Common pedi skin disease

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Common pediatric skin problems Viruses may involve the skin either by dissemination to skin during a systemic viral infection accompanied by viral replication in skin (viral exanthem) or by producing a virus-induced skin tumor. viral exanthems are commonest.

Transcript of Common pedi skin disease

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Common pediatric skin problems

Viruses may involve the skin either by dissemination to skin during a systemic viral infection accompanied by viral replication in skin

(viral exanthem) or by producing a virus-induced skin tumor.

viral exanthems are commonest.

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Viral Exanthems

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Viral Exanthems…

• Important causes of child morbidity• Overlooked

• Exanthems: – Symmetric, diffuse skin eruptions caused by viral illnesses.– Macules, papules, pustules, vesicles, wheals or purpura.

• Enanthems: – Oral mm eruptions– Papules, vesicles, erosions, ulcerations or petechiae

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SHOW PICTURE
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Viral exanthems• Classification Scheme of childhood exanthems

– 1st disease ~ Measles– 2nd disease ~ Scarlet fever– 3rd disease ~ Rubella– 4th disease ~ Filatov-Dukes ds (an atypical Scarlet fever)

– 5th disease ~ Erythema infectiosum – 6th disease ~ Roseola infantum

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Viral Exanthems:• Etiologies

– DNA: Erythema infectiosum, exanthem sabitum, Varicella

– RNA: Measles and Rubella

• Transmission– Respiratory droplets/direct contact

– Developed world• Universal immunization• Dx~ advances in viral culture, serology, PCR and EM

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Viral Exanthems…

• Clues for clinical diagnosis– Primary lesion within the exanthem/Emphasis ~ skin

lesions– Time of appearance of the eruption against systemic sxs– Enanthem– Distribution of eruptions– Progression of eruptions

• How fast• Pattern of progression

– Other symptoms

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DDx of Viral Exanthems

Erythematous eruptions

morbilform– Measles– Rubella– Erythema infectiosum– Roseola infantum– CMV– Infectious Mononucleosis

Vesiculopustular lesions– HSV infection– Varicella & Herpes zoster– Kaposi’s Varicelliform erup.

Purpuric lesions– Atypical measles– Congenital rubella– Congenital CMV

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Viral Exanthems…

• Common Exanthems – Measles

– Rubella

– Varicella and Zoster

– Erythema infectiosum

– Roseola infantum

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Measles

• Rubeola, Morbilli

• The greatest killer of children in history.

Epidemiology• Global

– Affects 50 million people annually – Causes more than ONE million deaths per yr.

– Developing countries ~ morbidity and mortality

– Age of onset: > 45% before 9 months of age– Case fatality rate ⇨ 0.1 - 0.2% Vs 2 -10% (post Vs vaccine)

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Measles…

Epidemiology…

Ethiopia/ 2002-2003– 3,797 cases– 5th major cause of death in CU5– 4% attributable deaths ~ 19,000– Global share ~ 2%

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Measles…Etiology

– Measles virus, genus Morbillivirus ,(Paramyxoviridae)

– Single stranded RNA virus

Transmission– Respiratory droplets

– Infected person conatagious• before onset of rash

• up to 5 days after lesions appeared• Attack rate ~ >90%....100%• Asymptomatic infection…rare

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Measles…Pathogenesis• Entry thru respiratory tract epithelium

⇊• Replication occur in the regional lymph nodes

⇊• Hematogenous dissemination: skin and mm

⇊• Viral replication: skin and mm

• Infection of antigen-presenting cells ⇨immunosuppression.

• Following infection ⇨ shift from CMI to Humoral immunity occurs.

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Measles…Clinical Features• The course divided into three distinct phases:

I. Asymptomatic period– IP of 10 or 11 days following exposure

II. Prodrome phase – Lasts 3 to 4 days– Coryza, fever a striking palpebral conjunctivitis with photophobia, and a “barking” cough.

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Measles…

III. Onset of the rash– Persists longer than 5 to 6 days.– As exanthem progress, systemic signs subside

– Koplik's spots • Pathognomonic lesions • Tiny bluish white spots with red background/halo• On buccal mucosa opposite lower 2nd molars/inner lip• Usually appear 24 to 48 hrs before the rash (2nd febrile

day)

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The exanthem• Begins on the fourth febrile day

• Erythematous macules and papules– Behind ears, forehead at hairline– Spread: centrifugally and inferiorly– Face, trunk, extremities, palms and soles– Reach the feet ~ 3rd day

• Lesions fade away in order of appearance• Resolution: 4 – 6 days

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Measles…

Systemic signs– Generalized LAP, NVD– Splenomegally– Myelo/encephalitiis– Secondary infection

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Measles…DDx

Drug eruption Rubella Syphilis Leucocytoclastic vasculitis

Diagnosis Clinical

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Measles…Laboratory

– CytologyThe measles virus, a paramyxovirus, replicates within keratinocytes

and induces increased nuclear volume within the epidermal cells, producing multinucleated giant cells (Warthin- Finkeldy cells).

– Culture – Serology

• DFA

– PCR

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ManagementTreatment

– Symptomatic:• Hydration• Vit A supplementation

– Antibiotics

Prevention– MMR – Vaccine schedule: when exactly ??

• Maternal Ab– Affluent Society: 12-15 months and 11 -12 yrs, booster dose/college– Developing nations: three doses ~ 6-9; 15 mo; before KG– Ethiopina coverage ~ 51%

• Addis Ababa

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Measles…

Prognosis• Self limited• MR ~ 10% in poor countries

ComplicationsAcute

– Otitis M, Pneumonia, Encephalitis, Thrombocytopenia, PEM

Chronic– Subacute Sclerosing Panencephalitis

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Rubella

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Rubella

• German measles or ‘three day measles’

• Incidence ~ US: ↓ 99% since 1969. – 2001 ~ least cases

• Rubella virus, RNA virus.

• Age of onset– Before immunization ~ Children < 15 yrs– Currently ~ young adults

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• Transmission– Postnatal ~ Inhalation of droplets; – Congenital ~TORCH;

– Moderately contagious except in susceptible – Maximum communicabilty:

• 2 days before and 5-7 days after rash

– UP to 40% are asymptomatic

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Rubella…

Pathogenesis– Respiratory epithelium ⇨ 10 viremia ⇨ replication

in RES ⇨ 20 viremia ⇨peripheral blood monocytes ⇨entire body [Secretions, CSF, Urine].

Clinical features– IP: 14 – 21 dys– Characterstic signs: Lymphadenopathy

• Retoauricular, • Post. cervical and • sub. occipital.

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Rubella…• Exanthems

– Erythematous, maculopapular rash– 1st day ~ spreads to the face, trunk and extremities– 2nd day ~ facial exanthem fades.– 3rd day ~ exanthem fades completely with out residual pigmentary Δ

• Enanthems – Rose colored spots or petechiae on soft palate: Forchheimer’s sign

• Systemic signs – LAP– Splenomegally– Arthritis

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Rubella…DDx

– Other exanthems– Drug reactions

Diagnosis– Clinical ~ especially during epidemic– Laboratory

• Serology

• Culture

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Rubella…Management

– Symptomatic treatment– PEP: IV IG ~ for non immune, pregnant women who refuse abortion

– Immunization• Live attenuated virus

• Schedule– At 12 to 15 months of age– All non-immune prepubescent– All non immune postpubescent females NOT conceiving in 3 months

Prognosis– Post natal: usually mild and with no consequence

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Chicken Pox

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• Etiology: – VZV, infects 98% of adult population

• Age of onset– ~90% of cases in children younger than 10 yrs; – ~5% in persons greater than 15 yrs

• Transmission– Routes:

• Airborne droplets• Direct contact

– Pts are contagious: several days before rashes till last crop of vesicles.

– Crusts are NOT infectious– IP~14 dys; range 10 to 23 days– Varicella is 3x more infectious than Zoster.

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Pathogenesis

• Mucosa of URT and oropharynx

⇊• Local replication and 10 viremia AND replicates in cells of RES

⇊• Dissemination to the skin and mm

⇊• During the course of the varicella, the virus passes from the

skin lesion to the sensory nerves ⇛ ⇛ travels to the sensory ganglia ⇛ ⇛ establishes local infection.

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Clinical Features

• Prodrome– Chracterstically absent in children OR mild

• Exanthems appear with in 2-3 days after prodrome.

• Skin lesions– Usually quite pruritic– Vesicular lesions seen in successive crops– Scanty in children Vs much more dense in adults

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Distribution

• Lesions evolve rapidly– Paules ⇛ vesicles ⇛become umblicated and rapidly

evolve to ⇛pustules ⇛crust over 8-12 hrs period.– With subsequent crops all stages of evolution noted

simultaneusly:• Papules, vesicles, pustules, crusts

• Crusts fall off in 1-3 weeks time:– Leaving behind characterstic punched out permanent

scars…

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Erythematous halo

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1st lesions appear on the face and scalp

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Lesions at all stages

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Scattered

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Diffuse

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Rapidly evolving lesions

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Mild

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Extensive

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Clinical Features

Mucus membranes– erosions

• commonly on palate.

• Also on conjunctiva, larynx, pharynx, nose and trachea.

Pneumonitis ~ commonly in immunocmpromised pts

CNS ~ cerebral ataxia and encephalitis

Bacterial superinfection– Most commonly S. aureus and and group A Strept.– Impetigo, Echthyma and Cellulitis.

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Diagnosis

– Clinical– Tzanck smear– VZV Ag detection – Culture– Serology

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Management

• Antiviral agents– If began with in 24 hrs after onset of varicella, it

decreases severity.– Course not affected otherwise

• Treatment of secondary bacterial infections

• Symptomatic therapy

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Course and prognosis

Children• Self limited in healthy children

• Commonest complications vary with age– Children younger than 5yrs of age

• Bacterial superinfection

– Children 5-11 years of age• Varicella encephalitis

• Reye’s syndrome

Adults– Severe– Longer period

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Prevention

VZV immunization

– Prevents symptomatic primary VZV infection

– Up to 80% efficacy– A live attenuated varicella vaccine FDA 1995

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Erythema infectiosum and

Roseola infantum

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Erythema infectiosum

– Fifth disease– Human parvovirus B 19– IP: 4-14 days– Respiratory droplets– Symptomatic in 20-60% of cases– Characterstic

• Edematous, confluent plaques

• Slapped cheek appearance

• Spares nasal bridge, periorbital

– Treatment• Symptomatic

Roseola infantum

– Sudden rash, exanthem sabitum

– HHV – 6 & 7– Affected age: 6 to 24 months– Pathogenesis: UK– IP: 5-15 days– Characterstic

• Blanchable macules, papules

• Trunk and neck

• High grade fever ~ up to 40 c

• Rashes appear as fever subsides

– Management ~ symptomatic

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VIRUS-INDUCED TUMORS

• Certain viruses, such as human papillomaviruses and molluscum contagiosum viruses, do not destroy keratinocytes but induce keratinocyte proliferation, resulting in benign tumors of skin.

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Molluscum Contagiosum

Clinical features

• White or yellow-white 1-6 mm discrete papules with a central umbilication are seen

• Caused by a poxvirus that induces epidermal cell proliferation.

• Molluscum type I is believed to be responsible for common lesions on the extremities, head, and neck.

• Types 2 and 3 are most often associated with genital lesions in the adolescent or young adult.

The child is contagious as long as active lesions are present.

Untreated molluscum may require 1-5 years to resolve.

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Exercise

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