Infections Of The Respiratory tract Flashcards
Populations at risk
Infants,children,elderly, post operative patients, unconscious patients, smokers, children with genetic disorders, malnutrition
Most common respiratory virus infections of human
Influenza, RSV, rhinoviruses, measles, adenovirus,cytomegalovirus
Cell types in the lung
Type 1 pneumocyte: flat cell covers 90% of the alveolar wall surface but represent only 40%of the total cells - cannot regenerate - control fluid movement between airspace and interstitum
Type 2 pneumocyte: granular rounded cell representing 60% of the total epithelial cells but only 3% of the alveolar space - generate surfactant essential for respiratory function l
Lung macrophages - cellular host defence
FLara cell: wTery proteinous secretion which assists surfactant and mucin action
Lung infection
Infiltration of alveoli during infection - full of immune cells = can’t function anymore so no gas exchange
Epidemiology of RSV
- predictable epidemic pattern
- occurs only in temperate climates in winter
- summer month essentially disappears
- major case of hospitalisation of children
Human RSV
- entire population infected by 10 years of age
- repeated infection occurs but the severity of symptoms reduces with age
-represents a major disease threat in the elderly population especially in institutions - aerosol transmission
Incubation 2-8 days - starts in the LT, then to RT
Primary infection
Infection rare before 4 weeks of age - maternal antibody
All symptoms and the infection all depends on the dose and antibody
Disease include bronchiolitis, pneumonia, otitis media, respiratory wheeze
Contributory factors
RSV antigenic subgroups
- immunisation and protection experiments in mice identified two potential antigenically distinct groups of RSV
- using monoclonal antibodies two antigenic subgroups - A and B
Font differ in capacity to cause disease
Molecular epidemiology of RSV
- sequence analysis can distinguish between members of the two subgroups
- gene encoding the attachment protein is the most variable (50% sequence differences) while the nucleoprotein gene shows the least variability
Pneumovirus infections in vivo
- necrosis and sloughing off of mucosal epithelium > come off and enter lumen
- interstitial inflammation > blocks respiratory
- mucus secretion > blocks further
- these lead to bronchial plugs
Antibody response
IgM- appears within 5 - 10 days post infection
IgG - peaks 20-30 days after symptoms then decline
IgA - appears after IgG and IgM and peaks at days 8-13
IgE - cell bound on the mucosal surface - more likely in parasitic
Histology of RSV infection
Group 1 - control animal showing minimal perivascular inflammation
Group 2 - showing mild interstitial infiltration 7 days after primary RSV
Pneumonia virus of infection
- disease same as RSV
- dose dependent fashion of how extreme pneumonia produced
Process of infection
1) attachment of virus to cell surface glycosaminoglycan
2) interaction of the fusion protein with host cell surface molecules
3) fusion of the virus envelope with the PM
4) introduction of the nucleocapsid complex into the cytoplasm
5) transcription and translation of virus mRNA (high from 5’ and low 3’)
6) replication of the virus genome
7) assembly
8) release through budding from the apical surface of the cell
In situ hybridisation PVM infected lungs
- 2 days pi: detect virus RNA within cells, sliver grains infected cell, detecting specific RNA
- 3 days pi: much more widespread, focuses of high level and the radiating outwards, observe animals behave wells
- 4 days pi: large quantities of virus, terminal bronchioles - massively infected, still displaying a lot of symptoms
- 5 days pi: infection has passed the terminal bronchioles and other alveoli and other alveoli
- 8 days pi: if dose given that they can recover from
