symptoms such as shortness of breath. If left untreated, diphtheria toxin may enter the bloodstream, causing damage to the kidneys, nerves, and heart. Extremely rare complications include suffocation and partial paralysis. A vaccine, DTaP, effectively prevents the disease and is mandatory in the United States for participation in public education and some professions (exceptions apply). The first step of C. diphtheriae infection involves the toxigenic bacteria colonizing a mucosal layer. In young children, this typically occurs in the upper respiratory tract mucosa. In adults, the infection is limited mostly to the tonsillar region. Some unusual sites of infection include the heart, larynx, trachea, bronchi, and anterior areas of the mouth including the buccal mucosa, the lips, tongue, and the hard and soft palate. The bacteria have a number of virulence factors to help them localize on areas of the respiratory tract, many of which are yet to be fully understood as diphtheria does not affect many model hosts such as mice. One common virulence factor that has been studied in vitro is DIP0733, a multi-functional protein that has shown to have a role in bacterial adhesion to host cells and fibrogen-binding qualities. In experiments with mutant strains of the C. diphtheriae, adhesion and epithelial infiltration decreased significantly. The ability to bind to extracellular matrices aids the bacteria in avoiding detection by the body's immune system. 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. Once the bacteria have localized in one area, they start multiplying and create the inflammatory pseudomembrane. Individuals with faucial diphtheria typically have the pseudomembrane grow over the tonsil and accessory structures, uvula, soft palate, and possibly 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. 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