Nail Infection — Causes, Onychomycosis vs Paronychia, Terbinafine & Treatment — Symptoms, Causes & Treatment | MyMedicPlus

Nail infections encompass two main clinical entities: onychomycosis (fungal nail infection — also called tinea unguium) and paronychia (infection of the nail fold — the skin surrounding the nail). Onychomycosis is the most common nail disorder worldwide, affecting approximately 10% of the general population and rising steeply with age (up to 50% of adults over 70). It is caused by dermatophytes (85–90% — predominantly Trichophyton rubrum and T. interdigitale), yeasts (5–10% — Candida species), and non-dermatophyte moulds. Paronychia is acute (bacterial — Staphylococcus aureus, Streptococcus) or chronic (fungal — Candida, from repeated wet work exposure). Both conditions cause significant functional impairment and psychosocial distress, and can serve as entry points for secondary bacterial infection — particularly in immunocompromised patients and those with diabetes.

Onychomycosis causes: dermatophytes (85–90%) — Trichophyton rubrum (most common globally), T. interdigitale (previously T. mentagrophytes var. interdigitale), Epidermophyton floccosum; Candida species (5–10%) — C. albicans predominantly affects fingernails of those with chronic wet-work exposure; non-dermatophyte moulds (1–5%) — Scopulariopsis brevicaulis, Fusarium, Aspergillus. Risk factors for onychomycosis: advanced age (prevalence doubles per decade over 40); diabetes mellitus (peripheral vascular disease and immune dysfunction); tinea pedis (athlete's foot — the most common precursor; up to 30% of untreated tinea pedis progresses to onychomycosis); peripheral vascular disease; nail trauma; immunosuppression (HIV, transplant recipients); communal facilities (swimming pools, gym changing rooms). Paronychia causes: Acute paronychia: bacterial infection — Staphylococcus aureus (most common), Streptococcus pyogenes, less commonly gram-negatives; precipitated by nail biting, finger sucking, nail trauma, manicure injuries, ingrown toenails. Chronic paronychia: predominantly non-infectious (repeated irritant or allergic contact dermatitis from wet work — hairdressers, kitchen workers, healthcare workers); secondary colonisation with Candida albicans is common; occasionally caused by psoriasis or lichen planus affecting the nail fold.

Onychomycosis clinical presentations: Distal and lateral subungual onychomycosis (DLSO — most common): begins at the distal or lateral free edge; subungual hyperkeratosis (thickening of nail bed — chalky, crumbly material); onycholysis (separation of nail plate from nail bed); yellow-white or brown discolouration; nail plate becomes brittle and thickened. Superficial white onychomycosis (SWO): white powdery patches on the nail plate surface — predominantly caused by T. interdigitale on toenails. Proximal subungual onychomycosis (PSO): white discolouration starting from the lunula (proximal nail fold) — indicates proximal infection — associated with immunosuppression (HIV/AIDS); consider HIV testing. Total dystrophic onychomycosis: complete nail plate destruction — severe long-standing disease. Paronychia: Acute: rapid-onset hot, red, tender swelling of the nail fold — fluctuant when pus has accumulated; may spontaneously discharge pus; fever if severe. Chronic: persistent redness, swelling, and tenderness of the nail fold (proximal or lateral) over months to years; nail plate may become ridged, discoloured, and dystrophic; characteristic loss of the cuticle (eponymium); multiple nails often affected simultaneously.

Clinical diagnosis alone is insufficient for onychomycosis — 50% of clinically suspected fungal nail infections are due to other causes (psoriasis, lichen planus, trauma, pachyonychia). Laboratory confirmation is essential before prescribing systemic antifungal therapy. Nail clipping and subungual scraping: sample from the most proximal active disease edge; place in a small container or folded paper. Microscopy: direct KOH (potassium hydroxide) preparation — dissolves keratin; visualises fungal hyphae under light microscope; rapid (result same day); sensitivity 60–80%; does not identify species. Culture: grows on Sabouraud dextrose agar at room temperature for 3–6 weeks; identifies species — essential for planning treatment (dermatophyte versus Candida versus mould has treatment implications); sensitivity 50–60%. PCR (molecular testing): most sensitive and specific (above 90%); rapid results; increasingly available in specialist centres. Dermatoscopy (epiluminescence microscopy): ruin appearance, longitudinal streaks, jagged proximal edge — aids clinical diagnosis and distinguishes from mimics. Dermoscopy of nail: subungual keratosis, colour patterns — differentiates from psoriasis, melanonychia, or haematoma. Biopsy of nail plate/bed: rarely required — if PCR and culture both negative and clinical concern remains, periodic acid-Schiff (PAS) staining of nail biopsy demonstrates fungi. Acute paronychia: clinical diagnosis — swab of pus for culture and sensitivity guides antibiotic choice if not responding to empirical treatment.

Onychomycosis — topical therapy (for limited disease — less than 50% nail plate involvement, no lunula involvement, fewer than 3 nails): amorolfine 5% nail lacquer (Loceryl) — applied weekly to affected nails after filing and degreasing; 9–12 months for toenails; cure rate approximately 50% for mild disease; no significant systemic side effects. Ciclopirox 8% nail lacquer (Penlac) — applied daily; similar efficacy to amorolfine. Efinaconazole 10% solution (Jublia) — newer; applied daily for 48 weeks; higher cure rates (17–18% mycological + clinical cure) but expensive. Onychomycosis — systemic therapy (gold standard for moderate-severe disease): Terbinafine 250 mg daily — allylamine antifungal (squalene epoxidase inhibitor); dermatophyte onychomycosis: 6 weeks for fingernails, 12–16 weeks for toenails; complete cure rate 50–75% at 48 weeks; superior to azoles for dermatophytes. Itraconazole pulse therapy: 400 mg/day for 1 week, repeated monthly (2 pulses for fingernails, 3 pulses for toenails); azole — broader spectrum including Candida and moulds; equivalent to terbinafine for dermatophytes; suitable when terbinafine is contraindicated (liver disease). Fluconazole 150–300 mg weekly: alternative azole, particularly for Candida onychomycosis. Monitoring: LFTs at baseline and at 6 weeks for terbinafine (rare hepatotoxicity — 1 in 45,000 cases; stop if symptomatic); warn patients about drug interactions (itraconazole — CYP3A4 inhibitor). Acute paronychia treatment: mild: warm soaks (epsom salt) 3–4 times daily; topical antibacterial; allow spontaneous drainage. If fluctuant: incision and drainage under local anaesthesia — release pus, no excision of tissue. Antibiotics (oral amoxicillin-clavulanate, flucloxacillin, or cefalexin if beta-lactam allergy) — for spreading cellulitis or systemic features. Chronic paronychia treatment: avoid wet work — the single most important intervention; protective gloves; allow the proximal nail fold to regrow the cuticle (eponymium); topical steroid (mometasone, clobetasol) + antifungal (clotrimazole) cream — reduces inflammation and secondary Candida colonisation; Swiss roll technique (marsupialization of the proximal nail fold) for refractory cases.

Permanent nail dystrophy (long-standing or recurrent onychomycosis causes irreversible nail plate damage — the matrix, once destroyed, cannot regenerate healthy nail tissue despite successful mycological cure). Secondary bacterial cellulitis (fissured, dystrophic nails provide entry points for Staphylococcus aureus and Streptococcus — particularly dangerous in diabetic patients and those with peripheral vascular disease; may progress to ascending limb infection or osteomyelitis). Diabetic foot complications (untreated onychomycosis in diabetic patients — combined with peripheral neuropathy and vascular disease — significantly increases the risk of plantar ulceration and serious secondary infection requiring hospitalisation). Felon (acute paronychia extending to the deep pulp space of a fingertip — surgical emergency requiring incision and drainage to prevent osteomyelitis and finger ischaemia). Drug-related hepatotoxicity from systemic antifungal treatment (terbinafine — rare, approximately 1 in 45,000 patients; LFT monitoring recommended).

Preventing onychomycosis: treat tinea pedis (athlete's foot) promptly and completely — it is the most common precursor to toenail fungal infection; apply antifungal powder or spray to footwear; wear moisture-wicking socks; wear footwear (flip-flops) in communal wet areas (swimming pools, gym showers, changing rooms); dry between toes thoroughly after bathing; avoid sharing nail clippers, files, or footwear; keep nails trimmed short and filed smooth to reduce subungual space for fungal colonisation. Diabetic patients and those with peripheral vascular disease should have regular podiatric review — early detection and treatment of onychomycosis prevents complications. Preventing paronychia: avoid nail biting and finger sucking; handle cuticles gently — do not cut them (cuticle is a protective barrier against moisture and micro-organisms); wear waterproof gloves for wet work; avoid repeated manicure injuries; treat ingrown toenails early.

See your GP or pharmacist if: one or more nails become thickened, discoloured (yellow, white, or brown), crumbly, or separate from the nail bed — especially in toenails; symptoms have been present for more than 3 months; nail changes are causing pain, difficulty wearing shoes, or secondary skin infection. Laboratory confirmation (nail clipping with KOH and culture) is required before prescribing oral antifungal treatment — do not take terbinafine or itraconazole without a positive mycological result. Seek urgent assessment for: acute paronychia with spreading redness, fever, and systemic illness — requires urgent drainage and antibiotics to prevent felon (deep space hand infection) or sepsis; rapidly spreading infection in a diabetic patient with nail problems; immunocompromised patients (chemotherapy, transplant, HIV) with nail infections — systemic spread of fungal infection is a risk.