viral 20encephalitis by LBY2ks


									     Viral Encephalitis
Dan Karlin, Jenny Richmond, Chiemi Suzuki
         BIO 4158: Microbiology and Bioterrorism
                       Dr. Zubay
                     April 20, 2004
   Introduction
   History and epidemiology
   Molecular biology
   Weaponization
   Clinical manifestations
   Preparednes and continued surveillance
   Encephalitis is an acute inflammatory process affecting the brain
   Viral infection is the most common and important cause, with
    over 100 viruses implicated worldwide
   Symptoms
       Fever
       Headache
       Behavioral changes
       Altered level of consciousness
       Focal neurologic deficits
       Seizures
   Incidence of 3.5-7.4 per 100,000 persons per year
       Causes of Viral Encephalitis
   Herpes viruses – HSV-1, HSV-2, varicella zoster virus, cytomegalovirus,
    Epstein-Barr virus, human herpes virus 6
   Adenoviruses
   Influenza A
   Enteroviruses, poliovirus
   Measles, mumps, and rubella viruses
   Rabies
   Arboviruses – examples: Japanese encephalitis; St. Louis encephalitis virus;
    West Nile encephalitis virus; Eastern, Western and Venzuelan equine
    encephalitis virus; tick borne encephalitis virus
   Bunyaviruses – examples: La Crosse strain of California virus
   Reoviruses – example: Colorado tick fever virus
   Arenaviruses – example: lymphocytic choriomeningitis virus
          What Is An Arbovirus?
   Arboviruses = arthropod-borne viruses
   Arboviruses are maintained in nature through
    biological transmission between susceptible
    vertebrate hosts by blood-feeding arthropods
   Vertebrate infection occurs when the infected
    arthropod takes a blood meal
        Major Arboviruses That Cause
   Flaviviridae
     Japanese encephalitis
     St. Louis encephalitis
     West Nile

   Togaviridae
     Eastern equine encephalitis
     Western equine encephalitis

   Bunyaviridae
       La Crosse encephalitis
West Nile Virus
                West Nile Virus
   Flavivirus
   Primary host – wild birds
   Principal arthropod
    vector – mosquitoes
   Geographic distribution -
    Africa, Middle East,
    Western Asia, Europe,
    Australia, North
    America, Central

       History of West Nile Virus
   1937 - West Nile virus isolated from woman in Uganda
   1950s – First recorded epidemics in Israel (1951-1954,
   1962 – Epidemic in France
   1974 – Epidemic in South Africa. Largest ever West
    Nile epidemic.
   1996 – Romanian epidemic with features similar to
    those of the North American outbreak. 500 cases and
    50 deaths.
   1999 – Russian outbreak. 40 deaths.
      West Nile Virus: 1999 New York
   Crows dying in and around Queens
    in late summer
   27 deaths among captive birds in
    the Queens and Bronx zoos
   Concomitant human infection of
    apparent encephalitis in the same
   Outbreak was first attributed to St.
    Louis encephalitis, but tissue
    samples from dead crows
    confirmed that it was West Nile
   59 human cases requiring
    hospitalization, including 7 deaths
    Spread of West Nile Virus in the US
   2000 – spread throughout New
    England and Mid-Atlantic regions.
        18 new human cases reported
   2001 – spread throughout the
    entire eastern half of the US
        64 cases reported, with NY, FL
         and NJ accounting for 60%
   2002 – spread westward across
    Great Plains into Western US.
    Reached California by Labor Day.
        By end of 2002 cumulative human
         cases > 3900, with > 250 deaths
   2003 – US, Canada, Mexico
        9,858 cases reported to CDC,
         including 262 deaths in 45 states
         and D.C.
West Nile Activity in the US –
 Reports as of April 7, 2004
West Nile Activity in the US –
Counties Reporting Cases as of
       March 24, 2004
                   West Nile Virus 2004:
                   BREAKING NEWS
   April 13, 2004 – Ohio may have first 2004 West Nile Case
       79 year old man from Scioto County, OH was admitted April 1 with viral
        meningitis and encephalitis which rapidly progressed to coma over 2 days.
            Initial IgM antibody titers were positive for West Nile virus and he
             complained of itching from insect bites upon admission
       Has been treated with blood-pressure drugs to control over-response by
        the immune system to West Nile virus, causing brain inflammation.
            Previously unresponsive and paralyzed.
            Can now open his eyes and shake his head in response to questions, but still
             cannot talk.
St. Louis Encephalitis
           St. Louis Encephalitis
   Flavivirus
   Most common
    human pathogen in the
   Leading cause of
    epidemic flaviviral
History of St. Louis Encephalitis
   1933 – virus isolated during St. Louis and Kansas City,
    MO epidemic
   1940’s – virus spread to Pacific Coast
   1959-1971 – virus spread to Southern Florida
   1974-1977 – last major epidemic. Over 2,500 cases in
    35 states.
   1990-1991 – South Florida epidemic. 226 cases and 11
   1999 – New Orleans outbreak. 20 reported cases.
St. Louis Encephalitis
Japanese Encephalitis
                Japanese Encephalitis
   Flavivirus related to St. Louis
   Most important cause of arboviral
    encephalitis worldwide, with over
    45,000 cases reported annually
   Transmitted by culex mosquito,
    which breeds in rice fields
        Mosquitoes become infected by
         feeding on domestic pigs and wild
         birds infected with Japanese
         encephalitis virus. Infected
         mosquitoes transmit virus to
         humans and animals during the
         feeding process.
History of Japanese Encephalitis
   1800s – recognized in Japan
   1924 – Japan epidemic. 6125 cases, 3797 deaths
   1935 – virus isolated in brain of Japanese patient who
    died of encephalitis
   1938 – virus isolated from Culex mosquitoes in Japan
   1948 – Japan outbreak
   1949 – Korea outbreak
   1966 – China outbreak
   Today – extremely prevalent in South East Asia.
    30,000-50,000 cases reported each year.
  Distribution of Japanese
Encephalitis in Asia, 1970-1998
Eastern Equine
      Eastern Equine Encephalitis
   Togavirus
   Caused by a virus transmitted to
    humans and horses by the bite of
    an infected mosquito.
   200 confirmed cases in the US
   Average of 4 cases per year
   States with largest number of cases
    – Florida, Georgia, Massachusetts,
    and New Jersey.
   Human cases occur relatively
    infrequently, largely because the
    primary transmission cycle takes
    place in swamp areas where
    populations tend to be limited.
          History of Eastern Equine
   1831 – First recognized as a disease in horses. Over 75
    horses died in 3 counties in Massachusetts.
   1845-1912 – epizootics in Northeast and Mid-Atlantic
   1933 – virus isolated from horse brains
   1938 – association of human disease with epizootics.
    30 cases of fatal encephalitis in children living in same
    area as equine cases.
   1947 – largest recorded outbreak in Louisiana and
    Texas. 13,344 cases and 11,722 horse deaths
Western Equine
     Western Equine Encephalitis
   Togavirus
   Mosquito-borne
   639 confirmed cases in
    the US since 1964
   Important cause of
    encephalitis in horses
    and humans in North
    America, mainly in the
    Western parts of the US
    and Canada
         History of Western Equine
   Early 1900’s – epizootics of viral encephalitis in
    horses described in Argentina
   1912 – 25,000 horses died in Central Plains of
   1930 – San Joaquin Valley, CA outbreak. 6000
    cases in horses. Virus isolated from horse brains
   1938 – virus isolated from brain of a child
La Crosse Encephalitis
              La Crosse Encephalitis
   Bunyavirus
   On average 75 cases per year reported
    to the CDC
   Most cases occur in children under 16
    years old
   Zoonotic pathogen that cycles between
    the daytime biting treehole mosquito,
    and vertebrate amplifier hosts
    (chipmunk, tree squirrel) in deciduous
    forest habitats
   Most cases occur in the upper
    Midwestern state, but recently cases
    have been reported in the Mid-Atlantic
    region and the Southeast
   1963 – isolated in La Crosse, WI from
    the brain of a child who died from
Summary – Confirmed and Probable
    Human Cases in the US
Virus            Years          Total cases

Eastern Equine   1964-2000      182

Western Equine 1964-2000        649

La Crosse        1964-2000      2,776

St. Louis        1964-2000      4,482

West Nile        1999-present   > 9,800
 Molecular Biology of
Viruses that can Cause
  Viral Encephalitis
      • Flaviviridae: West Nile Virus
 • Togaviridae: Eastern and Western
                   Equine Encephalitis
      • Bunyaviridae: La Crosse Virus
•Japanese Encephalitis Virus
• St. Louis encephalitis virus
       • West Nile Virus
    Flavivirus: Virus Classification
   Family Flaviviridae
   3 Genera
       Flavivirus, Pestivirus, Hepacivirus
   Flavivirus - 12 Serogroups
       Japanese encephalitis virus serogroup
            Includes West Nile Virus (WNV), St. Louis Encephalitis,
             and others
Scanned images of West Nile virus isolated
from brain tissue from a crow found in New
Viral Replication Cycle
Genome Structure
                          Viral Genome
   Positive Strand RNA Genome
   1 ORF – Genome encodes single polyprotein which is
    subsequently cleaved
       5’ portion
            3 structural proteins
       3’ portion
            7 non-structural proteins
   Genome also includes 5’ and 3’ noncoding regions
    which have functional importance
Secondary structure loops
        3’ Stem Loop of Plus Strand
   Tertiary interactions of 3’ non-coding region serve to
    stabilize and compact the 3’ region of the genome and
    may also create binding sites for cellular and/or viral
   Pseudoknots – Formed by interactions between 3’ stem
    loop and adjacent nucleotides
       PK1 May be important for minus strand replication
   Interacts with cellular proteins
       P104, EF-1α, and p84
    Conserved Secondary and Tertiary
    Terminal RNA Structures in Minus
   Stem loop structures at 5’ and 3’ ends are conserved
    across flavivirus species suggesting a functional
    importance for these groups.
   Minus strand stem loops may play a role in facilitating
    the formation of replication complexes and in releasing
    newly synthesized minus strands from plus strands.
   In addition, its interaction with cellular proteins is
    important for replication.
     Viral Proteins: Structural and
   Structural Proteins
       Capsid (C), Membrane (M), Envelope (E)
   The envelope - receptor binding
       Dimers of E protein arrange their β sheets in a head to tail
        formation which lie flat on top of the lipid bilayer. The distal
        portions of these proteins are anchored in the membrane
   Non-Structural Multifunctional Proteins
       NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5
   Many functions of non-structural proteins have yet to
    be determined
      Viral Non-Structural Proteins
   NS1- may play a role in flavivirus RNA synthesis; it has been shown to be
    essential for negative strand synthesis
   NS2A, NS2B, NS4A, NS4B - may facilitate the assembly of viral replication
    complexes by an unknown mechanism
   NS3: Multifunctional
      Proteolytic function upon association with NS2B
      RNA triphosphatase function thought to be important for the synthesis
        of the 5’ cap structure
      Helicase and NTPase activity
      Its activity may be upregulated through interaction with phosphorylated
   NS5
        RNA dependent RNA polymerase
        Methyltransferase domain thought to be required for formation of the 5’ cap
Model for Closed-Loop Complex
  Formation in Flaviviruses

 •  Eastern Equine Encephalitis Virus
  • Western Equine Encephalitis Virus

• Venezuelan Equine Encephalitis Virus
   Family: Togaviridae
       Genus: Alphavirus
   49S Single Stranded Genome
       ~11700 Nucleotides
   3’ end: Five potential structural proteins
       C, E3, E2, 6K, and E1
   5’ end: Unknown number of non-structural proteins
    probably involved in replication
   Genome has an opposite orientation from the
Alphavirus Structure

    Alphaviruses: Protein Function
   E1and E2 glycoprotein heterodimers form trimers that appear as
    knobs on the surface of the virion
       E1 – transmembrane glycoprotein with 2 to 3 N-linked glycosylation sites
       E2 - glycoprotein with 1 to 2 N-linked glycosylation sites, contains short
        intracytoplasmic tail and hydrophobic stretch of amino acids that serves
        as the fusion peptide for viral entry
   Capsid protein has a conserved N-terminal region which binds
    RNA and a C-terminal region which interacts with the
    cytoplasmic tail of E2 as well as capsid proteins
   E3 and 6K proteins are signal sequences for E2 and E1,
    respectively, and are largely cleaved off from the mature virion
                 Replication Cycle
   Proposed Model: E1 glycoprotein interacts with proteins on the
    cell surface. E2 binds to cellular proteins and receptor-mediated
    endocytosis takes place.
   In acidified endosomal compartment, glycoproteins fuse with
    membrane and the nucleocapsid is released.
   Virion RNA serves as mRNA, translation of non-structural
    proteins begins
   Structural proteins are transcribed as polyprotein
   E2 and E1 travel from ER to the Golgi
   At cellular membrane regions containing E1 and E2
    heterodimers interact with nucleocapsids and viral particles bud
    from the cell surface
  La Crosse Virus
La Crosse Virus

   Genome - single strand of negative sense RNA
   Four structural proteins
      Two external proteins

      Two associated with RNA to form nucleocapsid

   Matrix proteins absent from Bunyaviruses, therefore
    capsid proteins and envelope glycoproteins directly
    interact prior to budding

 Transmission Cycle is Key to
    Mosquito vector
                                                   Incidental infections

West Nile virus

     Bird reservoir hosts                 Incidental infections

   Vector, Vector, Vector
       In areas around NYC mosquitoes are extremely
        ubiquitous during the summer months
   Mosquitoes are already virulent, further genetic
    engineering is unnecessary
   A fully effective cure is not available
   Diagnosis is difficult
   Widespread Panic would be generated as the
    outbreak progresses
           The Iraq Connection
   The US shipped various pathogens, including
    WNV, to Iraq in the 1980s
   In 1999 following the West Nile Virus outbreak
    in NYC there were fears that Iraqi bioterrorism
    was involved
   Investigations by the CDC and the CIA found
    no evidence of bioterrorism in the 1999
     WNV as a low-tech Bioweapon:
      Possible Connection to 1999
   Gather mosquitoes in an endemic area
   Incubate mosquitoes with a food source
   Put them to sleep
   Place mosquitoes in a matchbox
   Board plane to US
   Take bus from airport; Release mosquitoes from
    bus window
   Wait for outbreak
                                     Source: Dr. Ilya Trakht
Clinical Considerations
                    Case Study
In August 2002, a 91 year old male from Northern Staten Island
who presented initially with sudden onset of fever, left lower
extremity weakness, inability to walk, and possibly some transient
and mild AMS, was admitted to a Staten Island hospital.

He was not considered to have aseptic meningitis or encephalitis
and WN virus infection was not considered at that time. After
being discharged, he was evaluated by a neurologist for persistent
left leg weakness and inability to walk.

In April 2003, the neurologist reported this case to the DOHMH
as a possible polio case. Serological specimens were forwarded
to the NYSDOH where they tested positive for WN virus.
Clinical Considerations
                         Patient History
   Detailed history critical to determine the likely cause of encephalitis.
   Prodromal illness, recent vaccination, development of few days → Acute
    Disseminated Encephalomyelitis (ADEM) .
   Biphasic onset: systemic illness then CNS disease → Enterovirus encephalitis.
   Abrupt onset, rapid progression over few days → HSE.
   Recent travel and the geographical context:
        Africa → Cerebral malaria
        Asia → Japanese encephalitis
        High risk regions of Europe and USA → Lyme disease
   Recent animal bites → Tick borne encephalitis or Rabies.
   Occupation
        Forest worker, exposed to tick bites
        Medical personnel, possible exposure to infectious diseases.
                          History cont.
   Season
       Japanese encephalitis is more common during the rainy season.
       Arbovirus infections are more frequent during summer and fall.
   Predisposing factors:
       Immunosuppression caused by disease and/or drug treatment.
       Organ transplant → Opportunistic infections
       HIV → CNS infections
            HSV-2 encephalitis and Cytomegalovirus infection (CMV)
   Drug ingestion and/or abuse
   Trauma
                Initial Signs
   Headache
   Malaise
   Anorexia
   Nausea and Vomiting
   Abdominal pain
                   Developing Signs
   Altered LOC – mild lethargy to deep coma.
   AMS – confused, delirious, disoriented.
   Mental aberrations:
       hallucinations
       agitation
       personality change
       behavioral disorders
       occasionally frank psychosis
   Focal or general seizures in >50% severe cases.
   Severe focused neurologic deficits.
               Neurologic Signs
   Virtually every possible focal neurological
    disturbance has been reported.
   Most Common
     Aphasia
     Ataxia

     Hemiparesis with hyperactive tendon reflexes

     Involuntary movements

     Cranial nerve deficits (ocular palsies, facial weakness)
Other Causes of Encephalopathy
   Anoxic/Ischemic conditions
   Metabolic disorders
   Nutritional deficiency
   Toxic (Accidental & Intentional)
   Systemic infections
   Critical illness
   Malignant hypertension
   Mitochondrial cytopathy (Reye’s and MELAS syndromes)
   Hashimoto’s encephalopathy
   Traumatic brain injury
   Epileptic (non-convulsive status)
   CJD (Mad Cow)
               Differential Diagnosis
   Distinguish Etiology
        (1) Bacterial infection and other infectious conditions
        (2) Parameningeal infections or partially treated bacterial meningitis
        (3) Nonviral infectious meningitides where cultures may be negative (e.g.,
         fungal, tuberculous, parasitic, or syphilitic disease)
        (5) Meningitis secondary to noninfectious inflammatory diseases
   MRI
        Can exclude subdural bleeds, tumor, and sinus thrombosis
   Biopsy
        Reserved for patients who are worsening, have an undiagnosed lesion
         after scan, or a poor response to acyclovir.
   Clinical signs cannot distinguish different viral encephalitides
     Differential Diagnosis cont.
                         Encephalopathy         Encephalitis
Fever                    Uncommon               Common
Headache                 Uncommon               Common
AMS                      Steady deterioration   May fluctuate
Focal Neurologic Signs   Uncommon               Common
Types of seizures        Generalized            Both
Blood: Leukocytosis      Uncommon               Common
CSF: Pleocytosis         Uncommon               Common
EEG: Diffuse slowing     Common                 +Focal
MRI                      Often normal           Focal Abn.
Clinical Considerations
Clinical Considerations
      Laboratory Diagnosis
               Laboratory Diagnosis
   Diagnosis is usually based on CSF
     Normal glucose
     Absence of bacteria on culture.

     Viruses occasionally isolated directly from CSF
            Less than half are identified
   Polymerase Chain Reaction techniques
       Detect specific viral DNA in CSF
                           NYSDOH PCR
                         Viral Encephalitis Letter of Agreement for
              Physician Ordered Testing by Polymerase Chain Reaction (PCR)

    NYSDOH's Wadsworth Center offers the following tests on CSF for viral encephalitis:
    PCR testing for a panel of viruses, including: herpes simplex, varicella zoster, cytomegalovirus,
    Epstein-Barr virus, enteroviruses, St. Louis encephalitis (SLE), eastern equine encephalitis (EEE),
    California encephalitis (including LaCrosse and Jamestown Canyon viruses), Powassan and West
    Nile (WN) viruses, and
    Enzyme-linked immunoassay (ELISA) for WN virus.
    If there is insufficient quantity of CSF (less than 1.0 ml) to conduct both ELISA and PCR for
    WN virus, please consider the following in determining which test is most appropriate for your
    ELISA is more sensitive than PCR for WN viral testing and should be considered when there is
    stronger suspicion of WN virus than other viruses.
    PCR is less sensitive for WN virus, but tests for a wide range of viruses. PCR should be
    considered if viruses other than WN virus are suspected.

Please note your testing priority below or on the viral encephalitis/meningitis case report
    form. If PCR testing is desired, the agreement below must be completed.
         Viral Encephalitis PCR Panel West Nile Virus ELISA Antibody Testing
Clinical Considerations
      Disease Progression
            Disease Progression
   Worsening neurologic symptoms
   Vascular collapse and shock
     May be due to adrenal insufficiency.
     Loss of tissue fluid may be equally important.

   Homeostatic failure
   Decreased respiratory drive
Clinical Considerations
   When HSE cannot be ruled out, Acyclovir must
    be started promptly (before the patient lapses
    into coma) and continued at least 10 days for
    maximal therapeutic benefit.
   Rocky Mountain spotted fever should also be
    considered, and empiric treatment with
    Doxycycline is indicated.
Suspected HSE Treatment Plan
   Acyclovir is a synthetic purine nucleoside
    analogue with inhibitory activity against HSV-1
    and HSV-2, varicella-zoster virus (VZV),
    Epstein-Barr virus (EBV) and cytomegalovirus
       In order of decreasing effectiveness
   Highly selective
                      Acyclovir Action
   Thymidine Kinase (TK) of uninfected cells does not use acyclovir as a
   TK encoded by HSV, VZV and EBV2 converts acyclovir into acyclovir
   The monophosphate is further converted into diphosphate by cellular
    guanylate kinase and into triphosphate by a number of cellular enzymes.
   Acyclovir triphosphate interferes with Herpes simplex virus DNA polymerase
    and inhibits viral DNA replication.
   Acyclovir triphosphate incorporated into growing chains of DNA by viral
    DNA polymerase.
   When incorporation occurs, the DNA chain is terminated.
   Acyclovir is preferentially taken up and selectively converted to the active
    triphosphate form by HSV-infected cells.
   Thus, acyclovir is much less toxic in vitro for normal uninfected cells because:
    1) less is taken up; 2) less is converted to the active form.
                    Supportive Therapy
   Fever, dehydration, electrolyte imbalances, and convulsions require treatment.
   For cerebral edema severe enough to produce herniation, controlled
    hyperventilation, mannitol, and dexamethasone.
        Patients with cerebral edema must not be overhydrated.
        If these measures are used, monitoring ICP should be considered.
   If there is evidence of ventricular enlargement, intracranial pressure may be
    monitored in conjunction with CSF drainage.
        Outcome is usually poor.
        For infants with subdural effusion, repeated daily subdural taps through the
         sutures usually helps.
        No more than 20 mL/day of CSF should be removed from one side to prevent sudden
         shifts in intracranial contents.
        If the effusion persists after 3 to 4 weeks of taps, surgical exploration for possible
         excision of a subdural membrane is indicated.
   Synthetic adrenocortical steroid
   Potent anti-inflammatory effects
   Dexamethasone injection is generally
    administered initially via IV then IM
   Side effects: convulsions; increased ICP after
    treatment; vertigo; headache; psychic
Clinical Considerations
       Patient Prognosis
   The mortality rate varies with etiology, and epidemics due to the
    same virus vary in severity in different years.
       Bad: Eastern equine encephalitis virus infection, nearly 80% of survivors
        have severe neurological sequelae.
       Not so Bad: EBV, California encephalitis virus, and Venezuelan equine
        encephalitis virus, severe sequelae are unusual.
       Approximately 5 to 15% of children infected with LaCrosse virus have a
        residual seizure disorder, and 1% have persistent hemiparesis.
   Permanent cerebral sequelae are more likely to occur in infants,
    but young children improve for a longer time than adults with
    similar infections.
       Intellectual impairment, learning disabilities, hearing loss, and other
        lasting sequelae have been reported in some studies.
             Prognosis w/ Treatment
   Considerable variation in the incidence and severity of sequelae.
        Hard to assess effects of treatment.
   NIAID-CASG trials:
        The incidence and severity of sequelae were directly related to the age of the
         patient and the level of consciousness at the time of initiation of therapy.
        Patients with severe neurological impairment (Glasgow coma score 6) at initiation
         of therapy either died or survived with severe sequelae.
        Young patients (<30 years) with good neurological function at initiation of
         therapy did substantially better (100% survival, 62% with no or mild sequelae)
         compared with their older counterparts (>30 years); (64% survival, 57% no or
         mild sequelae).
   Recent studies using quantitative CSF PCR tests for HSV indicate that clinical
    outcome following treatment also correlates with the amount of HSV DNA
    present in CSF at the time of presentation.
                 Glasgow Coma Scale
   Test          Response                 ____Score
   Eye           None                            1
   Opening       To pain                         2
                 To verbal stimuli               3
                 Spontaneously                   4
   Best          None                            1
   Verbal        Incomprehensible words          2
   Response      Inappropriate words             3
                 Disoriented conversation        4
                 Oriented conversation           5
   Best          None                            1
   Motor         Abnormal extension              2
   Response      Abnormal flexion                3
                 Flexion withdrawal              4
                 Localizes pain                  5
   ______________Obeys commands         _________6 _
                 Total score                     3-15
Clinical Considerations
   None for most Encephalitides
   JE
       Appears to be 91% effective
       There is no JE-specific therapy other than supportive care
       Live-attenuated vaccine developed and tested in China
            Appears to be safe and effective
            Chinese immunization programs involving millions of children
       Vero cell-derived inactivated vaccines have been developed in
            2 millions doses are produced annually in China and Japan
   Several other JE vaccines under development
Public Health
  Endemic Prevention
             Infection Control
   CDC’s “Three Ways to Reduce your West
    Nile Virus Risk”
     Avoid mosquito bites
     Mosquito-proof your home

     Help your community
           Avoid Mosquito Bites
   Apply Insect Repellent Containing DEET
   Clothing Can Help Reduce Mosquito Bites
       Cover up
   Be Aware of Peak Mosquito Hours
       Dusk to dawn are peak mosquito biting times for
        many species.
          Mosquito-Proof Home
   Drain Standing Water
   Install or Repair Screens
         Community-Wide Efforts
   Clean Up Breeding Grounds
   Ensure Safe Blood Supply
   Mosquito Control Programs
       Controversial
   Surveillance
                   Blood Supply
   NYC Policy Statement reflecting FDA policy:
    “To reduce WN transmission through blood
    components…. Blood donations will be screened for
    WN virus RNA… using nucleic acid amplification tests
    (NAT). In the event of a NAT-reactive donation,
    blood centers will remove and quarantine all blood
    components associated with the donation and notify
    the state or local health department. In addition, blood
    testing centers have added screening questions to
    identify and exclude persons with fever and headache in
    the week prior to donation.”
    Mosquito Control Programs
NYC DOHMH Statement:
“ We hope that spraying of adulticides will not be
  required this summer. However, if there is a
  threat of an outbreak of human illness and
  spraying is deemed necessary, targeted adult
  mosquito control measures (via ground or aerial
  spraying of pesticides) may be required.”
             Mosquito Control
   But wait, there’s more:
   Same Memo:
    Confirmed or suspected cases of pesticide
    poisoning must be reported to the New York
    State Department of Health’s Pesticide
    Poisoning Registry at (800)-322-6850, and to the
    New York City Poison Control Center at (212)-
            What’s Being Sprayed
   The adulticides used during the last three seasons in
    New York City is Sumithrin, a pyrethroid.
   Although pyrethroids are among the least toxic
    insecticides, they are nerve poisons, and act upon the
    sodium ion channels in nerve cell membranes.
   Inhaling pyrethroid insecticides can cause coughing,
    wheezing, shortness of breath, runny or stuffy nose,
    chest pain, or difficulty breathing.
   Skin contact can cause a rash, itching, or blisters.
   Sumithrin is not very toxic to mammals, but it is highly
    toxic to bees and fish.
            Crop-Dusting NYC?
   Aerosolized liquids sprayed over large areas of
    the city.
   Terrorism concern?
   New vector for urban area.
Public Health
“Since 2000, the NYC DOHMH has conducted comprehensive
arthropod-borne disease surveillance and control. In 2003,
efforts will again focus on mosquito control through reduction
of breeding sites and application of larvicides. In addition,
comprehensive mosquito, avian and human data collected during
the 2000-2002 seasons have allowed NYC DOHMH to develop
more sensitive surveillance criteria for determining the level of
WN viral activity in birds and mosquitoes that may indicate a
significant risk for a human outbreak. These indicators will be
monitored citywide to identify areas at risk for human
   Standing Water Reporting
The Department of Health & Mental Hygiene is
now accepting reports of standing water.
However, we will not be able to visit and treat
all reported nuisances. Therefore we are
encouraging City residents and business owners
to take immediate action to eliminate standing
water on their property.
               Dead-Bird Reporting
   Online form
   The Department of Health & Mental Hygiene is now
    accepting reports of dead birds. Only a sample of dead
    birds that meet specific criteria will be picked up and
    tested for the West Nile virus. However, your report of
    a dead bird is extremely important to us because dead
    bird reports may indicate the presence of West Nile
    virus. If you do not receive a call back from the
    Department of Health within two business days of
    making your report, please dispose of the bird.
             Mosquito Testing
“Five pools of mosquitoes collected in New York City have
tested positive for West Nile (WN) virus. These include a pool
of Culex salinarius, a human biting mosquito, collected on July 15,
in the Willowbrook Park area of Staten Island, a pool of Culex
restuans, primarily a bird-biting mosquito, collected from
Brookville Park, Queens on July 17, a pool of Culex pipiens, a
mosquito that bites both birds and humans, collected from the
Hunts Point area of the Bronx on July 18, a pool of Culex species
collected from Jamaica Bay, Queens on July 16, and a pool of
Culex salinarius collected from Greenwood Cemetery, Brooklyn
on July 21. These positive pools are the first evidence of West
Nile (WN) virus in New York City in 2003”
          Disease Reporting
“The New York City Department of Health and
Mental Hygiene (NYC DOHMH) is again
requesting that during the peak adult mosquito
season, from June 1 – October 31, 2003, all
suspected cases of viral encephalitis (all ages) and
viral meningitis (adults only) be reported
immediately by telephone or facsimile and that
appropriate laboratory specimens (cerebrospinal
fluid and sera) be submitted promptly for testing
for West Nile (WN) virus.”

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