Viral Encephalitis

Dan Karlin, Jenny Richmond, Chiemi Suzuki

BIO 4158: Microbiology and Bioterrorism Dr. Zubay April 20, 2004

Roadmap

Introduction History and epidemiology Molecular biology Weaponization Clinical manifestations Preparednes and continued surveillance

Introduction

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

http://www.cdc.gov/ncidod/dvbid/arbor/schemat.

Major Arboviruses That Cause Encephalitis

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 America

http://www.walgreens.com/images/library/healthtips/july02/westnile

History of West Nile Virus

1937 - West Nile virus isolated from woman in Uganda 1950s First recorded epidemics in Israel (1951-1954, 1957) 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 Outbreak

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 area Outbreak was first attributed to St. Louis encephalitis, but tissue samples from dead crows confirmed that it was West Nile virus 59 human cases requiring hospitalization, including 7 deaths

Spread of West Nile Virus in the US

2000 spread throughout New England and MidAtlantic 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 9,858 cases reported to

2003 US, Canada, Mexico

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 mosquitotransmitted human pathogen in the US Leading cause of epidemic flaviviral encephalitis

History of St. Louis Encephalitis

1933 virus isolated during St. Louis and Kansas City, MO epidemic 1940s 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 deaths. 1999 New Orleans outbreak. 20 reported cases.

St. Louis Encephalitis

Japanese Encephalitis

Japanese Encephalitis

Flavivirus related to St. Louis encephalitis 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, 19701998

Eastern Equine Encephalitis

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 1964-present 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

History of Eastern Equine Encephalitis

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 regions 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

Western Equine Encephalitis

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 Encephalitis

Early 1900s epizootics of viral encephalitis in horses described in Argentina 1912 25,000 horses died in Central Plains of US 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 encephalitis

Summary Confirmed and Probable Human Cases in the US Virus Years Total cases
Virus Years Total cases Eastern Equine Western Equine La Crosse St. Louis West Nile 1964-2000 1964-2000 1964-2000 1964-2000 182 649 2,776 4,482

1999-present > 9,800

Molecular Biology of Viruses that can Cause Viral Flaviviridae: West Nile Virus Encephalitis

Togaviridae: Eastern and Western Equine Encephalitis Bunyaviridae: La Crosse Virus

Flavivirus

Japanese Encephalitis Virus St. Louis encephalitis virus West Nile Virus

Family Flaviviridae 3 Genera

Flavivirus: Virus Classification

Flavivirus, Pestivirus, Hepacivirus Japanese encephalitis virus serogroup

Flavivirus - 12 Serogroups

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 York.

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 7 non-structural proteins

3 portion

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 proteins Pseudoknots Formed by interactions between 3 stem loop and adjacent nucleotides

PK1 May be important for minus strand replication P104, EF-1, and p84

Interacts with cellular proteins

Conserved Secondary and Tertiary Terminal RNA Structures in Minus Strand

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 Non-Structural

Structural Proteins

Capsid (C), Membrane (M), Envelope (E) Dimers of E protein arrange their 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 NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5

The envelope - receptor binding

Non-Structural Multifunctional Proteins

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 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

Togavirus

Eastern Equine Encephalitis Virus Western Equine Encephalitis Virus Venezuelan Equine Encephalitis Virus

Togavirus

Family: Togaviridae

Genus: Alphavirus ~11700 Nucleotides C, E3, E2, 6K, and E1

49S Single Stranded Genome

3 end: Five potential structural proteins

5 end: Unknown number of non-structural proteins probably involved in replication Genome has an opposite orientation from the Flaviviruses

Alphavirus Structure

http://www.cdc.gov/ncidod/dvbid/arbor/alphavir.htm

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 nonstructural 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

Bunyaviridae
La Crosse Virus

La Crosse Virus

http://www.virology.net/Big_Virology/BVRNAbunya.html

Bunyaviruses

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

Bioweaponization

http://www.cdc.gov/ncidod/dvbid/arbor/index.htm

Transmission Cycle is Key to Weaponization

Mosquito vector
Incidental infections

West Nile virus

Bird reservoir hosts

Incidental infections

http://www.cdc.gov/ncidod/dvbid/westnile/conf/February_2003.htm

Bioweaponization

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

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 outbreak

WNV as a low-tech Bioweapon: Possible Connection to 1999 outbreak Gather mosquitoes in an endemic

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 Dr. Ilya Trakht Source: Wait for outbreak

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
Diagnosis

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. Immunosuppression caused by disease and/or drug treatment. Organ transplant Opportunistic infections HIV CNS infections

Predisposing factors:

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,

Other Causes of Encephalopathy

Anoxic/Ischemic conditions Metabolic disorders Nutritional deficiency Toxic (Accidental & Intentional) Systemic infections Critical illness Malignant hypertension Mitochondrial cytopathy (Reyes and MELAS syndromes) Hashimotos 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 Can exclude subdural bleeds, tumor, and sinus thrombosis Reserved for patients who are worsening, have an undiagnosed lesion after scan, or a poor response to acyclovir.

MRI

Biopsy

Differential Diagnosis cont.

Encephalitis Fever Common Headache AMS fluctuate Focal Neurologic Signs Types of seizures Blood: Leukocytosis Common CSF: Pleocytosis EEG: Diffuse slowing +Focal Encephalopathy Uncommon Uncommon Common Steady deterioration May Uncommon Common Generalized Both Uncommon Uncommon Common Common

Clinical Considerations
Radiology

MRI

MRI

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
NEW YORK STATE DEPARTMENT OF HEALTH (NYSDOH) 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 patient: 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.

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
Treatment

Treatment

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

Acyclovir is a synthetic purine nucleoside analogue with inhibitory activity against HSV-1 and HSV-2, varicella-zoster virus (VZV), EpsteinBarr virus (EBV) and cytomegalovirus (CMV)

In order of decreasing effectiveness

Highly selective

Acyclovir Action

Thymidine Kinase (TK) of uninfected cells does not use acyclovir as a substrate. TK encoded by HSV, VZV and EBV2 converts acyclovir into acyclovir monophosphate. 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.

Dexamethasone

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 disturbances

Clinical Considerations
Patient Prognosis

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

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 Eye Opening

Response ____Score None 1 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 Response Abnormal flexion 3 Flexion withdrawal 4 Localizes pain 5 ______________Obeys commands _________6 _ Total score 3-15

Clinical Considerations
Vaccination

Vaccination

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 China

2 millions doses are produced annually in China and Japan

Public Health Considerations

Endemic Prevention

Infection Control

CDCs 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

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, theres more: Same Memo: Confirmed or suspected cases of pesticide poisoning must be reported to the New York State Department of Healths Pesticide Poisoning Registry at (800)-322-6850, and to the New York City Poison Control Center at (212)-764-7667.

Whats 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,

Crop-Dusting NYC?

Aerosolized liquids sprayed over large areas of the city. Terrorism concern? New vector for urban area.

Public Health Considerations

Surveillance

Surveillance
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 transmission.

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

http://www.nyc.gov/html/doh/html/wnv/wnvbird.html

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,

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