Symptom Eliciting Mechanism of Diseases
Exotoxins causes diseases in different organisms in different ways and these diseases are elicited differently depending on the individual bacterial species. There is a different exotoxin that is released to elicit disease in an organism. Pathogens find a way into the host through contaminated food and water and physical contacts amongst hosts. Once inside the host, they interfere with the normal functioning of the host’s body systems. The paper aims at looking at the different symptom eliciting mechanisms and how this topic influences the nurse profession.
The host’s immune system usually retaliates by making efforts to eliminate the disease-causing pathogens. For instance, in the case of viral diseases, fever is experienced as a symptom since the body increases its temperature in an attempt to kill the virus since high temperature deprives them the chance of surviving. The pathogens, however, are equipped with defensive mechanisms to destroy cells of the host that provides host immunity and protection from foreign disease-causing microorganisms. Bacteria mainly produce toxins that are either proteinaceous (exotoxins) or non -proteinaceous (endotoxins). Basing on amino acid structure and functions, the exotoxins are grouped into three groups, (1)A-B toxins classified to be a toxin type 3 (2) Superantigens toxins a type 1 toxin and (3) Membrane -disrupting toxins, the type 2 toxins.
A-B Toxins
A significant number of bacteria have been discovered to have the A-B toxins e. g vibrio cholerae, Escherichia coli, among others. A-B toxins are made up of two components, component A and B, where component A performs the role of carrying enzymatic activities. In contrast, component B is involved in the toxin binding and delivery processes (Dal Peraro & Van Der Goot, 2016). Component A is found to be characterized by a varying range of enzymatic activity, which ranges from proteolytic, e.g., tetanus activity to ADP\-ribosylations activity, e.g., cholera. Membrane disrupting toxins destroys the plasma membrane, thus damaging the host cells. They are fond of attacking the macrophages, white blood cells, and red blood cells. Clostridium perfringens, staphylococcus aureusaresome of the few bacterial species that produce these types of toxins. They are the causal agents of diseases like tissue necrosis and gas gangrene. Superantigens- the type 1 toxins are antigens that catalyze the production of large numbers of T cells and also stimulate the T-cells to produce cytokine- a substance that triggers immune responses and inflammatory responses that may result into deadly and high fevers and reduced blood pressure. The most susceptible cells to the effects of superantigen toxins are the T cells and macrophages. Microorganisms causing disease, i.e., viruses and bacteria utilize the three mechanisms to cause diseases, and in the process, symptoms of the diseases are manifested. A-B toxins are protein complexes made up of two components, component A and B. They are synthesized as a single polypeptide, and the two portions separate during proteolytic cleavage. Several species of pathogenic bacteria are known to secrete it. The toxins are known to disrupt internal cell function, thus classified as type 3 toxin. Portion A is the active portion that inactivates the signal pathway enzymatically hence affecting the host cell functions while portion Bis are known to carry out binding processes by binding exotoxin molecules onto the surface of the host’s cell membrane and also decides on the cell type to which the toxins will have an effect on. They catalyze the same reaction, although they target different cells. After the toxin binds on the cell membrane, it is moved across the cell membrane. The A-B toxins enter by endocytosis during which the two components split up, and the A part enters into the cell cytoplasm directly. The catalytic reaction by component A of most A-B toxins follows, and they remove the ADP-ribosyl group from coenzyme NAD and covalently attaches it to a few host cell proteins by ADP -ribosylation. This results in interruption of the normal function of the host’s proteins, which thus dictates the damage type to cause. At this point, symptoms of the bacterial disease manifest itself. The host defends itself from the toxin by producing antitoxin antibodies that will prevent the toxins from attaching itself to the host’s cell membrane. Bacteria species utilizing this mechanism include Escherichia coli, Vibrio cholerae, and Corynebacterium diphtheriae.
Super-antigens Toxins
Superantigens are classified to be a type 1toxin and are responsible for the production of T cells and catalyze the production of cytokine from the T cells. Bacterial species are responsible for the production of these exotoxin types include streptococcus pyogenes and staphylococcus aureus. These bacterial species have the ability to produce T lymphocytes through the interaction with varying domains of the beta chain of the receptor of T cell antigens. Superantigens inhibit normal cell processes by bridging T cell receptors (TCR) and major histocompatibility molecules (MCH) molecules resulting in division and differentiation of the T cells giving rise to cells referred to as the effector cells. The resulting effector cells release T cell factors. Considering T cells count that share the Vβ domains is high, most T cells are activated by the superantigens despite their differences in antigen specify resulting to significant disruption of systems hence symptoms similar to that of septic shocks such as multiple organ failures and serious injuries of tissues are exhibited ( Seilie & Wardenburg, 2017, December). The latest research has discovered that superantigens activate another signalling pathway in the T cells when Scr family kinase and Lck are absent by making heterotrimeric guanine nucleotide-binding protein active. This discovery opens up the possibility of coming up with therapeutic reagents that can be used to control diseases resulting from the superantigens. Bacteria species utilizing this mechanism include S. aurelia and S. pyogenes. They cause toxic shock and food poisoning. Superantigens are found to cause high stimulation of the immune cells, which in turn leads to overproduction of cytokines that trigger immune and inflammatory responses hence deadly high fevers, reduced blood pressure, which are the symptoms of diseases the bacterial pathogens producing the toxins cause.
Membrane disrupting toxins
Membrane-disrupting toxins also referred to as pore-forming toxins, and a type 2 toxin usually destroys the cell membrane of host cells by disrupting the phospholipid by layer in the cell membranes. There are two types of these toxins. These are hemolysin and leucocidins. They do insert holes in the cell membrane causing contents of the cytoplasm to leak out. This can also result in cell lysis. Its primary role is to kill professional phagocytes like macrophages, but some of the bacterial tend to use it as an escape route from phagosomes into the cells of the host. Damaged cells release DAMPs- the danger-associated molecular patterns, which in turn attaches to pattern recognition receptors (PRRS) that cause inflammatory cytokines release. Further tissue damage results from this inflammatory response that reduces blood pressure. Clostridium birefringent is a bacterial species that utilize this kind of mechanism to elicit symptoms of gas gangrene; clostridium difficile causes the manifestation of antibiotic-associated colitis symptoms (Nowrouzian et al. 2019).
Professional Application
It is key for nurses to understand how the mechanism works since they work in hospital settings and interact with patients. Understanding how symptoms are elicited and the types of pathogens utilizing the toxins helps them to observe accurate symptoms of a disease they suspect and thus will be able to administer the appropriate care and medication to the patient. It is thus vital for nurses to expand their knowledge for them to deliver medical services effectively. It gives the nurse an ability to understand the process and progress of a disease necessary in creating an effective partnership with the medical staff in making correct decisions based on the states of the infection.
Conclusion
There are three different mechanisms that elicit symptoms of disease in a host, and this includes A-B toxins, superantigens, and Membrane disrupting toxins. The host immune cells recognize and respond to substances that are toxic to the cells of the host. Body cells release an exotoxin that elicits a disease, the body cells respond differently and therefore elicit the diseases in different ways. Understanding how an infection is elicited provides information essential for designing a treatment plan for a patient. It is easier to understand how to resolve a medical condition when you understand the complications involved through the knowledge of the bacterial species eliciting the symptoms of the disease.
References
Dal Peraro, M., & Van Der Goot, F. G. (2016). Pore-forming toxins: ancient, but never really out of fashion. Nature Reviews Microbiology, 14(2), 77.
Nowrouzian, F. L., Ljung, A., Nilsson, S., Hesselmar, B., Adlerberth, I., &Wold, A. E. (2019). Neonatal gut colonization by Staphylococcus aureus strains with certain adhesins and superantigens is negatively associated with subsequent development of atopic eczema. British Journal of Dermatology, 180(6), 1481-1488.biology (Vol. 72, pp. 101-116). Academic Press.
Seilie, E. S., &Wardenburg, J. B. (2017, December). Staphylococcus aureus pore-forming toxins: The interface of pathogen and host complexity. In Seminars in cell & developmental b