Parasites And Their Virulence

.. d eventual collapse (Georgi and Georgi 1990). Host immobility increases the opportunities for female mosquitoes to find and feed upon hosts (Read and Harvey 1993). Infected dogs have large numbers of D. immitis microfilaria in their circulatory systems, again increasing the likelihood of ingestion by the insect. Many infected dogs eventually die from heartworm, but in the process the parasite has ensured transmission.

Similar debilitating effects have been observed in tapeworm-stickleback interaction; infected sticklebacks must swim nearer the water’s surface due to an increased rate of oxygen consumption caused by the parasite (Keymer and Read 1991). Parasitized sticklebacks are more likely to be seen and eaten by birds, the next host in the life cycle. Many horizontally transmitted parasites manipulate specific aspects of host behavior to facilitate transmission between species. Host fitness is severely impaired in such interactions. The digenean D.

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spathaceum invades the eyes of sticklebacks, increasing the likelihood of successful predation by birds (Milinski 1990). D. dendriticum migrate to the brains of infected ants, causing them to uncontrollably clamp their jaws onto blades of grass, ensuring ingestion by sheep (Esch and Fernandez 1993, Combes 1991). Infection of a mammalian brain by rabies (Lyssavirus spp.) alters the host’s behavior, increasing the chance of conflict with other potential hosts, while accumulation of rabies virus in the salivary glands ensures that it is spread by bites (Krebs, J. W.

et al. 1995). Horizontally transmitted parasites which target nervous tissue increase transmissibility by modifying the host into a suicidal instrument of transmission. Transmission factors determining parasitic virulence are the spatial element in a spatial-temporal dynamic. Host density directly determines the virulence of parasites which depend upon a single host species (Herre 1993). Virulence may be increased when transmission necessitates insect vectors or consumption of the primary host by another species.

Virulence varies inversely with the distance between potential hosts; this distance is magnified when it is measured between different species. THE EQUILIBRIUM MODEL It has been proposed that there is a coevolutionary arms race between parasite and host, as the former seeks to circumvent the defensive adaptations of the latter (Esch and Fernandez 1993). In this view, parasitic virulence is the result of a dynamic stalemate between host and parasite. This exemplifies the red queen hypothesis, which predicts continued stalemate until the eventual extinction of both species. Benton (1990) notes that the red queen hypothesis ignores the potential for compromise in such a system.

Snails (Biomphalaria glabrata) resistant to Schistosoma mansoni are at a selective disadvantage due to the costs associated with resistance (Esch and Fernandez 1993). A high level of virulence persists in the system because the snail cannot afford to mount an adequate defense. The arms race hypothesis assumes that the host population can successfully counter increasing parasitic virulence with resistance over an extended period of time. Although an arms race may be sustainable in some fraction of parasite-host interactions, many hosts (such as B. Glabrata) cannot participate indeterminately. An alternative explanation for the reduced virulence of congruently evolved hosts and parasites is the prudent parasite hypothesis (Esch and Fernandez 1993), in which parasitic virulence decreases in response to host mortality.

Parasites which are too virulent drive their hosts, and themselves, to extinction. Parasites which are less virulent persist in the host population. The prudent parasite hypothesis helps to account for the variation in coevolutionary outcome by linking host population dynamics with virulence, but it fails to describe the individual selective forces which modulate virulence over time. The prudent parasite hypothesis serves as the theoretical framework in which the factors determining parasitic virulence can be synthesized. Antia et al.

(1993) and Lenski and May (1994) propose a tradeoff between transmissibility and induced host mortality which predicts that parasites will evolve toward a level of virulence which strikes an equilibrium in the parasite-host system. Equilibrium models suggest that P. intestinalis, which evolved a higher (yet appropriate) level of virulence in its host (Ebert 1994), is a prudent parasite. Antia et al. (1993) use an equation developed by May and Anderson in 1983 to examine the tradeoffs in parasite-host interaction: Ro = (BN) / (a + b + v). Ro is the net reproductive rate of a parasite, B is the rate parameter for transmission, N is host density, a is the rate of parasite induced host mortality, b is the rate of parasite-independent host mortality and v is the rate of recovery of infected hosts.

Parasite populations grow when transmission or host density increase, when host mortality decreases or when hosts recover slowly. Studies have established a positive correlation between transmissibility (B) and host mortality (a) (Ebert 1994, Antia et al. 1993, Lenski and May 1994). Parasite populations which exhibit high transmissibility (i.e. virulence) within a host population are simultaneously lowering host density. When host density is low, parasites which exhibit high virulence may kill their hosts before contact with new hosts occurs. Thus, transmissibility is a spatial factor which describes the likelihood of contact between hosts and, ultimately, between a parasite and its host.

Lenski and May (1994) propose an evolutionary sequence in which parasite populations adapt to the changes they cause in host density (Fig. 1). A parasite suprapopulation is likely to include a range of genotypes which are expressed in different potential levels of virulence (Lenski and May 1994). When host density is high, more virulent parasites are successful and host density is reduced. At a lower density of hosts, less virulent strains of the parasite are at a selective advantage as they increase host survival during infection and allow more time for transmission to occur.

Also, more virulent strains of the parasite are prone to induce mortality in entire subsets of the host population, driving themselves to extinction along with their hosts. This pattern repeats over time, lowering virulence with each adjustment to declining host population size. Extinction of the host population is avoided when sufficient variation is present in the parasite population (Lenski and May 1994). The evolutionary sequence may be reversed to explain evolution toward higher virulence when parasitic virulence is below the equilibrium level. More virulent strains of the parasite outcompete less virulent strains when host density is above equilibrium. Conservation of virulence over time occurs when a stable equilibrium is maintained. Conserved virulence may be high (Lenski and May 1994), but it reflects stability within a system dictated by a unique set of transmission factors. Many parasites must reach a certain population size within the host to be successfully transmitted, while in certain systems, sacrifice of one host facilitates transmission to the next host (i.e.

interspecies transmission). The inclusiveness of the equilibrium model gives it great potential for accurate predictability of a broad range of parasite-host interactions. CONCLUSION Traditional assumptions about the factors determining parasitic strategy have been largely apocryphal, ignoring contradictory evidence (Esch and Fernandez 1993). Equilibrium models synthesize the temporal (i.e. evolutionary) factors and spatial (i.e. transmission) factors characteristic of parasite-host systems.

Time is required to modulate virulence, while spatial factors such as host density and transmission strategy determine the direction of the modulation. The development of an inclusive, accurate model has significance beyond theoretical biology, given the threat to human populations posed by pathogens such as HIV (Gibbons 1994). Mass extinctions such as the Cretaceous event may have resulted from parasite-host interaction (Bakker 1986), and sexual reproduction (i.e. recombination of genes during meiosis) may have evolved to increase resistance to parasites (Holmes 1993). Parasitism constitutes an immense, if not universal, influence on the evolution of life, with far-reaching paleological and phylogenetic implications. A model which synthesizes the key factors determining parasitic virulence and can predict the entire range of evolutionary outcomes is crucial to our understanding of the history and future of species interaction. Science Essays.