Onychomycosis (Fungal Nail Infection / Tinea Unguium)

• Yellow-brown discoloration starting at the distal/lateral nail edge
• Onycholysis (nail plate separating from the nail bed)
• Subungual hyperkeratosis (chalky debris under the nail)
• Multiple fingers affected

Definition

• Andrews' Diseases of the Skin, p. 351

Epidemiology

• Affects up to 14% of the general population
• More common in older individuals and increasing in children/adolescents
• More common in men than women
• Up to 40% of toenail onychomycosis patients have concurrent tinea pedis
• Fitzpatrick's Dermatology, p. 2967

Etiology (Causative Organisms)

• Andrews' Diseases of the Skin, p. 351

Risk Factors

• Advanced age
• Male sex
• Nail trauma
• Immunosuppression (HIV/AIDS, diabetes mellitus, organ transplant)
• Peripheral vascular disease
• Wearing tight shoes / occlusive footwear
• Use of communal locker rooms, pools, showers
• Family members with onychomycosis (contagious)

• Fitzpatrick's Dermatology, p. 2967

Clinical Types

1. Distal Lateral Subungual Onychomycosis (DLSO) - Most Common

• Invasion starts at the distal edge or lateral corner of the nail
• Whitish-to-brownish-yellow opacification at the distal nail edge
• Spreads proximally as a streak
• Leads to subungual hyperkeratosis, nail thickening, and eventual onycholysis
• This is what is shown in the uploaded image

2. White Superficial Onychomycosis (WSO)

• Direct invasion of the dorsal nail plate surface
• White, sharply bordered chalky patches on toenail surfaces
• Caused by T. interdigitale and non-dermatophyte molds

3. Proximal Subungual Onychomycosis (PSO)

• Fungus enters via the proximal nail fold
• White-to-beige opacity seen on the proximal nail plate
• Spreads distally; can destroy the entire nail
• Marker for HIV infection - screen all PSO patients

4. Candida Onychomycosis

• Massive nail destruction and hyperkeratosis
• Seen in chronic mucocutaneous candidiasis, other immunodeficiency states, and infants

5. Total Dystrophic Onychomycosis

• End-stage disease; entire nail plate destroyed
• Can result from progression of any of the above types
• Fitzpatrick's Dermatology, p. 2967-2968; Andrews' Diseases of the Skin, p. 349-351

Diagnosis

• Andrews' Diseases of the Skin, p. 351

Differential Diagnosis

• Nail psoriasis - pitting, oil-drop discoloration, salmon patches; skin/joint involvement
• Lichen planus - rough nails, pterygium formation; oral/skin lesions
• Eczema / contact dermatitis - affects adjacent nail fold
• Traumatic onycholysis - history of injury
• Yellow nail syndrome - all 20 nails, associated with lymphedema/pleural effusion
• Norwegian (hyperkeratotic) scabies - generalized hyperkeratosis
• Melanoma - must always rule out in pigmented nail changes
• Andrews' Diseases of the Skin, p. 351

Treatment

Topical Therapy (mild/distal disease, contraindication to systemic)

Systemic (Oral) Therapy - First Line for Most Cases

• Adults: 250 mg/day for 6 weeks (fingernails) or 12 weeks (toenails)
• Children >40 kg: 250 mg/day; 20-40 kg: 125 mg/day; <20 kg: 62.5 mg/day
• Mycologic cure ~70% (toenails), ~80% (fingernails)

• 200 mg twice daily for 1 week per month
• 2 months for fingernails; 3-4 months for toenails
• Good for Candida and non-dermatophyte molds too

• 150-300 mg once weekly for 6-12 months
• Comparable efficacy; convenient once-weekly dosing

• Andrews' Diseases of the Skin, p. 351-352; Fitzpatrick's Dermatology, p. 2968-2969

Combination & Mechanical Approaches

• Combination topical + oral can improve clearance rates
• Nail trimming and debridement help deliver medication to the site
• Nd:YAG laser therapy: 50-60% cure rate after multiple sessions
• Surgical or chemical nail avulsion (40% urea) for refractory cases - a recent systematic review (Mycoses, 2025) confirmed 40% urea as an effective adjuvant to antifungals

For Candida Onychomycosis

• Itraconazole 400 mg/day pulse (1 week/month) for 4-12 weeks, OR
• Fluconazole 50 mg/day or 300 mg/week for similar duration
• Topical + systemic combination improves outcomes

Prevention and Recurrence

1. Keep feet clean and dry - dry between toes thoroughly after washing
2. Wear breathable footwear - avoid tight, occlusive shoes
3. Use antifungal powder or spray in shoes and socks
4. Avoid walking barefoot in communal areas (pools, gym locker rooms, showers)
5. Treat concomitant tinea pedis - it's a major reservoir for nail reinfection (30% of cases co-exist)
6. Don't share nail clippers, files, or footwear
7. Change socks daily; use moisture-wicking materials
8. Topical antifungal lacquers after cure can be used as maintenance
9. Manage systemic risk factors - optimal diabetes control, improve peripheral circulation
10. Treat household contacts if infected

• Fitzpatrick's Dermatology, p. 2968-2969; Andrews' Diseases of the Skin, p. 351

When to Urgently Seek Care

• Diabetic patients or those with peripheral neuropathy: onychomycosis significantly increases risk of bacterial cellulitis - treat promptly
• Any suspicion of PSO (proximal white opacity under the nail): screen for HIV
• Spreading redness, warmth, swelling, or pus around the nail - possible secondary bacterial infection

Important Note

Why Hydrophobia Occurs in Rabies

First, Understand the Virus's Path to the Brain

1. The virus is inoculated via a bite into muscle/skin
2. It replicates briefly in muscle, then binds to nicotinic acetylcholine receptors at the neuromuscular junction
3. It enters peripheral nerve axons and travels centripetally (toward the CNS) via retrograde fast axonal transport at up to ~250 mm/day
4. It replicates in spinal cord motor neurons and dorsal root ganglia, then ascends rapidly to the brain
5. Once in the CNS it spreads widely via axonal connections - the brainstem and limbic system are particularly heavily infected
6. After CNS infection is established, it spreads centrifugally back out to salivary glands, skin, cornea - this is why saliva is infectious

• Harrison's Principles of Internal Medicine 22e, p. 1695

The Core Mechanism of Hydrophobia

Step-by-step breakdown:

1. Virus infects the brainstem - especially near the nucleus ambiguus

2. Attempting to swallow water triggers violent spasms

• The diaphragm
• The pharyngeal muscles (throat)
• The laryngeal muscles (voice box)
• Accessory respiratory muscles

"Hydrophobia: involuntary, painful contraction of the diaphragm and accessory respiratory, laryngeal, and pharyngeal muscles in response to swallowing liquids... These symptoms are probably due to dysfunction of infected brainstem neurons that normally inhibit inspiratory neurons near the nucleus ambiguus, resulting in exaggerated defense reflexes that protect the respiratory tract."

• Harrison's Principles of Internal Medicine 22e

3. Classical conditioning creates the "phobia" component

• Seeing water
• Hearing water (splashing, running taps)
• Smelling it
• Or just being offered a drink

• Bradley and Daroff's Neurology in Clinical Practice, p. 1675

Aerophobia - The Same Mechanism

"Up to 80% of patients may exhibit hydrophobia or aerophobia, spasms of pharyngeal and nuchal muscles lasting from 1 to 5 minutes, triggered by swallow attempts or tactile, auditory, visual, and olfactory stimuli."

• Bradley and Daroff's Neurology in Clinical Practice

Why the Virus "Wants" This to Happen (Evolutionary Perspective)

The Hypersalivation + Pharyngeal Dysfunction = "Foaming at the Mouth"

• Hypersalivation (from autonomic dysfunction - the virus infects the salivary glands and their autonomic supply)
• Pharyngeal paralysis/spasm (patient cannot swallow)

• Harrison's Principles of Internal Medicine 22e, p. 1695

Clinical Note - Hydrophobia as a Diagnostic Sign

"The findings of hydrophobia with resultant gagging and hypersalivation are so characteristic of rabies infection that in many developing countries, water is offered to the patient as a diagnostic test."

• Rosen's Emergency Medicine

Summary Table