1,142 research outputs found
Evaluating undercounts in epidemics: response to Maruotti et al. 2022
Maruotti et al. 2022 used a mark-recapture approach to estimate bounds on the
true number of monkeypox infections in various countries. These approaches are
fundamentally flawed; it is impossible to estimate undercounting based solely
on a single stream of reported cases. Simulations based on a Richards curve for
cumulative incidence show that, for reasonable epidemic parameters, the
proposed methods estimate bounds on the ascertainment ratio of roughly independently of the true ascertainment ratio. These methods
should not be used
Can hot temperatures limit disease transmission? A test of mechanisms in a zooplanktonâfungus system
Thermal ecology theory predicts that transmission of infectious diseases should respond unimodally to temperature, that is be maximized at intermediate temperatures and constrained at extreme low and high temperatures. However, empirical evidence linking hot temperatures to decreased transmission in nature remains limited.We tested the hypothesis that hot temperatures constrain transmission in a zooplanktonâfungus (Daphnia dentiferaâMetschnikowia bicuspidata) disease system where autumnal epidemics typically start after lakes cool from their peak summer temperatures. This pattern suggested that maximally hot summer temperatures could be inhibiting disease spread.Using a series of laboratory experiments, we examined the effects of high temperatures on five mechanistic components of transmission. We found that (a) high temperatures increased exposure to parasites by speeding up foraging rate but (b) did not alter infection success postâexposure. (c) High temperatures lowered parasite production (due to faster host death and an inferred delay in parasite growth). (d) Parasites made in hot conditions were less infectious to the next host (instilling a parasite ârearingâ or âtransâhostâ effect of temperature during the prior infection). (e) High temperatures in the freeâliving stage also reduce parasite infectivity, either by killing or harming parasites.We then assembled the five mechanisms into an index of disease spread. The resulting unimodal thermal response was most strongly driven by the rearing effect. Transmission peaked at intermediate hot temperatures (25â26°C) and then decreased at maximally hot temperatures (30â32°C). However, transmission at these maximally hot temperatures only trended slightly lower than the baseline control (20°C), which easily sustains epidemics in laboratory conditions and in nature. Overall, we conclude that while exposure to hot epilimnetic temperatures does somewhat constrain disease, we lack evidence that this effect fully explains the lack of summer epidemics in this natural system. This work demonstrates the importance of experimentally testing hypothesized mechanisms of thermal constraints on disease transmission. Furthermore, it cautions against drawing conclusions based on field patterns and theory alone.A free Plain Language Summary can be found within the Supporting Information of this article.A free Plain Language Summary can be found within the Supporting Information of this article.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/151821/1/fec13403-sup-0001-Summary.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151821/2/fec13403_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151821/3/fec13403.pd
Simple guide to starting a research group
Conducting cutting-edge research and scholarship becomes more complicated with each passing year; forming a collaborative research group offers a way to navigate this increasing complexity. Yet many individuals whose work might benefit from the formation of a collaborative team may feel overwhelmed by the prospect of attempting to build and maintain a research group. We propose this simple guide for starting and maintaining such an enterprise
Toward a comprehensive system for constructing compartmental epidemic models
Compartmental models are valuable tools for investigating infectious
diseases. Researchers building such models typically begin with a simple
structure where compartments correspond to individuals with different
epidemiological statuses, e.g., the classic SIR model which splits the
population into susceptible, infected, and recovered compartments. However, as
more information about a specific pathogen is discovered, or as a means to
investigate the effects of heterogeneities, it becomes useful to stratify
models further -- for example by age, geographic location, or pathogen strain.
The operation of constructing stratified compartmental models from a pair of
simpler models resembles the Cartesian product used in graph theory, but
several key differences complicate matters. In this article we give explicit
mathematical definitions for several so-called ``model products'' and provide
examples where each is suitable. We also provide examples of model
stratification where no existing model product will generate the desired
result
A H2O2-producing glyoxal oxidase is required for filamentous growth and pathogenicity in Ustilago maydis
Persistence, extinction and spatio-temporal synchronization of SIRS cellular automata models
Spatially explicit models have been widely used in today's mathematical
ecology and epidemiology to study persistence and extinction of populations as
well as their spatial patterns. Here we extend the earlier work--static
dispersal between neighbouring individuals to mobility of individuals as well
as multi-patches environment. As is commonly found, the basic reproductive
ratio is maximized for the evolutionary stable strategy (ESS) on diseases'
persistence in mean-field theory. This has important implications, as it
implies that for a wide range of parameters that infection rate will tend
maximum. This is opposite with present results obtained in spatial explicit
models that infection rate is limited by upper bound. We observe the emergence
of trade-offs of extinction and persistence on the parameters of the infection
period and infection rate and show the extinction time having a linear
relationship with respect to system size. We further find that the higher
mobility can pronouncedly promote the persistence of spread of epidemics, i.e.,
the phase transition occurs from extinction domain to persistence domain, and
the spirals' wavelength increases as the mobility increasing and ultimately, it
will saturate at a certain value. Furthermore, for multi-patches case, we find
that the lower coupling strength leads to anti-phase oscillation of infected
fraction, while higher coupling strength corresponds to in-phase oscillation.Comment: 12page
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