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PARAMYXOVIRUSESDr. Nehal Draz
Myxoviruses
Orthomyxo viruses
Paramyxo viruses
-Smaller-Segmented RNA genome-Liable to Agic variation
-Larger-Single piece of RNA - Not liable to Agic variation
Influenza viruses- Parainfluenza- Mumps vairus- Measles virus- Respiratory syncytial virus
Myxo = affinity to mucin
Large Spherical envelopped
Unsegmented –ve sense RNA
The lipid envelope is associated with 2-virus specific glycoptns; Haemaglutinin-Neuraminidase (HN) ptn& fusion (F) ptn
Respiratory Sncytial Virus
Commonest cause of bronchitis & pneumonia among infants< 1yr.
Causes repeated infections throughout life, usually associated with moderate- to severe cold –like symptoms
Severe lower respiratory tract disease may occur at any age, especially elderly & those with compromised cardiac, pulmonary or immune systems
Laboratory Diagnosis
Specimens: nasal secretions-nasopharyngeal aspirate
1- Direct virus demonstration:- DIF: for detection of viral Ag- RT-PCR for detection of viral RNA2- Viral isolation:- nasal secretions inoculated onto (HeLa)- Growth is recognized by development of
CPE in the form of giant cells & syncytia
Treatment
Symptomatic treatment for mild disease
Oxygen therapy & may be mechanical ventilation in children with severe disease
Ribavirin aerosol
No vaccine is yet available
Human Parainfluenza Viruses(1,2,3,4)
HPIVs are second to RSV as a common cause of lower respiratory tract disease in young children
Similar to RSV, HPIVs can cause repeated infections throughout life, usually upper respiratory tract illness
Can also cause severe lower respiratory tract infections ammong immunocompromised patients
Each of the four HPIVs has different clinical & epidemiologic features
The most distinctive clinical feature of HPIV-1& HPIV-2 is croup
HPIV-3 is more associated with bronchiolitis & pneumonia
HPIV-4 is infrequently detected, because it is less likely to cause severe disease
Croup (laryngotracheobronchitis difficulty in breathing, hoarseness and a seal bark-like coughing
Laboratory Diagnosis
Specimens: nasal secretion-nasopharyngeal aspirate- bronchoalveolar lavage
1- Direct virus demonstration:- DIF: for detection of viral Ag- RT-PCR for detection of viral RNA2- Viral isolation:- Specimens are inoculated onto (MKTC)- Growth is recognized by hemadsorption
using guinea pig RBCs or by direct IF
3- Serological tests: Based on Nt, HI, or ELISA for
detection of IgM or IgG Paired acute & convalescent sera are
necessary for IgG detection A four fold or more rise in the titre
indicates infection
Mumps Viruss
Causes epidemic parotitis ( non suppurative inflammation of parotid)
Mode of transmission: Via aerosols & fomites The virus is secreted in urine so
urine is a possible source of infection
saliva
Pathogenesis & clinical picture
Infects children 5-15years Replicates in the nasopharynx
®ional LNs Incubation period: 2-25 d
viremia
Lasts 3-5 d
meninges
glands
-Salivary-Pancreas-Testes-ovaries
Long life immunity due to IgG neutralizing Abs
Severe aseptic meningitis in adults Orchitis in adult males which might
cause sterility Pancreatitis Oophritis & thyroiditis
Complications
Laboratory Diagnosis
Specimens: - saliva - CSF - urine1- Direct virus demonstration:- RT-PCR for detection of viral RNA2- 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
3- serology: ELISA is used for detection of IgM or
IgG For IgG, paired acute & convalescent
sera are necessary Four fold or more rise in IgG titer
indicates infection
Prevention
Mumps vaccineActive immunization
-Live attenuated-Given by subcutaneous injection-Long term immunity-Monovalent form or MMR vaccine
Measles virus
Causes measles (robeola) One of the most contagious respiratory
infections It can nearly affect every person (in a given
population) by adolescence, in the absence of immunization programs
Mode of transmission: - Large repiratory droplet -airborne
Most infectious in the early stageBefore the rash appears
Pathogenesis & clinical picture
Replication initially in the upper & lower respiratory tract
Followed by LNs replication Viremia & growth in a variety of
epithelial tissue Incubation period: 1-2 wks In 2-3 days, no rash but fever,
running nose, cough & conjunctivitis
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 days
A 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 vessels
The rash lasts from 3-7 d & may be followed by skin exfoliation
2-Koplick spots
3-Maculopapular rash
4-Skin exfoliation
Persist 1-3 daysDisappear after the rash onset Lasts for 3-7 days
1-Respiratorysymptoms
2-3 days
Long life immunity due to IgG neutralizing Abs
The virus invades the body via blood vessels reaches surface epithelium first in the respiratory tract where there are only 1-2 layers of epithelial cells Then in mucosae (Koplik's spots) and finally in the skin (rash).
complications
I- Respiratory Otitis media & bacterial pneumonia:
common Giant cell pneumonia in patients
with impaired CMI ( rare but fatal)II- Neurological Postinfectious encephalitis. Few
days after the rash (1:1000) Subacute sclerosing panencephalitis
(SSPE) (1:100.000)
Laboratory Diagnosis
Specimens: nasal secretions-nasopharyngeal aspirate or swab- urine
1- Direct virus demonstration:- DIF: for detection of viral Ag- RT-PCR for detection of viral RNA2- 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
3- serology: ELISA is used for detection of IgM or
IgG For IgM single serum specimen 1-2
wks after the rash onset For IgG, paired acute & convalescent
sera are necessary Four fold or more rise in IgG titer
indicates infection
Prevention
Active immunization
Mumps vaccine
-Live attenuated-Given by subcutaneous injection-Long term immunity-Monovalent form or MMR vaccine
Passive immunizationMeasles IGs
- For immunocompromised patients-Intramuscular within 6 days of exposure-Prevent measles symptoms in 80% of cases
Rubella Virus
Causes German measles which is the mildest of common viral exanthems
It is a member of rubiviruses but not an arbovirus
Envelopped +ve sense ss RNA Posseses hemaglutinating ability
Diseases
1- German measles: acute febrile illness with rash & lymphadenopathy affecting children & young adults
2- Congenital Rubella Syndrome: Serious abnormalities of the fetus as a consequence of maternal infection during early pregnancy
Postnatal rubella (German measles) Pathogenesis & clinical picture
Mode of transmission: droplet Initial viral replication occurs in the
respiratory mucosa followed by multiplication in the cervical lymph nodes
Viremia develops with spread to other tissues. As a result the disease symptoms develop in 50% of cases after an incubation period of 12-23 days
Possibly 50% of infections are apparently subclinical
Fever & malaise (prodromal symptoms) for 1-2 days
Maculopapular rash appears on the face,then the trunk, then the extremities and disappears within 3 days
Suboccipital and postauricular lymphadenopathy
Extremely rare complications, self limiting encephalopathy
complications
Extremely rare (1/6000) Rubella encephalopathy 6 days after the rash appears Complete recovery with no sequalae
Laboratory Diagnosis
Specimens: nasal secretions-nasopharyngeal aspirate or swab
1- Direct virus demonstration:- DIF: for detection of viral Ag- RT-PCR for detection of viral RNA2- Viral isolation:- nasal secretions inoculated onto
(MKTC)- Growth is recognized by interference
with coxsakie virus
3- serology: ELISA is used for detection of IgM or
IgG For IgM single serum specimen For IgG, paired acute & convalescent
sera are necessary Four fold or more rise in IgG titer
indicates infection
Congenital rubella
Congenital rubella is a group of physical problems that occur in an infant when the mother is infected with the virus that causes German measles.
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.
Risk factors for congenital rubella include:
Not getting the recommended rubella immunization
Contact 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.
Clinical picture
Transient symptoms: growth retardation, anemia &
thrombocytopenia Permanent defects: congenital heart
diseases, total or partial blindness, deafness & mental retardation
Progressive rubella panencephalitis:Extremely rare slow virus disease,
develops in teens with death within 8 yrs
Laboratory Diagnosis
Detection of maternal IgM or rising IgG in serum
Then, detection of rubella Ag in the amniotic fluid by DIF
Live newborn: detection of IgM antirubella Abs in the serum of the baby by ELISA
Stillbirth: virus isolation on MKTC
During Pregnancy After Birth
Prevention of congenital rubella
-Women in the childbearing age-School age children
Pregnancy should be avoided 3 months after vaccination
vaccinate
Maternal rubella infection confirmed during the first trimester????
Therapeuticabortion
Contains 3 live attenuated viruses: mumps, measles and rubella
Given in 2 doses The first dose: to children 12-15
months of age by subcutaneous injection
MMR
Why not before that?
Contraindications?
When is the second dose?
Thank you