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Influenza secrets do you know
This document discusses influenza viruses and pandemics. It covers the taxonomy and anatomy of influenza viruses, noting there are three types (A, B, C) that can infect humans. Type A is of most concern as it can undergo antigenic shift, resulting in new subtypes that have caused past pandemics like the 1918 Spanish flu. The document outlines the influenza virus life cycle and how it is transmitted. It also discusses diagnosis of both human and avian influenza, noting some strains of avian H5N1 can cause severe disease in humans.
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Influenza secrets do you know
- 1. Influenza Drama Premierjohn Secrets Behind Him Let us Start Enjoy 1
- 2. The premier johnof the drama Pandemics Spanish flue A (H1N1) 1918 Asian flue A (H2N2) 1957 Hong Kong flue A (H3N3) 1968 Russian flue A (H1N1) 1977 2
- 3. What we willspeak about Introduction Family orthomyxoviridae Influenza virus Anatomy Naming Zoonosis Transmission to human How? 3
- 4. Influenza Pathogenethis 4 7 DAYS POST-INFECTION
- 5. Influenza life cycle Steps 5
- 6. Diagnosis Theact of professional 6
- 7. Classification Influenzais one of orthomyxoviridae ss(-) RNA virus minus sense single strand RNA virus 7
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- 9. HA protein -attachment, fusion HA 9 S S S S S S cell enzymes acid pH
- 10. anatomy orthomyxoviridae10 HA - hemagglutinin NA - neuraminidase helical nucleocapsid (RNA plus NP protein) lipid bilayer membrane polymerase complex M1 protein type A, B, C : NP, M1 protein sub-types: HA or NA protein
- 11. ORTHOMYXOVIRUSES 11 HA- hemagglutinin NA - neuraminidase helical nucleocapsid (RNA plus NP protein) lipid bilayer membrane polymerase complex M1 protein
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- 14. From inside himself infuenza 14
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- 16. ORTHOMYXOVIRUSES 16 pleomorphic influenza types A,B,C febrile, respiratory illness with systemic symptoms
- 17. Family orthomyxoviridae Influenza A B and C Only A and B can cause Human disease Influenza A infect awide variety of mammals And tends undergo antigenic changes 17
- 18. Virus character Enveloped (80-120 nM ) Segmented negative stranded RNA 8 segment A and B 7 segments c Total genome size average 13.6 Average 0.89 – 2.34 kb each segment 18
- 19. type A, B,C : NP, M1 protein sub-types: HA or NA protein 19 HA - hemagglutinin NA - neuraminidase helical nucleocapsid (RNA plus NP protein) lipid bilayer membrane polymerase complex M1 protein
- 20. Influenza Asubtypes 15 hemagglutinine 9 Neuraminidase subtypes Subtypes of type A Important for human H1N1 H2N2 20
- 21. Antigentic shift drift Antigenic shift Completely new HA subtype Only with influenza A Assocaited with pandemics Antigenic drift Relatively minor subtype changes Influenza A and B EPIDEMIC and regional out break 21
- 22. Influenza virus 3types Type A Associated with widespread epidemic Pandemic TYPE B infrequently associated with regional wide spread epidemic Type C associated with sporadic cases minor localized disease 22
- 23. How to nameinfluenza virus Type ABC citystrain#year isolatedglycoprotein HA (1-15) NA ( 1-9) eg. AHONG KONG031968H3N3 World wide pandemics= pandemic 1918-1919 influenza pandemic caused 2o million deathes 1947 asian influenza 23
- 24. Influenza changes rapidely Antigenic drift substitution in HA and NA This can increase the escape from the immune system Antigenic shift assortment of gene segment in cells Infected by different strain avian gene substituted with human strain gene Swine can replicate both strain This can open up for infection of new host Both make it difficult to obtain good vaccine 24
- 25. 25 Influenza AViruses to Humans Human virus Reassortant virus Transmission of Avian Non-human virus 15 HAs 9 NAs
- 26. where 26 where do “new” HA
- 27. Timeline of Emergenceof Influenza Viruses in Humans 27 H9 1998/9 1918 1957 1968 1977 1997 2003 H1 H1 B H2 H7 H5 H5 Spanish Influenza Asian Influenza Russian Influenza Avian Influenza Hong Kong Influenza H3 Pandemic vaccines Regular vaccines 1918
- 28. Influenza Virus Types& Subtypes in Humans (Trivalent Vaccine) Type A Seasonal epidemics caused by H3N2, H1N1, and H1N2 subtypes Pandemics (caused by new subtypes) Type B No subtypes Seasonal epidemics only 28
- 29. Timeline of Emergenceof Influenza Viruses in Humans 29 H9 1998/9 1918 1957 1968 1977 1997 2003 H1 H1 B H2 H7 H5 H5 Spanish Influenza Asian Influenza Russian Influenza Avian Influenza Hong Kong Influenza H3 Pandemic vaccines Regular vaccines
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- 32. History of antigenicshift 32
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- 38. Influenza pandemics Antigenic shift has occurred at least 3 times in the past, each time resulting in highly lethal pandemics. All three pandemics in the 20th century spread world wide within 1 year of detection 1918 Spanish flu (H1N1) which caused the death of 20-40 million people 1957 Asian flu (H2N2) 1968 Hong Kong flu (H3N2). This subtype still circulates today. 38
- 39. Lessons from thepast Hospital in pandemic Photo of the caution taken by officials during the influenza epidemic of 1918 39 .
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- 41. 41 TRACHEAL MUCOSANORMAL 7 DAYS POST-INFECTION pathogenesis NORMAL TRACHEAL MUCOSA 3 DAYS POST-INFECTION Lycke and Norrby Textbook of 3 DAYS DAYS POST-INFECTION POST-INFECTION
- 42. changes DECREASEDCLEARANCE RISK BACTERIAL INFECTION VIREMIA RARE 42
- 43.
- 44. Diagnosis Avianinfluenza 44
- 45. Avian influenza Thehighly pathogenic form of avian influenza A was first recognized in Italy in 1878 45
- 46. Highly pathogenic Thisstrain 46 It is extremely contagious and rapidly fatal in birds with a mortality approaching 100%.
- 47. All outbreaksof the highly pathogenic form of avian influenza have been caused by subtypes H5 and H7. 47
- 48. The virusmultiplies in the intestines of these birds and is shed in saliva, nasal secretions and feces. 48
- 49. A singlegram of contaminated feces contains enough virus to infect 1 million birds The virus can survive in contaminated manure for up to 3 months and in contaminated water up to 30 days. Birds that survive infection excrete virus for at least 10 days, orally and in feces, thus facilitating further spread. 49
- 50. H5N1 hasjumped the species barrier on 2 separate occasions in the recent past causing severe disease in humans. The first documented human infection by H5N1 occurred in Hong Kong, China in 1997. 18 people were hospitalized, 6 died. The entire domestic bird population of Hong Kong, 1.5 million birds, was culled in 3 days. Human infection stopped after all chickens were culled. Limited human-to-human transmission of H5N1 was documented. 50
- 51. How do peopledie? Unlike influenza viruses we are more familiar with in which respiratory symptoms dominate, H5N1 replicates in a wide range of cell types This results in severe disseminated disease affecting multiple organs and causing high mortality. 51
- 52. Presentation Patientswith documented H5N1 typically present to the hospital 2-6 days after the onset of fever and cough. Other early symptoms include sore throat, runny nose and myalgia's. SOB develops in 1 to 5 days. At admission all patients have clinically apparent pneumonia with either patchy or interstitial infiltrates. Leukocyte count is normal or decreased, and transaminases may be mildly to moderately elevated. Patients go on to develop disseminated disease affecting multiple organs Secondary bacterial infection has not been a factor 52
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- 54. There are 2classes of drugs available that are effective against the influenza virus: The M2 inhibitors: amantidine and ramantidine The neuraminidase inhibitors: oseltamivir and zaminivir In preliminary studies H1M5 has been shown to be resistant to the M2 inhibitors 54
- 55. Another interesting bitof information H5N1 infection has been confirmed in a single household of domestic cats in Thailand. 14 of 15 cats in the household died. One dead cat was known to have contact with a dead chicken. Up to now, domestic cats were not been considered susceptible to infection with influenza viruses although some older studies from the 1970s reported experimental infection of domestic cats under laboratory conditions. 55
- 56. Diagnosis Therole of profetional How it is down At what level 56
- 57. avian Historyof high mortality Clinical signs nervous signs Diarhae Sudden death 57
- 58. diagnosis PM The respiratory digestive system Multiorgans affected 58
- 59. Laboratory diagnosis Sample Live bird Tracheal swap Cloacal swap Faeces Dead bird Organs faeces 59
- 60. identification Procedures Inoculation of 9-11day old emryonated chicken eggs followed by Haemagglutination immunodiffusion test Confirm presence of influenza virus Subtype determination with nonspecific antisera Strain virulence evaluation of intravinouspathogencity index (IVPI) in 4-8 week old chicken 60
- 61. Serology Testsavailable ELISA Detect antibodies to AI virus Doesn’t distinguish subtypes AGID Agar gel diffusion Both within 1 week of infection HI haemagglutination I inhibition test Serotype specific test Available for each H subtype HI titers are positive a few days later than ELISA 61
- 62. Enzyme linked immunabsorbantassay (ELISA) 62 Sample to be tested virus capturing antibody Enzyme -> colour Detecting antibody
- 63. Haemagglutination (HA) 63 virus No virus
- 64. Haemagglutination 64 Dilution 2 4 8 16 32 64 128 256 512 1024 prozone titre No virus
- 65. immunoflourscent Ableto detect antibodies to specific neuraminidase subtype 65
- 66. RT -PCR Reverse transcriptase polymerase chain reaction Able to detect virus at very low level The presence of subtype H5or H& can be confirmed BY using H5 or H7 specific primer 66
- 67. Human FEVER HEADACHE MYALGIA COUGH RHINITIS OCULAR SYMPTOMS 67
- 68. Clinical finding SEVERITY VERY YOUNG ELDERLY IMMUNO-COMPROMISED HEART OR LUNG DISEASE 68
- 69. PULMONARY COMPLICATIONS CROUP (YOUNG CHILDREN) PRIMARY INFLUENZA VIRUS PNEUMONIA SECONDARY BACTERIAL INFECTION Streptococcus pneumonia Staphylococcus aurous Hemophilius influenzae 69
- 70. MORTALITY MAJORCAUSES OF INFLUENZA VIRUS- ASSOCIATED DEATH BACTERIAL PNEUMONIA CARDIAC FAILURE 90% OF DEATHS IN THOSE OVER 65 YEARS OF AGE 70
- 71. DIAGNOSIS ISOLATION NOSE, THROAT SWAB TISSUE CULTURE OR EGGS SEROLOGY RAPID TESTS provisional - clinical picture + outbreak 71
- 72. hours of incubtion48 IPA on MDCK cells infected by A/H1N1 72
- 73. Prevention by vaccine inactivated egg grown sub-unit vaccine for children reassortant live vaccine approved 2003 for healthy persons (those not at risk for complications from influenza infection) ages 5-49 years 73
- 74. Prevention of Influenza Avoid close contact with people who are sick Stay home when you are sick Cover Your Cough Frequent hand washing Avoid touching eyes, nose or mouth Antiviral drugs 74
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- 76. Drugs preventive RIMANTADINE (M2) type A only AMANTADINE (M2) type A only ZANAMIVIR (NA) types A and B, not yet approved for prevention OSELTAMIVIR (NA) types A and B 76
- 77. Treatment drug RIMANTADINE (M2) type A only, needs to be given early AMANTADINE (M2) type A only, needs to be given early ZANAMIVIR (NA) types A and B, needs to be given early OSELTAMIVIR (NA) types A and B, needs to be given early 77
- 78. Avian influenza vaccine Convential vaccine Inactivated oil emulsion vaccine used world wide Recominant vaccine Vector I LT vaccine or pox Heteroglogous vaccine In avian influenza contain the same agglutinine Adifferent Neuramindase 78