3 things happen to a (-)ssRNA virus when it enters a cell

A
  1. It must be transcribed into (+)RNA by the RNA-d,RNA-p it brought with it
  2. multiple copies of (-)RNA are made from the (+)RNA,
  3. some (+)RNA are transcribed into viral proteins
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13
Q

How does a (-)dsRNA virus work

A

Just like a (-)ssRNA virus. Must bring its own RNA-d,RNA-p

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14
Q

What must all RNA viruses code for

A

RNA-dependent, RNA-polymerase

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15
Q

What must Retroviruses code for

A

RNA-dependent, DNA-polymerase (reverse transcriptase)

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16
Q

What is horizontal transmission

A

person to person

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17
Q

What is vertical transmission

A

Mom to fetus transplacentally or to baby during birthing

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18
Q

What is a carrier

A

Chronically infected, asymptomatic individual

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19
Q

What is the iceberg effect

A

Reference to how many infected people are asymptomatic

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20
Q

If antimicrobial defenses are intact, how do microbes infect an individual

A
  1. Microbial attachment/penetration 2. biting arthropod 3. skin wound/animal bite
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21
Q

If antimicrobial defense are not intact, how do microbes infect an individual

A

They just waltz right in

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22
Q

What is the public health consequence of a disease with a large iceberg effect

A

It makes spread of the disease much more likely since asymptomatically infected individuals are still infectious, but can’t be isolated

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23
Q

What is a recurrent illness

A

One you never get rid of, like Herpes

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24
Q

What happens if the number of microorganisms exceed the disease threshold in an individual

A

Then the individual will display disease symptoms. Until this threshold is reached, the individual will display no signs or symptoms

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25
Q

Disease potential =

A

(virulence)(dose)/host resistance

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26
Q

Which antibody do humans make the most of

A

IgA; more than all the other antibodies combined

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27
Q

How does IgA from an infection at a particular site get to another site

A

multiplying daughter B-cells migrate to other mucosal sites

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28
Q

How does IgA get presented on a mucosal surface

A

It binds to a poly-Ig Fc receptor on the basolateral side, which is then taken up by epithelial cells and extruded to the outer or lumen-surface

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29
Q

What is the role of poly-Ig Fc receptor

A

It tags IgA for uptake and secretion by epithelial cells and a portion of it remains attached to IgA to help it resist proteases

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30
Q

What is the role of IgA

A

Block colonization by binding fimbrae; neutralize by covering spike

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31
Q

What is the benefit of taking the Salk polio vaccine

A

It’s killed so it can’t cause disease

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32
Q

What is the drawback to taking the Salk polio vaccine

A

It is administered intravenously so it doesn’t create an IgA response. Thus a person can still get polio and be contagious

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33
Q

What is the benefit of taking the Sabin polio vaccine

A

It generates an IgA and IgG response, so you can’t get polio

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34
Q

What is the drawback to taking the Sabin polio vaccine

A

It is attenuated which means it can mutate to be pathogenic

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35
Q

What is the bystander effect in regards to the Sabin vaccine

A

It is a live virus, so the vaccinated person will shed it, potentially infecting other people. This effectively inoculates them too!

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36
Q

Can a baby be passively protected from polio

A

Yes, because polio is prevented by IgA

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37
Q

What family does polio belong to

A

Picornaviridae

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38
Q

What type of virus is polio

A

Enterovirus; non-enveloped (+)ssRNA

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39
Q

How many serotypes of polio are there

A

3, so it’s easy to develop a vaccine

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40
Q

How is polio spread

A

oral-fecal route

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41
Q

Where does a polio infection start

A

it enters through the mouth and begins replicating in the pharynx, GI tract, and local lymphatics

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42
Q

At what point of infection does clinical pathology from polio present

A

Once the virus enters the blood (viremia)

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43
Q

What tissue does polio virus target

A

Motor neuron fibers in the spinal cord

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44
Q

What is the iceberg effect of polio

A

~95% are asymptomatic

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45
Q

What percent of polio cases are paralytic

A

~0.5%

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46
Q

What is the reservoir for polio

A

Humans

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47
Q

What is the communicability of polio

A

7-10 days before onset; virus is present in stool for 3-6 weeks

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48
Q

What vaccine does the US use for polio

A

Salk, since 2000

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49
Q

When was the last polio case in the US reported

A

1981

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50
Q

When was the last case of polio in the Western hemisphere

A

1991

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51
Q

What was the goal for global polio eradication

A

2000, clearly not met

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52
Q

Why hasn’t polio been eradicated yet

A

Because Polio isn’t as scary as say smallpox, compliance isn’t so great in some countries. Plus they kill the WHO doctors

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53
Q

What countries are still endemic with polio

A

Nigeria, Pakistan, Afganistan. Syria recently had a polio pop-up along with other infectious diseases because of mass displacement and fighters imported from Pakistan, and now Iran has polio too thanks to Syria.

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54
Q

What causes the flu

A

Influenza virus and only influenza virus. None of that 24hr stomach bug stuff

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55
Q

What family does influenza virus belong too

A

orthomyxovirus

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56
Q

What type of virus is influenza

A

Enveloped, (-)ssRNA

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57
Q

Why do you have to get the flu vaccine every year

A

Because influenza is a highly mutable virus, every year there is a different strain

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58
Q

What proteins are commonly mutated in influenza type A virus

A

Neuraminidase (N) and hemagglutinin (H)

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59
Q

How do particularly virulent strains of influenza emerge

A

From a creature that is co-infected with 2 influenza virus, which can then inappropriately package proteins and make a hybrid virus AKA shift mutation

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60
Q

What is a shift mutation

A

A major change; creation of new subtype associated with a pandemic.

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61
Q

What is a drift mutation

A

A minor change, mostly point mutations

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62
Q

What does ‘endemic’ mean

A

normal rate of a disease in a particular area

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63
Q

What does ‘epidemic’ mean

A

Higher rate than is normal in a particular area

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64
Q

What does ‘pandemic’ mean

A

world-wide epidemic

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65
Q

What does the H protein do

A

Initial viral binding to a cell

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66
Q

What does the N protein do

A

Helps new virus bud off the cell

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67
Q

What is interesting about influenza virus’ genome

A

It is segmented, allowing it to swap genes, and each gene is wrapped in a capsid.

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68
Q

What is the standout feature of influenza virus replication

A

it occurs in the nucleus instead of the cytoplasm like all the other RNA viruses

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69
Q

Does influenza virus code for RNA-d,RNA-p

A

Yes, all RNA viruses do. It must bring functional RNA-d, RNA-pol in with it as well

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70
Q

The Spanish flu was an H1N1 virus, as is the 2009 Swine flu. Why didn’t massive amounts of people die from Swine flu

A

Although they have the same spike proteins, they have enough genetic drift to be very different

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71
Q

How is influenza virus transmitted

A

Via respiratory droplets, which can be spread airborne or by hands

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72
Q

What part of the body does influenza virus normally infect

A

respiratory epithelium only; no viremia

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73
Q

How long is influenza virus contagious in an individual

A

Virus is shed in respiratory secretions for 5-10 days

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74
Q

What is the incubation of influenza virus

A

Symptoms normally show in 1-4 days

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75
Q

What is the clinical presentation of influenza infection

A

Abrupt onset of fever, myalgia, sore throat, non productive cough, headache, shortness of breath.

76
Q

What clinical features are not present in influenza infection

A

There is no stuffy nose and no mucus in the throat (unless there is a secondary infection)

77
Q

What does the severity of an influenza infection depend upon

A

an individual’s prior experience with antigenically related variants

78
Q

What is the fatality rate of influenza

A

~0.5-1 per 1,000 cases

79
Q

Why do influenza infections always peak in the winter

A

Low vit D, people are inside much more, the envelope is much more stable in cooler temperatures

80
Q

How many strains of influenza virus are there

A

3; A, B, and C

81
Q

Who does type A influenza infect

A

Humans and animals in any age group (which is kinda scary), causing moderate to severe illness, epidemics and pandemics

82
Q

Who does type B influenza infect

A

humans only, primarily affects only children and elderly, causing milder epidemics

83
Q

Who does type C influenza infect

A

Humans, it is rarely reported disease causing and is thus not medically important

84
Q

How many people died in the Spanish Flu (1918-1919)

A

50-100 million worldwide

85
Q

What kinds of influenza vaccines are available

A

inactivated and attenuated

86
Q

What is the inactivated influenza virus vaccine composed of

A

Saline solution with stripped off viral spikes administered intravenously

87
Q

What is the attenuated influenza virus vaccine composed of

A

A highly mutated (non-pathogenic) influenza virus

88
Q

Why doesn’t the flu vaccine provide 100% immunity

A

Because the scientists are just guessing which strains will be prevalent

89
Q

How many strains of influenza are included in the flu vaccine

A

it is trivalent; this year H1N1, H3N2, and some B strain.

90
Q

Why does the flu vaccine need to be administered yearly

A

Because the spike subtypes mutate so rapidly, there is a new strain out every year

91
Q

What is efficacy of the flu vaccine this year

A

~60%

92
Q

What type of virus is herpes

A

Enveloped, dsDNA genome

93
Q

What is unique about herpes’ replication cycle

A

Although it is a DNA virus, it replicates and assembles in the nucleus, including acquiring its envelope

94
Q

How long does a herpes infection last

A

It is a life-long infection

95
Q

What is the disease pattern of a herpes infection

A

Often there is an initial infection and illness, and then the virus goes latent and commonly has multiple relapses.

96
Q

What are the treatments for herpes

A

Because herpes has a large genome providing multiple targets, there are antiviral therapies available (acyclovir)

97
Q

Which herpes viruses do we all probably have

A

HHV-7, HHV-6, and Varicella-Zoster (HHV-3)

98
Q

What is HHV-1

A

Herpes simplex virus-1

99
Q

Which strains of herpes are latent in neurons

A

HHV-1,2,3

100
Q

What pathology does HHV-1 cause

A

Cold sore, oral ulcers (67% of Americans have it)

101
Q

What is HHV-2

A

Herpes simplex virus-2

102
Q

What pathology does HHV-2 cause

A

Genital herpes (25% of Americans have it)

103
Q

What is HHV-3

A

Varicella-Zoster

104
Q

What pathology does HHV-3 cause

A

Initially it causes Chickenpox; relapses as shingles (100% of adults have it)

105
Q

What is HHV-4

A

Epstein-Barr virus

106
Q

Where is HHV-4 latent

A

B-cells

107
Q

What pathology does HHV-4 cause

A

Infectious Mono, Burkitt’s lymphoma

108
Q

What is HHV-5

A

Cytomegalovirus

109
Q

Where is HHV-5 latent

A

Lymph/mono

110
Q

What pathology does HHV-5 cause

A

Congenital infection; generally very mild but could cross the placenta and cause some issues

111
Q

Where are HHV-6 and 7 latent

A

T-cells, mono, macs

112
Q

What pathology does HHV-6 and7 cause

A

roseola infantum

113
Q

What is HHV-8

A

Kaposi’s sarcoma virus

114
Q

Where is HHV-8 latent

A

lymphocytes

115
Q

What pathology does HHV-8 cause

A

Kaposi’s sarcoma, which is rare outside of AIDS

116
Q

How are most herpes virus spread

A

By mucosal contact

117
Q

What is the first stage of herpes infection

A

primary infection; viremia

118
Q

What is the second stage of herpes infection

A

Secondary infection; latent virus begins replicating but antibodies in the blood keep the relapse local

119
Q

When is HSV-1 (HHV-1, herpes simples virus-1) normally acquired

A

In the first 5 years of life

120
Q

How does HSV-1 virus shed

A

in saliva

121
Q

What is a sign of primary HSV-1 infection

A

a lip lesion, but 85% are asymptomatic

122
Q

If the primary HSV-1 infection is asymptomatic, is the person still infectious

A

Yep. They shed the virus in saliva.

123
Q

Where can secondary HSV-1 lesions appear

A

Normally in the mouth or gums and lips, but can be spread by contact with an open wound to hands, arms, and eyes

124
Q

Why is HSV-1 specific for oral, and HSV-2 specific for genitalia

A

Because of what their spikes bind, however it is possible to have HSV-1 and HSV-2 in either place

125
Q

How long is HSV-2 transmittable

A

From shortly before the lesion appears to about 20 days later when it is finally healed

126
Q

What are 2 unique features of HHV-3 (Varicella-Zoster, VZV)

A
  1. there is a vaccine for it 2. it is spread via respiratory droplets instead of mucosal contact
127
Q

When did the HHV-3 vaccine become available

A

1996

128
Q

What is the first stage of an HHV-3 infection

A

a 2 week incubation phase where the virus infects lung mucosa and local lymph nodes

129
Q

What is the second stage of an HHV-3 infection

A

Viremia with rash and papules, which appear predominantly on the trunk for 2 weeks

130
Q

What is the mortality of a primary HHV-3 infection

A

Children are 1:100,00
Adults are 1:5,000
Immunocompromised are 1:10

131
Q

Who is most at risk for developing complications from VZV?

A

pregnant women and their baby, auto immune, and immunosupressed

132
Q

What diseases are caused by HHV-4(Epstein-Barr)

A

Infection mononucleosis and burkett’s lymphoma

133
Q

How long is someone with EBV infectious

A

The individual sheds small amounts of virus in their saliva for the rest of their life

134
Q

What population develops Burkett’s lymphoma and/or nasopharyngeal cancer fro EBV

A

EBV with a malaria co-infection or immunosupression

135
Q

How is infectious mononucleosis characterized

A

fever, sore throat, swollen spleen and lymph nodes, increase in mononuclear cells, and fatigue

136
Q

Who is most at risk in a Cytomegalovirus infection

A

A fetus/baby whose mom is infected for the first time

137
Q

What happens to a baby if its mom gets a primary HHV-5 infection

A

It can suffer neural sequela. 1% of pregnancies do actually, and CMV is #1 cause of mental retardation

138
Q

What is the key characteristic of hepatitis viruses

A

They routinely replicate in and damage hepatocytes

139
Q

Which hepatitis viruses are stable

A

HAV and HEV because they are non-enveloped (naked)

140
Q

Which hepatitis viruses are not stable

A

HBV, HCV, HDV

141
Q

What is the route of transmission for HAV and HEV

A

fecal-oral

142
Q

What is the main route of transmission for HBV, HCV, and HDV

A

Exchange of bodily fluids (blood, semen, saliva, mother’s milk, etc)

143
Q

What hepatitis viruses cause chronic infection

A

HBV, HCV, HDV

144
Q

Which hepatitis viruses have vaccines

A

HAV and HBV (HDV indirectly)

145
Q

Who is most at risk from HEV

A

Pregnant women around the Indian ocean (strain is rare in US)

146
Q

What virus family does HAV belong to

A

RNA Picornavirus

147
Q

How many serotypes of HAV are there

A

just one worldwide which is why the vaccine was relatively easy to develop

148
Q

What kind of iceberg effect does HAV have

A

96% of kids infected are asymptomatic

149
Q

What percentage of adults with a primary HAV infection will be hospitalized

A

20%

150
Q

What is the infection progression of HAV

A

Food/mucosa/IV to gut mucosa to liver via blood

151
Q

What is the treatment if an individual as at risk of dying from an HAV infection

A

Inject with pooled IgG

152
Q

What virus family dos HBV belong to

A

DNA Hepadnavirus

153
Q

How many infected people end up with a chronic infection

A

about 10%

154
Q

How many serotypes of HBV are there

A

Just one worldwide

155
Q

What puts someone at high risk for HBV

A

doing anything that has to do with blood, sex, or birth

156
Q

Why is prenatal HBV screening super important

A

Because 90% of infants will be infected if mom has HBV, and 90% of those will become chronically infected

157
Q

Why can you get HBV from an accidental needle stick

A

although there is little blood on a used needle, there are 10^8 infectious particles in one ml of blood, so yeah.

158
Q

Are individuals who are chronically infected with HBV always symptomatic or infectious

A

Not always symptomatic but always infectious

159
Q

What happens to the liver in a hepatitis virus infection

A

It is damaged because the immune system constantly kills infected cells, but never makes enough antibody to bind up all the viruses, so hepatocytes keep getting infected

160
Q

How do hepatitis viruses cause liver cancer

A

Virus could insert its DNA into an oncogene or turn off a regulatory gene

161
Q

What super annoying about HBV

A

It is very hardy for an enveloped virus and can survive for up to 2 weeks in a drop of blood on a table.

162
Q

What is interesting about HBV’s replication cycle

A

It replicates entirely in the nucleus and so must code for RNA-d, DNA-pol

163
Q

What sort of immune response in necessary to kill a viral infection

A

A robust T-cell and antibody (b-cell) response

164
Q

When is a hepatitis virus infection considered chronic

A

If the free anti-HBsAg levels haven’t risen and HBsAg levels haven’t fallen in 6 months, the infection is chronic

165
Q

What’s missing from HDV’s genome

A

It has only one gene to code for a capsid, but still needs spikes which it gets from HBV

166
Q

What happens from a HBV/HDV co-infection

A

The simultaneous infection is more likely to be acute with signs and symptoms and hospitalization

167
Q

What happens from a HBV/HDV super infection

A

Being infected with HDV after being infected with HBV greatly increases the chances of a chronic infection, and of pathology

168
Q

What is an attenuated vaccine

A

One in which the bug is merely mutated to be non-pathogenic in humans

169
Q

What is an inactivated vaccine

A

One in which the pathogen in dead: Toxoid, killed, conjugate, or sub-unit

170
Q

What are the 4 obvious benefits of an attenuated vaccine

A
  1. Small does required 2. few boosters needed 3. creates good immune memory 4. increases Tc, Th, and sIgA levels
171
Q

What are the 3 obvious benefits of an inactivated vaccine

A
  1. Shelf stable 2. no reversions to pathogenic strain 3. immunodeficient ppl are not at risk
172
Q

What are 3 obvious drawbacks to an attenuated vaccine

A
  1. Unstable 2. possible reversion to pathogenic strain 3. immunodeficient people at risk
173
Q

What are 4 obvious drawbacks to an inactivated vaccine

A
  1. Large does required 2. many boosters needed 3. create poor immune memory 4. Mainly an IgG response
174
Q

How does a person/doctor/country decide which type of vaccine for a given pathogen to use

A

Weigh risks vs benefits

175
Q

What is herd immunity

A

When a significant portion of the population has been immunized, a pathogen can’t spread to individuals who have not developed immunity

176
Q

What are blocking antibodies

A

Mom’s IgG in baby blocks vaccinations, which is why they start at 2 mo

177
Q

Which childhood vaccines are attenuated

A

Rotavirus, influenza, MMR, and Varicella-Zoster

178
Q

What are the characteristics of a t-dependent response

A

This response is present in babies at birth: Th-cell is activated, IgM->IgG, booster response, good immune memory

179
Q

What are the characteristics of a t-independent response

A

This response develops by 2yo: poor immune memory and no Th-cell activation or class switching

180
Q

What causes a t-independent response

A

A massive first signal (antigen dose)

181
Q

What kind of bacteria is Haemophilus influenzae

A

gram-negative rod

182
Q

How is H. influenzae spread

A

Via respiratory droplets

183
Q

What area the 3 major virulence factors of H. influenzae

A

Capsule, IgA protease, LPS

184
Q

What are the 3 main causes of bacterial meningitis

A

S. pneumoniae, N. meningitidis, H. influenzae

185
Q

What is a hapten

A

compound that is antigenic but not immunogenic

186
Q

What is a conjugate vaccine

A

Hapten bound to a carrier protein that is immunogenic

Microbiology (4 decks)

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