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COMMON VIRAL EXANTHEMAS (MEASLES, CHICKENPOX & RUBELLA) Dr SARIKA GUPTA (MD,PhD),Assistant Professor.

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Presentation on theme: "COMMON VIRAL EXANTHEMAS (MEASLES, CHICKENPOX & RUBELLA) Dr SARIKA GUPTA (MD,PhD),Assistant Professor."— Presentation transcript:

1 COMMON VIRAL EXANTHEMAS (MEASLES, CHICKENPOX & RUBELLA) Dr SARIKA GUPTA (MD,PhD),Assistant Professor

2 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

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4 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

5 Measles-Pathogenesis  4 phases: Incubation period Prodromal illness Exanthematous phase Recovery

6 Measles-Pathogenesis Incubation period: measles virus migrates to regional lymph nodes primary viremia- disseminates 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

7 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

8 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

9 Measles-Clinical Features  Koplick’s spots: spread to involve the lips, hard palate & gingiva  They also may occur in conjunctival folds

10 Measles-Clinical Features  Temperature rises abruptly as rash appears & may reach upto 40 O C  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 hours

11 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

12 Measles-Clinical Features  Diarrhoea: more common in malnourished & small children  Severe cases: generalized lymphadenopathy including cervical & mesenteric lymph nodes  Mild splenomegaly

13 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

14 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

15 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

16 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

17 Measles-Complications  Due to the pathogenic effects of the virus on the respiratory tract & immune system Risk factors for complications  Children 20 years of age  Severe malnutrition  Vitamin A deficiency  Immunocompromised persons

18 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

19 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

20 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

21 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

22 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)

23 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 months of age

24 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

25 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%

26 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

27 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 wk, 11% at wk & 24% at wk  After 16 wk of gestation: defects uncommon

28 Rubella-Clinical Features POSTNATAL INFECTION  Incubation period: 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

29 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

30 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

31 Rubella-Differential Diagnosis  Mild form of measles  Scarlet fever  Roseola infantum  Enteroviral infections  Drug fever  Infectoius mononucleosis  Erythema infectiosum

32 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

33 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

34 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

35 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%)

36 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

37 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

38 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

39 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

40 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

41 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

42 Chickenpox-Clinical Fetures  Prodromal symptoms: fever (moderate), malaise, anorexia, headache & occasionally mild abdominal pain, 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 hr

43 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

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

45 Chickenpox-Differential Diagnosis Vesicular rashes caused by  Herpes simplex virus  Enterovirus  Rickettsial pox  S. aureus  Drug reactions  Contact dermatitis  Insect bites

46 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

47 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

48 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

49 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

50 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

51 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

52 Chickenpox-Treatment  Foscarnet is the only drug for the treatment of acyclovir-resistant VZV infections (in children infected with HIV)

53 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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