User:Ash0315/sandbox

citations did not transfer so they were manually entered into the main article but not here many links are in the group sandbox.

Pathology
C. diphtheriae causes an acute, highly transmittable infection known as Diphtheria that primarily implants in the upper respiratory tract but can also occur in the heart. As the primary method of spread is through particles expelled when an infected individual coughs or sneezes, the most common area of implantation and lesions is the nasopharyngeal tract. The mechanism of action of C. diphtheriae involves planting itself in a certain area of tissue and releasing an exotoxin. This exotoxin is absorbed in the blood, which in turn kills heart, kidney, and nerve cells by blocking protein synthesis. Toxigenic strains in susceptible individuals can cause disease by multiplying and secreting diphtheria toxin into either skin or nasopharyngeal lesions. The diphtheritic lesion is often covered by a pseudomembrane composed of fibrin, bacterial cells, and inflammatory cells. Diphtheria toxin can be proteolytically cleaved into two fragments - an N-terminal fragment A (catalytic domain), and fragment B (transmembrane and receptor binding domain). Fragment A catalyzes the NAD+ -dependent ADP-ribosylation of elongation factor 2, thereby inhibiting protein synthesis in eukaryotic cells. Fragment B binds to the cell surface receptor and facilitates the delivery of fragment A to the cytosol.

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Pathology[edited]
The mechanism of action for C. diphtheriae involves the bacteria establishing itself on a mucosal layer, typically within the respiratory tract, ulcerating it, and creating an inflammatory pseudomembrane which can then form lesions. This is the localized action of C. diphtheriae. It also has a metastatic component wherein the bacteria will release a potent toxin that enters the bloodstream and causes issues to the system at whole but notably the heart, lymph nodes, and brain.

The first step of C. diphtheriae infection involves the bacteria being introduced into the system and planting itself on a mucosal layer. In young children, this typically occurs in the upper respiratory tract mucosa. In adults, faucial diphtheria is more common wherein the primary site of infection is typically the posterior mouth or upper pharynx region. Some unusual sites of infection include the heart, larynx, trachea, bronchi, and anterior areas of the mouth including the buccal mucosa, the lips, the tongue, and the hard and soft palate. The bacteria has a number of virulence factors to help it localize on areas of the respiratory tract, many of which are yet to be properly researched as diphtheria does not affect many model hosts such as mice. One common virulence factor that has been researched extensively in vitro is DIP0733, a multi-functional protein that has shown to have a role in bacterial adhesion to host cells as well as fibrogen-binding qualities. In experiments creating a mutant strand of the ''Cor. diphtheriae'', adhesion and epithelial infiltration decreased significantly. Furthermore, the ability to bind to extracellular matrix aids the bacteria in avoiding detection by the body's immune system.

Once the bacteria has localized in one area, it starts multiplying to create the inflammatory pseudomembrane. In patients with faucial diphtheria typically have the pseudomembrane grow over the tonsil and accessory structures, uvula, soft palate, and possibly also the nasopharyngeal area. In upper respiratory tract diphtheria, the pseudomembrane can grow on the pharynx, larynx, trachea, and bronchi/bronchioles. The pseudomembrane starts off white in color and then later becomes dirty-gray and tough due to the necrotic epithelium.

When respiratory tract diphtheria causes psuedomembrane formation on the trachea or bronchi will decrease efficiency of airflow. Over time, the diffusion rate in the alveoli decreases due to the lower airflow and decreases the partial pressure of oxygen in the systemic circulation which can cause cyanosis and suffocation.

Diphtheria toxin can be proteolytically cleaved into two fragments - an N-terminal fragment A (catalytic domain), and fragment B (transmembrane and receptor binding domain). Fragment A catalyzes the NAD+ -dependent ADP-ribosylation of elongation factor 2, thereby inhibiting protein synthesis in eukaryotic cells. Fragment B binds to the cell surface receptor and facilitates the delivery of fragment A to the cytosol.

Lead[edit]
* all work on lead b/c the article one is really bad :') * Diphtheria is caused by the adhesion and infiltration of the bacteria into the mucosal layers of the body, primarily affecting the respiratory tract and the subsequent release of an endotoxin. The pathogen has both, a localized effect in terms of skin lesions, as well as a metastatic, proteolytic effects on other organ systems in severe cases. Originally a major cause of childhood mortality, diphtheria has been almost entirely eradicated from the United States due to the vigorous administration of the diphtheria vaccination in the 1910s. Lack of public resources and the bacteria's specificity has lead to a diminished understanding of the pathogen as model animals such as mice are not susceptible.