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.pdf
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/westnilea.jpg
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 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
mosquito-transmitted
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
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
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, 1970-1998
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 areas where
populations tend to be limited.
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 11,722 horse deaths
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 1900’s – 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
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
Flavivirus
•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
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
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
proteins
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
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)
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
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
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
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 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
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 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
outbreak
WNV as a low-tech Bioweapon:
Possible Connection to 1999
outbreak
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
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.
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
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.
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
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),
Epstein-Barr 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 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); (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
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
Several other JE vaccines under development
Public Health
Considerations
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)-
764-7667.
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
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, 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.”