Mathematical models can project how infectious diseases progress to show the likely outcome of an epidemic (including in plants) and help inform public health and plant health interventions. Models use basic assumptions or collected statistics along with mathematics to find parameters for various infectious diseases and use those parameters to calculate the effects of different interventions, like mass vaccination programs. The modelling can help decide which intervention(s) to avoid and which to trial, or can predict future growth patterns, etc.
History The modelling of infectious diseases is a tool that has been used to study the mechanisms by which diseases spread, to predict the future course of an outbreak and to evaluate strategies to control an epidemic. The first scientist who systematically tried to quantify causes of death was John Graunt in his book Natural and Political Observations made upon the Bills of Mortality, in 1662. The bills he studied were listings of numbers and causes of deaths published weekly. Graunt's analysis of causes of death is considered the beginning of the "theory of competing risks" which according to Daley and Gani is "a theory that is now well established among modern epidemiologists". The earliest account of mathematical modelling of spread of disease was carried out in 1760 by Daniel Bernoulli. Trained as a physician, Bernoulli created a mathematical model to defend the practice of inoculating against smallpox. The calculations from this model showed that universal inoculation against smallpox would increase the life expectancy from 26 years 7 months to 29 years 9 months. Daniel Bernoulli's work preceded the modern understanding of germ theory. In the early 20th century, William Hamer and Ronald Ross applied the law of mass action to explain epidemic behaviour. The 1920s saw the emergence of compartmental models. The Kermack–McKendrick epidemic model (1927) and the Reed–Frost epidemic model (1928) both describe the relationship between susceptible, infected and immune individuals in a population. The Kermack–McKendrick epidemic model was successful in predicting the behavior of outbreaks very similar to that observed in many recorded epidemics. Recently, agent-based models (ABMs) have been used in exchange for simpler compartmental models. For example, epidemiological ABMs have been used to inform public health (nonpharmaceutical) interventions against the spread of SARS-CoV-2. Epidemiological ABMs, in spite of their complexity and requiring high computational power, have been criticized for simplifying and unrealistic assumptions. Still, they can be useful in informing decisions regarding mitigation and suppression measures in cases when ABMs are accurately calibrated.
Assumptions Models are only as good as the assumptions on which they are based. If a model makes predictions that are out of line with observed results and the mathematics is correct, the initial assumptions must change to make the model useful.
Rectangular and stationary age distribution, i.e., everybody in the population lives to age L and then dies, and for each age (up to L) there is the same number of people in the population. This is often well-justified for developed countries where there is a low infant mortality and much of the population lives to the life expectancy. Homogeneous mixing of the population, i.e., individuals of the population under scrutiny assort and make contact at random and do not mix mostly in a smaller subgroup. This assumption is rarely justified because social structure is widespread. For example, most people in London only make contact with other Londoners. Further, within London then there are smaller subgroups, such as the Turkish community or teenagers (just to give two examples), who mix with each other more than people outside their group. However, homogeneous mixing is a standard assumption to make the mathematics tractable.
Types of epidemic models
Stochastic "Stochastic" means being or having a random variable. A stochastic model is a tool for estimating probability distributions of potential outcomes by allowing for random variation in one or more inputs over time. Stochastic models depend on the chance variations in risk of exposure, disease and other illness dynamics. Statistical agent-level disease dissemination in small or large populations can be determined by stochastic methods.
Deterministic When dealing with large populations, as in the case of tuberculosis, deterministic or compartmental mathematical models are often used. In a deterministic model, individuals in the population are assigned to different subgroups or compartments, each representing a specific stage of the epidemic. The transition rates from one class to another are mathematically expressed as derivatives, hence the model is formulated using differential equations. While building such models, it must be assumed that the population size in a compartment is differentiable with respect to time and that the epidemic process is deterministic. In other words, the changes in population of a compartment can be calculated using only the history that was used to develop the model.
Kinetic and mean-field Formally, these models belong to the class of deterministic models; however, they incorporate heterogeneous social features into the dynamics, such as individuals' levels of sociality, opinion, wealth, geographic location, which profoundly influence disease propagation. These models are typically represented by partial differential equations, in contrast to classical models described as systems of ordinary differential equations. Following the derivation principles of kinetic theory, they provide a more rigorous description of epidemic dynamics by starting from agent-based interactions.
Sub-exponential growth A common explanation for the growth of epidemics holds that 1 person infects 2, those 2 infect 4 and so on and so on with the number of infected doubling every generation. It is analogous to a game of tag where 1 person tags 2, those 2 tag 4 others who've never been tagged and so on. As this game progresses it becomes increasing frenetic as the tagged run past the previously tagged to hunt down those who have never been tagged. Thus this model of an epidemic leads to a curve that grows exponentially until it crashes to zero as all the population have been infected. i.e. no herd immunity and no peak and gradual decline as seen in reality.
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