Keys To Managing Severe Onychomycosis

Myron Bodman, DPM

Given the prevalence of onychomycosis and its varied clinical presentation, this author discusses the evolution of diagnostic testing and offers insights on the roles of various modalities in the treatment of severe onychomycosis.

Onychomycosis is a common infection that is increasing in incidence. Meissner (of Meissner’s corpuscle fame) first described onychomycosis in 1895.1 The most frequent culture cause of onychomycosis is Trichophyton rubrum, which has evolved over time to become more pathogenic. The previous thinking was that T. rubrum was just a contaminant but since the Vietnam War, it has become the dominant causative organism.

   In addition, Zaias and colleagues have reported that patients are genetically susceptible to dermatophyte infections in an autosomal dominant pattern.2 This helps to explain the rising incidence and recurrence rates of onychomycosis.

   The clinical types of onychomycosis have been updated to better categorize the wide variety of clinical presentations. Hay and Baran categorized the clinical growth patterns of onychomycosis as distal lateral subungual onychomycosis, white superficial onychomycosis, proximal subungual onychomycosis, endonyx onychomycosis and Candidal onychomycosis.3 Patients may have a combination of these subtypes simultaneously.

   Total dystrophic onychomycosis or severe onychomycosis refers to the most advanced form of any of the subtypes. This form of onychomycosis is a later stage of the chronic subungual dermatophyte infection that may take 10 to 15 years to develop. It is not only the most difficult stage to clear but is also the type with the highest risk of associated subungual ulceration, secondary bacterial infection and possible gangrene.

   The incidence of onychomycosis is increasing in the United States, reportedly affecting 6 to 12 percent of the population.4 There has been a sevenfold increase in cases over the last 20 years.

   Severe onychomycosis in patients with diabetes and patients with peripheral arterial disease increases the risk of secondary bacterial infection, nail bed ulceration and subsequent amputation.5,6 Onychomycosis and concurrent diabetes triple a patient’s risk of toe ulceration, infection and gangrene.

   As McCarthy points out, severe onychomycosis poses the greatest problem in patients with diabetic peripheral neuropathy.7 Just as constrictive footwear can cause pressure necrosis of the skin in patients with improperly fitting shoes, thickened, mycotic nails can cause pressure necrosis of the nail bed in those with diabetes. Sharp, brittle, infected nails can also abrade or gouge skin on the adjacent toes, and may even pierce the skin.

   In both cases, patients with diabetes often do not recognize these minor ulcerations because of decreased sensation. These ulcerations, if left untreated, have the potential to lead to secondary bacterial infection.7-10 The photo at the bottom on the right illustrates a foot with severe onychomycosis that developed a nail-induced ulceration.

How To Assess The Severity Of Onychomycosis

One generally determines clinical severity by the infection’s duration, degree of involvement and thickness of the fungally infected nail plate. Additionally, host resistance, genetic susceptibility and the pathogenicity of the particular fungal strain help account for a particular patient’s overall infection severity and helps predict the likelihood of cure.

   We can better define the clinical severity of onychomycosis in terms of area of involvement, proximity to the nail root and thickness in a standardized scoring system called the Onychomycosis Severity Index.11 This parallels the Psoriasis Severity Index that clinicians have long used to compare patient responses to various therapeutic methods in a standardized way.


A great article on "fungus nail" involvement with methods, drugs & outcome by my friend Dr. Ron Bodman. I also noticed over the years that there is most definitely an immune system involvement in nail fungus & C. albicans infection. As we say in WV, "it runs in the family." I have seen patients with specific toenails involved & some of their offspring have identical involvement. Some people do not have the ability to defend against the fungus organisms. They are then resistant to curative measures & tend to become reinfected after treatment.

We know fungi like a dark, warm, moist place to grow with a food source. I would like to suggest that perhaps contributing factors leading to an increase in nail & skin fungal infections over the last 20+ years may be connected to external changes in clothing & shoe gear. Over this time, we have seen a real increase in the use of artificial fibers such as nylon and polyester in socks/hosiery. These fabrics do not absorb moisture & raise the local temperature of the foot. There is no wick action with these fibers . Once again, today's shoe gear is entirely or mostly artificial uppers & lowers. These have the same characteristics. The feet are warmer, wetter, dark & there is little or no air circulation. The insoles/linings of the shoes are plastic fibers. The soles are rubber/vinyl.

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