viral encephalitis

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Information about viral encephalitis
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Published on March 15, 2008

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Viral Encephalitis:  Viral Encephalitis Dan Karlin, Jenny Richmond, Chiemi Suzuki BIO 4158: Microbiology and Bioterrorism Dr. Zubay April 20, 2004 Roadmap:  Roadmap Introduction History and epidemiology Molecular biology Weaponization Clinical manifestations Preparednes and continued surveillance Introduction:  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:  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?:  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 Slide6:  http://www.cdc.gov/ncidod/dvbid/arbor/schemat.pdf Major Arboviruses That Cause Encephalitis:  Major Arboviruses That Cause Encephalitis Flaviviridae Japanese encephalitis St. Louis encephalitis West Nile Togaviridae Eastern equine encephalitis Western equine encephalitis Bunyaviridae La Crosse encephalitis Slide8:  http://www.cdc.gov/ncidod/dvbid/arbor/worldist.pdf West Nile Virus:  West Nile Virus 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:  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:  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:  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 – Reports as of April 7, 2004 West Nile Activity in the US – Counties Reporting Cases as of March 24, 2004:  West Nile Activity in the US – Counties Reporting Cases as of March 24, 2004 West Nile Virus 2004: BREAKING NEWS:  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 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:  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:  St. Louis Encephalitis Japanese Encephalitis:  Japanese 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:  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:  Distribution of Japanese Encephalitis in Asia, 1970-1998 Eastern Equine Encephalitis:  Eastern Equine Encephalitis 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:  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 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:  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 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:  Summary – Confirmed and Probable Human Cases in the US Molecular Biology of Viruses that can Cause Viral Encephalitis:  Molecular Biology of Viruses that can Cause Viral Encephalitis Flaviviridae: West Nile Virus Togaviridae: Eastern and Western Equine Encephalitis Bunyaviridae: La Crosse Virus Flavivirus:  Flavivirus Japanese Encephalitis Virus St. Louis encephalitis virus West Nile Virus Flavivirus: Virus Classification:  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.:  Scanned images of West Nile virus isolated from brain tissue from a crow found in New York. Viral Replication Cycle:  Viral Replication Cycle Genome Structure:  Genome Structure Viral Genome:  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:  Secondary structure loops 3’ Stem Loop of Plus Strand:  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:  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:  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:  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:  Model for Closed-Loop Complex Formation in Flaviviruses Togavirus:  Togavirus Eastern Equine Encephalitis Virus Western Equine Encephalitis Virus Venezuelan Equine Encephalitis Virus Togavirus:  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:  Alphavirus Structure http://www.cdc.gov/ncidod/dvbid/arbor/alphavir.htm Alphaviruses: Protein Function:  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:  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:  Bunyaviridae La Crosse Virus La Crosse Virus:  La Crosse Virus http://www.virology.net/Big_Virology/BVRNAbunya.html Bunyaviruses:  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 Bioweaponization Slide59:  West Nile virus Mosquito vector Bird reservoir hosts Transmission Cycle is Key to Weaponization Incidental infections Incidental infections http://www.cdc.gov/ncidod/dvbid/westnile/conf/February_2003.htm Bioweaponization:  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 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:  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:  Clinical Considerations Case Study:  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:  Clinical Considerations Diagnosis Patient History :  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.:  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:  Initial Signs Headache Malaise Anorexia Nausea and Vomiting Abdominal pain Developing Signs:  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:  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:  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:  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.:  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 Radiology MRI:  MRI MRI:  MRI Clinical Considerations:  Clinical Considerations Laboratory Diagnosis 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:  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:  Clinical Considerations Disease Progression 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:  Clinical Considerations Treatment 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:  Suspected HSE Treatment Plan Acyclovir:  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:  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:  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:  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:  Clinical Considerations Patient Prognosis 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:  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:  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:  Clinical Considerations Vaccination 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:  Public Health Considerations Endemic Prevention Infection Control:  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 :  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 :  Mosquito-Proof Home Drain Standing Water Install or Repair Screens Community-Wide Efforts:  Community-Wide Efforts Clean Up Breeding Grounds Ensure Safe Blood Supply Mosquito Control Programs Controversial Surveillance Blood Supply:  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:  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:  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:  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?:  Crop-Dusting NYC? Aerosolized liquids sprayed over large areas of the city. Terrorism concern? New vector for urban area. Public Health Considerations:  Public Health Considerations Surveillance 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:  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:  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:  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:  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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