Myxovirus

Introduction
• Myxovirus – Enveloped RNA viruses characterised by ability to absorb onto
mucoprotein receptors on erythrocytes , causing hemagglutination (Clumping
of RBC ).
• Myxa – Mucus… Affinity of the virus to mucins
• Includes Influenza, Mumps, New castle disease and Parainfluenza viruses.
• Classified into 2 groups
• Orthomyxoviridae - Influenza viruses
• Paramyxoviridea - Mumps, New castle disease and Parainfluenza viruses.
 Paramyxovirus
• Important pathogens of infants and children,
responsible for a major part of Acute Respiratory
Infections.
• Also most contagious diseases in childhood
called Measles & Mumps are caused by
Paramyxovirus.
• Spherical in shape ,sizes ranges from 100 to 300
nm,
• Filamentous forms, up to several micrometres in
length up to 800 nm
• Linear Ss RNA molecule
• Antigenically stable
 Morphology
• Nucleocapsid is surrounded by a Lipid envelop ,has
the matrix protein at it’s base and transmembrane
glycoproteins spikes.
• Longer spike - Hemagglutinin ( H ), also possess
Neuraminidase ( N ) activity, called as H or HN
protein.
• Responsible for absorption of the virus to the host
cell surface.( Especially binding with RBC ) and
Initiates viral attachment & Infection.
• Second spike is “F” protein, responsible for fusion of
the viral envelop with plasma membrane of the host
cells ,leads to early step of infection
• Cell to cell fusion ,forms the giant cells
• Divided into Rubulavirus, Parainfluenza,
Morbillivirus, Pneumovirus
 Mumps (Rubulavirus)
Acute infectious disease commonly affecting children,
Characterised by Non suppurative enlargement of Parotid
glands.
Properties
1.Possessing both Hn and F proteins.
2.Agglutinates the erythrocytes of fowls,Guniea pig, Humans.
3.Hemagglutination is followed by Haemolysis and Elution at
37℃.
4.It is labile, being rapidly inactivated at room temperature or
exposure to formaldehyde.
5.It is antigenically stable and two complement fixing antigens
can be recognised, as in influenza viruses – The soluble ( S )
antigen and Viral ( V ) antigen
Clinical features
• Infection through Inhalation of infective droplets & Conjunctiva.
• Replicates in URT Cervical nodes disseminated through blood
to various organs
• Incubation period – 12 to 25 days
• First sign – Parotid swelling – Initially unilateral ,when it progress may become
bilateral , Includes fever ,local pain, tenderness, but Not warm or erythematous.
• Resolves within a week
• Complications – Epididymo -orchitis at 3rd pubertal age in Boys, results in
unilateral ,swelling,pain.If become bilateral then it leads to Testicular atrophy,
Sterility, Low sperm count.
• Pleocytosis
• Abnormal increased cell count in CSF especially Lymphocytes
• Meningitis is seen 60% of cases, Aseptic meningitis, sometime leads to
deafness

• Transmission
• By direct contact ,airborne droplets ,fomites contaminated with infective
saliva and also infected person urine.
• The virus is detectable in the saliva for a week before & a week or 2 after
onset of parotitis.
• Epidemic in children 5-15 age
• Humans are only host.
• Infection start to begin when a person in the late incubation or early clinical
stage of illness
Immunity
• Antibody response occur against both internal & surface antigen
• Internal antigen ( S ) – Appears early, within 3-7 days after onset of symptoms but
disappears after six months.
• Demonstration of antibody to S antigens shows current or recent infection.
• Surface antigen ( V ) – Anti body takes a month to appear ,persist for a year.

• LAB DIAGNOSIS
• Typical cases – No need of Lab diagnosis
• Atypical cases need virus isolation & serological test.
• The virus can be isolated
• Saliva - 4-5 days
• Urine - up to 2 weeks
• CSF - 8 – 9 days of onset
• IgM-ELISA
• Complete Fixation test - Positive
Vaccination
• Live virus vaccination
• Subcutaneous injection, either alone or in combination with Measles
and Rubella vaccines ( MMR vaccine) .
• Protection for at least 10 years
• Contraindication:
• Pregnancy
• Immunodeficiency and hypersensitivity to neomycin or egg protein
 Measles
• Measles is a highly contagious febrile illness, fatal for
small children
• Also called as Rubeola
• Spherical in shape, But Pleomorphic
• 120-250 nm in diameter
• Morphology as like Paramyxovirus
• Coiled nucleocapsid surrounded by Lipoprotein
• Carrying H spikes on its surface but No neuraminidase
• “F” Protein mediates cell fusion and Haemolytic
activities
• Labile and Readily inactivated by heat, UV, Ether and
Formaldehyde
• After an incubation period of 8-12 days, measles is
typically a 7-11 days illness with a prodromal phase of
2-4 days followed by an eruptive phase of 5-8 days.
 Pathogenesis & Clinical manifestations
• Prodromal phase of measles:
• The prodromal phase is characterized by fever
and three (C’s –1. Coryza of nose,
2.Conjunctivitis usually associated with
photophobia
3.Cough , also with Koplik’s spots and
lymphopenia.
The cough and coryza reflects an intense
inflammatory reaction involving the mucosa of the
respiratory tract.
• Koplik’s spots are small, bluish white ulceration
of the buccal mucosa.
• The fever and cough persists until the rash
appears and then subside within 1-2 days.
• The rash starts on the head and the spreads
progressively to the chest, the trunk and down
the limbs which appears as light pink, discrete
maculopapular that coalesce to form blotches
and becomes brownish in 5-10 days. The
fading rash resolves with leaving of scales in
affected area.
• ii. Modified measles:
• Modified measles occurs in partially immune
persons such as infants with residual maternal
antibody.
• Koplik’s spots are usually absent and rash is
mild.
• Atypical
• Atypical measles occurs in individuals who received the older inactivated vaccine and
later exposed to a wild strain.
• It may also rarely occur in persons vaccinated with attenuated vaccine.
• It is characterized by a prolonged high fever, pneumonitis and the rash.
• The rash characteristically begins peripherally and may be urticarial, maculopapular,
hemorrhagic or vesicular.
Symptoms of measles include:
• Rash that starts on the face and spreads to the chest and legs
• High fever
• Cough
• Runny nose
• Sore throat
• Pink eye (also called conjunctivitis)
• Tiny white spots in the mouth
Complications
• Pneumonia is life threatening complications of measles, caused by secondary bacterial
infections.
• Giant cells pneumonia is serious complication in children and adults with
Immunodeficiencies conditions.
• Complications involving CNS are the most serious.
• Acute encephalitis occurs in about 1:1000 cases.
• Post infections encephalomyelitis is an autoimmune disease associated with an immune
response to myelin base protein.
• Subacute sclerosing panencephalitis (SSPE) is a rare late complications of measles,
occurs with an incidence of about 1:300000 cases.
• SSPE is a degenerative disease of the CNS caused by persistent measles infection. The
disease begins 5-15 years after a case of measles.
• It is characterized by progressive mental deterioration, involuntary movements muscle
rigidity and coma the condition is associated with the presence of an extremely high
measles antibody titers in the blood and CSF.
• Other complications of measles include bronchopneumonia, laryngotracheobronchitis
(croup), diarrhea.
• Measles includes labor in some pregnant women, resulting in spontaneous abortion or
premature delivery. The virus may across the placenta and infect the fetus during maternal
measles.
Laboratory diagnosis of measles:
•Typical measles is reliably diagnosed on clinical grounds.
•Laboratory diagnosis is necessary in case of modified or atypical measles.
1. Specimens:
•Respiratory specimens, conjunctival specimen, urine, blood and brain tissue.
•Specimens are collected during the prodromal stage and the period following until 2 days
after the appearance of the rash.
2. Microscopy:
•Demonstration of multinucleated giant cells measuring up to 100 nm in diameter in Giemsa
stained smears is diagnostic of measles.
•Immunofluorescent study of exfoliated respiratory cells in nasopharyngeal secretion virus
particles.
3. Antigen detection:
•Measles antigen can be detected directly in epithelial cells in respiratory secretions, urinary
sediments, pharyngeal secretions by direct immunofluorescent antibody test.
4. Isolation and identification of virus:
•Nasopharyngeal and conjunctival swabs, blood samples, respiratory secretions and urine
collected from a patient during febrile period are appropriate sources of viral isolation.
•Growth can be obtained in primary human or monkey kidney cells.
•Growth occurs slowly with CPE containing both intra-nuclear and intra-cytoplasmic
inclusion bodies in 7-10 days.
5. Serology:
•Serologic confirmation of measles depends on a 4 fold rise in antibody tilter between acute
phase and convalescent phase sera or demonstration of measles specific antibody in a single
specimen drawn between 1 and 2 weeks after the onset of rash.
•ELISA
•Haemagglutinin Inhibition assay
Treatment and control of measles
• Ribavirin either intravenous or in aerosol form is evaluated now a days to treat severely
affected adults and immunocompromised individuals with acute measles or SSPE.
• Vitamin A treatment in developing countries has reduced mortality and morbidity.
• Active immunization
• The vaccine is available in monovalent form in combination with live attenuated Rubella
vaccine (MR) and live attenuated rubella and mumps vaccine (MMR)- currently used for
universal immunization of children.
• Efficacy – 95 % (90-98%)
• Duration of immunity- life long
• Schedule- 2 doses – first at the age of 9 month- second at the age of 2 years
• Passive immunization
• Pooled sera containing antibody against measles virus confess passive
immunity to infants and susceptible contacts of measles cases.