Pathogenicity Mechanisms
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Pathogenicity Mechanisms
Introduction
Human host immunity has undergone cycles of advancement, resulting in a well-organized and robust pathogen defense system. Furnished by time and condition immune system has been able to develop three significant defense layers comprising physical barriers, innate immune, and adaptive immune systems that synergistically operate to their efficiency. However, human beings continue facing exponentially rising threats from pathogens, and according to (Woolhous & Gaunt., 2007), infectious diseases are currently rated as the number one human killer. The trend raises worrying concerns about the reliability of the immune system on defending the host from pathogens. Unfortunately, as the immune system advances in defense mechanisms, pathogens evolve and develop strategies to beat immune system responses (Mañes, del Real, & Martínez-A., 2003). There are several mechanisms through which disease-causing microbes have adopted or advanced to bypass the immune system and elicit their disease symptoms, but this paper will discuss common ones; capsule production, toxins, and adhesins.
Adhesins
Creating contact with the host is crucial in the pathogen attack (Ribet & Cossart., 2015). All the communication sites, such as skin, mucous membranes, and others, have an unsuitable environment to the invaders’ attachment. Secretions from the protective layers such as gastric juice, saliva, and sweat are meant to wash microbes and reduce their chances of colonization (Crawford & Wilson., 2015). Some microbes elude the washing by producing binding substances, which help them stick to several host tissues. By adhering to host tissues, the pathogens can multiple and initiate their invasion (Sadikot et al., 2005).
Adhesive complexes (adhesins) expressed by some pathogens are either polysaccharides or polypeptides in nature. The protein molecules component forms the appendages (fimbriae) and hair-like structures that attach pathogens to host tissue surface. Other proteins in the complex contribute to the structural strength of the fimbriae. The use of the binding structure for adherence is common in gram-negative bacteria (Neisseria species, V cholera, E Coli, P aeruginosa, among others). Some microbes also use fimbriae polypeptide complexes (protein adhesives that do not form structures) in binding. Afimbrae use has been observed in mycobacterial pathogens mainly; Streptococcus spp, Staphylococcus spp. The other adhesive composition, which is the polysaccharides are part of the microbes’ cellular membrane.
With these complexes molecules, the pathogens can enhance their adherence to the host. Some bacteria have been known to utilize more than one adhesion mechanism to ensure they stick on the host for long periods. At the point of interaction with the host tissue, the pathogen creates a receptor-ligand synergy which might be of either; protein-carbohydrate or protein-protein in nature with host surface molecules, which include; glycoproteins, glycolipids, and extracellular matrix proteins. In some instances, the invaders also have to rely entirely on their structure and complex chemicals to fix the job. At the host tissue surface, the receptors stick to an afimbrial polypeptide complex on the pathogen surface for adherence.
Capsule production
Capsules refer to exopolysaccharides, which form the coating on extracellular surface molecules produced by pathogens. It has been established that capsules are specific to different species of microbes as they utilize different chemicals in their manufacture. Production of capsules is among the best mechanisms that enhance microbes’ virulence by ensuring that pathogens take longer to clear from infected regions. Capsules play significant roles in protecting pathogens from the immune responses and effects of medicines. The capsules shield the microbes’ phagocytosis by interfering with immunological surveillance such as restraining opsonization by antibodies, which is meant to provide signals for macrophages and other phagocytes. Lack of pathogen signals induces an inflammatory response as the phagocytes produce excess inflammatory cytokines to eliminate the pathogens’ threat. This series of reactions results in damage to host tissues.
Some bacteria species have been known to produce capsules include; Pseudomonas aeruginosa, Streptococcus pneumonia, and Neisseria meningitides. The pneumococcus capsular polysaccharide is one of the prime virulence factors characterized by the bacteria. Studies estimate that there exist more than 85 capsular types different from each other. Among the capsules, about a quarter are known to cause invasive diseases that affect the global population. Structural differences in their polysaccharides chemicals determine the type of capsules. For example, the P aeruginosa capsule comprises of alginate (guluronic acid and acetylated mannuronic).
Toxins
Toxins are inherent components of microbes’ biological weapons. They are proteinaceous or non-proteinaceous compounds secreted by pathogens to kill the host cells. Some of the non-proteinaceous toxins are; teichoic acids elucidated by Gram-positive microbes and LPS (endotoxin) by Gram-negative organisms. On the other hand, Proteinaceous toxins are usually enzymes that are delivered to host tissues by (1) discharge into the adjacent milieu and (2) direct injection into the host tissues and cells cytoplasm using type III secretion systems. Pathogens can inject the toxins in host cells using other diverse range of mechanisms. Pathogens exotoxins (Proteinaceous toxins) are grouped into four categories in relation to their amino acid structure and functions; A-B toxins, pore-forming toxins, proteolytic toxins, and other toxins.
A-B toxins are produced by several pathogens but are commonly used in by bacteria; Vibrio cholerae, Bordetella pertussis, and Corynebacterium diphtheria, among many others. The toxins consist of two subunits; A-one that possesses enzymatic activity ranges from ADP ribosylating activity in pertussis, diphtheria, and cholera to proteolytic activities in tetanus. Proteolytic toxins digest specific host cell proteins resulting in some manifestation of clinical symptoms of the disease. A typical example is the synaptobrevins effect of botulinum that hinders the release of neurotransmitters leading to host paralysis. The second unit B, is responsible for the delivery of toxins into the host and also plays the role of binding the pathogen to the host tissues.
Several microbes, especially Gram-negative pathogens elicit Pore-forming toxins. The toxins create a pore in host cells hence inducing lysis. The group of pore-forming toxins continue growing but are all under the RTX family (Repeat arginine (R) threonine (T) X motif within each toxin). In addition to these toxins, other microbes have possessed toxins in the form of immunoglobulin A (IgA) protease, which is a stable heat toxin that activates guanylate cyclase. Some other microbes possess toxins that modify the host cell cytoskeleton. Studies indicate that pathogens utilize toxins for a series of actions but mainly disruption of immune surveillance system and destruction of host defense structural integrity to enable them to establish and keep infection.
Impact of pathogenic mechanism knowledge to Nurses
Knowledge of the pathogenicity mechanism has varsity importance on how healthy workers execute their responsibilities. For instance, the information has led to the grouping of pathogens in different types of pathogenic mechanisms hence developing specific tool and approaches to efficiently diagnosis, prognosis, and clinical management of the resulting infectious disease
Pathogenicity knowledge also fashions health practitioners’ excellent understanding of complex interactions between microbes and the host and can utilize such information in controlling the disease. For instance, vaccines and other therapeutic approaches can be used strategically to deal with the infectious diseases which have shown resistance to certain medications.
References
Crawford, A., & Wilson, D. (2015). Essential metals at the host-pathogen interface: nutritional immunity and micronutrient assimilation by human fungal pathogens.FEMS yeast research, 15(7).
Mañes, S., del Real, G., & Martínez-A, C. (2003). Pathogens: raft hijackers. Nature Reviews Immunology 3(7), 557-568.
Ribet, D., & Cossart, P. (2015). How bacterial pathogens colonize their hosts and invade deeper tissues. Microbes and infection, 17(3), 173-183.
Sadikot, R. T., Blackwell, T. S., Christman, J. W., & Prince, A. S. (2005). Pathogen–host interactions in Pseudomonas aeruginosa pneumonia. American journal of respiratory and critical care medicine, 171(11), 1209-1223.
Woolhouse, M., & Gaunt, E. (2007). Ecological origins of novel human pathogens. Critical reviews in microbiology, 33(4), 231-242.