Upper Respiratory Tract Infections.pptx

7/30/2019 Upper Respiratory Tract Infections.pptx

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Upper Respiratory Tract Infections

Dr M. Kothalawela

Infection 2

2009/10 batch


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Burden of URI

Significant morbidity

and direct health care

costs

Direct costs of $ 17billion annually

Occasionally leads to

fatal illness

Excessive use of

antibiotics a major

issue


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Common URI terms are defined as

follows:

Rhinitis - Inflammation of the nasal mucosa

Rhinosinusitis or sinusitis - Inflammation of the nares and paranasalsinuses, including frontal, ethmoid, maxillary, and sphenoid

Nasopharyngitis (rhinopharyngitis or the common cold) -Inflammation of the nares, pharynx,hypopharynx, uvula, and tonsils

Pharyngitis - Inflammation of the pharynx, hypopharynx, uvula, andtonsils

Epiglottitis (supraglottitis) - Inflammation of the superior portion ofthe larynx and supraglottic area

Laryngitis - Inflammation of the larynx

Laryngotracheitis - Inflammation of the larynx, trachea, andsubglottic area

Tracheitis - Inflammation of the trachea and subglottic area


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The Common Cold (Rhinitis)

Children average 8 per year, adults 3 Etiologies :

Rhinoviruses 30 to 35% Coronaviruses about 10% Miscellaneous known viruses about 20% Influenza and adenovirus-30% Presumed undiscovered viruses up to 35% Group A streptococci 5% to 10%

Parainfluenza was the first respiratory virus isolated(1955)

Seasonal variation Rhinovirus early fall Coronavirus- winter


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Describe the scientific basis of

A person may have more than one episode of

common cold while get only one episode of

chickenpox for life


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The common cold


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Transmission of rhinoviruses

Direct contact is the most efficientmeans of transmission: 40% to 90%

recovery from hands.

Infectious droplet nuclei Brief exposure (e.g., handshake)

transmits in less than 10% of instances

Kissing does not seem to be a commonmode of transmission.


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Clinical characteristics

Incubation period 12-72 hours

Nasal obstruction, drainage, sneezing,

scratchy throat

Median duration 1 week but 25% can last 2

weeks

Pharyngeal erythema is commoner withadenovirus than with rhino or coronavirus


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Acute bacterial sinusitis

Epidemiological studies suggest 1 billion cases of viralrhinosinusitis occur annually in the US

Of these0.5-2% are complicated by bacterial sinusitis

Viral infection--> obstruction of ducts and compromise ofmucocilary blanket--> acute infection from virulent organisms(most often S. pneumoniae and H. influenzae)--> opportunisticpathogens

Nose blowing generates high intranasal pressures that depositbacteria into the sinus cavity

More common in adults than in children


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Paranasal sinuses


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Sinusitis

Community acquired bacterial sinusitis S.pneumoniae

H. influenzae

S. pyogenes Nosocomial sinusitis

Seen in critically ill, mechanically ventilated

S. aureus

Pseudomonas aeruginosa

Serratia marcescens

fungal


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Clinical features

Clinical features

Sneezing

Nasal discharge

Facial pressure

Fever

Purulent drainage

Headache

Sinus imaging not routinely recommended


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Acute sinusitis: complications

Maxillary: usually uncomplicated

Ethmoid: cavernous sinus thrombosis-serious

Frontal: osteomyelitis of frontal bone; cavernous

sinus thrombosis; epidural, subdural, or intracerebralabscess; orbital extension

Sphenoid: Rare; extension to internal carotid artery,cavernous sinuses, pituitary, optic nerves; common

misdiagnoses include ophthalmic migraine, asepticmeningitis, trigeminal neuralgia, cavernous sinusthrombosis


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Chronic sinusitis

The previous patient had an invasive aspergillus

sinusitis as a result of chronic high dose steroid

therapy, resulting in occlusion of carotid artery and

invasion into the brain. She died in a month. Bacterial: Cultures show a variety of opportunistic

pathogens including anaerobes but problem is

mainly anatomic, not microbiologic

Fungal: suspect especially when a single sinus is

involved;


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Spectrum of fungal sinusitis

Simple colonization

Sinus mycetoma (fungus

ball)

Allergic fungal sinusitis

Acute (fulminant)

invasive sinusitis

(notably, rhinocerebralmucormycosis)

Chronic invasive fungal

sinusitis


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Acute pharyngitis

Inflammatory syndrome of the pharynx

Most cases are viral

Most important bacterial cause is Streptococcus

pyogenes (15-20%)

Presents with sore or scratchy throat

In severe bacterial cases there may be

odynophagia, fever, headache


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Acute pharyngitis: physical exam

Viral: edema and hyperemia of tonsilsand pharyngeal mucosa

Streptococcal: exudate and hemorrhageinvolving tonsils and pharyngeal walls

Epstein-Barr virus (infectious mono):may also cause exudate, with

nasopharyngeal lymphoid hyperplasia


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Pharyngoconjuntival fever

Adenoviral pharyngitis

Pharyngeal erythema and exudate may

mimic streptococcal pharyngitis Conjunctivitis (follicular) present in 1/3 to

1/2 of cases; commonly unilateral but

bilateral in 1/4 of cases


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Vincents angina and Quinsy

Vincents angina: anaerobic pharyngitis

(exudate; foul odor to breath)

Ludwigs angina- cellulitis of dental origin

Quinsy: peritonsillitis/peritonsillar abscess.

Medial displacement of the tonsil; often

spread of infection to carotid sheath


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Diphtheria

Classic diphtheria (Corynebacteriumdiphtheriae): slow onset, then markedtoxicity

Arcanobacteriumhemolyticum (formerlyCornyebacteriumhemolyticum): exudativepharyngitis in adolescents and young adultswith diffuse, sometimes pruritic

maculopapular rash on trunk andextremities


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Diphtheria

fibrous pseudomembrane with necrotic epithelium and leukocytes


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Miscellaneous causes of pharyngitis

Primary HIV infection

Gonococcal infection

Diphtheria Yersiniaentercolitica (can have fulminant

course)

Mycoplasmapneumoniae

Chlamydiapneumoniae


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Treatment

Symptomatic

Penicillin for Strep throat

Macrolides for pen allergic patients Add an anti-anaerobic agent for Vincents and

Ludwigs angina


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Acute laryngotracheobronchitis (croup)

Children, most often in 2nd year

Parainfluenza virus type 1 most often in U.S.A. butother agents are Mycoplasma pneumoniae, H.influenza

Involvement of larynx and trachea: stridor,hoarseness, cough

Subglottic involvement: high-pitched vibratory

sounds Can lead to respiratory failure (2% get hospitalized)


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Acute epiglottitis

A life-threatening cellulitesof the epiglottis andadjacent structures

Onset usually sudden (as

opposed to gradual onset ofcroup); drooling, dysphagia,sore throat

H. influenzae the usual

pathogen both in children(the usual patients) andadults


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Acute suppurative

parotitis

Uncommon, but highmorbidity andmortality

Usually associated withsome combination ofdehydration, old age,

malnutrition, and/orpostoperative state

S. aureus the usual

pathogen


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Deep fascial space infections of the

head and neck

Several syndromes according to anatomic

planes

Can complicate odontogenic or oropharyngeal

infection

Ludwigs angina: bilateral involvement of

submandibular and sublingual spaces (brawny

cellulitis at floor of mouth)


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Deep fascial space infections of the

head and neck (2)

Lemierre syndrome: suppurative

thrombophlebitis of internal jugular vein

(Fusobacterium necrophorum)

Retropharyngeal space infection: contiguous

spread from lateral pharyngeal space or

infected retropharyngeal lymph node;

complications include rupture into airway,

septic thrombosis of internal jugular vein


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Severe acute respiratory distress

syndrome (SARS)

Caused by a previously

unrecognized coronavirus

genome has now been

sequenced. Clinical manifestations are similar

to those of other acute

respiratory illnessesnotably,

influenza

Cases in U.S.associated mainly

with travel or as secondary

contacts


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SARS: Radiographic findings

Early: a peripheral/pleural-based opacity (ground-glass or

consolidative) may be the only

abnormality. Look especially at

retrocardiac area.

Advanced: widespread

opacification (ground-glass or

consolidative) tending to affect

the lower zones and often

bilateral. Pleural effusions,

lymphadenopathy, and

cavitation are not seen.


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Disease Possible organisms Preferred specimen


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Disease Possible organisms Preferred specimen


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Lower respiratory tract infections

\


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Respiratory tract


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Anatomy of lower respiratory tract-

Trachea

Trachea 11-12cm tube,

thickened by cartilage, which extends fromthe larynx into the thoracic cage.

It is lined with pseudostratified epithelium,containing ciliated and mucous-secreting cells,and branches to form the left and rightprimary bronchi.

It represents the change from upper to lowerrespiratory tract.


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Bronchi

One primary bronchus supplies each lung. -

lined with pseudostratified, ciliated epithelium

and, on entering the lungs, divide to form the

secondary lobar bronchi, one for each lobe ofthe lungs.

Each secondary bronchus divides to produce

tertiary bronchi, which in turn produce thebronchioles


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Bronchial tree

This successive branching produces a

bronchial tree of ever decreasing diameter

which is characterised by a gradual loss of

cartilage, increase in smooth muscle withinthe wall and change from columnar to

cuboidal epithelium.

16 divisions in neonates 23 divisions in adults


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Lungs

Each lung is divided by fissures into lobes: 2 in the left(superior and inferior), 3 in the right (superior, middle andinferior). The lobes are further subdivided into lobules.

The lungs are housed in a pleural membrane.

Within the lobules, the bronchial tree is now at the level ofthe bronchioles and subsequently the alveoli. It is estimatedthat the adult human lung contains 300 million alveoli, whichcollectively offer a total surface area of 70m2 for gaseousexchange.

The lungs therefore, are primarily composed of alveoli, the

capillaries of the pulmonary circulation and connective tissue.Adequately perfused lungs may consist of 40% by weight ofblood in the circulation.


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Normal Host Defence Mechanisms

Mucocilliary escalator

Phagocytosis

Alveolar macrophages

Lysozymes

IgA

Interferons


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Bronchitis

Inflammation of the bronchial tubes

Tissues become irritated

More mucous then usual produced

Results in cough


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Acute bronchitis

Only lasts for a few weeks

Generally viral in origin

Rhinovirus, parainfluenzae, RSV and Influenza

Can get secondary bacterial overgrowth

H. influenzae

S. pneumoniae

S.aureus

Mycoplasma and Chlamidiya


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Chronic respiratory diseases

BronchiectasisLocalised, irreversible dilation of part of thebronchial tree

COPD

This is a term used for a number of conditionsincluding-

Emphysema

Alveoli lose their elasticity resulting in shortness of

breath Chronic bronchitis


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COPD

Acute exacerbations generally caused by

viruses (rhinoviruses, parainfluenza)

Secondary bacterial invasion is extremely

common (H.influenzae, Moraxella)


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Pneumonia

Inflammation of the alveoli of the parenchyma

of the lung with consolidation and exudation

Cough

Pleuritic pain

Production of purulent sputum Fever


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Pneumonia

Risk factors

COPD

Diabetes

Cardiac / Renal failure

Immunosuppression

Reduced levels consciousness Anything that inhibits the gag / cough reflex


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Community acquired pneumonia

S. pneumoniae

H. influenzae

Moraxella

K. pneumoniae(Friedlanders bacillus)

Pasturella N. meningitidis


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Hospital acquired pneumonia

Risk factors include mechanical ventilation

Enterobactericiae

Acinetobacter

Pseudomonas apecies

S.aureus (MRSA)


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Atypical pneumonia

Mycoplasma pneumoniae (Eaton agent)

Obligate human pathogen

Epidemics occur at 4-6 year intervals

Spread requires close contact

Common in children


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Atypical pneumonias

Chlamydia pneumoniae

Chlamydia psittaci

Legionairres disease

Q fever (Coxiella burnetti)

Hantavirus (ARDS)


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Investigations for pneumonia

Blood culture

Resp specimens/blood for viruses, chlamydia& mycoplasma

Urine for legionella & pneumococcal antigentesting

Sputum

BAL

Pleural fluid


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Pneumocystis jiroveci- stains

Panel A shows typical pneumocystis cystforms in a bronchoalveolar-lavagespecimen stained with Gomorimethenamine (x100). Thick cyst walls andsome intracystic bodies are evident.WrightGiemsa staining can be used for

rapid identification of trophic forms of theorganisms within foamy exudates, asshown in Panel B (arrows), inbronchoalveolar-lavage fluid or inducedsputum but usually requires a highorganism burden and expertise ininterpretation (x100). Calcofluor white is afungal cyst-wall stain that can be used for

rapid confirmation of the presence of cystforms, as shown in Panel C (x400).Immunofluorescence staining, shown inPanel D, can sensitively and specificallyidentify both pneumocystis trophic forms(arrowheads) and cysts (arrows) (x400).
http://content.nejm.org/content/vol350/issue24/images/large/09f2.jpeghttp://content.nejm.org/content/vol350/issue24/images/large/09f2.jpeg


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Overview

A. Basic Virology

B. Flu, Seasonal flu, Avian flu, Swine flu and

Pandemic Flu

C. Transmission

D. Specimen Collection and Transport

E. Infection Control


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A. Influenza viruses

Three main types Influenza A

Influenza B

Influenza C

Influenza A Human, Mammals and Birds

Influenza B- Humans only, Only one sub type-(But different strains)


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Th A t A i


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The Agent A virus Are Members of Ortho Myxo viridae family

Ortho Straight

Myxo- Love mucus

Consists of Protein container covered with spikes & a 8 segmentedgenome

Two types of spikes H type to attach the respiratory epithelium (Pathogencity)

N type To break up the cell and spread further within host Infectmore cells

H type is antigenic and antibodies formed against it, Only homotypic protection

17 H types and 9 M types (These are used to name the differentviruses)


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Influenza A subtypes

Different subtypes causes infections in

different species

Generally Avian Viruses cause infections in

birds

Human Strains cause infections in humans

Inter species spread is minimal species

barrier

But occur @ Human animal interface


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Sub types

Source Subtypes

Avian Influenza

viruses Any

type may be

present but H5,

H7 and H9 arecommon

Influenza A (

H5)

H5N1, H5N2, H5N3, H5N4, H5N5, H5N6, H5N7,

H5N8, and H5N9

Influenza A

(H7)

H7N1, H7N2, H7N3, H7N4, H7N5, H7N6, H7N7,

H7N8, and H7N9.

Influenza A

(H9)

H9N1, H9N2, H9N3, H9N4, H9N5, H9N6, H9N7,

H9N8, and H9N9

Swine origin H1, H2 and H3 H1N1, H1N2, H2N1, H3N1, H3N2, and H2N3

Prominent

Human

H1N1, and H3N2

Human and Avian subtypes are


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Human and Avian subtypes are

different

Difference @ Human subtype Avian Sub types

Overole Genetic

differences

52 key genetic differences exist between human

and avian sub types

PB2 RNA

polymerase gene

Position 627 in RNA

polymerase all human

subtypes- codes for

LYS

Same position codes for

GLU

Until discovery of H5 N1

Binding to Sialic

acid receptors

2-3 sialic acid

receptors

2-6 sialic acid receptors

Swine types binds to the both 2-3 and 2-6

sialic acid receptors


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Pig-Man Interface

Man- Bird interface

B.


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1. Flu Common term used to describe clinical manifestation of

infection caused by influenza virusesInfluenza A, B, and C

Clinical feature

Fever* or feeling feverish/chills Cough

Sore throat

Runny or stuffy nose

Muscle or body aches

Headaches Fatigue (tiredness)

Some people may have vomiting and diarrhea, though this ismore common in children than adults.

B


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2. Seasonal Flu Flu, which shows epidemic spread in certain Seasonal flu

Usually due to human adapted sub types Seasonal flu in northern hemisphere -October and as late as May

Seasonal flu in southern hemisphere-

In each flu season- 15% to 20% of population get flu during aseason with average of 36,000 deaths (USA)

Risk groups Elderly,

patients with chronic Respiratory infections,

Diabetics,

residents in Long term Care

These human adapted strains may change the antigenic

structure in due to changes occur in genomeantigenic drift


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Seasonal Flu. Every year, the public health officials of northern hemisphere look out for

Virological Surveillance for Infkuenza A and B and Novel Viruses

Outpatient Illness Surveillance (ILI) and SARI

Mortality Surveillance - from influenza A like illnesses

Influenza-Associated Pediatric Mortality SurveillanceSystem

Hospitalization Surveillance from SARI and ILI

Summary of the Geographic Spread of Influenza

In parallel, a surveillance is going on in southern hemisphere as well

We too, carry out them in smaller scale ILI, SARI, and Sentinel sitesurveillance too.

National Influenza Reference Centre in MRI

B


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3 Avian Flu(Bird Flu) Flu in birds

May be due to two types of agents HPAI

LPAI

All are due to Influenza A viruses LPAI virus- causes Milder disease HPAIsevere disease and may cause death among large

herds

If found to be positive in a herd- CULLING is advices

in order to prevent further spread So far not reported in SL

A rare possibility of transferring to humans at Humananimal interface High Mortality


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B


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B

4. Swine Influenza

Also known as pig influenza,

swine flu,

hog flu and

pig flu

Infection by one of several types of swineinfluenza viruses SIV or S-OIV (Virusesendemic to pigs)

H1N1, H1N2, H2N1, H3N1, H3N2, and H2N3.

Swine Flu


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Swine Flu

B


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B

5. Pandemic Flu

When usually influenza illnesses spread acrosscontinents with huge mortality among humans

Usually due to appearance of novel virus strain which

is transmissible from person to person

As the people lack immunity to Large numberssuccumbed Cytokine Storm

Due to major change of genome due to re-assortment


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Pandemic Influenza Viruses

Are Novel viruses

Due to re-assortment, Completely new virus

where no one is immune

Ex 1918 1919 (spanish flu) Killed 20 to 50 million

H1N1

1957 1958(Asian flu) Killed 3 million- H2N2 1968 1969 (Hong Kong flu)Killed 1 million- H3N2

2009 2010Killed 18,000 world wideH1N1


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C.Transmission


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Infected asymptomatic and Infected symptomatic

When Sneeze or talkDirect spread Up to 6 feet through droplets

Indirect spread- via surfaces and fomites through contact

Flu is contagious Healthy adults with disease -infectious one day before

symptoms to 5 to 7 d after become sick

Children - infectious >>7 days

Some may get asymptomatic disease- but stillspread the disease


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D Specimen collection and


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D. Specimen collection and

transportation


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National Influenza Centre


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Sample collection

Personal Protective Equipment N95 mask, gloves,gown

Timing : Early as possible (


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E I f i C l


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E. Infection Control

Prevent Infection transmission

Upper Respiratory Tract Infections.pptx

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