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JAPANESE ENCEPHALITIS phase 3.pptx oknnnn
- 1. CM 8.1 Describe anddiscuss the epidemiological and control measures including the use of essential laboratory tests at primary care level for communicable disease (Japanese Encephalitis) Dr.Parimita Roychoudhury Assistant Professor, DMCH, Dhubri
- 2. LEARNING OBJECTIVES • Atthe end of the session students will be able to 1.Define and differentiate between Acute Encephalitis syndrome and Japanese Encephalitis 2.Enumerate and Describe the epidemiological triad of Japanese Encephalitis 3.Describe the clinical features and differential diagnosis of Japanese Encephalitis 4.Describe the Laboratory diagnosis 5.Describe the Prevention and control methods of Japanese Encephalitis
- 3. Vector- living organismthat transmits an infectious agent from an infected animal to a human or another animal a) Invertebrate type : Arthropod vector fall into 7 categories. (1) Diptera - flies and mosquitoes (2) Siphonaptera - fleas (3) Orthoptera - cockroaches (4) Anoplura - sucking lice (5) Hemiptera - bugs, including kissing bugs (6) Acarina - ticks and mites (7) Copepoda - cyclops b) Vertebrate type — Mice, rodents, bats.
- 4.
- 5. AES • Any personof any age who develops acute onset of fever & change in mental status (confusion, disorientation, coma, inability to talk, new onset seizure- excluding simple febrile seizure). • Cause- virus, bacteria, fungus, parasites, spirochetes, chemical/ toxins. • Group of diseases having similar S/S. JE • Common cause of AES. • A PATIENT WILL COME WITH S/S OF AES NOT JE.
- 7. EPIDEMIOLOGY, PREVENTION AND CONTROL OFJAPANESE ENCEPHALITIS 7
- 8. INTRODUCTION 8 •JE is azoonotic disease transmitted by mosquito •Case-fatality rate among those with encephalitis can be as high as 30% •24 countries in the WHO South-East Asia and Western Pacific regions have endemic JEV transmission •There is no cure for the disease
- 9. History of JE •1870-Japan “Summer Encephalitis” epidemic • 1924-Great epidemic in Japan ,case fatality 62% • 1940 to 1954-Epidemic in China,Korea,India • 1983-Immunization in human first started in Korea • 2006 –JE vaccine introduced after campaign in endemic districts in India
- 10. DISTRIBUTION OF JEIN INDIA 10 ICMR
- 11. •The disease isendemic in 21 states. Assam, Bihar, Haryana. Uttar Pradesh, Karnataka, West Bengal and Tamil Nadu report out-breaks every year and contribute about 80 per cent of cases and deaths
- 12. ASSAM HISTORY • 1963-Serologicalevidence • 1976- First epidemic in Upper Assam • 1978- Virus isolation from Brain tissue at AMCH • 1978, 1982, 1986 -Greater magnitude epidemic. Most affected districts are Dibrugarh, Dhemaji, Lakhimpur, Sivasagar, Jorhat, Golaghat, Tinsukia & Sonitpur. 12
- 13. ASSAM 13 2017 2018 20192020 (23 July2020) 0 500 1000 1500 2000 2500 3000 2077 1492 2603 331 178 183 345 48 AES and deaths due to AES AES DEATH due to AES Years Numbers
- 14. 2017 2018 20192020 (23 July2020) 0 100 200 300 400 500 600 700 605 509 633 183 87 94 155 24 JE cases and death JE Death due to JE (Case Fatality rate) Years Number NVBDCP
- 15. EPIDEMIOLOGY of JapaneseEncephalitis
- 16. Agent Family Flaviviridae Genus Flavivirus(group B Arbovirus) Genomes SS RNA Serotypes Nakayama, Beijing • Temperature- Destroyed by heating for 30min above 56 degree. • Chemical/Disinfectants- Inactivated by common detergents, 70% ethanol, 3- 8% formaldehyde, 2% glutaraldehyde, 1% sodium hypochlorite. • Sensitive to UV light and gamma irradiation. 16
- 17. Hosts 17 Human host- • Bimodalage distribution • Children & young adults (<15years)- 85% • Elderly (>60years)- 10% • 1 clinical case suggests 300-1000 infections Natural host Amplifier host Dead end host Ergot, heron
- 18. Enviroment • Temperate- Latesummer/early autumn Tropical- Year round • Endemic in temperate & tropical regions of Asia. • Epidemics- Paddy season (monsoon & post monsoon) • Primarily rural areas. It has spread to new areas d/t agricultural development supported by irrigation programme 18
- 19.
- 20. Vector 20 Culicine mosquitoes- Culex tritaeniorhynchus,Culex vishnui and Culex pseudovishnui Breed in water mainly in paddy fields, rice cultivation, shallow ditches and pools. Primarily outdoor resting in vegetation (exophilic) and other shaded places but in summer may also rest in indoors.
- 21.
- 22. • Human tohuman transmission has not so far been recorded Man is an incidental dead-end host • Cattle and buffaloes may also be infected with the JE virus; although they may not be natural hosts of JE virus, they act as "mosquito attractants” • 9-12 days incubation period, they can transmit the virus to other hosts
- 23.
- 24. PRODROMAL STAGE ACUTEENCEPHALITIS CONVALESCENCE & SEQUELAE • IP- 5-15 days • Lasts- 1-6 days • Nonspecific –acute fever headache malaise • No CNS S/S. • Fever 38- 40.7 C • Headache, muscular rigidity, seizure, nuchal rigidity. • Altered sensorium, Coma. • Focal CNS signs. • Extra pyramidal signs (dystonia, choreoathetosis and coarse tremors). • Temp & ESR touch normal • 25% develop motor and intellectual deficit. • Neuropsychiatric sequel 30-50%. • Case fatality rate 20-40% 24 CLINICAL FEATURES
- 25.
- 26. LABORATORY DIAGNOSIS 26 TENTATIVE Antibody detection Heamagglutination InhibitionTest (HI), Compliment Fixation Test (CF), Enzyme Linked Immuno-Sorbant Assay (ELISA) for IgG (paired) and IgM (MAC) antibodies, etc. ELISA (Serum, CSF) Antigen Detection RPHA, IFA, Immunoperoxidase etc. Genome Detection RTPCR DEFINITIVE Virus isolation CSF, Brain IgM ELISA is the method of choice provided samples are collected 3- 5(within 7 days) days after the infection
- 27. 27 Specimen collection- • 4days after onset for isolation. • 5 days after onset for IgM ab. Laboratories- • District sentinel surveillance laboratories • National laboratories/ Referral laboratories
- 28.
- 29. DIFFERENTIAL DIAGNOSIS 29 Meningitis Febrile convulsions Rey’s syndrome Rabies Cerebral malaria Toxic encephalopathy Patientwith fever, altered sensorium lasting more than 6 hours, no skin rash and other known causes of encephalitis excluded *Fever with rash excludes JE *AES with symmetrical signs & fever likely to be Cerebral Malaria
- 30.
- 31. Field based management(case definition) 31 Suspected case Acute fever of 5-7 days + altered mental status + new seizure (except febrile) Probable case Suspected case in geographical/ temporal proximity of a confirmed case Confirmed case Suspected case with anyone- 1. JE specific IgM 2. 4 fold raised IgG 3. Isolation of virus/ag/ nucleic acid AES d/t other agent Suspected case in which diagnostic test is performed and aetiological agent other than AES/JE is identified AES d/t unknown agent Suspected case in which NO diagnostic test is performed/ no aetiological agent is identified/ test results are indeterminate
- 32.
- 33. WHAT HAVE WELEARNT TILL NOW……… • Viral infection • Fever • +Altered sensorium HOW DO WE START MANAGEMENT- • History • Clinical examination (General & Systemic)
- 34. MANAGEMENT OF CASES •Symptomatic and supportive • Refer to nearest FRU if anyone develops- Lethargy, Convulsions, Unconsciousness • Refer to higher center directly if develops- Shock, Needs ventilator, Unmanageable cyanosis. • Suspected case referred should be confirmed with 2 diagnostic test- 1. RT-PCR 2. Detection of- virus ag/ genome. 34
- 35. Management A, B, C,D Referral note should include history and clinal examination findings….WHY
- 37. The treatment ofthe patients may require as follow:- 1.) Management of Airways and Breathing. 2.) Management of Circulation. 3.) Control of Convulsion and Intracranial pressure 4.) Control of Temperature 5.) Fluid and Electrolytes and Calories/ Nutrition 6.) General management 7.) Specific treatment of any for treatable cause 8.) Investigations, Sample Collection & Transportation 9.) Reporting of a case 10.) Rehabilitation.
- 41.
- 42. PREVENTION & CONTROL 42 LEVELSOF PREVENTION ACTIVITES Primordial Primary IEC, vector control, Vaccination Secondary Diagnosis & Management of cases Tertiary Rehabilitation
- 43. PRIMARY LEVEL 43 Vector control Personal protective measures Controlof pig Vaccination
- 44. Vector Control Fogging Duringcontainment of JE outbreak Anti- larval operations Environmental measures (neem as fertilizer in fields, Alternate drying & wetting water management) Larvivorous fish Gambusia affinis ,Guppy Bio larvicides Bacillus thuringiensis, Israelensis, B sphaericus 44
- 45. Fogging • Affected village-Aerial/ground fogging with ULV insecticides (Malathion, Pyrethrum). Uninfected village- Falling within 2-3km radius of infected village. • Pre requisites of fogging- I. Done in outdoor situations. II. Downwind to upwind situation. III. Direct to all resting sites. IV. Medium/dry fog type. 45
- 46.
- 47. Personal protective measures •LLITBN- Pyrethroid • Curtains • Repellants • Proper clothing 47
- 48. Control of Pig •Immunization- Inactivated/ attenuated vaccines. • Challenge- difficult to ensure complete coverage due to rapid breeding & limited vaccine effectiveness. • Slaughtering of pig • Mosquito proof piggeries • Segregating pigs 4-5km away from human habitations 48
- 49. Vaccination in human •3 types of vaccines- 1. Inactivated brain derived and purified type- Nakayama/ Beijing strain 2. Cell culture derived- Inactivated- Beijing P-3 strain,Kolar 821564XY 3. Cell culture derived- Live attenuated- SA 14-14-2 strain • Recommended for- Children, Laboratory staff, Travellers (Visiting >30days) • Dose & Schedule- 0.5ml for <3years, 1ml for >3years. 2 dose 1 month apart Booster- 1year, every 3rd year till 15 years 49
- 50. Secondary level • Fieldbased management (Case definitions) • Laboratory diagnosis • Management of cases 50
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- 53. • Periodicity ofReports- I. Daily report- Outbreak situation II. Weekly report- Transmission period III. Monthly report- Inter-epidemic period. • Forms- I. AESF 1/1A- From states II. AESF 2/2A- Districts III. AESF 3- Line listing form IV. AESF 4- Case investigation form 53
- 56. MORTALITY/ MORBIDITY 56 Swine High mortalityin piglets. Death rare in adult pigs. Equine Morbidity- 2% during outbreak. Mortality 5%(upto 30%) Humans Mortality 5-35%. 20-40% but may reach 58% & over, higher in children. Serious neurologic sequelae 33-50%. MORTALITY MORBIDITY
- 57.