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MICR223 > MODULE 2 - Epidemiology of Infectious Diseases and Principles of Antimicrobial Therapy > Flashcards

MODULE 2 - Epidemiology of Infectious Diseases and Principles of Antimicrobial Therapy Flashcards

1
Q

what is epidemiology?

A

the study of distribution and determinants of health-related states or events (including disease) in specified populations and the application of this study to the control of disease and other health problems

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2
Q

what does epidemiology involve?

A

counting cases or health events and describes them in terms of time, place and person

dividing the number of cases by appropriate denominator to calc rates

comparing these rates over time or for different groups of people

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3
Q

what are the 5 W’s of epidemiology?

A

what - health issue of concern (case definition)

who - person (age, gender, ethnicity etc.)

where - place

when - time

why/how - causes, risk factors, modes of transmission

first 4 are descriptive epidemiology, 5th is analytical epidemiology

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4
Q

what is cholera?

A

acute diarrhoea illness which can lead to dehydration, coma and death

intestinal infection with vibrio cholera and transmission by contaminated food or water

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5
Q

how is frequency (how many) important to epidemiology?

A

relationship of no. of health events to population size allows comparison of disease occurrence across different populations

measures are prevalence and incidence

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6
Q

how is pattern important to epidemiology?

A

occurrence of health events by time (when), place (where), and person (who)

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7
Q

what is prevalence?

A

the proportion of a population that have the disease at a given point in time (i.e. existing cases)

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8
Q

how do you calculate prevalence?

A

prevalence = number w disease/total number in population

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9
Q

what is incidence proportion?

A

proportion of people who develop a disease during a specified time period (i.e. new cases)

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10
Q

how do you calculate incidence proportion?

A

incidence proportion = number who develop disease during a time period/total number at risk at the start of time period

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11
Q

what is the incidence rate?

A

how quickly people are developing the disease (i.e. new cases)

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12
Q

how do you calculate the incidence rate?

A

incidence rate = number of people who develop disease during time period/number of person-years at risk

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13
Q

what are determinants?

A

the causes and other factors that influence the occurrence of disease and other health-related events

i.e. identify the risk factor which leads to the disease via a causal pathway

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14
Q

what measures are associated with determinants?

A

relative risk

risk difference/attributable risk

odds ratio

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15
Q

what is relative risk (risk ratio) and how do you calculate it?

A

relative risk = incidence in exposed group/incidence in non-exposed group

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16
Q

how do you calculate the risk difference?

A

incidence of exposed group MINUS incidence of comparison group

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17
Q

when would you use an odds ratio?

A

when you don’t know the number of people exposed and is risk cannot be calculated

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18
Q

how do you calculate an odds ratio?

A

odds of exposure = number of exposures/number of non-exposures

odds ratio = odds of exposure in cases/odds of exposure in controls

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19
Q

what are the two main types of studies in epidemiology?

A

observational (cross-sectional, cohort, case-control)

experimental (randomised controlled trials)

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20
Q

what is a cross-sectional study?

A

observational

randomly select sample of source population

at same point in time measure exposures of interest and outcome of interest

calculate prevalence of exposures and outcomes

descriptive only

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21
Q

what is a cohort study?

A

observational

randomly select a sample of source population

measure exposure state of participants at beginning of study

group participants by exposed or not

follow-up for period of time

count who develops the outcome during follow-up

calculate incidence, relative risk and risk difference

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22
Q

what is a case control study?

A

observational

select cases with outcome of interest

select controls (without the outcome of interest) from the same source population

measure exposure status of both cases and controls

calculate odds ratio

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23
Q

what is a randomised controlled trial?

A

experimental

randomly select a sample of the source population

randomise sample participants into groups (intervention or control)

follow-up participants for period of time

measure outcome

calculate incidence, relative risk, and risk difference

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24
Q

what is a confounding factor?

A

a third variable distorting results

independently associated with exposure or outcome

does not sit on causal pathway

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25
Q

what is bias?

A

systematic error e.g. selection bias (differences between the groups or how they behave during study)

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26
Q

what does precision involve in epidemiological studies?

A

95% confidence intervals

P-values (probability that observed result would occur when null hypothesis is true)

sample size

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27
Q

how do you calculate infection rate?

A

cases per year/total population

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28
Q

how do you calculate mortality rate?

A

fatal cases per year/total population size

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29
Q

how do you calculate case fatality rate

A

fatal cases/cases of disease

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30
Q

how do you calculate infection fatality rate

A

fatal cases/cases of infection (including asymptomatic cases)

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31
Q

how do you calculate the secondary attack rate?

A

person exposed who then became infected/total persons exposed

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32
Q

what is R?

A

average number of people each person with a disease goes on to infect

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33
Q

what is R0?

A

assumes everyone in population is susceptible to infection and no control measures (however during epidemic people become infected or immune and are no longer susceptible)

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34
Q

what is Rt

A

effective reproduction number

potential for epidemic spread at a specific time (t) the under control measures in place

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35
Q

what happens if Rt > 1

A

virus will spread out and disease will become epidemic

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36
Q

what happens if Rt = 1

A

virus will spread locally and disease is endemic

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37
Q

what happens if Rt < 1

A

virus will stop spreading and disease will disappear eventually

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38
Q

what are the tasks of epidemiology in public health?

A
  1. public health surveillance
  2. field investigation
  3. analytic studies
  4. evaluation
  5. policy development

(1 and 2 are outbreak identification, 2 and 3 are outbreak investigation)

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39
Q

what does sporadic mean?

A

occasional cases of infection (no common source)

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40
Q

what does endemic mean?

A

infection is always present in the community

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41
Q

what does epidemic mean?

A

sudden increase in incidence of an infection locally

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42
Q

what does re-emerging mean?

A

previously a major threat, decreased dramatically, and now increasing again

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43
Q

what does pandemic mean?

A

a global epidemic

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44
Q

what does zoonotic mean?

A

disease transmitted from animals to humans

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45
Q

what does enzoonotic mean?

A

endemic transmission in animals (endemic in animals)

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46
Q

what does epizootic mean?

A

epidemic in animals

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47
Q

what is measles?

A

a respiratory disease caused by measles morbillivirus (fever, cough, conjunctivitis followed by head to toe rash)

can have serious complications

highly contagious and been circulating for thousands of years

vaccine available

most deaths are children <5

sporadic in NZ

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48
Q

because of the high R0 of measles, what do you need to do to prevent sporadic outbreaks becoming epidemics?

A

high vaccination levels

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49
Q

what is rhinovirus?

A

endemic (always present in community)

respiratory virus responsible for most common colds

> 100 different types meaning reinfection v common

detected all year round and can cause complications e.g. pneumonia

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50
Q

what is the definition of outbreak?

A

same as epidemic (sudden increase in incidence of an infection locally) but used for more limited geographic area

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51
Q

when do epidemics occur?

A

when a pathogen and susceptible hosts are present in adequate numbers, and the pathogen can be transmitted from a source to the susceptible hosts

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52
Q

what might an epidemic result from?

A

recent increase in amount or virulence of pathogen

recent introduction of the pathogen into a setting where it has not been before

enhanced mode of transmission so that more susceptible persons are exposed

change in the susceptibility of the host to the pathogen e.g dropping immunisation rates

factors that increase host exposure or involve introduction through new portals of entry

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53
Q

what is monkeypox?

A

a zoonotic orthodox DNA virus

human-to-human transmission through large respiratory droplets, close/direct contact with skin lesions, fomites

only recently efficient human-to-human transmission

2022 outbreak sexual contact main means of transmission

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54
Q

what is syphilis?

A

re-emerging

STI with severe long-term consequences if untreated

Treponema pallidum subsp pallidum

spirochete

primary infection - painless ulcer
secondary - disseminates through body causing rash/swollen lymph nodes
(those are two most infectious stages)
latent/asymptomatic phase
tertiary syphilism - gummas, neuro/cardio issues

congenital syphilis (mother to baby) can occur

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55
Q

what are the three types of plague which occur from yersinia pestis?

A

bubonic - buboes, fever, headache, chills, 30-60% fatality, can lead to next two

septicaemic - fever, weakness, shock, chills, abdominal pain

pneumonic - fever, headache, weakness, rapid developing pneumonia, 100% fatality, airborne

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56
Q

what is plague (Black Death)?

A

caused by yersinia pestis

enzoonotic between fleas and rodents

humans and domestic animals can become infected from flea bites - highest risk during epizootic cause fleas jump from dead hosts

little genetic change since Black Death

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57
Q

what is Spanish flu (influenza)?

A

has segmented genome where each segment encodes a different gene and it can reassert the segments between different viruses if you get co-infection (antigenic shift)

can change and evade immune response by:

  • accumulation of mutations (antigenic drift)
  • genetic reassortment of genetic segments (antigenic shift)
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58
Q

what are the two major surface proteins of spanish flu/influenza and what does reassortment of these result in?

A

haemagglutinin (HA)

neuraminidase (NA)

reassortment of HA and NA results in major changes in antigenicity giving it pandemic potential

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59
Q

what are the usual reservoirs for influenza?

A

wild birds and infection usually asymptomatic

also can infect a wide range of host e.g. swine, humans but causes disease in these

potential for zoonotic infection and pandemics

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60
Q

what are the possible outcomes of a pathogen entering a person?

A

it could be immediately eliminated

it could replicate which could then lead to elimination also, transmission, colonisation of normal microflora, asymptomatic or symptomatic infection

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61
Q

what does a bacteria need to do to be successful?

A

colonise a host, reproduce a lot and transmit to a new host

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62
Q

from a pathogens perspective, causing disease can be…

A

helpful (e.g. helps it transmit), neutral or unhelpful (clears it out of host)

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63
Q

would the coughing and sneezing disease symptoms caused by rhinovirus help it reproduce?

A

yes cause it leads to more transmission

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64
Q

would the penile discharge caused by chlamydia help it reproduce?

A

no cause people less likely to have sex so less transmission

65
Q

would the disease symptoms caused by tetanus (paralysis) help it reproduce?

A

no - we are just an incidental host and tetanus usually lives in the soil

66
Q

would the accesses caused by MRSA help it reproduce?

A

nah cause more likely to isolate yourself but also maybe yes cause it could make transmission easier

67
Q

what is an acute infection?

A

remains in host short-term and causes short-lived disease

68
Q

what is a chronic infection?

A

remains in host long-term (persistently replicating) and can cause disease or be asymptomatic

69
Q

what is an asymptomatic infection?

A

remains in host (persistently replicating) but no symptoms of disease

70
Q

what is a latent infection?

A

remains in host (dormant/not replicating) and shows no symptoms of disease

71
Q

what is reactivation?

A

latent infectious agent starts replicating again, which can be asymptomatic or result in disease

72
Q

what is colonisation/carriage?

A

part of normal microflora

73
Q

what is environmental/animal reservoir?

A

humans are not main reservoir

74
Q

what are the differences/similarities between latent infection and asymptomatic infection?

A

in latent infection host shows no symptoms and the pathogen isn’t replicating

in asymptomatic infection there are also no symptoms but pathogen is replicating

75
Q

what is a chronic infection like with hepatitis C?

A

asymptomatic but high level of replication then disease occurs later on

76
Q

what is a chronic infection like with HIV?

A

symptomatic early on but then immune system controls it and person is asymptomatic for ages but during this time virus infection CD4 T cells and eventually these are lost and person gets immunocompromised and loses control of virus

77
Q

what is HSV and VZV (chickenpox) infection like?

A

latent infection (once infected it won’t go away) and can reactivate later on

78
Q

what type of infection do rhinovirus and influenza cause?

A

acute infection

79
Q

outline the key points of Salmonella enterica serovar Typhi (typhoid fever) infection?

A

human restricted pathogen, acute infection causes disease (headache, fever, GI symptoms), not normal microflora, not sick during chronic carrier state, always replicating/contagious

chronic asymptomatic infection occurs after acute infection in gall bladder of 3-5% of infected (can go on for decades and infected highly contagious but asymptomatic)

80
Q

outline the key point of Varicella zoster virus infection?

A

human restricted pathogen, acute infection causes disease, not normal microflora, not sick during latency, not contagious during latency, can reactivate and become contagious

in primary infection cause chickenpox (varicella) (airborne transmission) but then immune system controls so it sets up latency in neurons

reactivation can occur with loss of immune control causing herpes zoster (shingles)

81
Q

what might favour overgrowth of a pathogen such as Candida albicans?

A

normal flora disruption with antibiotics allowing candida (part of normal microflora in digestive tract) to overgrow

immunosuppression

82
Q

is Candida albicans colonisation common or uncommon?

A

common - grows at many mucosal sites on the skin

83
Q

does Candida albicans have human carriage?

A

yes cause commonly colonises skin

84
Q

what types of infection does Candida albicans cause?

A

acute, chronic and asymptomatic (also disease doesn’t really help transmission and is related to load)

85
Q

what are the two types of disease caused by Candida albicans?

A

mucocutaneous and invasive

86
Q

what are the main aspects of cryptosporidium infection?

A

protozoal parasite which can form oocysts and has animal reservoir

causes acute and self limiting disease in immunocompetent host and chronic disease in immunocompromised host

87
Q

what are the main aspects of tuberculosis infection?

A

causes acute (latent tb), chronic and latent infection which can reactivate and then transmit (post primary/ extra pulmonary tb)

airborne transmission and most people clear the acute infection

has a human reservoir

88
Q

what is streptococcus agalactiae (group B streptococci)?

A

beta-haemolytic streptococci which is part of normal GI tract microflora in 20-40% of people and causes different disease in different hosts

neonatal infection (infection soon after birth) causing bacteraemia, meningitis, pneumonia

invasive disease in elderly and immunocompromised hosts (soft tissue, bone, joint infections)

invasive disease (food borne from raw fish) causing bacteraemia, meningitis (animal reservoir!)

89
Q

how does group B streptococci cause neonatal infection and what are the three types?

A

pregnant woman vagina and/or rectum may be colonised with group B strep (10-30%) and can transmit to neonate during or after birth and occasionally during pregnancy

congenital infection (spread during pregnancy) leading to still birth

early onset infection during delivery can cause meningitis

late-onset infection (>1 week post natal) more likely to cause meningitis and mode of infection unclear

leading cause of sepsis, pneumonia and meningitis in infants, causes acute infection and involves human carriage

90
Q

what antibiotic treatment is there for neonatal infection caused by group B strep (GBS)?

A

giving antibiotics during birth if we know woman colonised can prevent early onset disease (called intrapartum antibiotic prophylaxis) but doesn’t prevent late onset disease

91
Q

what is meningitis?

A

infection of the meninges and subarachnoid space

92
Q

what is a reservoir?

A

the habitat in which the agent normally lives, grows and multiplies

93
Q

bacterial isolates of the same species are related to differing degrees, what is a way we can exploit this for epidemiological purposes?

A

strain typing

94
Q

what is the core genome?

A

genes common to all strains within a species

these are defining genes of a species

e.g. any individual E. coli you sequence will have around 4800 genes in its genome, but only around 3000 common to all E. coli genomes (core genome)

95
Q

what is the pan-genome?

A

entire set of genes from all strains within a clade

e.g. E. coli pan genome >16000 (remember a single E. coli has 4800 genes)

96
Q

what causes genetic differences between bacterial isolates?

A

horizontal gene transfer (conjugation, transformation and transduction)

97
Q

why can two different E. coli have very different capacity to make people sick?

A

due to genomic plasticity within bacterial species

98
Q

what is a strain?

A

a genetic variant or subtype of a micro-organism within a species

99
Q

why do we need to subtype?

A

to link, source and track infections and epidemics

e.g. if you got swabs from three infected individuals in hospital and culture and isolate them, are they all the same strains or different, if all same strains could be an outbreak, is the swab from a nurse same as patient i.e. she infected him and so on

100
Q

what is a point source outbreak?

A

all coming from one food vehicle

101
Q

what is subtyping used to determine?

A

similarity between bacterial isolates

102
Q

what are some non DNA-based ways to distinguish strains?

A

antimicrobial susceptibility pattern (antibiogram)

serotyping

phage typing

103
Q

what are some DNA-based ways to distinguish strains?

A

restriction length polymorphism

amplified length polymorphism

rule field gel electrophoresis

multi locus sequence typing

genome sequencing

104
Q

what is serotyping?

A

using antibodies to detect specific surface antigens (H, K and O) to see if different strains have the same ones

composition of antigens varies so much between bacteria that they are antigenically distinct

so an antibody that can bind to one might not be able to bind to another i.e. they are different serotypes

105
Q

what are some common surface antigens in bacteria assessed during serotyping?

A

flagella (H antigen)

capsule (K antigen)

lipopolysaccharide (O antigen)

106
Q

of the 700 E. coli serotypes, what antigens determine serogroup and what ones determine serotype?

A

O antigen determines serogroup

O + H antigens determine serotype

107
Q

what is E. coli strain O157:H7?

A

makes cell wall antigen O157 and flagella antigen H7 (which are not responsible for making people sick). However, when we see O157 and H7 they usually accompany other highly undesirable genes e.g. shiga toxins which help it adhere to gut

108
Q

why is E. coli strain O157:H7 so good at making people sick?

A

it has a variable gene collection including two shiga toxins and genes that help it adhere to gut

109
Q

how do we do a serotype test?

A

latex beads are coated with antibody, if they encounter their antigen (while being stirred with bacteria) they agglutinate (make a clump)

110
Q

what does phage typing look at?

A

do strains have the same susceptibility to the same bacteriophages

uses a broad collection of bacteriophage to determine the susceptibility to those different viruses i.e. how well can these viruses replicate (if well they will lyse bacterial cell)

111
Q

how does phage typing work?

A

successful phages multiply and cause lysis

there is a diverse collection of bacteriophages

each phage has a different mechanism of action so it will act on a different set of molecular targets. Therefore different strains which have genetic differences will be differentially susceptible to each phage

112
Q

how is phage typing done in real life?

A

entire plate is bacterial lawn

divide in a grid, inoculate one unique phage per square

each spot with lysis represents susceptibility to that phage

the “which phages kill it” pattern can be used to distinguish strains

113
Q

what is a real-world application for phage typing?

A

can be used to distinguish S. aureus strains

it is fast and cheap

114
Q

what is restriction fragment length polymorphism (RFLP)?

A

to look at variations in DNA sequence of presence/absence of certain bits of DNA

to do it: purify DNA from isolate of interest, cut with restriction enzymes which recognise particular sequences (usually short enzymes) in DNA, separate through gel electrophoresis, blot it and prove against insertion sequences or other repetitive regions

115
Q

restriction fragment length polymorphism patterns are mainly determined through what?

A

through the specific combination of restriction enzymes and DNA probes

116
Q

what are the steps of amplified fragment length polymorphism (AFLP)?

A
  • digest DNA with two restriction enzymes (frequent cutters)
  • ligate restriction fragments with end-specific adapters
  • selective amplification of fragments by PCR
  • analysis by automated DNA sequencer or gel electrophoresis

all we are measuring is whether restriction sites have been gained or lost and whether there’s deletions in between

117
Q

what is pulse field gel electrophoresis (PFGE)?

A

gold standard for typing

differs from RFLP and AFLP in that it uses restriction enzymes but it uses ones which are rare cutters within the genome resulting in large fragments of DNA which can’t move seperate from standard gel electrophoresis. So to get them to move through gel we use PFGE. If there is a mutation in restriction enzymes site (can’t detect mutations outside of restriction sites cause large fragments) we see different numbers of bands

118
Q

what are the steps to multi-locus sequencing typing (MLST)?

A

amplification of seven housekeeping genes (sequences constrained because of essential function of encoded protein)

sanger sequencing

identify species specific alleles by comparison to database

assignment of sequence type

119
Q

what does multi-locus sequencing typing do?

A

uses DNA sequencing to uncover allelic variants in several conserved genes

120
Q

what are the downfalls of multi-locus sequencing typing?

A

use of highly conserved housekeeping genes often fails to detect the variability of closely related strains

sequencing seven genes is costly and time consuming

121
Q

what are the pros and cons of whole genome sequencing (WGS)?

A

pros: exactly which genes are there, exactly which mutations are present, you can do things you cannot do with other subtyping methods i.e. much higher sub typing resolution

cons: still relatively slow and expensive

122
Q

Streptococcus pneumoniae has over 90 capsular serotypes, what does this mean in regards to serotyping it?

A

genome sequencing shows that sometimes serotyping is very inaccurate due to capsular switching

123
Q

why are heavy metals antimicrobial?

A

because they are toxic to cells and not specifically bacterial ones so fuck everything up

key point is they are non-specific

e.g. mercury binds to and damages many proteins very non-specifically

124
Q

what is the principle that every antimicrobial works on?

A

maximise toxicity to pathogen while minimising toxicity to host

125
Q

every drug has a therapeutic dose and a toxic dose, what is the therapeutic index calculated from and what does it mean?

A

calculated from the ratio of the toxic dose to the therapeutic (effective) dose

a higher therapeutic index means a safer drug

126
Q

which is better for an antimicrobial, a narrow therapeutic margin or a wide therapeutic margin and why?

A

wide therapeutic margin is better cause bigger gap between therapeutic dose and toxic dose

127
Q

what is the easiest way to make a highly effective and safe drug?

A

target cell processes that humans don’t have

this means there will be a good therapeutic index and a wide therapeutic margin

128
Q

can you target two different types of microbes e.g. bacteria and protozoa?

A

yes but its uncommon

129
Q

why is penicillin selectively toxic for bacteria?

A

it inhibits cell wall synthesis by inhibiting peptidoglycan cross linking

peptidoglycan has a glycan backbone with N-acetyl muramic acid and N-acetyl glucosamine alternating and the glycan backbones are given stability by peptide bridges which require a transpeptidase to join them up. This links the peptide chains together which results in the peptidoglycan layer having structural strength which is important for bacteria’s survival

penicillin binds to the penicillin binding proteins (transpeptidases) and activates them preventing cross linking of peptidoglycan layer

130
Q

why has penicillin got a good therapeutic index?

A

peptidoglycan cell wall processes (which it targets) are specific to bacteria

131
Q

what is the most important part of penicillin and what does modifying it do?

A

the beta-lactam ring because it irreversibly binds to PBP

modifying the R group alters its spectrum and pharmacokinetics

modifying beta-lactam ring creates other classes of beta-lactam

132
Q

what does it mean if a drug is bactericidal and give example?

A

they kill their targets

e.g. penecillin

133
Q

what does it mean if a drug is bacteriostatic and give example?

A

keep the bacteria from growing when drug is present but the bacteria can start growing again as soon as the drug is gone

e.g. sulphonamides

134
Q

why is the difference between bacteriostatic-bactericidal important and what is the 60:40 rule?

A

the difference important for immunocompromised patients where you might need to use bactericidal drug rather than a bacteriostatic one you would have used for immunocompetent person who’s immune system could’ve done the rest

60:40 rule is to cure someone this should be 60% by their own immune system and 40% the antibiotic

this is because a fully functioning immune system is best for antimicrobial therapy

135
Q

what are pharmacokinetics?

A

what does the body do to the drug

136
Q

what are pharmacodynamics?

A

what the drug does to the bug

137
Q

what are the four main questions to ask when deciding on the right drug to use for an infection?

A

what do we know about the bacteria?

what do we know about the host?

what kind of infection and where does the drug need to go?

what do we know about how the drug behaves?

138
Q

when might it be a good idea to use antimicrobials in combination?

A

if we don’t know whats causing the infection

if infection is polymicrobial

to preven emergence of resistance

synergy (two antibiotics work better when combined)

combining will allow reduction of dose of a toxic antimicrobial

139
Q

what is the disk diffusion test?

A

each disk saturated with antibiotic and is dropped on bacterial lawn creating a gradient of antibiotic

zone of inhibition size corresponds to the diffused concentration of antibiotic that will inhibit bacteria growth

140
Q

what are the three possible outcomes of the disk diffusion test when testing multiple antibiotics?

A

indifference (antibiotics don’t affect one another)

synergy (one makes the other work better)

antagonism (one inhibits the other)

141
Q

what are some common benefits and drawbacks of antibiotics?

A

benefits: shorter less severe infection, cure infection, prevent infection (prophylactic), reduced morbidity and mortality

drawbacks: side effects, allergies, resistance emergence, secondary infections

142
Q

what are some common mechanisms of antimicrobial resistance?

A

modifying antibiotic target (antibiotics target specific cell processes) e.g. MRSA have a new penicillin binding protein that can cross-link peptidoglycan in presence of beta-lactam cause it doesn’t bind beta-lactam

inactivate the antibiotic e.g. beta-lactamases produced which hydrolyse beta-lactam ring

restrict access of antibiotic to its target e.g. decreasing permeability so antibiotic can’t get into cell or efflux pumps which pump out antibiotic

143
Q

what are the two kinds of resistance bacteria can have to an antibiotic?

A

innate resistance - chromosomally encoded and predictable i.e. they always genetically have been

acquired resistance - encoded on chromosome or plasmid, not predictable

144
Q

what is antibiotic-mediated selection

A

lots of germs (a few drug resistant)

antibiotics kill bacteria causing illness as well as good bacteria protecting the body from infection

the drug-resistant bacteria are now allowed to grow and take over

145
Q

how does antibiotic use promote resistance by selecting for point mutations that confer resistance?

A

lots of germs (a few drug resistant)

antibiotics kill bacteria causing illness as well as good bacteria protecting body from infection

drug-resistant bacteria now allowed to grow and take over

point mutations lead to resistance

146
Q

what is an example of a point mutation causing antibiotic resistance?

A

no quinolone binding

147
Q

how does antibiotic use promote resistance by selecting for bacteria that have acquired genes by horizontal gene transfer?

A

antibiotics kill of all germs expect drug resistant so the drug resistant can take over

some bacteria give their drug resistance to other bacteria causing more problems

148
Q

what is an example of antibiotic resistance being acquired through horizontal gene transfer?

A

acquisition of mega gene encoding PBP2A that doesn’t bind beta-lactams

149
Q

why is horizontal gene transfer more preferable to bacteria than a point mutation when it comes to gaining antibiotic resistance?

A

its easier and better to acquire resistance genes from other microbes

just cause a lot more difficult to get an effective mutation occurring when the best methods selected for and can just be got from your neighbour

150
Q

which came first, antibiotic use or antibiotic resistance?

A

antibiotic resistance e.g. soil microbes

cause antibiotics are from the environment and have been around forever

151
Q

do antibiotics treat viruses?

A

no

152
Q

is it only misuse of antibiotics that creates a selection pressure for antibiotic resistance?

A

nah even appropriate use

any use does

153
Q

why is antibiotic resistance such a major problem for agriculture?

A

it is used way more than in normal medical treatment

e.g. for growth promotion, prophylaxis, disease treatment

it also doesn’t go away when antibiotic usage is stopped

154
Q

what makes MRSA resistant?

A

MRSA has a gene called mecA which encodes a penicillin-binding protein (PBP2A) that gives resistance to all beta-lactams

mecA acquired through HGT not point mutation

MRSA can also gain other resistance genes and is only treatable with vancomycin

155
Q

what is Pantone-valentine leukocidin (PVL)?

A

a clinically important pore-forming S. aureus toxin which forms pores in monocytes and neutrophils leading to lysis

there are also many other S. aureus pore forming toxins this one just most important

156
Q

what is MSSA?

A

methicillin sensitive s. aureus

if it acquires mecA it becomes MRSA

157
Q

are the genes for methicillin resistance and PVL acquired together?

A

NO but they often are

PVL acquired by transduction

both acquired independently but you do often end up with both in the same organism

158
Q

true or false - MRSA often carries resistance genes for other antibiotics?

A

true

159
Q

how can using one antibiotic select for resistance of another antibiotic?

A

there is often cross resistance and these gene care genetically linked i.e. travel together on the same plasmid etc

MICR223 (7 decks)

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