Week 10 + 11 + pre-midterm material Flashcards

1
Q

outbreak

A

2 or more cases than the expected amount of cases for that illness

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2
Q

endemic

A

constant presence of a disease/infectious agent within a given area or population

disease or infectious agent keeps on reoccurring

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3
Q

epidemic

A

more cases than usually expected/ an excess of illnesses over time or at a specific time

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4
Q

pandemic

A

epidemics that have spread from where it started to other parts of the world

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5
Q

sporadic case

A

single occurrence of a disease or is infrequent enough that there’s no noticeable pattern or connection to other cases

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6
Q

How does the epidemic triangle allow for the emergence of an epidemic

A

Host
- the host/population needs to be susceptible to the disease

Agent
- microorganisms can evolve to become more infectious and can adopt mechanisms that changes its ability to cause a disease or cause a severe disease

Environment
- physical or social environment can change to make transmission more or less likely

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7
Q

What are the types of cases

A

Index: The first case that has been identified
Primary: the case that brings the infection into the population
Secondary: infected by the primary case
Tertiary: infected by the secondary case

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8
Q

what is surveillance done for and what are the 2 types

A

Done to look for any patterns or records of the infection by collecting and analyzing pop-level health information to guide the design of interventions

Passive Surveillance: collecting data in a passive way - waiting for reports from hospitals, doctors billing codes and notifiable diseases

Active Surveillance:actively trying to gather data - sending routine letters to doctors asking them to report on acute flaccid paralysis from polio vaccine

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9
Q

What are notifiable diseases

A

Cases that need to be reported due to the increase in the risk of spread

  • infectious + non-infectious diseases
  • poses threat of epidemic spread
  • reporting is done on several levels
  • list of reportable diseases change
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10
Q

What are the steps in outbreak management and control

A

1. Establish the existence of an outbreak
- Goal is to identify a cluster of cases that exceeds the expected amount of cases by chance alone

  • Minimum number is not needed, it depends on the expected amount of cases

2. Confirm the diagnosis
- Sometimes the first indication of an outbreak, but sometimes the info is not available during early stages of an outbreak investigation

3. Define what makes up a case and count cases as they occur
- Developing a case definition sometimes includes the microbiologic diagnosis

  • Can include person, place, and time
  • Case definitions can be redefined as the investigation continues
  • There are probable cases and confirmed cases (what are the advantages + disadvantages to each)

4. Perform descriptive epidemiology to determine who is at risk
- Want to know about the exposure, which demographic is affected, etc.

5. Formulate hypotheses on the causes and implement initial control measures

6. Test the hypothesis through the analysis of surveillance data

7. Evaluate the response and re-adjust hypotheses + control measures accordingly

(4-7)
- Conducts active case finding

  • For each case - data is collected on demographics, risk factors, + exposures
  • Create reports to help create a hypothesis on who is at risk
  • Usually uses standardized questionnaires to try to figure out exposures

8. Communicate info on the progress of the outbreak to partners + the public
- Inform people of the risk and how to reduce it and reduce the risk of spread

  • When to seek care

9. Plan for long term prevention and control

(5,7,9)
- Manage cases
> need for isolation
> infection control measures (cover wounds, avoid public spaces)

  • Manage contacts
    > symptom assessment, post-exposure prophylaxis
  • Environmental actions
    > food recall
    > social distancing
  • Infection prevention and control
    > masks
  • Vaccination
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11
Q

What do epidemic curves show and what do the shapes of it show

A

It allows us to track the emergence of an outbreak

Has the number of new cases plotted against date of onset

Shapes can show…
- Nature of the disease
- Mode of transmission
- Number of cases
- Incubation period
- Outliers in time or place

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12
Q

What are the 5 types of epidemic curves

A

Point Source
- Everyone gets exposed at the same time and they get the disease at different times - causing for people to have varying incubation periods

  • There is no ongoing exposure

Continuous Source
- Exposure continues until it gets controlled and there’s less cases

  • Exposure is the same

Intermittent Outbreak
- Irregular repeated exposures/intermittent exposure where each result in a small amount of cases

  • no propagated spread

Index Case w/ Limited Spread
- An index case results in secondary transmission due to person to person contact with containment

  • Can have a peak that happens for a long time
  • Shows what would happen in a vaccinated population

Propagated Spread
- An index case results in secondary + tertiary transmission

  • Peaks get separated with 1 incubation period between them (incubation periods should equal each other) and will merge into 1 large peak
  • Similar to index case spread but does not have a control - shows what would happen in an unvaccinated population

-

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13
Q

What is an incubation period, why is it important, and what are the characteristics

A

Delay between the infection/exposure and the appearance of first symptoms/signs

Can help us to determine the time of exposure and the identify of the antigen

Characteristics:
- Time between exposure to the infectious agent and the onset of symptoms

  • Each infectious disease has a specific incubation period with variation
  • Length of incubation period depends on how long it takes for the agent to multiply enough to cause symptoms
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14
Q

What is a latent period

A

The delay between infection and the time of infectiousness

A person can have a shorter latent period than incubation period - can transmit the agent without showing symptoms making them high risk of transmitting the disease

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15
Q

How to calculate:
Minimum Incubation Period
Maximum Incubation Period
Average Incubation Period

A

Minimum Incubation Period
1st case - exposure

Maximum Incubation Period
Last case - exposure

Average Incubation Period
Middle case/peak - exposure

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16
Q

What are the 3 types of transmission?

A

Contact
Vehicle
Vector

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17
Q

What is contact transmission

A
  • Person to person
  • Vertical transmission

Characteristics:
- Direct contact required
- Transmission in utero/womb during pregnancy or at the time of delivery

  • Droplet transmission
    Characteristics:
  • Carried by droplets over distances of 1 meter or less
  • Indirect contact transmission
    Characteristics:
  • Transmission through inanimate objects/fomites
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18
Q

What is vehicle transmission

A
  • Foodborne transmission
  • Waterborne transmission

Characteristics:
- Occurs through consumption of contaminated food or water

  • Airborne transmission

Characteristics:
- Occurs through tiny respiratory particles/aerosols floating in the air over distances of more than 1 metre

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19
Q

What is vector transmission

A
  • Mechanical
  • Biological

Characteristics:
- Occurs through living organisms
- Can be carried without the animal being infected (mechanical) or through infection of the animal (biological)

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20
Q

What are some prevention strategies

A
  • Vaccination
  • Hand hygiene
  • Personal protective equipment
  • Quarantine + isolation
  • Health education

Direct Contact:Cover wounds

Indirect Contact:clean fomites, use materials once

Droplet:masks, visors

Airborne:masks, ventilation, negative pressure rooms

Food/Water:safe practices, chlorination

Vector:vector control, insect repellents, clothing, bed nets

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21
Q

What is epidemiology + types of epidemiology

A

The study of the distribution and determinants of health-related states and events in specified populations and the application of this study to control health problems

  • Infectious Disease
  • Environmental
  • Chronic Disease
  • Molecular
  • Genetic
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22
Q

What is the purpose of infectious disease epidemiology

A
  1. To determine the extent of a disease in a population
  2. To assess risks of exposure on developing disease
  3. To identify the cause of new syndromes
  4. To study the natural history and prognosis of disease
  5. To determine if a treatment is effective
  6. To identify disease prevention strategies
  7. To identify health service use needs and trends
  8. To provide a foundation for healthy public policy
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23
Q

What are the fundamental concepts in infectious disease epidemiology

A

The cause of a disease is known - it is a infectious agent with unique characteristics (biological characteristics)
- Infectious diseases are defined by the mode of transmission

Involves 2 or more populations: humans, infectious agents, vectors, animals

Dependency
- Events are not independent of each other
- A case can also be a risk factor

Not everyone is susceptible
- People can be immune via vaccination or previous exposure

Cases can be a source without showing symptoms or signs of the disease
- Inapparent infections and carrier states

Spectrum of disease
- Asymptomatic - death

Often times there needs to be urgency when it comes to preventing and controlling the disease to protect the public’s health

Mostly concerned with interventions over determination of risk

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24
Q

What are the biological characteristics of an infectious organism

A

Infectivity:Agent’s ability to cause an infection in the host
- # of infected/ # of susceptible x100

Pathogenicity:Agent’s ability to cause disease
- # with clinical disease/# of infected x100

Virulence:Severity of the disease after infection
- # of deaths or severe illness/# with disease x100

Disease can be very infectious but not pathogenic or vice versa

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25
Q

What is immunogenicity

A

Ability of an organism to create a immune response after an infection that is capable of providing protection against re-infection by the same or similar organisms

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26
Q

What is the inapparent infection + carrier state

A

Inapparent infection:Has the disease/is infected but is asymptomatic

  • Usually short-lived

Carrier state:Person or animal has the infectious agent, doesn’t show symptoms and can still transmit it to others

  • Usually long-term
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27
Q

What are the outcomes of an exposure to an infectious agent

A
  • No infection
  • Subclinical infection
  • Clinical infections w/ varying severity
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28
Q

What is descriptive epidemiology

A
  • The foundation of epidemiology and public health
  • Key way to discovering emerging + re-emerging pathogens
  • Characterize disease in terms of person, place, and time
  • Only observing for intervention not testing it
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29
Q

What are measures of association

A
  • Quantifies the relationship between exposure and disease among 2 groups
  • Can’t show causations, only how strongly 2 things are associated
  • Bradford hill criteria can be helpful to provide evidence for possible causal relationship
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30
Q

What is prevalence and the use of it

A

The number of existing cases of a disease at a point in time/ population

Numerator:people who are ill, have specific symptoms, or evidence of infection but asymptomatic

Denominator:number of people in the population who are susceptible to the disease or were exposed

Expressed as proportion or percentage

Use of prevalence
- Tells us how many people have the disease

  • Estimates the probability that an individual will have the disease during a point in time
  • Estimates the cost associated with the specific disease
  • Project health care and other policy needs or issues
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31
Q

What is Incidence
Cumulative Incidence
Incidence Rate and the use of cumulative incidence

A

of new cases of disease within a time period/ # of people at risk in the population at the BEGINNING of the specified time period

The measure of the risk of developing the disease within a specified period of time

Cumulative Incidence
# of new cases of disease during a time period/ # of people at risk in the population at the BEGINNING of the specified time period

Incidence Rate
- Measure of the rate of development of a disease in a population

  • Measures how quickly people are developing the disease

of new cases of disease during a time period/ # of person-years when people were at risk of developing the disease

  • Unit = person years of follow up (xx cases per 1000 person years of observation)

Use of cumulative incidence
- Estimates the probability that a person will develop the disease during a specific time period

  • Research on causes, prevention and treatment of disease
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32
Q

What is the relationship between prevalence + incidence

A

They are related to each other by duration of disease

Prevalence ~ Incidence x Duration

Can be seen using the bathtub model: incident cases/births/immigration/recoveries are coming in, bath water = prevalent cases, deaths/emigrations/recovery is going through the pipe

If disease duration is short = the prevalence almost equals the incidence

If disease duration is long = prevalence will include both new and previous cases and will be GREATER than incidence

33
Q

what were Robert Koch’s 4 postulates (statements that he claimed to be true without any evidence) and why may they not be true

A
  1. the suspected agent had to be present in all infected individuals
  2. the agent has to be isolated + grown in pure culture (it’s only the one agent in the culture)
  3. the cultured agent will cause the disease once injected into a healthy and susceptible host
  4. the agent that was injected into the host can then be reisolated
34
Q

what is microbiota
microbiome
dysbiosis
mycobiome

A

microbiota:a population of microbes that are in a area of an individual (example: GI tract)

the microbiota can be different across different sites of the body and can be different from person to person

microbiome: all of the genomes and genes of a microbiota

dysbiosis:
a change in the microbiota’s structure or function which creates a disruption in the homeostasis/balance between the microbial community and its host

mycobiome:
part of the microbiome consisting of the fungi that line in or on a host

35
Q

what is a cross-sectional study

A
  • information about exposure and disease status is collected all at once
  • temporal: point in time
36
Q

what is a case-control study

A
  • picks sample based on people who has disease and who doesn’t have disease
  • looks back in time to collect information about exposure
  • temporal: point in time or retrospective data
  • best to use this design for when the disease is rare
37
Q

what is a cohort study

A
  • picks sample based on people who have been exposed and who has not been exposed
  • follows sample over time to see if they develop the disease or not
  • temporal: follows subjects over time - either prospectively or retrospectively
38
Q

what is a clinical trial

A
  • picks sample based on people who have the same disease status but have been exposed to different things
  • sample gets followed over time to determine outcome
  • temporal: follows subjects over time - prospectively
39
Q

what is the Bradford Hill Criteria of Causation

A

-Temporality: cause comes first and then effect
- Strength of Association: stronger the association = more likely the relationship is causal
- Consistency: consistent findings from different studies and populations strengthens the likelihood that the relationship is causal
- Dose-response relationship: greater exposure = greater the incidence of the disease (disease is occurring more often in the population?)
- Biological Plausibility: if there’s a reasonable biological mechanism between exposure and disease known - this can increase the likelihood of there being a causal relationship
- Specificity: if the exposure influences a specific outcome or population with no other explanation
- Coherence: the findings between epidemiology and lab align with each other are draw to the same conclusion
- Experiment: causation is more likely if the evidence is based on randomized experiments
- Analogy: if there is known strong evidence of a casual relationship between a specific exposure and outcome - researchers should be more accepting of weaker evidence of there being a causal relationship between a similar exposure and outcome

40
Q

What is the cell membrane structure of gram positive + gram negative

A

Gram positive

  • Has multiple peptidoglycan layers
  • Is thick and rigid

Gram negative

  • Has one peptidoglycan layer in between his outer and cytoplasmic membrane
  • It is flexible, porous, and helps with regulating osmosis of the cell
41
Q

what methods can we use to identify the organism that has caused a disease?

A

mass spectroscopy using MALDI-TOF:
- a type of mass spectroscopy method
- laser is used to ionize protein molecules which come from bacterial isolate (pure culture of the bacteria)
- the now ionized molecules get put through a vacuum + the speed they travel at through the vacuum depends on its protein’s mass to charge ratio
- the different speeds of the molecules are presented on to a screen
- the speeds are unique to a species which can help identify the organism or the species of the organism

PCR - molecular based methods:
when we’re looking for a specific bacteria

  • can beSINGLEPLEX(1 pathogen) orMULTIPLEX(more than 1 pathogen that can cause the disease)
42
Q

what is susceptibility testing and what do they look for

A

it’s a test to see if a drug works against the pathogen

done in vitro - they put a bug and a specific concentration in a tube and look at the growth of the bug

they are looking for the lowest concentration of drug that can stop the pathogen from growing - this is call theMINIMUM INHIBITORY CONCENTRATION (MIC)

43
Q

what are the 3 AST (antimicrobial susceptibility testing) methods in the clinical micro lab

A

1. broth microdilution

the MIC is shown where the concentration has visibly stopped the bug’s growth - dark gray in this case or clear tube

2. gradient strip diffusion

the MIC is seen where the ellipse meets the strip

3. disk diffusion

measures the diameter of the area of growth inhibition

large enough = the bacteria is susceptible to this drug/drug works against the bacteria

too small = the bacteria is resistant to the drug

44
Q

what are latent viruses/infections

A

Latency: when the virus is hidden or inactivated in a host cell

  • when this occurs symptoms are not seen and can be difficult to detect

viruses can either…

  • have circular viral genome molecules which is outside of the host cell’s chromosome
  • have proviruses be integrated in the host cell’s genome
45
Q

what does an opportunistic infection mean

A

an infection caused by a microorganism that normally doesn’t cause a disease but can become pathogenic and cause a disease when the immune system becomes weak

46
Q

what are retroviruses + what does provirus mean

A

these are positive single stranded RNA viruses that create viral DNA

the DNA gets integrated into the host cell’s chromosome

Provirus= what the viral genome that gets integrated is called

47
Q

what are the 2 mechanism that causes for viruses to evolve and invade the immune system

A

Antigenic drift

  • point mutations (1 base) that causes slight change in the spike proteins/glycoproteins
  • forinfluenza- spike proteins HA + NA constantly have antigenic drift - this results in seasonal variations in influenza
  • vaccines are updated for each time the spike proteins change

Antigenic shift- big changes in spike protein from reassortment (mixing of genetic material)

  • forinfluenza- 2 different influenza viruses (viruses that come from different species) end up infecting the same host cell + exchange genetic material - this leads to a new strain with the new mix of HA/NA proteins
48
Q

what are the steps of the virus life cycle

there are 5 steps

A

1. attachment

  • viruses attach to the host cell via its receptors
  • viruses are tissue specific (tissue tropism) - they’re specific in the tissues they’re attacking

2. entry

  • either the virus or the genetic material enters the host cell

3. genome replication + gene expression

  • the genetic material gets replicated and those genes encode forviral proteins

4. assembly

  • new viruses or viral particles get assembled

5. release

  • new viral particles leave the cell and infect other cells
49
Q

what is Pre-Exposure Prophylaxis + Post-Exposure Prophylaxis

A

PrEP

  • people without HIV use this as a preventative measure
  • it is a cART - combination of antiretroviral therapy
  • decreases their chances of getting HIV
  • useful for when one partner has HIV and the other doesn’t or for people who inject drugs

PEP

  • it is a cART - combination of antiretroviral therapy
  • emergency method for people who have been exposed to HIV
  • they take it for a few months after exposure
  • they have to start taking it 72 hours after being exposed
50
Q

what is the structure of a virus

A

contains…

  • nucleic acid (DNA or RNA)
  • capsid/protein coat (this has the basic necessities/materials to create new virions)
  • MAY have envelope (small part of the host cell’s phospholipid bilayer when the virus buds off)
  • MAY have spikes (glycoproteins that allows virus to attach to the host cell’s receptors and enter)
51
Q

what are examples of fungi and their morphology

A

Yeasts

  • single cells
  • reproduces via budding

Mold

  • multicellular bodies
  • made up of filaments (protein) called hyphae
  • Septate Hyphaecan have walls between hyphae
  • Nonseptate Hyphaedoes not have walls between hyphae

Dimorphic Fungi

  • can be either yeasts or mold - depends onenvironment
  • 25 degrees = mold
  • 37 degrees = yeast
52
Q

what is the spectrum of antibiotics/antibacterial drugs + spectrum of activity

A

Spectrum of activity: the range or diversity of bacteria that the antibiotic targets

Narrow spectrum: targets only a certain group of pathogens (e.g. ONLY gram-positive)

Broad spectrum: targets a wide group of pathogens (e.g. both gp + gn)

53
Q

what are the 2 types of antibacterial drugs

A

1. Bactericidal: kills the target bacteria

2. Bacteriostatic: stops the growth of the bacteria but doesn’t kill it - causesreversible inhibitionwhich allows for bacteria to grow again once drug is eliminated

54
Q

what is the bacterial growth curve and which phase is the best for antibiotics to attack

A

1. Lag phase= NO increase in number of living bacteria

2. Log phase= exponential increase in number of living bacteria

  • actively dividing via binary fission
  • this phase is the best for antibiotics to target b/ this is where a lot of the bacteria is in the middle of being created + antibiotics can ruin this process - specifically antibiotics that target the synthesis of DNA, cell wall, and proteins

3. Stationary phase= number of living and dead bacteria is the same, there is no increase or decrease to the amount of living bacteria, the amount is staying the same

  • nutrients get used up and waste products accumulate
  • the synthesis of nucleic acids, proteins, and peptidoglycans slow down which also makes them less susceptible to antibiotics
  • in this phase - bacteria may go into survival mode by creating virulence factors or endospores

4. Death or Decline phase= exponential decrease in number of living bacteria

55
Q

Gram stain process

A

Step 1: Crystal Violet
Stains cells purple or blue

Step 2: Iodine
Makes the CV adhere to the cell walls
- Stains cells purple or blue

Step 3: Alcohol
Washes away the dye from gram-negative
- GP: purple or blue
- GN: colourless

Step 4: Safranin
Dyes GN cells
- GP: purple or blue
- GN: pink or red

56
Q

What are serologies

A

Looks for an antibody response to the pathogen

57
Q

How to make a fungi culture

A

Silver stain

58
Q

Similarities and differences between cell types

A

Virus
- acellular
- NO cell wall
- NO membrane, some have envelopes
- NO ribosomes
- Depends on host for replication
- Carries either DNA or RNA (ss or ds)

Bacteria
- Prokaryotic
- Peptidoglycan is the main component of the cell wall
- Has membrane without ergosterol
- 70s ribosome
- 1 chromosome in the cytoplasm + plasmid
- binary fission

Fungi
- Eukaryotic
- Chitin + glucan are main components of the cell wall
- Has membrane with ergosterol
- 80S ribosome
- Chromosome in nucleus, NO plasmids or extrachromosomal
- Sexual + non-sexual reproduction

Humans
- Eukaryotic
- NO cell wall
- Has membrane without ergosterol
- 80s ribosome
- Chromosomes in nucleus
- Sexual reproduction via meiosis

59
Q

Selective toxicity

A

Selectively kills or stops the growth of microbial targets causing minimal or no harm to hosts

Used for antimicrobial targets: antibacterial, antivirals, and antifungals

60
Q

5 bacterial targets exploited in the development of antimicrobial drugs

A

1. Cell wall
2. Plasma membrane
3. Ribosomes
4. DNA synthesis
5. Metabolic pathways

61
Q

Antiviral targets

A

Antiretrovirals targets enzymes that are necessary for HIV viral replication
- reverse transcriptase (creates viral DNA)
- integrase (integrates the viral dna into the host DNA)
- protease (releases the proteins to allow for HIV to mature)

62
Q

Antifungal therapy for polyenes, azoles, and echinocandins

A

Polyenes:
- Mechanism - binds to ergosterol to create pores in the cell membrane causing cell leakage and death

Azoles:
- Mechanism - stops ergosterol synthesis which disrupts cell membrane formation

Echinocandins:
- Mechanism - stops beta-D-glucan synthesis which is a key component of the fungal cell wall - leads to cell lysis

63
Q

Antimicrobial drug resistance
When does resistance occur
and what are the processes for viruses, bacteria, and fungi

A

Resistance happens when random mutations are able to overcome antimicrobials and get chosen and passed down to generations

Virus
- mutations in the enzymes (target site modification)

Bacteria
- Blocked entry (porins), pump out, inactivate drugs with enzymes, modify the target

Fungi
- modifies the cell wall/membrane

64
Q

HIV disease progression

A
  • Acute infection
  • Latency phrase
  • AIDS
65
Q

90-90-90

A

90% of the people who got diagnosed with HIV - we want 90% of those people to be on treatment - we want 90% of those people to be suppressed

66
Q

Mechanisms for antibiotic resistance

A

1. Efflux pump
- beta-lactams
- aminoglycosides

2. Blocked penetration
- tetracyclines
- beta-lactams

3. Inactivation by enzymes
- macrolides
- beta-lactams

4. Target modification
- vancomycin
- beta-lactams

67
Q

What is relative risk and odds ratio

A

Relative risk:Proportion of people with the disease among exposed/proportion of people with the disease among the unexposed

Odds ratio:odds of disease among exposed/odds of disease among unexposed

OR = 1= exposure does NOT affect odds of outcome
OR<1 = exposure is associated with lower odds of outcome
OR>1 = exposure is associated with higher odds of outcome

68
Q

What is definitive host

A

Host where the parasite develops into the adult stage

  • Most often/not always - where the sexual reproduction occurs
69
Q

What is the intermediate host

A

Only harbours the parasite for a short amount of time

  • Usually a developmental stage is completed here
70
Q

What is the paratenic host:

A

Similar to the intermediate host BUT does not have any developmental stages here

  • Can act as a safe reservoir for the the parasites to accumulate
71
Q

What is the dead-end host

A

Does NOT allow transmission back to the definitive host + prevents the parasite from completing its development

72
Q

What are neglected diseases and what are control strategies

A
  • Gets overlooked by entities that are vital in drug access
    (government, public health programs)
  • Not considered a high priority for the prevention or treatment because they don’t usually impact people who live in high-income countries
  • Lack visibility because they usually do not cause dramatic outbreaks that kill large numbers of people

Control strategies:
- Antiparasitics (albendazole)
- Vector control, sanitation/hygiene, food safety

73
Q

What is zoonoses

A

any disease or infection that can be naturally transmitted from vertebrate animals to humans

74
Q

What is a vector+ vector-borne disease

A

living organism that can transmit infectious pathogens between humans OR from animals to humans

vector-borne diseases
diseases carried by arthropods

75
Q

What are factors that increase risk of animal-person spread

A

Host (reservoir + human host)
- Source host can carry infection w/o disease
- Phylogenetic similarity b/w source host + recipient host

Pathogen
- Wide host range, infects many host organisms
- High mutation rate allows to adapt to new hosts
- Ability to live in harsh environments

Environment
- Interaction b/w source + recipient host
- Changing environment, behaviour, and climate
- Loss of biodiversity

76
Q

Spillover Event

77
Q

How can climate change increase the risk of infectious diseases

A

Directly
- Increased temperatures
- Drought
- Variable precipitation
- Extreme weather events

Vector-borne

Indirectly
- Impacts on migration, population density, anmal-human interactions, biodiversity, food production

78
Q

What is the one health approach

A

A collaborative and transdisciplinary framework that recognizes the interconnectedness b/w human health, animal health, and environmental health