quiz 2 info Flashcards
(120 cards)
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
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
3
Q
what makes something a pathogen?
A
that it creates damage or dysfunction in host’s tissue
4
Q
what do pathogens want?
A
to live and reproduce
5
Q
examples of reservoirs
A
animate: humans and animals (cows)
inanimate: soil
6
Q
example of portals of exit
A
urine/feces, respiratory or urogenital tract, oral/proboscis (mosquitoes)
7
Q
what is a reservoir?
A
pathogen’s habitat - can have multiple
where pathogens normally live, grow, and multiply
8
Q
why is it important to know a pathogen’s reservoir?
A
for proper public health response and treatment of outbreaks
9
Q
what’s an example of a pathogen that uses HUMANS as reservoirs?
A
smallpox and measles
10
Q
what’s an example of a pathogen that uses ANIMALS as reservoirs?
A
anthrax - sheep
plague - rodents
11
Q
what’s an example of a pathogen that uses INANIMATE things as reservoirs?
A
fungal agents
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
13
Q
what is an example of a pathogen and its corresponding portal of exit?
A
influenza viruses exit through the respiratory tract
14
Q
what are the routes of transmission?
A
direct: contact and droplet
indirect: airborne, vehicle, and vector
15
Q
example of direct contact infections
A
mono or gonorrhea
16
Q
example of droplet spread infections
A
pertussis or meningococcal meningitis
17
Q
example of airborne transmission infection
A
TB
18
Q
examples of vehicle transmitted infection
A
polio or hepatitis A virus
19
Q
example of vector transmitted infections
A
malaria or HAT
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
21
Q
examples of portals of entry
A
skin, mucous membranes, and blood
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
23
Q
example of infection using SKIN as portal of entry
A
rabies and pink eye
24
Q
example of infection using GI as portal of entry
A
E. coli and polio
25
example of infection using RESPIRATORY SYSTEM as portal of entry
diphtheria, strep throat, pertussis
26
example of infection using UROGENITAL SYSTEM as portal of entry
herpes and gonorrhea
27
examples of infections with multiple portals of entry
TB: respiratory or GI tract
gonorrhea: throat or genitals
28
analogy for specific receptors in class
pathogen only being able to "grab" onto chicken elbows and not human ones
** at least until there's a mutation
29
colonize
replicate
30
virulence factor
how sick the infection/disease makes you
31
adhesion is a ___ ___
virulence factor
32
once in the body, the pathogen must ___ and ___
colonize and multiply
33
the initial inoculum of a pathogen is ___ sufficient
rarely
infection usually only comes after the pathogen has a chance to adhere and multiply
34
why is adherence a virulence factor?
the better a pathogen can adhere or to more places, the better is can be a pathogen
35
examples of adherence mechanisms
slime capsules, pili, and fimbrae
36
example of adherence
HIV binding to immune cell receptors
37
what are slime capsules?
bacterial carbohydrate-protein coating that helps pathogens "stick" non-specifically
38
what are pili?
little tails on bacteria that allow them to swim around and hook/velcro to tissue
39
what are fimbriae?
hair-like projections on bacteria (usually gram negative) that help it adhere
40
inoculum
dose
41
methods of attachment and penetration
specific enzymes to digest extracellular matrix
42
example of specific enzyme to digest extracellular matrix
neuraminidase from influenza virus (HN)
-> breaks down sialic acids on glycoproteins
43
phrasing to use when describing pathogen's invasive mechanisms
"___ binds to ___ receptor in ___ system and uses ___ mechanism"
44
how are we affected by the different complexes of influenza?
we need to adjust annual flu vaccines on complexes that are present
45
methods of withstanding host defense/immune system
hiding inside host cell
being hard to catch
changing appearance
blending in
killing immune cells directly
46
what types of pathogens typically hide in host cells?
all viruses and a few bacteria (like TB)
47
how can pathogens play hard to catch to avoid host defense systems?
slime capsule can make them "slippery"
48
example of "hard to catch" pathogen
anthrax - slime capsule
49
examples of pathogens that change their appearance to avoid host defense systems
HIV and influenza
50
why is it hard to vaccinate for "blending in" pathogens?
we try to target specific pathogens with vaccines, but blending in can allow the body to overlook them
51
what does "not antigenic" mean
that it doesn't stand out
relevant to "blend in" method
not recognized by immune system
52
examples of pathogens that kill immune cells directly
some viruses - HIV
bacteria with leukocidins
53
what do vaccines allow our bodies to do?
make quicker, stronger responses to infection
54
what are some ways that pathogens can get in the way of our treatments?
make it difficult to produce a vaccine
being drug resistance - viruses can become adaptive
55
how can pathogens induce damage or disrupt host tissue functions?
direct damage by pathogen: toxins or kill cells directly
indirectly: cause immune system response (my ex: fever)
56
what are the types of toxins?
exotoxins and endotoxins
57
what do exotoxins do?
damage membranes
inhibit protein synthesis
inhibit signal transduction
stimulate immune system
58
what type of pathogen can make toxins?
bacteria
59
how do toxins work?
substance secreted by bacteria to interfere with normal biological functions
60
how do exotoxins work?
damage membranes
think: poking hole in a balloon
61
what is an example of a disease that uses an exotoxin?
diphtheria
62
what can result from inhibition of protein synthesis by exotoxins?
cell death
63
what can result from inhibition of signal transduction by exotoxins?
interference with intra and extracellular communication
64
what is an example of an infection that uses an exotoxin that inhibits signal transduction?
tetanus - muscles contract uncontrollably, death by uninterrupted and prolonged diaphragm contraction
65
what's an infection that inhibits signal transduction with an exotoxin?
severe cholera - cells flush out a lot of water bc they can't communicate with each other
66
what's an example of an infection that stimulates the immune system?
staph a
67
what are the two ways signal transduction can be inhibitted?
ion transport (cholera)
nerve/muscle junction (tetanus)
68
what are endotoxins?
nonspecific LPS (lipopolysacchrarides) complexes on gram negative bacteria that cause fever
are antigenic
69
how is gonorrhea a successful pathogen?
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
how is cholera a successful pathogen?
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
how is HIV a successful pathogen?
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
importance of fungal diseases
probably kill more people than HIV and malaria
are developing a drug resistance
73
why don't we recognize fungal diseases more?
they often go undiagnosed
74
what is the pathogenicity of fungal infections?
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
what is the goal of antibiotics?
directly kill the pathogen
inhibit reproduction of the pathogen
76
what do antivirals do?
try to interfere with viral life cycle
much more difficult bc they utilize host cells
77
why are antibiotics challenging to make?
avoid side effects or allergic reactions
variety of strains
methods of delivery
stable storage
cost
resistance
78
why does having multiple strains make it hard to produce antibiotics?
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
why does having multiple methods of AB delivery pose as a challenge?
shots need trained medical personnel
having liquid availability would be best for kids, but this isn't necessarily feasible
80
why is stable storage an AB challenge?
not keeping within specific temp needs (room temp or fridge) can lead to AB degradation
81
what are the mechanisms of AB?
inhibit cell wall synthesis/function
inhibit nucleic acid synthesis/function
inhibit protein synthesis
82
what is an example of an AB that inhibits CELL WALL synthesis?
penicillin - only works on gram positive bacteria
cells can't survive w/o cell wall, effectively kill bacteria
external issue
83
what does inhibiting nucleic acid synthesis result in?
genetic issues for bacterial cells
84
what does inhibition of protein synthesis do?
cause functional issues for bacterial cells
85
what are common side effects of AB?
rash, loose stools/diarrhea, and stomach upset
86
what are rare reactions to AB use?
severe allergic reaction, severe or bloody diarrhea, kidney or liver damage with long term use of some AB
87
what makes a bacteria have a gram positive cell wall?
has very thick protein carbohydrates in cell wall
ex: peptidoglycan
no outer membrane
88
what makes a bacteria have a gram negative cell wall?
thinner cell wall surrounded by lipids
has lipopolysaccharides in outer membrane
89
why is knowing gram -/+ important?
to properly identify bacteria
properly target with AB
determine how dangerous the bacteria is
90
additional modes of action by AB*
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
how are microbes of interest in terms of emerging world diseases?
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
what are some of the most dangerous antibiotic resistant diseases?
c diff
carbapenem-resistant enterobacteria (group, abbreviated CRE)
93
what are some serious antibiotic resistant pathogens?
MRSA
DR-TB
vancomycin resistant enterococci
94
what causes ABR?
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
what are typical bacterial genetics?
single circular chromosomes
96
what is the extra genetic material bacteria can have?
plasmids
97
what are plasmids?
small circular pieces of DNA
often contain genes that make things more virulent (ABR, toxin production)
97
how can plasmids be shared between bacteria?
conjugation
98
what are the different methods of bacterial genetic exchange?
conjugation
transformation
transduction
transposons
recombination
** only focusing on transformation, transduction, and conjugation
99
what does penicillin do?
prevent formation of peptidoglycan -> can't form cell wall
100
what is bacteria DNA conjugation?
make a bridge between cells and exchange genetic material
physical connection
101
what is bacterial DNA transformation?
pick up DNA, usually from a dead bacteria in the environment
102
what is bacterial DNA transduction?
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
what are ways that bacteria fight back against antibiotics?
make cell wall impermeable
use efflux pump
inactive AB
alter metabolic pathway
change target protein
104
how can bacteria enable methods of fighting back against AB?
changes to DNA/chromosomes/plasmids, require an increased dosage of AB or need a different one
105
what does AB interfering with bacteria growth/replication allow for?
immune system to kick in
106
how does AB interfere with bacterial growth/replication?
target differences between bacteria and eukaryotic cells
like cell wall components
107
how does bacteria respond to penicillin?
destroy it or change the shape of target protein
108
what do sulfonamides do?
interfere with folic acid synthesis -> part of DNA synthesis
109
how do bacteria respond to sulfonamides?
over produce PABA and change shape of target protein
110
what does macarolides do?
bind to ribosomes to inhibit protein synthesis
111
what do bacteria do to fight back against macarolides?
decrease permeability to drug (gram -) and change target protein shape
112
what does cipro do?
bind to enzyme to prevent DNA synthesis
113
how do bacteria respond to cipro?
increase efflux pump and change shape of target protein
114
why is changing the shape of the target protein a difficult way to interfere with AB abilities?
changing the shape of a protein can change its function, so there is a fine line between the two
115
what human behaviors are promoting ABR?
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
what are some factors in ABR in developing countries?
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
what is part of the reasno AB in agriculture is such an issue?
former misconceptions that they didn't matter
can actually cause small scale outbreaks
118
how do we research AB on petri dishes?
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
what's an example of a bacteria that uses endotoxins?
some strains of E. coli
gram negative
