It is probable that there are many other examples of symbiotic virus‐parasitoid/parasite relationships awaiting discovery. However, not all wasp parasitoids have relationships with viruses and these inject toxins that cause similar disruptions to the host immune response and host development.
1.2.7 The Concept of Harm
The term ‘harm’ is often employed when describing interactions between organisms but is particularly pertinent to any discussion of host: parasite relationships. Unfortunately, harm is a difficult term to define and is not always easy to measure. For example, parasites are usually much smaller than their host and a single parasite may have such a minor impact that its effect on the physiology and well‐being of the host is too trivial to measure. By contrast, a large number of the same parasite could cause serious illness or even death. Similarly, a low parasite burden may have little impact upon a healthy, well‐nourished adult host, but the same number of parasites infecting an unhealthy, starving young host may prove fatal. Consequently, harbouring a pathogen (being infected) and expressing the signs and symptoms of being infected (suffering from a disease) are not necessarily synonymous. A common analogy is that a single glass of water will not harm you and may even do you good, but the rapid consumption of a thousand glasses of water would kill you. Does that mean that water is beneficial or poisonous? Clearly, it can be both and, likewise, harm is dependent upon the context in which it is being considered. For human parasites, one should also consider the context and psychological consequences. Among some poor communities, being infected by lice and parasitic worms may be considered an unremarkable fact of everyday life. By contrast, in affluent communities, the very thought of harbouring worms inside the body or being bitten by fleas may cause mental torment far above any physical harm caused. It is therefore not a good idea to make the ability to record measurable harm as a pre‐requisite for the classification of the relationship between two organisms. Indeed, in certain instances, low levels of parasitic infection may benefit the well‐being of the host (Maizels 2020). Nevertheless, many parasite species have the capacity to cause morbidity, that is, a diseased state, and some may cause mortality (death). We discuss the possible beneficial consequences of low parasite burdens in more detail in Chapter 12.
The morbidity that parasite infections induce is often reflected in a reduction in the host’s fitness as measured in terms of its growth or reproductive output. This is often attributed to the direct pathogenic effect of the parasite, such as through the loss of blood and the destruction of tissues or competition for resources. For example, many gut helminths act as so‐called kleptoparasites (literally, thieving parasites) and compete with their host for nutrients within the gut lumen. However, the situation is far more complicated than this. Although a functional immune system is crucial for an organism to protect itself against pathogens, immune systems are energetically costly and when nutrients are limiting, it must trade these costs against other physiological processes. Ilmonen et al. (2000) demonstrated this by injecting one group of breeding female pied flycatchers (Ficedula hypoleuca) with a diphtheria‐tetanus vaccine and a control group with a saline solution. The vaccine was not pathogenic and did not induce an infection, but it activated the birds’ immune system. They found that birds injected with the vaccine exhibited a lower feeding effort, invested less in self‐maintenance and had a lower reproductive output, as determined by fledgling quality and number. The authors therefore concluded that the energetic consequences of activating the immune system can be sufficient to reduce the host’s breeding success.
1.3 Parasite Hosts
A parasite host is an organism on or in which the parasite lives and from which it derives its nutrition. The host is usually not related taxonomically to the parasite although this is not always the case (see intra‐specific parasites). Most parasites are highly host specific and only infect one host species or a group of closely related species. This is because all hosts represent a unique challenge in terms of the complex adaptations the parasite requires to evolve to identify, invade, and survive within/upon them. Nevertheless, a few parasite species, exploit a wide range of hosts. For example, the protozoan parasite Toxoplasma gondii infects, grows, and asexually reproduces in virtually all warm‐blooded vertebrates although sexual reproduction only takes place within the small intestine of cats.
Hosts can be divided into classes, depending upon the role they play in the parasite’s life cycle. The ‘definitive’ (or final) host is the one in, or on, which the parasite reaches maturity and undergoes sexual reproduction, whilst the ‘intermediate’ host is the one in which the parasite undergoes its developmental stage(s). There may be just one or several intermediate hosts and the parasite may or may not undergo asexual reproduction during this time, but it cannot develop into an adult or reproduce sexually. In this way, some parasites exploit their hosts to maximum effect by combining the reproductive power of asexual reproduction in the larval stage with the advantages of sexual reproduction during the adult stage.
Parasites devote more of their energies to reproduction than free‐living animals because they do not have to worry about food, shelter, and fluctuations in environmental conditions. This is important because the chances of any offspring locating and establishing themselves within a suitable host are very low. The completion of a parasite’s life cycle sometimes depends upon the death of the intermediate host and the subsequent consumption of the larval form by the definitive host. In this situation, the parasite is often very pathogenic in its intermediate host but has relatively minor effects on the definitive host. The intermediate host is not always killed or consumed by the definitive host. For example, after undergoing asexual reproduction in the snail intermediate host, the cercariae of the liver fluke Fasciola hepatica physically and chemically bore their way out and swim off to transform into metacercariae attached to aquatic vegetation. The snail survives the damage to its tissues, and the lifecycle is completed when the metacercaria are consumed by the sheep definitive host (see Section 5.2.1.1.1 for more details).
Parasites of Parasites
Viruses infect several parasitic protozoa such as Leishmania spp. (Rossi and Fasel 2018) and Giardia lamblia (Janssen et al. 2015) but, at the time of writing, there was surprisingly little evidence of their presence in helminths – though this is probably because few scientists have looked for them. Some workers suggest that viruses could be used to combat parasite infections (Hyman et al. 2013), but there is increasing evidence that many of the viruses found in parasitic protozoa contribute to their pathogenicity (Gómez‐Arreaza et al. 2017).
Parasites are also infected by prokaryotic (e.g., bacteria) and eukaryotic (e.g., fungi and protozoa) parasites. Those parasites that infect other parasites are known as hyperparasites. For example, the microsporidian Nosema helminthorum is parasitic on the tapeworm Moniezia expansa that lives within the small intestine of sheep and goats (Canning and Gunn 1984). Sheep become infected by the tapeworm when they accidentally ingest oribatid mites containing the cysticercoids of M. expansa. Subsequently, the sheep must consume the infective cysts of N. helminthorum and these must then penetrate the tegument (tapeworms lack a gut of their own) of the tapeworm. Within the tapeworm, N. helminthorum reproduces and causes numerous raised opaque bleb‐like patches but is not especially pathogenic. Related microsporidia affect various other platyhelminth parasites (Canning 1975; Sokolova and Overstreet 2020), but there are remarkably few reports of them infecting parasitic nematodes (e.g., Kudo and Hetherington 1922). The discovery of microsporidia infecting the free‐living nematode Caenorhabditis elegans has opened the potential of developing a laboratory model for studying both nematode immunity and the biology of microsporidia (Zhang et al. 2016). This is because C. elegans is a commonly used model organism whose full genome is known. Several