Paramyxoviridae contains viruses that are transmitted via the respiratory route and can cause localized respiratory infections or disseminate throughout the body. Parainfluenza viruses resemble orthomyxoviruses in morphology but are larger and pleomorphic, with a helical symmetry, 18nm nucleocapsid, and negative-sense RNA genome. They cause respiratory infections in children and have six structural proteins, including envelope glycoproteins, that help mediate attachment and fusion to host cells. Human parainfluenza viruses are a major cause of lower respiratory tract infections in young children.

2. • Paramyxoviridae contains a group of viruses; which are
transmitted via the respiratory route following which :
• They may cause localized respiratory infections in children
e.g. respiratory syncytial virus & the parainfluenza viruses)
or
• They may disseminate throughout the body to cause highly
contagious diseases of childhood such as mumps (parotid
enlargement) & measles(rashes).

3. • Parainfluenza viruses
resemble Orthomyxoviruses
in morphology but are larger
& pleomorphic.
• Size : 100 – 300 nm, rarely
800nm, Rarely large
filaments & giant forms
seen.
• Symmetry : Helical
• Nucleocapsid : 18nm
• Genome : Negative sense,
linear, single stranded , non
– segmented RNA

4. • Six structural Proteins :
Which form capsid,
polymerase, matrix protein
( underlies the envelop),&
envelop glycoproteins.
• Envelop : Nucleocapsid is
surrounded by a host
derived lipid envelop in
which the following virus
coded peplomers
(glycoproteins ) are
inserted.

5. • F – Glycoprotein : Present in all myxoviruses. Mediate
membrane fusion. Also have hemolysin activity ( except
in pneumoviruses).
• Larger Glycoproteins – Help in attachment to the host
cells. May be either H or HN or G type –
1. HN Glycoproteins – Have both haemagglutinin &
neuraminidase activities e.g. in parainfluenza & mumps
viruses
2. H Glycoproteins – Have only haemagglutinin activity
e.g. in measles.
3. G Glycoproteins – No haemagglutinin & neuraminidase
activities. Help in attachment e.g. in respiratory syncytial
virus.

6. • Paramyxoviridae family - Divided into two subfamilies -
Paramyxovirinae & Pneumovirinae.
Subfamilies Paramyxovirinae Pneumovirinae
Genera Respirovirus Rubulavirus Morbillivirus Henipavirus Pneumovirus Metapneumovirus
Human
Viruses
Parainfluenza
1, 3
Mumps
Parainfluenza
2, 4a, 4b
Measles Hendra
Nipah
(Zoonotic)
Respiratory
Syncytial
virus
Human
metapneumovirus

7. • Human parainfluenza viruses – one of the major causes of
lower respiratory tract infections in young children. Has 5
serotypes.
• Type 1 and 3 – Genus Respirovirus.
• Type 2, 4a, 4b – Genus Rubulavirus.

8. • Transmission by respiratory route ( By direct salivary contact or
by large – droplet aerosols).
• Incubation Period – 5 to 6 days.
• Virus multiplies locally and cause various respiratory
manifestations.
• Mild common cold syndrome like rhinitis, pharyngitis.
• Laryngotracheobronchitis ( croup) – with type 1 & 2 viruses.
• Bronchitis & Pneumonia
• Reinfection.

9. • Worldwide in distribution
• Type 3 – Most prevalent serotype & exists as endemic
throughout the year with annual epidemics during spring.
• Type 1 & Type 2 – Less common. Tend to cause epidemics
during rainfall or winter.
• Type 4a & 4b cause milder illness and are most difficult to
isolate.
• Parainfluenza viruses – Important cause of outbreaks in
pediatric wards, day care centers & in schools.

10. • Antigen detection : Viral antigens in the infected exfoliated
epithelial cells of nasopharynx – Detected by direct
immunofluorescence by using specific monoclonal antibodies. It
is rapid but less sensitive.
• Viral isolation :
1. Specimens – Nasal washes, bronchoalveolar lavage fluid, lung
tissue. Specimens to be inoculated as early as possible.
2. Tissue culture – Primary monkey kidney cell line – most
sensitive. Other cell lines used – LLC – MK2.
3. Produce little or no cytopathic effects
4. Viral growth detected by performing haemadsorption using
guinea pig erythrocytes or Ag detection by direct IF.

11. •Serum antibodies : Can be measured by neutralization test,
haemagglutination inhibition test or ELISA. Presence of IgM or
fourfold rise of IgG titer – Indicative of active infection.
• Reverse transcriptase PCR : Highly specific & sensitive. But
available only in limited settings.

12. • Most common cause of parotid gland enlargement in children. In
severe cases, it can also cause orchitis & aseptic meningitis.
• PATHOGENESIS :
 Transmission – Through respiratory route via droplets, saliva, &
fomites.
 Primary replication – Occurs in the nasal mucosa or upper
respiratory mucosa → infects mononuclear cells & regional lymph
nodes→ spills over to blood stream resulting in viremia →
dissemination.
 Target sites – Mumps virus has special affinity for glandular
epithelium. Classic sites – salivary glands, testes, pancreas,
ovaries, mammary glands, & central nervous system.

13. • CLINICAL MANIFESTATIONS :
• Incubation period – 7 – 23 days (Average 19 days).
• Inapparent infection – Half of the infected persons are either
asymptomatic or present with non specific symptoms such as
fever, myalgia, & anorexia( more common in adults).
• Bilateral parotitis – Acute non – suppurative parotid gland
enlargement, present in 70 – 90% cases. Rarely may be unilateral.
• Epididymo – orchitis – Next most common presentation. 15 – 30
% cases.
• Aseptic meningitis – Occurs in < 10% cases with a male
predominance , self limiting
• Oophoritis – In about 5% of females
• Atypical mumps – Absent parotitis, directly presents as aseptic
meningitis.

14. • EPIDEMIOLOGY –
• Endemic worldwide. Peak in winter & spring.
• Period of communicability – Pts are infectious from 1 wk. before
to 1 wk. after the onset of symptoms. It is shed in saliva,
respiratory droplets, & urine.
• Source – Clinical & subclinical cases. No carrier state.
• Reservoir – Humans are the only reservoir of infection.
• Incidence – 100 – 1000 cases per 10000.
• Age – 5 – 9 years. No age spared.
• Immunity – One attack – lifelong immunity.

15. • LABORATORY DIAGNOSIS –
• Specimens – Buccal or oral swab, CSF, Saliva, urine
• Antigen detection – By direct IF test
• Viral isolation – 1. Primary monkey kidney cells, 2. Shell viral
technique. Cytopathic effect – cell rounding & giant cell formation.
• Serum Abs – By ELISA, neutralization test, haemagglutination
inhibition test.
• RT – PCR – Detects viral RNA.
• TREATMENT –
• No specific antiviral drug. T/t – mostly symptomatic

16. • PROPHYLAXIS –
• LIVE ATTENUATED VACCINE – From Jeryl Lynn or RIT 4385, or
Urabe strain. It is prepared in chick embryo cell line.
• MUMPS VACCINE IS AVAILABLE AS – 1. Trivalent MMR vaccine
(Live attenuated Measles – Mumps – Rubella vaccine) or 2.
Quadrivalent MMR – V vaccine ( contains additional live
attenuated varicella vaccine) or 3. Monovalent mumps vaccine (
not commonly used)
• Schedule – 2 doses of MMR is given by IM route at 1 yr. & 4 – 6
yr.(before starting school)
• Efficacy – 90% after second dose.

17. • Measles is an acute, highly contagious childhood disease,
characterized by fever, respiratory symptoms, followed by typical
maculopapular rash.
• PATHOGENESIS –
 Transmission – Via respiratory route through droplet inhalation &
aerosols.
 Spread – Virus multiplies locally in the respiratory tract →Then
spreads to regional lymph nodes → enters the blood stream in
infected monocytes (primary viremia)→ further multiplies in
reticuloendothelial system → spill over into blood ( secondary
viremia)→ disseminates to various sites.
 Target sites – Predominantly the virus is seeded in the epithelial
surfaces of the body, including skin, respiratory tract &
conjunctiva.

18. • CLINICAL MANIFESTATIONS –
• Incubation period – 10 days to 3 wks.
1. PRODROMAL STAGE – lasts for 4 days.
Characterized by – Fever – On day 1
i.e. 10th day of inf.
• Koplik’s spots - are pathognomic of
measles, appear on 12th day of inf. – 1
mm white to bluish spot surrounded by
an erythema on buccal mucosa near 2nd
lower molar. Rapidly spread to entire
buccal mucosa & fades away on onset of
rash.
• Non specific symptoms – Cough, coryza,
nasal discharge, redness of eye, diarrhea
or vomiting.

19. • CLINICAL MANIFESTATIONS –
2. Eruptive stage –
• Maculopapular dusky red rashes after 4
days of fever ( i.e. 14th day of infection).
Typically appear first behind the ears→
spread to face, arm, trunk & legs→ then
fade in the same order after 4 days of
onset.
3. Post Measles Stage –
• Characterized by weight loss, weakness
,disorientation , chronic illness.

20. • COMPLICATIONS –
• Secondary bacterial infections – Otitis media,
Bronchopneumonia.
• Recurrence of fever or failure of fever to subside with rash.
• Giant cell pneumonitis ( Hecht’s pneumonia) in
Immunocompromised pts. Acute Laryngotracheobronchitis &
diarrhoea.
• CNS complications –
1. Post measles encephalomyelitis
2. Measles inclusion body encephalitis
3. Subacute sclerosing panencephelitis

21. • LABORATORY DIAGNOSIS :
• Specimen – Nasopharyngeal swab
• Antigen detection by using anti –
nucleoprotein antibodies.
• Virus isolation –
1. Monkey or human kidney cells or Vero /
hSLAM cell line – produces CPE as
multinucleated giant cells ( Warthin – Finkeledy
cells.
2. Shell viral culture
• Antibody detection – Against nucleoprotein Ag
by ELISA or neutralization tests.
• Reverse – transcriptase PCR – detects viral
RNA.

22. • PROPHYLAXIS –
• Live attenuated vaccine – Strains used –
Edmonston strain, Schwartz strain ,
Edmonston - Zagreb strain , Moraten strain.
• Vaccine is prepared in chick embryo cell
line.
• Vaccine available in lyophilized form & has
to be reconstituted with distilled water & to
be used within 4 hours. Stored at -200 C
• Dose – One dose (0.5ml) containing > 100
infective viral units & is administered
subcutaneously.

23. • PROPHYLAXIS –
• Combined vaccines – MMR or MMR – V
vaccines
• Contacts – Measles immunoglobulin –
0.25 mg / kg/body wt.

24. • EPIDEMIOLOGY –
• Source – Cases are only source of infection.
• Reservoir – Humans only
• Infective material – Virus shed in secretions of nose, throat, &
respiratory tract of cases of measles.
• Period of communicability - Pts. Are infectious from 4 days
before to 4 days after the onset of rash.
• Secondary attack rate – high
• Age – Children 6 months to 3 years in developing countries &
older children > 5 yrs. In developed countries.

25. • RSV is a major respiratory pathogen of young children & is the
most common cause of LRTI ( Bronchiolitis & pneumonia) in
infants.
• PATHOGENESIS –
• Transmission – Direct contact( contaminated fingers, fomites, self
inoculation onto conjunctiva or anterior nares or by large
droplets.
• Spread – It replicates locally in the epithelial cells of nasopharynx
 spread to LRT  cause bronchiolitis & pneumonia
• Pathology – Peribronchiolar infiltration by lymphocytes.
Submucosal edema, Necrosis of bronchiolar epithelium &
formation of plugs consisting of mucus, cellular debris & fibrin
which occlude the smaller bronchioles.

26. • CLINICAL MANIFESTATIONS –
• I.P. – 3 – 5 days . Most common cause of LRTI in infants < 1 yr.
• Symptoms – Running nose, fever, accompanied by cough,
wheezing, & dyspnoea.
• In Adults – RSV produces influenza like URTI. Occasionally can
cause LRTI
• Recurrent infection – Common both in children & adults.

27. • LABORATORY DIAGNOSIS –
• Ag Detection – Direct IF test detecting virus on exfoliated cells &
ELISA detecting Ag in nasopharyngeal secretions.
• Virus Isolation – HeLa & HEp – 2 cell lines for RSV isolation .
Characteristic CPE – Syncytium formation.
• Antibody Detection – IF, neutralization tests, ELISA.
• Reverse Transcriptase PCR – Viral RNA.

28. • Not a myxovirus . Also c/a German measles.
• MORPHOLOGY - Belongs to Togaviridae family & is the only
member under genus Rubivirus. It is enveloped, SS RNA virus
measuring 50 – 70 nm. Envelop contains two types of spike – like
glycoproteins E1 & E2. Only one serotype. Humans only reservoir.
• Types of infections – Post natal or congenital
• Transmission – spreads from person to person by respiratory
droplets via upper respiratory mucosa.
• Spread – Replicates locally in nasopharynx  L.N.  viremia after
7 – 9 days  Rash

29. • CLINICAL FEATURES –
• I.P. – 14 days . Infection subclinical in 20%
• Rash – generalized & maculopapular in nature.
• Lymphadenopathy
• Forchheimer spots – Pin head sized petechie on soft palate &
uvula.
• Complications – Arthralgia and Arthritis.

30. • LABORATORY DIAGNOSIS –
• Specimens – Nasopharyngeal & Throat swab.
• Virus Isolation – In monkey or rabbit origin cell lines & then
growth detected by viral interference. Shell viral technique.
• Antibody Detection – By HAI or ELISA
• CONGENITAL RUBELLA SYNDROME – Has teratogenic effect.
Transmission to fetus if mother is infected during first trimester .
• Causes ear defect, ocular defect, cardiac defect & CNS defects.

31. • VACCINATION –
• RA 27/3 is live attenuated vaccine for rubella prepared from
human diploid fibroblast cell line. Available singly or in
combination of mumps & measles – MMR.
• Schedule – Single dose (0.5 ml) of vaccine is administered
subcutaneously.