PubMed · 14326669
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H NORIKI. 1965-02-15. [INFECTIOUS HEPATITIS FROM A BASIC STANDPOINT].. https://pubmed.ncbi.nlm.nih.gov/14326669/
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The endemic persistence of infectious diseases can often not be understood without taking into account the relevant heterogeneities of host mixing. Here, we consider spatial heterogeneity, defined as 'patchiness' of the host population. After briefly reviewing how disease persistence is influenced by population size, reproduction number and infectious period, we explore its dependence on the level of spatial heterogeneity. Analysis and simulation of disease transmission in a symmetric meta-population suggest that disease persistence typically becomes worse as spatial heterogeneity increases, although local persistence optima can occur for infections with oscillatory population dynamics. We obtain insight into the dynamics that underlie the observed persistence patterns by studying the infection prevalence correlation between patches and by comparing full-model simulations to results obtained using simplified patch-level descriptions of the interplay between local extinctions and between-patch transmissions. The observed patterns are interpreted in terms of rescue effects for strong spatial heterogeneity and in terms of between-patch coherence and synchronization effects at intermediate and weak levels of heterogeneity.
Quasi-experimental study designs, sometimes called nonrandomized, pre-post-intervention study designs, are ubiquitous in the infectious diseases literature, particularly in the area of interventions aimed at decreasing the spread of antibiotic-resistant bacteria. Little has been written about the benefits and limitations of the quasi-experimental approach. This article outlines a hierarchy of quasi-experimental study design that is applicable to infectious diseases studies and that, if applied, may lead to sounder research and more-convincing causal links between infectious diseases interventions and outcomes.
The spread of infectious diseases near the epidemic threshold is investigated. Scaling laws for the size and the duration of outbreaks originating from a single infected individual in a large susceptible population are obtained. The maximal size of an outbreak n(*) scales as N(2/3) with N the population size. This scaling law implies that the average outbreak size [n]scales as N(1/3). Moreover, the maximal and the average duration of an outbreak grow as t(*) approximately N(1/3) and [t] approximately ln N, respectively.