C. Ralph Daniel

Onychomycosis in children: Prevalence and treatment strategies

BACKGROUND Onychomycosis is observed less frequently in children than adults. Until recently management of onychomycosis in children included topical formulations, oral griseofulvin, and in some cases deferral of treatment. OBJECTIVE We attempted to determine the prevalence of onychomycosis in North American children 18 years old or younger attending our dermatology offices (three Canadian, two U.S.) and to report the groups experience using fluconazole, itraconazole, and terbinafine for onychomycosis. METHODS We undertook a prospective, multicenter survey in which all children, regardless of presenting complaint, were examined for onychomycosis by a dermatologist. In instances of clinical suspicion appropriate nail samples were obtained for light microscopy and culture. RESULTS A total of 2500 children under age 18 were examined in the five-center survey (1117 males and 1383 females, mean +/- S.E. age: 11.2 +/- 0.1 years). There was one child with fingernail and ten with mycologically confirmed toenail dermatophyte onychomycosis. The overall prevalence of onychomycosis was 0.44%. Considering those children whose primary or referring diagnosis was not onychomycosis or tinea pedis, the prevalence of onychomycosis was 0.16%. Outside the survey we have seen six other children with dermatophyte onychomycosis; these 17 cases form the basis for the remainder of the report. Of the 17 children, eight (47%) had concomitant tinea pedis infection, and in 11 (65%) a sibling, parent, or grandparent had onychomycosis or tinea pedis. Management included topical terbinafine (two patients: one cured, one failed therapy), topical ketoconazole (one patient: clinical improvement), oral fluconazole (two patients: one cured, one had Downs syndrome and was noncompliant), oral itraconazole (four patients: three cured with subsequent recurrence at follow-up in one patient, one lost to follow-up), oral terbinafine (five patients: four cured with subsequent recurrence at follow-up in one patient, one failed therapy). One child received no therapy following discussion with the parents, one was lost to follow-up and one was found to have asymptomatic hepatic dysfunction with hepatitis C at pretherapy bloodwork. CONCLUSION The prevalence of onychomycosis in our sample of North American children 18 years old or younger was 0.44% (n = 2500). In the subset of children whose primary or referring diagnosis was not onychomycosis, the prevalence of onychomycosis was 0.16%. Children with onychomycosis should be carefully examined for concomitant tinea pedis, and their parents and siblings checked for onychomycosis and tinea pedis. The newer oral antifungal agents fluconazole, itraconazole, and terbinafine may be effective and well-tolerated in the treatment of onychomycosis in this age group. These drugs should be carefully evaluated in a larger cohort of children with onychomycosis.

The spectrum of nail disease in patients with human immunodeficiency virus infection.

There are no known pathognomonic nail signs of human immunodeficiency virus (HIV) infection. However, several presentations should increase the index of suspicion. (1) Proximal white subungual onychomycosis or superficial white onychomycosis, especially of the fingernails, is present. Trichophyton rubrum appears to cause both most commonly in HIV-infected patients. Periungual dermatophyte involvement and involvement of all 10 fingernails is unusual in non-HIV-infected persons. (2) Candida is a primary pathogen of the nail bed and nail plate especially if many nails are involved. (3) A destructive, almost granulomatous-like psoriatic involvement of the nails is present. (4) Squamous cell carcinoma of the nail bed in a young adult. There are no clinical trails to confirm the efficacy of therapy mentioned in this article. The treatment suggestions are empirical and are the personal views of the authors.

Candida infection of the nail : role of Candida as a primary or secondary pathogen

Candida species are commonly found in the nail unit.1–3 Candida albicans is most likely to be the pathogen.1–4 Other Candida species including C. tropicalis, C. krusei, C. parapsilosis, and C. guilliermondii, etc. have also been implicated, but to a lesser extent.1,3 The status of Candida as a primary or secondary pathogen in certain nail disorders is open to question (Table 1). For the purposes of this discussion, a primary pathogen will be one that directly invades the nail plate or nail plate and bed. A secondary pathogen will be one that secondarily affects the nail folds, hyponychium or nail bed after trauma, moisture, contact irritants, etc., have first altered the structure of the nail unit.

Factors that may affect the response of onychomycosis to oral antifungal therapy

With the advent of the newer oral antifungals available to treat onychomycosis, the majority of patients respond to therapy. However, there may be subsets of patients who exhibit poor response or failure. Possible explanations for this may be grouped into categories, including: (i) patient characteristics; (ii) organisms causing or associated with the nail infection; (iii) nail characteristics; and (iv) local diseases involving the nail.

Nails in systemic disease

Nail plate and nail unit abnormalities may be helpful as diagnostic tools or as a part of the puzzle for confirmation of systemic disease. There are specific and nonspecific nail signs, which can be seen involving one or more nails, that occur simultaneously or secondary to systemic disease. Occasionally these clues can be diagnostic, while most are nonspecific reaction patterns. Nail changes occur in the nail plate as a result of nail matrix abnormalities caused by systemic disease and other systemic insults such as reactions to medications. In this article we review some of the more common nail signs that can be used to help diagnose systemic disease.

Treatments of tinea pedis

The severity of tinea pedis infection determines the course of treatment required. Mild infections may be resolved using a topical agent. More severe presentations (eg, dermatophytosis complex) may require treatment that eliminates the bacterial and fungal infection. Some topical monotherapies may exhibit both antifungal and antibacterial activity. In other instances, it may be necessary to combine an antifungal agent with an antibacterial agent. If inflammation is present, an agent with known anti-inflammatory action may need to be used. The chronic presentation of tinea pedis (dry type) sometimes does not respond well to topical therapy. In such instances, systemic antifungal therapy is required to ensure that adequate concentrations of the therapeutic agent are present at the site of infection.

Grading simple chronic paronychia and onycholysis.

the treatment of New World CL cases, an uncontrolled trial in which 13 Ecuadorian patients with CL were treated with 400 mg/day of oral itraconazole for a minimum of 3 months was carried out. The authors reported that prolonged and high-dose treatment regimens with itraconazole were not effective treatments for the majority of the patients with mucocutaneous leishmaniasis. It appears that more appropriately designed RCTs are needed to provide stronger evidence regarding the therapeutic efficacy of itraconazole, particularly in New World CL.

Traditional management of onychomycosis

The traditional management of onychomycosis includes mechanical, chemical, and surgical approaches, as well as topical and oral antifungal medications. Topical preparations have been consistently disappointing, and the tendency in later years has been to rely on two systemic agents-griseofulvin and ketoconazole-for management of more severe or recalcitrant infections. However, both drugs require a long duration of therapy (4 to 6 months for fingernails, 10 to 18 months for toenails). Even with such prolonged treatment, the overall success rate is only about 15% to 30% for toenail infections and 50% to 70% for fingernail infections. Furthermore, both griseofulvin and ketoconazole have numerous potential side effects and drug/drug interactions. Therefore, laboratory monitoring should be performed during the course of treatment with these agents and they should be used only after evaluation of the patients current medical status and a review of concomitant medications.

The nail and Koebner-like phenomenon

If an area on the skin of a psoriatic patient is repeatedly traumatized, psoriasis may arise or worsen in that area (Koebner phenomenon). 2 The same holds true for psoriasis of the nails and also for lichen planus, but perhaps to a lesser extent. In this communication, we report the case of a 45-year-old Caucasian man who presented with chronic dermatitis of the hands, palms (Fig. 1), and face due to epoxy resins. He was occupationally exposed to epoxy derivatives at work and could not change his occupation because he was a craftsman skate-maker for agonistic teams. Previous treatment had included topical steroids and antihistamines. The clinical examination revealed nail changes suggestive of nail psoriasis (Fig. 2), and we considered the possibility that he had psoriasis koebnerized by contact allergy. This hypothesis was supported by the optimal results obtained on treating the patient with oral acitretin 50 mg/day (Fig. 3). We have reported this case because it is a typical example of how nail psoriasis can be koebnerized by allergic contact dermatitis. Contact allergy is, in fact, a traumatic event for nails. The Koebner phenomenon is very important in psoriasis, but as this case there are other nail disorders that can be worsened by trauma. To make a difference from psoriasis, we will talk of Koebner-like phenomenon. In chronic paronychia, for example, a Koebner-like phenomenon is important in the diathesis of the disease. Initially, the seal between the nail plate and nail fold, usually the proximal nail fold, is disrupted. This commonly occurs in the form of physical trauma (such as overaggressive manicuring) or chemicals/contactants. The subsequent inflammatory reaction impairs keratinization of the nail fold, preventing the formation of a new cuticle. The damaged nail matrix then interferes with normal nail growth. Once the seal is broken, moisture, irritants, and, possibly, yeasts (the latter are controversial) perpetuate the disorder. 3–5

Commentary: The illusory tinea unguium cure

O nychomycosis is a common disorder and makes up approximately half of the nail disorders and 30% of the dermatophytoses we see as dermatologists. In older individuals the prevalence is high and likely approaches 60% or more in those older than 70 years. During the 1990s, onychomycosis was ‘‘hot,’’ not in any small part because of the onychomycosis treatment battles between orally administered terbinafine and itraconazole. Since 1996, however, no new Food and Drug Administrationeapproved systemic drugs for onychomycosis have come to market. During this time, the use of griseofulvin for tinea unguium has greatly diminished because of the greater efficacy of terbinafine and itraconazole. Topical ciclopirox lacquer is the latest onychomycosis drug to be approved in the United States, but its efficacy in providing a complete cure as a monotherapy is unacceptably low. This situation is compounded as longterm follow-up of patients treated for tinea unguium has been lacking. Indeed, the article by Piraccini et al is a welcome addition to the literature. This was a 7-year prospective study limited to patients who had achieved a complete (clinical and mycological) cure with either terbinafine or itraconazole. Of 73 patients, 41 also used topical amorolfine after achieving cure. ‘‘The administration of systemic terbinafine to treat the first episode of onychomycosis seemed to provide better long-term success in those patients with a complete response. . ..’’ The statistical value was difficult to access because 59 patients were treated with terbinafine and only 14 with itraconazole.