resp viruses Flashcards
(27 cards)
what are resp tract vriuses:
* Diverse group of viruses that affect respiratory tract
1. Upper respiratory tract infection (URTI)
‘—-’, — , —
2. Lower respiratory tract infection (LRTI) — , — , —
3. Viruses involved in generalised viral infections
— or—- pneumonitis
May initially present as — & then progress to —
common cold , sinusitis , phargytis
penumonia m bronchitis , bronchiolotis
chickenbox or measles
URTI to LRTI
common viral resp syndroms:
1- bronchiolotis causes by —
other causes:
Influenza viruses
Parainfluenza viruses
Adenoviruses
Rhinoviruses
2- common cold casues by – , — , —
other causes:
Parainfluenza viruses
Enteroviruses
Adenoviruses
Human metapneumoviruses
RSV
3- croup caused by —
otehr : Influenza viruses
RSV
4- influezna like illness causes by — , –
other causes:
Parainfluenza viruses
Adenoviruses
5- penumonia: causes by — , — , —
others:
Adenoviruses
Parainfluenza viruses
Enteroviruses
Rhinoviruses
Human metapneumoviruses
Other Coronaviruses
respiratory syntial virus ( RSV)
rhinovirus , conronvirus , RSV
parainfluenza viruses
infuelza virus , SARS CoV-2
SARS CoV-2 RSV influezna viruses
transmission of resp viruses:
Direct spread: principal route is from — via —
Indirect spread: person touches a surface or
object contaminated with infectious droplets( —- ) & then touches his/her mouth, nose or eye
spread:
* —
– i.e. coughing, sneezing
* —
– person touches a surface or object contaminated with infectious droplets (fomite) & then touches
mouth, nose or eye
* —
– Of normal or colonizing flora
* —
– i.e. intubation, instrumentation
* Larger particles settle — , smaller ones may remain airborne for —
person to person
resp droplets
fomite
droplet
fomite
aspiration
direct
quickly
1-2 hours
infection control : how to prevent spread of resp virus:
* Prevent — in the first place
where possible
- —- - influenza
* Specific infection control measures to
prevent trasmission
- — precautions (as for ALL
patients)
PLUS
- — precautions
PLUS
- Point of care — assessment (PCRA)
infection
immuisation
standard
droplet
risk
common cold: — , — with — , nasal — & — (—- ), sore throat, cough, headache, & mild
malaise. Fever usually absent. Not systemically ill
— common, is —
* caused by — , — , — ,
* Rapid — changes
Symptomatic treatment; — likely
mild URTI
sneezing
nasal congestion and discharge ( rhinorrhoea)
very common
self limiting
cornoavirus rhinovirus adenovvirus
genetic
no vaccines
Influenza viruses are classified on the basis of —- into 3 distinct types: A, B & C
Influenza A viruses infect a range of — &—- species
– — influenza in humans
* Responsible for — and —
* — are the original main reservoir;
– Generally do not cause disease in the — host
» multiply in the — leading to a high — load → — → —
– ‘Avian influenza’ primarily affects wild — ;
* — may become infected; humans are — infected
core proteins
mamalian and avain species
seasonal
annual epidemics and occasional pandemics
birds
avain
GIT
faceal load
human
human to human
aquatic fowl
domestic birds
rarely
Influenza types B & C restricted to—
– Influenza B viruses
* cause outbreaks every — but are not associated with —
– Influenza C
* — & typically causes — disease
influenza virus:
Genome – — segments
Antigens project from the — = —
* — (HA) [e.g., H1, H2 & H3]
* — (NA) [e.g., N1, N2]
humans
2-4
pandemics
uncommon , milder
8
envelope = subtypes
haemagglutin
neuraminidase
biological features and their impact on epidemology :
“Antigenic Drift”
* — antigenic change
* — errors by the viral — result in amino acid — in surface —
- —-
* — immunity in population, little in infants, some— immunity in adults
* Outbreaks of variable severity; usually most severe — & — (– most severe)
minor
transcpriton
dna polymerase
subsituition
glycoprptoien
yearly epidemics
partial
cross reacting
eldelry and young
h3
biological features and their impact on epidemology:
“Antigenic Shift”
- – antigenic change
- Genes “ — ” between different —
- Genetic — occurs when two different
viruses simultaneously – a host cell resulting in a — virus with newsurface or internal
proteins, leading to a —
* Novel surface proteins = — population
immunity.
* High attack rate, excess morbidity &
mortality in all age groups
major
swapped
strains
re assortmenet
infect
novel virus
pandemic
little
pathogensis of influenza infection :
1- Droplets on — membranes
Enters via — cells, attaches to— epithelium
2- Haemagglutinin (HA)
binds to — on —
Neuramidase (NA)–
cleaves — (in resp — ) to allow — of virus from cell and prevents —
(+ is a — target)
3-Antigenic shift / drift
antigens not
recognised by host
immune system
Virus induced lymphocyte
dysfunction
- Interferon (clinical features)
4- Diffuse inflammation of
trachea & bronchi – may
progress to ulcerative
necrotizing trachea-
bronchitis
Loss of cilia - Mucociliary
damage facilitates bacterial
superinfection
5- droplet spread
musucous memebrnae
resp epithelial cells
columnar epithelium
receptor
host cells
sialic acid
resp epithelium
release
clumping
Rx
influenza infection:
* — respiratory illness due to influenza A, B or C
* — outbreaks & — worldwide, &
unpredictable —
– 1918 pandemic: spread worldwide within 9 months
causing up to 40,000,000 deaths; more than in WWI
* Usually — infection (uncomplicated
influenza)
* Associated with increased morbidity & mortality in certain high-risk populations ( — influenza)
acute
seasonal
epidemics
pandemics
self limiting
complicated
infleuzna clinical:
* — onset of fever, cough & myalgia lasting only a few days with more — weakness & —
* 95% of exposed individuals who become symptomatic, do so within —
* Incubation period — days before
* Infectious for up to 7 days after
This is NOT the ‘common cold’ where symptoms are mild & largely, upper respiratory
influenza complications:
1-* Primary influenza pneumonia
2-* Secondary bacterial pneumonia:
* — pneumoniae
* — influenzae
* —-
* Myositis/myocarditis
* CNS: Seizures/encephalopathy/encephalitis
* — Syndrome
* Encephalopathy & liver failure
* Now very rare
* Death
abprupt
presistent weakness and depression
3 days
1-2 days
streptoccous penumoea
haemphilis influenza
staphlycoccus aureus
reyes
influezna treatment:
* Mainly supportive;
– —
– —
* If hospitalised
– — & — care review if clinically indicated
* Antivirals - — inhibitors
– Oseltamivir (Can also be used as —- in exposed at risk patients)
– Zanamivir (inhaled)
– (Peramivir & baloxivir)
* Advise future —
influeza vaccination:
Inactivated virus should be given each year in advance
of the influenza season (Sept/Oct)
Recommended
1. Any individual > — of age at increased risk of influenza or its complications
2. Those at increased risk of transmitting influenza to a person at high risk for complications
– Healthcare workers
– May be considered for family, carers & household contacts of
patients at increased risk
3. All children > — < —
Live — vaccine
anti pyretic
analgesia
oxygen and critical care
neuramidinase
prophylaxis
vaccination
>6 months
>2 <12
intransael
info :
at risk groups
Adults or children (>6 months) with any of the following
– Chronic illness requiring regular medical follow-up
– Immunosuppression due to disease or treatment
– All persons aged 65 or more
– All pregnant women (any gestation) & up to 6 weeks
postpartum
– Morbid obesity
– Children & adults on long-term aspirin therapy
– Residents of nursing homes & other long stay
facilities
– Pig / poultry / waterfowl workers
healthcare worker vaccination
Healthcare workers, usually healthy adults, are likely to
have excellent response to vaccination unlike some
patients
* Hospitalised patients can acquire influenza from
infected healthcare workers, visitors or other
patients
* About 30% of people infected with influenza are — but can still be infectious
* Influenza can kill a — patient
asymptomatic
vulnerbale
resp syncytial virus:
* Most common severe — respiratory tract infection in — & —
* Commonest cause of hospital — in young children
* May affect —
* Usually — respiratory symptoms in — & —
* Severe disease if —
* Worldwide distribution: Typical seasonality in temperate climates
* — the norm
* Source of infection for an infant or young child is typically adults &
older children
* – infectious: Spread facilitated by — places, crèche/preschool attendance, other siblings attending school etc
lower
infacts and younf children
hospital admissions
adults
upper
older children n audlts
immunocormpromised
re infection
highly
croweded
RSC bronchiolitis: — inflammatory injury of the –
* Respiratory — with — , nasal — , —
* Apnoea
* Irritability
* Cyanosis
* Prominent intercostal retraction indicating — airway obstruction
acute
bronchioles
disteess
tahcyponea , nasal flaring and wheeze
lower
treatmenet for RSV:
No effective — available
– High risk children, — immunisation with palivizumab
during peak season – given monthly & no lifelong immunity
* Treatment mainly — :
– —
– —
* Antiviral – —
– Consider for high-risk infants with severe disease
– However clear benefit not conclusively demonstrated
* Isolate with — precautions
- new developments in rsv treatment :
* 2 forms of passive immunisation for infants against
RSV have been authorised recently in EU
1. Nirsevimab:
— acting monoclonal antibody, can be administered –
2. RSVpreF (Abrysvo, produced by Pfizer) — vaccine provides — protection through — antibody transfer
* 2 forms of RSV vaccine for — people, have been
approved –
1. RSVPreF3 (Arexvy, produced by GSK)
2. RSVpreF (Abrysvo, produced by Pfizer)
vaccines
passive
supportive
antipyrtic
oxygen
ribavirin
doplet
long acting
directly
maternal
infact
transplacental
older ppl
1- parainfluenza virus:
* Epidemiology
– — serotypes – Types 1 – 4 (4a & 4b)
– 6 – 9% of respiratory viral infections
* Biological features and pathogenesis
– Incubation period of 3 – 6 days
– — (laryngotracheobronchitis) in children
* presents as a – , — cough in the middle of the — , can also cause—-
* 2nd most common cause of — respiratory hospitalisation
– Moderate-to-severe infection in
immunocompromised patients
* Treatment:
– —
2- adenovirus;
* Epidemiology
– Many different serotypes (~50)
* Biological features and pathogenesis
– Cause – , — & —
– RTIs include
* “Common cold”,
* Pharyngitis
* Bronchitis,
* Bronchiolitis
* —- winter & spring,
– more common in— than — & in –
four
croup
harsh brassy cough
night
bronchiolitis
childhood
supporitve
RTI , diarohera , conjucivtis
penumonia
boy > girls
immunocompromsed
general comments:
* History (including vaccination history) & examination
* Respiratory sample
– Nasopharyngeal aspirates/ throat swabs / broncho-
alveolar lavage / sputum
* Which tests?
– — to detect viral nucleic acid in specimens
* often done as part of a ‘multiplex’ test – e.g. check for influenza virus & RSV in a —
– Serology – not routine; time taken to mount
antibody response
– Cell culture – — , not done diagnostically
NAAT/PCR
throat swab
slow
1- avian influenza:
* Disease of — (all species) caused by —
* — avian influenza sub types
* Generally replicate — in
humans
* Don’t transmit well to —
* — reservoir of potential infection
* — mutations, — of new genes,
especially – —
2- MERS-COV:
* Viral respiratory disease caused by a —
(MERS‐CoV) first identified in 2012.
* Majority of human cases due to —
infections
– Doesn’t seem to pass easily from person-to-person unless there is — contact, e.g. providing unprotected care to a patient
* — likely to be a major reservoir host & an animal source of MERS infection in humans
– However, exact role of camels in transmission of the virus & the
exact route(s) of transmission are unknown
birds
influena A
15
ineffienctly
humans
extensive
rapid
accquisiton
H5 N1
cornovirus
human to human
direct contact
camels
MERS-COV:
* Index case, United Arab Emirates
(UAE), Sept. 2012
* Globally 2613 laboratory confirmed
cases
– Majority reported from Saudi Arabia (2196 cases, including 855 related deaths) with a case–fatality ratio of 39%.
* – > — :
– — community cases
– — clusters
– — acquisition
– — cases
* ¾ cases underlying disease
* Incubation period —
m >f
spordic
family
Nosocomial
imported
12 days
SARS-COV-2:
* — , — respiratory syndrome coronavirus 2 (SARS-CoV-2)
causing — disease 2019 (COVID-19)
* Identified 7/1/2020
– Increase in – of unknown aetiology in Wuhan, China
during Dec 2019
– Novel Coronavirus:
1-* — virus
– —-sense single-stranded RNA virus
2-* — virus
– Identified 7/1/2020
* 15/2/2020 – 104 strains had been sequenced
* 24/3/2020 – genomic and proteomic
compositions identified
– Coronaviruses
* Not new
* Build on what we know
severe acute
conoavirus
pneumonia
ra virus
+ve
labile virus
info:
* 4 endemic
Coronaviruses
* OC43,
* 229E,
* NL63
and
* HKU1
SARS-COV-2:
* Pathogenesis related to function of— & —-
* Has – main structural proteins:
– S = –
– E = –
– N = –
– M = –
* – non-structural proteins & —
accessory proteins
* Binds to— receptor in —
and other tissues
- variants:
* SARS-CoV-2 evolves over time (like other viruses)
* Most mutations have no impact on viral —
* Certain variants have emerged rapidly within populations with evidence for
enhanced — or — implications; these are considered variants
of concern
structural
non structral protiens
4
spike
envelope
neucleopasid
memrbane
16
5-8
ACE2
lungs
viral function
transmission or clinical implication
transmission:
Spread:
* Primarily via respiratory —
* Also:
– —
– Contact with — surfaces and transfer to — membranes
Incubation period: — days with median of — days
Infectivity depends on — and — of illness
* Transmission can occur 1-3 days — symptom onset.
– Peak viral load — after the first week of symptoms.
– mild to moderate COVID-19 may shed virus for up to — following onset of symptoms.
– severe COVID-19 may shed virus for up to —
* Asymptomatic persons can transmit the virus, but for —
periods
droplets
aersoles
contaminated
mucus
1-14
5-6
stage and severity
before
declined
10 days
20 days
shorter
