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emerging world diseases > quiz 2 info > Flashcards

quiz 2 info Flashcards

1
Q

what are the sections of the chain of infection?

A

infectious agent begins in reservoir, portal of exit, mode of transmission, portal of entry, susceptible host

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2
Q

what makes a successful pathogen?

A

survives passage from one host to the next

attaches and penetrates host tissue

withstands (even if temporarily) host immune/defense system

induces damage or disrupts function of host tissues

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3
Q

what makes something a pathogen?

A

that it creates damage or dysfunction in host’s tissue

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4
Q

what do pathogens want?

A

to live and reproduce

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5
Q

examples of reservoirs

A

animate: humans and animals (cows)

inanimate: soil

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6
Q

example of portals of exit

A

urine/feces, respiratory or urogenital tract, oral/proboscis (mosquitoes)

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7
Q

what is a reservoir?

A

pathogen’s habitat - can have multiple

where pathogens normally live, grow, and multiply

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8
Q

why is it important to know a pathogen’s reservoir?

A

for proper public health response and treatment of outbreaks

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9
Q

what’s an example of a pathogen that uses HUMANS as reservoirs?

A

smallpox and measles

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10
Q

what’s an example of a pathogen that uses ANIMALS as reservoirs?

A

anthrax - sheep

plague - rodents

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11
Q

what’s an example of a pathogen that uses INANIMATE things as reservoirs?

A

fungal agents

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12
Q

what is a portal of exit?

A

path that a pathogen uses to leave its host

usually related to where the pathogen is localized

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13
Q

what is an example of a pathogen and its corresponding portal of exit?

A

influenza viruses exit through the respiratory tract

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14
Q

what are the routes of transmission?

A

direct: contact and droplet

indirect: airborne, vehicle, and vector

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15
Q

example of direct contact infections

A

mono or gonorrhea

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16
Q

example of droplet spread infections

A

pertussis or meningococcal meningitis

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17
Q

example of airborne transmission infection

A

TB

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18
Q

examples of vehicle transmitted infection

A

polio or hepatitis A virus

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19
Q

example of vector transmitted infections

A

malaria or HAT

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20
Q

what is a portal of entry?

A

how a pathogen enters a susceptible host

provides access to tissues the pathogen can multiply or a toxin can act in

** usually highly specific

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21
Q

examples of portals of entry

A

skin, mucous membranes, and blood

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22
Q

why are portals of entry highly specific?

A

if the pathogen can’t take advantage of that tissue, it can’t do damage or survive

needs to be able to grab onto a very specific receptor

cholera won’t infect someone if it only sits on healthy, unbroken skin

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23
Q

example of infection using SKIN as portal of entry

A

rabies and pink eye

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24
Q

example of infection using GI as portal of entry

A

E. coli and polio

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25
Q

example of infection using RESPIRATORY SYSTEM as portal of entry

A

diphtheria, strep throat, pertussis

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26
Q

example of infection using UROGENITAL SYSTEM as portal of entry

A

herpes and gonorrhea

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27
Q

examples of infections with multiple portals of entry

A

TB: respiratory or GI tract

gonorrhea: throat or genitals

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28
Q

analogy for specific receptors in class

A

pathogen only being able to “grab” onto chicken elbows and not human ones

** at least until there’s a mutation

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29
Q

colonize

A

replicate

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30
Q

virulence factor

A

how sick the infection/disease makes you

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31
Q

adhesion is a ___ ___

A

virulence factor

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32
Q

once in the body, the pathogen must ___ and ___

A

colonize and multiply

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33
Q

the initial inoculum of a pathogen is ___ sufficient

A

rarely

infection usually only comes after the pathogen has a chance to adhere and multiply

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34
Q

why is adherence a virulence factor?

A

the better a pathogen can adhere or to more places, the better is can be a pathogen

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35
Q

examples of adherence mechanisms

A

slime capsules, pili, and fimbrae

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36
Q

example of adherence

A

HIV binding to immune cell receptors

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37
Q

what are slime capsules?

A

bacterial carbohydrate-protein coating that helps pathogens “stick” non-specifically

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38
Q

what are pili?

A

little tails on bacteria that allow them to swim around and hook/velcro to tissue

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39
Q

what are fimbriae?

A

hair-like projections on bacteria (usually gram negative) that help it adhere

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40
Q

inoculum

A

dose

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41
Q

methods of attachment and penetration

A

specific enzymes to digest extracellular matrix

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42
Q

example of specific enzyme to digest extracellular matrix

A

neuraminidase from influenza virus (HN)
-> breaks down sialic acids on glycoproteins

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43
Q

phrasing to use when describing pathogen’s invasive mechanisms

A

“___ binds to ___ receptor in ___ system and uses ___ mechanism”

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44
Q

how are we affected by the different complexes of influenza?

A

we need to adjust annual flu vaccines on complexes that are present

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45
Q

methods of withstanding host defense/immune system

A

hiding inside host cell

being hard to catch

changing appearance

blending in

killing immune cells directly

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46
Q

what types of pathogens typically hide in host cells?

A

all viruses and a few bacteria (like TB)

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47
Q

how can pathogens play hard to catch to avoid host defense systems?

A

slime capsule can make them “slippery”

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48
Q

example of “hard to catch” pathogen

A

anthrax - slime capsule

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49
Q

examples of pathogens that change their appearance to avoid host defense systems

A

HIV and influenza

50
Q

why is it hard to vaccinate for “blending in” pathogens?

A

we try to target specific pathogens with vaccines, but blending in can allow the body to overlook them

51
Q

what does “not antigenic” mean

A

that it doesn’t stand out

relevant to “blend in” method

not recognized by immune system

52
Q

examples of pathogens that kill immune cells directly

A

some viruses - HIV

bacteria with leukocidins

53
Q

what do vaccines allow our bodies to do?

A

make quicker, stronger responses to infection

54
Q

what are some ways that pathogens can get in the way of our treatments?

A

make it difficult to produce a vaccine

being drug resistance - viruses can become adaptive

55
Q

how can pathogens induce damage or disrupt host tissue functions?

A

direct damage by pathogen: toxins or kill cells directly

indirectly: cause immune system response (my ex: fever)

56
Q

what are the types of toxins?

A

exotoxins and endotoxins

57
Q

what do exotoxins do?

A

damage membranes

inhibit protein synthesis

inhibit signal transduction

stimulate immune system

58
Q

what type of pathogen can make toxins?

A

bacteria

59
Q

how do toxins work?

A

substance secreted by bacteria to interfere with normal biological functions

60
Q

how do exotoxins work?

A

damage membranes

think: poking hole in a balloon

61
Q

what is an example of a disease that uses an exotoxin?

A

diphtheria

62
Q

what can result from inhibition of protein synthesis by exotoxins?

A

cell death

63
Q

what can result from inhibition of signal transduction by exotoxins?

A

interference with intra and extracellular communication

64
Q

what is an example of an infection that uses an exotoxin that inhibits signal transduction?

A

tetanus - muscles contract uncontrollably, death by uninterrupted and prolonged diaphragm contraction

65
Q

what’s an infection that inhibits signal transduction with an exotoxin?

A

severe cholera - cells flush out a lot of water bc they can’t communicate with each other

66
Q

what’s an example of an infection that stimulates the immune system?

A

staph a

67
Q

what are the two ways signal transduction can be inhibitted?

A

ion transport (cholera)

nerve/muscle junction (tetanus)

68
Q

what are endotoxins?

A

nonspecific LPS (lipopolysacchrarides) complexes on gram negative bacteria that cause fever

are antigenic

69
Q

how is gonorrhea a successful pathogen?

A

a) only has human host

b) is transferred by sexual contact (even during childbirth)

c) attaches to receptors in epithelial cells with pili (genital, eye, throat, rectum, sperm)

d) evades host defense system by changing pili and protein II (acts like slide capsule) to avoid phagocytosis

e) induces damage through sepsis, growth in genital tract, and inflammation by immune response

70
Q

how is cholera a successful pathogen?

A

a) uses humans or biofilm to stay in water reservoirs

b) transfers by vehicle, aided by biofilm

c) attaches to receptor of epithelial cells (triggers biofilm synthesis if not already present) and uses pili to attach

d) evades defense system by using biofilm

e) induces damage by producing a toxin and disrupting host cell signaling

71
Q

how is HIV a successful pathogen?

A

a) host in humans (HIV-1), HIV-2 and SIV can infect simians but doesn’t make them ill

b) transferred via blood or bodily fluids (semen), and mother-child transfer

c) attaches to CD4 receptors in immune cells (uses additional CCR5 in t-helper cells and macrophages)

d) evades host defense system by hiding in host cell, living in macrophages to access brain, and antigenic changes

e) induces damage by killing t-helper cells, interrupting immune response, kills CD4 cells

72
Q

importance of fungal diseases

A

probably kill more people than HIV and malaria

are developing a drug resistance

73
Q

why don’t we recognize fungal diseases more?

A

they often go undiagnosed

74
Q

what is the pathogenicity of fungal infections?

A

found in GI and mouth of most healthy adults and on many womens vaginas

are able to cross blood-brain barrier

are opportunistic (immunocompromised, HIV infection, attaches to implanted medical devices)

common nosocomial infection

75
Q

what is the goal of antibiotics?

A

directly kill the pathogen

inhibit reproduction of the pathogen

76
Q

what do antivirals do?

A

try to interfere with viral life cycle

much more difficult bc they utilize host cells

77
Q

why are antibiotics challenging to make?

A

avoid side effects or allergic reactions

variety of strains

methods of delivery

stable storage

cost

resistance

78
Q

why does having multiple strains make it hard to produce antibiotics?

A

can use for different strains but don’t always have time to figure out which one is most effective

can create antibiotic resistances or kill good bacteria

79
Q

why does having multiple methods of AB delivery pose as a challenge?

A

shots need trained medical personnel

having liquid availability would be best for kids, but this isn’t necessarily feasible

80
Q

why is stable storage an AB challenge?

A

not keeping within specific temp needs (room temp or fridge) can lead to AB degradation

81
Q

what are the mechanisms of AB?

A

inhibit cell wall synthesis/function

inhibit nucleic acid synthesis/function

inhibit protein synthesis

82
Q

what is an example of an AB that inhibits CELL WALL synthesis?

A

penicillin - only works on gram positive bacteria

cells can’t survive w/o cell wall, effectively kill bacteria

external issue

83
Q

what does inhibiting nucleic acid synthesis result in?

A

genetic issues for bacterial cells

84
Q

what does inhibition of protein synthesis do?

A

cause functional issues for bacterial cells

85
Q

what are common side effects of AB?

A

rash, loose stools/diarrhea, and stomach upset

86
Q

what are rare reactions to AB use?

A

severe allergic reaction, severe or bloody diarrhea, kidney or liver damage with long term use of some AB

87
Q

what makes a bacteria have a gram positive cell wall?

A

has very thick protein carbohydrates in cell wall

ex: peptidoglycan

no outer membrane

88
Q

what makes a bacteria have a gram negative cell wall?

A

thinner cell wall surrounded by lipids

has lipopolysaccharides in outer membrane

89
Q

why is knowing gram -/+ important?

A

to properly identify bacteria

properly target with AB

determine how dangerous the bacteria is

90
Q

additional modes of action by AB*

A

target cell membrane - not great bc our cells also have cell membranes, but can have topical applications

ex: colistin

target other metabolic processes - like folic acid pathways to interrupt DNA production

ex: sulfonamides

91
Q

how are microbes of interest in terms of emerging world diseases?

A

they can adapt super well and have great and rapid genetic variation

formerly overcome diseases can make a comeback through these adaptations, such as resistances

92
Q

what are some of the most dangerous antibiotic resistant diseases?

A

c diff

carbapenem-resistant enterobacteria (group, abbreviated CRE)

93
Q

what are some serious antibiotic resistant pathogens?

A

MRSA

DR-TB

vancomycin resistant enterococci

94
Q

what causes ABR?

A

quick bacterial and viral replication rates with high mutation rates

selective pressure eliminating those that don’t have resistance -> left with stronger pathogens

human behaviors promoting

95
Q

what are typical bacterial genetics?

A

single circular chromosomes

96
Q

what is the extra genetic material bacteria can have?

A

plasmids

97
Q

what are plasmids?

A

small circular pieces of DNA

often contain genes that make things more virulent (ABR, toxin production)

97
Q

how can plasmids be shared between bacteria?

A

conjugation

98
Q

what are the different methods of bacterial genetic exchange?

A

conjugation

transformation

transduction

transposons

recombination

** only focusing on transformation, transduction, and conjugation

99
Q

what does penicillin do?

A

prevent formation of peptidoglycan -> can’t form cell wall

100
Q

what is bacteria DNA conjugation?

A

make a bridge between cells and exchange genetic material

physical connection

101
Q

what is bacterial DNA transformation?

A

pick up DNA, usually from a dead bacteria in the environment

102
Q

what is bacterial DNA transduction?

A

presence of a virus as an intermediate

bacteriophage = virus infects bacteria

virus infects bact A, uses it and leaves while taking some genetic material with, then infects bact B and leaves some bact A DNA there

103
Q

what are ways that bacteria fight back against antibiotics?

A

make cell wall impermeable

use efflux pump

inactive AB

alter metabolic pathway

change target protein

104
Q

how can bacteria enable methods of fighting back against AB?

A

changes to DNA/chromosomes/plasmids, require an increased dosage of AB or need a different one

105
Q

what does AB interfering with bacteria growth/replication allow for?

A

immune system to kick in

106
Q

how does AB interfere with bacterial growth/replication?

A

target differences between bacteria and eukaryotic cells

like cell wall components

107
Q

how does bacteria respond to penicillin?

A

destroy it or change the shape of target protein

108
Q

what do sulfonamides do?

A

interfere with folic acid synthesis -> part of DNA synthesis

109
Q

how do bacteria respond to sulfonamides?

A

over produce PABA and change shape of target protein

110
Q

what does macarolides do?

A

bind to ribosomes to inhibit protein synthesis

111
Q

what do bacteria do to fight back against macarolides?

A

decrease permeability to drug (gram -) and change target protein shape

112
Q

what does cipro do?

A

bind to enzyme to prevent DNA synthesis

113
Q

how do bacteria respond to cipro?

A

increase efflux pump and change shape of target protein

114
Q

why is changing the shape of the target protein a difficult way to interfere with AB abilities?

A

changing the shape of a protein can change its function, so there is a fine line between the two

115
Q

what human behaviors are promoting ABR?

A

overconsumption and non-compliance by patients

improper diagnoses and misuse by physicians

using incorrect, expired, or not full dosage

sharing of medications

use of antimicrobials in agriculture

116
Q

what are some factors in ABR in developing countries?

A

unskilled practitioners and lack of infrastructure (refrigeration, distance to resources)

cultural beliefs and crowded/unhygienic conditions

low literacy rates (can’t read bottle)

poor quality AB and ability to purchase w/o prescription

117
Q

what is part of the reasno AB in agriculture is such an issue?

A

former misconceptions that they didn’t matter

can actually cause small scale outbreaks

118
Q

how do we research AB on petri dishes?

A

soak a piece of paper in antibiotic solution and place it on petri dish with bacteria growing on it

zone of inhibition created around paper as AB diffuses out

bigger zone = more effective AB, smaller = antibiotic can get in easier

119
Q

what’s an example of a bacteria that uses endotoxins?

A

some strains of E. coli

gram negative

emerging world diseases (4 decks)

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