Transcript Diphtheria, Pertusis & tetanus

COMMON VIRAL
EXANTHEMAS (MEASLES,
CHICKENPOX & RUBELLA)
Dr SARIKA GUPTA (MD,PhD),Assistant Professor
Measles-Etiology
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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 vaccinationNO OUTBREAKS
Measles-Pathogenesis
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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
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4 phases:
Incubation period
Prodromal illness
Exanthematous phase
Recovery
Measles-Pathogenesis
Incubation period: measles virus migrates to
regional lymph nodes
primary viremiadisseminates the virus to the
reticuloendothelial system
secondary
viremia spreads virus to body surfaces
The prodromal illness begins after the
secondary viremia; associated with epithelial
necrosis, giant cell formation & virus shedding
With onset of the rash, antibody production
begins & viral replication & symptoms begin to
subside
Measles-Transmission
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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
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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
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Koplick’s spots: spread
to involve the lips,
hard palate & gingiva
They also may occur
in conjunctival folds
Measles-Clinical Features
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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
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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
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Diarrhoea: more common in malnourished & small
children
Severe cases: generalized lymphadenopathy including
cervical & mesenteric lymph nodes
Mild splenomegaly
Measles-Diagnosis
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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
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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
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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
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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
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Due to the pathogenic effects of the virus on the
respiratory tract & immune system
Risk factors for complications
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Children <5 years of age & adults >20 years of age
Severe malnutrition
Vitamin A deficiency
Immunocompromised persons
Measles-Complications
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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
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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
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Measles encephalitis in immunocompromised patientsfrom 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
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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
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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
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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
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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
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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
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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
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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 1112 wk, 11% at 13-14 wk & 24% at 15-16 wk
After 16 wk of gestation: defects uncommon
Rubella-Clinical Features
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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
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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
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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
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Mild form of measles
Scarlet fever
Roseola infantum
Enteroviral infections
Drug fever
Infectoius mononucleosis
Erythema infectiosum
Rubella-Diagnosis
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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
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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
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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
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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
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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
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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
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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)
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Varicella is an acute febrile rash illness
Caused by VZV which is a neurotropic human αherpesvirus
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
Incubation period (10-21 days): replication
in the local lymphoid tissue
primary
viremia-disseminates the virus to the
reticuloendothelial system
secondary
viremia spreads virus to body surfaces
leading to widespread cutaneous lesions
During the late incubation period-VZV
transported back to the mucosa of the upper
respiratory tract & oropharynx, permitting
spread to susceptible contacts 1-2 days
before the appearance of rash
Host immune responses limit viral replication
and facilitate recovery from infection
Immunocompromised child-continued viral
replication -disseminated infection
Chickenpox (Varicella)
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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
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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
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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
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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
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Vesicular rashes caused by
Herpes simplex virus
Enterovirus
Rickettsial pox
S. aureus
Drug reactions
Contact dermatitis
Insect bites
Chickenpox-Diagnosis
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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
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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
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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
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Chickenpox-Complictions
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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
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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
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Foscarnet is the only drug for the treatment of
acyclovir-resistant VZV infections (in children infected
with HIV)
Chickenpox-Prevention
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Since persons with chickenpox are infectious for 1-2
days before the onset of rash isolation only reduces the
spread
Individual protection NECESSARY (vaccine)