Rashes in pediatricsShilpa R Singh MD

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

Transmission

• Respiratory tract or conjunctivae through droplet carrying virus

• Infectious from 3 days before up to 4-6 days after the onset of rash

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

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

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 5 - 6 days

Can see desquimation in severe cases

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

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

rubeola (nine-day or red measles)

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

Treatment and Prevention

• Supportive

• No prophylactic antibiotics

• Vitamin A ( 6 months – 2 yrs , hospilatized , malnutrition other complications )

• Vaccination 2 dosages , 1st dose 12- 15 months , 2nd dose 4 -6 yrs of age

• MMR – live vaccine , do not give to pregnant or immunosuppressed

Rubella (german measles)

Rubella virus (Togaviridae )

Little or no prodrome in children

In adolescents - 1-5 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

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

Forchheimer spot

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 14-21 days

Complications - rare in childhood - arthritis, purpura thrombocytopenia, mild encephalitis

rubella (german Measles)

Congenital Rubella Syndrome

• Deafness

• Ocular - Cataract , Retinopathy

• Heart – PDA , Pulmonary artery stenosis , Pulmonary valve stenosis

• Low birth weight

• Neonatal Purpura

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

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

varicella (chickenpox)

Hallmark - lesions in all stages of evolution

All scabs slough off 10-14 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

Varicella Lesions

varicella (chickenpox)

Occurs year-round, peaks in late autumn and late winter through early spring

Incubation period ranges from 10-20 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

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

varicella (chickenpox)

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

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

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

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

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

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

erythema infectiosum (fifth disease)

Question 10 month old infent is seen in clinic with history of fever up to 39.44 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

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

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 10-15 days

roseola infantum (exanthem subitum)

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 30-50 days (shorter, 14-20 days, in transfusion-acquired infection)

Don’t usually see “classic mono” in young children

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

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

Infectious mononucleosis

Complications:

pneumonia

hemolytic anemia and thrombocytopenia

icteric hepatitis

acute cerebellar ataxia, encephalitis, aseptic meningitis, myletis, Guillain-Barre

rarely myocarditis and pericarditis

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

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

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

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

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

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 24-72 hours

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

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

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

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

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

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

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)

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

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

herpes zoster (shingles)