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Japanese Encephalitis
 

Japanese Encephalitis

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  • The first historic mention of Japanese encephalitis occurred during the “summer encephalitis” outbreaks in the late 1870’s. The next documented epidemic in Japan occurred in 1924 with 6,125 human cases resulting in 3,797 human deaths (62% case-fatality rate). The virus was first isolated in Japan in 1935 from a fatal human case of encephalitis. In 1938, the virus was first isolated from its primary vector species, Culex tritaeniorhynchus .
  • In 1940, JE was first identified in China and in 1949 it was identified in Korea during a major epidemic that resulted in 5,548 human cases. In 1954 the virus was recognized in India and a major epidemic occurred in 1978 with over 6,000 human cases occurring. In 1983, in South Korea, JE immunizations started in children as young as age 3 except in endemic areas where the vaccine was recommended in children even younger. From 1983 to 1987 the JE vaccine was available in the U.S. on an investigational basis.
  • JE virus infection occurs throughout the temperate and tropical regions of Asia. Although initially prevalent in Japan in the late 1800’s, control methods (vaccination and pesticides) have reduced the incidence of the disease in this country. Currently, the disease occurs in China, India, Nepal, Philippines, Sri Lanka and Northern Thailand. Occasionally sporadic cases of disease occur in Indonesia and northern Australia. An estimated 50,000 cases of JE occur globally each year, with 10,000 deaths and nearly 15,000 disabled. The disease has not occurred in the rest of the world. Photo shows distribution of Japanese encephalitis.
  • JE in pigs causes high mortality for newborn piglets. However there is close to zero mortality for adult pigs. Death from JE in equines is rare; when outbreaks occur, mortality rates of 5% or less have been reported. JE can be quite severe for humans. One in 300 infections results in symptomatic disease and mortality rates can vary from 5-35% depending on intensive care facilities of the region. Approximately 33-50% of the patients with symptomatic disease, who survive, have major neurologic sequelae within 1 year. This can include seizures, paresis or movement disorders. Children (ages 2-10 years) and the elderly are at the highest risk.
  • Clinical diagnosis of JE should be suspected in horses demonstrating fever and signs of central nervous system disease. In swine a tentative diagnosis of JE is based on the birth of litters with a high percentage of stillborn and weak piglets. Definitive diagnosis of JE in animals is by virus isolation. Samples of blood, cerebral spinal fluid (in horses), spinal cord and portion the brain can be used for this process. The brain should be submitted as one half fixed in 10% buffered formalin and one half unfixed. JE diagnosis can be tentatively diagnosed by the demonstration of a rise in titer (paired samples 14 days apart) by neutralization, hemagglutination inhibition (HI), immunofluorescence (IF), complement fixation (CF) and ELISA tests. These tests are not definitive for JE due to cross reactivity of Flaviviruses.
  • Post mortem lesion in humans are a pan-encephalitis. Infected neurons are scattered throughout the CNS. Occasional microscopic necrotic foci are present with the thalamus being affected severely. The photo shows a section of brain taken from a patient with Japanese encephalitis. This gross pathology can be found in all of the arbovirus encephalitides. The perivascular congestion and hemorrhage, may be diffuse or focal, and is seen predominantly in cortical gray and deep gray matter. Photo from Gary Baumbach, MD., Department of Pathology, University of Iowa, College of Medicine, http://www.vh.org/adult/provider/pathology/CNSInfDisR2/Text/203.html.
  • Human cases of JE may be suspected in persons visiting endemic areas and demonstrating neurological sign accompanied by a fever. A tentative diagnosis of JE can be based on a four-fold rise in antibody titer using several methods, such as hemagglutination inhibition (HI), immunofluoresent antibody titer (IFA), complement fixation (CF) or IgG ELISA. Caution should be used when interpreting these results since cross-reactivity can occur with other flaviviruses. Additionally, the antibody response may have already peaked by the time the patient presented for care and there for fail to demonstrate a rise in titer. Additionally, demonstration of JE specific IgM in serum or CSF may be useful in acute phases of the disease. Definitive diagnosis of JE is done by viral isolation. Samples of CSF can be used. Brain tissue can be used for virus isolation in post-mortem situations. There is no specific treatment for JE and supportive care is recommended.
  • The mortality rate in piglets can be quite high from JE. This reduction in number of offspring can have an great economic impact for the swine market. Additionally, equine deaths due to an outbreak of JE can result in a 2-5% mortality rate. These losses can impact the income potentially provided by these animals. Although JE is not currently found in the U.S., the transmitting vectors are, as is the potential for the disease. Since humans are also quite susceptible to JE, the need for immunization of the population and treatment of affected persons can lead to an great economic demand to the public and the medical community. Additionally, vector control measures will be needed to aid and protect the population.
  • JE has significant public health impact. Swine and birds can serve as reservoirs, as well as, amplifiers of the virus. This contributes to the spread of the disease, as has been occurring over the last 100 years. Although JE is not currently found in the U.S., the transmitting vectors are. Additionally, importation of infected, amplifying swine is always possible. Rapid identification and diagnosis will be important for protecting the public and our livestock from this disease.

Japanese Encephalitis Japanese Encephalitis Presentation Transcript

  • TOPIC : JAPANESE ENCEPHALITIS
    • PRESENTED BY : Dr Tshering Choden Bhutia
  • “ WELCOME”
    • JAPANESE ENCEPHALITIS
  • “ INTRODUCTION ”
    • SYNONYMS: Japanese B Encephalitis, Arbovirus B Encephalitis, Mosquito-Borne Encephalitis, Russian Autumnal Encephalitis, Brain Fever, Summer Encephalitis.
    • Definition: JE is an inapparent to acute arboviral infection of horses, pigs and humans. It’s a zoonotic disease i.e. infecting mainly animals and incidentally man.
  • AETIOLOGY :
    • Family : Flaviviridae
    • Genus: Flavivirus
    • Virions : Spherical, lipoprotein-enveloped particles being 40-50nm in diameter, 3 structural and 7 non-structural proteins
    • Genome : Single stranded positive sense RNA of molecular weight 3 × 10 6 daltons
    • Antigenic Structure : Hemagglutinins, Complement Fixing and Neutralising Antigens
  • FLAVIVIRUS
    • FLAVIVIRUS
  • Flavivirus Genome
  • Resistance To Physical And Chemical Action
    • Temperature : Destroyed by heating for 30mins above 56°C; Thermal Inactivation Point is 40°C
    • pH : Inactivated in acid environment of 1-3 (Stable in alkaline environment of pH 7-9)
    • Chemicals/Disinfectants : Inactivated by organic & lipid solvents, common detergents, phenol iodophors, 70% ethanol, 3-8% formal dehyde, 2% gluteraldehyde, 1% sodium hypochlorite
    • Survival : Sensitive to UV light & gamma irradiation
  • ARBOVIRUSES (ABV):
    • Viruses of vertebrates biologically transmitted by hematophagus insect vectors
    • Special characteristic : Ability to multiply in arthropods
    • Worldwide in distribution but far more numerous in tropical than in temperate zones
    • India : Over 40 ABV detected, >10 are known to produce human disease
  • Taxonomy Of Some Important Arboviruses FAMILY GENUS IMPORTANT SPECIES Togaviridae Alphavirus Chikungunya, Mayaro, O’nyong-nyong, EEE,WEE,VEE virus etc Flaviviridae Flavivirus Japanese Encephalitis, West Nile, Dengue types 1, 2, 3,4, KFD, MVE, Yellow fever virus Bunyaviridae Bunyavirus Phlebovirus Nairovirus Hantavirus California encephalitis, Oropouche, Turlock Rift valley fever, Sandfly fever virus Ganjam virus, Nairobi sheep disease virus Prospect hill, Hantan, Seoul, Puumala Reoviridae Orbivirus African horse sickness, Blue tongue viruses Rhabdoviridae Vesiculovirus Vesicular stomatitis virus, Chandipura virus
  • HISTORY
    • 1870’s : Japan
      • “ Summer encephalitis” epidemics
    • 1924 : Great epidemic in Japan
      • 6,125 human cases; 3,797 deaths
    • 1935 : First isolated
      • From a fatal human encephalitis case
    • 1938 : Isolated from Culex tritaeniorhynchus
  • HISTORY (contd.)
    • 1940-1978
      • Disease spread with epidemics in China, Korea and India
    • 1983 : Immunization in South Korea
      • Started as early as age 3
      • Endemic areas started earlier
    • 1983-1987 : Vaccine available in U.S. on investigational basis
  • EPIDEMIOLOGY
    • Geographical Distribution
    • Hosts
    • Transmission
    • Morbidity and Mortality
  • Geographic Distribution
    • Endemic in temperate and tropical regions of Asia
    • Reduced prevalence in Japan
    • Has not occurred in U.S
    • India - Epidemics
    Japan China Korea Indonesia India Philipines
  • HOSTS • Horses are the primary affected domestic animals of JE though essentially a dead-end host ; other equids (donkeys) are also susceptible • Pigs act as “ amplifiers” of the virus producing high viraemias which infect mosquito vectors • The natural maintenance reservoir for JE virus are birds of the family Ardeidae ( herons and egrets) Contd..
  • PIG - AMPLIFYING HOST
    • EGRET {RESERVOIR HOST}
    • POND HERON
    • Humans are vulnerable to this disease and this disease is a primary public health concern in Asia; humans are considered a dead-end host
    • • Other subclinically infected animals which likely do not contribute to spread include: cattle, sheep, goats, dogs, cats, chickens, ducks, wild mammals, reptiles and amphibians
    … Although they (birds) do not demonstrate clinical disease they do generate high viraemias upon infection
  • LIFE CYCLE OF JAPANESE ENCEPHALITIS
    • TRANSMISSION
    • JE presents two recognised epidemiologic patterns in Asia:
    • Late summer/early autumn-associated epidemic disease of northern temperate areas
    • - Large numbers of mosquitoes feed on Ardeid birds
    • (spring season)
    • - Ardeid birds migrate between rural and urban
    • ecosystems introducing JE virus(spring season);
    • these birds also amplify virus
    • - Increased vector activity leads to spill-over and
    • infection of swine by mosquito vectors shared by
    • birds and pigs
    • - Infection of pigs produces additional amplification
    • of virus; also large populations of vector-accessible
    • swine with rapid generational overturn facilitate JE
    • virus infection (summer)
    • - with profusion of JE virus circulating, mosquitoes of
    • horses and humans also transmit agent to these
    • hosts; usually sporadic & localised epizootics or
    • epidemics (late summer or early autumn)
    • Year-round endemic disease of southern tropical areas
    • - continual cycle between birds, swine & mosquitoes
    • - principal vectors: Culex tritaeniorhynchus and Culex
    • gelidus
    • minor sporadic outbreaks in horses and humans
    • during monsoon season
    • Actual transmission of JE virus occurs by means of Mosquitoes
    • - Principally Culex species mosquitoes ; Culex
    • tritaeniorhynchus is important as it has a wide
    • host range that includes birds, horses, swine and
    • humans
    • - C. tritaeniorhynchus oviposits in flooded
    • fields (fish ponds, rice paddies and ditches)
    • & is most active at twilight hours
  • Culex tritaeniorhynchus ( Cx vishnui group)
    • CULEX MOSQUITO BITING HUMAN
    • A TYPICAL BREEDING HABITAT FOR MOSQUITOES
  • - Aedes spp. of mosquitoes have also been implicated - JE virus has been isolated from other species of mosquitoes (i.e. Anopheles and Mansonia ) but their role is unclear - vertical transmission in mosquitoes has been documented
    • JE virus cycles in Ardeid birds by means of
    • mosquitoes
    • Although horses may produce viraemias sufficient
    • to infect mosquito vectors, their populations are
    • usually inadequate to maintain the virus or have
    • any important epidemiological impact
    • Sources of virus :
    • Water birds of the family Ardeidae; herons and egrets
    • Mosquito vectors as described above
    • Once infected, swine amplify JE virus and high titres in
    • blood, provide more infectious agent to vectors
    • - JE virus could be transmitted in boar semen
    • Overwintering of epizootic/epidemic JE virus has not
    • been elucidated
    • - introduction of JE virus strains from endemic areas
    • - hibernating mosquitoes may maintain virus; also
    • through transovarial passage
    • - maintenance in reptiles, amphibians or bats
  •  
  • Morbidity/Mortality
    • Swine
      • High mortality in piglets
      • Death rare in adult pigs
    • Equine
      • Morbidity: 2%, during an outbreak
      • Mortality: 5%
    • Humans
      • Mortality: 5-35%
      • Serious neurologic sequelae: 33-50%
  • DYNAMICS OF JE TRANSMISSION Environment Vector Mosquito Host - Amplifying Host - Carrier Victim-Accidental Full Recovery Death Recovery with residual complications
  • PATHOGENESIS
  • JE IN ANIMALS (Most commonly seen in late summer to early fall)
    • A} HORSE:
    • Incubation period :
    • 4 to 14 days (experimentally determined)
    • 8 to 10 days ( average range)
    • Subclinical disease is most common , clinical signs if present vary, disease usually presents itself in sporadic or localised clusters
    • THREE SYNDROMIC MANIFESTATIONS IN HORSE
  • Three Syndromic manifestations :
    • Transitory Type Syndrome :
    • -Moderate fever lasting 2-4 days
    • -Inappetance, Impaired Locomotion, Congested or Jaundiced Mucosa; most commonly with swift recovery of 2-3 days
    • Lethargic Type Syndrome :
    • -Variable febrile periods (as high as 41°C)
    • - Pronounced Stupor, Bruxism, Chewing Motions
    • Difficulty in Swallowing, Petechiation of Mucosa,
    • Paralysis; Recovery usually occurs within about a
    • week
    • 3) Hyper excitable Type Syndrome :
    • - High fever (41°C or higher)
    • - Profuse sweating & muscle tremor, aimless wandering
    • - Behavioral changes manifested by aggresion, loss of vision, collapse, coma & death;
    • - Neurologic sequelae may result; 5% mortality in horses (upto 30%)
    • - Morbidity Rates < 1% to 1.4%
    • - Case Fatality Rate (CFR) :
    • In Outbreaks vary - 5 to 15%
    • Severe Epizootics - 30 to 40%
    • B} JE IN SWINE :
    • Incubation Period:
    • -Not been clearly established
    • Signs of disease manifested as early as 3 days
    • but viraemia & accompanying fever may
    • appear within 24hrs post inoculation
    • In Swine most commonly JE manifests as a Reproductive disease;
    • Reproductive Losses - 50 to 70%
    a) Abortion in Sows: Still births or mummified fetuses; usually at term b) Reduced No. & Motility of Sperm In Boars
  • STILLBORN FETUSES
    • Live born piglets most often demonstrate neurologic signs of tremors & convulsions & may die soon after birth
    • Mortality in non-immune, infected piglets can approach 100%
    • Mild febrile disease or subclinical disease in
    • non-pregnant females
    • Natural infection results in long lasting immunity
    • Mortality is near Zero in adult swine
  • LESI0NS
    • A} IN HORSES:
    • - P.M. gross lesions of CNS associated with JE are, in general, non-specific
    • - Histopathologic examination reveals a non- suppurative encephalomyelitis with apparent perivascular cuffing; phagocytic destruction of nerve cells & focal gliosis
    • - Blood vessels appear dilated with numerous mononuclear cells.
    • B} IN SWINE:
    • - Litters of infected sows contain mummified or stillborn fetuses; some fetuses dark in appearance
    • - Evidence of congenital neurologic damage; hydrocephalus, cerebellar hypoplasia & spinal hypomelinogenesis observed in some litters
    • - Also subcutaneous oedema
  • DIFFERENTIAL DIAGNOSIS
    • EQUINE:
    • - WEE, EEE, other viral encephalatides, Hendra virus, Rabies, Neurotoxins, Toxic encephalitis
    • SWINE:
    • - Myxovirus-parainfluenza 1, Corona virus, Menangle virus, Porcine Parvovirus, Porcine Reproductive and Respiratory Syndrome
  • SAMPLING
    • Before collecting or sending any samples from animals with a suspected foreign animal disease; the proper authorities should be contacted
    • Samples should be sent under secure conditions & to authorized laboratories to prevent the spread of the disease
  • Diagnosis in Animals:
    • Clinical
      • Horses: Fever and CNS disease signs
      • Swine: High number of stillborn piglets
    • Laboratory Tests
      • Definitive: Viral isolation
        • Blood, spinal cord, brain, CSF
      • Rise in antibody titre
        • Neutralization, HI, IF, CF, ELISA
        • Cross reactivity of Flaviviruses
  • TREATMENT IN ANIMALS:
    • No effective treatment
    • Supportive Care:
    • - Antipyretics
    • - Anticonvulsants
    • - Maintenance of Nutrition
    • - Treatment of Secondary Bacterial Infection
    • JE IN MAN : CLINICAL FEATURES
    • Incubation Period - 5 to 15 days
    • Only 1 in 300 to 1 in 1000 infections develop into encephalitis, rest asymptomatic
    • Course of disease- 3 stages: a} Prodromal stage: Fever, headache and malaise. Duration- 1 to 6 days.
    • b} Acute encephalitic stage: Fever, 38 to 40.7°C,
    • nuchal rigidity, focal CNS signs, convulsion
    • & altered sensorium progressing in many
    • cases to coma.
    • c} Late stage and sequelae: Temperature & ESR touch normal level, neurological signs
    • become stationary
    • Case Fatality Rate (CFR) :
    • -Varies between 20-40% but it may reach 58% & over , higher in children
    • 30-50% of the people that survive the infection develop paralysis, brain damage, or other serious permanent sequelae
    • Average period between the onset of illness & death is about 9 days
    • In utero infection possible:
    • - Abortion of fetus
  •  
  • Post Mortem Lesions
    • Pan-encephalitis
    • Oedema and congestion of brain & meninges
    • Infected neurons scattered throughout CNS
    • Occasional microscopic necrotic foci
    • Thalamus generally severely affected
  • Differential Diagnosis
    • Meningitis
    • Febrile Convulsions
    • Rey’s Syndrome
    • Rabies
    • Cerebral Malaria
    • Toxic Encephalopathy
  • Diagnosis and Treatment In Man:
    • Clinical
    • Laboratory Tests
      • Tentative diagnosis
        • Antibody titer : HI, IFA, CF, ELISA
        • JE-specific IgM in serum or CSF
      • Definitive diagnosis
        • Virus isolation : CSF sample, brain
        • Treatment:
        • - No Specific treatment
      • - Supportive care
  • PREVENTION AND CONTROL
    • A} SANITARY PROPHYLAXIS :
    • Housing of animals in-doors in screened stabling can provide protection from mosquitoes
    • - Especially during active JE outbreaks & during peak vector activity (usually dusk to dawn)
    • -Insecticides, repellants & fans also
    • provide protection
    • Vector control reduces transmission
    • IN AFFECTED VILLAGES:
    • -Aerial or ground fogging with ultra low volume insecticides
    • -Spraying should cover vegetation around houses, breeding sites & animal shelters
    • IN UNINFECTED VILLAGES :
    • - Those falling within 2-3 km radius of infected villages should also receive spraying as a preventive measure
    • Use of mosquito nets should be advocated
  • B} MEDICAL PROPHYLAXIS
    • VACCINATION OF SWINE & HORSES:
    • - Modified Live or Inactivated Vaccines
    • Vaccination of swine prevents reproductive disorders & directly impacts JE viral amplification; especially in enzootic areas
    • - vaccinated breeding sows & boars; protects animals, reduces amplification, ensures healthy litters & decreases likelihood of aspermia
    • Vaccines also protect horses from clinical disease & possible sequelae
    • VACCINATION OF HUMAN BEINGS :
    • - Currently 3 types of JE vaccines in large scale use are:
    • 1. Mouse Brain-derived Purified & Inactivated Vaccine (Nakayama or Beijing strain of JE virus)
    • 2. Cell Culture Derived Inactivated JE Vaccine (Beijing P-3 strain)
    • 3. Cell Culture Derived, Live Attenuated Vaccine ( SA 14 – 14 – 2 strain of JE virus)
  •  
    • C} AGRICULTURAL PRACTICES :
    • - water management practice of Paddy cultivation-
    • At least one dry day every week will conserve water, reduce larval population increase rice grain yield, and reduce the emission of methane into the environment thereby reducing the Global warming effect. Using neem products as fertilizers will also reduce the mosquito population
    • D} Animal Reservoir :
    • JE was controlled in Japan by vaccinating the pig population. But this is unlikely to be possible in India since there is no centralized pig rearing. So all pig rearing practices should be undertaken at least 5 Kms away from human habitations and all measures to promote pig husbandry (Bank Loans) should be subject to this condition
  • JE - GLOBAL SCENARIO
    • Major public health disease in Asia
    • Virus first isolated in Japan in 1935
    • As per WHO estimates 50 thousand serious cases and 10 thousand deaths each year
    • Disease is prevalent in Indian Sub-continent, Nepal, India, Sri Lanka and some areas in Bangladesh
  • Global scenario contd…,
    • Other SE Asian countries reporting cases include:
    • Myanmar, Thailand, Cambodia, China
    • Indonesia, Laos, Vietnam, Malaysia, Philippines, Taiwan,
    • Hong Kong and
    • Korea
  • JE Vaccines : Today Vaccine Type Strain & Substrate Producer Licensure & distribution Inactivated Nakayama Mouse Brain Biken (Japan); Green Cross (South Korea); CRI (India); Vabiotech (Vietnam); GPO (Thailand) International Local& Region Local Local & India Local & Region Beijing 1 Mouse Brain Kaketsuken; Biken; Kitasota (Japan) Production stopped; Bulk storage P3 PHK or Vero Multiple (China) Domestic Live, Attenuated SA14-14-2 on PHK Chengdu; Wuhan; Lanzhou ( China) China; India, Nepal, South Korea, Sri Lanka
  • In Pipeline Vaccine type and strain Producer Status Commercial Strategy Inactivated, Vero cell derived Beijing 1 Biken; Kaketsuken Phase 3 Japan –pediatric ?International [Licensure: 2008] Inactivated Vero Cell derived SA14-14-2 [IC51] Intercell; Biological E Pediatric ( 1-3 years in India) Phase 2 Traveler & Military Pediatric [2009] Live , recombinant, Vero Cell derived SA14-14-2 pr M&E in 17 D YF backbone Acambis; BBIL Clinical (Ph2 in Adult; ph 2 pediatric initiated in India) Traveler & Military Pediatric [2009]
  • JAPANESE ENCEPHALITIS IN INDIA
    • 1952 - First evidence of JE viral activity by
    • VRC (NIV) during sero-surveys for arbo-viruses.
    • 1955 - First human case of JE.
    • 1958 - First viral isolation from JE case.
    • 1973 - First outbreak- Bankura and Burdwan in West Bengal.
    • 1976 - Repeat outbreak in Burdwan.
    • 1978 -Widespread occurrence of suspected JE cases.
      • -National level monitoring initiated by NMEP in 1978.
      • -Initiation of immunization using inactivated mouse
      • brain vaccine
  • JE ENDEMIC AREAS IN INDIA Number of endemic districts: 135; Population: 330 million JE affected areas
    • Andhra Pradesh
    • Assam
    • Bihar
    • Haryana
    • Kerala
    • Karnataka
    • Maharashtra
    • Manipur
    • Nagaland
    • Tamil Nadu
    • Uttar Pradesh
    • West Bengal
  • Frequency of Japanese Encephalitis episodes in India (1996-2007 ) Repeat Occurrences No. of States with reported JE cases: 15
  • YEAR TOTAL CASES (INDIA) TOTAL DEATHS (INDIA) 2005 6,527 1,682 2006 2,832 658 2007(JULY) 391 92 4,017 (WHO) 2008 294 (WHO) 2009 2,868 (U.P) 505
    • FOR CLINICAL MANAGEMENT OF JAPANESE ENCEPHALITIS FOLLOWING DEFINITIONS ARE FOLLOWED BY:
    • GOVT. OF INDIA,
    • DIRECTORATE OF NATIONAL VECTOR BORNE
    • DISEASES CONTROL PROGRAMME, DELHI
  • Case Definition : Suspected case . Acute onset of fever (≤ 7 days) . change in mental status With/ without . New onset of seizures (excluding febrile seizures) . (Other early clinical findings - may include irritability, somnolence or abnormal behaviour greater than that seen with usual febrile illness)
  • Probable Cases Suspected case in close geographic and temporal relationship to a laboratory-confirmed case of JE in an outbreak Acute Encephalitis Syndrome due to other agent - A suspected case in which diagnostic testing is performed and an etiological agent other than JE is identified Acute Encephalitis Syndrome due to unknown agent - A suspected case in which no diagnostic testing is performed / no etiologicaI agent was identified / test results were indeterminate
  • JE CASE CLASSIFICATION, NICD, NEW DELHI
    • SUSPECT:
    • A CASE THAT IS COMPATIBLE WITH THE
    • CLINICAL DESCRIPTION
    • PROBABLE:
    • A SUSPECT CASE WITH PRESUMPTIVE
    • LABORATORY RESULTS
    • CONFIRMED:
    • A SUSPECTED CASE THAT IS LABORATORY
    • CONFIRMED
  • Economic Impact
    • 1} Animals :
      • Porcine
        • High mortality in piglets
      • Equine
        • Up to 5% mortality rate
        • 2} Humans:
        • Medical cost for immunization and medical treatment
  • Public Health Significance :
    • Vectors in U.S.
    • Disease has spread in last 100 years
    • Reservoirs: swine and birds
    • Human mortality
    • Animals deaths
      • Lost income
  • “ THANK YOU”