Competing for blood: the ecology of parasite resource competition in human malaria–helminth co‐infections

Ecological theory suggests that co‐infecting parasite species can interact within hosts directly, via host immunity and/or via resource competition. In mice, competition for red blood cells (RBCs) between malaria and bloodsucking helminths can regulate malaria population dynamics, but the importance of RBC competition in human hosts was unknown. We analysed infection density (i.e. the concentration of parasites in infected hosts), from a 2‐year deworming study of over 4000 human subjects. After accounting for resource‐use differences among parasites, we find evidence of resource competition, priority effects and a competitive hierarchy within co‐infected individuals. For example reducing competition via deworming increased Plasmodium vivax densities 2.8‐fold, and this effect is limited to bloodsucking hookworms. Our ecological, resource‐based perspective sheds new light into decades of conflicting outcomes of malaria–helminth co‐infection studies with significant health and transmission consequences. Beyond blood, investigating within‐human resource competition may bring new insights for improving human health.     

Host defence versus intraspecific competition in the regulation of infrapopulations of the flea Xenopsylla conformis on its rodent host Meriones crassus

Mechanisms that regulate parasite populations may influence the evolution of hosts and parasites, as well as the stability of host-parasite dynamics but are still poorly understood. A manipulation experiment on the grooming ability of rodent hosts (Meriones crassus) and flea (Xenopsylla conformis) densities on these hosts successfully disentangled two possible regulating mechanisms: (i) behavioural defence of the host and (ii) intraspecific competition among parasites, and revealed their importance in suppressing the feeding of fleas. Moreover, the results suggest that flea competition is direct and is not mediated by host grooming, immune response, or parasite-induced damage to the host. These mechanisms, together with interspecific competition and density-dependent parasite-induced host damage, may limit the parasite burden on an individual host and may prevent parasites from overexploiting their host population.     

The evolution of reduced antagonism—A role for host–parasite coevolution

Why do some host–parasite interactions become less antagonistic over evolutionary time? Vertical transmission can select for reduced antagonism. Vertical transmission also promotes coevolution between hosts and parasites. Therefore, we hypothesized that coevolution itself may underlie transitions to reduced antagonism. To test the coevolution hypothesis, we selected for reduced antagonism between the host Caenorhabditis elegans and its parasite Serratia marcescens. This parasite is horizontally transmitted, which allowed us to study coevolution independently of vertical transmission. After 20 generations, we observed a response to selection when coevolution was possible: reduced antagonism evolved in the copassaged treatment. Reduced antagonism, however, did not evolve when hosts or parasites were independently selected without coevolution. In addition, we found strong local adaptation for reduced antagonism between replicate host/parasite lines in the copassaged treatment. Taken together, these results strongly suggest that coevolution was critical to the rapid evolution of reduced antagonism.     

Relative helminth size in crustacean hosts: in vivo determination, and effects of host gender and within-host competition in a copepod infected by a cestode

Crustaceans are important hosts for a number of helminth parasites, and they are increasingly used as models for studying the physiology, ecology and evolution of parasite-host interactions. In ecological studies, this interaction is commonly described only in terms of prevalence and number of larvae per infected host. However, the volume of helminth parasites can vary greatly, and this variation can potentially give important insights into the nature of a parasite-host relationship. It may influence and be influenced, for example, by within-host competition, host size, growth, and life history. Here we present a simple method that allows rapid approximation of the absolute and relative volumes of cestode larvae within copepod hosts of various developmental stages (nauplii, copepodites and adults). The measurements are taken in vivo without much disturbance of the animals, i.e. the technique allows study of growth and development of the parasites in relation to that of their hosts. The principles of this technique can be adopted to other helminth parasites and other crustacean hosts. Using this method in the copepod Macrocyclops albidus infected with the cestode Schistocephalus solidus, we found that the relative parasite size (= `parasite index') ranged from 0.5% to 6.5% of host size 14 days after infection. It was greater in male than in female hosts. With increasing number of parasites per host, the total parasite volume increased while the mean volume of the individual parasites decreased. The magnitude of the observed parasite indices, the large variation that was found within a sample of 46 infected adult copepods, and the observed correlates suggest that this new index can indeed be an important measure of parasite success and its pathogenecity.     

On the capacity of macroparasites to control insect populations

A graphical model of the population dynamics of macroparasites and their hosts is developed. Three principal means by which the parasites can be regulated are considered: reduction in host density as a result of parasite-induced host mortality, reduction in host density as a result of parasite-induced host sterility, and competition among parasites within multiply-infected hosts. The means by which parasites are regulated has a major effect on the degree to which they can depress host population densities. In particular, a parasite that sterilizes its host is expected to reduce host density more than one that causes an equivalent decline in host fitness through increased mortality. A special case of the model is developed for herbivorous insects that, in the absence of parasites, are limited by larval food resources. Parasites that are regulated via parasite-induced host sterility will control the insect populations below the level set by larval resources if the threshold host density for the parasites (N(T)) is less than the ratio of carrying capacity to net reproductive rate of the insects (K/R). Data are presented showing that all three means of parasite regulation, but especially parasite-induced host sterility, can operate in Howardula aoronymphium, a nematode parasite of mycophagous Drosophila flies. Data from a field cage experiment show that, if these nematodes are regulated primarily via reductions in host density due to this sterility, the parameters N(T), K, and R are such that Howardula is likely to play an important role in controlling Drosophila populations. However, this conclusion must be tempered by the fact that these nematodes also cause increased host mortality and experience within-host competition, making the conditions for parasite control of the flies more stringent.     

Aquaculture-induced changes to dynamics of a migratory host and specialist parasite: a case study of pink salmon and sea lice

Exchange of diseases between domesticated and wild animals is a rising concern for conservation. In the ocean, many species display life histories that separate juveniles from adults. For pink salmon (Oncorhynchus gorbuscha) and parasitic sea lice (Lepeophtheirus salmonis), infection of juvenile salmon in early marine life occurs near salmon sea-cage aquaculture sites and is associated with declining abundance of wild salmon. Here, we develop a theoretical model for the pink salmon/sea lice host–parasite system and use it to explore the effects of aquaculture hosts, acting as reservoirs, on dynamics. Because pink salmon have a 2-year lifespan, even- and odd-year lineages breed in alternate years in a given river. These lineages can have consistently different relative abundances, a phenomenon termed “line dominance”. These dominance relationships between host lineages serve as a useful probe for the dynamical effects of introducing aquaculture hosts into this host–parasite system. We demonstrate how parasite spillover (farm-to-wild transfer) and spillback (wild-to-farm transfer) with aquaculture hosts can either increase or decrease the line dominance in an affected wild population. The direction of the effect depends on the response of farms to wild-origin infection. If aquaculture parasites are managed to a constant abundance, independent of the intensity of infections from wild to farm, then line dominance increases. On the other hand, if wild-origin parasites on aquaculture hosts are proportionally controlled to their abundance then line dominance decreases.     

Dose-independent virulence in phoretic mites that parasitize burying beetles

Virulence, the negative impact of parasites on their hosts, typically increases with parasite dose. Parasites and hosts often compete for host resources and more parasites will consume more resources. Depending on the mechanism of competition, increasing host resources can benefit the host. Additional resources can also be harmful when the parasites are the main beneficiaries. Then, the parasites will thrive and virulence increases. While parasite dose is often easy to manipulate, it is less trivial to experimentally scale host resources. Here, we study a system with external host resources that can be easily manipulated: Nicrophorus burying beetles reproduce on vertebrate carcasses, with larger carcasses yielding more beetle offspring. Phoretic Poecilochirus mites reproduce alongside the beetles and reduce beetle fitness. The negative effect of mites could be due to competition for the carrion between beetle and mite offspring. We manipulated mite dose and carcass size to better understand the competition between the symbionts. We found that mite dose itself was not a strong predictor of virulence. Instead, the number of mite offspring determined beetle fitness. At larger doses, there was strong competition among adult parental mites as well as mite offspring. While increasing the carcass size increased both host and parasite fitness, it did surprisingly little to alleviate the negative effect that mites had on beetles. Instead, relative virulence was stronger on large carcasses, indicating that the parasites appropriate more of the additional resources. Our results demonstrate an ecological influence on the selection of parasites on their hosts and suggest that virulence can be dose-independent in principle.     

THE INFLUENCE OF HOST DEMOGRAPHY ON THE EVOLUTION OF VIRULENCE OF A MICROSPORIDIAN GUT PARASITE

It is predicted that host exploitation should evolve to maximize parasite fitness and that virulence (= parasite-induced host mortality) evolves along with the rate of host exploitation. If the life expectancy of a parasite is short, it is expected to evolve a higher rate of host exploitation and therefore higher virulence because the penalty to the parasite for killing the host is reduced. We tested this hypothesis by keeping for 14 months the horizontally transmitted microsporidian parasite Glugoides intestinalis in mono-clonal host cultures (Daphnia magna) under conditions of high and low host background mortality. High host mortality, and thus parasite mortality, was achieved by replacing weekly 70–80% of all hosts in a culture with uninfected hosts from stock cultures (Replacement lines). In the low-mortality treatment no replacement took place. Contrary to our expectation, parasites from the Replacement lines evolved a lower within-host growth rate and virulence than parasites from the Nonreplacement lines. Across lines we found a strong positive correlation between within-host growth rate and virulence. We did further experiments to answer the question why our data did not support the predictions. Sporophorous vesicles (SVs, spore clusters) were smaller in doubly infected than in singly infected host-gut cells, indicating that competition within cells bears costs for the parasite. Due to our experimental protocol, the average life span of infections had been much higher in the Nonreplacement lines. Since the number of parasites inside a host increases with the time since infection, long-lasting infections led to high frequencies of multiply infected host-gut cells. Therefore, we speculated that within-cell competition was more severe in the Nonreplacement lines and may have led to selection for accelerated within-host growth. SVs in the Nonreplacement lines were indeed significantly larger. Our results point out that single-factor explanations for the evolution of virulence can lead to wrong predictions and that multiple infections are an important factor in virulence evolution.     

Parasites promote host gene flow in a metapopulation

Local adaptation is a powerful mechanism to maintain genetic diversity in subdivided populations. It counteracts the homogenizing effect of gene flow because immigrants have an inferior fitness in the new habitat. This picture may be reversed in host populations where parasites influence the success of immigrating hosts. Here we report two experiments testing whether parasite abundance and genetic background influences the success of host migration among pools in a Daphnia magna metapopulation. In 22 natural populations of D. magna, immigrant hosts were found to be on average more successful when the resident populations experienced high prevalences of a local microsporidian parasite. We then determined whether this success is due to parasitism per se, or the genetic background of the parasites. In a common garden competition experiment, we found that parasites reduced the fitness of their local hosts relatively more than the fitness of allopatric host genotypes. Our experiments are consistent with theoretical predictions based on coevolutionary host-parasite models in metapopulations. A direct consequence of the observed mechanism is an elevated effective migration rate for the host in the metapopulation.     

When parasites disagree: Evidence for parasite‐induced sabotage of host manipulation

Host manipulation is a common parasite strategy to alter host behavior in a manner to enhance parasite fitness usually by increasing the parasite's transmission to the next host. In nature, hosts often harbor multiple parasites with agreeing or conflicting interests over host manipulation. Natural selection might drive such parasites to cooperation, compromise, or sabotage. Sabotage would occur if one parasite suppresses the manipulation of another. Experimental studies on the effect of multi‐parasite interactions on host manipulation are scarce, clear experimental evidence for sabotage is elusive. We tested the effect of multiple infections on host manipulation using laboratory‐bred copepods experimentally infected with the trophically transmitted tapeworm Schistocephalus solidus. This parasite is known to manipulate its host depending on its own developmental stage. Coinfecting parasites with the same aim enhance each other's manipulation but only after reaching infectivity. If the coinfecting parasites disagree over host manipulation, the infective parasite wins this conflict: the noninfective one has no effect. The winning (i.e., infective) parasite suppresses the manipulation of its noninfective competitor. This presents conclusive experimental evidence for both cooperation in and sabotage of host manipulation and hence a proof of principal that one parasite can alter and even neutralize manipulation by another.     

Coinfecting parasites can modify fluctuating selection dynamics in host–parasite coevolution

Genetically specific interactions between hosts and parasites can lead to coevolutionary fluctuations in their genotype frequencies over time. Such fluctuating selection dynamics are, however, expected to occur only under specific circumstances (e.g., high fitness costs of infection to the hosts). The outcomes of host–parasite interactions are typically affected by environmental/ecological factors, which could modify coevolutionary dynamics. For instance, individual hosts are often infected with more than one parasite species and interactions between them can alter host and parasite performance. We examined the potential effects of coinfections by genetically specific (i.e., coevolving) and nonspecific (i.e., generalist) parasite species on fluctuating selection dynamics using numerical simulations. We modeled coevolution (a) when hosts are exposed to a single parasite species that must genetically match the host to infect, (b) when hosts are also exposed to a generalist parasite that increases fitness costs to the hosts, and (c) when coinfecting parasites compete for the shared host resources. Our results show that coinfections can enhance fluctuating selection dynamics when they increase fitness costs to the hosts. Under resource competition, coinfections can either enhance or suppress fluctuating selection dynamics, depending on the characteristics (i.e., fecundity, fitness costs induced to the hosts) of the interacting parasites.     

Does timing matter? How priority effects influence the outcome of parasite interactions within hosts

In nature, hosts are exposed to an assemblage of parasite species that collectively form a complex community within the host. To date, however, our understanding of how within-host–parasite communities assemble and interact remains limited. Using a larval amphibian host (Pacific chorus frog, Pseudacris regilla) and two common trematode parasites (Ribeiroia ondatrae and Echinostoma trivolvis), we experimentally examined how the sequence of host exposure influenced parasite interactions within hosts. While there was no evidence that the parasites interacted when hosts were exposed to both parasites simultaneously, we detected evidence of both intraspecific and interspecific competition when exposures were temporally staggered. However, the strength and outcome of these priority effects depended on the sequence of addition, even after accounting for the fact that parasites added early in host development were more likely to encyst compared to parasites added later. Ribeiroia infection success was reduced by 14 % when Echinostoma was added prior to Ribeiroia, whereas no such effect was noted for Echinostoma when Ribeiroia was added first. Using a novel fluorescent-labeling technique that allowed us to track Ribeiroia infections from different exposure events, we also discovered that, similar to the interspecific interactions, early encysting parasites reduced the encystment success of later arriving parasites by 41 %, which could be mediated by host immune responses and/or competition for space. These results suggest that parasite identity interacts with host immune responses to mediate parasite interactions within the host, such that priority effects may play an important role in structuring parasite communities within hosts. This knowledge can be used to assess host–parasite interactions within natural communities in which environmental conditions can lead to heterogeneity in the timing and composition of host exposure to parasites.     

Effects of maternal parasite load on offspring life-history traits in the common lizard (Lacerta vivipara)

We studied the effect of maternal ectoparasite load (measured at parturition) on the life-history traits of the offspring of the host Lacerta vivipara, the European common lizard. The ectoparasite, a mite belonging to the family Laelapidae, had a detrimental effect on its host: parasite load was associated with increased host mortality, and was negatively correlated with host body mass. Parasite load was persistent over time, suggesting that parasite load can be predictable. Offspring of highly parasitised mothers had higher values of several fitness components early in life than offspring of parasite-free mothers or lightly infested mothers. This was expressed in terms of increased F₁ yearling growth rate, and reproductive investment at first reproduction (measured as F₂ hatchling mass). These results are interpreted as a host adaptation to attenuate the impact of parasites. Indeed, if high parasite loads arise from long exposure time to a constant population of parasites, and if the negative effects of parasites are additive over time, hosts could reduce the impact of parasites simply by investing more during the earlier stages of life. Naturally, having better performance early in life should lead to higher mortality rates and/or lower fecundity later in life.     

Dose effects and density-dependent regulation of two microparasites of<Emphasis Type="Italic"> Daphnia magna</Emphasis>

Individual hosts constitute a limited resource for parasites, suggesting that density-dependent effects may play a role in within-host growth and parasite regulation. This hypothesis has been tested for several helminth parasites, but not for microparasites. We therefore examined dose-response patterns for the microparasitic bacterium Pasteuria ramosa and the fungus Metschnikowiella biscuspidata infecting the planktonic crustacean Daphnia magna. With increasing numbers of transmission stages administered to the host we found that host fecundity and survival and parasite transmission-stage production declined. Using a k-value analysis, a method that quantifies the strength of density dependence, we found for both parasites that density dependence acted at all doses, indicating the absence of a minimum density below which parasite fitness is density- independent. At low doses density was exactly compensated, but it was overcompensated at high doses. Overcompensation at high doses was weak for P. ramosa, but high for M. biscuspidata. At the two highest doses M. biscuspidata killed its hosts before any transmission stages were produced. Our data indicate that density dependence is expressed through retarded spore development in P. ramosa, but through both host mortality and reduced parasite fecundity in M. biscuspidata. A further experiment (P. ramosa only) revealed that in well-fed hosts more parasite transmission stages are produced than in poorly fed hosts, suggesting that competition for host resources retards P. ramosa development. Our data for P. ramosa, but not for M. biscuspidata, are largely consistent with assumptions made in models on microparasite epidemiology. We draw attention to the relevance of dose effects and within-host competition for the evolution of virulence. Received: 15 July 1999 / Accepted: 14 September 1999     

THE EVOLUTION OF PARASITISM IN THE RED ALGAE: MOLECULAR COMPARISONS OF ADELPHOPARASITES AND THEIR HOSTS1

In several groups of parasites including insect, flowering plant, fungal, and red algal parasites, morphological similarities of the parasites and their specific hosts have led to hypotheses that these parasites evolved from their hosts. But these conclusions have been criticized because the morphological features shared by parasite and host may be the result of convergent evolution. In this study, we examine the hypothesis, originally put forth by Setchell, that adelphoparasitic red algae, that is, parasitic red algae that are morphologically very similar to their hosts, evolved from their specific red algal hosts. Rather than comparing morphological features of parasites and hosts, small-subunit 18S nuclear ribosomal DNA and the internal transcribed spacer regions (ITSs) of the nuclear ribosomal repeat are compared for five parasites, their hosts, and related nonhosts from four red algal orders. These comparisons reveal that each of these adelphoparasites has evolved either directly from the host on which it is currently found, or it evolved from some other taxon that is closely related to the modern host. The parasites Gardneriella tuberifera, Rhodymeniocolax botryoides, and probably Gracilariophila oryzoides evolved from their respective hosts Sarcodiotheca gaudichaudii, Rhodymenia pacifica, and Gracilariopsis lemaneiformis, respectively. The parasite Faucheocolax attenuata evolved from either Fauchea laciniata or Fauchea fryeana and subsequently radiated onto the other host species. Presently this parasite is found on both hosts. Lastly, some parasitic genera such as Plocamiocolax are polyphyletic in their origins. A species of Plocamiocolax from an Antarctic Plocamium cartilagineum appears to have evolved from its host whereas the common Plocamiocolax pulvinata that occurs along the west coast of North America likely evolved from Plocamium violaceum and radiated secondarily onto its present day host, Plocamium cartilagineum.     

Turnover in local parasite populations temporarily favors host outcrossing over self‐fertilization during experimental evolution

The ubiquity of outcrossing in plants and animals is difficult to explain given its costs relative to self‐fertilization. Despite these costs, exposure to changing environmental conditions can temporarily favor outcrossing over selfing. Therefore, recurring episodes of environmental change are predicted to favor the maintenance of outcrossing. Studies of host–parasite coevolution have provided strong support for this hypothesis. However, it is unclear whether multiple exposures to novel parasite genotypes in the absence of coevolution are sufficient to favor outcrossing. Using the nematode Caenorhabditis elegans and the bacterial parasite Serratia marcescens, we studied host responses to parasite turnover. We passaged several replicates of a host population that was well‐adapted to the S. marcescens strain Sm2170 with either Sm2170 or one of three novel S. marcescens strains, each derived from Sm2170, for 18 generations. We found that hosts exposed to novel parasites maintained higher outcrossing rates than hosts exposed to Sm2170. Nonetheless, host outcrossing rates declined over time against all but the most virulent novel parasite strain. Hosts exposed to the most virulent novel strain exhibited increased outcrossing rates for approximately 12 generations, but did not maintain elevated levels of outcrossing throughout the experiment. Thus, parasite turnover can transiently increase host outcrossing. These results suggest that recurring episodes of parasite turnover have the potential to favor the maintenance of host outcrossing. However, such maintenance may require frequent exposure to novel virulent parasites, rapid rates of parasite turnover, and substantial host gene flow.     

Response of a root hemiparasite to elevated CO2 depends on host type and soil nutrients

Although elevated CO₂ may affect various forms of ecological interactions, the effect of elevated CO₂ on interactions between parasitic plants and their hosts has received little attention. We examined the effect of elevated CO₂ (590 μl l⁻¹) at two nutrient (NPK) levels on the interactions of the facultative root hemiparasite Rhinanthus alectorolophus with two of its hosts, the grass Lolium perenne and the legume Medicago sativa. To study possible effects on parasite mediation of competition between hosts, the parasite was grown with each host separately and with both hosts simultaneously. In addition, all combinations of hosts were grown without the parasite. Both the parasite and the host plants responded to elevated CO₂ with increased growth, but only at high nutrient levels. The CO₂ response of the hemiparasite was stronger than that of the hosts, but depended on the host species available. With L. perenne and M. sativa simultaneously available as hosts, the biomass of the parasite grown at elevated CO₂ was 5.7 times that of parasites grown at ambient CO₂. Nitrogen concentration in the parasites was not influenced by the treatments and was not related to parasite biomass. The presence of the parasite strongly reduced both the biomass of the hosts and total productivity of the system. This effect was much stronger at low than at high nutrient levels, but was not influenced by CO₂ level. Elevated CO₂ did not influence the competitive balance between the two different hosts grown in mixture. The results of this study support the hypothesis that hemiparasites may influence community structure and suggest that these effects are robust to changes in CO₂ concentration. Received: 17 August 1998 / Accepted: 3 March 1999     

Bioenergetic theory predicts infection dynamics of human schistosomes in intermediate host snails across ecological gradients

Epidemiological dynamics depend on the traits of hosts and parasites, but hosts and parasites are heterogeneous entities that exist in dynamic environments. Resource availability is a particularly dynamic and potent environmental driver of within‐host infection dynamics (temporal patterns of growth, reproduction, parasite production and survival). We developed, parameterised and validated a model for resource‐explicit infection dynamics by incorporating a parasitism module into dynamic energy budget theory. The model mechanistically explained the dynamic multivariate responses of the human parasite Schistosoma mansoni and its intermediate host snail to variation in resources and host density. At the population level, feedbacks mediated by resource competition could create a unimodal relationship between snail density and human risk of exposure to schistosomes. Consequently, weak snail control could backfire if reductions in snail density release remaining hosts from resource competition. If resource competition is strong and relevant to schistosome production in nature, it could inform control strategies.     

Nestling sex predicts susceptibility to parasitism and influences parasite population size within avian broods

Vertebrate hosts differ in their level of parasite susceptibility and infestation. In avian broods, variation in susceptibility of nestlings to ectoparasites may be associated with non‐uniform distributions of parasites among brood mates, with parasites concentrating feeding on the most vulnerable hosts. The presence of a highly susceptible nestling in a brood can benefit the remaining young by reducing the parasite pressure they experience; however, from a parasite’s perspective, broods with fewer susceptible hosts may provide effectively fewer resources than broods of the same size containing a greater abundance of susceptible hosts, and this could limit the number of parasites that a host brood can sustain. To test whether variation in number of susceptible hosts affects the number of parasites in bird nests, we first examined the role of host sex and induced immunity (via methionine supplementation) on susceptibility of mountain bluebirds Sialia currucoides to parasitism by blow flies Protocalliphora spp. We then assessed the effect of variation in number of susceptible hosts on the number of parasites inhabiting the nest. Only females showed a benefit of methionine supplementation, gaining mass more rapidly following supplementation compared to males. This suggests that females are more susceptible to parasites in this system; this was further supported by parasite feeding trials, in which parasites extracted larger blood meals from female than male hosts. Finally, the abundance of parasites in nests was predicted by brood sex ratio: broods containing more female young harboured more parasites. Hence, within‐brood variation in host susceptibility to parasites can not only influence the costs of parasitism for individual nestlings, but may also have consequences for the size of parasite populations within nests. If patterns of maternal investment affect the abundance of nest‐dwelling parasites, these interactions may be important for understanding fitness consequences of maternal resource allocation in many vertebrate hosts.     

Egg mimicry by the Pacific koel: mimicry of one host facilitates exploitation of other hosts with similar egg types

When brood parasites exploit multiple host species, egg rejection by hosts may select for the evolution of host‐specific races, where each race mimics a particular host's egg type. However, some brood parasites that exploit multiple hosts with the ability to reject foreign eggs appear to have only a single egg type. In these cases, it is unclear how the parasite egg escapes detection by its hosts. Three possible explanations are: 1) host‐specific races are present, but differences in egg morphology are difficult for the human eye to detect; 2) the brood parasite evolves a single egg type that is intermediate in appearance between the eggs of its hosts; 3) or the parasite evolves mimicry of one of its hosts, which subsequently allows it to exploit other species with similar egg morphology. Here we test these possibilities by quantifying parameters of egg appearance of the brood‐parasitic Pacific koel Eudynamys orientalis and seven of its hosts. Koel eggs laid in the nests of different hosts did not show significant differences in colour or pattern, suggesting that koels have not evolved host‐specific races. Koel eggs were similar in colour, luminance and pattern to the majority of hosts, but were significantly more similar in colour and luminance to one of the major hosts than to two other major hosts, supporting hypothesis 3. Our findings suggest that mimicry of one host can allow a brood parasite to exploit new hosts with similar egg morphologies, which could inhibit the evolution of host defences in naïve hosts.