Antibiotic-associated diarrhea (AAD) results from an imbalance in the colonic microbiota caused by antibiotic therapy. Microbiota alteration changes carbohydrate metabolism with decreased short-chain fatty acid absorption and an osmotic diarrhea as a result. Another consequence of antibiotic therapy leading to diarrhea is overgrowth of potentially pathogenic organisms such as "Clostridium difficile". It is defined as frequent loose and watery stools with no other complications.

Meta-analyses have concluded that probiotics may protect against antibiotic-associated diarrhea in both children and adults. Evidence is insufficient, however, regarding an effect on rates of "Clostridium difficile" colitis.

However, citing conflicting data in the studies, other sources claim that the use of probiotics has failed thus far to meet the standard of medical care required for evidence-based medicine. Demonstration of the efficacy of probiotics is needed by randomized, double blind, placebo-controlled trials.

Efficacy of probiotic AAD prevention is dependent on the probiotic strain(s) used and on the dosage. Up to a 50% reduction of AAD occurrence has been found. No side-effects have been reported in any of these studies. Caution should, however, be exercised when administering probiotic supplements to immunocompromised individuals or patients who have a compromised intestinal barrier because of the risk of an infection caused by the probiotic supplements.

"Clostridium difficile", also known more commonly as "C. diff", is known to account for 10 to 20 percent of antibiotic-associated diarrhea cases. The reasoning for this, is that the antibiotics administered for the treatment of certain diseases processes such as inflammatory colitis also inadvertently kills a large portion of the gut flora, the normal flora that is usually present within the bowel. With this lower amount of "healthy" bacteria present, the overgrowth of "C. diff" is then responsible "for elaborating the enterotoxin".

Nickel allergy results in a skin response (rash) after the skin comes in direct and sustained contact with any item which releases a large amount of free nickel from its surface. The skin reaction can occur at the site of contact, or sometimes spread beyond to the rest of the body. Cutaneous exposure can cause localized erythematous, pruritic, vesicular, and scaly patches. Ingestion of nickel may cause a systemic reaction, that will affect a larger skin surface. Examples of systemic reactions can include hand dermatitis, baboon syndrome, or generalized eczematous reactions.

Within the workplace, individuals may be exposed to significant amounts of nickel, airborne from the combustion of fossil fuels, or from contact with tools that are nickel-plated. Historically, workplaces where prolonged contact with soluble nickel has been high, have shown high risks for allergic contact nickel dermatitis. For example, nickel dermatitis was common in the past among nickel platers. Due to improved industrial and personal hygiene practices, however, over the past several decades, reports of nickel sensitivity in workplaces, such as the electroplating industry, have been sparse. In the workplace, exposure reduction includes personal protection equipment and other risk management measures.

Wallerian degeneration is a process that results when a nerve fiber is cut or crushed and the part of the axon distal to the injury (i.e. farther from the neuron's cell body) degenerates. This is also known as anterograde or orthograde degeneration. A related process known as 'Wallerian-like degeneration' occurs in many neurodegenerative diseases, especially those where axonal transport is impaired. Primary culture studies suggest that a failure to deliver sufficient quantities of the essential axonal protein NMNAT2 is a key initiating event.

Wallerian degeneration occurs after axonal injury in both the peripheral nervous system (PNS) and central nervous system (CNS). It occurs in the axon stump distal to a site of injury and usually begins within 24–36 hours of a lesion. Prior to degeneration, distal axon stumps tend to remain electrically excitable. After injury, the axonal skeleton disintegrates, and the axonal membrane breaks apart. The axonal degeneration is followed by degradation of the myelin sheath and infiltration by macrophages. The macrophages, accompanied by Schwann cells, serve to clear the debris from the degeneration.

Schwann cells respond to loss of axons by extrusion of their myelin sheaths, downregulation of myelin genes, dedifferentiation and proliferation. They finally align in tubes (Büngner bands) and express surface molecules that guide regenerating fibers. Within 4 days of the injury, the distal end of the portion of the nerve fiber proximal to the lesion sends out sprouts towards those tubes and these sprouts are attracted by growth factors produced by Schwann cells in the tubes. If a sprout reaches the tube, it grows into it and advances about 1 mm per day, eventually reaching and reinnervating the target tissue. If the sprouts cannot reach the tube, for instance because the gap is too wide or scar tissue has formed, surgery can help to guide the sprouts into the tubes. Regeneration is efficient in the PNS, with near complete recovery in case of lesions that occur close to the distal nerve terminal. However recovery is hardly observed at all in the spinal cord. One crucial difference is that in the CNS, including the spinal cord, myelin sheaths are produced by oligodendrocytes and not by Schwann cells.

Wallerian degeneration is named after Augustus Volney Waller. Waller experimented on frogs in 1850, by severing their glossopharyngeal and hypoglossal nerves. He then observed the distal nerves from the site of injury,

which were separated from their cell bodies in the brain stem.

Waller described the disintegration of myelin, which he referred to as "medulla", into separate particles of various sizes. The degenerated axons formed droplets that could be stained, thus allowing studies of the course of individual nerve fibres.