Hyperparasitism, a Mutualistic Phenomenon

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.

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.


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.


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.


1964 ◽  
Vol 42 (5) ◽  
pp. 745-765 ◽  
Author(s):  
T. Burnett

Two populations of Trialeurodes vaporariorum (Westw.) and its chalcid parasite Encarsia formosa Gahan were reared on tomato plants in the greenhouse at 72–76 °F for 26 weeks. Although the abundance of both species fluctuated with peaks of increasing amplitude, the population that was initially larger remained so throughout the period of sampling because the parasite inflicted similar rates of mortality in both cases. The fluctuations of the two separate populations were synchronized throughout the period of propagation. Host mortality, which resulted either from almost immediate killing of host scales following attack by adult parasites or from death of host larvae following parasitization and development of parasite progeny, was determined by parasite density, host size, and possibly by a number of other factors such as the age structure of host larval populations, age of adult parasites, and succulence of leaves on which the host larvae developed. The interaction of host and parasite produced cycles in the age structures of host and parasite populations that, in turn, influenced the interaction of the two species. The death of host larvae following attack by adult parasites was a form of host protection, as it ensured the rapid decline in the abundance of the parasite population and was, therefore, the primary factor in the maintenance of the host–parasite system.


Parasitology ◽  
1980 ◽  
Vol 81 (2) ◽  
pp. 405-421 ◽  
Author(s):  
Anne E. Keymer

SUMMARYAn experimental study of the effects of parasitism by H. diminuta on the intermediate host, Tribolium confusum, is described. No density- dependent constraints on parasite establishment within individual hosts are evident, although a reduction in cysticercoid size at high parasite burdens is demonstrated. The relationship between parasite burden, host mortality and host fecundity is investigated. Host mortality is linearly related to parasite burden, whereas the relationship between parasite burden and host fecundity is non-linear. There is no difference in viability between eggs from infected and uninfected females. The generative causes of these effects are not investigated experimentally, although it is postulated that survival is related to the degree of damage to the midgut wall caused by parasite penetration, and fecundity to the biomass of parasites harboured by the host. The significance of these effects is discussed in relation to the overall dynamics of the host-parasite association.


Author(s):  
Jose M. Riascos ◽  
Viviana Villegas ◽  
Ignacio Cáceres ◽  
Jorge E. Gonzalez ◽  
Aldo S. Pacheco

Jellyfish display strong population variability. Competitive interactions between fish and jellyfish have been depicted as a major mechanism controlling this variability. Biological associations involving jellyfish are, however, more diverse than predation–prey interactions and remain poorly understood. Parasitic associations in particular may have relevant effects on jellyfish host populations. We studied basic patterns (temporal patterns of parasite intensity–biomass and the distribution pattern of parasites among hosts) of the association between the parasitic anemone Peachia chilensis and its scyphozoan host, Chrysaora plocamia. The mean number of parasites per host (MI) was high (average = 465) and showed significant differences during the pelagic life phase of the medusa. The mean biomass of parasites per host was also significantly different among months but showed a different temporal pattern to that of MI, which may reflect recruitment pulses of parasitic larvae. The mean biomass of P. chilensis per host averaged 56.3 mg ash-free dry mass, which represents a trophic flow of energy probably linking pelagic and benthic food webs. The distribution of parasites among hosts was best fitted to the negative binomial distribution model, as typical for host–parasite systems. We concluded that the parasite-induced host mortality and reduction of fecundity, represented by parasitic castration, is restricted to a few hosts and is therefore under the expected levels that characterize the dynamic equilibrium of host–parasite systems.


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.


2021 ◽  
Author(s):  
Huajing Wang ◽  
Shuo Li ◽  
Zhao Cui ◽  
Tingting Qin ◽  
Hang Shi ◽  
...  

ABSTRACTMalaria is a fatal disease that presents clinically as a continuum of symptoms and severity, which are determined by complex host-parasite interactions. Clearance of infection is believed to be accomplished by the spleen and mononuclear phagocytic system (MPS), both in the presence and absence of artemisinin treatment. The spleen filters infected RBCs from circulation through immune-mediated recognition of the infected RBCs followed by phagocytosis. Using different strains of mice infected with P. berghei K173 (PbK173), the mechanisms leading to splenomegaly, histopathology, splenocyte activation and proliferation, and their relationship to control of parasitemia and host mortality were examined. Survival time of mice infected with PbK173 varied, although the infection was uniformly lethal. Mice of the C57BL/6 strain were the most resistant, while mice of the strain ICR were the most susceptible. BALB/c and KM mice were intermediate. In the course of PbK173 infection, both strains of mice experienced significant splenomegaly. Parasites were observed in the red pulp at 3 days post infection in all animals. All spleens retained late trophozoite stages as well as a fraction of earlier ring-stage parasites. The percentages of macrophages in infected C57BL/6 and KM mice were higher than uninfected mice on 8 dpi. Spleens of infected ICR and KM mice exhibited structural disorganization and remodeling. Furthermore, parasitemia was significantly higher in KM versus C57BL/6 mice at 8 dpi. The percentages of macrophages in ICR infected mice were lower than uninfected mice, and the parasitemia was higher than other strains. The results presented here demonstrate the rate of splenic mechanical filtration and the splenic macrophages likely contribute to an individual’s total parasite burden. This in turn can influence the pathogenesis of malaria. Finally, different genetic backgrounds of mice have different splenic mechanisms for controlling malaria infection.


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