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Dynamical Models of Epidemics: from Black Death to SARS. D. Gurarie CWRU. History. Epidemics in History – Plague in 14th Century Europe killed 25 million – Aztecs lost half of 3.5 million to smallpox – 20 million people in influenza epidemic of 1919 Diseases at Present
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Dynamical Models of Epidemics: from Black Death to SARS D. Gurarie CWRU
History Epidemics in History – Plague in 14th Century Europe killed 25 million – Aztecs lost half of 3.5 million to smallpox – 20 million people in influenza epidemic of 1919 Diseases at Present – 1 million deaths per year due to malaria – 1 million deaths per year due to measles – 2 million deaths per year due to tuberculosis– 3 million deaths per year due to HIV – Billions infected with these diseases History of Epidemiology . Hippocrates's On the Epidemics (circa 400 BC) . John Graunt's Natural and Political Observations made upon the Bills of Mortality (1662) . Louis Pasteur and Robert Koch (middle 1800's) History of Mathematical Epidemiology . Daniel Bernoulli studied the effect of vaccination with cow pox on life expectancy (1760) . Ross's Simple Epidemic Model (1911) . Kermack and McKendrick's General Epidemic Model (1927)
Geographic Distribution -1990 Schistosomiasis • Chronic parasitic trematode infection • 200-300 million people worldwide • Significant morbidity (esp. anemia) • Premature mortality • Life-cycle is complex, requiring species-specific intermediate snail host • Optimal control strategies have not been established.
Smallpox: XVIII century • Known facts: • Short duration (10 days), high mortality (75%) • Life-long immunity for survivors • Prevention: immunity by inoculation (??) • Problem: could public health (life expectancy) be improved by inoculation? Daniel Bernoulli 1700-1782 “I simply wish that, in a matter which so closely concerns the well-being of mankind, no decision shall be made without all the knowledge which a little analysis and calculation can provide.” Daniel Bernoulli, on smallpox inoculation, 1766
Bernoulli smallpox model (1766) 1) Population cohort of age a, n(a), mortality m(a) 2) Small pox effect Caveat: if inoculation mortalityf is included one would needf<.5% for success!
Modeling issues and strategies • State variables for host/parasite • “mean” or “distributed” (deterministic/stochastic) • Prevalence or level/intensity • Disease stages (latent,…) • Susceptibility and infectiousness • Transmission • Homogeneous (uniformly mixed populations): “mass action” • Heterogeneous: age/gender/ behavioral strata, spatially structured contacts • Environmental factors • Multi-host systems, parasites with complex life cycles, …. • Goals of epidemic modeling • Prediction • Risk assessment • Control (intervention, prevention)
Box (compartment) diagrams S I Birth Death SI S I R SIR recruitment SEIR SEIR S S E E I I R R V V S – Susceptible E – Exposed I – Infectious R - Removed V – Vaccinated … Total population: N = S+I+…
S I b SIR with immunity S I R b m Residual S(∞)>0 SIR-type modelsRoss, Kermak-McKendrick • Population size is large and constant • No birth, death, immigration or emigration • No recovery • No latency • Homogeneous mixing SI Basic Reproduction number: R0=bN/m R0>1 – endemic R0<1 - eradication
I S R m b d endemic epidemic SIR with loss of immunity • Control • R0=“transmissiom”x”pop. density”/”recovery”<1. Hence critical density N>m/b • to sustain endemic level • (ii) Vaccination removes a fraction of N from transmission cycle: so eradication • (equilibrium I<0) requires (1-1/R0) fraction of N vaccinated
(1-n)d l X X Z Y m m+dn m “Smallpox cohort” SIR
Growth models: variable population N(t) Const recruitment Linear growth due to S (Voltera-Lotka) Linear growth rate due to S,I
HIV/AIDS and STD • Variable population N=S+I • Natural growth a for S • Mortality m=10/year for I • Transmission: b S I/(S+I) • = mean number of partners/per I • S/(S+I) probability of infecting S (S-fraction of N) Typical collapse Conclusion: Transm. treatment Treatment w/o prevention of spread can only increase g (collapse!)
AIDS for behavioral groups: 6D model Parameters: Initial state
Heterogeneous transmission for distributed populations • SIR type are only conceptual models • Idealize transmissions and individual characteristics (susceptibilities) • Real epidemics requires heterogeneous models: • age structure • spatial/behavioral heterogeneity, etc.
Age structured models (smallpox) Continuous population strata n(a,t), age “a”, time “t” Discrete population bins: n=(na) Normal growth Infection
Example: 15-bin system with linear growth and structured transmission Age bins: red (young) to blue (old) High survival Low survival
Fisher’s Equation (1937) Original motivation: spread of a genetype in a population) • Infection: S(x,t), I(x,t)– (distributed) susceptibles and infectives • Population density is constant N • No birth or death • No recovery or latent period • Only local infection • Infection rate is proportional to the number of infectives • Individuals disperse diffusively with constant D
Solutions: propagating density waves Spreading wave in uniform medium with const pop. density Spreading wave with variable pop. density (red) • Problems: • Equilibrium, Basic Reproduction Number? • Speed of propagation (traveling waves)? • Parameters for control, prevention?
Some current modeling issues and approaches • Spatial/temporal patterns of outbreaks and spread • Stochastic modeling • Cellular Automata and Agent-Based Models • Network Models (STD)