Invasion and spread of alien species can drive ecosystem changes, such as, the dynamics of infectious diseases. The non-native, marine gastropod Crepidula fornicata has become established across European coastlines over the last century, but there remains little insight into its disease carrying capacity and potential role as a source/sink of parasites. To address this knowledge gap, we surveyed limpets from two sites in South Wales, UK for signatures of disease/pathology using polymerase chain reaction-based methods (haemolymph) and histology (solid tissue). We encountered trematode-like parasites in ~1% individuals (5 out of 462). Three limpets displayed gross damage in the gonad, i.e. castration, and encysted metacercariae were found in the muscle of two other individuals. On the basis of 28S rDNA and internal transcribed spacer 2 genomic targets, we identified the gonad-infecting trematodes as members of the family Microphallidae – putative novel species related to the genus Longiductotrema. Earlier reports suggest that C. fornicata is not a host for trematode parasites in either its native or alien range but may act as a sink due to its filter feeding lifestyle. We provide clear evidence that C. fornicata is parasitized by at least one trematode species at two sites in Wales, UK, and likely act as a spillback or accidental host among native littorinids.

Bradynema listronoti is a parasitic nematode described from infected specimens of the carrot weevil Listronotus oregonensis. Prevalence of infection by B. listronoti under field conditions was followed over a period of 16 years in an untreated carrot field. Susceptibility of different carrot weevil life stages was evaluated as well as the impact of infection on fecundity and mortality. Gene expression in infected and uninfected carrot weevils was also compared to evaluate the impact of the parasite on the host transcriptome. Prevalence of B. listronoti in carrot weevil populations was sustained over the years ranging from 20 to 63%. All the weevil stages exposed to B. listronoti inoculum were susceptible to infection, larvae being more vulnerable (59 ± 8% infected) compared with pupae (4 ± 3% infected) and adults (7 ± 3% infected). The fecundity of infected female weevils was greatly reduced (60-fold) due to an inhibition of the maturation of the reproductive system. Transcriptomic analyses revealed that this parasitic castration may have been triggered by the inhibition of reproductive hormone production. The B. listronoti–L. oregonensis interaction represents a case of parasitic castration with a unique potential for biological control of an important pest of carrots.

Parasitic castration is a strategy used by parasites to minimize damage to the host by consuming its reproductive system, which results in the morphological alteration of the host. We determined that the forewing shape and density of the antennal sensilla of field-collected adult male mantids (Hierodula formosana), infected by horsehair worms (Chordodes formosanus) was partially feminized (intersexuality), and both male and female mantids infected by horsehair worms exhibited allometric changes in their wings and walking legs. In addition, the testes of most infected male adults disappeared or reduced in size, whereas the number of ovarioles in infected female adults was unaffected. The infection mainly influenced the structures related to host reproduction and locomotion, suggesting unbalanced energy exploitation and the reduction of parasitic virulence. In addition, the intersexuality of infected male adults indicated that sexual differentiation in insects, which researchers have considered to be an autonomous process, was influenced by the infection. The similarity of the antennae of infected male adults with those of last-instar female nymphs suggested that parasitic juvenilization may cause such feminization, but the mechanism of parasitic influence on insect sex characteristics should be studied further.

Host castration represents a mechanism used by parasites to exploit energy resources from their hosts by interfering with their reproductive development or to extend host lifespan by removing risks associated with reproductive activity. One of the most intriguing groups of parasitic castrators is represented by the insects belonging to the order Strepsiptera. The macroparasite Xenos vesparum can produce dramatic phenotypic alterations in its host, the paper wasp Polistes dominula. Parasitized female wasps have undeveloped ovaries and desert the colony without performing any social task. However, very little attention has been given to the parasitic impact of X. vesparum on the male phenotype. Here, we investigated the effects of this parasite on the sexual behaviour and the morpho-physiology of P. dominula males. We found that, differently from female wasps, parasitized males are not heavily affected by Xenos: they maintain their sexual behaviour and ability to discriminate between female castes. Furthermore, the structure of their reproductive apparatus is not compromised by the parasite. We think that our results, demonstrating that the definition of X. vesparum as a parasitoid does not apply to infected males of P. dominula, provide a new perspective to discuss and maybe reconsider the traditional view of strepsipteran parasites.

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.

Parasitism is defined in various ways as an intimate relationship in which one partner, the parasite, lives on or in another, the host, generally at the expense of the latter. Parasitism commonly results in a unique array of host physiological responses and adaptations. Most studies of the physiological effects of parasitism have focused on the pathological consequence of infection and disease. While many physiological changes contribute to pathogenesis, it is now recognized that parasitic infections at sub-clinical levels also produce physiological effects that either ameliorate or may not contribute to the disease process. Moreover, these physiological changes are often manifested by altered host behaviour. Behavioural studies have enabled an ecological- and evolutionary-oriented evaluation of host responses. In this fashion, physiological effects may be assessed as to whether they affect fitness and confer benefit or harm to one or both of the symbionts involved. We briefly examine how these physiological responses, specifically neural, endocrine, neuromodulatory, and immunomodulatory components, may interact to modify host behaviours. We consider the adaptiveness of these responses and how the behavioural patterns elicited may simultaneously appear adaptive for the parasite as well as the host. In addition, we address how parasite-host physiological and behavioural interactions may be altered during the course of parasitism.

Reproductive parameters of Ligula intestinalis-infected roach (Rutilus rutilus) which were held under long-tem laboratory conditions with unlimited food supply were investigated. Although uninfected and infected roach showed no difference in condition factor and both groups deposited perivisceral fat, the gonadosomatic-index was significantly lower in infected female and male roach. Quantitative histological analysis revealed that gonad development was retarded upon parasitization in both genders. In contrast to the phenotype described in the field, infected females were able to recruit follicles into secondary growth, but a high percentage of secondary growth follicles underwent atresia. In both genders, the histological data corresponded well with reduced expression of pituitary gonadotropins and lowered plasma concentrations of sex steroids, as revealed by real-time RT-PCR and ELISA, respectively. Furthermore, a reduction of vitellogenin mRNA and modulated expression of sex steroid receptors in the liver was demonstrated. Like in the field, there was a significant adverse impact of L. intestinalis on host reproductive physiology which could not be related to parasite burden. Our results show, for the first time, that maintenance under laboratory conditions can not abolish the deleterious effect of L. intestinalis on gametogenesis in roach, and indicate a specific inhibition of host reproduction by endocrine disruption.

Relative growth and reproductive biology of Munida rutllanti were investigated for the first time in the Adriatic Sea. A total of 938 individuals were analysed. Sex-ratio differed statistically from the expected 1:1. Six individuals exhibited secondary sex characteristics of both males and females. Carapace length of males ranged from 10.5 to 21.5 mm, while in females it ranged from 11.2 to 19.4 mm. Sexual dimorphism was observed in seven morphometric characters. Ovigerous females were first observed in summer and later in autumn with higher frequency. Realized fecundity showed wide variation (273–3250 eggs) and positive correlation between the brood and female size. An epicaridean isopod Pleurocrypta sp., parasitizing the gill chamber of both sexes was isolated and its effect on the oogenesis was studied by histological examination of host reproductive system. Growth inhibition, modification of secondary sex characteristics, as well as retardation of oogenesis and failure of oviposition, are repercussions of bopyrid infestation. Given the small prevalence (7.85%) of the bopyrid in the M. rutllanti Adriatic population, we assume that for the moment there is no severe effect on the host population dynamic.

Infection with digenetic trematodes causes an inhibition or complete cessation of fecundity in their intermediate hosts, freshwater snails. It has been demonstrated in the host–parasite combination Lymnaea stagnalis–Trichobilharzia ocellata that the action of the female gonadotropic hormones upon their target organs is inhibited by the peptide schistosomin. Schistosomin is produced in the central nervous system of the snail and released upon parasitic infection. In order to study the in vitro release of schistosomin, a bioassay was developed. Central nervous systems were incubated with either an acetic acid or a methanolic extract of larval stages of Trichobilharzia ocellata (miracidia, mother sporocysts, cercariae). The incubation media were chromatographed using HPLC and released schistosomin (-like material) was tested for bioactivity in the calfluxin bioassay. The in vitro release of schistosomin was only induced with a methanolic extract of cercariae. The nature of the cercarial factor is discussed.

Myxobolus cerebralis is the causative agent of whirling disease that has significant economical and ecological impacts on trout populations. Although intensive studies have been conducted to understand its effects on and interactions with its fish host, only limited information is available about how and to what extent M. cerebralis affects its oligochaete host, Tubifex tubifex. We investigated the effects of M. cerebralis on survival, growth, reproduction, and feeding activity of T. tubifex. Mature, immature and juvenile worms were exposed to myxospores and their infection prevalence, mortality, sexual development, reproduction and spore production were compared with unexposed worms. The parasite affected neither survival nor growth but inhibited clitellar development and reduced cocoon production by over 80%. Numbers of actinospores released from mature worms were nearly 9-fold higher than that of immature worms. When non-clitellated infected worms were kept at 30°C for 4 days, spore release ceased and they re-developed a clitellum. These results suggest parasite-induced castration. Comparative monitoring of defecation rate revealed that M. cerebralis reduced feeding activity of T. tubifex by approximately 40%. Low energy intake and impaired energetic allocation may be the underlying mechanism behind reduced fecundity of infected T. tubifex.

The present work reports the existence of parasitic castration induced by the bopyrid isopod Argeiopsis inhacae parasitizing the branchial chamber of female Stenopus hispidus. Parasitized and unparasitized females of S. hispidus displayed similar intermoult periods (14 ± 2 d) and exhibited similar mating behaviours. However, despite exhibiting typical mating behaviour, parasitized females were never able to produce any egg clutch when paired with unparasitized males; neither displayed the typical ‘dorsal bright green spot’ evidencing the presence of large vitellogenic oocytes. The idea that bopyrid infections generally lead to the ‘reproductive death’ of the decapod host is reinforced and the apparent existence of a heavily sex-biased infection towards females in S. hispidus may just be a consequence of the still limited number of surveyed specimens.

According to the Red Queen hypothesis for sex, cross-fertilization should be positively associated with the probability of exposure (risk) to virulent parasites. Unfortunately, risk is difficult to measure in the wild, and prevalence of infection is often substituted for risk. Here I suggest that prevalence of infection may not generally suffice as a surrogate for risk, since the Red Queen model can make opposite predictions depending on the distribution of risk in the wild. Specifically, the results of a matching-alleles model suggest that asexual populations should be more infected than sexual populations, when (1) the variance in risk among populations is small, and (2) the mean risk of exposure to parasites is near the point where selection switches to favouring sex over asex. If, however, the variance in risk among populations is large, sexual reproduction should be positively associated with the prevalence of infection. In addition, the coefficient of variation for reproductive mode should increase sharply at the switch point. In light of these results, I re-evaluated data from two studies on the distribution of males in 95 populations of a freshwater snail (Potamopyrgus antipodarum). Populations of these snails are often mixtures of sexual and asexual individuals, and the frequency of males is correlated with the frequency of sexual females in the population. The results show a large, highly skewed variance among populations for prevalence of infection by larval trematodes. The results also show a positive, significant relationship between prevalence of infection and the frequency of males, with a sharp increase in the coefficient of variation at intermediate prevalence. In addition, experimental studies suggest that some of the necessary conditions of the Red Queen hypothesis are also met in this system. Specifically, the most common trematode infecting these snails is (1) adapted to infecting local host populations of the snail, and is (2) more infective to clones that were common in the recent past. It is too early to know if the parasite theory is sufficient to explain the widespread distribution of sex. I suggest that the theory is not sufficient, but that parasites in combination with mutation accumulation in clonal lines may explain the maintenance of sex in species that occasionally produce apomictic mutants.