Parasites And Their Virulence Essay Example For Students

Parasites And Their Virulence Essay ABSTRACT Why do some parasites kill the host they depend upon while others coexist with their host? Two prime factors determine parasitic virulence: the manner in which the parasite is transmitted, and the evolutionary history of the parasite and its host. Parasites which have colonized a new host species tend to be more virulent than parasites which have coevolved with their hosts. Parasites which are transmitted horizontally tend to be more virulent than those transmitted vertically. It has been assumed that parasite-host interactions inevitably evolve toward lower virulence. This is contradicted by studies in which virulence is conserved or increases over time. A model which encompasses the variability of parasite-host interactions by synthesizing spatial (transmission) and temporal (evolutionary) factors is examined. Lenski and May (1994) and Antia et al. (1993) predict the modulation of virulence in parasite-host systems by integrating evolutionary and transmissibility factors. INTRODUCTION Why do certain parasites exhibit high levels of virulence within their host populations while others exhibit low virulence? The two prime factors most frequently cited (Esch and Fernandez 1993, Toft et al. 1991) are evolutionary history and mode of transmission. Incongruently evolved parasite-host associations are characterized by high virulence, while congruent evolution may result in reduced virulence (Toft et al. 1991). Parasites transmitted vertically (from parent to offspring) tend to be less virulent than parasites transmitted horizontally (between unrelated individuals of the same or different species). Studies in which virulence is shown to increase during parasite-host interaction, as in Eberts (1994) experiment with Daphnia magna, necessitate a synthesis of traditionally discrete factors to predict a coevolutionary outcome. Authors prone to habitually use the word decrease before the word virulence are encouraged to replace the former with modulate, which empha sizes the need for an inclusive, predictive paradigm for parasite-host interaction. Evolutionary history and mode of transmission will first be considered separately, then integrated using an equation discussedby Antia et al. (1993) and a model proposed by Lenski and May (1994). Transmission is a spatial factor, defined by host density and specific qualities of host-parasite interaction, which gives direction to the modulation of virulence. Evolution is a temporal factor which determines the extent of the modulation. The selective pressures of the transmission mode act on parasite populations over evolutionary time, favoring an equilibrium level of virulence (Lenski and May 1994). DOES COEVOLUTION DETERMINE VIRULENCE? Incongruent evolution is the colonization of a new host species by a parasite. It is widely reported that such colonizations, whensuccessful, feature high virulence due to the lack of both evolved host defenses and parasitic self-regulation (Esch and Fernandez 1993, Toft et al. 1991). Unsuccessful colonizations must frequently occur when parasites encounter hosts with adequate defenses. In Africa, indigenous ruminants experience low virulence from Trypanosoma brucei infection, while introduced ruminants suffer fatal infections (Esch and Fernandez 1993). There has been no time for the new host to develop immunity, or for the parasite to self-regulate. Virulent colonizations may occur regularly in epizootic-enzootic cycles. SinNombre virus, a hemmorhagic fever virus, was epizootic in 1993 after the population of its primary enzootic host, Peromyscus maniculatus, had exploded, increasing the likelihood of transmission to humans (Childs et al. 1995). Sin Nombre exhibited unusually high mortality in human populations (Childs et al. 1995), which were being colonized by the parasite. It is assumed that coevolution of parasite and host will result in decreased virulence (Esch and Fernandez 1993, Toft et al. 1991). Sin Nombre virus was found to infect 30.4 % of the P. maniculatus population, exhibiting little or no virulence in the mice (Childs et al. 1995). Similar low levels of virulence have been found in the enzootic rodent hosts of Yersinia pestis (Gage et al. 1995). In Australia, decreased grades of virulence of myxoma virus have been observed in rabbit populations since the virus was introduced in 1951 (Krebs C. J. 1994). Many of the most widespread parasites exhibit low virulence, suggesting that success in parasite suprapopulation range and abundance may be the result of reduction in virulence over time. Hookworms are present in the small intestines of one-fifth of the worlds human population and rarely induce mortality directly(Hotez 1995). Evolution toward a higher level of virulence has been regarded as an unexplainable anomaly. Parasites which do less harm presumably have an advantage throughout a long coevolutionary association with their hosts. Eberts (1994) experiment with the planktonic crustacean Daphnia magna and its horizontally transmitted parasite Pleistophora intestinalis suggests that coevolution does not determine the direction of the modulation of virulence. Virulence decreased with the geographic distance between sites of origin where the host and parasite were collected (Ebert 1994). Thus, the parasite was significantly more virulent in hosts it coexisted with in the wild than it was in novel hosts. Many viruses, such as Rabies (Lyssavirus spp.), persist in natural populations while maintaining high levels of virulence in all potential hosts (Krebs, J. W. 1995). Ex tinction is not an inevitable outcome of increased virulence (Lenski and May 1994). Increased or conserved virulence during coevolution callsinto question long held assumptions about the effect of coevolution on parasitic virulence (Gibbons 1994). Parasitic virulence frequently changes over coevolutionary time, but the length of parasite-host association does not account for the virulence of the parasite. Transmission has been identified as the factor which determines the level of parasitic virulence (Read and Harvey 1993). TRANSMISSION AND THE DIRECTION OF MODULATION Herres (1993) experiment with fig wasps (Pegoscapus spp.) and nematodes (Parasitodiplogaster spp.) illustrates the effect of transmission mode on parasitic virulence. When a single female wasp inhabited a fig, all transmission of the parasite was vertical, from the female to her offspring. The parasites fitness was intimately tied to the fecundity of the host upon which it had arrived. When a fig was inhabited by sever al foundress wasps, horizontal transmission between wasp families was possible. In the figs inhabited by a single foundress wasp, Herre found that less virulent species of the nematode were successful, while in figs containing multiple foundress wasps, more virulent species of the nematode were successful. Greater opportunity to find alternate hosts resulted in less penalty for lowering host fecundity. More virulent nematodes had an adaptive advantage when host density was high and horizontal transmission was possible. When host density was low, nematodes which had less effecton host fecundity ensured that offspring (i.e. future hosts) would be available. Christopher columbus - american hero or portuguese EssayAn alternative explanation for the reduced virulence of congruently evolved hosts and parasites is the prudent parasitehypothesis (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 virulenc e 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 (Ebert1994), 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 mortalitydecreases 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 theequilibrium 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