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This image shows a large erythematous lesion with diffuse and ill-defined borders suggestive of celullitis of the foot. The pinna is not involved in cellulitis of face. All the other features mentioned are that of erysipelas.

Milians's ear sign is used to distinguish between erysipelas and cellulitis of the facial region, where there is involvement of ear in erysipelas and sparing in cellulitis, as there is no deeper dermal tissue and subcutaneous fat in the pinna.

Current usage tends to regard erysipelas as a form of cellulitis rather than a distinct entity, so that the definition of cellulitis would include inflammation of dermal as well as subcutaneous tissue.

Similarities include the presence of group A beta-hemolytic streptococci gt; Staphylococcus aureus, Hemophilus influenza and often a region of portal of entry for infection like tinea or trauma.

Usually the disease settles over 1–2 weeks with appropriate systemic antibiotics like Flucloxacillin

Note: St. Anthony's Fire is also used for ergotism caused by the fungus Claviceps purpura as it causes burning sensations resulting in gangrene of limbs.

The image below shows erysipelas, with well demarcated raised margins.

Erysipelas(St.Anthony's fire)

Infection of superficial derma l lymphatics

Raised and sharply demarcat ed edge that spreads by perip heral extension

Blistering is common with su perficial hemorrhage

Extends over the ear

Cellulitis

Suppurative inflammation in volving the subcutaneous tiss ue

Diffuse, ill-defined margins

Severe cellulitis may show bu llae and progress to dermal n ecrosis

Does not extend over the ear

The above image is suggestive of staphylococcus which causes sycosis, folliculitis, and furunculosis.

Scarlet fever is caused by Streptococcus pyogenes.

The coral pink fluorescence in the groin region on Wood's Lamp examination is characteristically seen in erythrasma. Coral pink fluorescence is due to the presence of porphyrins.

Corynebacterium minutissimum is the bacterium responsible for erythrasma and the conversion of aminolaevulinic acid to protoporphyrin.

The palms and soles are frequently affected. The rash starts over the face and spreads centrifugally to the extremities (more affected) and the trunk.

Smallpox is caused by the variola virus and was eradicated from the world in May 1980.

Fever, headache, and malaise appear 10-14 days after infection. Lesions are monomorphic (lesions within an area are at the same stage) and initially vesicular/pustular which then dry, scab over, and finally, heal. Skin scarring is common following recovery.

Incubation perio d

Transmission

Prodrome Rash

Pock appearance

Evolution of poc ks

Scab formation Scab separation Infectivity

Smallpox(variola) 10-14 days

Respiratory viral sheddingTh rough contact with the fluid f ound in the patient's sores.R arely airborne route.

Fever and malaise for 2–4 da ys before the onset of rash

Centrifugal spread˜sually on palms and solesAxilla is usu ally freeRash on extensor sur faces

Vesicle > Pustule >˜mbilicat ed > Scab

Synchronous (monomorphic)

10–14 days after onset of ras h

14–28 days after onset of ras h

From the onset of exanthem until all scabs separate

Chickenpox(varicella) 14–21 days

Aerosolized droplets from na sopharyngeal secretions.’y d irect cutaneous contact with vesicle fluid from skin lesions. Airborne transmission rarely

Minimal to none

Centripetal distributionSeldo m on palms and soles; appea rs in cropsAxilla affectedRas h on flexor surfaces

Macule > Papule > Vesicles o n erythematousbase > Pustul e > Scab

Asynchronous

4–7 days after onset of rash

Within 14 days after onset of rash

From 1 day before rash until all vesicles become scabs. Sca bs are non-infectious.

The above image shows shiny, pearly white, umbilicated papules which are suggestive of molluscum contagiosum.

The peak incidence is between 2-5 years. The incubation period is around 14 days-• months. It is mainly caused by type-I molluscum contagiosum virus (MCV-1) in children and type-II (MCV2) in adults and HIV patients. ™ew lesions develop along the line of trauma (pseudo-Koebner phenomenon). Sexually transmitted molluscum contagiosum may be present over the genital area.

Microscopic examination of the lesions shows eosinophilic inclusions called Henderson-Patterson bodies.

The condition is usually self-limiting but treatment is required for non-resolving symptomatic lesions. Destruction with cantharidin, trichloroacetic acid, diluted liquefied phenol, or surgical removal are a few options.

The above image showing small, red hemorrhagic pustules with the given scenario is suggestive of orf or ecthyma contagiosum.

It is caused by the parapox virus. The commonly affected sites are hands and forearms. Lymphadenitis, lymphangitis, and fever are often present.

It presents with a single lesion—a small, firm, red, or reddish-blue papule that develops after 5–6 days at the site of contact with an infected animal (mostly sheep and goats) and enlarges into a hemorrhagic pustule. The epidermis of an orf lesion shows ballooning degeneration of keratinocytes with eosinophilic cytoplasmic inclusions.

Treatment is usually not necessary, and the lesions heal after 3-6 weeks.

The presence of fever, along with painful sores in the mouth and small, tense vescicles with surrounding erythema on the palms and soles in a child point towards the diagnosis of

hand-foot-mouth disease. The most common cause of which worldwide is coxackievirus A16.

Spread is by droplets or faecal contamination and the incubation period is 7 days. The fever is generally mild, and is followed by the appearance of lesions. The characteristic lesions are slightly oval, with a grey blister roof and a narrow rim of erythema. The oral lesions are aphthoid and are less painful than aphthous ulcers.

Only symptomatic treatment is given. The lesions generally disappear in 7 - 10 days.

The above image shows small, closely grouped vesicles on an inflamed base which are suggestive of herpes labialis or cold sore.

It is caused by HSV-1 (less frequently HSV-2) and commonly affects the face.

The lesions are painful and pruritic. Fever is often present which subsides in 3–5 days followed by the initial vesicular lesions becoming pustular and then crusted before healing in 7–10 days without scarring. Recurrent herpetic lesions are vesicular and ulcerative and tend to occur in the same region.

Treatment: Oral acyclovir 200 mg and topical 5 acyclovir can be used for treatment. In case of resistance to acyclovir, foscarnet or cidofovir can be used.

Option A: Varicella presents with papules and vesicles with a centripetal distribution associated with systemic symptoms of fever and malaise.

Option C: Molluscum contagiosum presents with shiny, pearly white umbilicated papules.

Option D: Whitlow presents with painful swelling of the fingertips and periungual area due to herpes infection by inoculation.

The above scenario is suggestive of active primary genital herpes in the mother. In the case of neonatal transmission, the mortality is high.

Herpes simplex infection of a baby within 28 days of birth is called neonatal herpes. HSV-2 is more commonly implicated than HSV-1. It is usually acquired vertically from the mother or postnatally by contact with nongenital sites.

Features of neonatal herpes:

• Vesicular eruption
• Inflamed and ulcerated mucosae
• Disseminated disease:
• Lethargy
• Seizures
• Respiratory distress
• Hepatosplenomegaly with hepatitis
• Thrombocytopenia.

Primary genital herpes infection in the mother at the time of delivery is associated with a high risk of transmission to the baby during vaginal delivery. Hence cesarean section is indicated and prophylactic aciclovir should be considered for the neonate.

Neonatal herpes is treated with highdose intravenous acyclovir followed by oral acyclovir for 6 months.

The image below shows neonatal herpes. A scalp monitor was associated with infection in this infant.

In case of resistance to acyclovir, foscarnet or cidofovir can be used to treat herpes. They act on viral DNA polymerases thus blocking DNA replication.

The above image showing multiple vesicular lesions on the trunk is suggestive of chickenpox or varicella caused by the varicella-zoster virus. It is non-contagious after the lesions have crusted.

Most infections occur before the age of 5 but can occur in older children and adults. The lesions develop in 3-5 crops and are polymorphic (present at different stages in each site). In 2–4 days, a dry crust forms leaving a shallow pink depression which, in the absence of secondary infection, heals without scarring.

Most common complication is secondary bacterial infection. Varicella confers lasting immunity and second attacks are uncommon.

Varicella-zoster virus (VZV) is a human herpesvirus that causes varicella (chickenpox) as a primary infection and then remains in a latent form in the dorsal root ganglia for a variable period after which it can reactivate to cause herpes zoster (shingles).

The above image shows unilateral, painful, grouped vesicles in a single dermatome suggestive of herpes zoster or shingles. The mucous membranes within the affected dermatomes are involved in shingles.

Herpes zoster/shingles is an acute cutaneous segmental eruption due to the reactivation of latent varicella-zoster virus from dorsal root ganglia. An earlier infection with varicella is essential before zoster can occur.

The first symptom of zoster is usually pain, 1-3 days after which the lesions appear. Occasionally, the pain may not be followed by the eruption (‘zoster sine eruptione’). The patients are infectious, both from the virus in the lesions and nasopharynx.

The most commonly involved dermatomes in decreasing order of frequency are thoracic gt; cervical gt; trigeminal gt; lumbosacral. The incidence of ophthalmic zoster increase with age. The posterior nerve roots and ganglia show inflammatory changes.

Herpes zoster ophthalmicus is a variant of zoster involving the ophthalmic division of the trigeminal nerve (V1). Herpes zoster oticus/Ramsay Hunt syndrome is another variant involving the geniculate ganglion and presents with ipsilateral facial nerve palsy, otalgia and vesicles over external ear.

Zoster is a self-limiting infection but it is painful and carries a risk of secondary infection and post-herpetic neuralgia. Analgesia and treatment of secondary infections are sufficient for mild infections.

Indications for antivirals in VZV (Acyclovir 800 mg):

• Painful zoster infections in adults
• Facial zoster at any age
• Immunocompromised

Post-herpetic neuralgia is most frequent when the trigeminal nerve is involved.

The commonest and most intractable complication of zoster is post-herpetic neuralgia. It

is generally defined as persistence or recurrence of pain more than 1-3 months after the onset of zoster. The pain may be a continuous burning pain with hyperaesthesia or a spasmodic shooting type or pruritic paraesthesia may also occur. Allodynia (pain caused by normally innocuous stimuli) is often the most distressing symptom and occurs in most people with postherpetic neuralgia.

A tricyclic antidepressant such as amitriptyline or nortriptyline is useful for hyperaesthesia and constant burning pain.

The above image showing a white corrugated plaque over the lateral border of the tongue in an HIV-infected patient which cannot be rubbed off is suggestive of oral hairy leukoplakia. It is due to the reactivation of Epstein-’arr Virus (E’V) infection.

Other conditions associated with E’V infection are:

• Glandular fever
• Rash triggered by ampicillin
• ’urkitt's Lymphoma
• Nasopharyngeal carcinoma
• E’Vassociated lymphoproliferative disease
• Agerelated E’Vassociated ’cell lymphoma

Roseola infantum is the most common exanthematic fever in children under the age of 2 years.

Roseola infantum or exanthema subitum is an acute febrile illness with a maculopapular eruption. It is also called the 6th disease. Causative organisms are HHV-6 and HHV-7.

It begins with an abrupt onset of fever for 3–5 days followed by an eruption of discrete rosepink maculopapular rash on the neck and trunk which may later spread to other areas and then fade, leaving no scaling or pigmentation. The lesions may have surrounding pallor. Nagayama spots which are red papules over the palate are pathognomonic. Cervical and occipital lymph nodes are usually enlarged.

Treatment is symptomatic.

Kaposi varicelliform eruption or eczema herpeticum is a widespread viral skin infection that causes localized or mild vesicular eruptions in a patient with preexisting skin disease (most commonly in atopic dermatitis).

The implicated viruses are:

• HSV-1 (most common)
• HSV2
• VZV
• Coxsackie A6 and A16 (eczema coxsackium)
• Vaccinia (eczema vaccinatum)

It presents with fever and vesicles that are widely disseminated and may become hemorrhagic. The skin is painful and generally erythematous. The fever subsides in 4 to 5 days and the pustules heal with crusting, leaving some permanent scarring.

Oral or intravenous acyclovir is used for the treatment depending on the severity of the infection. The image below shows an ecxema herpitcum eruption in a child.

Verruca vulgaris or common wart is most commonly caused by human papillomavirus-2 (HPV-2)

but is also related to types 1, 4, 27, and 57.

Common warts are usually asymptomatic. They show acanthosis, hyperkeratosis,

and papillomatosis and present as firm papules with a rough horny surface. The most commonly affected sites are on the backs of the hands and fingers, and, in children on the

knees. Pseudo-Koebner phenomenon may be observed.

Treatment is usually with topical agents such as salicylic acid, caustics, glutaraldehyde, formalin, or with laser, cryotherapy, surgical removal.

verruca vulgaris.

The clinical scenario and image describe a sharply defined, painful, rough keratotic papule (sago grain appearance) seen on the pressure point of the sole. This is suggestive of

a deep palmoplantar wart or Myrmecia wart. It is usually caused by human papillomavirus-1

(HPV-1).

The superficial form of plantar warts is called mosaic warts which are caused by HPV-2. They present as a plaque of closely grouped small warts and are usually painless.

Option A: Verrucous warts present as asymptomatic skin colored papules and plaques with rough surfaces.

Option ’: Filiform warts are finger-like projections mainly due to HPV-2.

Option C: Planar warts are flat surfaced lesions and hence the name. They are mainly due to HPV3 and 10.

The above image shows rough finger-like growth over the vulva which is suggestive of condyloma acuminata. It is caused by human papillomavirus (HPV-6 gt; HPV-11).

It is also called genital/venereal warts and has high infectivity. It is acquired most commonly after sexual contact but may also occur non-sexually.

Imiquimod and podophyllotoxin are both the first-line drugs used in the treatment of genital warts.

Topical immunomodulation with imiquimod cream is approved for the treatment of genital warts, superficial basal cell carcinoma, and actinic keratoses. It is not used for the treatment of squamous cell carcinoma.

Imiquimod is an FDA-approved drug that acts by stimulating toll-like receptors 7 and 8 of macrophages, monocytes, and dendritic cells and induces apoptosis.

The given image shows cryotherapy which is used for the treatment of certain conditions like warts. The main disadvantage of this procedure is pain.

Cryotherapy is a physician-administered treatment modality and it uses dimethyl ether spray, carbon dioxide snow, or liquid nitrogen to produce cold thermal damage to the skin.

Liquid nitrogen produces the coldest freeze and is most commonly used in practice. It is applied using a cotton wool bud or a cryospray until a rim of iced tissue (seen as a white discoloration) develops around the lesion. The freeze is maintained for 5–30 sec. Scarring is unlikely with freezing times under 30 secs.

Cryotherapy is considered relatively safer in pregnancy.

The above image shows the characteristic 'slapped cheek appearance' seen in erythema infectiosum caused by parvovirus B19.

It evolves in three phases:

• First phase - sudden onset diffuse and macular, asymptomatic erythema of the cheeks, (slapped cheek). Prodromal symptoms may or may not be present.
• Second phase - begins after 1–4 days, with discrete erythematous macules and papules on the proximal extremities and later the trunk.
• Third phase - Recurring stage, the eruption is greatly reduced or invisible, only to recur after
• the patient is exposed to heat or sunlight, or in response to crying or exercise.

Only about 7 of children with erythema infectiosum have arthralgias, whereas 80 of adults have joint involvement.

A maculopapular rash is not seen in zoster (shingles).

Shingles cause vesicular lesions that are grouped together and specific to a dermatome.

Maculopapular rashes are seen in:

• Rubella
• Dengue (febrile phase)
• Measles
• Chikungunya (acute infectious phase)
• Erythema infectiosum
• Zika virus
• West Nile virus
• Infectious mononucleosis

Type of ra sh

Macule

Papule Vesicle

Description

Flatlesion with a well-circum scribed change in skin color

< 1 cm

Elevated solidskin lesion < 1 cm

Smallfluidcontaining blister

The above image shows multiple vesicles amp; crusts clustered on an inflamed base around the lips which is characteristic of herpes labialis or cold sore.

It is commonly caused by herpes simplex virus type 1(HSV-1) and rarely by herpes simplex virus type 2 (HSV-2). It begins with a prodrome of pain, burning, and tingling followed by the appearance of erythematous papules. The papules then become vesicular and may ulcerate.

It is treated with oral acyclovir 200 mg and 5 topical acyclovir.

Option B: Herpangina or vesicular pharyngitis is characterized by the presence of ulcerating small vesicles on the oral fauces and the posterior pharyngeal wall. It is commonly caused by the coxsackie virus.

Option C: Molluscum contagiosum is characterized by pearly white, wart-like umbilicated papules. It is caused by the pox virus.

Option D: Impetigo is characterized by golden yellow or honey-coloured crusts that form after the rupture of pustulating vesicles. Non-bullous impetigo is caused by both S. aureus and streptococcus. Bullous impetigo is caused by S. aureus.