Host life-history variation in response to parasitism

Parasitology ◽  
1985 ◽  
Vol 90 (1) ◽  
pp. 205-216 ◽  
Author(s):  
D. J. Minchella

Over half of all living species of plants and animals are parasitic, which by definition involves intimate association with and unfavourable impact on hosts (Price, 1980). This paper will only consider parasites whose ‘unfavourable impact’ adversely affects the birth and/or mortality rates of their hosts (Anderson, 1978). Most organisms are potential hosts and must deal with the problem of parasitism. The probability of parasitic infection of a host is influenced by both environmental and genetic factors. Traditionally it was assumed that a host was either resistant or susceptible to a particular parasite and therefore the interaction between a parasite and potential host had only two possible outcomes: either the resistant host rebuffed the parasitic attack and remained uninfected or the parasite successfully invaded and significantly reduced the reproductive success of the susceptible host. This approach, however, ignored the intraspecific genetic variation present within both host and parasite populations (Wakelin, 1978). Since the outcome is determined by the interaction of a finite set of host genes and parasite genes, genetic variation in host susceptibility and parasite infectivity (Richards, 1976; Wakelin, 1978) suggests that more than two outcomes are possible. Variation in host and parasite genomes does not begin and end at the susceptibility/infectivity loci. Other genes may also influence the outcome of host–parasite interactions by altering the life-history patterns of hosts and parasites, and lead to a variety of outcomes.

2018 ◽  
Author(s):  
Jacob W. Malcom ◽  
Thomas E. Juenger ◽  
Mathew A. Leibold

ABSTRACTBackgroundIdentifying the molecular basis of heritable variation provides insight into the underlying mechanisms generating phenotypic variation and the evolutionary history of organismal traits. Life history trait variation is of central importance to ecological and evolutionary dynamics, and contemporary genomic tools permit studies of the basis of this variation in non-genetic model organisms. We used high density genotyping, RNA-Seq gene expression assays, and detailed phenotyping of fourteen ecologically important life history traits in a wild-caught panel of 32Daphnia pulexclones to explore the molecular basis of trait variation in a model ecological species.ResultsWe found extensive phenotypic and a range of heritable genetic variation (~0 < H2< 0.44) in the panel, and accordingly identify 75-261 genes—organized in 3-6 coexpression modules—associated with genetic variation in each trait. The trait-related coexpression modules possess well-supported promoter motifs, and in conjunction with marker variation at trans- loci, suggest a relatively small number of important expression regulators. We further identify a candidate genetic network with SNPs in eight known transcriptional regulators, and dozens of differentially expressed genes, associated with life history variation. The gene-trait associations include numerous un-annotated genes, but also support several a priori hypotheses, including an ecdysone-induced protein and several Gene Ontology pathways.ConclusionThe genetic and gene expression architecture ofDaphnialife history traits is complex, and our results provide numerous candidate loci, genes, and coexpression modules to be tested as the molecular mechanisms that underlieDaphniaeco-evolutionary dynamics.


2020 ◽  
Vol 287 (1930) ◽  
pp. 20201017
Author(s):  
James R. Whiting ◽  
Muayad A. Mahmud ◽  
Janette E. Bradley ◽  
Andrew D. C. MacColl

Seasonal disease and parasitic infection are common across organisms, including humans, and there is increasing evidence for intrinsic seasonal variation in immune systems. Changes are orchestrated through organisms' physiological clocks using cues such as day length. Ample research in diverse taxa has demonstrated multiple immune responses are modulated by photoperiod, but to date, there have been few experimental demonstrations that photoperiod cues alter susceptibility to infection. We investigated the interactions among photoperiod history, immunity and susceptibility in laboratory-bred three-spined stickleback (a long-day breeding fish) and its external, directly reproducing monogenean parasite Gyrodactylus gasterostei . We demonstrate that previous exposure to long-day photoperiods (PLD) increases susceptibility to infection relative to previous exposure to short days (PSD), and modifies the response to infection for the mucin gene muc2 and Treg cytokine foxp3a in skin tissues in an intermediate 12 L : 12 D photoperiod experimental trial. Expression of skin muc2 is reduced in PLD fish, and negatively associated with parasite abundance. We also observe inflammatory gene expression variation associated with natural inter-population variation in resistance, but find that photoperiod modulation of susceptibility is consistent across host populations. Thus, photoperiod modulation of the response to infection is important for host susceptibility, highlighting new mechanisms affecting seasonality of host–parasite interactions.


Parasitology ◽  
1998 ◽  
Vol 116 (S1) ◽  
pp. S47-S55 ◽  
Author(s):  
J. C. Koella ◽  
P. Agnew ◽  
Y. Michalakis

SummarySeveral recent studies have discussed the interaction of host life-history traits and parasite life cycles. It has been observed that the life-history of a host often changes after infection by a parasite. In some cases, changes of host life-history traits reduce the costs of parasitism and can be interpreted as a form of resistance against the parasite. In other cases, changes of host life-history traits increase the parasite's transmission and can be interpreted as manipulation by the parasite. Alternatively, changes of host's life-history traits can also induce responses in the parasite's life cycle traits. After a brief review of recent studies, we treat in more detail the interaction between the microsporidian parasite Edhazardia aedis and its host, the mosquito Aedes aegypti. We consider the interactions between the host's life-history and parasite's life cycle that help shape the evolutionary ecology of their relationship. In particular, these interactions determine whether the parasite is benign and transmits vertically or is virulent and transmits horizontally.Key words: host-parasite interaction, life-history, life cycle, coevolution.


2005 ◽  
Vol 288 (5) ◽  
pp. R1226-R1236 ◽  
Author(s):  
Mauricio Avigdor ◽  
Shannon D. Sullivan ◽  
Paul D. Heideman

Natural variation in neuroendocrine traits is poorly understood, despite the importance of variation in brain function and evolution. Most rodents in the temperate zones inhibit reproduction and other nonessential functions in short winter photoperiods, but some have little or no reproductive response. We tested whether genetic variability in reproductive seasonality is related to individual differences in the neuronal function of the gonadotropin-releasing hormone network, as assessed by the number and location of mature gonadotropin-releasing hormone-secreting neurons under inhibitory and excitatory photoperiods. The experiments used lines of Peromyscus leucopus previously developed by selection from a wild population. One line contained individuals reproductively inhibited by short photoperiod, and the other line contained individuals nonresponsive to short photoperiod. Expression of mature gonadotropin-releasing hormone (GnRH) immunoreactivity in the brain was detected using SMI-41 antibody in the single-labeled avidin-biotin-peroxidase-complex method. Nonresponsive mice had 50% more immunoreactive GnRH neurons than reproductively inhibited mice in both short- and long-day photoperiods. The greatest differences were in the anterior hypothalamus and preoptic areas. In contrast, we detected no significant within-lines differences in the number or location of immunoreactive GnRH neurons between photoperiod treatments. Our data indicate that high levels of genetic variation in a single wild population for a specific neuronal trait are related to phenotypic variation in a life history trait, i.e., winter reproduction. Variation in GnRH neuronal activity may underlie some of the natural reproductive and life history variation observed in wild populations of P. leucopus. Similar genetic variation in neuronal traits may be present in humans and other species.


2018 ◽  
Author(s):  
Elizabeth ML Duxbury ◽  
Jonathan P Day ◽  
Davide Maria Vespasiani ◽  
Yannik Thüringer ◽  
Ignacio Tolosana ◽  
...  

AbstractIt is common to find considerable genetic variation in susceptibility to infection in natural populations. We have investigated whether natural selection increases this variation by testing whether host populations show more genetic variation in susceptibility to pathogens that they naturally encounter than novel pathogens. In a large cross-infection experiment involving four species of Drosophila and four host-specific viruses, we always found greater genetic variation in susceptibility to viruses that had coevolved with their host. We went on to examine the genetic architecture of resistance in one host species, finding that there are more major-effect genetic variants in coevolved host-parasite interactions. We conclude that selection by pathogens increases genetic variation in host susceptibility, and much of this effect is caused by the occurrence of major-effect resistance polymorphisms within populations.


2021 ◽  
Vol 95 ◽  
Author(s):  
A.A. Davis ◽  
J.T. Vannatta ◽  
S.O. Gutierrez ◽  
D.J. Minchella

Abstract Host–parasite coevolution may result in life-history changes in hosts that can limit the detrimental effects of parasitism. Fecundity compensation is one such life-history response, occurring when hosts increase their current reproductive output to make up for expected losses in future reproduction due to parasitic infection. However, the potential trade-offs between this increase in quantity and the quality of offspring have been relatively unexplored. This study uses the trematode, Schistosoma mansoni, and its snail intermediate host, Biomphalaria glabrata, to better understand how this host life-history response, fecundity compensation, impacts host reproduction. Measures of host reproductive output as well as offspring hatching success and survival were collected to assess the reproductive consequences of infection. Infected snails exhibited fecundity compensation by increasing the number of eggs laid and the overall probability of laying eggs compared to uninfected snails. Parental infection status did not play a significant role in hatching or offspring survival to maturity. Offspring from a later reproductive bout demonstrated a higher hatching success rate. Overall, the lack of an apparent trade-off between quantity and quality of offspring suggests that infected parental snails invest more resources towards reproduction not only to increase reproductive output, but also to maintain the fitness of their offspring, possibly at the expense of their own longevity.


2015 ◽  
Vol 84 (3) ◽  
pp. 625-636 ◽  
Author(s):  
Brittany F. Sears ◽  
Paul W. Snyder ◽  
Jason R. Rohr

Parasitology ◽  
2007 ◽  
Vol 134 (10) ◽  
pp. 1355-1362 ◽  
Author(s):  
A. RIVERO ◽  
P. AGNEW ◽  
S. BEDHOMME ◽  
C. SIDOBRE ◽  
Y. MICHALAKIS

SUMMARYParasitic infection is often associated with changes in host life-history traits, such as host development. Many of these life-history changes are ultimately thought to be the result of a depletion or reallocation of the host's resources driven either by the host (to minimize the effects of infection) or by the parasite (to maximize its growth rate). In this paper we investigate the energetic budget of Aedes aegypti mosquito larvae infected by Vavraia culicis, a microsporidian parasite that transmits horizontally between larvae, and which has been previously shown to reduce the probability of pupation of its host. Our results show that infected larvae have significantly less lipids, sugars and glycogen than uninfected larvae. These differences in resources were not due to differences in larval energy intake (feeding rate) or expenditure (metabolic rate). We conclude that the lower energetic resources of infected mosquitoes are the result of the high metabolic demands that microsporidian parasites impose on their hosts. Given the fitness advantages for the parasite of maintaining the host in a larval stage, we discuss whether resource depletion may also be a parasite mechanism to prevent the pupation of the larvae and thus maximize its own transmission.


2017 ◽  
Vol 284 (1863) ◽  
pp. 20171176 ◽  
Author(s):  
Andrés Valenzuela-Sánchez ◽  
Benedikt R. Schmidt ◽  
David E. Uribe-Rivera ◽  
Francisco Costas ◽  
Andrew A. Cunningham ◽  
...  

The decline of wildlife populations due to emerging infectious disease often shows a common pattern: the parasite invades a naive host population, producing epidemic disease and a population decline, sometimes with extirpation. Some susceptible host populations can survive the epidemic phase and persist with endemic parasitic infection. Understanding host–parasite dynamics leading to persistence of the system is imperative to adequately inform conservation practice. Here we combine field data, statistical and mathematical modelling to explore the dynamics of the apparently stable Rhinoderma darwinii – Batrachochytrium dendrobatidis (Bd) system. Our results indicate that Bd-induced population extirpation may occur even in the absence of epidemics and where parasite prevalence is relatively low. These empirical findings are consistent with previous theoretical predictions showing that highly pathogenic parasites are able to regulate host populations even at extremely low prevalence, highlighting that disease threats should be investigated as a cause of population declines even in the absence of an overt increase in mortality.


2021 ◽  
Author(s):  
Annabell A Davis ◽  
Jonathan Trevor Vannatta ◽  
Stephanie O Gutierrez ◽  
Dennis J Minchella

Host-parasite coevolution may result in life-history changes in hosts that can limit the detrimental effects of parasitism. Fecundity compensation is one such life-history response, occurring when hosts increase their current reproductive output to make up for expected losses in future reproduction due to parasitic infection. However, the potential trade-offs between quantity and quality of offspring produced during fecundity compensation are relatively unexplored. This study uses the trematode, Schistosoma mansoni, and its snail intermediate host, Biomphalaria glabrata, to better understand the impacts of this host life-history response. Measures of host reproductive output as well as offspring hatching success and survival were collected to assess the reproductive consequences of infection. Infected snails exhibited fecundity compensation (increase in the number of eggs laid compared to controls) and had a higher probability of laying any eggs at all. Infection status did not play a significant role in hatching or offspring survival to maturity. However, the age of the parental snail had a significant impact on hatching success, as offspring from older parents demonstrated a higher hatching success rate. Overall, the lack of an apparent trade-off between quantity and quality of offspring suggests that infected parental snails invest more resources towards reproduction in order to maintain the fitness of their offspring, possibly at the expense of their own longevity.


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