Regardless of how they are classified, all living things follow Darwin's theory of natural selection. A nice illustration are microbial pathogens. The immune system of the host must be constantly attacked if these organisms are to not only survive but also thrive there. Furthermore, there are a variety of ways in which these infections cause disease. Nevertheless, Alberts et al. (2002) contend that all pathogens, regardless of the mechanism employed to cause infection, rely upon their ability to colonize the host, attain a suitable niche, evade the host's defence measures, replicate, and leave the infected host for another (p. 1423). As such, colonization is the first step of infection. Nevertheless, most parts of the human body are covered by the skin, which provides a strong first line of defense, mucosal surfaces consisting of a single epithelial layer, such as those found in the lungs and the small intestine, are more susceptible sites for infection.
The protective barriers in the human body are lined by normal flora, which competes with pathogenic fungi and bacteria. Yet, exceptions from this behaviour do occur, as it can be observed in viruses which seem to prefer sites of lower microorganism densities for infection. With this brief outline of the basic stages of infection, it is important to underscore that both hosts and pathogens undergo constant evolution to survive. Janeway, et al. (2001) contends that pathogens have developed elaborate approaches to evade the host's defense measures (p. 425). As such, the aim of this paper is to present a concise discussion on diversity in microbial pathogens in relation to pathogenesis and immune evasion. The paper will focus on fungal pathogens.
Diversity in Fungal Pathogens
Over a million species of fungi are in existence but only a small percentage of the total number can be considered true pathogens, capable of causing illnesses in individuals with fully functional immune systems. However, fungal infections still present inimitable challenges to the immune system of their host. Brown (2011) contends that the majority of fungal pathogens (comprising commensals - Candida or saprophytes, Aspergillus) are, opportunistic as they cause diseases when the host's immune system is weak or there is a breach in the physical defense barrier (p. 1). Certainly, fungal infections emanating from compromised immune systems have been on the rise over the past few years. The same study highlights that diseases caused by fungi are the major cause of morbidity and mortality in individuals with altered immune systems. The increase of incidences of fungal diseases has necessitated studies aimed at understanding mechanisms that trigger natural and adaptive anti-fungal protection. Understanding these mechanisms is crucial in comprehending how fungal pathogens generate diversity at their surfaces and how this contributes to the pathogenesis and immune evasion.
Fungi Recognition in Hosts
Studies conducted on this subject revealed that phagocytic cells (dendritic cells, macrophages, monocytes, and neutrophils) are essential for the recognition and protection against fungal pathogens. Intrinsically, defects in any of these phagocytic cells may result in a susceptibility to fungal infection. Hohl et al. (2009) contend that although the natural reaction facilitated by macrophages and neutrophils is sufficient to control most fungal infections, comprehensive anti-pathogen protection necessitates an adaptive reaction. Dendritic cells initiate and direct adaptive response. In addition to this, other cells, such as monocytes, aid this process. The process results in an immune response comprising various fungal-distinct components. Nevertheless, contends that protection in all instances requires the amplification of the anti-fungal functions of phagocytes. Essentially, phagocytes achieve inherent recognition of fungal pathogens in hosts.
Fundamentally, this recognition is accomplished by sensing cell wall constituents, although argues that certain internal components, such as DNA, may be detected. Cell walls of fungi are primarily made up of carbohydrate polymers, which are effective in preserving the rigid structure, giving the microorganism its shape and offering protection. Nevertheless, asserts that in some species of fungi, such as C. albicans, internal components are exposed. Furthermore, the dynamic nature of the cell wall allows for significant change, especially during morphological transitions, a common occurrence in fungi. Nather and Munro (2008) identified at least three causes of cell wall variation (p. 137). These three are changes in the cell wall composition, protein alteration, and differential glycosylation. The same study reveals the reversible transitions of C albicans between the yeast form and the filamentous configuration. This change in morphology can help in comprehending the virulence of C. albicans. It is also imperative to note that the configuration of the cell wall differs from one species of fungi to another and between the varying morphological layouts. The membrane-attached pattern recognition receptors (PRRs) are the primary detectors of fungal components. Detection can be either direct or indirect. Direct detection is by host's phagocytes while indirect or opsonic is through membrane-coupled opsonic receptors.
Diversity in Fungi Aiding Immune Evasion
The processes through which pathogens adapt to their host are varied. However, Calo et al. (2013) assert that advances made through studies have highlighted some ways in which these microorganisms achieve these remarkable achievement. These processes employ an array of diversity initiators ranging from the mode of reproduction, prions, aneuploidy, and mutations. These generators are depicted in Figure 1. Schmid-Hempel (2009) contends that studies have revealed the correlation between immune evasion by parasites and pathogenesis. In essence, the advent of virulence may be a sign of immune evasion. As discussed earlier in this paper, it is important to highlight that pathogens, in this case fungi, evade immunity by altering the composition of their cell wall. By doing so, these pathogens become "invisible" to the PRRs. In this section, the discussion follows the different ways in which pathogens alter their cell surfaces to facilitate the immune evasion.
Mode of Reproduction
According to Calo et al. (2013), sexual and parasexual means of reproduction have the capability of introducing the diversity in cell surfaces and ultimately aiding immune evasion. Heitman (2010) contends that studies have proven that pathogenic fungi and parasites reproduce sexually rather than by clonal division or sexually as was thought before (p. 86). Calo et al. (2013) contend that these modes of reproduction promote, to some extent, an exchange of genetic materials. Nevertheless, the author is keen on highlighting that, in many instances, inbreeding is involved helping to preserve desired genomic configurations. As a result, these pathogenic microbes spawn limited genetic diversity, which may result in the immune evasion. Inherently, pathogenic microorganisms reproduce either sexually or parasexually. Parasexual reproduction involves cell-cell fusion. Genetic diversity is achieved through autonomous chromosomal assortment. Parasexuality has been observed in C. albicans. On the other hand, sexual reproduction facilitates evolution through either removal of deleterious mutations or combination of beneficial alleles. In essence, the modes of reproduction discussed facilitate adaptation of pathogenic fungi to the slow evolving host body and, as such, aid the immune evasion.
Aneuploidy
In humans, aneuploidy is deleterious as seen in the genetic condition Down's syndrome. Nevertheless, aneuploidy can be beneficial. According to Calo et al. (2013), it results in drug resistance in fungi. Moreover, this facilitates rapid adaptive advancement, aiding immune evasion. Torres et al. (2010) contend that these pathogenic fungi contain mutations that enable the microorganisms to tolerate aneuploidy by facilitating throughput toxic proteins in stoichiometric imbalance (p. 71). It is important to highlight that these genotypic variations dictate the phenotypic appearance of these pathogens so any disparity will lead to an alteration of the cell surface aiding immune evasion.
Hsp90 Facilitated Evolution
Jarosz and Lindquist (2010) contend that the protein chaperone Hsp90 can facilitate immune evasion in pathogenic fungi (p. 1820). In essence, this chaperone system is capable of altering the correlation between phenotypes and genotypes, particularly under stressful environments. Furthermore, Jarosz and Lindquist (2010) contend that the above process kick-starts an evolutionary process which promotes the formation of genetically intricate traits (p. 1821). Moreover, Calo et al. (2013) assert that Hsp90 may act in two ways as an initiator for variability. The first method is through transporting altered cell regulators. The second technique is through the interaction of the Hsp90 chaperone system and calcineurin (cell signal regulator), permitting distribution of new traits, such as drug resistance to an assorted range of fungal species.
Prions
Originally, prions were observed because of their ability to cause mammalian diseases. Nevertheless, prions also occur in fungi and can be either harmful or beneficial. Calo et al. (2013) contend that prions can facilitate a bridge between protein homeostasis and the microorganisms' stress reactions, as such promoting phenotypic flexibility. As a result, pathogenic cells can propagate and thrive under different conditions.
Conclusion
All organisms have to conform to the Darwinian selection. Owing to their complexity, some organisms evolve at a more rapid rate than other do. This phenomenon applies in particular when observed the relationship between pathogens and their hosts. As discussed in the essay, pathogens hinge their survival on colonizing their host, attaining a sustainable niche then exiting the infected host for uninfected one. Innate immune systems in hosts are designed to identify the attack and eliminate such pathogens. PRRs are used to detect and eliminate pathogenic fungi. As such, pathogens have evolved aiding them to evade these immune systems through altering their surface appearance. The above discussion has outlined briefly some of the mechanisms these pathogenic microorganisms employ to attain immune evasion., paying particular attention to C. albicans.
References
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