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

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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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