ungi are parasitic organisms, classified as members of  the Fungus Kingdom.  Unlike plants, they contain no chlorophyll, surviving by breaking down and consuming plants and animals, living or dead. 

Since they are unable to synthesize glucose, fungi use enzymes to extract sugar and amino acids from organic matter.  They require no light, growing well in caves and cisterns.  During a late summer's night in the wood, subterranean fungal tubules (mycelia) produce, as seen by the light of morn-a fairy ring of toadstools.

Basics and History of Dermatophytoses:

Dermatophyte fungal organisms feed exclusively on keratin, a protective protein found in non-living dermal structures, i.e. hair, toenails, fingernails, and the outer layer of skin.  Two genera of fungi account for most dermatophytoses: Trichophyton and Microsporum.  Occasionally, yeasts attack, such as Candida albicans (monilia-vaginal moniliasis, thrush, etc.) or Malassezia furfur (tinea versicolor).

Tinea comes from Latin for "gnawing worm" and means "ringworm" in medicalese.  Dermatophytes cause ringworm in various areas of the human body-on the smooth skin of the body, it's called tinea corporis;  scalp, it's tinea capitis;  beard-tinea barbae; crotch-tinea cruris;  hands-tinea manum; feet-tinea pedis; fingernails, toenails-tinea unguium (L. tinea "ringworm" + unguis "a nail" > unguium "nails") or onychomycosis  (Greek onycho "nail" + mycosis "fungal infection).

Tinea corporis infection first appears on the skin as a red pimple, then an expanding circle with central clearing, producing a red ring. On a nail, the infection moves as an arc from the point of origin.  Persistently moist skin conditions, as in the feet and toe area particularly, promote tinea unguium.  Occlusiveness through clothing, intertrigenous areas (axillae, groin areas), plasters, bandaids, polishes and paints, artificial applications such as acrylic nails, orthopedic devices, etc. especially with exertion and increased rates of perspiration promotes hydration of the skin and increases the risk of fungi taking "root."

The fungal cause of ringworm was identified in 1843 by Gruby, who named it Trichomyces tonsurans, now Trichophyton tonsurans, a cause of tinea capitis, seen often in children.   People with diabetes, HIV, circulatory insufficiency of the feet and legs (PVD), aging people, estrogen deficiency, the wearing  of artificial nails (acrylic or "wraps"), and chronic nail polish use have increased rates of tinea unguium.  A crack in the skin or a nail may allow entry of a fungal organism, which germinates under favorable conditions (moisture, keratin, darkness, warmth, physical support, and presence of essential building blocks for its growth) and becomes a ringworm.

Tinea capitis and tinea corporis may result from zoophilic transmission of M. canis from dogs or cats to the scalp or hairless skin of  children.  Fungal infections arise  from soil, people, animals and fomites (hairbrushes, upholstery, etc.).  "Dandruff" may represent shedding of infectious cell parts from the scalp of an individual suffering from tinea capitis.  Couples rubbing  toes under the sheets at night may spread tinea unguium from one to another.  

Schönlein in 1837 identified the fungal organism responsible for Favus ( tinea favosa).  Originally named  Achorion schönleinii, today called Trichophyton schönleinii.^[1]    Favus (L. "honeycomb") is a chronic tinea capitis, usually appearing in childhood.  Adult cases are often cases of childhood favus unsuccessfully or not treated.   Improved standards of living and medical care have greatly reduced the incidence of favus  in developed countries; however, Favus persists in eastern Sub-Saharan Africa and India.   See photos: http://www.ifd.org/pictures/Tincap3.jpg  and http://en.wikipedia.org/wiki/Favus

Eichstedt identified in 1846 the yeast responsible for pityriasis versicolor-now called tinea versicolor.  Eichstedt named it Microsporon furfur, today called Malassezia furfur.  Other Tineas are caused by T. mentagrophytes, Microsporum canis (from dogs and cats-usually causes Tinea capitis or corporis in children), and other fungi responsible for various superficial fungal infections.  

Lilienthal published in 1876 the association of Vidium albicans, a yeast now called Candida albicans, with mycosis vaginalis,^[2] a disease now called vaginal moniliasis. Yeasts, such as C. albicans, can invade the nails, throat (thrush), esophagus  (monilial esophagitis), and more, especially in immunocompromised  people. 

Pathopysiology:

In a typical frontal nail attack, the fungus takes advantage of minor trauma at the end of the nail plate, where an uplift injury has partially separated plate from bed.  The fungal organism grows inward toward and along the cuticle. The creature digests and erodes the overlying nail plate, leaving detritus in its wake, causing discoloration, separation, and thickening of the plate.

The nail plate grows out from the matrix, near the lunula, pushing detritus and fungus distally.  Fingernails grow twice as quickly as toenails, and this outflow ("glacier of keratin") has a protective effect, concerning the establishment of onychomycosis.  This sweeping effect partially accounts for the lower rate of established tinea unguium in fingers vs. toes. 

Trivia: Longer and more highly used digits sport the fastest growing nails.  One type of onychomycosis attacks the face or top of the nail plate.  Its digestive enzymes drill down through the plate, leaving white discoloration over entry into the subungual space. 

Tinea pedis (foot ringworm) is often associated with tinea unguium.  Maceration and fissures may form between the toes, especially between the fourth and fifth toes.  These openings allow bacterial entry into surrounding soft tissue, which may lead to cellulitis in immunocompromised persons, such as diabetics, requiring immediate intervention.. 

A unique type of tinea unguium is seen with HIV infection, wherein separation of the nail plate occurs at the nail matrix, leaving a white plaque near the lunula.

Clinical Review

Tinea unguium is very common, especially involving a great toenail, occurring in 4%-14% of the population, increasing with age.  The diagnosis involves clipping a piece of contaminated nail or collecting detritus, treating it with a few drops of 10% to 20% KOH solution, warmed for hair or nails, allowing better visualization of fungal hyphae.  A culture of such a fragment for fungi is confirmatory.  Histological exam may be needed in difficult cases.  Wood's light (UV) may show fluorescence in a few dermatophytoses.

Many people with toenail fungus  do not obtain treatment because they lack symptoms,  or it's covered by their footwear, or they believe the cost and risk of treatment outweigh the benefit, or they don't know they have it! 

A recent survey of health care providers revealed many make a clinical diagnosis and start treatment.   Some providers and patients choose "watchful waiting" or ignore the problem, but patients with pain, embarrassment, vocational issues, and risk factors for bacterial cellulitis should and usually do receive appropriate therapy.

Treatment:

Mechanical/physical: wear diabetic or box-toed shoes, change leather shoes daily (rotate every 48 hours), regular podiatric care, especially patients with diabetes.  

Topical: creams, ointments, powders (in sock and shoes), ciclopirox 8% nail polish-nontoxic, less costly, slightly less effective. Treat concomitant tinea pedis topically.

Medical: Systemic antifungals-beware of costs, including hepatic toxicity and drug-drug interactions.  Short term effectiveness 70-80%; longterm <50%.  Weigh benefit to risk ratio.  May be highly and relatively rapidly effective. 

Surgical debridement by a podiatrist/surgeon: reducing nail plate thickness, trimming nail margins to reduce shoe pressure. 

Surgical extraction: must ablate the affected nail matrix to prevent post-op growth of a deformed, painful "claw" nail from a partially functional residual matrix. 

Case: A 35 year old waiter was laid off work because of the unsightly condition of his finger nails.  Waiters were not allowed to wear gloves  while taking orders or serving customers.   The finger nails were completely involved, with thickened longitudinal brown furrows; on the side, the toes were severely invilved, as well.  

Past medical history: No liver disease, toxin exposures, or surgeries.

He had a negative family and personal history for diabetes.  No vascular disease.

Social history: smoker, 1 pack per day.  Alcohol 6 beers per week.  Happily married with 5 healthy children. Wife-housewife.  Three  years in the US, from Guatemala.

Review of systems: no liver disease, no jaundice, no hepatitis now or past.

He was informed that this treatment incurs a 25% to 30% relapse rate.^[3]   He chose to proceed eagerly with antifungal therapy.  Systemic Lamisil (terbinafine) was prescribed for a course of  12 weeks.  He was instructed not to consume beer or any other form of alcohol while undergoing therapy.  He tolerated the treatment well.  Liver function remained normal throughout the course of therapy. 

His fingernails were clear at three months.  

He resumed his position as a waiter.  His florid case of tinea unguium raises the possibility of  an inherited defect of cell-mediated immunity, leaving him open to attack by cell-walled organisms.   

In 3 months-the time necessary for finger nail regrowth-he may have a recurrence and need to find work at a place where he can wear gloves or not need them-or, undergo another round of systemic antifungal medication, this time using antifungal nail polish as a concomitant drug or given as a chaser.

References:

 http://www.ifd.org/pictures/Tincap3.jpg

http://en.wikipedia.org/wiki/Favus

[1] Diseases of the Skin including the Exanthemata. Ferdinand Hebra, MD and Moriz Kaposi, MD. 1880; pp.116-117.

[2] A Treatise on Diseases of the Skin. S. Lilienthal, MD 1876

[3] David de Berker, M.R.C.P. "Fungal Nail Disease." N Engl J Med. 2009;360:2108-16.

Also see   NEJM.org