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Common Viral Exanthemas (Measles, Chickenpox & Rubella) : DR Sarika Gupta (MD, PHD), Assistant Professor

This document discusses common viral exanthemas including measles, chickenpox, and rubella. It provides details on the etiology, pathogenesis, transmission, clinical features, diagnosis, complications, treatment, and prevention of measles. Key points include that measles is caused by a paramyxovirus, has an incubation period of 8-12 days, and symptoms include Koplik's spots, a maculopapular rash, and complications can include pneumonia and encephalitis. Rubella is caused by a togavirus and can cause fetal damage and congenital rubella syndrome if a woman is infected during pregnancy.

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0% found this document useful (0 votes)
157 views52 pages

Common Viral Exanthemas (Measles, Chickenpox & Rubella) : DR Sarika Gupta (MD, PHD), Assistant Professor

This document discusses common viral exanthemas including measles, chickenpox, and rubella. It provides details on the etiology, pathogenesis, transmission, clinical features, diagnosis, complications, treatment, and prevention of measles. Key points include that measles is caused by a paramyxovirus, has an incubation period of 8-12 days, and symptoms include Koplik's spots, a maculopapular rash, and complications can include pneumonia and encephalitis. Rubella is caused by a togavirus and can cause fetal damage and congenital rubella syndrome if a woman is infected during pregnancy.

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ashigha
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We take content rights seriously. If you suspect this is your content, claim it here.
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COMMON VIRAL

EXANTHEMAS (MEASLES,
CHICKENPOX & RUBELLA)

Dr SARIKA GUPTA (MD,PhD),Assistant Professor


Measles-Etiology
 An acute viral disease
 Highly contagious
 Measles virus is a single-stranded, lipid-enveloped
RNA virus in the family Paramyxoviridae and
genus Morbillivirus
 Humans are the only host of measles virus
 Maintenance of >90% immunity through vaccination-
NO OUTBREAKS
Measles-Pathogenesis
 Necrosis of the respiratory tract epithelium & an
accompanying lymphocytic infiltrate
 Small vessel vasculitis on the skin & on the oral
mucous membranes
 Warthin-Finkeldey giant cells: pathognomonic for
measles, formed by fusion of infected cells, with up
to 100 nuclei and intracytoplasmic and intranuclear
inclusions
 Measles virus also infects CD4+ T cells, resulting in
suppression of the Th1 immune response
Measles-Pathogenesis
 4 phases:
Incubation period
Prodromal illness
Exanthematous phase
Recovery
Measles-Pathogenesis
Measles-Transmission

 Through the respiratory tract or conjunctivae


 Following contact with large droplets or small-droplet
aerosols in which the virus is suspended
 Patients are infectious from 3-4 days before to up
to 4-6 days after the onset of rash
Measles-Clinical Features
 High fever, an enanthem, cough, coryza,
conjunctivitis & a prominent exanthem
 Incubation period: 8-12 days
 Prodromal phase: mild fever, conjunctivitis with
photophobia, coryza, a prominent cough & KOPLIK’S
SPOTS
 Koplik spots: enanthem & the pathognomonic sign of
measles
 Appear 1 to 4 days prior to the onset of the rash
 Discrete red lesions with bluish white spots in the
center on the inner aspects of the cheeks at the level
of the premolars
Measles-Clinical Features
 Koplick’s spots: spread
to involve the lips,
hard palate & gingiva
 They also may occur
in conjunctival folds
Measles-Clinical Features
 Temperature rises abruptly as rash appears & may
reach upto 40OC
 Measles rash: generalized, maculopapular,
erythematous, confluent
 The rash begins on the face around
the hairline & behind the ears
 It then spreads downward
to the neck, trunk, arms, legs
& feet over next 24-48 hours
Measles-Clinical Features

 The rash fades over about 7 days in the same


progression as it evolved
 Leaves a fine, browny, branny desquamation of skin
 Severity of disease: related to the extent &
confluence of rash
 Rash: may be absent in immunocompromised children
 Hemorrhagic measles (black measles): bleeding from
mouth, nose or bowels
Measles-Clinical Features

 Diarrhoea: more common in malnourished & small


children
 Severe cases: generalized lymphadenopathy including
cervical & mesenteric lymph nodes
 Mild splenomegaly
Measles-Diagnosis
 Almost always based on clinical and epidemiologic
findings (history of contact)
 Fever of at least 3 days with at least one of three C
(cough, coryza, conjuctivitis)
 Decreased total white blood cell count, with relative
lymphocytosis
Measles-Diagnosis
 IgM antibody in serum: appears 1-2 days after the
onset of the rash & remains detectable for about
1 mo
 Demonstration of a fourfold rise in IgG antibodies in
acute & convalescent specimens collected 2-4 wk
later
 Viral isolation from blood, urine or respiratory
secretions by culture or rt-PCR
Measles-Differential Diagnosis

 Rubella-rashes & fever are less striking


 Roseola infantum (exanthem subitum)- rash appear as
the fever disappears
 Echovirus
 Coxsachie
 Adenovirus
 Infectious mononucleosis
 Scarlet fever-diffuse fleshy papular rash with “goose
flesh” texture
Measles-Differential Diagnosis
 Meningococcemia-rashes are similar but NO
conjuctivitis & cough
 Kawasaki disease- no cough, elevations of neutrophils
and acute-phase reactants; the characteristic
thrombocytosis
 Drug fever
Measles-Complications
 Due to the pathogenic effects of the virus on the
respiratory tract & immune system
Risk factors for complications
 Children <5 years of age & adults >20 years of age
 Severe malnutrition
 Vitamin A deficiency
 Immunocompromised persons
Measles-Complications

 Pneumonia- giant cell pneumonia (direct viral


infection) or superimposed bacterial infection
(Streptococcus pneumoniae, Haemophilus influenzae
& Staphylococcus aureus)
 Croup, tracheitis or bronchiolitis
 Acute otitis media
 Sinusitis and mastoiditis
 Retropharyngeal abscess
 Activation of pulmonary tuberculoses
Measles-Complications

 Diarrhea & vomiting


 Appendicitis- obstruction of the appendiceal lumen
by lymphoid hyperplasia
 Febrile seizures
 Encephalitis- 1-3/1,000 cases of measles;
postinfectious, immunologically mediated process, not
due to a direct viral effect
Measles-Complications

 Measles encephalitis in immunocompromised patients-


from direct damage to the brain by the virus
 Thrombocytopenia
 Myocarditis
 Bacteremia, cellulitis & toxic shock syndrome
 Measles during pregnancy-high maternal morbidity,
fetal wastage & stillbirths & congenital
malformations in 3% of live born infants
Measles-SSPE
 Fatal degenerative disease of central nervous system
 Chronic complication of measles
 Result from a persistent infection with an altered
measles virus that is harbored intracellularly in the
CNS for several years
 Usually after 7-10 year the virus apparently regains
virulence & attacks the cells in the CNS
 Change in personality, gradual onset of mental
deterioration & myoclonus
 Measles vaccination protects against SSPE
Measles-Treatment
 SUPPORTIVE
 Maintenance of hydration, oxygenation & comfort
 Antipyretics-comfort and fever control
 Vitamin A supplementation-reduced morbidity and
mortality from measles
 Single dose of 200,000 IU orally for children
≥1 yr of age (100,000 IU for children 6 mo–1 yr
of age and 50,000 IU for infants <6 mo of age)
Measles-Prevention
 Isolation- from 7 days after exposure to 4-6 days after
the onset of rash
 Vaccine or immunoglobulin- vaccine is effective in
prevention or modification of measles only if given within
72 hr of exposure. Immune globulin may be given up to 6
days after exposure to prevent or modify infection.
 Immune globulin-for susceptible household contacts
younger than 6 months of age, pregnant women &
immunocompromised persons
 Immunization during an outbreak-immunize infant as
young as 6 months of age; additional dose at 12-15
months of age
Rubella
 Rubella (German measles or 3-day measles)
 Mild exanthematous disease of infants & children
 Major clinical significance- fetal damage as part of
the congenital rubella syndrome
 Etiology: Rubella virus; RNA virus of genus Rubivirus
under family Togaviridae
 Humans are the only known host
Rubella-Epidemiology
 Transmission-through oral droplet or transplacental
route
 Virus is shed in nasopharyngeal secretions 7 days
before exanthem & upto 7-8 days after its
disappearance
 Rubella susceptibility among women of child bearing
age in India- 4%-43%
Rubella-Pathogenesis
 Infection virus replication in the respiratory
epithelium spreads to regional lymph nodes
viremia viral shedding from the nasopharynx
 Cellular & tissue damage in the infected fetus: tissue
necrosis, reduced cellular multiplication time,
chromosomal breaks & production of a protein
inhibitor causing mitotic arrests
 Most distinctive feature of congenital rubella:
chronicity
 Ongoing tissue damage and reactivation
Rubella
 Risk factor for severe congenital defects: stage of
gestation at the time of infection
 Maternal infection during the 1st 8 wk of gestation:
most severe & widespread defects
 Risk for congenital defects: 90% for maternal
infection before 11 wk of gestation, 33% at 11-
12 wk, 11% at 13-14 wk & 24% at 15-16 wk
 After 16 wk of gestation: defects uncommon
Rubella-Clinical Features
POSTNATAL INFECTION
 Incubation period: 14-21 days
 Prodrome: low-grade fever, sore throat, red eyes with
or without eye pain, headache, malaise, anorexia &
lymphadenopathy (suboccipital, postauricular &
anterior cervical lymph nodes)
 Rash: begins on the face & neck as small, irregular
pink macules that coalesce & it spreads centrifugally
to involve the torso & extremities, where it tends to
occur as discrete macules
Rubella-Clinical Features
 Rash: fades from the face as it extends to the rest
of the body so that the whole body may not be
involved at any 1 time
 The duration of the rash is generally 3 days & it
resolves without desquamation
Rubella-Clinical Features
 About the time of onset of the rash, examination of
the oropharynx- reveal tiny, rose-colored lesions
(Forchheimer spots) or petechial hemorrhages on the
soft palate
 Subclinical infections are common (25-40%)
 Polyarthritis or arthralgia-common in adult females
 Lab findings: Leukopenia, neutropenia & mild
thrombocytopenia
Rubella-Differential Diagnosis
 Mild form of measles
 Scarlet fever
 Roseola infantum
 Enteroviral infections
 Drug fever
 Infectoius mononucleosis
 Erythema infectiosum
Rubella-Diagnosis
 Supportive history of exposure or consistent clinical
findings
 Rubella specific IgM enzyme immunosorbent assay (4-72
days)
 Fourfold rise in IgG in sequential sera
 Rubella virus culture from nasopharynx & blood by tissue
culture system or PCR
 WHO definition of PROBABLE infection: fever,
maculopapular rash, lymphadenopathy or
arthralgia/arthritis
 WHO definition of CONFORMED infection: probable
case with IgM positivity within 28 days of onset of rash
Rubella-Complications
 Postinfectious thrombocytopenia 
 Arthritis- classically involves the small joints of the
hands
 Encephalitis-a postinfectious syndrome following acute
rubella & a rare progressive panencephalitis
manifesting as a neurodegenerative disorder years
following rubella
 Guillain-Barré syndrome, peripheral neuritis
 Myocarditis
Congenital Rubella Syndrome
 Result of in utero fetal infection
 Classical CRS triad: cataract, sensorineural hearing
loss & congenital heart disease
Clinical manifestations:
 Intrauterine growth restriction, postnatal mental &
motor retardation
 Bilateral/unilateral cataract, salt-and-pepper
retinopathy, microphthalmia
 Nerve deafness
 Meningoencephalitis at birth
Congenital Rubella Syndrome
 Patent ductus arteriosus, pulmonary artery stenosis,
VSD & ASD, myocarditis
 Hepatitis
 Dermal erythropoiesis (blueberry muffin lesions)
 Thrombocytopenic purpura
 Anemia
 Hepatosplenomegaly
 Microcephaly
 Interstitial pneumonitis
 Delayed manifestations: Diabetes mellitus (20%),
thyroid dysfunction (5%)
Rubella-Treatment
 No specific treatment available for either acquired
rubella or CRS
 Supportive treatment- antipyretics and analgesics
 Intravenous immunoglobulin or corticosteroids-for
severe, nonremitting thrombocytopenia
 Hearing screening- important, early intervention
improve outcomes
Rubella-Treatment
Management of exposed pregnant women
 Rubella antibody status is tested immediately result
positive mother is immune no further action
 Rubella antibody status negative repeat samples
after 1-2 weeks negative 1st specimen & positive
test result in either the 2nd or 3rd specimen
seroconversion suggesting recent infection
termination of pregnancy
Rubella-Treatment
Management of congenital rubella syndrome
 Children with CRS may excrete the virus in
respiratory secretions up to 1 yr of age
 Isolation & contact precautions maintained unless
repeated cultures of urine and pharyngeal secretions
have negative results
 Isolation at home my be required for 1 year
 Care of CRS infants require multidisciplinary team
 Prognosis poor
 PREVENTION by IMMUNIZATION
Chickenpox (Varicella)
 Varicella is an acute febrile rash illness
 Caused by VZV which is a neurotropic human α-
herpesvirus
 Secondary attack rate: 90%
 Transmission: by airborne spread or through direct
contact with skin lesions
 Varicella results from inoculation of the virus onto the
mucosa of the upper respiratory tract & tonsillar
lymphoid tissue
Chickenpox-Pathogenesis
Chickenpox (Varicella)
 Transportation of virus in a retrograde manner through
sensory axons to the dorsal root ganglia throughout the
spinal cord establishment of virus latent
infection in the neurons subsequent reactivation 

herpes zoster, a vesicular rash that usually is


dermatomal in distribution
Chickenpox-Clinical Fetures
 Prodromal symptoms: fever (moderate), malaise,
anorexia, headache & occasionally mild abdominal pain,
24-48 hours before the rash appears
 These symptoms resolve within 2-4 days after the
onset of the rash
 Varicella rash often appear first on the scalp, face, or
trunk
 The initial exanthem consists of intensely pruritic
erythematous macules that evolve through the papular
stage to form clear, fluid-filled vesicles
 Clouding & umbilication of the lesions begin in 24-48 hr
Chickenpox-Clinical Fetures
 While the initial lesions are crusting, new crops form on
the trunk & then the extremities
 The simultaneous presence of lesions in various
stages of evolution is characteristic of varicella
 The distribution of the rash is predominantly central
or centripetal

Pearl on a rose patel


Chickenpox-Clinical Fetures
 The average number of varicella lesions is about 300
(10-1500)
 Hypopigmentation or hyperpigmentation of lesion sites
persists for days to weeks in some children
 Severe scarring is unusual unless the lesions were
secondarily infected
Chickenpox-Differential Diagnosis

Vesicular rashes caused by


 Herpes simplex virus
 Enterovirus
 Rickettsial pox
 S. aureus
 Drug reactions
 Contact dermatitis
 Insect bites
Chickenpox-Diagnosis
 CLINICAL
 Leukopenia during the 1st 72 hours after onset of
rash; followed by a relative & absolute lymphocytosis
 Elevated hepatic enzymes
 Specific diagnosis of VZV infection: needed in
immunocompromised children
Chickenpox-Complictions
 Mild thrombocytopenia, petechiae (common); purpura,
hemorrhagic vesicles, hematuria & gastrointestinal
bleeding (rare)
 Cerebellar ataxia, encephalitis, Guillian-Barre
syndrome, transverse myelitis
 Pneumonia
 Nephritis, nephrotic syndrome, hemolytic-uremic
syndrome
 Arthritis
 Myocarditis, pericarditis
 Pancreatitis
Chickenpox-Complictions
 Orchitis
 Secondary bacterial infections of the skin (group A
streptococci & S. aureus): impetigo, cellulitis,
lymphadenitis & subcutaneous abscesses; varicella
gangrenosa- more invasive skin infections
Congenital Varicella Syndrome
 In infants born to women who have varicella before
20 wk of gestation
Characterized by
 Cicatricial skin scarring in a zoster-like distribution,

limb hypoplasia
 Neurologic abnormalities: microcephaly, cortical

atrophy, seizures & mental retardation


 Eye abnormalities: chorioretinitis, microphthalmia &

cataracts
 Renal abnormalities: hydroureter & hydronephrosis

 Autonomic nervous system abnormalities: neurogenic

bladder, swallowing dysfunction & aspiration pneumonia


Chickenpox-Complictions
 If a baby is born <4 days after onset of maternal
varicella or upto 2 days before the onset: high risk
for severe varicella & a high mortality rate
Chickenpox-Treatment
 Supportive treatment for fever & itching
Indications for acyclovir in children:
 Malignancies
 BMT
 Chmotherapy or high dose steroid treatment
 HIV infection
 Severe vaicella
 Chronic skin disease
 Long term salicylate therapy
 Chlidren >12 years
Treatment should be initiated within 24 hr of the onset of
rash
Chickenpox-Treatment
 Foscarnet is the only drug for the treatment of
acyclovir-resistant VZV infections (in children infected
with HIV)
Chickenpox-Prevention
 Since persons with chickenpox are infectious for 1-2
days before the onset of rash isolation only reduces the
spread
 Individual protection NECESSARY (vaccine)

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