Infective Dermatoses
Skin infections are usually presented as a list of organisms with a list of drugs. Two questions do far more work.
How deep is the infection? The skin has layers, and infection at each layer produces a recognisable clinical picture with a completely different level of urgency. Depth is a ladder that runs from trivial to lethal in four rungs.
Where is the lesion active? An expanding annular lesion with central clearing and a scaly advancing border is fungal, and the border is where the organism lives, which is why that is where you scrape.
A third consideration is specific to India and has changed practice in the last few years: dermatophyte infection here is now frequently terbinafine-resistant, so the drug that used to work reliably often does not.
1. The Depth Ladder
| Depth | Infection | Border | Urgency |
|---|---|---|---|
| Epidermis | Impetigo | Superficial crust, golden | Topical treatment |
| Upper dermis and lymphatics | Erysipelas | Sharp, raised, palpable edge | Oral antibiotics |
| Deep dermis and subcutis | Cellulitis | Indistinct, not palpable | Systemic antibiotics, admission if severe |
| Fascia | Necrotising fasciitis | Rapidly advancing, skin may look deceptively normal | Immediate surgery |
The palpable, sharply demarcated edge of erysipelas is the useful sign, and it exists because infection is confined to the upper dermis and its lymphatics, which have a defined limit. Cellulitis extends into loose subcutaneous tissue, so it has no clear boundary.
Necrotising fasciitis
Pain out of proportion to the visible findings is the hallmark, and it is the earliest sign. The infection travels along fascial planes, which have a poor blood supply, so the overlying skin may look unremarkable while the tissue beneath is dead.
Later features are systemic toxicity, skin anaesthesia over the affected area, crepitus, bullae and dusky discolouration, but waiting for these is waiting too long.
The LRINEC score, using C-reactive protein, white cell count, haemoglobin, sodium, creatinine and glucose, supports the diagnosis and is significantly higher than in cellulitis, but it does not exclude the diagnosis and must never delay surgical exploration.
Treatment is urgent, radical surgical debridement with broad-spectrum antibiotics. Antibiotics alone do not work, for the same reason they fail in any dead tissue: they arrive through blood that no longer reaches it.
The recurrent cellulitis problem
Cellulitis recurs in the same limb far more often than chance would predict, and the reason is mechanical rather than microbial.
Each episode damages dermal lymphatics, which impairs drainage, which produces oedema, which impairs local immune surveillance and predisposes to the next episode. The cycle is self-reinforcing and eventually produces the thickened, cobblestoned skin of chronic lymphoedema.
Breaking the cycle means treating the portal of entry rather than only the infection. Interdigital tinea pedis, fissured heels and venous eczema are the usual entry points, and treating them prevents more recurrences than any antibiotic choice does. Compression and elevation address the oedema, and prophylactic penicillin is considered where episodes remain frequent.
2. Bacterial Infections
Impetigo is superficial and usually staphylococcal, producing golden crusts. The bullous form results from exfoliative toxin cleaving desmoglein 1, which is the same mechanism as staphylococcal scalded skin syndrome, differing only in whether the toxin acts locally or systemically.
Folliculitis, furuncle and carbuncle form a depth series within the follicle: inflammation of the follicle, a deeper abscess of one follicle, and a coalescing abscess of several follicles with multiple draining sinuses.
Recurrent boils warrant a look for a cause: diabetes, nasal carriage of Staphylococcus aureus, anaemia or immunosuppression.
Erythrasma is a corynebacterial infection of flexures that fluoresces coral-red under Wood light, distinguishing it from tinea, which does not.
3. Dermatophyte Infection and the Indian Problem
Dermatophytes invade keratin, so they affect skin, hair and nails but never mucosa. The classic lesion is annular with central clearing and an active scaly border.
Scrape the edge, not the centre. The centre has already been cleared by the immune response and often yields nothing.
Potassium hydroxide mount of the scrapings shows septate branching hyphae, and culture identifies the species when needed.
The change that matters
Until recently, terbinafine was reliable first-line treatment. Indian dermatology has since seen an epidemic of chronic, recurrent, extensive and treatment-resistant dermatophytosis.
The principal organism is Trichophyton indotineae, and terbinafine resistance is common, with reported resistance in the region of 70 per cent of isolates in published series. Resistance is conferred by point mutations in the squalene epoxidase gene, of which F397L is the best characterised.
The organism is anthropophilic and has now spread internationally from the Indian subcontinent, so it is no longer only a local problem.
Two clinical consequences follow.
Itraconazole has become the practical first-line oral agent in much of Indian practice, at adequate doses and for adequate duration, with terbinafine reserved or used after susceptibility considerations.
Topical corticosteroid misuse is a major driver. Over-the-counter combination creams containing a potent steroid with an antifungal and an antibacterial are widely available in India. The steroid suppresses inflammation, so the lesion loses its raised scaly edge and its annular shape, becoming an ill-defined erythematous patch that no longer looks like ringworm. This is tinea incognito, and it delays diagnosis while the infection extends.
The tinea family
| Site | Name | Distinguishing feature |
|---|---|---|
| Scalp | Tinea capitis | Children; hair loss with scaling; needs oral treatment |
| Body | Tinea corporis | Annular with active edge |
| Groin | Tinea cruris | Spares the scrotum, unlike candidiasis |
| Foot | Tinea pedis | Interdigital maceration or moccasin scaling |
| Nail | Onychomycosis | Distal subungual thickening and discolouration |
Tinea capitis always requires systemic treatment, because topical agents cannot reach the fungus within the hair shaft. Kerion is the boggy inflammatory mass produced by a vigorous immune response and can scar if untreated.
Pityriasis versicolor is caused by Malassezia, which is a yeast rather than a dermatophyte. It produces hypopigmented or hyperpigmented scaly macules on the trunk with fine scale on stretching, and potassium hydroxide shows the spaghetti and meatballs appearance of short hyphae with spores.
4. Scabies
Scabies is caused by Sarcoptes scabiei burrowing in the stratum corneum, and the symptoms are an allergic response to the mite and its products rather than to the burrowing itself.
This explains the delay: itch begins four to six weeks after a first infestation, once sensitisation has developed, but within a day or two on re-infestation.
Itch is worst at night, lesions favour finger webs, wrists, axillae, periumbilical skin, genitalia and, in infants, the palms, soles and scalp. The burrow is the pathognomonic lesion.
Crusted or Norwegian scabies occurs in the immunosuppressed, the elderly and the neurologically impaired. It carries a huge mite burden, is highly contagious, and is often minimally itchy because the immune response that produces itch is absent.
Treatment
Permethrin 5 per cent is first-line, applied to the whole body from the neck down, and to the scalp and face in infants, left on overnight and repeated after a week.
All household and close contacts are treated simultaneously, whether or not they itch, since they may be within the incubation period.
Oral ivermectin is used in extensive disease, crusted scabies, institutional outbreaks and where topical treatment cannot be applied reliably, and mass drug administration with ivermectin has been shown to reduce community prevalence of both scabies and impetigo in northern India.
Post-scabetic itch persists for weeks after successful treatment, and mistaking it for failure leads to repeated unnecessary applications and irritant dermatitis. Permethrin resistance is a genuine and growing concern, mediated by sodium channel mutations and detoxifying enzyme activity, but persistent itch alone is not evidence of it.
5. Viral Infections
Herpes zoster follows reactivation in a dorsal root ganglion, producing a painful dermatomal eruption that does not cross the midline. Ophthalmic involvement with lesions on the nose tip, the Hutchinson sign, indicates nasociliary nerve involvement and threatens the eye.
Antivirals are most effective started within 72 hours. Zoster in a young adult without obvious cause should prompt consideration of HIV infection.
Molluscum contagiosum produces umbilicated pearly papules and is self-limiting in children, usually resolving over months without scarring. Extensive molluscum in an adult, particularly on the face, suggests immunosuppression and warrants HIV testing.
Viral warts are caused by human papillomavirus and are treated by destruction or immune stimulation rather than by any antiviral, since no drug clears the virus from infected keratinocytes.
Herpes simplex produces grouped vesicles on an erythematous base that recur at the same site, and eczema herpeticum is its dangerous form, in which the virus disseminates across skin already damaged by atopic dermatitis and requires urgent systemic aciclovir.
Hand, foot and mouth disease, usually coxsackievirus, gives oral ulcers with acral vesicles in young children.
6. Candidiasis and the Moist Skin
Candida is a commensal that becomes pathogenic when the local environment changes, which is why the disease is usually a marker of something else.
It favours moist, occluded, macerated sites: submammary and inguinal folds, the napkin area, the angles of the mouth, and the nail folds of people whose hands are constantly wet.
Three features separate candidal intertrigo from tinea, and they are reliably examined.
Candidiasis produces satellite lesions, small pustules and papules scattered beyond the main red area, which dermatophytes do not.
Candidiasis involves the scrotum; tinea cruris characteristically spares it. That single observation resolves most groin rashes.
Candidiasis is beefy red and macerated with a ragged edge, rather than annular with central clearing.
Oral candidiasis in an adult who is not on antibiotics, inhaled steroids or immunosuppression should raise the question of undiagnosed diabetes or HIV infection, and recurrent vulvovaginal candidiasis is a recognised presentation of new diabetes.
7. Infections Weighted Heavily in India
Cutaneous tuberculosis takes several forms, and two are examined repeatedly.
Lupus vulgaris is the commonest form in India, a slowly extending plaque with apple-jelly nodules seen on diascopy, typically on the head and neck. Scrofuloderma results from direct extension from an underlying tuberculous node or bone, producing undermined ulcers and sinuses with tethered scarring.
Post-kala-azar dermal leishmaniasis follows treated visceral leishmaniasis, usually months to years later, producing hypopigmented macules, papules and nodules, characteristically around the face. It matters epidemiologically because these patients act as a reservoir maintaining transmission between outbreaks, so treating them is a public health intervention rather than a cosmetic one.
The differential of a hypopigmented patch in India therefore has to include leprosy, pityriasis versicolor, post-kala-azar dermal leishmaniasis, pityriasis alba and vitiligo, and it is separated on sensation, scale and distribution.
Leishmaniasis and other tropical infections
Cutaneous leishmaniasis, transmitted by the sandfly, produces a painless nodule that ulcerates with a raised indurated edge, classically on exposed skin. In India the visceral form dominates, but the cutaneous form occurs in Rajasthan and adjoining areas.
Cutaneous larva migrans produces a serpiginous, intensely itchy advancing track on the feet or buttocks after contact with soil or sand contaminated by animal hookworm larvae. It is self-limiting because the larvae cannot complete their life cycle in humans, but treatment with ivermectin or albendazole shortens it considerably.
Deep fungal infections such as chromoblastomycosis and mycetoma occur in barefoot agricultural workers, producing chronic verrucous plaques or a swollen foot with discharging sinuses containing grains. Mycetoma is separated into actinomycetoma, which is bacterial and responds to prolonged antibiotics, and eumycetoma, which is fungal and often needs surgery.
8. Worked Examples
Example 1. A 40-year-old presents with a rapidly spreading painful leg over 12 hours. The skin looks mildly erythematous but he is in severe pain and has a heart rate of 128. What is the concern and what is the priority?
Necrotising fasciitis. Pain out of proportion to the visible findings is the hallmark and the earliest sign, and the reason the skin looks deceptively unimpressive is that the infection tracks along fascial planes beneath it.
The priority is urgent surgical exploration with radical debridement, alongside broad-spectrum antibiotics and resuscitation. The LRINEC score may support the diagnosis but a low score does not exclude it and must never delay surgery. Antibiotics alone fail because dead fascia has no blood supply to deliver them.
Example 2. A 32-year-old has had extensive itchy annular lesions on the trunk and groin for eight months, treated repeatedly with a combination cream from a pharmacy. The lesions are now ill-defined and lack a raised edge. Explain what has happened and how you would manage it.
This is chronic recurrent dermatophytosis modified by topical corticosteroid, that is tinea incognito. The over-the-counter combination cream contains a potent steroid, which suppresses the inflammatory response that produces the raised scaly border and the annular shape, so the lesion no longer looks like ringworm while the fungus continues to spread.
Management begins with stopping the combination cream and confirming the diagnosis with a potassium hydroxide mount from the active edge. Systemic treatment is required given the extent and chronicity, and in current Indian practice itraconazole at adequate dose and duration is the practical first-line agent, because Trichophyton indotineae with squalene epoxidase mutations makes terbinafine resistance common. Treat the household, wash and sun-dry clothing and bedding, and counsel explicitly against returning to steroid-containing creams.
Example 3. A family of five presents with itch worst at night. The father has burrows in the finger webs. His 2-year-old has lesions on the palms and soles. Two family members have no symptoms. How do you treat them?
Treat all five simultaneously. Permethrin 5 per cent is applied to the whole body from the neck down in the adults and older children, and additionally to the scalp and face in the 2-year-old, since infants characteristically have palmar, plantar and scalp involvement. It is left on overnight and repeated after one week.
The asymptomatic members are treated regardless, because itch begins only four to six weeks after a first infestation once sensitisation has developed, so they may be infested but not yet symptomatic. Clothing and bedding are laundered hot or sun-dried. Warn the family that itch may persist for several weeks after successful treatment as an allergic phenomenon, and that this is not treatment failure.
Example 4. Why should the edge of a ringworm lesion be scraped rather than the centre?
Because the fungus lives at the advancing margin. The annular appearance arises because the dermatophyte spreads centrifugally through the stratum corneum while the immune response clears the older, central portion behind it. By the time the lesion is visibly annular, the centre contains little or no viable fungus, so scrapings from it frequently yield a false negative potassium hydroxide mount and a negative culture.
The active scaly border is where hyphae are actively invading keratin, so scrapings taken there give the highest yield. The same logic applies to biopsy site selection and to judging whether treatment is working.
Example 5. A 28-year-old has a hypopigmented patch on the cheek. List the diagnoses you must separate and how you would do it.
The differential in India includes leprosy, pityriasis versicolor, post-kala-azar dermal leishmaniasis, pityriasis alba and vitiligo.
Sensation separates leprosy: definite loss of sensation within the patch is one of the cardinal signs and should be tested with the eyes closed against adjacent normal skin, along with palpation of peripheral nerves.
Scale separates pityriasis versicolor, which shows fine scale on stretching the skin and gives spaghetti and meatballs on potassium hydroxide mount.
Pigment separates vitiligo, which is depigmented rather than hypopigmented and appears chalk-white with accentuation under Wood light.
Post-kala-azar dermal leishmaniasis requires a history of treated visceral leishmaniasis, usually months to years earlier, and matters because these patients are a reservoir sustaining transmission. Pityriasis alba is a diagnosis of exclusion in a child with atopic tendency.
Summary
Depth decides urgency: impetigo, erysipelas, cellulitis, necrotising fasciitis.
Erysipelas has a sharp raised palpable edge; cellulitis does not.
Pain out of proportion is the earliest sign of necrotising fasciitis.
LRINEC supports the diagnosis but never delays surgery.
Bullous impetigo and scalded skin syndrome share one mechanism: exfoliative toxin cleaving desmoglein 1.
Erythrasma fluoresces coral-red under Wood light; tinea does not.
Dermatophytes invade keratin, so they never affect mucosa.
Scrape the active edge, not the cleared centre.
Indian dermatophytosis is now frequently terbinafine-resistant.
Trichophyton indotineae carries squalene epoxidase mutations, notably F397L.
Itraconazole has become the practical first-line oral agent in Indian practice.
Steroid-containing combination creams produce tinea incognito and delay diagnosis.
Tinea capitis always needs systemic treatment.
Pityriasis versicolor is caused by Malassezia and shows spaghetti and meatballs.
Scabies itch is an allergic response, so it begins four to six weeks after first infestation.
Treat all contacts simultaneously whether or not they itch.
Crusted scabies has a huge mite burden and may barely itch.
Post-scabetic itch persists for weeks and is not treatment failure.
Zoster in a young adult should prompt consideration of HIV.
Lupus vulgaris shows apple-jelly nodules; scrofuloderma extends from a node or bone.
Post-kala-azar dermal leishmaniasis is a transmission reservoir, so treating it is public health work.
