common pedi skin disease
TRANSCRIPT
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.
Viral Exanthems
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
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
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
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
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
Viral Exanthems…
• Common Exanthems – Measles
– Rubella
– Varicella and Zoster
– Erythema infectiosum
– Roseola infantum
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)
Measles…
Epidemiology…
Ethiopia/ 2002-2003– 3,797 cases– 5th major cause of death in CU5– 4% attributable deaths ~ 19,000– Global share ~ 2%
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
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.
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.
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)
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
Measles…
Systemic signs– Generalized LAP, NVD– Splenomegally– Myelo/encephalitiis– Secondary infection
Measles…DDx
Drug eruption Rubella Syphilis Leucocytoclastic vasculitis
Diagnosis Clinical
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
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
Measles…
Prognosis• Self limited• MR ~ 10% in poor countries
ComplicationsAcute
– Otitis M, Pneumonia, Encephalitis, Thrombocytopenia, PEM
Chronic– Subacute Sclerosing Panencephalitis
Rubella
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
• 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
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.
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
Rubella…DDx
– Other exanthems– Drug reactions
Diagnosis– Clinical ~ especially during epidemic– Laboratory
• Serology
• Culture
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
Chicken Pox
• 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.
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.
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
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…
Erythematous halo
1st lesions appear on the face and scalp
Lesions at all stages
Scattered
Diffuse
Rapidly evolving lesions
Mild
Extensive
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.
Diagnosis
– Clinical– Tzanck smear– VZV Ag detection – Culture– Serology
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
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
Prevention
VZV immunization
– Prevents symptomatic primary VZV infection
– Up to 80% efficacy– A live attenuated varicella vaccine FDA 1995
Erythema infectiosum and
Roseola infantum
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.
Treatment :- Removal of a papule is curative.04/12/23 73
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Exercise
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