Fungal nail disease

Published on 02/04/2015 by admin

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190 Fungal nail disease

Instruction

Look at this patient’s toenails.

Salient features

History

• Embarrassment from a cosmetic perspective

• Mechanical problems including the fact that nails get snagged in clothing, etc.

• History of diabetes.

Examination

• Nails are white, green or, occasionally, black when the infection is superficial or proximal (Fig. 190.1A,B).

• When the infection is distal there may be onycholysis (Fig. 190.1C,D; see Case 193).

image

Fig. 190.1 Onychomycosis. (A) Proximal subungal onychomycosis. (B) Superficial onychomycosis with a dry, white, powdery surface that can be easily scraped away. (C) Distal onychomycosis: early changes. (D) Distal onychomycosis: late changes where the infection has progressed along a linear channel.

(With permission from Habif 2009.)

Proceed as follows:

• Look at the fingernails: thickened, yellow or white nail with scaling under the elevated distal free edge of the nail plate

• Tell the examiner that you would like to look for underlying immunodeficiency states such as HIV and circulatory disorders (Raynaud syndrome).

Diagnosis

This patient has fungal nail disease (lesion), which is usually caused by Trichophyton or Candida (aetiology), and it is cosmetically unacceptable to the patient (functional status).

Advanced-level questions

What do you understand by the term onychomycosis?

It refers to a fungal infection of nails. Diagnostic criteria (J Am Acad Dermatol 2007;56:939–44) include:

• Clinical primary criteria:

• White/yellow or orange/brown patches or streaks

• Clinical secondary criteria:

• Onycholysis
• Subungual hyperkeratosis/debris
• Nail-plate thickening.

Note: Tinea pedis often occurs concomitantly with pedal onychomycosis, and tinea manuum with infected fingernails.

• Laboratory criteria:

• Positive microscopic evidence
• positive culture of dermatophyte.

What are the different causative organisms?

• Dermatophytes (ringworm, tinea unguium): Trichophyton rubrum, T. interdigitale (toenails are more commonly affected than fingernails). T. rubrum infection is associated with distal or lateral involvement of the nail plate that spreads proximally, eventually affecting the whole nail; this may be associated with proximal subungual nail dystrophy associated with separation of the nail from the bed. T. interdigitale infection, characteristically seen in patients with AIDS, produces superficial white onychomycosis with crumbly white areas on the nail surface.

• Yeasts: Candida albicans, C. parapsilosis (fingernails are more commonly affected than toenails).

• Non-dermatophytes (moulds): Fusarium, Scopulariopsis brevicaulis (toenails are more commonly affected than fingernails).

Does the clinical picture vary according to the nature of the infecting organism?

Yes, as follows:

• Dermatophytes: distal or lateral nail involvement spreading proximally, proximal subungual dystrophy, superficial white dystrophy, white or yellow thickened nails, crumbling of nail plate, adjacent web or skin involvement may be present.

• Candida: chronic paronychia, shiny red bolstered nailfold, almost exclusively affects finger nailfolds, loss of cuticle, pus exuding from under nailfold, usually proximal nail involvement, distal nail dystrophy (associated with circulatory disorders), total dystrophic onychomycosis, nails white, green or occasionally black.

• Non-dermatophyte: superficial white onychomycosis, solitary nail involvement, colour of the nail may be influenced by the nature of infecting mould (e.g. the nails are white with Fusarium, white, yellow, brown or green with S. brevicaulis).

What are the patterns of fungal nail involvement?

Distal lateral subungual onychomycosis.

Superficial white onychomycosis.

Proximal white subungual onychomycosis.

Total dystrophic onychomycosis (i.e. all the previous three sites are affected).

Is laboratory diagnosis essential before starting treatment?

Yes, for the following reasons:

• Antifungal treatment is prolonged and the causative organism may be non-fungal

• To identify contacts of the patient

• To exclude mixed infection

• To optimize treatment as certain fungi are less responsive to treatment.

What are the poor prognosis factors?

• Areas of nail involvement >50%

• Significant lateral disease

• Subungual hyperkeratosis >2 mm

• White/yellow or orange/brown streaks in the nail

• Total dystrophic onychomycosis (with matrix involvement)

• Non-responsive organisms (e.g. Scytalidium mold)

• Immunosuppression

• Diminished peripheral circulation.

Mention some non-fungal nail infections

Bacterial nail infection, e.g. Pseudomonas aeruginosa (green or blackish discoloration of the nails), Staphylococcus aureus (causes acute paronychia or whitlow).

How are specimens obtained for mycological diagnosis?

Scrapings are taken with a blunt scalpel as proximally as possible in the nail:

• In distal and lateral onychomycosis, specimens are taken from the proximal part of the diseased portion of the nail and subungual material

• In superficial white onychomycosis, the scrapings are taken from the diseased nail surface

• In proximal white mycosis, the scrapings are taken from the nail surface.

In the laboratory, 20–30% potassium hydroxide is added to part of the specimen to macerate nail keratin before direct microscopy and the rest of the specimen is inoculated on different media.

What is the recommended treatment for onychomycosis?

• Dermatophyte infections (BMJ 1995;311:1277–81):

• Localized distal nail disease: tioconazole with undecylenic acid paint, amorolfine paint weekly and 40% urea paste for dissolution
• Proximal or extensive nail disease: terbinafine, itraconazole, fluconazole, griseofulvin and amorolfine nail paint. Data have suggested that terbinfaine is the treatment of choice for onychomycosis (Lancet 1998;351:541, BMJ 1999;318:1031–5).

• Candidal infections:

• Chronic paronychia (localized): imidazole creams or paints, nystatin ointment, terbinafine cream; there is insufficient evidence on the effects of topical antifungal agents in people with frequently infected toenails (BMJ 2001;322:288–9)
• Distal infection: tioconazole with undecylenic acid paint, amorolfine nail paint
• Severe infection or severe chronic paronychia: itraconazole.

• Non-dermatophyte (mould) onychomycosis:

• Localized disease: tioconazole with undecylenic acid paint, amorolfine paint weekly, 40% urea paste for dissolution or even avulsion of the nail
• Persistent disease: itraconazole.

Mention some fungal infections that do not respond to oral treatment

Scopulariopsis, Scytalidium, Fusarium and Acremonium spp.

What is the definition of cure in fungal nail infections?

Cure in fungal nail infections is defined by the absence of clinical signs or the presence of negative nail culture and/or microscopy results with one or more of the following minor clinical signs (J Am Acad Dermatol 2007;56:939–44):

• Minimal distal subungual hyperkeratosis

• Nail-plate thickening.

Persistent onychomycosis is suggested at the end of the observation period by:

• White/yellow or orange/brown streaks or patches in or beneath the nail plate

• Lateral onycholysis with subungual debris.

Although nail appearance will usually continue to improve after therapy is stopped, the nails may have a persistent abnormal appearance even where therapy has been effective.

What information is available about the genetic susceptibility to fungal nail infections?

One study reported an autosomal recessive form of susceptibility to chronic mucocutaneous candidiasis that was associated with homozygous mutations in CARD9—the gene encoding the caspase recruitment domain containing protein 9. The patients had low numbers of Th17 cells (helper T cells that produce interleukin 17) (N Engl Med Med 2009;361:1727).

Another study reported a mutation leading to replacement of Tyr-238 in the β-glucan receptor dectin-1 in a family in which four women had either recurrent vulvovaginal candidiasis or onychomycosis. This Tyr-238 polymorphism hampered the recognition of Candida β-glucan and was associated with an impaired cytokine response by monocytes and macrophages. The mutation did not, however, impair killing of Candida by neutrophils, which seems to prevent invasive fungal infections (N Engl Med Med 2009;361:1760).

Further reading

Denning DW, Evans EGV, Kibbler CC, et al. Fungal nail disease: a guide to good practice (report of a Working Group of the British Society for Medical Mycology). BMJ. 1995;311:1277-1281.

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