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- All Subjects: Persistence
- Creators: Smith, Hal
- Creators: Herman, Richard
- Status: Published
Motivated by the fact that understanding the dynamics of disease vector is crucial to understanding the transmission and control of the VBDs they cause, a novel weather-driven deterministic model for the population biology of the mosquito is formulated and rigorously analyzed. Numerical simulations, using relevant weather and entomological data for Anopheles mosquito (the vector for malaria), show that maximum mosquito abundance occurs when temperature and rainfall values lie in the range [20-25]C and [105-115] mm, respectively.
The Anopheles mosquito ecology model is extended to incorporate human dynamics. The resulting weather-driven malaria transmission model, which includes many of the key aspects of malaria (such as disease transmission by asymptomatically-infectious humans, and enhanced malaria immunity due to repeated exposure), was rigorously analyzed. The model which also incorporates the effect of diurnal temperature range (DTR) on malaria transmission dynamics shows that increasing DTR shifts the peak temperature value for malaria transmission from 29C (when DTR is 0C) to about 25C (when DTR is 15C).
Finally, the malaria model is adapted and used to study the transmission dynamics of chikungunya, dengue and Zika, three diseases co-circulating in the Americas caused by the same vector (Aedes aegypti). The resulting model, which is fitted using data from Mexico, is used to assess a few hypotheses (such as those associated with the possible impact the newly-released dengue vaccine will have on Zika) and the impact of variability in climate variables on the dynamics of the three diseases. Suitable temperature and rainfall ranges for the maximum transmission intensity of the three diseases are obtained.
+ 1 phage, with explicit nutrient, where the jth phage strain infects the first j bacterial strains, a perfectly nested infection network (NIN). This system is subject to trade-off conditions on the life-history traits of both bacteria and phage given in an earlier study Jover et al. (2013). Sufficient conditions are provided to show that a bacteria-phage community of arbitrary size with NIN can arise through the succession of permanent subcommunities, by the successive addition of one new population. Using uniform persistence theory, this entire community is shown to be permanent (uniformly persistent), meaning that all populations ultimately survive.
It is shown that a modified version of the original NIN Lotka-Volterra model with implicit nutrient considered by Jover et al. (2013) is permanent. A new one-to-one infection network (OIN) is also considered where each bacterium is infected by only one phage, and that phage infects only that bacterium. This model does not use the trade-offs on phage infection range, and bacterium resistance to phage. The OIN model is shown to be permanent, and using Lyapunov function theory, coupled with LaSalle’s Invariance Principle, the unique coexistence equilibrium associated with the NIN is globally asymptotically stable provided that the inter- and intra-specific bacterial competition coefficients are equal across all bacteria.
Finally, the OIN model is extended to a “Kill the Winner” (KtW) Lotka-Volterra model
of marine communities consisting of bacteria, phage, and zooplankton. The zooplankton
acts as a super bacteriophage, which infects all bacteria. This model is shown to be permanent.
overall dynamics of the system and how they depend on the incidence
function. I consider both an epidemic and endemic perspective of the
model, but in both cases, three classes of incidence
functions are identified.
In the epidemic form,
power incidences, where the infective portion $I^p$ has $p\in(0,1)$,
cause unconditional host extinction,
homogeneous incidences have host extinction for certain parameter constellations and
host survival for others, and upper density-dependent incidences
never cause host extinction. The case of non-extinction in upper
density-dependent
incidences extends to the case where a latent period is included.
Using data from experiments with rhanavirus and salamanders,
maximum likelihood estimates are applied to the data.
With these estimates,
I generate the corrected Akaike information criteria, which
reward a low likelihood and punish the use of more parameters.
This generates the Akaike weight, which is used to fit
parameters to the data, and determine which incidence functions
fit the data the best.
From an endemic perspective, I observe
that power incidences cause initial condition dependent host extinction for
some parameter constellations and global stability for others,
homogeneous incidences have host extinction for certain parameter constellations and
host survival for others, and upper density-dependent incidences
never cause host extinction.
The dynamics when the incidence function is homogeneous are deeply explored.
I expand the endemic considerations in the homogeneous case
by adding a predator into the model.
Using persistence theory, I show the conditions for the persistence of each of the
predator, prey, and parasite species. Potential dynamics of the system include parasite mediated
persistence of the predator, survival of the ecosystem at high initial predator levels and
ecosystem collapse at low initial predator levels, persistence of all three species, and much more.
Hundreds of thousands of people die annually from malaria; a protozoan of the genus Plasmodium is responsible for this mortality. The Plasmodium parasite undergoes several life stages within the mosquito vector, the transition between which require passage across the lumen of the mosquito midgut. It has been observed that in about 15% of parasites that develop ookinetes in the mosquito abdomen, sporozoites never develop in the salivary glands, indicating that passage across the midgut lumen is a significant barrier in parasite development (Gamage-Mendis et al., 1993). We aim to investigate a possible correlation between passage through the midgut lumen and drug-resistance trends in Plasmodium falciparum parasites. This study contains a total of 1024 Anopheles mosquitoes: 187 Anopheles gambiae and 837 Anopheles funestus samples collected in high malaria transmission areas of Mozambique between March and June of 2016. Sanger sequencing will be used to determine the prevalence of known resistance alleles for anti-malarial drugs: chloroquine resistance transporter (pfcrt), multidrug resistance (pfmdr1) gene, dihydropteroate synthase (pfdhps) and dihydrofolate reductase (pfdhfr). We compare prevalence of resistance between abdomen and head/thorax in order to determine whether drug resistant parasites are disproportionately hindered during their passage through the midgut lumen. A statistically significant difference between resistance alleles in the two studied body sections supports the efficacy of new anti-malarial gene surveillance strategies in areas of high malaria transmission.
Obesity has reached epidemic proportions all around the world, and it has doubled in prevalence in both adults and children in over 70 countries from 1980 to 2015 (Afshin et al., 2017). Excessive weight gain in this proportion has been shown to negatively affect human cognition, reward neurocircuitry, stress responsiveness, and quality of life (Morris et al., 2015). Obesity is an example of a complex interaction between the environment (i.e., high-fat diets) and heredity (i.e., polygenic patterns of inheritance). The overconsumption of a high-fat diet (HFD) is an environmental factor that commonly induces weight gain (Hariri & Thibault, 2010). Two dietary-induced phenotypes have been observed in rats as a bimodal distribution of weight gain: obesity-prone (OP) and obesity-resistant (OR). Levin et al. (1997) investigated male and female HFD-fed Sprague-Dawley rats designated as OR when their weight gains were less than the heaviest chow-fed controls, and OP when their weight gains were greater than the heaviest chow-fed controls. OP rats showed greater weight gain, similar energy intake (EI), and similar feed efficiency (FE) compared to OR rats. Pagliassotti et al. (1997) designated male HFD-fed Wistar rats as OP and OR based on upper and lower tertiles of weight gain. OP rats displayed greater weight gain and EI than OR rats. These investigations highlight a predicament regarding rodent research in obesity: independent variables such as rat age, gender, strain, distribution of dietary macronutrients, and fatty acid composition of HFD and chow vary considerably, making it challenging to generalize data. Our experiment utilized outbred male Sprague-Dawley rats (5-6 weeks) administered a chow diet (19% energy from fat; 3.1 kcal/g) and a lard-based HFD (60% energy from fat; 5.24 kcal/g) over eight weeks. Separate rat populations were examined over three consecutive years (2017-2020), and independent obesogenic environmental variables were controlled. We investigated the persistence of weight gain, EI, and FE in HFD-fed rats inclusive of a population of designated OP and OR rats based on tertiles of weight gain. We define persistence as being p > 0.05. We hypothesize that the profiles (periodic data) of the dependent variables (weight gain, EI, FE) will be similar and persistent throughout the three separate years, but the magnitudes (cumulative data) of the dependent variables will differ. Our findings demonstrate that HFD, OP, and OR groups were persistent for periodic and cumulative weight gain, along with FE across the three consecutive independent years. Our findings also demonstrate impersistence for periodic EI in all groups, along with impersistence in cumulative EI for CHOW, OP, and OR groups. Therefore, our results allude to an inconsistent relationship between EI and weight gain, indicating that EI does not completely explain weight gain. Thus, the weakness between EI and weight gain relationship may be attributed to a polygenic pattern of inheritance, possibly signaling a weight setpoint regardless of EI.
Obesity has reached epidemic proportions all around the world, and it has doubled in prevalence in both adults and children in over 70 countries from 1980 to 2015 (Afshin et al., 2017). Excessive weight gain in this proportion has been shown to negatively affect human cognition, reward neurocircuitry, stress responsiveness, and quality of life (Morris et al., 2015). Obesity is an example of a complex interaction between the environment (i.e., high fat diets) and heredity (i.e., polygenic patterns of inheritance). The overconsumption of a high-fat diet (HFD) is an environmental factor that commonly induces weight gain (Hariri & Thibault, 2010). Two dietary-induced phenotypes have been observed in rats as a bimodal distribution of weight gain: obesity-prone (OP) and obesity-resistant (OR). Levin et al. (1997) investigated male and female HFD-fed Sprague-Dawley rats designated as OR when their weight gains were less than the heaviest chow-fed controls, and OP when their weight gains were greater than the heaviest chow-fed controls. OP rats showed greater weight gain, similar energy intake (EI), and similar feed efficiency (FE) compared to OR rats. Pagliassotti et al. (1997) designated male HFD-fed Wistar rats as OP and OR based on upper and lower tertiles of weight gain. OP rats displayed greater weight gain and EI than OR rats. These investigations highlight a predicament regarding rodent research in obesity: independent variables such as rat age, gender, strain, distribution of dietary macronutrients, and fatty acid composition of HFD and chow vary considerably, making it challenging to generalize data. Our experiment utilized outbred male Sprague-Dawley rats (5-6 weeks) administered a chow diet (19% energy from fat; 3.1 kcal/g) and a lard-based HFD (60% energy from fat; 5.24 kcal/g) over eight weeks. Separate rat populations were examined over three consecutive years (2017-2020), and independent obesogenic environmental variables were controlled. We investigated the persistence of weight gain, EI, and FE in HFD-fed rats inclusive of a population of designated OP and OR rats based on tertiles of weight gain. We define persistence as being p > 0.05. We hypothesize that the profiles (periodic data) of the dependent variables (weight gain, EI, FE) will be similar and persistent throughout the three separate years, but the magnitudes (cumulative data) of the dependent variables will differ. Our findings demonstrate that HFD, OP, and OR groups were persistent for periodic and cumulative weight gain, along with FE across the three consecutive independent years. Our findings also demonstrate impersistence for periodic EI in all groups, along with impersistence in cumulative EI for CHOW, OP, and OR groups. Therefore, our results allude to an inconsistent relationship between EI and weight gain, indicating that EI does not completely explain weight gain. Thus, the weakness between EI and weight gain relationship may be attributed to a polygenic pattern of inheritance, possibly signaling a weight setpoint regardless of EI.