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VIRAL INFECTIONS OF THE SKIN

Herpes Simplex Virus

  • HSV-1
  • HSV-2

Herpes Simplex Virus type-1(HSV-1)

  • Remains latent in trigeminal root ganglion.
  • HSV-1, is classically associated with facial infections- Gingivostomatitis and recurrent cold sores ( skin or lip)
  • Keratoconjuntivitis generally with lid swelling and vesicles, dendritic ulcers may be seen, (untreated repeated attacks may lead to visual impairment).
  • Meningoencephalitis (characterised by fever, headache and confusion).

HSV-1 causes cold sores on the mouth or lips.
HSV-1 infection
Orolabial HSV-1 infection

Diagnosis
  • PCR on CSF
  • RBC on CSF

Herpes Simplex Virus type-II (HSV-II)
  • Latent in sacral nerve ganglia.
  • Causes herpes genital infections: Painful vesicular lesions of genitals and anal area.
  • In neonates it may have one of these three presentations:
  • Disseminated with liver involvement.
  • Encephalitis
  • Skin, eyes or mouth



HSV-2 infection

Diagnosis
  • PCR on CSF ( for encephalitis)
  • Viral culture with fluorescent antibody stain to identify virus.

Treatment
  • Primary HSV
Famciclovir- 250 mg XTID
Valaciclovir- 500 mgX BID
Aciclovir- 200mg, 5 times a day
i.v Aciclovir- 5mg/Kg X TID (if severe and preventing oral intake
  • Recurrent HSV- 1 or 2
Aciclovir ointment 3-5 times/day
Oral aciclovir 200mg 6hrly
Famciclovir 250mgXBID
Valaciclovir 500mg daily
In immunocompromised (aciclovir 400mgXQID, famciclovir 500mgXBID, valaciclovir 1gXBID)

  • Severe complications
i.v. aciclovir 10mg/kgX TID (upto 20mg/kg in severe encephalitis)
  • Disease suppression
Aciclovir 400mgXBID
Famciclovir 250mgXBID
Valaciclovir 500mg daily


Varicella zoster virus (VZV)
  • The varicella zoster virus (VZV) is the cause of both varicella (chickenpox) and zoster(shingles).
  • The primary infection of varicella includes viraemia and a widespread eruption, after which the virus persists in dorsal root ganglion, usually sensory. Zoster is the result of reactivation of this residual latent virus.

Chickenpox
  • Humans are the only known reservoir of VZV.
  • Chickenpox is highly contagious.
  • VZV is dermo and neurotropic.
  • Spread by the aerosol route.

Clinical features
  • Clinically, chickenpox presents with a rash, low-grade fever, and malaise, although a few patients develop a prodrome 1–2 days before onset of the exanthem.
  • Disease is well tolerated in children.
  • It is more severe in adults, pregnant women and immunicompromosed.
  • Incubation period is 14-21 days, after which vesicular eruption begins( first on the mucosal surfaces followed by rapid dissemination in a centripetal distrubition.
  • New lesions occur every 2-4 days associated with fever.
  • The rash progresses from small pink macules to vesicles and pustules within 24hrs, followed by crusting.
  • Self-limiting cerebellar ataxia (rarely).
  • Maternal infection in early pregnancy carries a risk of neonatal damage, and disease within 5 days of delivery can lead to severe neonatal varicella.




Diagnosis
  • Dx is usually clinically obvious.
  • For confirmation of Dx: Aspiration of vesicular fluid and PCR or tissue culture.

Treatment

  • Varicella in the otherwise healthy child requires only symptomatic treatment. 
  • In some instances aciclovir is used in childhood chickenpox to reduce the severity and duration of the eruption.
  • Rest and analgesics are sufficient for mild attacks of zoster in the young. Soothing antiseptic applications may be helpful and secondary bacterial infection will require antibiotics.
  • Aciclovir, valaciclovir and famciclovir are required in the management of the immunocompromised or any case of pneumonitis.

Shingles

Herpes zoster (shingles) is a sporadic disease that results from reactivation of latent VZV from dorsal root ganglia.
Commonly seen in elderly.

Clinical features

  • Herpes zoster is characterized by a unilateral vesicular dermatomal eruption, often associated with severe pain. The dermatomes from T3 to L3 are most frequently involved. 
  • In children, reactivation is usually benign; in adults, it can be debilitating because of pain.
  • The onset of disease is heralded by pain within the dermatome, which may precede lesions by 48–72 h; an erythematous maculopapular rash evolves rapidly into vesicular lesions.
  • When branches of the trigeminal nerve are involved, lesions may appear on the face, in the mouth, in the eye, or on the tongue. Zoster ophthalmicus is usually a debilitating condition that can result in blindness in the absence of antiviral therapy.
  • In the Ramsay Hunt syndrome, pain and vesicles appear in the external auditory canal, and patients lose their sense of taste in the anterior two-thirds of the tongue while developing ipsilateral facial palsy. The geniculate ganglion of the sensory branch of the facial nerve is involved.
  • CNS involvement may follow localized herpes zoster: myelitis or encephalitis.






Treatment
  • In severe infection and in the immunocompromised:
Early therapy with aciclovir 800mgX 5times daily or valaciclovir1g X TID, or i.v aciclovir 10mg/kg X TID
Reduce early and late onset pain esp. in pt. >65yrs.
  • Post-herpetic neuralgia:
Aggressive analgesia and the use of transcutaneous nerve stimulation.
Plus amitriptyline 25-100mg daily or gabapentin 300mg daily increasing slowly to 300mg BID or more.

Human Papillomavirus Infections

Human papillomaviruses (HPVs) selectively infect the epithelium of skin and mucous membranes. These infections may be asymptomatic, produce warts, or be associated with a variety of both benign and malignant neoplasias.

Clinical Manifestations
  • The clinical manifestations of HPV infection depend on the location of lesions and the type of virus.
  • Common warts usually occur on the hands as flesh-colored to brown, exophytic, and hyperkeratotic papules. 
  • Plantar warts may be quite painful; they can be differentiated from calluses by paring of the surface to reveal thrombosed capillaries.
  •  Flat warts (verruca plana) are most common among children and occur on the face, neck, chest, and flexor surfaces of the forearms and legs.
  • Anogenital warts develop on the skin and mucosal surfaces of external genitalia and perianal areas .
  • Among circumcised men, warts are most commonly found on the penile shaft. Lesions frequently occur at the urethral meatus and may extend proximally.
  • Mosaic warts: mosiac like plaques of tightly packed individual warts.

Common wart

Plantar wart




Flat warts (verruca plana)



Anogenital warts

Mosaic warts
Treatment
  • Majority of cases of viral warts resolve spontaneously.
  • Initial t/t:
  • Salicylic acid or salicylic and lactic acid combination along with regular and frequent paring of the hyperkeratotic skin.
  • Cryotherapy using liquid nitrogen: As an alt. or in case of failure of above t/t.
  • Warts close to/under the nails: Cutting of nails and electrodesiccation or destructive therapy.
  • Other t/t:
  • Systemic retinoids, intralesional injections of bleomycin or interferon, application of diphencyprone or dinitrichlorobenzene, imiquimod.

Molluscum contagiosum
  • Molluscum contagiosum virus is an obligate human pathogen that causes distinctive proliferative skin lesions. These lesions measure 2–5 mm in diameter and are pearly, flesh-colored, and umbilicated, with a characteristic dimple at the center. A relative lack of inflammation and necrosis distinguishes these proliferative lesions from other poxvirus lesions. Lesions may be found—singly or in clusters—anywhere on the body except on the palms and soles and may be associated with an eczematous rash.
  • Molluscum contagiosum is highly prevalent in children and is the most common human disease resulting from poxvirus infection
  • Molluscum contagiosum can be associated with immunosuppression and is frequently seen among HIV-infected patients



Diagnosis

The diagnosis of molluscum contagiosum is typically based on its clinical presentation and can be confirmed by histologic demonstration of the cytoplasmic eosinophilic inclusions (molluscum bodies) that are characteristic of poxvirus replication.


Treatment


There is no specific systemic treatment for molluscum contagiosum, but a variety of techniques for physical ablation have been used. Cidofovir displays in vitro activity against many poxviruses, and case reports suggest that parenteral or topical cidofovir may have some efficacy in the treatment of recalcitrant molluscum contagiosum in immunosuppressed hosts.

BACTERIAL INFECTION

IMPETIGO

INTRODUCTION

  • Contagious superficial Pyogenic infection of the skin.


Two main clinical form are
  • Non – Bullous impetigo ( or Impetigo contagiosa of Tilbury Fox)

Causative organism – Staph. aureus, Streptococcus or both

  • Bullous Impetigo

Causative organism – Mainly Staph disease but rarely can be due to streptococci


Pathology 

Bullous impetigo 

  • Epidermis split just below the granular layer to form large blister


  • Neutrophils migrate through spongiotic epidermis to blisters cavity, which may also contain bacilli


  • Occasionally acanthotic cells may be seen


  • Dermis contains inflammatory infiltrate of Neutrophils and lymphocytes



Non – Bullous impetigo

  • Histology is similar except that blister formation is slight and transient 



Clinical Feature

  • In non-bullous impetigo, the initial lesion is a very thin-walled vesicle on an erythematous base. 
  • The vesicle ruptures so rapidly that it is seldom seen as such.
  • The exuding serum dries to form yellowish brown crusts.
  • The crusts eventually dry and separate to leave erythema, which fades without scarring.
  • The face, especially around the nose and mouth, and the limbs are the sites most commonly affected,



Non-bullous impetigo

  • In bullous impetigo, the bullae are less rapidly ruptured and become much larger;, and persist for 2 or 3 days.
  • After rupture thin, flat, brownish crusts are formed. Central healing and peripheral extension may give rise to circinate lesions.


  • Although the face is often affected, the lesions may occur anywhere.



Bullous impetigo
Treatment

  • Topical:

    Mupirocin or fusidic acid is active against both    organism.
    Washing with soap and water.
  • Oral:

    Antibiotics like Flucloxacillin or Erythromycinin severe cases.
  • Proper education


Complication 

  • Infective complication are uncommon in the absence of systemic disease or malnutrition


  • Cellulitis occasionally follow streptococcal disease


  • Post streptococcal glomerulonephritis 

Specially following S. pyogens infection

  • Scarlet fever, Urticaria and Erythema multiforme



Ecthyma 

Introduction 

Pyogenic infection of the skin characterized by the formation of adherent crusts, beneath which ulceration occur.

Aetiology 

Bacteriological status – Similar to Impetigo

  • Predisposing factors 

Poor hygiene 
Malnutrition 
Minor injuries 
Other skin condition, like scabies
IV drug abusers

Clinical Feature 

  • Small bullae or pustules on an erythematous base


  • Soon surmounted by hard crust of dried exudate, which increase in size by peripheral accretion.


  • The base may become indurated and a red edematous areola is often present.


  • Crust is removed with difficulty , to reveal a purulent irregular scar.




Ecthyema enduratum of Bazin


  • Healing occur after few weeks, with scarring


  • Common sites 

Buttocks, Thighs and Legs


Treatment 

  • Antibiotics' active against both staph. and streptococcus


  • Improve hygiene and nutrition 


  • Topical therapy either with sulconazole or miconazole clears lesions satisfactorily over 1 week.


  • Treatment of underlying disease – e.g.. Scabies



Erythrasma

  • Erythrasma is a mild, chronic, localized superficial infection of the skin caused by bacteria, known as C. minutissimum.


  • Clinical infection may occur at any age but is more common among adults than children.


  • Detected by Wood’s light examination- pink fluorescence


Clinical features

  • Asymptomatic or mild itch.


  • Erythrasma involves the toe clefts more frequently than any other site. 


  • As clinically manifest lesions it occurs most commonly in the groins, axillae and the intergluteal and submammary flexures. 





Treatment

  • Topical azole cream- cotrimazole, miconazole.
  • Topical antibiotics
  • Extensive cases: oral erythromycin

Cellulitis and Erysipelas 

Introduction 

  • Cellulitis is an inflammation of subcutaneous tissue which is usually infective.

  • Erysipelas is a bacterial infection of the dermis and upper subcutaneous tissue
  • Well defined, raised edge, reflecting more superficial (dermal) involvement (clinical hallmark)
  • It can sometime penetrate deep dermis and subcutaneous tissue to form cellulitis.

Bacteriology 

Group A beta hemolytic streptococci most of the time

Other organisms 
Group C or G streptococci
Group B streptococci in new borne
Staph aureus 



Predisposing factors:
DM
Vericose leg ulcer
        Tinea pedis

Clinical Features 


Erythema, heat swelling and pain.
In erysipelas, the edge of the lesion is well-demarcated and raised, but in cellulitis it is diffuse.
Blistering occur in both conditions.
Site
Cellulitis:
Legs
Erysipelas:
Lower extremities 
Face  - may spread to eyelids but orbital complications are rare



Cellulitis



Erysipelas

Dx

  • Specimens for bacteriological examination should be
  • taken from vesicle fluid or eroded or ulcerated surfaces, in addition to blood cultures.

Treatment
  • Antistreptococcal agent:
Phenoxymethylpenicillin
Erythromycin/ciprofloxacin- in case of penicillin sensitivity
          I.V antibiotics- in severe cases.

Folliculitis

Circumscribed infectious process that originate in the hair follicle and is defined by its anatomic features.

Mainly of two types
Superficial 
Located superficially

Deep 
It extend more deeply to produce perifollicular inflammation

Superficial folliculitis 
  • Subacute or chronic inflammation confined to ostium or extend slightly below it
  • Common condition which heals without scarring



Common causes

  • Staphylococcus auerus and coagulase negative staph


Physical 
  • Traumatic epilation
  • Adhesive plaster and dressing


Chemical injury 
  • Contact with mineral oils
  • Exposure to tar products
Sites 

  • Commom in children and common sites being scalp and limbs.


Lesion 

  • Present as small follicular papules or pin head pustules, which are rarely painful


  • Pus culture is sterile most of time and rarely coagulase negative staph can be isolated




Follicular impetigo of Bockhart

  • Variant of superficial folliculitis caused by staph. aureus 

  • Common in childhood age

Treatment 

  • Removal of causative agent in case of physical and chemical factors suspected

  • Mild staphylococcus
Self limiting 
Cleansing and local antiseptic

  • Severe
Topical and systemic antibiotics

  • Recurrent and persistent cases
Prophylaxis against staph in carriage sites


Deep folliculitis

Furuncle
  • A furuncle is an acute, usually necrotic, infection of a hair follicle with S. aureus.


  • Site:

Any site and common site are neck, buttocks and anogenital area.

  • Aetiology

S.aureus
M>F
Most common in adolescence and early adult life.
Tight clothes predisposes
The infecting strain of Staphylococcus is usually also present in the nares or the perineum

Clinical features

  • A furuncle first presents as a small, follicular, inflammatory nodule, soon becoming pustular and then necrotic and healing after discharge of a necrotic core to leave a violaceous macule and, ultimately, a permanent scar.


  • Occasionally, there may be fever and mild constitutional symptoms.





Treatment

  • Antistaphylococcal antibiotics.

Carbuncle
  • A carbuncle is a deep infection of a group of contiguous follicles with S. aureus, accompanied by intense inflammatory changes in the surrounding and underlying connective tissues, including the subcutaneous fat.


  • Aetiology

S.aerues
Common in men (middle or old age)
They may be seen in the apparently healthy but are more common in the presence of diabetes, malnutrition, cardiac failure, drug addiction or severe generalized dermatoses, such as exfoliative dermatitis or pemphigus, and during prolonged steroid therapy.


Clinical features

  • Very tender nodule associated with severe constitutional symptoms.


  • May be upto 10cm in size and discharge in several days.


  • Site: neck, shoulders and hips.





Treatment
  • Antistaphylococcal antibiotics

  • Diabetes and other possible underlying conditions should be sought.

Staphylococcal scalded skin syndrome
  • SSSS is an exfoliative dermatosis in which most of the body surface becomes erythematous and the necrotic superficial epidermis strips off.


  • Occurs predominantly in childern (esp. neonates)


Etiology

  • Staph. Aereus
  • Due to protease like effect of exfoliative toxins
  • Two of the toxins (A and B) cause disruption of the desmosomes by cleaving desmoglein-1 in the most superficial epidermis and also cause the split beneath the stratum corneum which leads to peeling of skin.



Clinical features

  • The initial event is usually a localized staphylococcal infection. This may be in the skin or at a distant or ‘occult’ site.
  • A few days later, patients develop fever, irritability and skin tenderness.
  • A widespread erythematous eruption follows, which progresses rapidly to blister formation.
  • The tender skin becomes gathered into folds and, as it shrinks, leaves raw areas which are extremely painful.
  • The condition usually heals within 7–14 days
  • Swabs and cultures of blister fluids do not usually grow the staphylococci, as the blisters are mediated by the toxins which are disseminated haematogenously. The staphylococci may be isolated from the original septic site.





Treatment


  • Systemic antibiotic:

Flucloxacillin

  • Supportive measures
  • Bacterial swabs from carrier sites- to exclude satph. Carrriage.