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FINAL Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

What kind of bacteria is yersinia pestis (gram negative or positive)

A

negative

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2
Q

form of plague associated with inflamed lymph nodes that cause buboes to form

A

bubonic

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3
Q

form of plague that causes skin hemorrhages and is associated with the black death

A

septacemic

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4
Q

form of plague that is associated with infection of the lungs

A

pneumonic

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5
Q

what is the difference between primary pneumonic and secondary pneumonic plague

A

primary is spread through aerosol droplets
secondary comes from other tissues

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6
Q

is there a vaccine available for the black plague

A

nah

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7
Q

the wild cycle of black plague transmission

A

Sylvatic

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8
Q

what mechanism of the black plague causes fleas to bite more

A

yersinia pestis forms a biofilm within the stomach of fleas causing them to feel “hungrier” and thus bite more.

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9
Q

what are the three cycles of bp transmission

A

sylvatic, urban and human

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10
Q

what kind of secretion does the yersinia pestis use

A

type 3

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11
Q

what kind of staining do you use for TB

A

acid fast

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12
Q

which virus is TB closely associated with

A

HIV

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13
Q

testing method of TB where size of bumps is diagnostic marker

A

mantoux test/ppd

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14
Q

What are the two stages of TB

A

latent and active

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15
Q

which bacteria type has many of its important virulence factors encoded in plasmids

A

y. pestis

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16
Q

where does TB infection begin

A

pulmonary alveoli

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17
Q

what are the three primary mechanisms TB uses to persist

A

blocking of cytokine signaling, blocking of phagosome maturation, and counteracting ROS

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18
Q

what state does mtb often go into inside of a granuloma

A

a dormant state. within this state drugs and host antimicrobial strategies are less effective

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18
Q

necrotic vs apoptotic macrophages (which is better for spreading bacteria)

A

necrotic. When they die the contents of that cell are released into the extracellular environment

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19
Q

inside the granuloma, what can the mtb use for an energy source

A

lipids from dead cell membranes

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20
Q

what are the components of a granuloma

A

epithelioid cells, multinucleated cells, foam cells, innate/adaptive cell types, and epithelial cells. Each of these contain few to no bacteria.

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21
Q

what are the three stages of granulomas

A

solid, necrotic, and caseating

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21
Q

in which stage of granuloma does tb exist as dormant

A

solid

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22
Q

what is the transition state between solid and caseating granulomas (TB is now active again)

A

necrotic

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23
Q

in which stage of the granuloma does it lose it’s rigidity due to decay at the center

A

caseating

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24
Q

does BCG prevent TB infection

A

no

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25
Q

what does BCG often cause in TB tests

A

false positives

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26
Q

what are the main modern gen vaccines used

A

live mycobacteria, subunit vaccines, naked dna and viral vectored, and double stranded rna capsules

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27
Q

TB is known for requiring what type of treatment

A

a cocktail of drugs

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28
Q

what class of bacteria is vibrio spp

A

gram negative

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28
Q

where is cholera typically found

A

in water or food sources that have been contaminated with feces from a person with cholera

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29
Q

what is vital for cholera to survive in water

A

biofilm

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30
Q

are there any known animal hosts for cholera

A

no, but technically they attach very easily to animals with high amounts of chitin in their shell

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31
Q

can antibiotics remove the effects of cholera?

A

no but they are effective in shortening the symptoms

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32
Q

true/false: all forms of cholera are pathogenic

A

no, there are two main types that make people sick

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33
Q

what kind of toxin is the cholera toxin

A

A-B translocation/type 3

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34
Q

what are the main targets of antibiotics

A

inhib of cell mebrane synthesis, protein translation, disruption of membrane, inhib of nucleic acid synth, disruption of bacterial dna, and inhibition of enzymes in dna replication

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35
Q

what are the resistance mechs of bacterial to antibiotics

A

limiting access of ab, enzymatic inactivation, modification of ab targets and failure to activate antibiotics

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36
Q

how are ab resistant genes regulated

A

repressors, translational attenuation, activators, and insertion/promoter mutations

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37
Q

mutations of ___ decrease diffusion of antibiotics into the cell

A

porins

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38
Q

which virus is near erradication

A

polio virus

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39
Q

smallpox is ___

A

erradicated

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40
Q

what did hershey and chase yield from their experiment

A

DNA is the molecule that mediates heredity. They found the irradiated DNA inside host cells but not the marked protein.

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41
Q

what is variolation

A

direct use of tissue from infected organism to introduce virus into immune system

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42
Q

which virus type requires RNADP ( brings its own RNADP)

A

negative rna type

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43
Q

which virus is similar and can be translated directly to a protein

A

positive rna type

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44
Q

how many dna families have envelopes

A

three

44
Q

which rna strand type is associated with being enveloped

A

single strand type

45
Q

not all + rna is mrna

A

true

45
Q

Viral genomes must make mRNA that can be read by
host ribozyme true/false

A

true

46
Q

what envelops negative strand rna viruses

A

helical nucleocapsids

47
Q

what is encoded by the viral genome

A

rep of viral genome, assembly and packaging of the genome, reg and tim of rep cycle, modulation of host defenses, and spread to other cells and hosts

48
Q

what is not encoded by the viral genome

A

ribozyme, trna, membrane and energy production

49
Q

what kind of replication for HPV 16

A

roling circle

50
Q

what kind of replication for HSV

A

linear

51
Q

what are the four main driving effects of viral evolution

A

large number of progeny, large number of mutants, quasi effects, and selection

52
Q

quasi species theory

A

Viral infections are initiated a population of particles, not a single virus, The large number of progeny produced are complex products of
selective forces inside the host, and The survivors that can re-infect a new host reflect the selective
forces outside the host

53
Q

is there a vaccine for measles

A

yes, created in 1963 and quite effective

54
Q

is there a vaccine for Ebola

A

not yet it is current under development

55
Q

what determines cell tropism

A

cell receptors for a virus, cell transcription factors that recognize virus promoters, ability of the cell to support viral replication, and physical barriers

56
Q

what are the 2 types of chronic persistent infections

A

true latency and persistence

57
Q

characteristics of a “persistent virus”

A

replicates constantly at a low level

58
Q

characteristics of a true latent virus

A

ceases replication after initial primary infection

59
Q

Rapid onset of disease symptoms result in eradication of the virus or death of the infected animal

A

acute infection

59
Q

what are the basic steps in the viral life

A
  1. absorption, penetration, uncoating, synth of viral nucleic acid and protein, assembly, and release
60
Q

what are the three pathways of persistent infection

A

integration into host genome, sporadic release but latent most of the time, and virus is constantly released without lysis of host cell membrane

61
Q

how is viral absorption affected by temperature

A

it is not affected, it acts independent of temp

62
Q

How do enveloped viruses enter the cell

A

fusion with the cell membrane through endosomes

63
Q

what is enveloped virus entry dependent upon

A

mediated by PH

64
Q

when does the eclipse phase of viral replication end?

A

it ends when the first viral particle is formed.

65
Q

where does protein synthesis occur for viral replication

A

in the cytoplasm

65
Q

where can nucleic acids be synthesized for viral replication

A

in the nucleus or the cytoplasm

66
Q

what is the transmission route for influenza a

A

respiratory

67
Q

what is the transmission route for the enterovirus

A

faecal-oral

68
Q

vertical transmission

A

transfer of virus to offspring

68
Q

what is the transmission route for hepatitis b

A

blood borne

69
Q

what is the transmission route for rabies

A

insects or animal vectors

70
Q

what is horizontal transmission

A

from one organism to another via direct or indirect

71
Q

what are plaque forming units

A

viruses that lyse cells and create holes in the monolayer of cells

71
Q

what does virulence depend on

A

dose, strain, host factors, and inocculation route

72
Q

what is the most common method used to propagate viruses

A

cell culturing

73
Q

what does the MOI ratio indicate

A

the ratio of virons to host cells

74
Q

what can we evaluate with MOI

A

the total number of cells that will be infected and the number of virons infecting each cell

75
Q

what is a lytic infection

A

virus entering cell and lysing/killing the cell in the process

76
Q

what are the innate receptors for viruses

A

NOD, TLR, AND RIG

77
Q

gram staining procedure

A

crystal violet, iodine, alcohol wash, and then application of safranin

78
Q

what does the clonal selection theory explain

A

how the immune system responds to different pathogens and develops specific immunity against different antigens

79
Q

RIG 1 is for

A

viruses

80
Q

what is a special function of TCRs

A

antigen recognition

81
Q

What causes differentiation and survival of tcrs

A

co-stimulation via B7CD28 and cytokines

82
Q

what do TCRs recognize

A

linear epitopes presented on MHC 1 and MHC 2 molecules

83
Q

how do TCRs mature

A

recombination

84
Q

what is the only cell type that does not express MHC’s

A

red blood cells

85
Q

what are MHC 1 molecules for

A

endogenous antigens

86
Q

what are MHC 2 molecules for

A

exogenous antigens

87
Q

which MHC class type Kill sinfected cells by perforin/granzyme or fas/fas-
ligand mediated cytotoxicity and restricts viral replication

A

MHC 1/CD8+

88
Q

which influenza type is only infectious to humans, causes less severe illness, and causes epidemics

A

Type B

89
Q

which mhc class type is required for B cell activation

A

MHC 2/ CD 4+

90
Q

what are the antibody mediated forms of protection

A

opsonization, activation of the complement, and neutralization

91
Q

Which influenza type is associated with more severe illness, regular epidemics, and able to cause pandemics. Also effects humans and animals

A

type A

92
Q

what are the surface proteins found on the influenza virus

A

hemagglutin and neuraminidase

92
Q

what kind of virus is the influensa virus

A

neg sense single stranded rna

93
Q

what is the mechanism that causes seasonal influenzas

A

error prone RDRP»>antigenic drift» seasonal influenza

94
Q

what is the difference between antigenic drift and antigenic shift in terms of viruses

A

antigenic drift occurs due to point mutations in hemaglutin and neuraminidase and thus slightly different antigenic profiles. Conversely antigenic shift occurs due reassortment of genes and explosive spread that has no existing immunity

95
Q

which antigenic type ( drift or shift) is associated with causing pandemics

A

shift

96
Q

What does influenza virus bind to

A

salic acid

97
Q

which surface protein binds to salic acid

A

HA

98
Q

which surface protein cleaves influenza

A

NA

99
Q

what regulates type 3 secretion

A

calcium and temp

100
Q

Where are MH2 molecules normally found

A

in adaptive/innate cells

101
Q

which influenza type is considered to be more severe

A

influenza type a

102
Q

where does the influenza virus replicate

A

inside the nucleus

103
Q

where does the influenza virus undergo protein synthesis

A

in the cytoplasm

104
Q

when is type three secretion most active

A

at low calcium and around 37 degrees celsius

105
Q

most of the plus strand rnas have a __ genomic RNA structure

A

single stranded

Medical Microbiology (3 decks)

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