Solving an Infectious Disease Model considering Its Anatomical Variables with Stochastic Numerical Procedures

The aim of the current work is to perform the numerical investigation of the infectious disease based on the nonlinear fractional order prey-predator model using the Levenberg–Marquardt backpropagation (LMB) based on the artificial neuron networks (ANNs), i.e., LMBNNs. The fractional prey-predator model is classified into three categories, the densities of the susceptible, infected prey, and predator populations. The statistics proportions for solving three different variations of the infectious disease based on the fractional prey-predator model are designated for training 80% and 10% for both validation and testing. The numerical actions are performed using the LMBNNs to solve the infectious disease based on the fractional prey-predator model, and comparison is performed using the database Adams–Bashforth–Moulton approach. The infectious disease based on the fractional prey-predator model is solved using the LMBNNs to reduce the mean square error (M.S.E). In order to validate the exactness, capability, consistency, and competence of the proposed LMBNNs, the numerical procedures using the correlation, M.S.E, regression, and error histograms are drawn.

An eco-epidemiological model with general functional response of predator to prey

We consider a nonautonomous eco-epidemiological model with general functions for predation on infected and uninfected preys as well as general functions associated to the vital dynamics of the susceptible prey and predator populations. We obtain persistence and extinction results for the infected prey based on assumptions on auxiliary systems constructed from the disease-free system. We moreover consider an iterative process that can improve the extinction results. We apply our results to general eco-epidemiological models that include several examples existent in the literature.

The visual ecology of selective predation: Are unhealthy hosts less stealthy hosts?

Predators can strongly influence disease transmission and evolution, particularly when they prey selectively on infected hosts. Although selective predation has been observed in numerous systems, why predators select infected prey remains poorly understood. Here, we use a model of predator vision to test a longstanding hypothesis as to the mechanistic basis of selective predation in a Daphnia-microparasite system, which serves as a model for the ecology and evolution of infectious diseases. Bluegill sunfish feed selectively on Daphnia with a variety of parasites, particularly in water uncolored by dissolved organic carbon. The leading hypothesis for selective predation in this system is that infection-induced changes in the appearance of Daphnia render them more visible to bluegill. Rigorously evaluating this hypothesis requires that we quantify the effect of infection on the visibility of prey from the predator’s perspective, rather than our own. Using a model of the bluegill visual system, we show that the three common parasites, Metschnikowia bicuspidata, Pasteuria ramosa and Spirobacillus cienkowskii, increase the opacity of Daphnia, rendering infected Daphnia darker against the background of downwelling light. As a result of this increased brightness contrast, bluegill can see infected Daphnia at greater distances than uninfected Daphnia – between 19-33% further, depending on the parasite. Pasteuria and Spirobacillus also increase the chromatic contrast of Daphnia. Contrary to expectations, the visibility Daphnia was not strongly impacted by water color in our model. Our work generates hypotheses about which parasites are most likely affected by selective predation in this important model system and establishes visual models as a valuable tool for understanding ecological interactions that impact disease transmission.

Effects of parasites and predators on nociception: decreases analgesia reduces overwinter survival in root voles (Rodentia: Cricetidae)

Growing evidence suggests that parasite-infected prey is more vulnerable to predation. However, the mechanism underlying this phenomenon is obscure. In small mammals, analgesia induced by environmental stressors is a fundamental component of the defensive repertoire, promoting defensive responses. Thus, the reduced analgesia may impair the defensive ability of prey and increase their predation risk. This study aimed to determine whether coccidia infection increases the vulnerability to predation in root voles, Microtus oeconomus (Pallas, 1776), by decreased analgesia. Herein, a predator stimulus and parasitic infection were simulated in the laboratory via a two-level factorial experiment, then, the vole nociceptive responses to an aversive thermal stimulus were evaluated. Further, a field experiment was performed to determine the overwinter survival of voles with different nociceptive responses via repeated live trapping. The coccidia-infected voles demonstrated reduced predator-induced analgesia following exposure to predator odor. Meanwhile, pain-sensitive voles had lower overwinter survival than pain-inhibited voles in enclosed populations throughout the duration of the experiment. Our findings suggest that coccidia infection attenuates predator-induced analgesia, resulting in an increased vulnerability to predation.

Dynamical of Ratio-Dependent Eco-epidemical Model with Prey Refuge

This paper discusses the dynamic analysis of three species in the eco-epidemiology model by considering the ratio-dependent function and prey refuge. The prey refuge is applied under the fact that infected prey has protection instincts that allow it to reduce predation risk. Here, we get the boundedness and three equilibrium points where are existence under certain conditions. In the model, three equilibrium points are locally asymptotically stable and one of the equilibrium points is globally asymptotically stable. We find that the system undergoes Hopf bifurcation around the interior equilibrium point by choosing as a bifurcation parameter. We also find a condition for uniform persistence. Finally, several simulations of numerical are performed not only to illustrate the analytical results but also to illustrate the effect of the prey refuge.

Analisis dinamik model predator-prey tipe Gause dengan wabah penyakit pada prey

This article studies the dynamics of a Gause-type predator-prey model with infectious disease in the prey. The constructed model is a deterministic model which assumes the prey is divided into two compartments i.e. susceptible prey and infected prey, and both of them are hunted by predator bilinearly. It is investigated that there exist five biological equilibrium points such as all population extinction point, infected prey and predator extinction point, infected prey extinction point, predator extinction point, and co-existence point. We find that all population extinction point always unstable while others are conditionally locally asymptotically stable. Numerical simulations, as well as the phase portraits, are given to support the analytical results.

Dynamics of an Eco-Epidemic Predator–Prey Model Involving Fractional Derivatives with Power-Law and Mittag–Leffler Kernel

In this paper, we consider a fractional-order eco-epidemic model based on the Rosenzweig–MacArthur predator–prey model. The model is derived by assuming that the prey may be infected by a disease. In order to take the memory effect into account, we apply two fractional differential operators, namely the Caputo fractional derivative (operator with power-law kernel) and the Atangana–Baleanu fractional derivative in the Caputo (ABC) sense (operator with Mittag–Leffler kernel). We take the same order of the fractional derivative in all equations for both senses to maintain the symmetry aspect. The existence and uniqueness of solutions of both eco-epidemic models (i.e., in the Caputo sense and in ABC sense) are established. Both models have the same equilibrium points, namely the trivial (origin) equilibrium point, the extinction of infected prey and predator point, the infected prey free point, the predator-free point and the co-existence point. For a model in the Caputo sense, we also show the non-negativity and boundedness of solution, perform the local and global stability analysis and establish the conditions for the existence of Hopf bifurcation. It is found that the trivial equilibrium point is a saddle point while other equilibrium points are conditionally asymptotically stable. The numerical simulations show that the solutions of the model in the Caputo sense strongly agree with analytical results. Furthermore, it is indicated numerically that the model in the ABC sense has quite similar dynamics as the model in the Caputo sense. The essential difference between the two models is the convergence rate to reach the stable equilibrium point. When a Hopf bifurcation occurs, the bifurcation points and the diameter of the limit cycles of both models are different. Moreover, we also observe a bistability phenomenon which disappears via Hopf bifurcation.

Occurrence of antibodies anti-Toxoplasma gondii among sheltered and free-roaming cats within a university campus

The present study aimed to assess anti-T. gondii antibodies in sheltered and free-roaming cats within a university campus that has an overlapping population of humans and livestock. A total of 51 cats were tested for anti-T. gondii antibodies using the indirect immunofluorescent antibody test. Overall, 8/51 cats (15.7%) were seropositive. Cats were more likely to be seropositive when free-roaming (p= 0.008) and with presence of skin lesions (p= 0.042), and less likely with < 1 year of age (p= 0.021), probably due to higher environmental exposure and infected prey consumption. The presence of seropositive free-roaming cats whose areas overlapped those occupied by humans and livestock may suggest an increased on-campus chance of T. gondii occurrence.

Predator-dependent transmissible disease spreading in prey under Holling type-II functional response

This paper focusses on developing two species, where only prey species suffers by a contagious disease. We consider the logistic growth rate of the prey population. The interaction between susceptible prey and infected prey with predator is presumed to be ruled by Holling type II and I functional response, respectively. A healthy prey is infected when it comes in direct contact with infected prey, and we also assume that predator-dependent disease spreads within the system. This research reveals that the transmission of this predator-dependent disease can have critical repercussions for the shaping of prey–predator interactions. The solution of the model is examined in relation to survival, uniqueness and boundedness. The positivity, feasibility and the stability conditions of the fixed points of the system are analysed by applying the linearization method and the Jacobian matrix method.