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

&regional 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