Medicine chapters

Bacterial, mycobacterial, fungal and viral skin infections

The common bacterial, mycobacterial (leprosy, cutaneous TB, cutaneous leishmaniasis), fungal and viral skin infections, how each looks, the key test and the drug of choice.

UHS PGET syllabus: Dermatology (5 MCQs), Bacterial and mycobacterial infections; fungal and viral diseases of the skinUpdated October 2026
In 30 seconds
  • Impetigo (Staph. aureus or Strep. pyogenes) gives honey-coloured crusts around the mouth and nose; cellulitis and erysipelas are deeper streptococcal or staphylococcal infections treated with flucloxacillin.
  • Leprosy ranges from tuberculoid (few anaesthetic patches, strong immunity, no bacilli) to lepromatous (many nodules, weak immunity, many bacilli); treat with WHO multidrug therapy.
  • Dermatophytes cause tinea (KOH shows hyphae); terbinafine is preferred for nails, griseofulvin for tinea capitis in children; herpes zoster needs antivirals within 72 hours.
On this page

Overview

Skin infections are the commonest skin problems seen in Pakistani clinics. Heat, humidity, overcrowding, diabetes and misuse of steroid creams all make them more common and more severe.

This chapter covers four groups:

  • Bacterial: impetigo, folliculitis, boils and carbuncles, cellulitis, erysipelas, necrotising fasciitis, erythrasma.
  • Mycobacterial and protozoal: leprosy, cutaneous tuberculosis, atypical mycobacteria and cutaneous leishmaniasis.
  • Fungal: dermatophytes (tinea), candida, Malassezia and deep mycoses.
  • Viral: herpes simplex, varicella zoster, warts, molluscum and orf.

Bacterial infections

Impetigo

  • Highly contagious superficial infection, mostly in children, spread by direct contact.
  • Organisms: Staphylococcus aureus (commonest) or Streptococcus pyogenes.
  • Non-bullous: red patches with golden or honey-coloured crusts, usually around the mouth and nose.
  • Bullous impetigo: toxin-producing Staph. aureus causes flaccid blisters that rupture.
  • Treatment:
    • Localised: topical fusidic acid; keep mupirocin for MRSA.
    • Widespread or bullous: oral flucloxacillin for 7 days (erythromycin or clarithromycin if penicillin-allergic).
    • Keep the child off school until lesions crust over or for 48 hours after starting antibiotics.
High-yield

Streptococcal impetigo can be followed by post-streptococcal glomerulonephritis (cola-coloured urine and facial puffiness a few weeks later). Antibiotics do not prevent this, unlike rheumatic fever after throat infection.

Staphylococcal scalded skin syndrome (SSSS)

  • Toxin (exfoliative toxin) from Staph. aureus splits the upper epidermis (granular layer).
  • Mostly in infants and young children: fever, tender red skin, then widespread peeling with a positive Nikolsky sign.
  • Mucous membranes are spared, unlike toxic epidermal necrolysis (TEN), which splits at the dermo-epidermal junction and involves mucosa.
  • Treat with intravenous anti-staphylococcal antibiotics and fluids.

Folliculitis, boils and carbuncles

LesionWhat it isKey points
FolliculitisSuperficial infection of hair folliclesSmall pustules; Staph. aureus; Pseudomonas after hot tubs; sycosis barbae in the beard
Furuncle (boil)Deeper infection of one folliclePainful red pus-filled lump; Staph. aureus
CarbuncleSeveral adjacent boils joined togetherLarge painful swelling with multiple draining openings, fever; classically on the nape of the neck or back in diabetics
  • Single boils: warm compresses; larger ones need incision and drainage.
  • Widespread, facial or recurrent: oral anti-staphylococcal antibiotics for 10–14 days.
  • Recurrent boils in healthy young adults: suspect a Staph. aureus strain making the Panton–Valentine leukocidin (PVL) toxin; swab, decolonise the nose and treat family contacts.
  • Always check blood glucose in recurrent boils or carbuncles.

Cellulitis and erysipelas

FeatureErysipelasCellulitis
DepthUpper dermis and lymphaticsDeeper dermis and subcutaneous fat
EdgeSharp, raised marginIll-defined
Common siteFace and legsLower leg
Usual organismStrep. pyogenesBeta-haemolytic streptococci and Staph. aureus
  • Both cause a hot, tender, red, swollen area with fever and malaise; blisters, lymphangitis and lymphadenopathy may occur.
  • Risk factors: lymphoedema, obesity, venous disease, diabetes, and toe-web tinea (a common entry point).
  • Swabs from intact skin are usually negative; ASO and anti-DNase B titres may confirm streptococcal infection.
  • Treatment: flucloxacillin (or erythromycin/clarithromycin if allergic), oral or intravenous depending on severity. Treat any toe-web fungal infection.
  • Up to half of patients have further episodes; long-term prophylaxis helps only while it is taken.

Necrotising fasciitis

  • Rapidly spreading, life-threatening infection along the fascial planes.
  • Type 1: mixed aerobes and anaerobes (after abdominal surgery, in diabetes). Type 2: group A streptococcus alone, often in previously healthy people.
  • Pain out of proportion to the skin signs is the key early clue; later dusky skin, blisters, crepitus and shock.
  • Very high CRP and white cell count; imaging may show gas but must not delay surgery.
  • Treatment: urgent surgical debridement plus intravenous antibiotics (benzylpenicillin plus clindamycin for group A strep; broad cover plus metronidazole if the organism is unknown).
High-yield

Clindamycin is added because it switches off toxin production, not just to widen cover.

Other bacterial infections

  • Ecthyma: deeper, punched-out ulcers with thick crust, from streptococci or staphylococci; linked to poor hygiene and malnutrition.
  • Ecthyma gangrenosum: necrotic ulcer with a black centre caused by Pseudomonas septicaemia in neutropenic patients.
  • Erythrasma: brown-pink scaly patches in the groin, axillae or toe webs, caused by Corynebacterium minutissimum; coral-pink fluorescence under Wood's lamp; treat with a topical or oral macrolide.
  • Gas gangrene: Clostridium perfringens in contaminated deep wounds; debridement plus benzylpenicillin and clindamycin.
  • Cutaneous anthrax: painless papule becoming an ulcer with a black eschar and marked oedema, in people handling animal hides or wool.

Mycobacterial infections

Leprosy (Hansen disease)

  • Cause: Mycobacterium leprae, an acid-fast bacillus that cannot be grown in culture (grows in mouse footpads and the nine-banded armadillo).
  • Spread is probably by nasal droplets after prolonged close contact; linked to poverty and crowding.
  • It prefers cool parts of the body: skin, peripheral nerves, nose, testes and eyes.
  • The type of disease depends on the patient's cell-mediated immunity (CMI).
FeatureTuberculoid (TT)Borderline (BT, BB, BL)Lepromatous (LL)
Cell-mediated immunityStrong (Th1, interferon)Unstable, in betweenWeak (Th2)
Skin lesionsFew, large, well-defined, hypopigmented or red, dry, hairless, anaesthetic patchesSeveral, less well definedMany, symmetrical papules, nodules, diffuse thickening
NervesOne or two thickened nerves near lesions, early damageMany nerves, severe damageSlow, symmetrical "glove and stocking" loss
Bacilli (slit smear)None or very fewVariableVery many
Lepromin testPositiveVariableNegative
OtherGranulomas around nervesMost unstable; prone to type 1 reactionsLeonine facies, loss of eyebrows (madarosis), nasal stuffiness and collapse, gynaecomastia
Memory hook

TT = Tough immunity, Tiny bacilli count. LL = Low immunity, Loads of bacilli.

Indeterminate leprosy is the earliest form: one or a few faint hypopigmented macules with slightly reduced sensation.

Diagnosis is mainly clinical, based on WHO cardinal signs:

  1. A hypopigmented or reddish skin patch with definite loss of sensation.
  2. Thickened peripheral nerves (ulnar, common peroneal, greater auricular) with loss of sensation or weakness.
  3. Acid-fast bacilli on a slit-skin smear.

Biopsy and PCR for M. leprae DNA can help.

WHO treatment classification:

  • Paucibacillary (PB): 5 or fewer skin lesions and no bacilli.
  • Multibacillary (MB): 6 or more lesions, or bacilli seen.
Regimen (adults)DrugsDuration
MultibacillaryRifampicin 600 mg monthly (supervised) + clofazimine 300 mg monthly (supervised) and 50 mg daily + dapsone 100 mg daily12 months
PaucibacillaryRifampicin 600 mg monthly (supervised) + dapsone 100 mg daily6 months

Leprosy care in Pakistan is provided through the national leprosy control programme and specialist centres, with drugs supplied by WHO. Regimens are revised from time to time, so check the current national guideline.

Lepra reactions (often after starting treatment):

FeatureType 1 (reversal reaction)Type 2 (erythema nodosum leprosum, ENL)
WhoBorderline leprosyLepromatous (and BL)
MechanismType IV (cell-mediated) hypersensitivityType III (immune complex)
FeaturesExisting lesions become red, swollen and painful; acute neuritis with sudden nerve palsyCrops of new painful red nodules, fever, arthralgia, iridocyclitis, orchitis, neuritis
TreatmentPrednisoloneAnalgesia, prednisolone (especially if eyes involved), clofazimine; continue MDT
High-yield

Do not stop multidrug therapy during a lepra reaction. Treat the reaction and continue the antileprosy drugs.

Exam trap

In a reversal reaction, the old lesions flare. In ENL, new tender nodules appear while old lesions are unchanged.

Patients with numb hands and feet need self-care education and protective footwear to prevent ulcers and deformity.

Cutaneous tuberculosis

FormHow it arisesAppearance
Lupus vulgaris (commonest)Post-primary, in people with good immunityRed-brown plaque or nodules, usually head and neck; "apple jelly" colour on diascopy; heals with scarring; risk of SCC in old scars
Tuberculosis verrucosa cutisRe-inoculation into skin of a previously infected person (prosector's wart)Warty plaque on hands, knees or buttocks
ScrofulodermaSpread from an underlying TB lymph node or boneCold abscess that breaks down into ulcers and sinuses with scarring, often in the neck
TuberculidesHypersensitivity to TB elsewhereErythema induratum (Bazin disease): tender nodules on the calves, may ulcerate; erythema nodosum on the shins

Treatment is the same as pulmonary TB with standard anti-tuberculous therapy; follow the national TB programme guideline.

Atypical mycobacteria

Mycobacterium marinum ("fish tank granuloma") gives a painless nodule on the hand after cleaning a fish tank or contact with unchlorinated water; nodules may spread up the lymphatics. Culture needs a low temperature; treat with combination antibiotics such as clarithromycin for several weeks.

Cutaneous leishmaniasis ("oriental sore")

  • Protozoan Leishmania (in Pakistan mainly L. tropica and L. major) spread by the bite of the sandfly. It is endemic in parts of Pakistan, especially Balochistan, Khyber Pakhtunkhwa and areas bordering Afghanistan.
  • A painless papule appears weeks to months after the bite at an exposed site (face, arms, legs), enlarges and ulcerates with a raised, red, indurated edge and crust ("volcano" ulcer).
  • Heals slowly over months to a year or more, leaving a depressed scar.
  • L. tropica can cause leishmaniasis recidivans (new papules at the edge of an old scar).
  • Diagnosis: Giemsa-stained slit-skin smear from the edge shows amastigotes (Leishman–Donovan bodies) in about 80%; biopsy, culture or PCR if negative.
  • Treatment: small lesions may heal alone; local options are cryotherapy or intralesional pentavalent antimony (sodium stibogluconate or meglumine antimoniate); multiple or large lesions need systemic antimony, amphotericin or an azole.
High-yield

Mucocutaneous leishmaniasis (espundia) is mainly a South American (L. braziliensis) disease, not the usual Pakistani sore.

Fungal infections

Dermatophytes (tinea, ringworm)

  • Three genera: Trichophyton, Microsporum and Epidermophyton. They live on dead keratin (stratum corneum, hair, nails).
  • Sources: other people (anthropophilic), animals (zoophilic, e.g. cats and dogs) or soil (geophilic).
  • Typical lesion: itchy, scaly, annular patch with an active raised edge and central clearing.
TypeSitePoints to know
Tinea capitisScalpMostly children; scaly bald patches with broken hairs; T. tonsurans and T. violaceum common in South Asia; Microsporum may fluoresce green under Wood's lamp
KerionScalpSevere inflammatory tinea capitis: boggy, pus-studded swelling with hair loss and tender neck nodes; often mistaken for an abscess; can leave scarring alopecia
Tinea corporisBodyAnnular ringworm
Tinea crurisGroinMen; spreads onto thighs; scrotum usually spared (unlike candida)
Tinea pedis (athlete's foot)Toe webs, solesWhite, macerated, fissured toe webs; entry point for cellulitis
Tinea unguiumNailsThick, crumbling, yellow-white nails starting at the distal edge; T. rubrum commonest
Tinea incognitoAnyRingworm altered by topical steroid; less scaly and spreading; flares when the steroid stops

Diagnosis: skin scrapings from the active edge, plucked hairs or nail clippings in 10% potassium hydroxide (KOH) show branching septate hyphae; culture on Sabouraud agar identifies the species.

Treatment:

  • Localised skin tinea: topical azole (clotrimazole, miconazole) or terbinafine cream for 1–2 weeks beyond clearing. Nystatin does not work on dermatophytes.
  • Widespread tinea, tinea capitis, tinea manuum and extensive tinea pedis: oral terbinafine or itraconazole (for about 1–2 months in skin disease).
  • Tinea capitis in children: oral griseofulvin (classic drug of choice; take with fatty food) or terbinafine. Topical treatment alone cannot reach the hair follicle.
  • Onychomycosis: oral terbinafine for 3–6 months (clears up to about 80%, but relapse is common) or pulsed itraconazole.
High-yield

Terbinafine blocks squalene epoxidase and is fungicidal; it is the drug of choice for dermatophyte nail infection. Griseofulvin binds fungal microtubules and is still used for tinea capitis in children.

Exam trap

A topical steroid (or a steroid–antifungal mix sold over the counter) on tinea makes it look better at first, then spread: tinea incognito. This is a major problem in Pakistan, where combination steroid creams are widely sold.

Id reaction (dermatophytid): an itchy vesicular rash on the hands or trunk in response to a distant fungal infection; it contains no fungus and settles when the tinea is treated.

Candida

  • Candida albicans is a commensal yeast of gut and vagina that overgrows on warm, moist, occluded skin.
  • Predisposing factors: diabetes, obesity, broad-spectrum antibiotics, steroids, pregnancy, immunosuppression, wet work, dentures.
  • Sites: intertrigo (groin, under breasts), napkin rash, vulvovaginitis, balanitis, oral thrush, chronic paronychia (in people whose hands are often wet) and nail infection.
  • Look: glazed red patch with a ragged peeling edge and satellite papules and pustules beyond the border; oral white plaques can be scraped off.
  • Treatment: topical azole or nystatin; treat the cause and exclude diabetes.
Exam trap

Satellite lesions and involvement of the scrotum point to candida, not tinea cruris.

Malassezia

Malassezia (formerly Pityrosporum) is a lipophilic yeast on oily skin. It causes:

  • Pityriasis versicolor: young adults in hot weather; fine scaly hypopigmented or pink-brown macules on the upper trunk. KOH shows short hyphae and round yeasts ("spaghetti and meatballs"). Treat with topical azoles or selenium sulphide/ketoconazole shampoo used on the body; oral itraconazole for resistant cases. Pigment takes months to return; recurrence is common.
  • Seborrhoeic dermatitis (see the eczema chapter).
  • Malassezia folliculitis: itchy uniform papules on the upper back and shoulders, mistaken for acne.

Deep (subcutaneous) mycoses

  • Follow traumatic implantation of soil fungi.
  • Sporotrichosis ("rose gardener's disease"): nodule at the site of a thorn prick with new nodules along the lymphatics; treat with itraconazole.
  • Mycetoma (Madura foot): swelling, sinuses and grains in the discharge, in barefoot rural workers; may be fungal (eumycetoma) or bacterial (actinomycetoma).
  • Chromoblastomycosis: warty plaques on the legs in the tropics.

Viral infections

Herpes simplex

  • HSV-1: usually oral; primary infection in childhood as gingivostomatitis; recurrences as cold sores. HSV-2: mainly genital.
  • The virus stays latent in sensory ganglia (trigeminal for oral, sacral for genital) and reactivates with fever, UV light, stress and immunosuppression.
  • Lesions: grouped vesicles on a red base, becoming crusted erosions.
  • Special forms: herpetic whitlow (finger, often health workers), eczema herpeticum (widespread punched-out erosions in atopic eczema; an emergency), herpes gladiatorum, keratitis.
  • HSV is the commonest trigger of recurrent erythema multiforme.
  • Tzanck smear shows multinucleated giant cells (also seen in VZV); PCR of a swab is the test of choice.
  • Treatment: oral aciclovir or valaciclovir for severe primary or genital infection; intravenous aciclovir for eczema herpeticum, neonates and the immunocompromised; aciclovir cream early for cold sores.

Varicella zoster virus

  • Primary infection is chickenpox; the virus then lies latent in the dorsal root ganglia.
  • Herpes zoster (shingles): reactivation, often in the elderly or immunosuppressed. Pain or tingling first, then a unilateral band of grouped vesicles in one dermatome, which does not cross the midline.
  • Complications: post-herpetic neuralgia (pain beyond the rash; commonest in the elderly), ophthalmic zoster (Hutchinson sign: vesicles on the tip of the nose suggest eye involvement), Ramsay Hunt syndrome (facial palsy with ear vesicles), motor weakness, dissemination.
  • Treatment: oral aciclovir, valaciclovir or famciclovir started within 72 hours of the rash, for 7–10 days; intravenous in the immunocompromised; good analgesia.
  • A shingles vaccine is available for older adults.
High-yield

Zoster in more than one dermatome or disseminated zoster in a young person should prompt an HIV test.

Human papillomavirus (warts)

TypeLookSite
Common wart (verruca vulgaris)Rough, keratotic papule; black dots (thrombosed capillaries)Hands, knees
Plantar wart (verruca)Flattened by pressure; black dots on paring; painfulSoles
Plane wartSmall, flat, skin-coloured; often in lines (Köbner)Face, back of hands
Filiform wartLong thin projectionsFace
Anogenital wartSoft, cauliflower-likeGenitals (HPV 6 and 11; see STI chapter)
  • Most warts clear by themselves over months to years.
  • Treatment: daily salicylic acid paint after paring is the mainstay; cryotherapy with liquid nitrogen; curettage and cautery or laser for stubborn warts.
Exam trap

Paring a plantar wart shows black dots and bleeding points; paring a corn or callus shows smooth layers of keratin.

Molluscum contagiosum

  • Caused by a poxvirus; common in children; spread by contact and autoinoculation.
  • Small pearly, dome-shaped papules with a central dimple (umbilication); a white cheesy core can be squeezed out.
  • Clears without treatment over months; options include cryotherapy, curettage or potassium hydroxide 5% lotion in children.
  • Genital molluscum in adults is usually sexually spread. Large or widespread facial lesions in an adult suggest HIV.

Orf

Poxvirus from sheep and goats (common around Eid al-Adha in people handling animals). A red papule on the hand becomes a blistering, pustular nodule and heals by itself in about 4–6 weeks, giving lasting immunity. It may trigger erythema multiforme.

Exam focus

Expect: organisms of impetigo and the link with post-streptococcal glomerulonephritis, carbuncle in a diabetic, erysipelas versus cellulitis, SSSS versus TEN, erythrasma under Wood's lamp, the leprosy spectrum (immunity, lepromin test, bacilli), WHO cardinal signs and MDT drugs, type 1 versus type 2 lepra reactions, lupus vulgaris and scrofuloderma, cutaneous leishmaniasis in Pakistan, tinea capitis and kerion, KOH findings, terbinafine for nails and griseofulvin for scalp, tinea incognito, candida satellite lesions, pityriasis versicolor, zoster timing of antivirals, and molluscum as a poxvirus.

Quick revision

  • Impetigo: Staph. aureus or Strep. pyogenes; honey crusts; fusidic acid or flucloxacillin; PSGN risk.
  • Carbuncle: joined boils, multiple openings, diabetics, nape of neck.
  • Erysipelas: sharp edge, face, Strep. pyogenes. Cellulitis: deeper, lower leg.
  • Necrotising fasciitis: pain out of proportion; urgent surgery.
  • Leprosy: TT strong CMI, few anaesthetic patches; LL weak CMI, many nodules and bacilli.
  • MB MDT: rifampicin + clofazimine + dapsone for 12 months; PB: rifampicin + dapsone for 6 months.
  • Type 1 reaction: borderline, type IV, neuritis, steroids. Type 2 (ENL): lepromatous, type III, nodules and fever.
  • Lupus vulgaris: apple jelly nodules on diascopy.
  • Oriental sore: sandfly, raised-edge ulcer, Giemsa smear, antimony.
  • Tinea: KOH hyphae; terbinafine for nails; griseofulvin for tinea capitis; kerion = inflammatory scalp tinea.
  • Pityriasis versicolor: Malassezia; spaghetti and meatballs; topical azoles.
  • Zoster: antivirals within 72 hours; risk of post-herpetic neuralgia.
  • Molluscum: umbilicated papules; poxvirus.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; Levinson's Review of Medical Microbiology and Immunology).

FAQ

What is the difference between a furuncle and a carbuncle?

A furuncle is a deep infection of one hair follicle; a carbuncle is several joined furuncles with many draining openings and fever, typical in diabetics.

Why is the lepromin test positive in tuberculoid leprosy?

Tuberculoid patients have strong cell-mediated immunity against M. leprae, so they mount a delayed hypersensitivity response; lepromatous patients cannot.

Should multidrug therapy be stopped during a lepra reaction?

No. The reaction is treated with steroids (and clofazimine for ENL) while multidrug therapy continues.

Why do topical creams fail in tinea capitis?

The fungus lives inside and around the hair shaft deep in the follicle, which only oral antifungals reach.

How is cutaneous leishmaniasis confirmed?

By finding Leishman–Donovan bodies on a Giemsa-stained smear or biopsy taken from the raised edge of the ulcer.