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Swine flu
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- 2. TOPICS TO BEDISCUSSED • INTRODUCTION • EPIDEMIOLOGY • RISK GROUPS • ETIOLOGY • PATHOGENESIS • CLINICAL FEATURES • COMPLICATIONS
- 3. INTRODUCTION • It iscaused 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 cased significant mortality among young people
- 4. EPIDEMIOLOGY • Latest pandemicof swine flu was first noted in Mexico in march 2009 • It spread worldwide affected nearly 195 countries and it ended in August 2010
- 6. • In Indiaoutbreak 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
- 9. • The averageincubation period is 1-3 days (maximum 7 days) • Transmission through contact with large particle respiratory droplets • Other body fluids and fomites also play a role in 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. RISK GROUPS • Age< 5 years & > 65 years • Obese individuals • Pregnancy • Persons with Asthma/ COPD or other chronic pulmonary diseases • Immuno compromised and ppl receiving Immuno suppressive therapy • Sickle cell anemia and other Hemoglobinopathies
- 11. • Long termaspirin therapy • CKD • Metabolic disease such as diabetes mellitus • Persons with Neuromuscular disorders, seizure disorders, cognitive dysfunction • People working in Health care institutions
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- 14. • It’s aRNA virus belonging to the family of Orthomyxoviridae • Three main genera - Influenza A, Influenza B, Influenza C • Influenza A is further sub-typed into 16 distinct H types & 9 distinct N types based on Hemagglutinin & Neuroaminidase antigens on the surface of the virus
- 15. • Every yearnew 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
- 17. PATHOGENESIS • Virus particlemay 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
- 20. COMMON CLINICAL FEATURES •Fever • Sore throat • Rhinorrhea • Myalgia & Arthralgia • Headache • Vomiting • Diarrhoea
- 22. EXTRA PULMONARY MANIFESTATION •CVS- Chest pain, hypotension • CNS- Seizures, lethargy, altered mental status, weakness or paralysis • OTHERS- Decreased urine output, cyanosis, dehydration
- 23. COMPLICATIONS • PULMONARY -Progressive viral pneumonia, Secondary bacterial pneumonia, ARDS • CNS - Encephalitis, Encephalopathy, GBS, ADEM • CVS - Myocarditis, Pericarditis • OTHERS – Renal failure, Rhabdomyolysis, Ryes syndrome, Hemophagocytosis, Multi organ failure syndrome
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