In areas where<unk> is endemic,<unk>  in the nasopharyngeal passageways is common. Its 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<unk> toxin into either skin or nasopharyngeal lesions. The diphtheritic lesion is often covered by a pseudomembrane composed of fibrin, bacterial cells, and inflammatory cells.<unk> 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.
Corynebacterium diphtheriae
Bacillus anthracis
Streptococcus bovis
Staphylococcus aureus
Corynebacterium pseudotuberculosis
Streptococcus pyogenes
Rhodococcus equi
Corynebacterium striatum