Modelling congenital transmission of Chagas’ disease

Raimundo, Silvia Martorano; Massad, Eduardo; Yang, Hyun Mo

doi:10.1016/j.biosystems.2009.11.005

Cited by 24 publications

(11 citation statements)

References 7 publications

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“…Thus, if R 0 is greater than 1, the disease is established in the population, and if R 0 is less than 1, the disease disappears. In the case of Chagas disease, the main component of the reproductive number is given by vector transmission, and when this is cut off, congenital transmission alone is incapable of perpetuating the disease [86,90]. There are very few attempts to estimate the R 0 of this disease, an exception being the study by Massad [91], who estimated it at R 0 = 1.25 for a region of Brazil.…”

Section: The Reproductive Number (R 0 )mentioning

confidence: 99%

Eco-Epidemiology of Chagas Disease in Chile

Lambarri¹,

Cifuentes²,

Ayala³

et al. 2018

Chagas Disease - Basic Investigations and Challenges

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There are four vector species of Chagas disease in Chile: Triatoma infestans, responsible for the domestic cycle; Mepraia spinolai, the main wild vector; and M. gajardoi and M. parapatrica, two coastal wild species whose importance as vectors is not well known. They are species of dry environments of the central-north region of Chile, whose best predictors of distribution are warm average temperatures and low rainfall. They are found in rock quarries, nests of birds, and small mammals, and T. infestans has sylvatic foci associated with a Bromeliaceae species. While human blood represents 70% of the diet of T. infestans, in M. spinolai this value is 7%, which means that a large part of Chagas disease in Chile is due to T. infestans. However, all species have high percentages of T. cruzi infection. Chagas disease in Chile follows the distribution of T. infestans, and although the cycle of domestic transmission by this vector is interrupted, there is still a constant prevalence and mortality and ascending incidences. Models predict that although climate change will not vary greatly the north-south distribution of vectors, it could increase the reproductive number of the disease, increasing risk areas of Chagas disease.

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Section: The Reproductive Number (R 0 )mentioning

confidence: 99%

Eco-Epidemiology of Chagas Disease in Chile

Lambarri¹,

Cifuentes²,

Ayala³

et al. 2018

Chagas Disease - Basic Investigations and Challenges

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show abstract

“…We only consider vector transmission, which is the main mode of transmission for T. cruzi within its endemic geographic area. Thus, we ignore vertical transmission (from mother to offspring) and "accidental" transmission due to blood transfusion, organ transfer or contaminated food [see 39,40,41]. Susceptible hosts can become infected through a vector's faeces laid close to a bite scar following a blood meal; the parasite may enter the body when hosts scratch themselves.…”

Section: Parasite Transmissionmentioning

confidence: 99%

Low virulence evolves as a bet-hedging strategy in fluctuating environment

Nguyen

Rajon

Fouchet

et al. 2015

Preprint

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The effect of fluctuating environmental conditions (i.e. environmental stochasticity) on the evolution of virulence has been broadly overlooked, presumably due to a lack of connection between the fields of evolutionary epidemiology and insect ecology. Practitioners of the latter have known for a long time that stochastic environmental variations can impact the population dynamics of many insects, some of which are vectors of infectious diseases. Here we investigate whether environmental stochasticity affecting a vector's life history can have an indirect impact on the evolutionarily expected virulence of the parasite, using Chagas disease as an example. We model the evolution of virulence using the adaptive dynamics framework, showing that parasite virulence should decrease when the vector's dynamics randomly change in time. The decrease is even more pronounced when environmental variations are frequent and ample. This decrease in virulence can be viewed as a bet-hedging strategy: when a parasite is at a risk of not being transmitted (e.g. because vectors are scarce), its best option is to stay in the host longerthat is, to be less virulent. Lowering virulence is thus very similar to increasing iteroparity, a well-known risk-spreading strategy, and should be expected to evolve whenever parasite transmission varies randomly in time.

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“…Let us show that the matrix A , given by equation (14), is an M -matrix [31] for big non-trivial equilibrium

{\overset{Q}{true}}_{MathClass-rel>}^{c}

, where T > is one of the coordinates.…”

Section: Appendix B: the Local Stability Of The Non-trivial Equilibrimentioning

confidence: 99%

Mathematical modeling of solid cancer growth with angiogenesis

Yang

2012

Theor Biol Med Model

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BackgroundCancer arises when within a single cell multiple malfunctions of control systems occur, which are, broadly, the system that promote cell growth and the system that protect against erratic growth. Additional systems within the cell must be corrupted so that a cancer cell, to form a mass of any real size, produces substances that promote the growth of new blood vessels. Multiple mutations are required before a normal cell can become a cancer cell by corruption of multiple growth-promoting systems.MethodsWe develop a simple mathematical model to describe the solid cancer growth dynamics inducing angiogenesis in the absence of cancer controlling mechanisms.ResultsThe initial conditions supplied to the dynamical system consist of a perturbation in form of pulse: The origin of cancer cells from normal cells of an organ of human body. Thresholds of interacting parameters were obtained from the steady states analysis. The existence of two equilibrium points determine the strong dependency of dynamical trajectories on the initial conditions. The thresholds can be used to control cancer.ConclusionsCancer can be settled in an organ if the following combination matches: better fitness of cancer cells, decrease in the efficiency of the repairing systems, increase in the capacity of sprouting from existing vascularization, and higher capacity of mounting up new vascularization. However, we show that cancer is rarely induced in organs (or tissues) displaying an efficient (numerically and functionally) reparative or regenerative mechanism.

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Modelling congenital transmission of Chagas’ disease

Cited by 24 publications

References 7 publications

Eco-Epidemiology of Chagas Disease in Chile

Eco-Epidemiology of Chagas Disease in Chile

Low virulence evolves as a bet-hedging strategy in fluctuating environment

Mathematical modeling of solid cancer growth with angiogenesis

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