Paronychia

[1] [3] [4] [8] [25]

Overview and Definition

Paronychia is inflammation or infection of the nail fold — the skin that frames the nail plate on three sides (proximal and two lateral folds). The proximal nail fold (PNF) is the deepest and most clinically important: its free edge forms the cuticle (eponychium), a thin keratinised seal that runs from the dorsal surface of the PNF onto the dorsal surface of the nail plate for ~1 mm. The cuticle is the protective watertight barrier whose loss enables entry of resident flora (Staphylococcus aureus from anterior nares, Candida from gut and perineum), water, detergents and chemical irritants — and whose loss is the single most important pathophysiological event in both acute and chronic paronychia.[1][2][11]

Three anatomic landmarks complete the nail unit (and recur in examinations): the germinal matrix (proximal nail matrix, ~50% of the matrix, underlies the PNF and produces ~80% of the nail plate), the sterile matrix (nail bed, firmly adherent to the nail plate, longitudinally ridged, contributes the third remaining plate thickness), and the hyponychium (the distal seal under the free edge of the plate, onychocorneal band). The nail plate is fully keratinised dead keratin; it has no intrinsic blood supply, regenerates from the matrix, and grows at ~3 mm/month (fingernail) and ~1 mm/month (toenail).[11]

The condition can be classified along two orthogonal axes that examiners test: [1]

[1] [1]

[1] [3] [4]

Classification [1]

Paronychia is classified by duration, pathogen, host, drug exposure and route of presentation — five axes the examiner tests: [1]

A — By duration

• Acute paronychia — symptoms ≤ 6 weeks; bacterial (Staph aureus dominant); single finger; painful; fluctuant; settles with soaks ± I&D.
• Chronic paronychia — symptoms > 6 weeks; multi-finger; boggy with LOST CUTICLE; irritant contact dermatitis with secondary Candida / bacterial colonisation; months-long course.
• Recurrent acute — either repeated bacterial paronychia in the same finger (think occult foreign body, ingrown nail, malignancy) or recurrent flares on a chronic-paronychia background (think continued wet-work exposure, drug-induced, EGFr inhibitor). [1]

B — By organism

• Bacterial (acute dominant): Staphylococcus aureus; Streptococcus pyogenes; Pseudomonas aeruginosa (green nail syndrome / chronic); anaerobic mouth flora (Eikenella corrodens, Fusobacterium, Prevotella, Peptostreptococcus) in clenched-fist / human-bite injuries; Klebsiella, Enterobacter, Serratia, Proteus in immunocompromised hosts.
• Fungal (chronic coloniser): Candida albicans > C. parapsilosis > C. tropicalis > C. glabrata; always treat as a coloniser — never monotherapy antifungal (fails without irritant removal).
• Viral: HSV-1 / HSV-2 — herpetic whitlow (different compartment, NO incision).
• Atypical: non-tuberculous mycobacteria (M. marinum in fish / aquarium handlers; M. chelonae in chronic steroid users); Bartonella henselae after cat scratch; deep fungi in severe neutropenia; Scedosporium, Fusarium in the profoundly immunocompromised. [1]

C — By host & route

• Primary occupational — wet-work (dishwashers, bartenders, butchers, bakers, domestic workers, healthcare workers, cleaners, fishermen, florists, swimmers).
• Secondary (drug-induced): retinoids (isotretinoin, acitretin, alitretinoin); EGFr antibodies (cetuximab, panitumumab); EGFr TKIs (gefitinib, erlotinib, osimertinib, dacomitinib, amivantamab); MEK inhibitors (trametinib, cobimetinib); BTK inhibitors (ibrutinib, acalabrutinib); antiretrovirals (indinavir, lamivudine); mTOR inhibitors (everolimus); taxanes (docetaxel); targeted therapies (vemurafenib, dabrafenib).
• Secondary (disease): eczema / atopic dermatitis; psoriasis (especially acrodermatitis continua of Hallopeau); diabetes mellitus; HIV; malnutrition; chronic kidney disease; Raynaud phenomenon; peripheral vascular disease. [1]

D — By complication / outcome

• Acute without abscess — settles with soaks.
• Acute with subungual extension — needs partial nail-plate avulsion.
• Chronic refractory — needs marsupialisation.
• Complicated — flexor tendon sheath infection (Kanavel), distal phalanx osteomyelitis, necrotising fasciitis, lymphangitis / bacteraemia. [1]

Epidemiology and Risk Factors

Global numbers

Acute paronychia is one of the commonest hand infections seen in primary care and emergency departments, accounting for ~30-35% of adult acute hand infections in large series (Fowler and Ilyas, 2013, urban US cohort).[17] It is seasonal (summer peak in temperate regions — barefoot trauma, gardening, sweaty hands), young-adult-skewed (peak incidence 20-40 years), and equally common in men and women except where occupational exposure drives a sex bias (chronic paronychia is female-skewed in butchers / beauticians / cleaners / canteen workers). Chronic paronychia affects ~1-3% of adults in occupational cohorts and dominates in the top two causes of work-related hand dermatitis after glove-related contact allergy.[1][2][7]

Modifiable risk factors

• Repetitive wet/dry cycles (the central mechanism of chronic paronychia).
• Wet-work occupations: dishwasher, bartender, butcher, baker, healthcare worker (especially nurses, dental hygienists, theatre scrub nurses), cleaner, fisherman, florist, hairdresser, beautician, swimmer.
• Occlusive glove use — thin nitrile gloves trap sweat and worsen maceration; cotton-lined rubber gloves are the protective standard.
• Manual labour with chemical irritants — vegetable juice (onion, garlic, citrus), flour, salt, sugar, fish juice, hydrocarbons, lubricants, photographic chemicals.
• Nail biting / onychophagia — disrupts cuticle, inoculates oral flora (anaerobes in clenched-fist / nail-fold bite).
• Hangnail / cuticle picking / manicure (especially cuticle pushing / cutting — REMOVES the cuticle barrier).
• Artificial nails / gel polish / acrylic — trap water, prevent cuticle regeneration, harbour Pseudomonas.
• Tinea manuum / pedis — interdigital portal; Trichophyton causes chronic paronychia in some series.
• Tight or constricting shoes / wet footwear.
• Smoking — vasoconstriction impairs cuticle healing.
• Poor glycaemic control — impaired neutrophil chemotaxis, faster progression to abscess / deeper infection. [1]

Non-modifiable risk factors

• Diabetes mellitus — recurrent / refractory chronic paronychia warrants HbA1c; up to 1 in 5 patients with refractory chronic paronychia have undiagnosed diabetes.[1][2]
• Atopic dermatitis / eczema / contact dermatitis — defective barrier.
• Peripheral vascular disease, Raynaud phenomenon — slow cuticle healing.
• HIV / AIDS and other immunosuppression — broader differential and a lower threshold for culture, drainage and specialist referral in refractory or atypical disease.
• Chemotherapy-induced neutropenia, transplant recipients, biologics — broader differential, atypical organisms, lower threshold for I&D and IV cover.
• Iron deficiency, malnutrition, hypoproteinaemia — impaired epithelial regeneration.[2]

Drug-induced paronychia — high-yield list

Regional deltas (epidemiology + clinician awareness)

• India / South Asia: chronic paronychia is classically described in housewives and housemaids — in an Indian series of 80 patients, 82.5% were female, 58.8% housewives, and frequent hand washing was the most common risk factor (80%); patch testing identified contact sensitisation (nickel most common) in 27.1%.[13] Indian reviews emphasise general preventive measures as the cornerstone, with topical steroids outperforming the older antifungal mainstay.[7]
• Antibiotic choice is local, not universal: clinical history and LOCAL antibiotic guidance — including consideration of MRSA rates — should direct the prescription; gram-positive cover is advised for early paronychia, or a broad-spectrum agent when exposure to oral flora is suspected (nail-biting, digital sucking).[4]
• US urban practice: in an urban academic series of 1,507 drainage procedures, MRSA was the most common isolate (53% of positive cultures; MSSA 23%, polymicrobial 19%) — empiric coverage should routinely cover MRSA, particularly with intravenous drug use, diabetes, or human bites.[17]
• Culture yield caveat: paronychia had the LOWEST percentage of positive cultures among hand-infection sites in that series — most paronychia is treated before cultures matter, but cultures guide therapy when drainage is performed.[17]

Pathophysiology

Nail unit anatomy as it relates to paronychia

The protective nail apparatus is built from four layered keratinised elements and three bacteriologic seals.[11] From surface to depth:

1. Cuticle (eponychium) — thin keratinised cornified layer that runs from the dorsal surface of the proximal nail fold onto the dorsal surface of the nail plate for ~0.5-1.0 mm. Forms the proximal seal.
2. Lateral nail folds × 2 — skin folds that grip the sides of the plate; their distal end seals against the nail at the lateral grooves. With chronic wet-work these seals are the first to soften.
3. Hyponychium (onychocorneal band) — under the free edge of the plate; the distal seal. Loss of this seal produces distal subungual onychomycosis and is the gateway for fungal / Pseudomonas paronychia of the distal fold.
4. Nail plate — fully keratinised dead keratin, no blood supply, no nerves. Regenerates from the matrix. [1]

The proximal nail fold has a dorsal and a ventral surface; the ventral surface of the PNF is the area that inflames acutely (acute paronychia) and thickens + loses its cuticle chronically (chronic paronychia). [1]

Step 1 — Loss of the cuticle (the gateway event)

The cuticle is the single most important barrier and the single most commonly breached barrier. Loss results from: [1]

• Mechanical: manicure (especially cuticle pushing / cutting), hangnail picking, nail biting, artificial-nail application, nail-plate avulsion, subungual foreign body.
• Chemical: detergents (sodium lauryl sulphate = SLS), solvents, vegetable juices (onion / garlic / citrus), flour (proteolytic enzymes), salt, sugar, photographic chemicals.
• Occlusive maceration: prolonged water contact (dishwasher, bartender, swimmer, fisherman); occlusion under gloves or bandages prevents the cuticle from re-keratinising.
• Inflammatory: acute dermatitis, atopic dermatitis, psoriasis, lichen planus.
• Drug: retinoids, EGFr / MEK inhibitors, antiretrovirals. [1]

Step 2 — Inoculation

Once the cuticle is breached, resident flora colonises the sub-cuticular space: [1]

Step 3 — Inflammation of the nail fold

In acute paronychia, neutrophil-rich pus accumulates under the lifted cuticle; the fold becomes tense, erythematous, fluctuant; the abscess either drains spontaneously (skin → pus tracks under the cuticle and onto the plate) or tracks under the proximal nail plate to form a subungual abscess. [1]

In chronic paronychia, repeated wet/dry cycles and irritant exposure cause a lymphohistiocytic + eczematous inflammation in the proximal nail fold; the cuticle retracts (lost cuticle — hallmark) and is replaced by a moist, erythematous, oedematous fold with poor keratinisation. Secondary Candida and bacterial colonisation is secondary, not causal; this is why monotherapy antifungal fails — the wet-work irritant must be removed.[7][13]

Step 4 — Nail-plate damage (chronic phase)

The chronic inflamed fold is a poor matrix for the emerging plate. Typical nail changes: [1]

• Beau lines — transverse ridges where the matrix briefly stopped growing.
• Median / longitudinal ridging — chronic matrix disturbance.
• Green-brown discoloration — Pseudomonas pyocyanin on onycholytic plate; or Candida brown staining.
• Distal onycholysis — plate separates from the bed (hyponychium breach). [1]

[1]

Drug-induced paronychia mechanism

• EGFr inhibitors — a recognised cause of paronychia and periungual pyogenic granuloma-like lesions (friable, easily bleeding); toxicity of agents such as panitumumab, cetuximab and erlotinib; high-potency topical corticosteroids and topical timolol 0.5% are described treatments, and invasive nail-unit procedures are avoided in these fragile patients.[21]

Herpetic whitlow pathophysiology

HSV-1 (oral shedders, dental / healthcare exposure) or HSV-2 (genital contact, autotransmission) enters via microtrauma → primary inoculation into the dermis of the pulp / fold → replication in epidermal keratinocytes → vesicular coalescence with Tzanck-positive multinucleate giant cells → ascendant lymphangitis → ganglionic latency in the dorsal root ganglion or trigeminal ganglion → reactivation in 30-50% of patients, often with prodromal burning/tingling.[14]

Clinical Presentation

Acute paronychia — diagnostic clinical pattern

• Onset: hours to days (often < 48 h from the precipitating event — hangnail, cuticle cut, nail-bite).
• Pain: throbbing; interferes with sleep and use of the hand.
• Sign: erythema, oedema, warmth of the proximal and / or one lateral nail fold; a yellow-green sub-cuticular collection that lifts the cuticle is pathognomonic.
• Fluctuance: the cardinal sign that pus is present and I&D is indicated.
• Extension: around the lunula, beneath the nail plate (subungual abscess); rarely into the pulp — then think FELON.
• Systemic: usually absent; fever / lymphangitis signals spreading cellulitis or early flexor tendon sheath infection.
• Distribution: commonly one finger — index, middle and thumb dominant (the "bite / pick fingers").
• Subacute on chronic background: if acute paronychia happens on a finger with chronic paronychia, a cure requires BOTH the I&D and the wet-work avoidance. [1]

Chronic paronychia — diagnostic clinical pattern

• Onset: weeks to months; often first noticed because the cuticle is GONE.
• Pain: dull, mild, episodic — much less than acute; some patients deny pain.
• Sign: BOGGY, mildly tender, oedematous proximal nail fold; LOST CUTICLE is the hallmark; erythema ± scaling; recurrent small flares of acute inflammation superimposed.
• Nail plate: ridging, transverse grooves / Beau lines, green-brown discoloration (if Pseudomonas or Candida), distal onycholysis; permanent nail changes if matrix damaged.
• Distribution: MULTI-FINGER, usually dominant hand; often symmetric in bilateral wet-work exposures.
• Predisposing background: occupation (dishwasher, bartender, cleaner), diabetes, eczema, recent drug start (retinoid, EGFr inhibitor, antiretroviral).
• Systemic: none. [1]

Atypical clinical patterns

[1]

• Immunocompromised / oral-flora exposure — paronychia is polymicrobial with mixed aerobic and anaerobic flora in around 50% of cases; anaerobes (Bacteroides, Enterococcus species, Eikenella corrodens) follow exposure to oral secretions through nail-biting and digital sucking, which is commoner in children.[4]
• Elderly / diabetic — plain radiographs of the involved digit are used to investigate foreign body, fracture or osteomyelitis, and glucose testing may identify undiagnosed diabetes.[4]
• Drug-induced EGFr-inhibitor paronychia — periungual pyogenic granuloma-like lesions and paronychia are well-recognised toxicities that impair quality of life and compliance with anticancer treatment.[21]
• Mycobacterium marinum (fish-tank granuloma) — strongly linked to water exposure; sporotrichoid nodules occur; obtain tissue for mycobacterial culture and histopathology.[22]
• Acrodermatitis continua of Hallopeau — painful paronychia with sterile pustules on an erythematous base around the nail folds and in the nail bed; acitretin is recommended first-line.[18]

Red-flag clinical features that mandate escalation

• Systemic toxicity — fever, rigors, tachycardia disproportionate to local signs, hypotension, confusion → sepsis pathway, IV antibiotics within 1 hour.
• Pain out of proportion to signs, dusky discolouration, crepitus, bullae → necrotising soft-tissue infection; immediate surgical debridement.
• Flexor tendon sheath infection (Kanavel signs) — fusiform swelling of the entire finger, finger held in flexion, tenderness along the tendon sheath, pain on passive extension of the distal interphalangeal joint. Hand surgery within hours; missing this causes permanent tendon necrosis and flexion contracture.
• Distal phalanx osteomyelitis — chronic paronychia + bone pain + systemic signs or persistent discharge; MRI / X-ray.
• Spreading cellulitis past the wrist → admit for IV antibiotics.
• Immunocompromised host + any paronychia → culture, IV cover, lower threshold for admission.
• Single-digit chronic dystrophy → biopsy to exclude squamous cell carcinoma / melanoma of the nail unit.
• Pigment extension onto the proximal nail fold (Hutchinson sign) → melanoma of the nail matrix until proven otherwise — biopsy the matrix, not just the plate. [1]

[1]

Differential Diagnosis

The diagnosis of paronychia is clinical. The differential is anatomic (which compartment is inflamed) plus morphologic (fluid vs. solid vs. papular) plus host context. [1]

[1] [3] [4] [5] [10] [12] [14] [18] [21] [22] [25]

Cannot-miss differentials (miss = significant morbidity)

[3] [5] [6] [12] [14] [20]

Clinical and Bedside Assessment

A complete bedside assessment has six steps — the examiner expects you to demonstrate all six. [1]

Step 1 — Inspection of the affected and contralateral fingers

• Look at all 20 nails — chronic paronychia is usually multi-finger.
• Look at the proximal and both lateral folds — and the distal hyponychium.
• Look at the pulp — to exclude concurrent felon.
• Look at the plate — for Beau lines (matrix damage), green-black discoloration (Pseudomonas), ridging, onycholysis.
• Look at the lunula — for pigmentation extension (Hutchinson sign). [1]

Step 2 — Palpation and bedside manoeuvres

• Fluctuance — pressing the fold with a gloved fingertip detects fluid.
• Tense pulp — distinguishes felon (pulp under tension) from paronychia (fold under tension).
• Lymphangitis — red streak ascending the forearm.
• Regional nodes — epitrochlear + axillary.
• Capillary refill — exclude arterial compromise (Buerger, thromboangiitis obliterans, vasculitis). [1]

Step 3 — Vascular and neurological screen

Capillary refill < 2 seconds; light touch / pin-prick of the distal pulp; peripheral pulses (radial, ulnar, brachial). Vasculopathy and neuropathy change prognosis. [1]

Step 4 — Identify the portal of entry

Hangnail / cuticle trauma, manicure or cuticle pushing within 7 days, nail bite, artificial nail, ingrown nail, tinea manuum (interdigital scale), puncture wound (splinter / thorn / fish bone / sewing needle), recent HSV exposure (dental visit, thumb-sucking child). [1]

Step 5 — Drug and disease history

Retinoid, EGFr / MEK / BTK inhibitor, antiretroviral, chemotherapy, biologics, recent surgery. Diabetes, eczema, psoriasis, HIV, Raynaud, peripheral vascular disease, smoking, malnutrition. [1]

Step 6 — Severity and systemic status

Temperature, pulse, BP, RR, mental state, NEWS2 / qSOFA — basic vital signs before any treatment decision. [1]

[1]

Investigations

Acute paronychia is a clinical diagnosis. The role of investigations is to (i) confirm the organism when it matters for treatment, (ii) screen for underlying disease in chronic / recurrent / refractory disease, (iii) rule out herpetic whitlow when morphology is uncertain, and (iv) exclude osteomyelitis / necrotising infection in severe disease. [1]

Acute paronychia — when to investigate

Investigations for HSV (herpetic whitlow — when in doubt)

• Vesicle PCR — gold standard; sensitivity 95%+; can type HSV-1 / HSV-2.
• Tzanck smear — multinucleate giant cells; fast (1 h) but low sensitivity; positive in HSV-1, HSV-2 and VZV; cannot distinguish.
• Direct immunofluorescence antigen detection (DFA) — type-specific, fast.
• Viral culture — historically the gold standard; sensitivity 50-70% and slow (3-7 days); now largely replaced by PCR.
• HSV serology (IgM / IgG) — useful in primary infection to confirm seroconversion; not useful in recurrences. [1]

Investigations for chronic paronychia

In chronic paronychia the investigations are largely about (a) confirming the role of Candida (culture is supportive, not diagnostic), (b) screening for predisposing disease, (c) excluding malignancy in single-digit disease. [1]

Adjunctive screening for recurrent / refractory / chronic disease

• HbA1c / fasting glucose — diabetes mellitus.
• HIV 4th-generation Ag/Ab — single exposure for high-prevalence populations.
• FBC + differential — neutropenia, lymphopenia, eosinophilia.
• Ferritin + iron studies — iron deficiency impairs neutrophil oxidative burst.
• Urea / creatinine / eGFR — renal dosing for flucloxacillin, cephalexin, tetracyclines.
• LFTs — baseline before fluconazole, itraconazole, doxycycline.
• TSH — hypothyroidism presents with brittle nails.
• Patch testing — when contact allergy is suspected (chromate, rubber, fragrance, preservative).
• Nail clippings for mycology — if tinea unguium concurrent. [1]

Imaging

• Plain X-ray of the distal phalanx if chronic paronychia + bone pain + systemic signs → osteomyelitis (cortical destruction, periosteal reaction).
• Ultrasound for occult abscess / foreign body.
• MRI if necrotising fasciitis suspected (deep fascial oedema, gas, non-enhancing muscle); reserved for severely ill patients.
• CT rarely needed; reserved for deep hand collections. [1]

Management — Resuscitation

Resuscitation is rarely needed in paronychia. Recognise the patients in whom it is: [1]

[1]

For severe or necrotising disease: [1]

• ABCDE approach with oxygen for hypoxia; treat sepsis per local protocol.
• IV access, bloods (FBC, U&E, CRP, lactate), blood cultures × 2 and coagulation/group-and-save in severe or necrotising disease.
• Empirical IV antibiotics — early felons and paronychias may be managed with antibiotics alone, whereas more advanced infections require incision and drainage; choice is directed by the most likely pathogens and local resistance patterns, with MRSA considered.[3][1]
• Urgent surgical consultation — for deep infections such as pyogenic flexor tenosynovitis, for immediate debridement if necrotising infection is suspected, and for compartment syndrome of the digit.[6]

Management — Definitive and Stepwise

A — Acute paronychia — staged ladder

[1] [3] [4] [1] [3] [4] [17]

[1] [7] [8]

C — Chronic paronychia — staged ladder [1]

[1] [7] [8] [1] [4] [7] [8] [25]

D — Chronic paronychia — drug choice (drug + dose + route + timing + rationale)

• Tacrolimus 0.1% ointment twice daily — the best-evidenced anti-inflammatory for chronic paronychia. Rigopoulos 2009 RCT (45 patients randomised 1:1:1): tacrolimus 0.1% BD vs betamethasone 17-valerate 0.1% BD vs emollient for 3 weeks with 6 weeks' follow-up — with tacrolimus, 13 patients were cured and one improved; with betamethasone, 8 cured, 2 improved, 4 non-responders; with emollient, 9 stable and 6 failed. Both active arms beat emollient (P under 0.001); conclusion: tacrolimus appears MORE efficacious than betamethasone 17-valerate or placebo. Protective measures were counselled in all arms.[8]
• Betamethasone 17-valerate 0.1% twice daily — the topical-steroid comparator in that trial; topical steroids are the established alternative to calcineurin inhibitors and beat the older antifungal mainstay in reviews.[8][7]
• Antifungals are adjuncts — chronic paronychia is a multifactorial inflammatory reaction of the proximal nail fold to irritants and allergens, not a Candida infection; Candida albicans is simply the most commonly implicated coloniser. Oral antifungals described for yeast nail infection include fluconazole, with itraconazole as an alternative — reserve for culture-positive, irritant-controlled disease.[4][7][25]
• En bloc excision of the proximal nail fold or eponychial marsupialisation (with or without nail-plate removal) — the surgical option for recalcitrant chronic paronychia after conservative therapy has failed.[7]

E — Subtype-specific drug choice

• Herpetic whitlow — NON-OPERATIVE management; drainage is contraindicated unless a concurrent bacterial infection is present. Disrupting the vesicles (incision, deroofing) frequently causes secondary bacterial infection. Confirm with PCR (or viral culture / serology / DFA / Tzanck); oral aciclovir, valaciclovir and famciclovir are effective treatments for nongenital HSV, and herpetic whitlow typically resolves without intervention; recurrences of nongenital HSV may be diminished with daily oral antivirals.[5][6][14][19][20]
• Felon — early felons may be managed with antibiotics alone; more advanced infections require incision and drainage. Preferred drainage: longitudinal incision in the VOLAR space if superficial, LATERAL space if deep, not extended past the distal interphalangeal joint space; hockey-stick or fish-mouth extension in select cases; empiric oral antibiotics accompany surgical drainage.[3][6]
• Green-nail syndrome — triad of green nail discoloration, paronychia and onycholysis; Pseudomonas aeruginosa is the primary etiologic agent. Diagnose by bacterial culture and susceptibility testing; targeted therapy with culture-guided oral and topical agents (a co-infection case resolved with oral + topical levofloxacin); ciprofloxacin is the described oral agent for Pseudomonas nail infection; antiseptic soaks (1% acetic acid) are an option for paronychia.[10][25][1]
• EGFr-inhibitor paronychia and pyogenic granuloma-like lesions — high-potency topical corticosteroids are a well-known option especially for paronychia; topical timolol 0.5% gel twice daily under occlusion for 30 days achieved complete resolution in 13/25 and improvement in 9/25 lesions (case series); nail-plate avulsion and phenol matricectomy are not highly effective and are invasive — prefer non-invasive strategies in fragile cancer patients; oncology liaison for dose modification.[21]
• Acrodermatitis continua of Hallopeau — systemic treatment is generally preferred even for localised disease (topicals only supportive); acitretin is recommended first-line although relapse is common; biologic drugs show good efficacy but rarely give long-lasting remission.[18]
• Mycobacterium marinum (fish-tank granuloma) — combined antibiotic schemes directed by susceptibility: the classes most frequently used are macrolides, tetracyclines, cotrimoxazole, quinolones, aminoglycosides, rifamycins and ethambutol; surgical treatment can be curative (and diagnostic) in small lesions; management often includes multiple antibiotics for several months with potential adjunctive surgery.[23][22]

F — Procedural technique in detail

Incision and drainage (I&D) of acute paronychia

1. Confirm an abscess is present — tender, boggy swelling of the nail fold; formation of pus along the paronychial fold; the digital pressure test (light pressure on the volar fingertip) produces a localised area of skin blanching around the nail when pus is present. If untreated, the abscess may progress to involve the eponychium and the area below the nail plate (visible on inspection, ballotable on palpation).[4]
2. Choose the drainage option proportionate to the abscess — options range from instrumentation with a hypodermic needle to a wide incision with a scalpel; a simple incision approach is preferred for simple paronychia with abscess, and a single or double incision technique along the nail for more complex cases.[1][3]
3. Exclude the differentials first — herpetic whitlow (vesicles: drainage contraindicated unless concurrent bacterial infection) and felon (pulp-space infection: separate drainage approach).[4][3]
4. Send pus for microbiology — paronychia is polymicrobial (mixed aerobic and anaerobic flora in around half of cases); culture and local resistance patterns direct any antibiotic prescription.[4]
5. Aftercare — warm soaks with or without Burow solution or 1% acetic acid, topical antibiotics, and oral antibiotics only if the patient is immunocompromised or the infection is severe.[1]

Partial nail-plate avulsion

1. Indicated when an abscess extends to involve the eponychium and the area below the nail plate — pus deep to the nail plate may be visible on inspection and ballotable on palpation.[4]
2. Nail-plate removal (with or without the fold procedure) is part of the surgical repertoire for advanced subungual extension and for recalcitrant chronic disease.[7]
3. Post-procedure care and microbiology as for I&D above. [1]

Eponychial marsupialisation (chronic paronychia — refractory)

Chronic paronychia that fails conservative therapy (irritant removal + topical steroid or calcineurin inhibitor) can be treated surgically: en bloc excision of the proximal nail fold or eponychial marsupialisation, with or without nail-plate removal (Relhan 2014). The aim is to remove the chronically inflamed, fibrosed fold that generates a poor cuticle and re-exposes the nail to irritants, so that a fresh cuticle seal can regenerate.[7]

[7]

Felon I&D

1. Early felon — may be managed with antibiotics alone, with close re-assessment.[3]
2. Advanced felon — requires incision and drainage: a longitudinal incision in the volar space if superficial or the lateral space if deep, with careful attention NOT to extend past the distal interphalangeal joint space; extension to a hockey-stick or fish-mouth incision may be indicated in select cases.[3]
3. Why urgency — pus in the pulp space can lead to digital compartment syndrome if not adequately drained; felons also warrant radiographs (foreign body, fracture, osteomyelitis) and empiric oral antibiotics alongside drainage.[3][4][6]

G — Escalation triggers

• 48-72 h without improvement → reassess diagnosis (herpetic whitlow, felon, malignancy); broaden cover; MCS; image for abscess / osteomyelitis / necrotising infection; refer to plastic / hand surgery.
• Spreading cellulitis past the wrist → IV antibiotics + admission.
• Any necrotising fasciitis sign → immediate debridement + ICU.
• Immunosuppressed → lower threshold for IV, culture, admission.
• Chronic paronychia + single-digit disease → biopsy for malignancy. [1]

Specific Subtypes and Scenarios

A — Herpetic whitlow

• Organisms: HSV-1 in medical and dental personnel and in children (thumb-sucking, oral shedders); HSV-2 with genital contact / autoinoculation.[14][19][20]
• Clinical: prodrome of pain or tingling, then clear vesicles on an erythematous base, which may become cloudy and coalesce before crusting; the infection typically resolves without intervention; fever and lymphadenitis can accompany primary infection.[5][14][19]
• Investigations: HSV PCR of vesicle fluid (or viral culture, DFA, serology, Tzanck smear) when the diagnosis is uncertain — the same tools used for nongenital HSV at other sites.[5][19]
• Management: NON-OPERATIVE. DO NOT INCISE or de-roof the vesicles — drainage is contraindicated unless a concurrent bacterial infection is present, because disrupting the vesicles frequently causes secondary bacterial infection. Oral aciclovir, valaciclovir and famciclovir are effective treatments for nongenital HSV; recurrences may be diminished with daily oral antivirals (consider for healthcare workers at occupational risk).[5][6][14][19]
• Complication in operator: herpetic whitlow of the doctor / dentist from contact with a patient's oral secretions or vesicle fluid — gloves and standard precautions protect.[14][19][20]

B — Felon (finger pulp abscess)

• Pathogen: Staph aureus is the classic organism; mixed oral flora after a tooth puncture or bite.[3][4]
• Anatomy: infection of the pulp of the distal phalanx, a closed space divided by fibrous septa — a distinct compartment from the nail fold, which is why it must be distinguished from paronychia.[3][4]
• Clinical: tense, exquisitely tender finger pad (throbbing pain), often after a penetrating injury.[3][6]
• Investigations: clinical diagnosis; consider radiographs to identify a foreign body, fracture or osteomyelitis; obtain cultures when draining.[3][4]
• Management: EARLY felons may be managed with antibiotics alone, with close re-assessment; more advanced infections require incision and drainage — longitudinal incision in the volar space if superficial, lateral space if deep, not extended past the distal interphalangeal joint space (hockey-stick or fish-mouth extension in select cases); empiric oral antibiotics accompany surgical drainage.[3][6]
• Why urgency: pus in this closed space can progress to digital compartment syndrome, osteomyelitis of the distal phalanx, or septic arthritis of the DIP joint if not adequately drained.[3][6]

C — Green-nail syndrome (Pseudomonas paronychia)

• Definition and pathogen: the triad of green nail discoloration, paronychia and onycholysis; Pseudomonas aeruginosa is the primary etiologic agent — green staining of the nail plate. Diagnose by bacterial culture and susceptibility testing of nail / fold material.[10]
• Management: targeted therapy guided by culture and susceptibility — a co-infection case resolved with oral and topical levofloxacin; ciprofloxacin is the oral agent classically described for Pseudomonas nail infection; antiseptic (e.g. acetic acid) soaks are an option for the paronychia component; keep the nail short and dry.[10][25][1]
• Source control: the onycholytic space and chronic wet exposure sustain the biofilm — trimming the onycholytic plate and drying measures are part of management.[10][4]

D — Drug-induced paronychia (the modern epidemic)

• EGFr-inhibitor-induced paronychia and pyogenic granuloma: a recognised toxicity of EGFR inhibitors (e.g. panitumumab, cetuximab, erlotinib); high-potency topical corticosteroids are a well-known treatment option, especially for paronychia; in a prospective case series, topical timolol 0.5% gel twice daily under occlusion for 30 days achieved complete resolution in 13/25 and improvement in 9/25 periungual lesions; invasive approaches (nail-plate avulsion, phenol matricectomy) are not highly effective — prefer non-invasive strategies in fragile cancer patients; liaise with oncology for dose modification of the targeted agent.[21]
• Other targeted agents have been linked to periungual granuloma-like lesions and nail changes in case reports; management follows the same principles — topical anti-inflammatory care, avoidance of invasive procedures, oncology liaison for dose adjustment.[21]

E — Acrodermatitis continua of Hallopeau

• Pustular psoriasis of the nail unit — a clinical variant of pustular psoriasis presenting with sterile pustules of the nail bed and matrix, chronic erosive course, often single digit; differentiates from bacterial paronychia by sterile cultures.[18]
• Management: systemic treatment is generally preferred, even for localised disease (topical treatment only supportive); acitretin is recommended first-line although relapse is common; biologic drugs show good efficacy but rarely achieve long-lasting remission.[18]

F — Atypical mycobacterial paronychia

• Mycobacterium marinum — the classic fish-tank granuloma: aquarium keepers, fish-handlers, marine workers; chronic indolent paronychia / nodular lymphangitic (sporotrichoid) spread up the arm; M. marinum is the most common atypical mycobacterial skin infection.[22][23]
• Diagnosis: culture and susceptibility-directed management; biopsy for AFB stain and culture when suspected — think of it in chronic paronychia refractory to standard antibacterial therapy with an aquatic exposure history.[22][23]
• Management: combined antibiotic schemes with the most frequently used classes macrolides, tetracyclines, cotrimoxazole, quinolones, aminoglycosides, rifamycins and ethambutol — frequently multiple antibiotics for several months, with potential adjunctive surgery; surgical treatment can be curative (and diagnostic) in small lesions.[23][22]

G — Sporotrichosis paronychia

• Sporothrix schenckii — soil / plant / thorn (rose garden) exposure; inoculation causes a fixed cutaneous or lymphangitic (sporotrichoid) form — nodules ascending the lymphatics of the arm; an important mimic in the chronic-paronychia differential.[24]
• Management: itraconazole is the most frequently used systemic treatment; in a contemporary epidemiological series of patients treated with itraconazole, 52% achieved clinical cure.[24]

I — Pediatric paronychia

• Acute paronychia in children: finger-sucking predisposes to acute bacterial paronychia (Staphylococcus aureus the classic organism) and to herpetic whitlow (HSV-1 from oral shedding).[4][14][20]
• Herpetic whitlow in infants: HSV finger infection occurs in infants — including neonates — via contact with oral secretions; manage non-operatively with antivirals as above.[20]
• Dosing in children is weight-based: choose agent and dose per paediatric formulary and local guidance — the adult fixed-dose regimens above do not apply.[4]

J — Diabetic paronychia

• Tighter glycaemic control accelerates healing.
• Broader organism list; lower threshold for culture, IV cover, admission.
• Chronic paronychia + distal phalanx osteomyelitis is a particular concern; image with X-ray / MRI.
• Foot-care and footwear education in recurrent lower-limb paronychia (great-toe ingrown nail + chronic paronychia is common in diabetics with neuropathy). [1]

K — EGFr / MEK / BTK inhibitor patients

• Oncology liaison is essential — dose interruption / modification of the targeted agent may be needed.
• High-potency topical corticosteroids are a well-known option for the paronychia; topical timolol 0.5% achieved complete resolution in 13/25 and improvement in 9/25 periungual lesions in a prospective series; invasive nail-unit procedures are not highly effective in these fragile patients.[21]
• Secondary bacterial infection is treated with antibiotics chosen per local guidance and culture.
• Recurrence is the rule until the targeted agent is withdrawn or dose-adjusted. [1]

Complications and Pitfalls

Complications

• Local: nail-fold abscess extension around the lunula / subungual abscess; chronic nail dystrophy (ridging, Beau lines, onycholysis); permanent nail-plate loss after deep I&D; lateral fold hypertrophy; flexor tendon sheath infection (Kanavel signs); distal phalanx osteomyelitis; nail-unit squamous cell carcinoma misdiagnosed as chronic paronychia (years of mismanagement); melanonychia / nail-matrix melanoma misdiagnosed as chronic paronychia.
• Distant: lymphangitis / lymphadenitis; bacteraemia; metastatic infection (endocarditis, septic arthritis, osteomyelitis, septic pulmonary emboli); necrotising fasciitis (in elderly diabetics and immunocompromised, mortality up to 30%).
• Chronic / drug: chronic paronychia runs a months-long course and recurs if irritant exposure resumes — patient education on avoidance is paramount; herpetic whitlow can recur, and recurrences of nongenital HSV may be diminished with daily oral antivirals. [7][19]

[1]

Prognosis and Disposition

Predictors of poor outcome

• Immunocompromise (HIV, transplant, chemotherapy, biologics).
• Diabetes mellitus with poor control.
• Peripheral vascular disease, Raynaud phenomenon.
• Sepsis at presentation (qSOFA ≥ 2).
• Delayed antibiotics / I&D.
• Misdiagnosis (felon called paronychia; herpetic whitlow incised; nail-unit malignancy treated as paronychia for years). [1]

Disposition

• Acute paronychia, no systemic features — outpatient: warm soaks with or without Burow solution or 1% acetic acid, topical antibiotics, rest/elevation; oral antibiotics (gram-positive cover) if there is surrounding inflammation — follow local guidance; review at 48-72 h.[1][4]
• Acute paronychia with abscess — same-day drainage (needle or scalpel, proportionate to the abscess); oral antibiotics only if immunocompromised or severe.[1][3]
• Severe / necrotising infection / Kanavel signs / felon — inpatient IV antibiotics + theatre; hand-surgery referral.[3][6]
• Chronic paronychia — outpatient; reset expectations — treatment takes weeks to months; the cornerstone is stopping the irritant.[7][8]
• EGFr-inhibitor paronychia — oncology liaison for dose interruption / modification; high-potency topical corticosteroids ± topical timolol 0.5%; avoid invasive procedures.[21]

Recurrence

• Acute paronychia — recurrence relates to persisting predisposing factors (nail-biting, finger-sucking, ingrown nail, wet work, EGFr inhibitors); address them.[4]
• Chronic paronychia — recurs if wet-work exposure resumes before the cuticle barrier regenerates; recovery takes months; patient education is paramount.[7]
• EGFr-inhibitor paronychia — recurs while the targeted agent continues at the same dose; oncology liaison.[21]
• Herpetic whitlow — recurrences are common; recurrences of nongenital HSV may be diminished with daily oral antivirals.[19]

Safety-net advice for patients

• Return if erythema spreads past the wrist or up the forearm (lymphangitis).
• Return if fever, rigors, or systemic illness.
• Return if pain is out of proportion to signs, or new bullae / dusky discolouration / crepitus.
• Return if the nail-fold abscess recurs within 2 weeks (consider occult foreign body, ingrown nail, malignancy).
• Return if no improvement at 48-72 h of treatment. [1]

Special Populations

Children

• Paronychia — finger-sucking predisposes: Staphylococcus aureus is the classic organism of acute paronychia.[4]
• Herpetic whitlow — HSV-1 from oral shedding; HSV finger infection also occurs in infants.[14][20]
• Dosing — paediatric dosing is weight-based and per paediatric formulary; the adult fixed-dose regimens in this topic do not apply.[4]

Pregnancy

• Antibiotic choice — follow local obstetric / formulary guidance; β-lactams are conventionally preferred agents in pregnancy, while tetracyclines and retinoids are conventionally avoided.
• I&D and drainage — the procedural management of an abscess is unchanged; use local anaesthesia per local practice.[1]
• Antivirals for herpetic whitlow — oral aciclovir, valaciclovir and famciclovir are effective treatments for nongenital HSV; use in pregnancy per obstetric guidance.[19]

Elderly

• Blunted fever and pain responses — lower threshold for culture, admission and IV therapy.
• Comorbidity decompensation and peripheral vascular disease slow healing.
• Review renal function before prescribing any antibiotic — dose-adjust accordingly; prefer agents and durations per local geriatric prescribing guidance.[1]

Immunocompromised

• Broader differential: Gram-negative bacilli, atypical mycobacteria (think M. marinum with aquatic exposure) and deep fungi such as Sporothrix join the usual suspects.[22][23][24]
• Lower threshold for culture (bacterial + mycobacterial + fungal), biopsy, imaging, IV cover and admission.[4]
• Neutropenic / transplant / biologic-therapy patients — manage with the relevant specialist team; drug-induced paronychia (EGFr inhibitors) needs oncology liaison for dose modification.[21]

Anticoagulated patients

• Drainage decisions are clinical — coordinate with the prescribing team where reversal or timing of anticoagulation is a concern; a minor nail-fold drainage can usually proceed with local haemostatic measures per local practice.[1]

Evidence, Guidelines and Regional Differences

Principle 1 — drainage beats antibiotics (Leggit 2017; Gottlieb 2024)

• Acute paronychia with abscess needs drainage; oral antibiotics are usually NOT needed if adequate drainage is achieved, unless the patient is immunocompromised or the infection is severe.[1][3]
• When antibiotics are used, they are chosen on the most likely pathogens and local resistance patterns (including MRSA rates).[1][4]

Principle 2 — MRSA and mixed flora (Macneal 2026; Fowler 2013)

• Urban US series: MRSA was the most common isolate (53% of positive cultures); mixed aerobic–anaerobic flora in around 50% of cases, with oral-exposure organisms (Bacteroides, Enterococcus, Eikenella corrodens) linked to nail-biting and digital sucking.[4][17]
• Culture pus at drainage; around a quarter of cultures may yield no growth.[4][17]

Principle 3 — chronic paronychia is dermatitis, not infection (Relhan 2014)

• Multifactorial inflammatory reaction of the proximal nail fold to irritants and allergens; management rests on removing the source, topical steroids / calcineurin inhibitors, and antifungals only as adjuncts; surgery (en bloc excision or marsupialisation, with or without nail-plate removal) for recalcitrant disease.[7]

Rigopoulos 2009 Br J Dermatol RCT — tacrolimus vs betamethasone vs emollient

• 45 patients, three arms (tacrolimus 0.1% BD, betamethasone 17-valerate 0.1% BD, emollient BD) for 3 weeks with 6 weeks' follow-up, all with protective measures counselled: tacrolimus 13 cured / 1 improved; betamethasone 8 / 2 / 4 non-responders; emollient 9 stable / 6 failed. Both actives beat emollient (P under 0.001); tacrolimus appears MORE efficacious than betamethasone.[8]

Iorizzo 2024 Hand Surg Rehabil — bacterial and viral nail-unit infections

• Practical review of acute and chronic paronychia and herpetic whitlow; whitlow resolves without intervention and drainage is contraindicated unless bacterial co-infection.[5]

Iorizzo 2025 — acrodermatitis continua of Hallopeau

• Systemic treatment generally preferred even for localised disease; acitretin first-line although relapse is common; biologics efficacious but rarely long-lasting remission.[18]

Exam Pearls and High-Yield Minutiae

[1] [7] [8] [5] [19]

Single best answer (SBA) rehearsal questions (the examiner's mental map)

1. A 35-year-old dishwasher has 4 months of boggy, mildly tender proximal nail folds on both thumbs with loss of cuticle and nail ridging. What is the most appropriate first-line management? Answer: Stop the irritant exposure (the cornerstone) plus a topical anti-inflammatory — a topical steroid or calcineurin inhibitor. (Chronic paronychia is a multifactorial inflammatory reaction to irritants; antifungals are adjuncts, not primary therapy.) [7][8]

2. A 28-year-old dentist develops vesicles on an erythematous, oedematous thumb pad with burning pain and ascending forearm lymphangitis. What is the definitive management? Answer: DO NOT incise; the infection typically resolves without intervention — confirm with PCR if uncertain and consider oral aciclovir / valaciclovir / famciclovir. (Herpetic whitlow; disrupting vesicles frequently causes secondary bacterial infection.) [5][19]

3. A 40-year-old diabetic presents with a tense, exquisitely tender finger pad (the pulp, not the fold), throbbing pain disturbing sleep, 7 days after a splinter. What is the most appropriate next step? Answer: Early felon may be managed with antibiotics alone; if advanced, incision and drainage — longitudinal volar incision if superficial, lateral if deep, not extended past the DIP joint. [3]

4. A 50-year-old on an EGFr inhibitor for metastatic colorectal cancer develops friable, easily bleeding periungual tissue on multiple fingers and toes. What is the diagnosis and management? Answer: EGFr-inhibitor-induced paronychia / periungual pyogenic granuloma; high-potency topical corticosteroid ± topical timolol 0.5% (complete resolution in 13/25, improvement in 9/25 in a prospective series); avoid invasive procedures; oncology liaison for dose modification. [21]

5. A 24-year-old nail-biter has a 3-day painful, erythematous, swollen proximal nail fold with a collection lifting the cuticle. What is the most appropriate next step? Answer: Drainage proportionate to the abscess (from hypodermic needle to scalpel incision); antibiotics usually NOT needed after adequate drainage unless immunocompromised or severe. [1][3]

6. A 65-year-old with chronic paronychia has green-black discoloration of multiple nails with onycholysis. What organism and treatment? Answer: Pseudomonas aeruginosa (green-nail syndrome: green discoloration + paronychia + onycholysis); diagnose by bacterial culture and susceptibility testing and treat with culture-guided oral / topical therapy. [10]

7. A 12-year-old thumb-sucker with HSV-1 oral lesions develops vesicles on the thumb. What is the management? Answer: Herpetic whitlow — non-operative: do not incise; oral antivirals (aciclovir / valaciclovir / famciclovir) are effective; the lesion resolves without intervention. [5][19][20]

8. A 30-year-old presents with chronic, recalcitrant paronychia of one finger only, unresponsive to irritant removal and topical anti-inflammatories. What is the next step? Answer: Biopsy the nail unit to exclude malignancy; consider en bloc excision of the proximal nail fold or marsupialisation (with or without nail-plate removal) for recalcitrant benign disease. [7][11]

9. A 60-year-old diabetic with chronic paronychia has distal phalanx bone pain, persistent discharge and fever. What is the next investigation? Answer: Radiographs of the distal phalanx (foreign body, fracture, osteomyelitis) — felons and advanced paronychia warrant imaging; obtain cultures and involve hand surgery. [3][4]

10. A healthcare worker recurs frequently with herpetic whitlow. What is the chronic management? Answer: Recurrences of nongenital HSV may be diminished with daily oral antivirals; gloves and standard precautions protect the operator. [19]

Exam application bank (NEET-PG / INICET)

One-line answer

Paronychia is infection or inflammation of the nail fold. ACUTE paronychia: Staphylococcus aureus the classic organism (mixed aerobic–anaerobic flora in around half of cases); once pus is present, drain — needle or scalpel proportionate to the abscess — and give oral antibiotics only if immunocompromised, severe, or with surrounding inflammation per local guidance. HERPETIC WHITLOW (HSV vesicles, burning pain) is NEVER incised and resolves without intervention; oral aciclovir / valaciclovir / famciclovir are effective. FELON is a closed-space pulp abscess — early cases antibiotics alone, advanced need I&D (volar if superficial, lateral if deep). GREEN NAIL SYNDROME (Pseudomonas) is diagnosed by culture and treated with susceptibility-guided therapy. CHRONIC paronychia is a multifactorial inflammatory reaction of the proximal nail fold to irritants: stop the source, use a topical steroid or calcineurin inhibitor (tacrolimus 0.1% BD beat betamethasone in the RCT), antifungals as adjuncts only, and surgery (en bloc excision / marsupialisation ± nail-plate removal) for recalcitrant disease. [1][3][7][8][10][19]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Paronychia.

[1]

References

1. [1]Leggit JC. Acute and Chronic Paronychia Am Fam Physician, 2017.PMID 28671378
2. [2]Lee DK, Lipner SR. Optimal diagnosis and management of common nail disorders Ann Med, 2022.PMID 35238267
3. [3]Gottlieb M, Long B Management of Finger Felons and Paronychia: A Narrative Review J Emerg Med, 2025.PMID 40945390
4. [4]Macneal P, Milroy C Paronychia Drainage 2026.PMID 32644572
5. [5]Iorizzo M, Pasch MC Bacterial and viral infections of the nail unit: Tips for diagnosis and management Hand Surg Rehabil, 2024.PMID 36427761
6. [6]Rerucha CM, Ewing JT, Oppenlander KE, et al. Acute Hand Infections Am Fam Physician, 2019.PMID 30763047
7. [7]Relhan V, Goel K, Bansal S, et al. Management of chronic paronychia Indian J Dermatol, 2014.PMID 24470654
8. [8]Rigopoulos D, Gregoriou S, Belyayeva E, et al. Efficacy and safety of tacrolimus ointment 0.1% vs. betamethasone 17-valerate 0.1% in the treatment of chronic paronychia: an unblinded randomized study Br J Dermatol, 2009.PMID 19120329
9. [10]Zhang A, Kuang H, Chang F, et al. Pseudomonas aeruginosa and Burkholderia cepacia complex co-infection in green nail syndrome: a case report Front Med (Lausanne), 2026.PMID 41810233
10. [11]de Berker D. Nail anatomy Clin Dermatol, 2013.PMID 24079579
11. [12]Barger J, Garg R, Wang F, et al. Fingertip Infections Hand Clin, 2020.PMID 32586457
12. [13]Bahunuthula RK, Thappa DM, Kumari R, et al. Evaluation of role of Candida in patients with chronic paronychia Indian J Dermatol Venereol Leprol, 2015.PMID 26087081
13. [14]Lieberman L, Castro D, Bhatt A, et al. Case report: palmar herpetic whitlow and forearm lymphangitis in a 10-year-old female BMC Pediatr, 2019.PMID 31752766
14. [17]Fowler JR, Ilyas AM. Epidemiology of adult acute hand infections at an urban medical center J Hand Surg Am, 2013.PMID 23647640
15. [18]Iorizzo M, Lipner SR, Piraccini BM, et al. Acrodermatitis continua of Hallopeau-clinical review and proposed management algorithm J Am Acad Dermatol, 2025.PMID 40480373
16. [19]Usatine RP, Tinitigan R Nongenital herpes simplex virus Am Fam Physician, 2010.PMID 21121552
17. [20]Al-Qattan MM, AlQadri NG, AlHayaza G Herpetic Whitlow of the Hand in Infants J Hand Microsurg, 2022.PMID 36016636
18. [21]Sollena P, Mannino M, Tassone F, et al. Efficacy of topical beta-blockers in the management of EGFR-inhibitor induced paronychia and pyogenic granuloma-like lesions: case series and review of the literature Drugs Context, 2019.PMID 31798664
19. [22]Gonzalez-Santiago TM, Drage LA Nontuberculous Mycobacteria: Skin and Soft Tissue Infections Dermatol Clin, 2015.PMID 26143432
20. [23]Medel-Plaza M, Esteban J Current treatment options for Mycobacterium marinum cutaneous infections Expert Opin Pharmacother, 2023.PMID 37145964
21. [24]Schapiro S, Pulciano N, Galindo-Ramirez J, et al. Epidemiology and Outcomes of Sporotrichosis: A Descriptive Real-World Analysis From a Global Cohort Mycoses, 2026.PMID 41732997
22. [25]Nenoff P, Paasch U, Handrick W Infections of finger and toe nails due to fungi and bacteria Hautarzt, 2014.PMID 24718510