Parasitology. Alan Gunn

pathogenic infections in humans and domestic animals and a simple laboratory model would prove extremely useful in the development of drug treatments etc.

A paratenic host, also sometimes referred to as a transport host, is one that a parasite enters but within which it cannot undergo further development. Paratenic hosts are not usually essential for a parasite to complete its life cycle although they may provide a useful bridge between the infective stage/intermediate host and definitive host. For example, the definitive hosts of the nematode Capillaria hepatica are primarily rodents although it infects several other species of mammals including dogs, cats, and pigs. Human infections are rare but potentially serious. The adult worms reside in the definitive host’s liver and their unembryonated eggs remain there until the host dies/ is killed and a scavenger/ predator consumes them (Figure 1.2). The unembryonated eggs pass through the gut of the scavenger/predator and then out with the faeces. This helps disperse the eggs in the environment. Development of the eggs to the infective stage occurs within the soil and takes several weeks or even months. If the definitive host’s body is not consumed, the eggs embryonate to the infective stage, but there will be little dispersal. Earthworms ingest infective embryonated eggs of C. hepatica whilst feeding on soil and detritus. Because many rodents consume earthworms, these probably facilitate the transfer of the nematode to its definitive host.

Figure 1.2 Life cycle of the nematode Capillaria hepatica illustrating the role of paratenic hosts in the transmission cycle. Drawings not to scale. 1 = A rodent becomes infected when it consumes embryonated eggs. These hatch in the small intestine, the larvae penetrate the gut, enter the circulation, and reach the liver. The larvae (L) moult become adult male (M) and female (F) worms and commence laying eggs. The unembryonated eggs remain in the liver. 2 = When the rodent dies its body decays and the unembryonated eggs enter the soil. If a scavenger eats the body, the unembryonated eggs pass through the gut and are dispersed. 3 = If a fox or other predator eats a live infected rodent, the unembryonated eggs are passed in its faeces. Scavengers and predators therefore act as dispersal hosts. 4 = The eggs embryonate to the infective stage in the soil. A rodent, human, or other susceptible mammal becomes infected when it consumes the infective eggs. 5 = Earthworms that consume infective eggs act as paratenic hosts if they are subsequently eaten by a rodent (or other susceptible mammal such as a pig). 6 = Humans are accidental, dead‐end hosts within whose liver the parasites can develop to adulthood and produce eggs.

1.4 Zoonotic Infections

      A zoonotic infection (zoonosis) is one that is freely transmissible between humans and other vertebrate animals. The transfer of Plasmodium falciparum malaria between two people by a mosquito is therefore not zoonosis because a mosquito is not a vertebrate and P. falciparum only infects humans. By contrast, a mosquito transmitting Plasmodium knowlesi from a monkey to a human would be an example of a zoonosis because the P. knowlesi infects both monkeys and humans and we are both vertebrates. A disease that is only transmitted between humans is called an anthroponosis and a good example would be P. falciparum.

      Many of the most important parasites in human and veterinary medicine are zoonotic infections. For example, pigs are the normal intermediate host of the pork tapeworm Taenia solium, and we are its definitive host. Therefore, pigs infect humans, and we infect pigs. Sometimes, humans are just one additional host within a parasite’s life cycle. For example, the blood fluke Schistosoma japonicum has many definitive hosts apart from humans, including dogs, cattle, pigs, and rats. Consequently, all these definitive hosts can shed eggs that will infect the snail intermediate hosts, and the resultant cercariae can infect all of them.

      The transmission of zoonotic parasites is usually heavily influenced by the nature of human: animal relationships. Therefore, they can be both simultaneously theoretically simple and recalcitrant to control. This is because their control often depends upon changing human behaviour, and this depends upon a complex mix of culture, religion, tradition, economics, personality, and politics. For example, theoretically, many zoonotic infections might be halted by simple acts of basic hygiene or the cooking of food. However, people are often unable or unwilling to change the way they live their life for all sorts of reasons. Zoonotic infections should not always be considered from the risks that they pose to us. Sometimes, wild animal populations can be threatened by the diseases that we transmit to them. We will consider specific instances of this throughout the book.

1.5 The Co‐evolution of Parasites and Their Hosts

Evolution can be defined as a change in gene frequency between generations, but for this to occur three criteria need to be met. First, there must be genetic variation within the population. If the population is genetically homogeneous, then variation can only occur sporadically through random mutation. The second criterion is that the variation must be heritable: if the variation cannot be passed on to offspring, then it will be lost regardless of the benefits it imparts. The third and final criterion is that the variation must influence the probability of leaving reproductively viable offspring. If the variation is beneficial, then the organism possessing it will leave more offspring; however, unless these are reproductively viable, the variation would be quickly lost from the gene pool. Parasites live in close association with their hosts and the two organisms will co‐evolve. The nature of the host: parasite relationship may therefore change with time. For example, provided the three criteria are met, the host will evolve resistance/susceptibility factors depending upon the pressure exerted by the parasite. Although ever greater resistance to infection may appear to be ‘ideal’, this is unlikely to arise if the energetic cost impacts on the ability to leave viable offspring. At the same time, the parasite will evolve virulence/avirulence factors that promote its own survival.

      It is often stated that long‐standing parasite: host relationships are less pathogenic than those that have established more recently. This is based on the reasoning that if the parasite kills its host, then it will effectively ‘commit suicide’ because it will have destroyed its food supply. Consequently, over time, it is to be expected that the parasite will become less harmful to its host – that is, it becomes less virulent. However, this assumption is questionable because a pathogen’s virulence often reflects its reproductive success. For example, let us consider two hypothetical strains, A and B, of the same nematode species that lives in the gut of sheep. Strain A is highly virulent and causes the death of the sheep whilst strain B is relatively benign and seldom causes any mortality. At first glance, one might expect that strain B would leave more offspring because its host lives for longer. However, if virulence was linked to the nematode’s reproductive output and the eggs were released at a time when they were likely to infect new hosts, then strain A would bequeath more of its genes to subsequent generations. Consequently, the proportion of strain A in the nematode population would increase with time and there would be constant selection for increasing virulence. The sheep and the parasites may eventually be driven to extinction by these changes, but individual animals (and humans) are almost always driven by their own immediate self‐interest rather than hypothetical future prospects.

1.5.1 The Red Queen’s Race Hypothesis

      The scenario described above naturally begs the question of, if this is true, why does life still exist today. This is because, on this basis, parasites and other pathogens should have killed everything off many millions of years ago. The answer is that the scenario is too simplistic and all host: parasite/pathogen relationships involve a complex array of competing factors. Consequently, the evolutionary endpoint of any relationship is case‐dependent. Sometimes the parasite becomes more virulent, and sometimes its virulence attenuates to an intermediate level, but one cannot assume that the natural endpoint is a mutually beneficial form of mutualism. Indeed, the relationship between a parasite and