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Measles:
anOverview
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Case 1
7 month female
From East RandPresented on 02/10/2003
Previously well
Not yet immunised against measles5 day history upper respiratory tract infectionsymptoms
Rash for 2 days went to clinic
Referred to JHB Hospital with serological evidenceof measles infection
No known contacts
Also had vomiting, diarrhoea
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On examinationThriving
Colour, hydration adequate
Miserable
Watering eyes, bilateral inflamed tympanic membranes
Rhinitis, nasal discharge
Shotty cervical lymphadenopathy
Cough, but no respiratory distress or chest signsDiffuse maculopapular rash, confluent areas, starting to turnbrown in some areas
Course
Patient admitted to ensure adequate fluid intakeDay 2 less vomiting
Ruptured left tympanic membrane
Discharged on Augmentin, Panado
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Case 2
8 year old boyFrom central JHB
Known HIV positive patient
Recent history cough, fever, malaise, poorappetite, sores on lips
Known TB contact father (on treatment)
Investigated for TB 1 month before
negativeNo known measles contacts
Apparently immunisations up to date
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On examinationToxic, but not marked respiratory distress
Reasonably wellgrown
Pink on nasal prong oxygen
Dry mucous membranes
Generalised lymphadenopathy
Not jaundiced
Diffuse scars/pigmentation from old rashes/folliculitisExcoriated lesion right forearm not from recent PPD
Head and neck
Severe conjunctivitis, no discharge
Unable to open mouth extensive labial sores Herpeslesions
Chest
Evidence of right upper lobe, left lingular pneumonia
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Cardiovascular system Mild cor pulmonale
Abdomen Generally tender, 4cm tender hepatomegaly
Central Nervous System Cooperative
Generalised decreased power
No neck stiffness No focal signs
ManagementTreated for bacterial pneumonia
Lasix for cardiac failure
Investigated for TB
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Course
Deteriorated in wardDay 3 noted to have swollen, red lips, circumoralerythema
Discharging eyes, unable to open them
? new rash on trunk difficult to seeIll-looking, more drowsy, withdrawn but rousable
Lumbar puncture performed, given Vitamin A, measlesserology sent
ResultsDay 6- patient demised; terminal event unknown
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Results
02/10/2003 WCC 10,7
Hb 10,1
Plts 257
CRP 160,3 U&E
128/4,3/96/14/7,9/45
06/10/2003 WCC 8,6
Hb 10,5
Plts 320
CRP 323
CSF no cells, normal,ADA 2,6
Blood cultures negative
Sputum negative Tuberculin skin test -
neg
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Measles(Rubeola)
Measles virus, genus Morbillivirus, familyParamyxoviridae
One serotype, humans only host
Virions spherical structures, 100 250 nmdiameter
Inner capsid composed of coiled RNA helix, 3proteins
Outer envelope matrix protein bearinghaemagglutinin(H) peplomer, fusion(F)protein (NB in cytopathic effects of virus)
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Epidemiology
Important cause of childhood mortality in developingcountriesBefore vaccine developed (1963) epidemics every 2 5 years, winter and springEpidemic - up to half a million cases reportedDeveloping countries mortality rate 1 10%Developed countries 0,3%Much fewer cases since live attenuated virus vaccinedeveloped
Developed countries Measles almost eradicated Outbreaks in older children, young adults, eg. College
campuses
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Developing countries Common, endemic, increases in winter and spring
First year of life, even 6 months of age
Sporadic cases, or outbreaks extensive
Epidemics facilitated by inadequate immunity, overcrowding
More cases complicated
Epidemics occur due to
Failure to immunise Primary vaccine failure (5%)
Waning immunity (rare)
Highly contagious, respiratory secretions
Contagious from 1-2 days before symptoms, 4 days after onset
of rashProdrome most infectious
Quarantine period 1 week after rash appears, longer forcomplicated measles
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Pathogenesis
Portal of entry respiratory tractRegional lymph nodesEnters bloodstream reticuloendothelial system(primary viraemia) target organs (secondaryviraemia)
Target organs epithelial, endothelial cellsEyes, skin, respiratory tract, gastrointestinal tract,including mouthEndothelial cells vasculitis
Koplik spots, rash due to immune responseto virus inendothelial cellsImmunocompromised patients may have norash
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Virus directly invades T lymphocytes lymphopenia
Decreases neutrophil function, chemotaxis
Decreased T helper cells - decreased reactivity toPPD
Fusionprotein causes typical multinucleated giantcells; also aids viral spread from cell to cell
Damage to entire respiratory tract + immuneparesis secondary bacterial infections
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Clinical features
Usually symptomatic
Incubation period (infection to symptoms) : 9-12 daysProdrome : 2-4 days Nonspecific symptoms fever, malaise, anorexia, headache Classical triad cough, coryza, conjunctivitis (with photophobia,
lacrimation)Enanthem: Koplik spots Just before rash appears 1-2 mm, bluish-white, bright red background
Buccal mucosa, opposite 2nd
molars Pathognomonic for measles Disappear soon after rash appears Entire buccal, labial mucosa may be reddened
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Exanthem:
Erythematous, non-pruritic, maculopapular
Hairline, behind ears
trunk
limbs, includingpalms, soles
Confluent, blotchy
Most ill at this time
Day 4 starts to fade (in order of appearance),turns brownish, desquamates
Fever settles after 4-5 days if persists, suspectsecondary infection
Lymphadenopathy, splenomegaly, diarrhoea, vomitingChest Xray may be abnormal, even in uncomplicatedcases
Entire illness 10 days
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Complications
1)Respiratory TractOtitis media most common
Laryngitis, croup, bronchitis due to measles itself
Secondary pneumonia viral,bacterial
Primary giant cell pneumonia due to measles (rare)
immunocompromised, malnourished patientsReactivation of TB
2)Gastrointestinal TractGastroenteritis can be severe, especially in already
malnourished patientsProtein-losing enteropathy
Mouth reactivation of Herpes severe stomatitis
Hepatitis, ileocolitis, appendicitis, mesenteric adenitis
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3)Eye Malnourished especially at risk Keratitis, keratoconjunctivitis Cause of blindness 3rd world Vitamin A preventive role in respect of infection
4)CNS Encephalitis uncommon Fever, headache, drowsiness, coma, seizures Earlier - direct viral effect in CNS Later immune response causing demyelination Significant morbidity, permanent sequelae mental retardation,
epilepsy Rarely transverse myelitis Subacute sclerosing panencephalitis extremely rare, 6-10 years
after infection. Progressive dementia, fatal. Interaction of hostwith defective form of virus
5)Other Glomerulonephritis, myocarditis, postinfective thrombocytopenic
purpura
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Lab findings
FBC, differential lymphopenia, neutropeniaU&E deranged due to dehydrationRaised transaminasesMeasles encephalitis raised protein, lymphocytes inCSF
Virus detection Microscopy of respiratory epithelial cells (throat swab)
giant cells Immunofluorescence detects Measles antigens Culture virus from respiratory secretions/ urine (1-2 weeks)
Serology IgM (1-2 days after onset of rash) IgG (rises after 10 days)
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Differential Diagnosis
Classic Measles Koplik spots, coryza, cough, conjunctivitisKawasaki disease, Scarlet fever, Ebstein Barr virus,Toxoplasmosis, drug reaction, MycoplasmaHistory of immunisation important
IMMUNITY TO MEASLESCell-associated virusProtection antibody-mediatedRecovery cell-mediatedImmunity usually lifelong
Passive maternal transfer of IgG shouldprotect up to 1 yearDeveloping countries higher viral burden + accelerateddegradation of antibodies (malnutrition, HIV, chronic immunestimulation) at risk much earlier
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Rationale for vaccination strategies (developing countries): Higher risk during 1st year BUTlower rates of seroconversion (60%
- 6 months, 80% - 9 months, 95% - 15 months)
1st vaccine at 9 months
2nd at 18 months NOTa booster rather a second chance at seroconversion
Developed countries routine MMR at 15 months, 2nd MMR at 4-5 years, or 12 years
The Vaccine: Live attenuated virus
Schwarz egg most common
Edmonston Zagreb (EZ) human diploid cell culture
Subcutaneous
Side effects occasional fever (5-7 days later), transient rash
Cold chain maintenance NB
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Contraindications
Severehypersensitivity to egg protein give EZ instead
Allergy to Neomycin
Severeimmunosuppression chemotherapy, congenital immunedeficiencies.NOTHIV (unless intercurrent severe febrile illness)
Pregnancy teratogenic
Defer
for 3 months after receiving immune globulin
for 6 weeks after receiving blood products
for 3 months after stopping immunosuppressive treatment
Mustgive HIV patients asymptomatic andsymptomatic, malnourishedpatients, TB patients
Failures
Primary failure 5%
Faulty storage
Pre-existing antibodies (maternally derived)
Simultaneous administration of vaccine and immunoglobulin
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Post-exposureWho is susceptible?
Consider susceptible unless: Proof of receipt of 2 doses of live vaccine, or 1 after 1st birthday
Proof of previous diagnosed measles infection
Laboratory evidence of immunity
Vaccinate within 72 hours of exposure
Immune globulin between 72-96 hours after exposure
Treatment
Supportive, symptom-directed
Antibiotics for otitis media, pneumoniaHigh doses Vitamin A in severe/ potentially severe measles/patients less than 2 years
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Measles in the HIV patient
Lower response to vaccineMay acquire lower titres of antibody from mother,higher rate of degradation of maternally acquiredantibodies
More likely malnourished, more susceptible to severeinfection, complications, higher mortality
May have had TB reactivate
If suspecting TB, PPD beforevaccine (anergy up to 1
month after)Measles may hasten progression of HIV