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Microbiology > Exam 2.2 > Flashcards

Exam 2.2 Flashcards

1
Q

What is the iceberg effect of measles

A

Essentially zero

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2
Q

How is measles spread

A

from person to person via respiratory droplets. Super contagious

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3
Q

What kind of virus causes measles and mumps

A

Paramyxovirus

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4
Q

What kind of genome does measles virus have

A

enveloped, (-)ssRNA

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5
Q

What kind of capsid does measles virus have

A

helical

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6
Q

How many measles virus serotypes are there

A

just 1

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7
Q

What kind of vaccine is the measles mumps and rubella vaccine (MMR)

A

attenuated

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8
Q

What factors increase death rate from measles infection

A

poverty that causes malnutrition

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9
Q

What percent of the population must be vaccinated against measles virus to have herd immunity

A

92-94% because it is so highly infectious

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10
Q

What is one unusual effect of a measles virus infection

A

It suppresses the immune system which allows for secondary infections

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11
Q

Is it possible to completely rid the world of measles, mumps and rubella viruses

A

Yes, because humans are the only reservoir for all three

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12
Q

What kind of genome does mumps virus have

A

(-)ssRNA, enveloped

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13
Q

How is mumps spread

A

from person to person via respiratory droplets

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14
Q

What tissue does measles virus initially infect

A

Lung epithelium and local lympathics

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15
Q

What tissue does mumps virus initially infect

A

Lung epithelium, and also potentially eyes and nose

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16
Q

After measles virus goes systemic, what tissue does it infect

A

Epi/endothelium, thus the characteristic measles rash

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17
Q

After mumps goes systemic, what tissue does it infect

A

Glands including salivary and testicular ducts, but especially the parotids

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18
Q

What is the most common permanent damage caused by mumps virus infection

A

Duct damage resulting in deafness or sterility

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19
Q

Who is especially at risk in a rubella infection

A

Baby has a 25% chance of severe birth defects if mom gets a primary rubella infection in the first trimester

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20
Q

What is the iceberg effect of mumps virus

A

25% of infected individuals don’t show signs and symptoms

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21
Q

What type of virus is Rubella

A

togavirus

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22
Q

what kind of genome does rubella virus have

A

(+)ssRNA, enveloped

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23
Q

How is rubella virus spread

A

from person to person via respiratory droplets

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24
Q

What tissue does rubella initially infect

A

respiratory tract.

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25
Q

What kind of virus is Respiratory Syncytial Virus

A

Paramyxovirus

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26
Q

What kind of genome does RSV have

A

(-)ssRNA, enveloped

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27
Q

How is RSV spread

A

from person to person via respiratory droplets

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28
Q

What tissue does RSV initially infect

A

Lung epithelium

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29
Q

What is the course of development of RSV infection

A

75% individuals develop UIR, 25% develop LRI and of those 3-5% require hospitalization

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30
Q

Who is most at risk for complications from RSV infection

A

kids with cystic fibrosis often die from RSV

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31
Q

Is it possible to eradicate RSV

A

No because there is no vaccine. But were there a vaccine then yes, because humans are the only reservoir

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32
Q

How many infected people are necessary to maintain an acute infection in a population

A

300,000

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33
Q

How many infected people are necessary to maintain a chronic infection

A

way less than 300,000 because it is always infectious

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34
Q

What sort of pathology do accidental hosts have

A

Super severe with high mortality rates

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35
Q

What sort of pathology do natural hosts have

A

little or no disease

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36
Q

What 2 things qualify a virus as ‘emerging’

A
  1. new infectious agents causing new disease 2. known disease increasing in incidence or geographical range
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37
Q

What kind of genome do most currently emerging disease have

A

ssRNA viruses because they have no spell checker mechanism and no proof reading strand which makes it easier to jump between species

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38
Q

What are arboviruses

A

viruses that have an arthropod vector (bugs and mites)

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39
Q

What is an emerging flavivirus

A

West Nile. We are accidental hosts; it kills crows

40
Q

What is an emerging togavirus

A

Chikunganya. mosquito vector; just mutated to infect different breeds and now is in the Caribbean (also rubella)

41
Q

What are roboviruses

A

Viruses that have a rodent vector

42
Q

What is an emerging bunyavirus

A

Hanta fever, which infects mice in the 4 corners region

43
Q

What is an emerging arenavirus

A

Lassa fever, which is like a less deadly version of ebola

44
Q

What is an emerging filovirus

A

Ebola. 70% death rate with a possible bat reservoir

45
Q

Which emerging viruses cause encephalitis

A

Chikungunya, West nile

46
Q

Which emerging viruses cause hemorrhagic fever

A

Hanta, Lassa, Ebola

47
Q

What causes a hemorrhagic fever

A

Complete use of all the clotting factors because the virus attacked the endothelium

48
Q

What is zoonosis

A

having a mammal or bird reservoir

49
Q

What is a dead end host

A

Accidental host in which the pathology is so severe you die before you have a chance to transmit the disease

50
Q

What is the mechanism of action in prion disease

A

Protease resistant proteins cause other proteins to misfiled to become protease resistant, which leads to a buildup of proteins (ameloid plaque)

51
Q

What are prions resistant to (in comparison to DNA)

A

Heat, formaldehyde, UV, Proteases

52
Q

What makes prion disease particularly insidious

A

It doesn’t even trigger an immune response because technically it is a host protein

53
Q

What was the first prion disease discovered

A

Scrapie, found in sheep

54
Q

What is Kuru

A

Human transmissible spongiform encephalitis

55
Q

What is the most common human transmissible spongiform encephalitis disease

A

Creutzfeldt-Jakob Disease (1:10,000,000/year)

56
Q

What is vCJD

A

Varient Creutzfeldt-Jakob disease, now thought to be caused by consumption of BSE infected beef, is the same except faster than CJD

57
Q

How does one get CJD

A

a prion could randomly misfold, or it could be transmitted by receiving brain products, like GH extracted from a cadaver

58
Q

What is Smallpox’s real name

A

Variola major

59
Q

What kind of genome does smallpox virus have

A

dsDNA, half enveloped, half not. Almost as large as the smallest bacteria

60
Q

How is smallpox virus spread

A

From person to person via respiratory route or from skin lesion once the rash develops

61
Q

What tissue does smallpox virus initially infect

A

Respiratory tract and then takes macrophage taxis to the lymph nodes

62
Q

What is the classic presentation of smallpox infection

A

Pox distributed more on extremedies and face (cmp to chicken pox) along with fever, etc

63
Q

What are the outcomes of smallpox infection

A

1/3 die 1/3 terribly scarred, 1/3 moderate-mild scarring on face and hands

64
Q

What is variolation

A

purposely infecting someone with a mild strain of smallpox as a sort of immunization

65
Q

What’s convenient about a cowpox infection in a human

A

It stays localized in the hands and is not deadly, but is similar enough to smallpox to give immunity to it.

66
Q

Who is the last person to die from smallpox

A

Jen Parker, a medical photographer, caught it from a research lab and died, as did her father(MI) and the researcher who caused her illness(suicide)

67
Q

What kind of virus is HIV

A

Retrovirus

68
Q

What type of genome do all retroviruses have

A

two copies of (+)ssRNA

69
Q

What is the significance of having 2 copies of the ssRNA

A

Even if a strand is mutated so that it can’t complete its “life”cycle, it still has a chance of infecting more cells or individuals because it can be carried by a “healthy” virus

70
Q

Why are you never “cured” from HIV

A

Because the virus integrates into the host genome where it can lay latent indefinitely

71
Q

What must be included in every retrovirus particle

A

along with the genome, reverse transcriptase, to turn RNA into DNA

72
Q

What are the 3 classes of exogenous retroviruses

A

Oncoviruses(tumor), lentiviruses (slow), spumaviruses (foamy)

73
Q

What is a human oncovirus

A

HTLV I causes human leukemias; rare STI

74
Q

What are the human lentiviruses

A

HIV 1 (immunodeficiency), HIV 2 (brain lesion)

75
Q

What a spumavirus

A

? cytopathic, no overt pathology

76
Q

What is an HERV

A

Human endogenous retrovirus is a virus that integrates itself into germ line genome.

77
Q

Are HERVs dangerous

A

They are degenerate and no longer pathogenic. In fact, they make up 8% of our genome and may even be involved in placenta formation and other aspects of health

78
Q

How is HIV transmitted

A

Mainly sexual transmission, but also needles and transplacental and even health care products. Needles, sex, and blood

79
Q

How many HIV carriers are there

A

40 million, with 2 million AIDS cases

80
Q

How does one increase one’s risk of getting HIV

A
  1. Have more sexual partners 2. Have sex with someone with a large viral load 3. Have lots of sex with someone who is HIV + 4. Lose genital epithelial barrier from a different STI (particularly Chlamydia)
81
Q

Where is HIV definitely increasing

A

Eastern Europe and central asia; USSR collapsed and with it went public health plus IV drug use up since Afghanistan war

82
Q

What are the 4 major gene segments in a retrovirus

A

gag, pro, pol, and env,

83
Q

What is an LTR

A

long, terminal repeat. Found at both ends of a retrovirus genome and serves as a promotor, for insertion stuff

84
Q

What does the GAG segment code for

A

proteins involved in viral structure, like the capsid

85
Q

What does the POL segment code for

A

Enzymes for replications, like integrase and REV

86
Q

What does ENV code for

A

proteins that stabilize the envelop, spikes, like GP41 and GP120

87
Q

What does PRO code for

A

Protease

88
Q

What does GP120 do

A

bind CD4 via CCR5 or CXR4

89
Q

What does GP41 do

A

helps HIV virus fuse with the cell membrane

90
Q

how is an HIV virion activated

A

It must bud off while protease cleaves the polyprotein into functional proteins

91
Q

After the one long strand of HIV mRNA is made, what happens

A

The section that codes for spike proteins is cleaved and the two strands are transcribed separately

92
Q

What is the one step of HIV viral replication that can’t be block (yet)

A

transcription and translation of viral DNA into mRNA and proteins

93
Q

What is R-5 tropic HIV

A

HIV with a high affinity for CCR5 receptor (found on macrophages)

94
Q

What is T-tropic or X-4 tropic HIV

A

HIV that has a high affinity for CXCR4 receptor (found on T-helpers)

95
Q

What is the receptor affinity progression in HIV

A

Normally starts as R-5 tropic and mutates to X-4 tropic

96
Q

What is the benefit and harm of the affinity progression of HIV

A

X-4 type is less infectious, but more damaging to the infected individual

97
Q

Why is HAART (drug cocktail) the gold standard treatment for HIV

A

Because using just one drug makes it super easy for the virus to mutate and avoid the drug

Microbiology (4 decks)

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