Structural damage to hair cells (primarily the outer hair cells) will result in hearing loss that can be characterized by an attenuation and distortion of incoming auditory stimuli. During hair cell death scars develop, which prevent potassium rich fluid of the endolymph from mixing with the fluid on the basal domain. The potassium rich fluid is toxic to the neuronal endings and can damage hearing of the entire ear. If the endolymph fluid mixes with the fluid on the basal domain the neurons become depolarized, causing complete hearing loss. In addition to complete hearing loss, if the area is not sealed and leakage continues further tissue damage will occur. The scars that form to replace the damaged hair cell are caused by supporting hair cells undergoing apoptosis and sealing the reticular lamina, which prevents fluid leakage. The cell death of two supporting hair cells rapidly expands their apical domain, which compresses the hair cell beneath its apical domain. Nerve damage
Recent studies have investigated additional mechanisms of NIHL involving delayed or disabled electrochemical transmission of nerve impulses from the hair cell to and along the auditory nerve. In cases of extreme acute acoustic trauma, a portion of the postsynaptic dendrite (where the hair cell transfers electrochemical signals to the auditory nerve) can rupture from overstimulation, temporarily stopping all transmission of auditory input to the auditory nerve. This is known as excitotoxicity. Usually, this sort of rupture heals within about five days, resulting in functional recovery of that synapse.
Cutaneous diphtheria is an infection of the skin by Corynebacterium diphtheriae. : 265   It is also known as "desert sore". See also
Diphtheria
Skin lesion


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