MICROBIOLOGY

Paramyxovirus
Dr. Duenas
RNA Enveloped Viruses 2 spikes in the envelope:
 Orthomyxovirus  Hemagglutinin
 Paramyxovirus – “Para of M’s = Measles & Mumps”, RSV , Parainfluenza  Neuraminidase
 Arbovirus
 Rhabdovirus Fusion protein  causes cell to cell fusion  Giant cell formation
 Retrovirus

All members of the Paramyxoviridae family initiate infection via the

respiratory tract

Whereas replication of the respiratory pathogen is limited to the respiratory

epithelia, measles and mumps become disseminated throughout the body
and produce generalized disease

Rubella virus, although classified as a togavirus because of its chemical and

physical properties, can be considered with the paramyxoviruses on an
epidemiologic basis

STRUCTURE & CHARACTERISTICS

 Single stranded
 Negative-sense
 Linear
 Non-segmented RNA virus
 All members are antigenically stable
It can give lifelong immunity since it is antigenically stable

Picture Above: Structure of Paramyxovirus

Most Paramyxoviruses contain 6 structural proteins:
 3 proteins complexed with viral RNA:
o N (nucleocapsid) – represents the major
internal/integral protein
o P & L – involved in polymerase activity

 3 proteins participate in the formation of viral envelope:

o M protein – Matrix proteins  important in assembly Lecture notes:
The most common composition of Paramyxovirus is protein (73%), least
Glycoproteins: composition is the RNA (1%)
o HN or G – for attachment Envelope proteins – M, HN, G, F
o F (fusion) – for membrane & hemolysin activity Integral proteins – N, P, L

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 MICROBIOLOGY
Paramyxovirus
Dr. Duenas

Lecture notes:
What is the genera of Measles? Morbilivirus
What is the genera of Mumps? Rubulavirus

In the case of measles virus, the receptor is the membrane CD46 or CD150
molecule

REPLICATION OF PARAMYXOVIRUSES
A. Virus Attachment, Penetration, and Uncoating
B. Transcription, Translation, and RNA Replication
o No dependence in the nuclear function, most abundant
class of transcripts produced by an infected cell is from the
N gene
C. Maturation by Budding
Picture Above: Measles Infection
Memorize this by heart. Incubation period is composed of initial viral
MEASLES VIRUS (RUBEOLA VIRUS) invasion, Prodromal phase (3 C’s+ P), and Onset of rash (1st day)
 Acute
 Highly infectious disease In the Prodromal phase, we should check for the presence of Koplik’s spots.
 Characterized by: After the seeing the presence of Koplik’s spots, in 2-7 days there will be
o Fever presence of rashes. After the rash, give 1-2 weeks, the rashes will subside
o Respiratory Symptoms and they would turn brown called brawny desquamation. At that time, CD8
o Maculopapular Rash and IgM would ↓, while IgG ↑
IgG  for chronic infection, IgM  acute infection
 Triad (3 C’s) + P  happens during Prodome peroid
o Cough
 Day 14  maculopapular rash
o Coryza
appear
o Conunctivitis
o Photophobia  As circulating antibodies became
detectable  Viremia disappears
 MOT: Droplet means
and fever decreases
 Incubation Period: 10-14 days

The rash is a result of:

Humans: the only natural host for measles virus
 Interaction of immune T cells with virus-infected cells in the small
blood vessels which lasts about 1 week
 In patients with defective cell-mediated immunity, no rash develops

Picture Above: Complications of Measles

Complications of Measles include PIE, MIBE and SSPE. The longest and greatest
complication of measles is SSPE (Subacute Sclerosing Panencephalitis).
Entry in the RT  multiply  Regional LN  Multiplication  Primary viremia
MIBE – Measles Inclusion Body Encephalitis
Reticuloendothelial System (RES) PIE – Postinfection Encephalomyelitis
Multiply  Secondary Viremia  Skin, Respiratory Tract , Conjunctivae 
Replication

 Entire events occur during the IP (8-15 days)

 Patients are contagious during:
o Prodromal phase (2-4 days)  3 C’s + P
o First 2-5 days of rash, when virus is present in tears,
nasal and throat secretions, urine, and blood

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 MICROBIOLOGY
Paramyxovirus
Dr. Duenas
Complications
 Otitis Media – most common (5-9%)
 Secondary bacterial pneumonia – most common life-threatening
complication (10% & 20-80%)
 Giant Cell pneumonia – in CMI deficient individuals
 CNS complications – most serious
o Acute encephalitis
o Postinfectious encephalomyelitis (Acute disseminated
encephalomyelitis)  Neurological sequelae
o SSPE – progressive mental deterioration, involuntary
movements, muscular rigidity and coma

Immunity
 Infection confers lifelong immunity
 Cellular immunity  essential for recovery and protection
 Immunoglobulin deficiency  recover from measles and resists
reinfection
 CMI deficiency  do very poorly
 Vaccine: live attenuated virus which lasts for 15 years
Lecture notes:
MIBE – Measles Inclusion Body Encephalitis  Seen during 1st year after measles Laboratory Diagnosis
If after the measles, 5-15 years later a child develops encephalitis, a differential 1. Viral RNA by RT-PCR
diagnosis could be SSPE 2. Virus isolation – difficult
SSPE  Rare late complication of measles infection
3. Serology – measles IgM antibody

Key Immunologic Features of Measles:

Treatment, Prevention & Control
 Highly contagious
 Vitamin A treatment – decrease morbidity and mortality
 Only one serotype
 Vaccine – MMR or MR, MMRV
 No animal reservoir
 Contraindications to vaccine:
 Inapparent infections are rare
o Pregnancy  to prevent congenital rubella syndrome
 Infections confers lifelong immunity
o Allergy to eggs or neomycin
o Immune compromise
Clinical Findings o Recent immunoglobulin administration
 Incubation Period: 8-15 days
 Prodromal phase (2-4 days)
o 3 C’s  Coryza, Cough, Conjunctivitis + Photophobia
o Fever, redness of eyes
o Koplik spots (pathognomonic)  “grains of salt” 
appear 2 days before the rash
 Opposite the 2nd molar tooth

 Eruptive phase (5-8 days)  maculopapular rash starting from the

head  chest  trunk  extremities  5-10 days  brownish 
desquamation
o Centrifugal rash – from head  extremities

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 MICROBIOLOGY
Paramyxovirus
Dr. Duenas
PARAINFLUENZA VIRUSES MUMPS VIRUS
 4 Serotypes  Acute, contagious
 Most common of croup  Single serotype
o Acute laryngotracheobronchitis (LTB) in children under 5  Neutralizing antibodies against the hemagglutinin
years of age (Parainfluenza 1 & 2)  Humans  natural hosts
 Manifestations: harsh cough & hoarseness  Epidemic parotitis  non-suppurative swelling involving the
 MOT: Respiratory droplets salivary glands
o In adults: mild URTI
o In infants & young children: severe LRTI
 IP: 2-5 days

Disease Virus Type

Minor URTI 1, 3, 4
Croup (laryngotracheobronchitis) 6 mos. 3 yrs. 1, 2
Bronchitis (bronchiolitis) <1 yr. of age 1, 3
Pneumonitis <1 yr. of age 1, 3

Clinical Manifestations:
 Low grade fever
 Coryza
 Pharyngitis
 Some degree of
bronchitis
MOT:
Complication:  Direct contact
 Otitis media – most  Airborne droplets
common  Fomites
o Bedbugs – according to Jawetz
 Thru saliva only

Primary replication  URT epithelial cells  viremia  salivary glands &

other areas (meninges, testes, pancreas, ovaries, breast)
Newcastle Disease Virus – actually a paramyxovirus in birds; an occupational Involvement of the parotid glands is not an obligatory step in the infectious
disease that produces conjunctivitis in humans process
IP: 2-4 weeks
Laboratory Diagnosis Virus shedding: 3 days before up to 9 days after onset of gland swelling
Isolation: Nasopharyngeal Secretions
 Continuous monkey kidney cell line (LLC-MK2) Clinical Findings
 Embryonic Human Kidney  Prodromal period – anorexia, malaise
 CPE – Detectable only with type 2  Enlargement of parotid glands – most characteristic feature
 Immunofluorescence  Central nervous system involvement – aseptic meningitis
 PCR  Mumps orchitis – lack of elasticity of the tunica albuginea
 Adsorption of Guinea pig RBC  1/3 of cases –subclinical
 To determine the specific type  HI test  50% - present with swelling involving one or both gland with pain
 ELISA  Aspetic meningitis (10-30%)

Treatment
 Contact isolation precautions 2 Complications:
 Restriction to visitors 1. Orchitis
 Isolation of infected patients o When bilateral  sterility
 Gowning and handwashing by medical personnel o Post-pubertal males have fibrous tunica albuginea which
resists expansion  pressure necrosis of the
 The antiviral drug ribavirin
spermatocytes
 No vaccine is available

2. Meningitis
o Benign, self-limiting
3. Post-infection encephalitis
4. Deafness

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 MICROBIOLOGY
Paramyxovirus
Dr. Duenas
Diagnosis Clinical Forms
 Clinical 1. “common colds” – adults and older children
 Isolation & Identification of the virus 2. Croup – 1-3 years old
o The most appropriate clinical samples for viral isolation 3. Bronchiolitis and pneumonia - <1 yr.; most common cause;
are saliva, cerebrospinal fluid, and urine characterized by low grade fever, cough, tachypnea, tachycardia,
o Culture  monkey kidney cells wheezes
o Immunofluorescence
o CPE Immunity
o Hemadsorption inhibition  Maternally transmitted neutralizing antibodies
 Nucleic acid detection  PCR  No vaccine is available today
 Serology  ELISA or HI  In older children & adults  mild infection like common colds
 Account for 1/3 of respiratory infections in bone marrow transplant
Treatment & Prevention patients
 No specific treatment o Because they are immunocompromised
 Immunization  MMR  2 doses  Important cause of otitis media in infants especially during winter
 Effectively prevented by live attenuated virus vaccine
 Immunity – persists 9-10 years Laboratory Diagnosis
 Natural infection – permanent immunity  Antigen detection – Immunofluorescence or ELISA
 Culture – Human heteroploid cell lines (HeLa cells & HEp-2 cells)
Immunity  Nucleic acid detection  PCR
 Permanent after single infection  Serology  Immunofluorescence, ELIS or Nt tests
 Passive immunity is transferred from mother to offspring; thus, it is
rare to see mumps in infants younger than 6 months Treatment & Prevention
 Supportive care – removal of secretions, administration of oxygen
RESPIRATORY SYNCYTIAL VIRUS (RSV)  Antiviral drug  Ribavirin  aerosol for 3-6 days
 Replication initially occur in the epithelial cells of the nasopharynx  Vaccine:
LRT  bronchiolitis & pneumonia o Immune globulin with high titer antibodies  marginal
 Most common cause of bronchiolitis & pneumonia in infants benefit
(6 weeks- 6 months; peak = 2 months) o Humanized antiviral monoclonal antibodies
 IP: 3-5 days
 MOT: Respiratory droplets HENDRA VIRUS & NIPAH VIRUS INFECTION
 Two Zoonotic paramyxoviruses
 New genus (Henipavirus)
 Natural hosts for both viruses  Fruit Bats
 Reasons for emergence:
o Ecologic chances (land use)
o Animal husbandry practices
 1998-1999  severe encephalitis due to Nipah virus in Malaysia
transmitted from pigs to humans
 Hendra virus  an equine virus  caused human fatalities in
Australia
 Classified as Biosafety Level 4 pathogens
 Human Metapneumovirus – cause respiratory tract infections similar
to RSV

REFERENCES
 PPT
 Virus shedding:  Microbiology Manual (2019)
o Infants & young children  1-3 weeks  Dr. Duenas Recordings
o Adults  1-2 days
 Severe infection in infants  immunopathogenic mechanism 
maternal antibodies passed to the infant may react to the virus 
damage cell in the respiratory tract

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