Parasite Toxicity: Parasite Evolution and Host Adaptation

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A parasite derives nutrients from its host through a mode of feeding known as parasitism. Parasites live inside or on the outside of the host’s body throughout its life cycle. A host can suffer from conditions caused by the parasite in all stages of the parasite’s life (Webster, 2009). A parasite can affect its host in quite a number of ways depending on the parasite’s species. Parasites produce some toxic substances that are dangerous to the host. The most devastating effects of a parasite to the host are related to the toxicity of the parasite. Some parasites evolve at a fast rate and therefore making it difficult for scientists to conduct research on the level of toxicity of a parasite over the evolution time. (Webster, 2009). However, a number of experts have argued that the level of toxicity of parasites to their hosts reduces over evolution time. This paper aims at evaluating the relevance of this notion.

Adaptation occurs at every level of an individual organism. However, empirical studies on parasite evolution present a different picture; the toxicity continues to decrease (Viney et al., 2002). Most importantly, some experts argue that the evolution of lower toxicity in response to limited parasite dispersal is a clear indication of adaptation at the group level. The effect of dispersal on reduced parasite toxicity can be understood in terms of adaptation. The process of adaptation is an evolutionary process that has prompted many researchers to develop an interest in studying it. According to Darwin’s theory of evolution, adaptation is a consequence of natural selection. In this case, the process of adaptation takes place through the action of natural selection (Viney et al., 2002). The process of natural selection is mediated through differential reproductive success and the associated genetic changes of the organism in question. This phenomenon is often passed to the organisms’ future generations. Increased dispersal reduces a parasite’s toxicity because dispersal subjects the parasite to different environments (Tinsley, 1999). Some of these environments hamper the production of toxins by the parasite. The reduction in parasite virulence is therefore attributed to increased dispersal (Tinsley, 1999).

The phenomenon of natural selection leads to the molecular evolution and ultimately changes the chemical and biological behavior of parasites. The Red Queen Hypothesis states that biotic interactions are a result of molecular evolution (Stearns & Hoekstra, 2005). According to this theory, species coexist in the ecosystem. However, adaptation is likely to change the manner in which species coexist. Consequently, one species may become more competent than the other. As a result, the less competent species becomes displaced from the system. This theory has been used by a number of scientists to explain the reduction in parasites’ toxicity on their hosts (Stearns & Hoekstra, 2005). This theory explains the fact that adaptation often alters the genetic material of various species including parasites within the ecosystem. As a result, the species acquires specific genes, which influence the overall outlook depending on the conditions dictated by the environment (Rosza et al., 2000). Consequently, the species may alter its chemical characteristics after some time. For example, toxins that were produced earlier might become irrelevant after the adaptation. Thus, their production or effect lessens over the course of evolution (Rosza et al., 2000). A reduction in the toxicity of parasites can be best explained using this hypothesis.

Biologists have conducted different studies to evaluate a reduction in the toxicity of Encephalitozoon cuniculi owing to changes in its mitochondria over time (Roger et al., 2006). Intracellular parasites undergo a number of cellular and genetic transformations during their lifetime. According to the current data on different genomes, E. cuniculi as a genome generates ATP through substrate-level phosphorylation only (Roger et al., 2006). Proliferating microsporidia have been known to recruit the host’s mitochondria. As a result, this parasite often tops up its ATP requirements by extracting some from its host. It has been found that E. cuniculi has genes that code vector proteins that resemble the host’s ADP/ATP transporters. Lewis and Campbell (2002) compared the sequences of four E. cuniculi ATP transporters to those derived from nucleotide transporters found in plastids and bacterial parasites, and those of previously characterized ATP/ADP translocases (Lewis & Campbell, 2002). The researchers learnt that the four E. cuniculi sequences differed from each other significantly. The researchers launched an investigation in order to understand why the four sequences were different from each other. The researchers used antisera to determine the expression and cellular location of the E. cuniculi transporters (Lewis & Campbell, 2002). The researchers attributed the differences in location and expression of E. cuniculi sequences to adaptation. According to the researchers, E. cuniculi have undergone changes in their genomic composition over time (Price, 1980).

The use of bacterial-like nucleotide transporters (NTTs) to acquire ATP from their hosts is a unique strategy (Price, 1980). This strategy often leads to stiff competition for ATP between the host and E. cuniculi. This competition is sometimes extremely toxic to the host. Other intracellular parasites like Leishmania and Plasmodium have been found to use transporters that are homologous to their hosts’ proteins (Price, 1980). The study conducted by Price (1980), suggests that microsporidia use NTTs to steal ATP from their hosts. Price’s study also suggests that Microsporidia have undergone evolutionary changes leading to changes in the expression and location of NNTs. However, the reasons as to why E. cuniculi has undergone these changes are not clear, but according to Price (1980) this might be due to changes in the ATP pathway in their hosts. The technique used by E. cuniculi to meet its ATP requirements by stealing extra ATP from the host often leaves the host literally starving (Lewis & Campbell, 2002). This is extremely toxic to the host during harsh conditions especially when food is scarce. During such conditions, the parasite significantly benefits because its energy requirements are less than those of the host. The study conducted by Tinsley (1999) suggests that this phenomenon seems to be reducing because E. cuniculi ATP transporters located in the parasites’ mitochondria normally change their genetic composition.

In another study conducted by Jean and Clark (2012), a completely new method was used to study the effect of evolution on toxicity. The researchers endeavored to evaluate how evolution in the host has contributed to low toxicity in parasites. According to Jean and Clark (2012), infectious diseases significantly influence the demography of humans, plants and animal populations. The host’s resistance to diseases varies with time and in the process affects disease patterns. In a number of host loci, variability has been reported in many instances (Hughes et al., 2012). For example, the manner in which the major histocompatibility complex influences disease expressions is a result of selective forces, which have been imposed by pathogens. It has also been found that at the molecular level, pathogen diversity influences the dynamics of epidemics (Price, 1980). For example, low HIV prevalence in a given region may be due to low genetic variation in that region. Other studies have revealed that there is a negative relationship between the general measure of pathogen diversity and disease incidences (Tinsley, 1999).

Furthermore, advanced genetic engineering studies have shown that there is a negative correlation between disease prevalence and population resistance biodiversity. The relationship between disease dynamics and host population genetic structure has not been properly investigated by genetic engineering experts (Roger et al., 2006). New diseases have continued to emerge due to pathogen evolution. Thus, it is paramount to study how evolution in the host has contributed to low toxicity in parasites. According to Lively and Dybdahl (2000), the current models examining host-pathogen co-evolution have been shaped by the gene for gene paradigm.

In addition, this theory indicates that the pathogen virulence gene and a resistant gene in the host must be present at the same time for a resistant reaction to take place. Lively and Dybdahl (2000) argue that the strength of the positive relationship between host resistance and pathogen virulence in the Linum Melampsora interaction, explains the potential for host variation to determine evolutionary trajectories of pathogen populations (Webster, 2009). Furthermore, pathogens in a low diversity host population are not normally favored by evolution. Lively and Dybdahl (2000) conclude that the parasite systems of plant and animal parasite systems play a major role in the transmission of diseases to the host. Pathogen isolates that resistant genes fight to overcome affect the rate of spore production. A reduction in spore production occurs when resistant genes are attacked by virulent pathotypes. From the study conducted by Webster, it can be noted that some hosts may undergo evolutionary changes which limit the toxicity of parasites (Webster, 2009). These findings support the notion that the toxicity of parasites to their hosts reduces over evolution time. This study is particularly important because it evaluates this phenomenon from the host’s perspective.

Furthermore, insect-borne parasites are known to adapt to changes in temperature and nutrition within the arthropod vector by lifecycle differentiation. Insect-borne parasites normally face immunological attacks and some nutrient deficiencies while in the arthropod vector (Webster, 2009). Most importantly, these parasites use specific cues to initiate changes in temperature and PH in the host’s body (Hurd et al., 1998). These changes are aimed at challenging the hosts by making them vulnerable. Molecules that are involved in the generation of these cues continue to evolve while there has been a significant reduction in the toxicity caused by insect-borne parasites owing to evolutionary changes. African trypanosomes, which are protozoan parasites, are some of the most harmful parasites known to man (Lewis & Campbell, 2002). These parasites are often transmitted by tsetse flies, and this requires the formation of bloodstream stumpy forms. This phenomenon is genetically predetermined. A stumpy inducing factor has been known to induce the formation of stumpy forms. When ingested by tsetse flies, stumpy forms differentiate into procyclical forms. Proteins associated with differentiation (PAD) are controlled by predetermined genetic factors. Tinsley (1999) argues that these genetic factors have undergone numerous changes as the parasites attempt to adapt to changes in the environment. Consequently, some of the changes that occur are overwhelmed by changes in the ecosystem. As a result, there has been a reduction in the toxicity of trypanosomes (Lewis & Campbell, 1980).

Recent research has found that the effects of a parasite on the host vary widely. The most devastating effects of a parasite to its host are related to the toxicity of the parasite. The study conducted by Hurd, Lane, and Chappel (1998) revealed that increased dispersal reduces a parasite’s toxicity because dispersal subjects the parasite to different environments. Some of these environments hamper the production of toxins by the parasite in question. This approach has also been used to explain a reduction in parasite virulence. Another study conducted by Hurd et al. (1998) used the Red Queen hypothesis to explain how the phenomenon of natural selection leads to the molecular evolution and ultimately changes the chemical and biological behaviors of parasites. Red Queen Hypothesis states that biotic interactions are a result of molecular evolution (Tinsley, 1999).

In addition, the study conducted by Hurd et al. (1998) indicates that the use of bacterial-like nucleotide transporters (NTTs) to acquire ATP from hosts is a unique strategy. This strategy often leads to stiff competition for ATP between the host and the parasite. This competition is sometimes extremely toxic to the host. Other intracellular parasites like Leishmania and Plasmodium have been found to use transporters that are homologous to their hosts’ proteins (Tinsley, 1999). The study conducted by Hurd et al. (1998) suggests that this phenomenon seems to be reduced owing to evolutionary changes in the genetic composition of E. cuniculi ATP transporters located in the parasite’s mitochondria.

On the other hand, Stearns and Hoekstra (2005) used a different approach to explain this phenomenon. The researchers endeavored to evaluate how evolution in the host has contributed to low toxicity in parasites. From the study conducted by these researchers, it can be noted that some hosts may undergo evolutionary changes, which limit the toxicity of parasites. These findings support the notion that the toxicity of parasites to their hosts reduces over evolution time. This study is particularly important because it evaluates this phenomenon from the host’s perspective.

In conclusion, parasites are known to adapt to changes in temperature and PH in the arthropod vector. These parasites use specific cues to initiate changes in temperature and PH in the host’s body or the host’s environment. This is aimed at challenging the hosts or making them vulnerable. Price (1980) argues that genetic factors have undergone numerous changes as the parasites attempt to get used to their new environment. In addition to that, some of the genetic changes that occur are overwhelmed by changes in the ecosystem (Price, 1980). As a result, there has been a reduction in the toxicity of trypanosomes. Thus, it can be argued that the toxicity of parasites to their hosts reduces over evolution time.

References

Clark, D. P., & Jean, N. P. (2012). Molecular biology. 2^nd ed. Waltham, MA: Academic Press.

Hughes, D. P., Brodeur, J., & Thomas, F. (2012). Host manipulation by parasites. London: Oxford University Press. Web.

Hurd, H. Lane, R. P., & Chappell, L. H. (1998). Parasite-insect interactions: Reciprocal manipulation. British Society for Parasitology Journal, 116 (35), 48-59.

Lively, C. M., & Dybdahl, M. F. (2000). Parasite adaptation to locally common host genotypes.Nature Journal, 405 (19), 128-145. Web.

Lewis, E., & Campbell, J. F. (2002). The behavioral ecology of parasites. Wallingford: CABI Publishers. Web.

Price, P. W. (1980). Evolutionary biology of parasites. Princeton, NJ: Princeton University Press.

Roger, M. J., Pedro, N., & Gonzalez, L. (2006). Allelopathy: a physiological process with ecological implications. Dordrecht, Netherlands: Springer Publishers.

Rosza, L., Reiczigel, J., & Majoros G. (2000). Quantifying parasites in samples of hosts. Journal of Parasitology, 86 (7) 228-232. Web.

Stearns, S. C. & Hoekstra, R. F. (2005). Evolution: an introduction. Oxford: Oxford University Press.

Tinsley, R. C. (1999). Parasite adaptation to environmental constraints. Cambridge: Cambridge University Press.

Viney, M. E., Read, A. F., & Chappell, L. H. (2002). Parasite variation: immunological and ecological significance. Cambridge University Press. Web.

Webster, J. P. (2009). Natural history of host-parasite interactions. London: Academic Publishers.

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Parasite Toxicity: Parasite Evolution and Host Adaptation

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