ID exam 2, class 1, epidemiology, ch 33

slides & anis notes from class done, no socrative

difference between infectious disease and non infectious disease epidemiology (4 each)

non ID: causation usually stable (eg smoking → lung cancer), risk factors change slowly, study one person’s exposure, eg cancer, heart disease
ID: causation is dynamic: pathogen reproduces/mutates/spreads, risk factors change rapidly (immunity, transmission, chains), must study chains of transmissions between people, eg measles, COVID

why does the difference between ID and non-ID important for epidemiologists (4)

cant just count cases - must understand transmission networks, must predict: will this die out or grow exponentially, prevention requires interrupting chains (not just protecting individuals), eg. how contagious is measles?

4 modes of transmission + egs

direct person to person (measles (airborne), COVID (respiratory droplets), HCV (blood/bodily fluids))
indirect (contaminated water (cholera), vectors (malaria via mosquito))
environmnetal (legionella from AC)
reservoir dynamics (some diseases need animal reservoirs (zoonoses), others only need humans

3 things that determine if transmission happens

contact frequency (does the infected person contact a susceptible person?), biological requirement (can the pathogen survive the route), immunity status (is the susceptible person immunologically vulnerable)

key insight about transmission probability and contact patterns

diseases with high transmission probability (eg measles) spread through casual contacts, diseases with low probability (eg HCV) need specific contact types

how do you call people who is the start person of an infection? how about people infected by that person? what about people infected by the people infected by the first person? etc.

index case, secondary cases, tertiary cases, etc.

R0 def

average number of new infections produced by one infected person in a completely susceptible population with NO interventions, contagiousness potential of a pathogen

critical threshold for R0

R0 = 1, after it, increases significantly faster, gold standard for outbreak control

effects on epidemic with diff R0

R0 <1 - epidemic dies out
R0 = 1 - endemic
R0 > 1 epidemic (exponential growth)

R0 formula

R0 = beta (measure of infectiousness) x c (number of contacts per infectious person per day) x D (duration of infectiousness)

what does R0 depend on (3)

how often infected people contact susceptible people (social structure), how easily the pathogen transmits (biology of pathogen), how long someone is contagious (pathogen biology + immune response)

does R0 ever really exist in real life?

no, its the theoretical potential in a completely susceptible population (which doesnt really exist)

what do we use instead of R0, what does it account for? (4)

Re (or Rt) - actual reproductive number right now, accounts for: some people are vaccinated (immune), some are naturally immune (had the disease), interventions are in place (masks, isolation, social distancing), only a fraction of population is susceptible

effective reproductive number formula

Re = beta (measure of infectiousness) x c (number of contacts per infectious person per day) x D (duration of infectiousness) x S (fraction of the population susceptible to the disease)
(OR just R0 x S)

how many people do we need to vaccinate to achieve herd immunity

depends on R0 - have to bring it < 1, calculate what S should be (and therefore how many need to be vaccinated), S = 1/R0, minimal coverage = 1 - S

steps of Re calculation

step 1 - how many are susceptible, calculate S
step 2 - calculate RE
step 3 - interpret Re, if under 1 → epidemic dies out!

Re changes over time during an outbreak (3 times), result

early outbreak: high susceptibility, Re close to R0, rapid growth
middle: susceptible people get infected, Re decreases, growth slows
late: fewer susceptibles left, Re drops below 1, outbreak ends
- why epidemics eventually burn out even without intervention

how does crowding help the spread of infection

increases the number of contacts ( c ) per time period

incidence vs prevalence

incidence: number of new cases occurring in a defined population over a defined time period (measures how fast the disease is spreading)
prevalence: number of existing cases (new+old) in a defined population at a given moment (measures how much disease is present rn)

5 reasons why nightclubs are superspreading hotspots

high contact rate (dancing, close proximity, touching), poor ventilation (indoors, crowded air), mixing (different people from different venues (multiple venues in the same night), distraction (people not thinking about transmission risk), duration (hours of exposure)
result: conditions maximize Re (all 3 components contact x transmission x duration)

what did COVID restrictions help with

directly impacts Re

how can you see if an epidemic is one outbreak + expl

phylogenetics: viruses mutate over time and we can track these mutations and compare virus genomes - can visualize the mutations in a phylogenetic tree

p-distance def

proportion of changes between sequences

central dogma of phylogenetics

genetic information flows vertically through time from ancestor to descendant, and organisms with more similar genetic sequences share more recent common ancestors

traditional vs genomic epi

traditional epi: person A was in contact with person B (if you can trace them)
genomic epi: person A and person C have nearly identical virus genomes so they could be in the same transmission chain (even if they didnt directly contact each other)

infectious diseases epidemiology concepts (3)

demonstrates transmission chain dynamics (one case → many secondary cases → international spread)
shows low R0 doesnt mean low impact (eg HCV R0 <1, but chains persist through specific contact networks eg MSM sexual networks)
illustrates effective surveillance using phylogenetics - genomics reveals clusters traditional contact tracing might miss

Exam q eg: Why does treating one TB patient reduce risk for their family?

TB is an infectious disease - would be transmittable otherwise

is R0 a constant? explain

no! it varies by population - eg measles in an isolated village is not the same as in a city, because contact patterns and transmission opportunities differ