2 Myxoviruses Paramyxo viruses Orthomyxo viruses Myxo = affinity to mucinMyxovirusesParamyxo virusesOrthomyxo virusesSmallerSegmented RNA genomeLiable to Agic variationLargerSingle piece of RNANot liable to Agic variation- Parainfluenza- Mumps vairus- Measles virus- Respiratory syncytial virusInfluenza viruses
3 Large Spherical envelopped Unsegmented –ve sense RNAThe lipid envelope is associated with 2-virus specific glycoptns; Haemaglutinin-Neuraminidase (HN) ptn& fusion (F) ptn
4 Respiratory Sncytial Virus Commonest cause of bronchitis & pneumonia among infants< 1yr.Causes repeated infections throughout life, usually associated with moderate- to severe cold –like symptomsSevere lower respiratory tract disease may occur at any age, especially elderly & those with compromised cardiac, pulmonary or immune systems
5 Laboratory DiagnosisSpecimens: nasal secretions-nasopharyngeal aspirate 1- Direct virus demonstration: - DIF: for detection of viral Ag - RT-PCR for detection of viral RNA 2- Viral isolation: - nasal secretions inoculated onto (HeLa) - Growth is recognized by development of CPE in the form of giant cells & syncytia
6 Treatment Symptomatic treatment for mild disease Oxygen therapy & may be mechanical ventilation in children with severe diseaseRibavirin aerosolNo vaccine is yet available
7 Human Parainfluenza Viruses(1,2,3,4) HPIVs are second to RSV as a common cause of lower respiratory tract disease in young childrenSimilar to RSV, HPIVs can cause repeated infections throughout life, usually upper respiratory tract illnessCan also cause severe lower respiratory tract infections ammong immunocompromised patients
8 Each of the four HPIVs has different clinical & epidemiologic features The most distinctive clinical feature of HPIV-1& HPIV-2 is croupHPIV-3 is more associated with bronchiolitis & pneumoniaHPIV-4 is infrequently detected, because it is less likely to cause severe diseaseCroup (laryngotracheobronchitisdifficulty in breathing, hoarseness anda seal bark-like coughing
9 Laboratory DiagnosisSpecimens: nasal secretion-nasopharyngeal aspirate- bronchoalveolar lavage 1- Direct virus demonstration: - DIF: for detection of viral Ag - RT-PCR for detection of viral RNA 2- Viral isolation: - Specimens are inoculated onto (MKTC) - Growth is recognized by hemadsorption using guinea pig RBCs or by direct IF
10 3- Serological tests:Based on Nt, HI, or ELISA for detection of IgM or IgGPaired acute & convalescent sera are necessary for IgG detectionA four fold or more rise in the titre indicates infection
11 Mumps VirussCauses epidemic parotitis ( non suppurative inflammation of parotid)Mode of transmission:Via aerosols & fomitesThe virus is secreted in urine so urine is a possible source of infectionsaliva
12 Pathogenesis & clinical picture Infects children 5-15yearsReplicates in the nasopharynx ®ional LNsIncubation period: 2-25 dLasts 3-5 dviremiaSalivaryPancreasTestesovariesglandsmeningesLong life immunity due to IgG neutralizing Abs
14 Complications Severe aseptic meningitis in adults Orchitis in adult males which might cause sterilityPancreatitisOophritis & thyroiditis
15 Laboratory DiagnosisSpecimens: - saliva - CSF - urine 1- Direct virus demonstration: - RT-PCR for detection of viral RNA 2- Viral isolation: - Specimens are inoculated onto (MKTC) or chick embryo - Growth is recognized by hemadsorption or by direct IF & by characteristic CPE giant cell formation
17 3- serology:ELISA is used for detection of IgM or IgGFor IgG, paired acute & convalescent sera are necessaryFour fold or more rise in IgG titer indicates infection
18 Prevention Active immunization Mumps vaccine Live attenuated Given by subcutaneous injectionLong term immunityMonovalent form or MMR vaccine
19 Measles virus Causes measles (robeola) One of the most contagious respiratory infectionsIt can nearly affect every person (in a given population) by adolescence, in the absence of immunization programsMode of transmission:- Large repiratory droplet-airborneMost infectious in the early stageBefore the rash appears
20 Pathogenesis & clinical picture Replication initially in the upper & lower respiratory tractFollowed by LNs replicationViremia & growth in a variety of epithelial tissueIncubation period: 1-2 wksIn 2-3 days, no rash but fever, running nose, cough & conjunctivitis
21 Koplick spots: slightly raised white dots, 2-3 mm in diameter are seen on the inside of the cheek shortly before rash onset persist for 1-3 daysA characteristic maculopapular rash extending from face to extremities involving palms & soles : this seems to be associated with T-cells attacking virally infected endothelial cells in small blood vesselsThe rash lasts from 3-7 d & may be followed by skin exfoliation
23 Disappear after the rash onset Lasts for 3-7 days 1-Respiratorysymptoms2-3 days2-Koplick spots3-Maculopapular rashPersist 1-3 daysDisappear after the rash onsetLasts for 3-7 days4-Skin exfoliationLong life immunity due to IgG neutralizing Abs
24 The virus invades the body via blood vessels reaches surface epitheliumfirst in the respiratory tract wherethere are only 1-2 layers of epithelial cellsThen in mucosae (Koplik's spots)and finally in the skin (rash).
25 complications I- Respiratory Otitis media & bacterial pneumonia: commonGiant cell pneumonia in patients with impaired CMI ( rare but fatal)II- NeurologicalPostinfectious encephalitis. Few days after the rash (1:1000)Subacute sclerosing panencephalitis (SSPE) (1: )
26 Laboratory DiagnosisSpecimens: nasal secretions-nasopharyngeal aspirate or swab- urine 1- Direct virus demonstration: - DIF: for detection of viral Ag - RT-PCR for detection of viral RNA 2- Viral isolation: - nasal secretions inoculated onto (MKTC) - Growth is recognized by development of CPE in the form of multinucleated giant cells containing both intranuclear & intracytoplasmic IBs
27 3- serology:ELISA is used for detection of IgM or IgGFor IgM single serum specimen 1-2 wks after the rash onsetFor IgG, paired acute & convalescent sera are necessaryFour fold or more rise in IgG titer indicates infection
28 Prevention Passive immunization Measles IGs Active immunization - For immunocompromised patientsIntramuscular within 6 days of exposurePrevent measles symptoms in 80% of casesActive immunizationMumps vaccineLive attenuatedGiven by subcutaneous injectionLong term immunityMonovalent form or MMR vaccine
29 Rubella VirusCauses German measles which is the mildest of common viral exanthemsIt is a member of rubiviruses but not an arbovirusEnvelopped +ve sense ss RNAPosseses hemaglutinating ability
30 Diseases1- German measles: acute febrile illness with rash & lymphadenopathy affecting children & young adults2- Congenital Rubella Syndrome: Serious abnormalities of the fetus as a consequence of maternal infection during early pregnancy
31 Postnatal rubella (German measles) Pathogenesis & clinical picture Mode of transmission: dropletInitial viral replication occurs in the respiratory mucosa followed by multiplication in the cervical lymph nodesViremia develops with spread to other tissues. As a result the disease symptoms develop in 50% of cases after an incubation period of daysPossibly 50% of infections are apparently subclinical
32 Fever & malaise (prodromal symptoms) for 1-2 days Maculopapular rash appears on the face,then the trunk, then the extremities and disappears within 3 daysSuboccipital and postauricular lymphadenopathyExtremely rare complications, self limiting encephalopathy
33 complications Extremely rare (1/6000) Rubella encephalopathy 6 days after the rash appearsComplete recovery with no sequalae
34 Laboratory DiagnosisSpecimens: nasal secretions-nasopharyngeal aspirate or swab 1- Direct virus demonstration: - DIF: for detection of viral Ag - RT-PCR for detection of viral RNA 2- Viral isolation: - nasal secretions inoculated onto (MKTC) - Growth is recognized by interference with coxsakie virus
35 3- serology:ELISA is used for detection of IgM or IgGFor IgM single serum specimenFor IgG, paired acute & convalescent sera are necessaryFour fold or more rise in IgG titer indicates infection
36 Congenital rubellaCongenital rubella is a group of physical problems that occur in an infant when the mother is infected with the virus that causes German measles.
37 Congenital rubella is caused by the destructive action of the rubella virus on the fetus at a critical time in development. The most critical time is the first trimester (the first 3 months of a pregnancy). After the fourth month, the mother's rubella infection is less likely to harm the developing fetus.The rate of congenital rubella has decreased dramatically since the introduction of the rubella vaccine.
38 Risk factors for congenital rubella include: Not getting the recommended rubella immunizationContact with a person who has rubella (also called the 3-day measles or German measles)Pregnant women who are not vaccinated and who have not had rubella risk infection to themselves and damage to their unborn baby.
39 Clinical picture Transient symptoms: growth retardation, anemia & thrombocytopeniaPermanent defects: congenital heart diseases, total or partial blindness, deafness & mental retardationProgressive rubella panencephalitis:Extremely rare slow virus disease, develops in teens with death within 8 yrs
40 Laboratory Diagnosis During Pregnancy After Birth Detection of maternal IgM or rising IgG in serumThen, detection of rubella Ag in the amniotic fluid by DIFLive newborn: detection of IgM antirubella Abs in the serum of the baby by ELISAStillbirth: virus isolation on MKTCDuring PregnancyAfter Birth
41 Prevention of congenital rubella vaccinateWomen in the childbearing ageSchool age childrenPregnancy should be avoided 3 months after vaccinationMaternal rubella infection confirmed during the first trimester????Therapeuticabortion
42 MMR Contains 3 live attenuated viruses: mumps, measles and rubella Given in 2 dosesThe first dose: to children months of age by subcutaneous injectionWhy not before that?When is the second dose?Contraindications?