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Rashes in pediatrics Shilpa R Singh MD
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Measles RNA virus , Paramyxoviridae Family Humans are the only host Incidence declined in 1963 after vaccine Current rate < 1case /1,000,000 population Infection imported from abroad, outbreaks occur in community with low vaccination
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Transmission Respiratory tract or conjunctivae through droplet carrying virus Infectious from 3 days before up to 4-6 days after the onset of rash
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Pathology Necrosis of respiratory tract epithelium and lymphocytic infiltrate Small vessel vasculitis on skin and oral mucosa Fusion of infected cell result in multinucleated giant cells Warthin – Finkeldey Giant cell , Pathognomonic
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Clinical Manifestation
Prodromal symptoms - fever, malaise, dry (occasional croupy) cough, coryza, conjunctivitis with clear d/c, marked photophobia 1 to 4 days prior to rash - Koplik spots on the buccal mucosa Koplik spots ( 50 – 70 %) - tiny, bluish-white dots surrounded by red halos on buccal mucosa opposite lower molars
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rubeola (nine-day or red measles)
Day 3 or 4 - blotchy, erythematous, blanching, maculopapular exanthem appears Rash begins at the hairline and spreads cephalocaudally and involves palms and soles Rash typically lasts days Can see desquimation in severe cases
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rubeola (nine-day or red measles)
Patients can be systemically ill Incubation period 9-10 days Patients contagious from 4 days prior to the rash until 4 days after the resolution of the rash Highly contagious - 90% for susceptible people
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rubeola (nine-day or red measles)
High morbidity and mortality common in children in underdeveloped countries Peak season is late winter to early spring Potential complications - OM, PNA, obstructive laryngotracheitis, acute encephalitis Vaccination is highly effective in preventing disease
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rubeola (nine-day or red measles)
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Diagnosis and Complications
Clinical Diagnosis Labs – Decreased White count ( Lymphocytes more than neutrophils ) Serum IgM ( Appears 1 -2 days after onset of rash , till 1 month ) Most common cause of death – Pneumonia Most common complication – Acute Otitis media Others – Tracheitis , bronchiolitis , febrile seizure , encephalitis , hemorrhagic measles ,keratitis , myocarditis
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Treatment and Prevention
Supportive No prophylactic antibiotics Vitamin A ( 6 months – 2 yrs , hospilatized , malnutrition other complications ) Vaccination 2 dosages , 1st dose months , 2nd dose 4 -6 yrs of age MMR – live vaccine , do not give to pregnant or immunosuppressed
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Rubella (german measles)
Rubella virus (Togaviridae ) Little or no prodrome in children In adolescents days of low-grade fever, malaise, headache, adenopathy, sore throat, coryza Exanthem - discrete, pinkish red, fine maculopapular eruption - begins on the face and spreads cephalocaudally Rash becomes generalized in 24 hours and clears by 72 hours
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rubella (german measles)
Suboccipital , post auricular and anterior cervical lymph nodes common Forchheimer spots - small reddish spots on the soft palate - can sometimes be seen on day 1 of the rash Arthritis and arthralgias - frequent in adolescents and young women - beginning on day 2 or 3 lasting 5-10 days Up to 25% of patients are asymptomatic - serology testing may be necessary to establish the diagnosis
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Forchheimer spot
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rubella (german Measles)
Important in establishing the diagnosis if the patient is pregnant or has been in contact c a pregnant woman Peaks in late winter to early spring Contagious from a few days before the rash to a few days after the rash Incubation period days Complications - rare in childhood - arthritis, purpura thrombocytopenia, mild encephalitis
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rubella (german Measles)
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Congenital Rubella Syndrome
Deafness Ocular - Cataract , Retinopathy Heart – PDA , Pulmonary artery stenosis , Pulmonary valve stenosis Low birth weight Neonatal Purpura
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Varicella (chickenpox)
Caused by varicella-zoster virus Highly contagious Brief prodrome of low-grade fever, URI symptoms, and mild malaise may occur Rapid appearance of puritic exanthem
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varicella (chickenpox)
Lesions appear in crops - typically have 3 crops Crops begin in trunk and scalp, then spread peripherally Lesions begin as tiny erythematous papules, then become vesicles surrounded by red halos Lesions began to dry - umbilicated appearance, then surrounding erythema fades and a scab forms
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varicella (chickenpox)
Hallmark - lesions in all stages of evolution All scabs slough off days Scarring not typical unless superinfected Cluster in areas of previous skin irritation Puritic lesions on the skin Painful lesions along the oral, rectal, and vaginal mucosa, external auditory canal, tympanic membrane
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Varicella Lesions
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varicella (chickenpox)
Occurs year-round, peaks in late autumn and late winter through early spring Incubation period ranges from days Contagious 1-2 days prior to rash until all lesions are crusted over Complications - secondary bacterial skin infections (GAS), pneumonia, hepatitis, encephalitis, Reye syndrome
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varicella (chickenpox)
Severe in the immunocompromised host - can be fatal Can have severe CNS, pulmonary, generalized visceral involvement (often hemorrhagic) Need to get varicella-zoster immunogloblin 96 hours post-exposure to possible varicella
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varicella (chickenpox)
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Adenovirus 30 distinct types
Variety of infections including conjunctivitis, URIs, pharyngitis, croup, bronchitis, bronchiolitis, pneumonia (occ fulminant), gastroenteritis, myocarditis, cystitis, encephalitis Can be accompanied by a rash - variable in nature Typically can see - conjunctivitis, rhinitis, pharyngitis c or s exudate, discrete, blanching, maculopapular rash
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adenovirus Can see anterior cervical and preauricular LAD, low-grade fever, malaise Peak season is late winter through early summer Contagious during first few days Incubation period 6-9 days
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Coxsackie hand-foot-and-mouth disease
Brief prodome - low-grade fever, malaise, sore mouth, anorexia 1-2 days later, rash appears Oral lesions - shallow, yellow ulcers surrounded by red halos Cutaneous lesions - begin as erythematous macules then evolve to small, thick-walled, grey vesicles on an erythematous base
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Coxsackie hand-foot-and-mouth disease
Highly contagious Incubation period 2-6 days Lasts 2-7 days Peak season summer through early fall If no cutaneous lesions - herpangina less painful and less intense than herpes gingivostomatitis
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erythema infectiosum (fifth disease)
Caused by Parvovirus B19 Affects preschool and young school aged children Peak incidence in late winter and early spring, but it is seen year round Characterized by rash - large, bright red, erythematous patches over both cheeks - warm, but non-tender
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erythema infectiosum (fifth disease)
Facial rash fades, then see a symmetrical, macular, lacy, erythematous rash on the extremities Resolution occurs within 3-7 days of onset Transmitted by respiratory secretions, replicates in the RBC precursors in the bone marrow Can cause aplastic crisis in patients with sickle cell disease, other hemogloblinopathies, and other forms in hemolytic anemia
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erythema infectiosum (fifth disease)
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Question 10 month old infent is seen in clinic with history of fever up to C (103 F ) for past 3 days . The child is playful and physical exam is unremarkable except for fever . No sick contacts at home . She does not attend day care .Of the folowing most likely virus causing this childs fever 1.Parvo virus 2. Herpes Simplex Virus 3. HHV-6 4. Epstein Barr virus (EBV ) 5. Cytomegalovirus
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roseola infantum (exanthem subitum)
Febrile illness affecting children 6-36 months Human herpesvirus 6 is causative agent Symptoms include: fever, usually >39 anorexia irritability these symptoms subside in 72 hours
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roseola infantum (exanthem subitum)
As fever defervenscences, usually an erythematous, maculopapular rash that appear on the trunk and then spread to the extremities, face, scalp, and neck Occurs year-round More common in late fall and early spring Incubation period thought to be days
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roseola infantum (exanthem subitum)
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Infectious mononucleosis
Acute self-limiting illness of children and young adults Caused by EBV Transmission by oral contact, sharing eating utensils, transfusion, or transplantation Incubation period days (shorter, days, in transfusion-acquired infection) Don’t usually see “classic mono” in young children
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Infectious mononucleosis
Prodrome - fatigue, malaise, anorexia, HA, sweats, chills lasting 3-5 days Symptoms fever - can have wide daily fluctuations pharyngitis c tonsillar and adenoidal enlargement c or s exudate, halitosis, palatal petechiae LAD - anterior cervical and posterior cervical - in classic cases, generalized LAD toward end of wk 1
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Infectious mononucleosis
Symptoms cont: splenomegaly - develops in 50% of patients in 2nd-3rd wk hepatomegaly in 10% of patients exanthem - erythematous, maculopapular, rubelliform rash in 5-10% of patients
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Infectious mononucleosis
Complications: pneumonia hemolytic anemia and thrombocytopenia icteric hepatitis acute cerebellar ataxia, encephalitis, aseptic meningitis, myletis, Guillain-Barre rarely myocarditis and pericarditis
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Infectious mononucleosis
Complications cont: upper airway obstruction from tonsillar and adenoidal enlargement seen more often in younger patients children < 5 yrs of age c obstruction are more likely to have secondary OM, recurrent bouts of OM, tonsillitis, and sinusitis splenic rupture
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Infectious mononucleosis
Diagnosis: classic finding - lymphocytosis (50% or more) c 10% atypical lymphocytes 80% or more of patients c elevated liver enzymes Monospot - detects heterophil antibodies - specific, not as sensitive - 85% of adolescents + and fewer younger patients specific EBV antibody titers and PCR
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Infectious mononucleosis
DDx If fever and exudative tonsillitis predominate GAS, diphtheria, viral pharyngitis If LAD and splenomegaly predominate CMV, toxo, malignancy, drug-induced mono If severe hepatic involvement viral hepatitis, leptospirosis
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herpes simplex infections
Primarily involve the skin and mucous surfaces Can be disseminated in neonates and immunocompromised hosts Produces primary infection - enters a latent or dormant stage, residing in the sensory ganglia - can be reactivated at any time
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herpes simplex infections
HSV-1 >90% of primary infections caused by HSV-1 are subclinical more common HSV-2 usually the genital pathogen usual pathogen of neonatal herpes
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herpes simplex infection
Diagnosis usually made clinically can scrap base of vesicle and a special stain - Giemsa-stained (Tzanck) ballooned epithelial cells c intranuclear inclusions and multinucleated giant viral cultures take hours
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Primary herpes simplex infections
Herpetic gingivostomatitis high fever, irritability, anorexia, mouth pain, drooling in infants and toddlers gingivae becomes intensely erythematous, edematous, friable and tends to bleed small yellow ulcerations c red halos seen on buccal and labial mucosa, tongue, gingivae, palate, tonsils
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primary herpes simplex infections
Herpetic gingivostomatitis yellowish white debris builds on the mucosal surfaces causing halitosis vesiculopustular lesions on perioral surfaces anterior cervical and tonsillar LAD symptoms last 5-14 days, but virus can be shed for weeks following resolution
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primary herpes simplex infections
Skin infections fever, malaise, localized lesions, regional LAD direct inoculation (usually cold sores) lesions are deep, thick-walled, painful vesicles on an erythematous base - usually grouped, but may be single lesions evolve over several days - pustular, coalesce, ulcerate, then crust over
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primary herpes simplex infections
Skin infections most common sites are lips and fingers or thumbs (herpes whitlow) eyelids and periorbital tissue infection can lead to keratoconjunctivitis - dx by dendritic ulcerations on slit lamp exam can lead to visual impairment - consult ophtho
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Recurrent herpes simplex infection
Triggers include fever, sunlight, local trauma, menses, emotional stress Seen most commonly as cold sores Prodrome of localized burning, itching or stinging before eruption of grouped vesicles
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recurrent herpes simplex infection
Vesicles contain yellow, serous fluid and are often smaller and less thick-walled than the primary lesions Vesicular fluid becomes cloudy after 2-3 days, then crusts over Regional, tender LAD
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herpes zoster (shingles)
Caused by varicella-zoster virus After primary infection, virus lies dormant in genome of sensory nerve root cell Postulated triggers include mechanical and thermal trauma, infection, debilitation as well as immunosuppression Lesions are grouped, thin-walled vesicles on an erythematous base distributed along the course of a spinal or cranial nerve root (dermatome)
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herpes zoster (shingles)
Lesions evolve from macule to papule to vesicle then crusted over a few days May have associated nerve root pain - not common in pediatrics - usually short-lived unless it involves a cranial nerve root dermatome +/- fever or constitutional symptoms Regional LAD common
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herpes zoster (shingles)
Thoracic, cervical, trigeminal, lumbar, facial nerve dermatomes (order of frequency) If cranial nerve involvement - prodrome of severe HA, facial pain, or auricular pain prior to the eruption Affected patients can transmit varicella, but less of a problem b/c lesions are often covered by clothing and the o/p is not involved in most cases
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herpes zoster (shingles)
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