- Swine flu, also known as H1N1, is caused by the influenza A H1N1 virus and causes respiratory illness. It was first detected in Mexico in 2009 and caused a global pandemic. - In India, it has caused periodic outbreaks since 2009, killing over 1000 people annually. The worst affected states have been Gujarat and Rajasthan. - The virus is transmitted through respiratory droplets from coughing and sneezing of infected individuals. It has an incubation period of 1-4 days. Symptoms include fever, cough, sore throat and body aches. Complications can include pneumonia.

1. Swine Flu (H1N1)
Dr Satyadeo Choubey

2. INTRODUCTION
• It is caused by Influenza virus (H1N1)
• It is usually a mild and self limited respiratory
illness
• It has potential to cause significant morbidity and
mortality
• 2009 pandemic influenza A (H1N1) virus is
continued to co-circulate following years along with
seasonal influenza A and it caused significant
mortality among young people

3. EPIDEMIOLOGY
• Latest pandemic of swine flu was first noted in
Mexico in march 2009
• It spread worldwide affected nearly 195
countries and it ended in August 2010

5. • In India outbreak killed:
2009 - 981 2012 - 405
2010 - 1763 2013 - 699
2011 - 75 2014 - 218
• 2015 outbreak became wide spread throughout
India. Gujarat & Rajasthan were the worst affected states
• 2009 pandemic strain is now responsible for the periodic
seasonal outbreaks of Influenza in India
• Almost 1000 people killed till August 2017 since Jan’17

8. • The average incubation period is 1-4 days (maximum 7
days)
• Transmission through contact with large infectious
respiratory droplets while coughing and sneezing
• Formites also play a role in transmission
• Close contact including hand shaking and hand to nose
transmission
• Viral shedding begins the day prior to symptom onset
and often to persist for 5-7 days, sometimes even longer
in children & immuno compromised

10. ETIOLOGICAL AGENT

12. • It’s a RNA virus belonging to the family of
Orthomyxoviridae
• Three main genera - Influenza A, Influenza B,
Influenza C
• Influenza A is further sub-typed into 18 distinct H
types & 9 distinct N types based on
Hemagglutinin & Neuroaminidase antigens on
the surface of the virus

13. • Every year new strains of influenza virus emerge as
its genes undergo point mutations leading to
‘Antigenic drift’
• This process helps the virus to evade host defense
mechanism
• Infuenza A virus has a 8 segmented genome with
eight single stranded RNA segments
• These genes get reassorted and produce a very
different strain altogether- “Antigenic shift”
• 2009 viral strain had undergone triple
reassortment and contain genes from the avian,
swine, and human viruses

15. • Around 1918, the ancestral virus, of avian origin, crossed the species boundaries
and infected humans as human H1N1.
• Soon after in America, where the human H1N1 was infecting pigs; it led to the
emergence of the H1N1 swine strain,.
• 1968, avian strain H1N1 infected humans again; this time virus met the strain
H2N2, and the reassortment originated the strain H3N2. This strain has remained
as a stable flu strain until now.
• The mid-1970s were important for the evolution of flu strains. First, the re-
emergence of the human H1N1 strain became a seasonal strain. Then, a small
outbreak of swine H1N1 occurred in humans, and finally, the human H2N2 strain
apparently became extinct.
• Around 1979, the avian H1N1 strain infected pigs and gave rise to Euroasiatic
swine flu and H1N1 Euroasiatic swine virus, which is still being transmitted in
swine populations.
• The critical moment for the 2009 outbreak was between 1990 and 1993. A triple
reassortment event in a pig host of North American H1N1 swine virus, the human
H3N2 virus and avian H1N1 virus generated the swine H1N2 strain.
• Finally, the last step in S-OIV history was in 2009, when the virus H1N2 co-infected
a human host at the same time as the Euroasiatic H1N1 swine strain. This led to
the emergence of a new human H1N1 strain, which caused the 2009 pandemic.

17. PATHOGENESIS
• Virus particle may settle on nasopharyngeal,
tracheobronchial, conjuctival, or other
respiratory mucosal epithelial cells.
• H1N1 2009 strain can also additionaly bind to the
2,3-linked sialic acid receptors that are present in
the lower respiratory tract and cause diffuse
alveolar damage and thereby causing pneumonia
in healthy individuals

22. COMMON CLINICAL FEATURES
• The hallmark of influenza is the sudden, rapid
onset of symptoms. Influenza symptoms may
include fever, chills, body aches, sore throat, non-
productive cough, runny nose and headache.
Gastrointestinal symptoms and muscle
inflammation occur more often in young children,
and infants can present with a sepsis-like
syndrome

23. Physical findings
• Fever: rapid onset, peaking at 38.400C (up to 41 0C,
especially in children), typically lasting 3 days (up to 4-8
days), gradually diminishing
• Face: flushed
• Skin: hot and moist
• Eyes: watery, reddened
• Nose: nasal discharge
• Ear: otitis
• Mucous membranes: hyperemic
• Cervical lymph nodes enlargement: (especially in children)

24. Course of Illness
• Severity varies from afebrile symptoms mimicking
common cold to severe prostration with or without
major respiratory signs and symptoms, especially in the
elderly.
• Fever and systemic symptoms typically last 3 days,
occasionally 5-8 days, and gradually diminish.
• Cough and malaise may persist more than 2 weeks. Full
recovery may take 1-2 weeks or longer, especially in
the elderly.

25. Complications (Children)
sinus or ear infections,
viral and bacterial pneumonia,
bronchiolitis,
croup,
dehydration (with or without
diarrrhoea)
febrile seizures,
severe dehydration ,
sepsis-like syndrome,
respiratory complications
( Bronchiolitis, Croup, Reactive
airway disease, Pneumonia),
Rhabdomyolysis,
encephalopathy /encephalitis
cardiac complications
(Myocarditis and Pericarditis).
Reye syndrome (with aspirin
use),
Toxic shock syndrome and
Sudden death (may be due to
cytokine dysregulation)

26. Complications Adults And Elderly
• Exacerbation of chronic illness
 Cardiac (congestive cardiac failure, coronary artery
disease);
 Chronic pulmonary disease (COPD),
• Respiratory complications include Bronchitis, Sinusitis,
Reactive airway disease and Pneumonia.
• Invasive bacterial co-infection (sepsis, pneumonia),
mainly from Staphylococcus aureus [MRSA, MSSA],
Streptococcus pneumoniae, and Hemophilous
influenza.

27. • Uncomplicated influenza: ILI (Influenza-like illness) may present
with fever, cough, sore throat, coryza, headache, malaise,
myalgia, arthralgia and sometimes gastrointestinal symptoms,
but without any features of complicated influenza.
• Complicated/severe influenza: Influenza requiring hospital
admission and/or with symptoms and signs of lower respiratory
tract infection (hypoxaemia, dyspnoea, tacchypnoea, lower chest
wall indrawing and inability to feed), central nervous system
involvement and/or a significant exacerbation of an underlying
medical condition.

30. 2009 H1N1 experience from west

31. Lab Diagnosis
• Routine hematological, Biochemical, Radiological investigations
• Confirmation of seasonal influenza (including HI N 1) infection is
through:
• • Real time RTPCR or gene-xpert
• • Isolation of the virus in culture or
• • Four-fold rise in virus specific neutralizing antibodies.
Laboratory testing of uncomplicated illness is NOT routinely
recommended, as it provides no advantage in the management
of individual patients.
• Testing can be considered for the patients: who meet the criteria
for complicated or severe influenza, where a laboratory diagnosis
will assist in patient management should undergo.

32. • In line with WHO recommendations, molecular diagnostics
(real-time multiplex PCR for influenza A and B virus or Gene
expert for influenza A and B virus) are currently the method
of choice for influenza virus detection.
• While specificity is high, the sensitivity of currently
available rapid-point-of-care or immunofluorescence tests
designed for direct detection of influenza A viruses is low
(59%-93%) and therefore they are not recommended for
diagnostic purposes.
• A negative Rapid Influenza Diagnostic Test (RIDT) result
does NOT exclude influenza and should not preclude
starting empiric antiviral treatment where sound
indications exist.

33. Specimen collection, storage and transportation
• Combined nasopharyngeal and oropharyngeal swabs in universal
transport medium (UTM) are preferred specimen.
• Flocked swabs should be used to collect specimens for a better
yield on PCR].
• Dacron or rayon swabs may be used if flocked swabs are not
available.
• Cotton wool budded swabs are not recommended.
• Once collected, these samples should be transported on ice to the
testing laboratory.
• The specimens must be refrigerated at 4°C if transport is expected
to be delayed.
• If the specimen(s) cannot be shipped within 72 hours of collection,
they should be kept frozen at -20°C. Avoid repeated freezing and
thawing of specimens.

34. Nasopharyngeal swabs (NPS)
• Carefully label the vial of UTM with patient identification information and date
of specimen collection.
• Gently insert the flocked swab through one nostril beyond the anterior nares
along the floor of the nasal cavity, until the pharyngeal wall is reached (swab
to reach depth equal to distance from nostril to outer opening of ear).
• Do not use more than minimal force if any obstruction is encountered.
• Rotate the swab three times against the nasopharyngeal wall and then
withdraw the swab slowly.
• Place the swab into UTM without touching it, snap off the tip at the marked
break point.
• Secure the cap.
• Transport the labelled swab

35. • Nasopharyngeal aspirates (NPA)
• Fill 5ml syringe with saline; attach catheter tubing to
syringe tip.
• Slowly insert the catheter into one nostril until the
pharyngeal wall is reached.
• Quickly inject saline into nostril and then aspirate the
recoverable nasopharyngeal specimen.
• Withdraw the catheter under suction, being careful
not to touch the tip.
• Inject the aspirated fluid into labelled UTM and
transport to the laboratory.

36. Anti-viral Medication
• Recommended as early as possible for any
patient with confirmed or suspected influenza
who
Has complicated or severe illness (including all
hospitalised patients)
 Is at higher risk for influenza complications
• ideally within 48 hours of symptom onset, and
should not be delayed while awaiting laboratory
confirmation.

37. Treatment how much effective
For uncomplicated influenza illness can reduce the duration of
symptoms by approximately 1 day when given within 48 hours of
onset of illness.
• Because of the large sample sizes required, no RCTs conducted
specifically to evaluate the effect of oseltamivir against severe
outcomes such as hospitalisation or death.
• Observational data suggest a benefit of oseltamivir treatment
against severe outcomes, although these may be subject to several
limitations.
• A meta-analysis of individual patient data reported lower risk of
mortality in patients treated with neuraminidase inhibitors
compared to those not treated.
• A meta-analysis showed a risk reduction in lower respiratory tract
complications and in hospital stay in the group that received
oseltamivir.

38. Adamantanes (amantadine and rimantadine) not recommended
for use due to high levels of resistance

39. Adverse effects (Oseltamivir)
• Generally well tolerated
• Gl side effects (transient nausea, vomiting) may increase with
increasing doses, particularly above 300 mg/day.
• Occasionally bronchitis, insomnia and vertigo.
• Less commonly angina, pseudo membranous colitis and peritonsillar
abscess have also been reported.
• Rare reports of anaphylaxis and skin rashes.
• In children, most frequently reported side effect is vomiting.
Infrequently, abdominal pain, epistaxis, bronchitis, otitis media,
dermatitis and conjunctivitis.
• There is no recommendation for dose reduction in patients with hepatic
disease.
• Fatal neuro-psychiatiric illness in children and adolescents has been
linked to oseltamivir, no scientific evidence of a causal relationship.

41. Supportive therapy
• IV Fluids.
• Propernutrition.
• Oxygen therapy/ ventilatory support.
• Antibiotics for secondary infection.
• Vasopressors for shock.
• Paracetamol or ibuprofen is prescribed for fever, myalgia and headache.
Patient is advised to drink plenty of fluids. Smokers should avoid smoking.
For sore throat, short course of topical decongestants, saline nasal drops,
throat lozenges and steam inhalation may be beneficial.
• Salicylate / aspirin is strictly contra-indicated in any influenza patient due
to its potential to cause Reye's syndrome.
• No role of steroids excpet for septic shock as per surviving sepsis
campaign guidelines

42. Protocol for the ventilator management of patient
with ALI/ARDS following Seasonal Influenza:
• Indications for Mechanical Ventilation:
Severe Respiratory Failure
Failure to achieve oxygen saturation of > or
equal to 90% (or pO2 of > or equal to 60 mm
Hg) on an FIO2 < 0.6.

43. Ventilator Settings:
• Pressure pre-set (controlled)
• Low tidal volume ventilator support
• Tidal volume — 6 ml/kg ideal body weight (Respiratory rate to a
maximum of 30- 35 per minute).
• Open lung strategy of ventilation with PEEP titration to keep the
lung recruited to achieve an FIO2 of < 0.5 and a saturation of >
90% or a PaO2 of > 60 mmHg
• Plateau (Pause) pressure not to exceed of > 30-35 mmHg.
• Alternative modes of ventilation APRV (Airway Pressure Release
Ventilation), IRV (Inverse Ratio Ventilation) in patients with
persistent Hypoxemia (SpO2 of < 88-90% with high PEEP & FIO2
> 0.8).
• Rescue therapy — recruitment manoeuvres, Sedation,
Neuromuscular Blockage & Prone Ventilations can be considered
if above oxygen goals are not met.

44. Prevention of influenza (Vaccine)
In general, influenza vaccines are most effective among children ≥ 2 years and
healthy adults.
• A meta-analysis including data from years when there was a mismatch between
vaccine and circulating strains estimated a pooled vaccine efficacy of 59% (95%
CI: 51-67) in healthy adults.
• Previous studies from South Africa have reported influenza VE estimates
from2005 to 2015 which ranged between 46% and 87% when there was a good
match and ranged between -14% and 38% when the circulating A(H3N2) strain
showed marked genetic drift.
• A randomised control trial conducted in South Africa has shown that when
pregnant women receive the influenza vaccine, their risk of developing influenza
is halved, as is the risk to their infants in the first 24 weeks of life.
• The vaccine has been shown not only to be efficacious for prevention of
influenza in both mothers and their infants but also safe.
• Trivalent influenza vaccine has been shown to provide protection in HIV-infected
adults without severe immunosuppression .
• In certain groups, including the elderly, immunocompromised individuals and
infants, influenza vaccine is less effective; however, it may reduce the incidence
of severe disease, e.g. bronchopneumonia, hospital admission and mortality.

51. Chemoprophylaxis
• Annual influenza vaccination is the best way to prevent
influenza.
• Antiviral chemoprophylaxis is currently NOT recommended.
However, WHO guidelines state that individuals at high risk of
severe disease who have been exposed to a patient with
influenza may benefit from presumptive treatment with a full
twice-daily 5-day course of antivirals, even if they do not show
signs and symptoms of infection.
• Alternatively, such patients can be monitored closely for early
signs of possible influenza infection, and given antiviral
treatment if they occur.

52. Infection prevention and control (IPC) considerations

53. Thank you