Transcript ORTHOMYXOVIRUS PARAMYXOVIRUS

ORTHOMYXOVIRUS
PARAMYXOVIRUS
Ma. Rosario L. Lacandula, MD, MPH
Department of Microbiology & Parasitology
College of Medicine
Our Lady of Fatima University
Orthomyxovirus
 Influenza virus
 Influenza A- pandemics and epidemics;
humans and animals
 Influenza B- epidemics; human virus
 Influenza C- mild respiratory tract infection
 Morphology:
 Segmented, ss genome,helical nucleocapsid
with outer lipoprotein envelope
 Envelope contain 2 spikes
 Hemagglutinin
 Binds to cell surface receptors( neuraminic acid/sialic
acid
 Neuramidase
 Enzymatic activity
 Internal antigens- M1 & NP proteins- type
specific, shows cross reactivity
 Antigenic Variations
 Antigenic shift
 Undergoes reassortment
 Results in changes of the H and N antigen
 Pandemics and epidemics
 Occurs with influenza A only
 Antigenic drift
 Change in the amino acid sequence of the H ag
 Occur both in A & B
 MOT: airborne respiratory droplets ( less than
10 um)
 Survive for short period on surfaces
 I.P. 18-72 hours
 Virus concentration in nasal and tracheal secretions
remains high for 24 to 48 hours
 Site of infection- epithelial cells of the
respiratory tract
 Recovery- interferons and CMI
 Humoral Immunity- ( IgG & IgA)protection
against reinfection, antibody against HA is
important
Symptoms and
complications
 1. Uncomplicated influenza
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Fever ( 38-40 C)
Myalgias, headache
Ocular symptoms- photophobia, tears, ache
Dry cough, nasal d/c
 2. Pulmonary complications/sequelae
 Croup( acute larygotracheobronchitis)
 Primary influenza pneumonia
 Secondary bacterial infection
 3 Non pulmonary complications
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Myositis
Cardiac complications
Encephalopathy
Reyes syndrome
Guillen-Barre syndrome
Diagnosis
 1. virus isolation
 Monkey kidney cell etc.
 No CPE
 2.serology
 Hemadsorption
 PCR
Chemotherapy
 Rimantadine and amantadine
 Zanamavir and oseltamivir
 Rest, liquids and anti febrile agents
PROPERTIES OF
ORTHOMYXOVIRUS AND
PARAMYXOVIRUS
Property
orthomyxovirus
paramyxovirus
viruses
Influenza A,B,C
Measles,mumps,
RSV,& parainfluenza
genome
Segmented
Non segmented
Virion RNA
polymerase
yes
yes
Capsid
helical
helical
Envelope
yes
yes
size
Smaller(110 nm)
Larger( 150 nm)
Surface spikes
H&N diff. spikes
H&N same spikes
Giant cell formation
no
yes
Envelope spikes
Virus
H
N
Fusion protein
Measles virus
+
-
+
mumps
+
+
+
RSV
-
-
+
Parainfluenza
+
+
+
Paramyxovirus
 Non segmented, ss genome; helical
capsid with outer lipoprotein envelope
 Envelope spikes: H & N and fusion
protein
MEASLES VIRUS
 Single serotype
 H- target of neutralizing Ab
 Humans are the natural host
Pathogenesis
 Receptor: CD46 on surface of
macrophages
 Rash-cytotoxic T cells attacking the virus
infected vascular endothelial cells in the
skin
 CMI- neutralizing the virus during viremic
phase
 MOT: droplet inhalation
 Hematogenous transplacental
Clinical
 IP 7-13 days
 Prodrome- high fever, 3C & P- infectious
 Koplick’s spots- buccal mucosa across
the molars- grains of salt surrounded by
red halo
 Rashes appears-starts below the ears
and spread throughout the body
undergoes brawny desquamation
Complications
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Encephalitis
Bacterial pneumonia
Giant cell pneumonia- defective CMI
Atypical measles- older inactivated
mealses
 SSPE-subacute sclerosing
panencephalitis
Mumps virus
 H and N + fusion protein on envelope
spikes
 Internal nucleocapsid protein- S Antigendetected in complement fixation test
 Humans are the natural host
 thermolabile
Mumps
 Nasal or URT epithelial cells- bloodsalivary glands, testes,ovaries, pancreas,
meninges and kidneys
 Shed in the saliva 2 days before to 9
days after the onset of salivary gland
swelling
 (+) virus in urine up to 14 days after
onset of symptoms
Clinical
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1/3 of patients subclinical
50% with swelling of the salivary glands
Pain and anorexia
Complications
 Orchitis-postpubertal-unilateral, bilateral-sterility
 aseptic meningitis
 Oophoritis-5%
 Pancreatitis- 4%
Immunity
 Ab vs HN glycoprotein- correlate with
immunity
 Ab vs S Ag- appear earliest, gone w/in 6
months
 Passive immunity from mother to offspringprotection during 1st 6 months of life
Diagnosis
 1. cell culture
 Specimen-saliva, spinal fluid or urine
 Monkey kidney cell
 CPE- cell rounding and giant syncytia formation
 2. serology- 4 fold rise in Ab titer in HI or CF
 Ab vs S antigen- current infection
 Ab Vs V antigen- past infection
 Prevention: vaccine, attenuated vaccine
Respiratory Syncytical
Virus
 Most important cause of pneumonia and
bronchiolitis in infants
 Fusion proteins- syncytia formation
 Humans and chimpanzees- natural host
 2 serotype: A & B
 MOT: respiratory droplet
Clinical
 1. infants- bronchiolitis, pneumonia
 2. young children- otitis media
 3. older children and adults- common
cold
 Diagnosis: immunofluorescence
 Isolation in cell culture- + CPE
 serology
Treatment
 Aerosolized Ribavirin
 Ribavirin + hyperimmune globulins
 Prevention
 NO VACCINE
 Palivizumab-prophylaxis, monoclonal ab vs.
fusion protein
Parainfluenza Virus
 Surface spikes: H & N same spike, fusion
on different spike
 Both humans and animals infected
 Four serotypes: 1, 2, 3 & 4
 MOT: respiratory droplet
 No viremia
 Clinical:
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1&2- major cause of croup; children < 6 y/o
Laryngitis
Pneumonia
Common cold- 4
Pharyngitis
Otitis media