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INFLUENZA
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Influenza-Objectives
• History
• Transmission
•
Clinical Features• Diagnosis
• Treatment
• Prevention
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History
• First described by Hippocrates in 412 BC
•
Influenza-like outbreaks have been clearlydocumented since 1173 AD.
•
Since 1580- 31 such possible influenzapandemics – global epidemics
• 3 in this century: in 1918, 1957 & 1968.
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• While pandemics can kill > 20 million people,
more people have died this century from
influenza complications that have occurred
during a seasonal epidemic, than from a
pandemic.
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INFLUENZA PANDEMICS
Name of Pandemic Date Deaths Case
Fatality rate
Subtype
Involved
Pandemic
severity
index
Asiatic ( Russian) Flu 1889-
1890
1 million 0.15 Possibly
H3N8
NA
Spanish Flu 1918-
1920
20-100
million
2 H1N1 5
Asian Flu 1957-
1958
1-1.5 million 0.13 H2N2 2
Hong Kong Flu 1968-
1969
0.75-1
million
<.0.1 H3N2 2
Swine Flu 2009-
2010
18,000 0.03 H1N1 NA
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History
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SEASONAL EPIDEMICS
• Worldwide, annual epidemics: 3-5 million casesof severe illness & about 250 000 - 500 000deaths.
• Illnesses result in hospitalizations & deathsmainly among high-risk groups (the very young,elderly or chronically ill).
• Most deaths associated with influenza inindustrialized countries - people age 65 or older.
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SEASONAL EPIDEMICS
• Influenza epidemics occur yearly during
autumn & winter in temperate regions.
• In some tropical countries, influenza viruses
circulate throughout the year with one or two
peaks during rainy seasons.
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EPIDEMIOLOGY
Influenza update N 185 - May, 2013 (WHO):
• Northern hemisphere: influenza season graduallycoming to an end with inter seasonal levels in North
America, Europe & northern Asia.
• A low level persistent transmission in a few countries:Canada and Egypt.
• Associated with increasing numbers of influenza type Bvirus appearing late in the season across NorthAmerica and parts of Europe
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EPIDEMIOLOGY
Prior to this, most commonly detected virus:
• North America- influenza A(H3N2)
• Europe - A(H1N1)pdm09
• Northern Asia - both viruses in varying proportions.
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Number of specimens positive for influenza by
subtype in the northern hemisphere
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• Tropics & Southern hemisphere- Low levels of
influenza activity, remains at inter-seasonal levels.
• Madagascar -epidemic since the beginning of April.
• In China- new cases of H7N9 have been reported
with 131 cases & 32 deaths to date
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Number of specimens positive for influenza by subtype in the
Southern hemisphere
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Number of specimens positive for influenza by subtype in the
Tropical South America Transmission Zone
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Epidemiology
• Worldwide there have been more than
440,000 laboratory confirmed cases of
pandemic Influenza H1N1 and over 5,700
deaths reported to the World HealthOrganization
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Epidemiology
• Trinidad and Tobago the most recent
epidemiological reports indicate 210
confirmed H1N1 laboratory confirmed cases
and five H1N1 deaths
• Males and females seem to be equally
affected.
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Epidemiology
• 57% of these cases fall within the 0-19 age
group and
• 37% within the 20-49 age range
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Epidemiology
• Important to note persons who died presented
with respiratory distress when admitted at the
hospital and had serious underlying risk factors
• Also the rest of the H1N1 cases treated in
Trinidad and Tobago were relatively mild and the
persons returned to their normal activities withinseven to ten days
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Etiology
• There are three types of influenza viruses: A, Band C.
• The influenza A and B viruses that routinely
spread in people (human influenza viruses)are responsible for seasonal flu epidemicseach year.
•
Influenza type C infections cause a mildrespiratory illness and are not thought tocause epidemics.
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Etiology
• Influenza A viruses can be broken down into
sub-types depending on the genes that make
up the surface proteins; the hemagglutinin (H)
and the neuraminidase (N).
• There are 17 different hemagglutinin subtypes
and 10 different neuraminidase subtypes.
• Influenza A viruses can be further broken
down into different strains
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Etiology
• CDC follows an internationally accepted namingconvention for influenza viruses.
• The approach uses the following components:
1. The antigenic type (e.g., A, B, C)
2. The host of origin (e.g., swine, equine, chicken, etc. Forhuman-origin viruses, no host of origin designation isgiven.)
3. Geographical origin (e.g., Denver, Taiwan, etc.)
4. Strain number (e.g., 15, 7, etc.)5. Year of isolation (e.g., 57, 2009, etc.)
6. For influenza A viruses, the hemagglutinin andneuraminidase antigen description in parentheses
(e.g., (H1N1), (H5N1)
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Pathophysiology
• Influenza viruses are encapsulated, negative-
sense, single-stranded RNA viruses of the
family Orthomyxoviridae.
• The core nucleoproteins are used to
distinguish the 3 types of influenza viruses: A,
B, and C. Influenza A viruses cause most
human and all avian influenza infections
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Pathophysiology
• The RNA core consists of 8 gene segments
surrounded by a coat of 10 (influenza A) or 11
(influenza B) proteins.
• Immunologically, the most significant surface
proteins include hemagglutinin (H) and
neuraminidase (N).
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Pathophysiology
• Major typing of influenza A occurs throughidentification of both N and H. Sixteen N and 9 Htypes have been identified.
• All hemagglutinins and neuraminidases infectwild waterfowl, and the various combinations ofH and N results in 144 combinations andpotential subtypes of influenza.
• The most common subtypes of human influenza
virus identified to date contain onlyhemagglutinins 1, 2, and 3 and neuraminidases 1and 2.
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Pathophysiology
• The variants are used to identify influenza A
virus subtypes.
• For example, influenza A subtype H3N2
expresses hemagglutinin 3 and neuraminidase
2.
• H3N2 and H1N1 are the most common
prevailing influenza A subtypes that infect
humans.
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Pathophysiology
• The viral RNA polymerase lacks error-checking
mechanisms and, as such, the antigenic drift
from year to year is sufficient to ensure a
significant susceptible host population.
• However, the segmented genome also has the
potential to allow re-assortment of genome
segments from different strains of influenza ina co-infected host.
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Pathophysiology
• In addition to humans, influenza also infects a
variety of animal species.
• More than 100 types of influenza A infect
most species of birds, pigs, horses, dogs and
seals. Influenza B has also been reported in
seals, and influenza C, rarely, in pigs.
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Pathophysiology
• Influenza A is a genetically labile virus, with
mutation rates as high as 300 times that of
other microbes.[14] Changes in its major
functional and antigenic proteins occur bymeans of 2 well-described mechanisms:
antigenic drift and shift.
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Pathophysiology
• Antigenic drift is the process by which inaccurate viralRNA polymerase frequently produces point mutationsin certain error-prone regions in the genes.
• These mutations are ongoing and are responsible for
the ability of the virus to evade annually acquiredimmunity in humans. Drift can also alter the virulenceof the strain.
• Drift occurs within a set subtype (eg, H2N2). For
example, AH2N2 Singapore 225/99 may reappear aswith a slightly altered antigen coat as AH2N2 NewDelhi 033/01.
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Pathophysiology
• Antigenic shift is less frequent than antigenic drift. In ashift event, influenza genes between 2 strains arereassorted, presumably during co-infection of a singlehost.
•
Segmentation of the viral genome, which consists of 10genes on 8 RNA molecules, facilitates geneticreassortment. Antigenic shift is less frequent thanantigenic drift. In a shift event, influenza genesbetween 2 strains are reassorted, presumably during
co-infection of a single host. Segmentation of the viralgenome, which consists of 10 genes on 8 RNAmolecules, facilitates genetic reassortment.
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Pathophysiology
• Such an antigenic shift can result in a virulent
strain of influenza that possesses the triad of
infectivity, lethality, and transmissibility and can
cause a pandemic.• Three such influenza pandemics have occurred in
recorded history: the 1918 Spanish influenza
(H1N1) pandemic and the pandemics of 1957(H2N2) and 1968 (H3N2). Smaller outbreaks
occurred in 1947, 1976, and 1977.
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Pathophysiology
• To date, the vast majority of cases of avian
influenza have been acquired from direct contact
with live poultry in emerging nations.
• Hemagglutinin type H5 attaches well to avianrespiratory cells and thus spreads easily among
avian species. However, attachment to human
cells and resultant infection is more difficult.• The reasons why humans can be infected with H5
are poorly understood.
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Pathophysiology
• To date, avian influenza remains a zoonosis, withno sustained human-to-human transmission.
• Family clusters have been reported but appear to
be almost always related to common exposures;however, limited human-to-human spreadthrough close proximity could not be officiallyruled out.
• In September 2004, one case in Thailandprobably involved daughter-to-mothertransmission; the mother died.
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Pathophysiology
• The pathophysiology of avian influenza differs
from that of normal influenza.
• Avian influenza is still primarily a respiratory
infection but involves more of the lower
airways than human influenza typically does.
• This is likely due to differences in the
hemagglutinin protein and the types of sialic
acid residues to which the protein binds.
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Pathophysiology
• Although this results in a more severe
respiratory infection, it probably explains why
few, if any, definite human-to-human
transmissions of avian influenza have beenreported: infection of the upper airways is
probably required for efficient spread via
coughing and sneezing.
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Pathophysiology
• In contrast to human influenza, most deaths
associated with avian influenza have been due
to primary viral pneumonia, with no evidence
of secondary bacterial infection.
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Pathophysiology
Reservoirs for avian influenza A
• Waterfowl, including ducks and geese, areconsidered to be the natural reservoirs for avian
influenza A. Most infections in these birds arebelieved to be asymptomatic.
• However, because these viruses can also infectand cause disease in domestic poultry and
because of the potential economic implications,substantial attention has been given to avianinfluenza.
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TRANSMISSION
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Transmission
• Transmission of influenza from poultry or pigs to
humans appears to occur predominantly as a
result of direct contact with infected animals.
• The risk is especially high during slaughter andpreparation for consumption; eating properly
cooked meat poses no risk.
•
Avian influenza can also be spread throughexposure to water and surfaces contaminated by
bird droppings.[23]
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Transmission
• Influenza viruses spread from human tohuman via aerosols created by coughs orsneezes of infected individuals.
• Influenza virus infection occurs afterinhalation of the aerosol by a person who isimmunologically susceptible.
• If not neutralized by secretory antibodies, thevirus invades airway and respiratory tractcells.
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Transmission
• Once within host cells, cellular dysfunction
and degeneration occur, along with viral
replication and release of viral progeny.
• Systemic symptoms result from inflammatory
mediators, similar to other viruses. The
incubation period of influenza ranges from 18-
72 hours.
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Transmission
• Viral shedding occurs at the onset of
symptoms or just before the onset of illness
(0-24 h). Shedding continues for 5-10 days.
• Young children may shed virus longer, placing
others at risk for contracting infection with the
virus.
• Shedding may persist for weeks to months inhighly immunocompromised persons.[5]
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Direct Transmission
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Airbone route
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Contaminated objects
• Hand to mouth
• Hand to nose
• Hand to eyes
HISTORY
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HISTORY
• Sore throat
• Cough
• Headache
• Fever, chills and rigors
• Myalgia
• Dyspnoea
• Weakness and Fatigue
• Vomiting
• Diarrhoea
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• Ask about contacts with the disease
• History of travel travel to places with
outbreaks
EXAMINATION
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EXAMINATION
• Patient looks unwell
• Altered mental status
Febrile to touch, Fever >38 oC
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RHINITIS, EYES WATERY AND RED PHARYNGITIS
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TACHYCARDIA LUNGS CLEAR
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Complications
• Reye’s Syndrome
• In children
– 2-12 days after onset of infection
– Severe fatty infiltration of the liver
– Cerebral edema
– Risk enhanced by use of salicylates
– Confusion LOC seizures
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Other complications
• Myositis
• Myocarditis
• Pericarditis
• CNS dysfunction
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Differential Diagnoses
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• Accurately diagnosing influenza A or B infection based
solely on clinical criteria is difficult because of theoverlapping symptoms caused by the various virusesassociated with upper respiratory tract infection (URTI).
• In addition, several serious viruses, including adenoviruses,
enteroviruses, and paramyxoviruses, may initially causeinfluenza like symptoms.
• The early presentation of mild or moderate cases offlavivirus infections (eg, dengue) may initially mimicinfluenza. For example, some cases of West Nile feveracquired in New York in 1999 were clinically misdiagnosedas influenza.
Differential Diagnoses
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Differential Diagnoses
• Acute Respiratory Distress Syndrome• Adenoviruses
• Arenaviruses
• Cytomegalovirus
• Dengue Fever• Echoviruses
• Hantavirus Pulmonary Syndrome
• HIV Disease
• Legionnaires Disease
• Parainfluenza Virus
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Diagnostics
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RIDT
• Rapid influenza diagnostic test (RIDT) – used
to detect the virus in nasal secretions and one
of the most common methods used to
diagnose this infection.
• It can help differentiate influenza from
other viral and bacterial infections with similar
symptoms that may be serious and must betreated differently.
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• Rapid flu tests are best used within the first 48 hours of theonset of symptoms to help diagnose influenza anddetermine whether or not antiviral drugs are a treatmentoption.
• Sometimes rapid tests are ordered to help identifyoutbreaks.
• Rapid tests vary in their ability to detect influenza.
• Some types can only detect influenza A; others can detectboth A and B but not distinguish between the two.
• Still others can detect and distinguish between influenza Aand B. However, none of them are able to differentiatebetween the strains of influenza A, such as H1N1.
Viral culture
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• Viral culture has been considered the "goldstandard" for diagnosing influenza, but it cantake up to 3 to 10 days for results.
• It can be used for confirmation of a positive
rapid test result.
• In this test, the influenza virus is actually grownand identified in the laboratory. It has theadvantage of identifying which viruses (A, B, oranother respiratory virus) and which strains ofvirus are present.
Viral culture
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Disadvantages
• The main disadvantages of the rapid influenza
antigen test are:
1) It will miss up to 30% of influenza cases, may
only detect 10-70% of 2009 H1N1 influenzainfections.
2) It will occasionally be positive when someone
does not actually have the flu.
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• Direct fluorescent antibody stain (DFA) – detectsinfluenza A or B virus in samples of nasal secretions.
•This method of testing is more specific than RIDT butrequires specialized equipment to perform and specialtraining to interpret, so it is usually not performed in adoctor's office.
• Samples are typically sent to a laboratory for testing. Anegative result with this test does not rule outinfluenza.
DFA
Viral culture
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Viral culture
• A rapid culture method, known as shell vialculture, may detect the presence of a respiratoryvirus in 24 to 48 hours, however, a traditionalviral culture performed in a large test tube may
require several days before the virus can bedetected.
• Growing the virus in culture is useful for
documenting which strains of influenza arecirculating in the community and which antiviralagents are effective in treating these viruses.
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Viral Culture
• Identifying these outbreaks can assist health careworkers in the prevention and treatment of theflu throughout a community.
• Influenza virus grown in culture can be sent to a
public health laboratory to determine if the strainof influenza A is the antigenic type (H5N1) foundin birds and chickens or the 2009 H1N1 influenzavirus.
•Viral cultures can also be used to identify otherviral infections that cause clinical symptomssimilar to the flu.
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• Real-time polymerase chain reaction (RT-PCR) – molecular testing is available that detects viral geneticmaterial in nasal secretions and is the most sensitivetest for influenza virus.
• However, this test is not widely available and resultscan take from one to several days.
•
These tests may be ordered to diagnose influenza Ainfection, especially in those who are seriously ill(hospitalized) and to help track influenza outbreaks.
RT-PCR
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Disadvantage of RT-PCR
• Some false negatives can occur with this
method.
• A new version of this test with specific
reagents directed toward the 2009 H1N1influenza virus was developed in April 2009 to
allow the detection of this novel flu virus.
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Antibody Tests
•
Influenza A or B antibody tests – these are bloodtests performed to detect the body's immuneresponse to an influenza infection.
• Acute and convalescent samples are required to
help confirm that a recent infection was due tothe flu.
• Antibody testing on single blood samples is notuseful. These tests are not done routinely and are
most often done for public health or researchpurposes.
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Treatment
Mild illness:Basic supportive care :
• antipyretics, such as paracetamol or acetaminophenfor fever or pain
• fluid rehydration and can be provided as needed.• Plenty rest
• Counseling pts- signs of progressive disease, when toseek medical attention
•Antiviral treatment is not necessary for people haveuncomplicated, or mild, illness and are not in a highrisk group for severe illness.
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ANTIVIRALS
Persons at higher risk for influenzacomplications
• children aged younger than 2 years;
• adults aged 65 years and older;
•persons with chronic pulmonary(including asthma), cardiovascular(except hypertension alone), renal,hepatic, hematological (includingsickle cell disease), metabolicdisorders (including diabetesmellitus) or neurologic and
neurodevelopment conditions(including disorders of the brain,spinal cord, peripheral nerve, andmuscle such as cerebral palsy,epilepsy, stroke, mental retardation
• persons with immunosuppression,e.g. HIV, including that caused bymedications
• women who are pregnant orpostpartum (within 2 weeks afterdelivery);
• persons aged younger than 19 years
who are receiving long-term aspirintherapy;
• persons who are morbidly obese (i.e.,BMI is 40 or greater)
• residents of nursing homes and otherchronic-care facilities
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ANTIVIRALS
2 classes available for treatment and prevention of influenza
1. ADAMANTANES
Include: amantadine and remantadine
MOA: inhibits the function of the M2 protein by blocking the ionchannel and thus stops the replication process virus to infect othercells
- Act against influenza A virus only.
- Come in a capsule or syrup form
side effects: The most frequent reactions are nausea, dizziness andinsomnia
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ANTIVIRALS
2. NEURAMINIDASE INHIBITORS
Includes: oseltamivir and zanamivir
MOA: bind to the active site on the viral neuraminidase, blocking its activity. Thus,virus particles cannot exit the cells as easily, and they tend to clump and notdisperse. This impedes their ability to infect more cells and attenuates thepatient's infection.
-effective against both influenza A and B infections.
-Zanamivir –inhaled powder
-Osetalmivir- capsules
Side effects: zanamivir may be associated with bronchospasm and may exacerbateasthma in some patients-. not recommended for persons with underlying airwaydisease
oseltamivir causes mild nausea and vomiting , which can be reduced by taking itwith food
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ANTIVIRALS
• Treatment is most effective when given within 48hoursafter the onset of illness, and the earlier the better.
• Recommended duration of treatment foruncomplicated illness is 5 days.
•
Patients with suspected influenza should completeantiviral treatment for a full treatment courseregardless of negative initial test results unless analternative diagnosis can be established and clinical judgment suggests that influenza is unlikely
• Supportive care such as oxygen therapy, intravenousfluids, and parenteral nutrition may be needed. Severecases may require ventilatory support with intubation
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TREATMENT
• a pulmonary specialist, a critical care specialist, aninfectious disease specialist, and the staff of the localpublic health department may all be consulted.
• Clinical laboratory personnel should also be informed
before potential isolates are sent to them.• hospital infection-control officers should be involved
early in the care of any patient who might have virus.
• Early involvement of the local public health
department and hospital infection control is necessaryto contain any outbreaks.
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Treatment
• Patients with influenza are at high risk for suchsecondary bacterial complications
• Antibacterial therapy plus antiviral treatment arerecommended for patients with community-acquired pneumonia when influenza also issuspected.
• likely bacterial pathogens associated with
influenza: S. pneumoniae, S. pyogenes, and S.aureus- including MRSA, especially forhospitalized patients .
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Treatment algorithm
• http://www.ncbi.nlm.nih.gov/pmc/articles/PMC139319/figure/f2-25/
l
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Viral Resistance
• Patients receiving antiviral medications who do not respond totreatment might have an infection with an antiviral-resistantinfluenza virus.
• In 2007-2008, a significant increase in the prevalence of oseltamivirresistance was reported among influenza A (H1N1) virusesworldwide. During the influenza season, 10.9% of H1N1 virusestested in the United States were resistant to oseltamivir.
• Oseltamivir resistance has been reported particularly amongimmunocompromised patients with 2009 H1N1 virus infection. hasmade this class of medications less useful clinically
• Infection-control measures are especially important for patientswho are immunocompromised to reduce the risk for transmissionof oseltamivir-resistant viruses
• In 2011 H3N2was found to be resistant to adamantanes
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Post exposure
• Postexposure chemoprophylaxis with neuraminidase inhibitorsgenerally should be reserved for those who have had recent closecontact with a person with influenza.
-family or other close contacts of a person with a suspected orconfirmed case who are at higher risk for influenza complicationsbut have not been vaccinated against the influenza virus strainscirculating at the time of exposure
-Unvaccinated health-care workers who have occupational exposuresand who did not use adequate personal protective equipment atthe time of exposure are also potential candidates forchemoprophylaxis
•
typically administered for a total of no more than 10 days after themost recent known exposure to a close contact known to haveinfluenza.
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Prevention
D fi i i
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Definitions
• Vaccine any preparation intended to
produce immunity to a disease by stimulating
the production of antibodies
• Immunization process whereby a person is
made immune or resistant to an infectious
disease, typically by the administration of avaccine
Wh h ld i d?
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Who should get vaccinated?
– High risk of having serious flu relatedcomplications
–People who live with or care for people at highrisk for developing flu-related complications.
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• Age : 6mths -4 yrs , >50 yrs
• Children aged 6 months to 18 years on long-term
ASA therapy Reye syndrome after infection
• Immunosuppression medication/ HIV
• Chronic pulmonary ( + asthma), cardiovascular (-
hypertension), renal, hepatic, neurologic,hematologic, or metabolic disorders (+ diabetes
mellitus)
• Health-care personnel
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• Health-care personnel
• Household contacts & caregivers of : – Children < 5yrs (esp. <6/12) & adults > 50 yrs
– people with medical conditions with higher risk of
severe complications from influenza
• Women who are pregnant
• People who are morbidly obese(BMI> 40)
V i f hild
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Vaccine for children
•
Recommended 6 months – 19
th
birthday
• 2009 H1N1 was not added to the seasonalvaccine until 2010-2011 flu season
• If did not get the 2009 H1N1 vaccine in 2009-2010 / seasonal flu vaccine in 2010-2011 or
later
not fully protected from 2009 H1N1 virusuntil they receive 2 doses of the 2012-2013 fluvaccine.
2 d i ti
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2 dose vaccination
• 1st dose – as soon as vaccine avaliable
• 2nd dose – 28 days after 1st
• reduced /no protection from a single dose ofvaccine.
• Approx. 2 weeks after the 2nd dose for protectionto begin.
• Protection lasts approx. 1 yr
Wh h ld t b i t d
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Who should not be vaccinated
1. Allergy to chicken eggs2. Previous severe reaction to an influenza
vaccine
3. Children age < 6/124. Moderately / severely ill with or without
fever after recovery then administervaccine
5. Hx of Guillain-Barre Syndrome (GBS) within 6weeks following receipt of influenza vaccine
Vaccination with egg allergy
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Vaccination with egg allergy
• 2012-2013 season
• CDC “administration of both full doses and split
doses of TIV have been tolerated by people with
egg allergies, without serious reactions”
• The Advisory Committee on Immunization
Practices (ACIP) experienced only hives fromconsuming eggs can receive TIV IM as long as
they are treated by a health care provider
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– familiar with the potential manifestations ofegg allergies &
– can be observed by a health care professional
for at least 30 minutes after receiving eachdose.
•
LAIV should not be used in these patients
T i l t i ti t d i (TIV)
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Trivalent inactivated vaccine (TIV)
• Injected muscle of the upper arm or thigh.• Used for healthy people*
– aged > 6/12
–chronic medical conditions
– women who are pregnant
* Healthy people people who do not have anunderlying medical condition that predisposesthem to influenza complications.
Live attenuated intranasal vaccine
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(LAIV)
• Eg. FluMist
• Adult 0.2 mL intranasally once /season
– 1 mL in each nostril
• Peads
– 2-8 yrs NOT previously vaccinated with intranasal
influenza vaccine: as adult then repeat dose in 46-
74 d – >8 years: Administer as in adults
Seasonal Influenza vaccine safety
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Seasonal Influenza vaccine safety
• 2012-2013 seasonal influenza vaccine
– Available August 2012
– protects against• influenza A H3N2 virus
• an influenza B virus &
• the 2009 (Influenza A) H1N1 virus
– Seasonal LAIV & TIV contain all 3 strains .
Adverse effects TIV
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Adverse effects - TIV
• Injection site reactions pain , redness, swelling resolve <2 days without treatment
• Fever, malaise, myalgia & other systemicsymptoms no previous exposure to the
influenza virus antigens in the vaccine e.g. youngchildren.
• Ocular or respiratory symptoms (e.g., red eyes,hoarse voice, cough etc) mild , resolve without
treatment• Immediate hypersensitivity reactions urticaria,
angioedema, anaphylaxis
Adverse Effect LAIV
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Adverse Effect - LAIV
• runny nose /nasal congestion (all ages)
• fever >100F age 2-6 yrs
• sore throat ( adults)
Screening for Vaccine
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Screening for Vaccine
• Ask about:
– Egg allergy
– Adverse events(eg. GBS) to prior doses of
influenza vaccine – Current Health status
• Children age 2- 4 years:
– Presence of wheeze / asthma in the past 12months
• USE TIV (NOT LAIV)
2013 2014 Influenza season
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2013- 2014 Influenza season
• Approved Feb.21st 2013 by ACIP
• TIV
– inactivated influenza vaccines
– replaced with the abbreviation IIV
• egg-based and cell culture-based trivalent inactivated
influenza vaccine (IIV3); and
• egg-based quadrivalent inactivated influenza vaccine
(IIV4).
2013 2014 Influenza season
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2013-2014 Influenza season
• RIV – recombinant hemagglutinin influenza vaccine
– available as a trivalent formulation (RIV3)
–
Produced in insect cells• LAIV
– live, attenuated influenza vaccine,
– available as a quadrivalent formulation (LAIV4)
• numeric suffix # of influenza virus antigenscontained in the vaccine.
Everyday preventative action to stop
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the spread of germs
1. Try to avoid close contact with sick people.
2. If you are sick with flu-like illness, CDC
recommends that you stay home for at least
24 hours after your fever is gone except toget medical care or for other necessities.
(Your fever should be gone without the use
of a fever-reducing medicine.)
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3. While sick, limit contact with others as much
as possible to keep from infecting them.
4. Cover your nose and mouth cough or
sneeze. Throw the tissue after use.
5. Wash hands often with soap and water / use
alco. Based hand rub.
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6. Avoid touching your eyes, nose and mouth.
7. Clean and disinfect surfaces and objects that
may be contaminated .
Public Health
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Public Health
• Enhanced surveillance
– with daily temperature taking
– prompt reporting with isolation
– Influenza update weekly
Thank You
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Thank You
References
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References
• Seneca H. Influenza: epidemiology, etiology, immunizationand management . J Am Geriatr Soc. 1980 Jun;28(6):241-50
• Palese P (January 2006). Making better influenza virus
vaccines? Emerging Infect . Dis. 12 (1): 61 –5
• Government of Trinidad and Tobago.
http://www.news.gov.tt/index.php?news=2346. 04
November, 2009 02:27:00
References
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References
• http://www.cdc.gov/flu/professionals/antivirals/antiviral-use-influenza.htm#indications
• http://www.who.int/csr/resources/publication
s/swineflu/clinical_management/en/
• http://www.ncbi.nlm.nih.gov/pmc/articles/P
MC3430703/
• http://emedicine.medscape.com/article/219557-clinical#a0256
References
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References
• http://www.cdc.gov/flu/about/disease/spread.htm
• http://cid.oxfordjournals.org/content/37/8/10
94.full.pdf