Ordinary Differential Equations (14): Epidemic Models and Epidemiology

In early 2020 the entire world watched a small system of ordinary differential equations decide policy. “Flatten the curve” was not a slogan; it was the intuition of a specific equation. Herd immunity was not a guess; it was the threshold $1 - 1/R_0$ derived in a single line. The SIR model — four lines of math, written down in 1927 by Kermack and McKendrick — turned out to be precise enough to drive trillion-dollar decisions.

This chapter builds that machinery from scratch. We start with the basic SIR model, derive every threshold and final-size relation analytically, and then layer on the realism: incubation periods (SEIR), asymptomatic transmission, vaccinations, and time-varying interventions (a stylised COVID-style scenario). Throughout, the goal is not to believe a forecast but to understand which mechanism a given parameter controls.

What You Will Learn#

• The SIR model as a 3-equation system: compartments, parameters, and the basic reproduction number $R_0 = \beta/\gamma$
• The threshold theorem ($R_0 > 1 \Leftrightarrow$ outbreak) and the final-size relation $S_\infty = S_0 e^{-R_0(1 - S_\infty)}$
• Closed-form expressions for the peak height $I^* = 1 - 1/R_0 - \ln R_0 / R_0$ and the herd-immunity threshold $1 - 1/R_0$
• The SEIR variant, latent-period dependence, and why it slows the initial growth rate
• COVID-19 extensions: asymptomatic compartment, intervention-induced time-varying $R_e(t)$ , reporting iceberg
• Network-level reproduction numbers and the role of super-spreaders
• Practical fitting: what $R_0$ , doubling time, and serial interval actually measure

Prerequisites: phase-plane analysis from Chapter 7 , nonlinear stability from Chapter 8 , numerical methods from Chapter 11 .

The SIR Model#

Split the population into three compartments:

• $S$ — susceptible (can catch the disease)
• $I$ — infectious (currently transmitting)
• $R$ — removed (recovered with immunity, isolated, or dead)

Two parameters carry all the physics:

• $\beta$ — transmission coefficient: average effective contacts per unit time, times probability of transmission per contact.
• $\gamma$ — removal rate: $1/\gamma$ is the average duration of infectiousness.

The total $S + I + R \equiv N$ is conserved (there are no births or deaths in the closed model), so the system is genuinely two-dimensional.

The basic reproduction number $R_0$ #

Threshold theorem. The disease-free equilibrium is locally stable iff $R_0 < 1$ . This number has a beautifully concrete meaning: it is the expected number of secondary infections caused by one typical infectious individual placed into a fully susceptible population. If each infected person infects fewer than one other, the chain dies out. If more than one, it explodes — at first.

What controls the peak?#

And the time of peak is when $S$ first crosses $1/R_0$ . Both quantities are determined by $R_0$ alone (with $\gamma$ setting the timescale).

Final size: who escapes?#

For $R_0 = 2.5$ and $S_0 \approx N$ , the equation gives $S_\infty / N \approx 0.107$ — about 89% of the population is infected by the end. Surprising, but a one-line consequence of the math.

Top-left: classic SIR time series for $R_0 = 2.5,\ 1/\gamma = 10$ d — $S$ collapses, $I$ peaks then dies, $R$ saturates. Top-right: phase portrait in $(S, I)$ — trajectories enter the upper half-plane, peak when crossing the vertical line $S = 1/R_0$ , and spiral toward the $S$ -axis. Bottom-left: cumulative incidence $1 - S$ asymptotes to the final-size value (red dashed line). Bottom-right: $S_\infty$ and $1 - S_\infty$ as functions of $R_0$ — the curve is steep just above 1, meaning small changes in $R_0$ cause huge changes in eventual reach.

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import numpy as np
import matplotlib.pyplot as plt
from scipy.integrate import solve_ivp

def sir(t, y, beta, gamma, N):
    S, I, R = y
    return [-beta*S*I/N, beta*S*I/N - gamma*I, gamma*I]

N, gamma = 1.0, 1/10
fig, ax = plt.subplots(figsize=(10, 5))
for R0 in [1.5, 2.0, 2.5, 3.0]:
    beta = R0 * gamma
    sol = solve_ivp(sir, [0, 200], [N - 1e-3, 1e-3, 0],
                    args=(beta, gamma, N),
                    t_eval=np.linspace(0, 200, 600))
    ax.plot(sol.t, sol.y[1], lw=2, label=f'R0 = {R0}')
ax.set_xlabel('Days'); ax.set_ylabel('Fraction infectious')
ax.legend(); plt.tight_layout(); plt.show()

Sensitivity to $R_0$ #

$R_0$ is the lever that determines outcomes. A factor-of-two change in $R_0$ can multiply peak demand on hospitals five-fold and pull the peak forward by weeks. The sensitivity is also analytic, which is rare.

Left: a family of $I(t)$ curves at $R_0 \in \{1.2, 1.6, 2.0, 2.5, 3.5, 5.0\}$ for fixed $1/\gamma = 10$ d. Higher $R_0$ -> higher and earlier peak. Middle: peak fraction infected (red) and time of peak (blue) versus $R_0$ . The black dashed line is the analytical formula $1 - 1/R_0 - \ln R_0 / R_0$ — spot on. Right: total fraction infected at the end (red) and the herd-immunity threshold $1 - 1/R_0$ (green dashed). Note that the final size always overshoots HIT — the epidemic does not stop the instant immunity reaches the threshold; it stops when transmission can no longer sustain itself, by which time many “extra” infections have happened.

Vaccination and Herd Immunity#

For $R_e \leq 1$ we need $v \geq 1 - 1/R_0$ . This is the herd-immunity threshold (HIT): the minimum fraction that must be immune for an introduced case to die out, on average.

For high-$R_0$ diseases combined with imperfect vaccines this can become infeasible ($v > 1$ ).

Top-left: $I(t)$ for vaccination coverages $v = 0,\ 0.20,\ 0.40,\ HIT,\ 0.85$ . At $v = HIT$ the curve is barely an outbreak; at $v = 0.85$ no outbreak occurs at all. Top-right: peak and additional infections versus coverage; the green region is post-HIT. Bottom-left: HIT versus $R_0$ with example diseases marked. Bottom-right: required coverage $v$ as a function of $R_0$ for vaccine efficacies $\mathrm{VE} \in \{0.5, 0.7, 0.9, 1.0\}$ — the “infeasible” red shading shows where high $R_0$ + low VE makes herd immunity unattainable through vaccination alone.

The picture also justifies the public-health emphasis on getting the laggards vaccinated: under a high-$R_0$ disease, the last 10% matters as much as the first 60%.

The SEIR Model#

The transition rate $\sigma$ has $1/\sigma$ = average latent duration. The basic reproduction number is unchanged: $R_0 = \beta/\gamma$ . So, do incubation periods matter?

The latent stage slows the early exponential growth, even though $R_0$ is unchanged. So at fixed $R_0$ , SEIR predicts a later, slightly lower peak than SIR. Equivalently: doubling time depends on the generation interval $T_g \approx 1/\sigma + 1/\gamma$ , not just on $R_0$ .

Top-left: full SEIR trajectory at $R_0 = 3,\ 1/\sigma = 5\ \text{d},\ 1/\gamma = 7\ \text{d}$ . Top-right: SEIR vs SIR at the same $R_0$ — SEIR peaks later and is slightly lower. Bottom-left: family of SEIR $I(t)$ for $1/\sigma \in \{0.5, 2, 5, 10, 20\}$ d — longer latent periods produce later, broader peaks. Bottom-right: initial growth rate $r$ as a function of latent period; doubling time on the right axis. As $\sigma \to \infty$ (instantaneous transition), SEIR recovers SIR.

A COVID-Style Extension#

Real epidemics need more than SEIR. COVID-19 introduced four mathematical wrinkles:

1. Asymptomatic transmission. A fraction $p$ of infections never develop symptoms but still spread (with reduced infectiousness $\kappa$ ).
2. Time-varying $\beta$ . Lockdowns, mask mandates, and behavioural changes alter transmission.
3. Reporting iceberg. Only a fraction of true cases gets detected; reported = $\rho \cdot I_s$ with $\rho < 1$ .
4. Variants. New strains restart the dynamics with a fresh $R_0$ .

We want $R_e(t) < 1$ . Two ways: shrink $\beta$ (interventions) or shrink $S/N$ (immunity).

Top-left: a stylised four-phase scenario — baseline $\beta = 0.6$ for 30 days, lockdown $\beta = 0.18$ for 30 days, partial relaxation $\beta = 0.30$ , then variant + relaxation $\beta = 0.40$ . Top-right: effective $R_e(t)$ — the lockdown phase pushes $R_e$ below 1 (green region) and the third wave climbs above 1 again. Bottom-left: reporting iceberg — the dashed black line is what surveillance would report ($\rho I_s$ ), far below the true infectious prevalence $I_s + I_a$ (purple). Bottom-right: counterfactual comparison of cumulative infected with vs without interventions. The gap is the cases averted — the policy benefit, expressed as a fraction of the population.

This is not a fit to real data — it is a clean cartoon of the structure that real fits use. The same equations, fitted to actual reported case time series with Bayesian inference, drove official forecasts in 2020-2022.

Network and Heterogeneous Models#

For scale-free networks ($P(k) \propto k^{-\alpha}$ with $2 < \alpha < 3$ ), $\langle k^2 \rangle$ diverges with system size. This means the epidemic threshold goes to zero — on such networks, even very low transmissibility can sustain an outbreak. Super-spreaders dominate the early dynamics in real epidemics; targeting them with contact tracing is disproportionately effective.

Two conceptual lessons:

• Average contact rate underestimates risk; the variance matters as much.
• Equal-coverage interventions waste resources; prioritise high-degree nodes.

Applications and Limits#

Where the math wins#

• Order-of-magnitude forecasting. Will hospitals overflow in 4 weeks? SEIR with the right $R_0$ gives a usable answer.
• Threshold reasoning. “How much vaccination do we need?” -> $1 - 1/R_0$ , divided by VE. No fit needed.
• Counterfactual comparison. “How many lives did the lockdown save?” -> Run with and without intervention; difference is the answer (subject to $R_0$ uncertainty).

Where it loses#

• Exact predictions. $R_0$ varies between settings, populations, weather, behavioural changes. Exact case counts beyond a few weeks are not reliable.
• Heterogeneity ignored. Age structure, geography, household clustering all matter; mean-field models give the wrong peak timing in detail.
• Behavioural feedback. People reduce contacts when they see the news. This is a closed-loop system, and ignoring the feedback inflates predicted peaks.

The right way to use the math is as a structured language for arguing about scenarios, not as a literal forecast.

Summary#

Exercises#

Conceptual.

1. Why does the SIR final size overshoot the herd-immunity threshold? Make the argument both intuitive and analytical.
2. The serial interval and the generation interval are both proxies for “time between successive infections”. Define them, and explain why they differ.
3. Two countries report the same case-doubling time. Could they have very different $R_0$ ? Use SEIR to argue.

Computational.

4. Solve the SIR system for $R_0 = 1.05, 1.5, 3.0$ and check the final-size formula numerically against the transcendental equation.
5. For SEIR at $R_0 = 3$ , plot the generation interval $1/\sigma + 1/\gamma$ versus the doubling time; verify that doubling time grows linearly with generation interval at fixed $R_0$ .
6. Implement the asymptomatic COVID model, fit it to your country’s first-wave reported time series with two free parameters ($\beta$ and start time), and compute $R_e(t)$ .

Programming.

7. Animate the family of SIR phase portraits as $R_0$ slides from 0.5 to 5.0.
8. Build a stochastic SIR (Gillespie algorithm) and compare its mean trajectory with the deterministic ODE for population sizes $N = 10^2,\ 10^4,\ 10^6$ . When does the deterministic limit kick in?
9. Implement an age-structured SIR with two age classes (children, adults) and a 2x2 contact matrix. Compute the next-generation matrix and find $R_0$ as its dominant eigenvalue.

References#

• Kermack & McKendrick, “A contribution to the mathematical theory of epidemics,” Proc. Roy. Soc. A 115 (1927)
• Anderson & May, Infectious Diseases of Humans, Oxford University Press (1991)
• Diekmann, Heesterbeek & Britton, Mathematical Tools for Understanding Infectious Disease Dynamics, Princeton (2013)
• Keeling & Rohani, Modeling Infectious Diseases in Humans and Animals, Princeton (2008)
• Brauer, Castillo-Chavez & Feng, Mathematical Models in Epidemiology, Springer (2019)
• Ferguson et al., “Impact of non-pharmaceutical interventions to reduce COVID-19 mortality,” Imperial College Report 9 (2020)
• Pastor-Satorras & Vespignani, “Epidemic spreading in scale-free networks,” Phys. Rev. Lett. 86 (2001)