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Parasites And Their Virulence Essay Research Paper

Parasites And Their Virulence Essay, Research Paper


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 Ebert’s (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 emphasizes 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 discussed


by 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, when


successful, 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. Sin


Nombre 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


world’s 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. Ebert’s (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). Extinction is


not an inevitable outcome of increased virulence (Lenski and May


1994). Increased or conserved virulence during coevolution calls


into 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


Herre’s (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 parasite’s fitness was intimately


tied to the fecundity of the host upon which it had arrived. When a


fig was inhabited by several 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 effect


on host fecundity ensured that offspring (i.e. future hosts) would be


available.


Low virulence is characteristic of many vertical transmission


cycles. Certain parasites avoid impairing their host’s fecundity by


becoming dormant within maternal tissue. Toxocara canis larvae reside


in muscles and other somatic tissues of bitches until the 42nd to 56th


day of a 70-day gestation, when they migrate through the placenta,


entering fetal lungs where they remain until birth (Cheney and Hibler


1990). A high proportion of puppies are born with roundworm infection,


which can also be transmitted from bitch to puppy by milk (Cheney and


Hibler 1990). If host density is low, a highly evolved vertical


transmission cycle (which exhibits low virulence in the parent)


ensures the survival of the parasite population.


High virulence is characteristic of horizontal transmission


cycles. In Herre’s (1993) experiment, more virulent parasites were


favored when host density was high and reduction of host fitness was


permissible. Certain parasites benefit from reduced host fitness,


particularly parasites borne by insect vectors (Esch and Fernandez


1993) and parasites whose intermediate host must be ingested by


another organism to complete the parasitic life cycle. By immobilizing


their host, heartworm (Dirofilaria immitis) and malaria (Plasmodium


spp.) increase the likelihood that mosquitoes will successfully ingest


microfilaria or gametocytes along with a blood meal. Heartworm


infestation causes pulmonary hypertension in dogs (Wise 1990),


resulting in lethargy and 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. 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.

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