THEORETICAL AND MATHEMATICAL APPROACH OF SOME REGULATION MECHANISMS IN A MARINE HOST-PARASITE SYSTEM

1995 ◽  
Vol 03 (02) ◽  
pp. 559-568 ◽  
Author(s):  
M. LANGLAIS ◽  
P. SILAN

Host-parasite systems offer such a complex behaviour that few quantitative analysis of their coupled dynamics have been performed. Many intertwinned factors play a role, such as intensity-dependent (intra or interspecific competition, pathogeny, immunological reactions) and/or intensity-independent (abiotic factors, host ethology). Most biomathematical approaches to host-parasite systems are concerned with infectious processes. Corresponding epidemiological models are not well-adapted to macroparasites whose demographical behaviour is quite specific: host mortality, parasite fertility and sometimes recruitment mechanisms depend on the amount of already fixed parasites on a given host and not on the mere existence of parasites. Overdispersion processes are fundamental and determine for a large part the regulation of both populations. A central issue is therefore a reliable description of these processes and their interactions with the global dynamics of the system. Our goal is to develop a mixed deterministic and stochastic model describing the dynamics of a host-parasite system (fish-helminth parasite) having a direct cycle within a marine environment. A dynamical analysis combining a deterministic approach and a stochastic one adapted to macroparasites allows the introduction of spatial and temporal heterogeneities. A particular effort is made towards the recruitment process.

Parasitology ◽  
2010 ◽  
Vol 137 (11) ◽  
pp. 1671-1680 ◽  
Author(s):  
J. F. MARQUES ◽  
M. J. SANTOS ◽  
H. N. CABRAL

SUMMARYMacroparasites are generally aggregated within their hosts with infection and aggregation levels resulting from a continuous arms race between maintaining high mating probability and host mortality low for which host and environmentally related factors contribute to some extent. Here, infection and aggregation patterns of the macroendoparasites infecting the flatfish Citharus linguatula, Arnoglossus laterna, Lepidorhombus boscii, Scophthalmus rhombus and Platichthys flesus in 3 areas along the Portuguese coast were analysed. Of the 21 macroendoparasite species found only 1 infected all hosts and most were host or area exclusive. For each host-parasite system, values of the indices varied between areas and macroendoparasites were not always aggregated; in fact, some macroendoparasites were generally uniformly distributed, which can be related to specific density-dependent regulation mechanisms. No general pattern was found for infection or aggregation levels of the 3 species infecting more than 2 hosts along the Portuguese coast, i.e. Lecithochirium rufoviride, Nybelinia lingualis and Anisakis simplex s.l., suggesting that regulation mechanisms are not species specific but are locally determined, with host ecology playing a significant role.


Parasitology ◽  
1969 ◽  
Vol 59 (3) ◽  
pp. 649-661 ◽  
Author(s):  
L. H. Ractliffe ◽  
H. M. Taylor ◽  
J. H. Whitlock ◽  
W. R. Lynn

Most epidemiological models assume that disease is the inevitable outcome of infection (see Bailey, 1957). Yet as Dubos (1965) has said; ‘Throughout nature, infection without disease is the rule rather than the exception’. There are, in fact, many diseases whose distribution cannot be explained solely by a consideration of the probabilities of host parasite encounters. In these cases, a diseased state is only one possible outcome of an interaction between parasite phenotypes, host phenotypes and the external environment. Haemonchosis is an example of such a disease and has been studied extensively in quantitative terms (see Whitlock & Georgi, 1968).


Parasitology ◽  
1978 ◽  
Vol 76 (2) ◽  
pp. 119-157 ◽  
Author(s):  
R. M. Anderson

SummaryThe nature of parasitism at the population level is defined in terms of the parasite's influence on the natural intrinsic growth rate of its host population. It is suggested that the influence on this rate is related to the average parasite burden/host and hence to the statistical distribution of parasites within the host population.Theoretical models of host–parasite associations are used to assess the regulatory influence of parasitic species on host population growth. Model predictions suggest that three specific groups of population processes are of particular importance: over-dispersion of parasite numbers/host, density dependence in parasite mortality or reproduction and parasite-induced host mortality that increases faster than linearly with the parasite burden. Other population mechanisms are shown to have a destabilizing influence, namely: parasite-induced reduction in host reproductive potential, direct parasite reproduction within the host and time delays in the development of transmission stages of the parasite.These regulatory and destabilizing processes are shown to be commonly observed features of natural host-parasite associations. It is argued that interactions in the real world are characterized by a degree of tension between these regulatory and destabilizing forces and that population rate parameter values in parasite life-cycles are very far from being a haphazard selection of all numerically possible values. It is suggested that evolutionary pressures in observed associations will tend to counteract a strong destabilizing force by an equally strong regulatory influence. Empirical evidence is shown to support this suggestion in, for example, associations between larval digeneans and molluscan hosts (parasite-induced reduction in host reproductive potential counteracted by tight density-dependent constraints on parasite population growth), and interactions between protozoan parasites and mammalian hosts (direct parasite reproduction counteracted by a well-developed immunological response by the host).The type of laboratory and field data required to improve our understanding of the dynamical properties of host–parasite population associations is discussed and it is suggested that quantitative measurement of rates of parasite-induced host mortality, degrees of over-dispersion, transmission rates and reproductive and mortality rates of both host and parasite would provide an important first step. The value of laboratory work in this area is demonstrated by reference to studies which highlight the regulatory influence of parasitic species on host population growth.


1963 ◽  
Vol 95 (7) ◽  
pp. 716-720 ◽  
Author(s):  
S. E. Flanders

AbstractHyperparasitism is a mortality factor that generally is beneficial to the continuous reproduction of the species involved.The parasites of a primary parasite of a phytophagous insect may exhibit two distinctive types of secondary relations to that insect. These types are defined as follows:Direct secondary parasitism: that type of host-parasite symbiosis where only the primary's parasitized host or the primary itself is attacked.Indirect secondary parasitism: that type of host-parasite symbiosis where the primary's phytophagous host is attacked whether parasitized or not parasitized.The host mortality caused by direct secondary parasitism may greatly exceed that caused by indirect secondary parasitism, this being manifested when the percentage of the primary parasitization of the phytophagous host is minimal.


1962 ◽  
Vol 94 (7) ◽  
pp. 673-679 ◽  
Author(s):  
T. Burnett

It is not unusual for parasite attack on insect hosts to have different consequences for individuals of the same species. An indication of the variation in types of alternative effects is given by a consideration of three host-parasite relationships. First, although most hosts in a population are susceptible to parasitization, some are immune to attack: about one in 3,000 larvae of the Mediterranean flour moth, Anagasta kühniella (Zeller), was found by Payne (1934) to be immune to attack by Bracon hebetor Say. Second, tile morphology of hosts may be modified differentially by parasitism: unhatched eggs of Aphdius platensis Brethes exert a juvenilizing effect on nymphs of Aphis craccivora Koch whereas parasite larvae sometimes cause the appearance of adult characters (Johnson, 1959). Third, some hosts are successfully parasitized whereas others are killed long before parasite progeny can mature: adult females of Metaphycus helvolus (Com.) kill the black scale, Saissetin oleae (Bern.), by parasitization, by mutilation with the ovipositor, and by host-feeding at wounds made by the ovipositor. Field tests showed that up to 97 per cent of a black-scale infestation may be killed by the parasite over a period of several months.


1994 ◽  
Vol 346 (1317) ◽  
pp. 283-293 ◽  

Genetic specificity occurs in many host-parasite systems. Each host can recognize and resist only a subset of parasites; each parasite can grow only on particular hosts. Biochemical recognition systems determine which matching host and parasite genotypes result in resistance or disease. Recognition systems are often associated with widespread genetic polymorphism in the host and parasite populations. I describe four systems with matching host—parasite polymorphisms: plant-pathogen interactions, nuclear—cytoplasmic conflict in plants, restriction enzymes in bacterial defence against viruses, and bacterial plasmids that compete by toxin production and toxin immunity. These systems highlight several inductive problems. For example, the observed patterns of resistance and susceptibility between samples of hosts and parasites are often used to study polymorphism. The detectable polymorphism by this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies that commonly occur in host-parasite systems. Another problem is that different matching systems may lead either to low frequencies of host resistance and common parasites, or to common resistance and rare parasites. Thus low levels of host resistance or rare parasites do not imply that parasitism is an unimportant evolutionary force on host diversity. Knowledge of biochemical recognition systems and dynamical analysis of models provide a framework for analysing the widespread polymorphisms in host-parasite genetics.


2021 ◽  
Author(s):  
Rimpi Pal ◽  
Afroz ◽  
Ayub Khan ◽  
MOHMAD AUSIF PADDER

Abstract Fractional order tumor-immune interaction models are being frequently used for understanding the complex behaviour of immune system and tumor growth. In this paper, a generalized fractional order tumor-immune interaction model has been developed by introducing immunotherapy (IL2) as third variable in the model. The study of generalized model is done by using conformable fractional order derivative. The stability analysis is done for both fractional order tumor model and its conformable fractional order version. By considering some biological fixed points for both versions of the model, the stability analysis around these fixed points shows that both the systems are stable at some fixed point under some stability conditions, which are defined in the model analysis. The numerical and graphical analysis is also done for both the systems by varying two parameters and keeping other parameters fixed for better understanding the dynamics of proposed model.


2015 ◽  
Vol 282 (1821) ◽  
pp. 20152097 ◽  
Author(s):  
Katja-Riikka Louhi ◽  
Lotta-Riina Sundberg ◽  
Jukka Jokela ◽  
Anssi Karvonen

Most studies of virulence of infection focus on pairwise host–parasite interactions. However, hosts are almost universally co-infected by several parasite strains and/or genotypes of the same or different species. While theory predicts that co-infection favours more virulent parasite genotypes through intensified competition for host resources, knowledge of the effects of genotype by genotype (G × G) interactions between unrelated parasite species on virulence of co-infection is limited. Here, we tested such a relationship by challenging rainbow trout with replicated bacterial strains and fluke genotypes both singly and in all possible pairwise combinations. We found that virulence (host mortality) was higher in co-infections compared with single infections. Importantly, we also found that the overall virulence was dependent on the genetic identity of the co-infecting partners so that the outcome of co-infection could not be predicted from the respective virulence of single infections. Our results imply that G × G interactions among co-infecting parasites may significantly affect host health, add to variance in parasite fitness and thus influence evolutionary dynamics and ecology of disease in unexpected ways.


Parasitology ◽  
1996 ◽  
Vol 113 (3) ◽  
pp. 303-309 ◽  
Author(s):  
S. T. Ashworth ◽  
C. R. Kennedy ◽  
G. Blanc

SUMMARYDensity-dependent effects of Anguillicola crassus larval infections in the copepod intermediate host were examined experimentally. Three species of copepods (Cyclops vicinus, C. viridis and C. fuscus) were subjected to a range of doses of larval A. crassus within infection arenas. Prevalence, intensity and parasite dispersion (variance: mean abundance) values increase and then approach an asymptote as infection dose increases. Infection parameters differ between species of copepod. Increasing temperature has a negative effect on the establishment of the parasite population within the intermediate host. Parasite-induced host mortality increases with dose. These mechanisms have the potential to regulate populations of A. crassus larvae within the copepod population and hence the whole suprapopulation.


Parasitology ◽  
1982 ◽  
Vol 85 (2) ◽  
pp. 373-398 ◽  
Author(s):  
R. M. Anderson ◽  
D. M. Gordon

SUMMARYThe paper examines the factors which generate various patterns of dispersion in the distribution of parasites within their host populations. Particular emphasis is placed on the role played by chance elements in the growth and decay of parasite populations and on the influence of different types of demographic processes. It is argued that observed distributions are dynamic, rather than static, entities generated by opposing forces, some acting to create over-dispersion and others acting to generate under-dispersion. Monte Carlo simulation experiments, based on probability models of the growth and decay of host and parasite populations, are used to study the dynamics of parasite dispersion. Attention is specifically focused on the role played by parasite-induced host mortality. It is shown that, for certain types of host–parasite associations, convex curves of mean parasite abundance in relation to age (age-intensity curves), concomitant with a decline in the degree of dispersion in the older age classes of hosts, may be evidence of the induction of host mortality by parasite infection. Empirical evidence is examined in light of this prediction. In general, however, simulation studies highlight the technical difficulties inherent in establishing clear evidence of parasite-induced host mortality from ecological studies of hosts and parasites in their natural habitats.


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