VIRGINIA EPIDEMIOLOGY BULLETIN

Robert B. Stroube, M.D., M.P.H., Health Commissioner Christopher Novak, M.D., M.P.H., Editor Suzanne R. Jenkins, V.M.D., M.P.H., Acting State Epidemiologist Vickie L. O’Dell, Layout Editor

January 2005 Volume 105, No. 1 Transmissible Spongiform Encephalopathies (TSEs)

A little over one year ago, on Decem- of diseases known as transmissible ber 25, 2003, the US Department of Agri- spongiform encephalopathies (TSEs). This a b culture (USDA) confirmed the diagnosis article is part of the Virginia Department of bovine spongiform encephalopathy of Health’s efforts to improve surveillance (BSE, or “mad cow disease”) in a single for TSEs in Virginia to better understand 1 dairy cow in Washington state. As a re- the disease as well as to detect any conversion sult, the USDA expanded and intensified changes in disease patterns. its national testing program for BSE. From June 1, 2004, to January 2, 2005, 167,476 Overview of TSEs alpha-helices beta-sheets cattle were tested. Not a single positive TSEs are a group of relatively rare pro- 2 animal was found. gressive neurodegenerative disorders that In May 2004, the New Jersey Depart- affect both humans and animals. They are Figure 1. (a) A healthy cellular ment of Health and Senior Services distinguished by long incubation periods, contains only alpha- (NJDHSS) and the Centers for Disease characteristic spongiform changes of the helices. (b) The pathogenic isoform Control and Prevention (CDC) reported brain associated with neuronal loss, and with alpha-helical structures on a suspected cluster of Creutzfeldt- the lack of a detectable immune or inflam- converted to beta-sheets.6 Jakob disease (CJD) cases (including one matory response. Unconventional agents Virginia resident) reportedly linked to the termed (or proteinacious infectious Garden State Racetrack in Cherry Hill, • Chronic Wasting Disease (CWD) in particles), abnormal isoforms of a normal deer and elk; New Jersey. Although there was public cellular protein encoded by a on chro- • Exotic ungulate encephalopathy concern that these deaths might have re- mosome 20, are considered the etiologic (EUE) in nyala and greater kudu; sulted from the consumption of meat con- agent by most scientists.4 An alternative taminated with the agent that causes BSE, hypothesis, the virino model, proposes that • Transmissible Mink Encephalopathy the study did not find a significantly el- the agent consists of a small nucleic acid, (TME) in mink; and evated number of cases of CJD or a and that this molecule is protected by the • Feline Spongiform Encephalopathy common etiology for the cases of CJD host prion protein. A third theory proposes (FSE) in cats. 3 that were identified. that TSEs are caused by conventional vi- While there is no evidence of contact However, incidents like these reinforce ruses. However, to date no -spe- or aerosol transmission for most prion dis- the need for healthcare providers to be cific nucleic acid has been detected in eases, they are infectious under some cir- aware of the previously low-profile group cases of TSE.5 cumstances, such as direct central ner- Known TSEs include: vous system inoculation or consuming con- Creutzfeldt-Jakob disease (CJD), taminated tissue. Prions are also charac- In This Issue: • New Variant CJD (vCJD), , terized by extreme resistance to conven- Transmissible Spongiform Gerstmann-Straüssler-Scheinker tional inactivation procedures including ir- Encephalopathies ...... 1 radiation, boiling, dry heat, and chemicals Index to Volume 104 ...... 5 (GSS), and Fatal Familial Insomnia (FFI) in humans; (formalin, alcohols). And while prion in- Office of Chief Medical Officer fectivity in purified samples is diminished • in sheep and goats; 2004 Report ...... 6 by prolonged digestion with proteases, Virginia Joins NEDSS ...... 7 • Bovine Spongiform Encephalopathy prion inactivation requires 1N NaOH, 4M Flu Corner ...... 7 (BSE) in cattle; guanidinium hydrochloride or isocyanate, tion (e.g., aphasia, 1979 through 1994, CJD was recorded as apraxia, dyslexia, dys- the cause of 3,642 deaths. The average graphia, agnosia, left- age at death was 67 years. Approximately right disorientation, uni- 98% of the deaths were among persons lateral neglect) may 45 years of age or older, and 80% of the occur.10 CJD deaths were among persons 60 years Myoclonus, often of age or older (Figure 4).4 provoked by sensory The average annual age-adjusted death stimuli, usually appears rate during the study period was 0.95 within the first six deaths per million persons in the US. This months of symptom is consistent with published estimates of onset. Cerebellar dis- the crude incidence worldwide of one case Figure 2. EEG typical of CJD, with diffuse one-hertz turbances occur and per million persons. The age-adjusted death triphasic waves.7 corticospinal tract in- rate of male patients was slightly higher volvement (such as than that of female patients, and most sodium hypochlorite (2% free chlorine con- extensor plantar reflexes, clonus, and hy- (95.2%) deaths were among whites.4 centration), or steam autoclaving at 132°C perreflexia) appear. Signs of basal gan- for 4.5 hours.8 glia involvement, such as hypokinesia, dys- Virginia CJD Epidemiology tonic posturing, Creutzfeldt-Jakob CJD is currently a reportable condi- cogwheel rigidity, tion in Virginia only if the ill person is less Disease (CJD) tremor, and than 55 years of age; therefore data on choreoathetoid The prototype TSE in hu- this condition are very limited. However, movements, may mans, Creutzfeldt-Jakob dis- a review of death certificate data in 2004 develop. In the fi- ease (CJD), is a rapidly fatal found a total of 72 cases of CJD from nal stage the pa- dementing illness that occurs 1986-2003 (annual range: 0 to 10 cases). tient loses all worldwide. Although 10% This suggests an overall incidence of CJD mental and physi- of cases are due to autoso- of 0.62 per million persons over the 18 cal functions. The mal dominant inheritance Figure 3. Spongiform changes in CJD year period. Among the five regions in Vir- patient may lapse (familial CJD), most cases (>90%) oc- ginia, the Northern region had the lowest into a coma and usually dies from an in- cur unpredictably in the population (spo- incidence (0.29/1,000,000 persons/year), fection, such as aspiration pneumonia, radic CJD). Less than 1% of cases are while the Eastern region had the highest precipitated by the bedridden, unconscious the result of iatrogenic transmission (0.96/1,000,000 persons/year). The rates state.10 (e.g., associated with receipt of con- in the 35 health districts (using 2002 popu- Neuropathologic evaluation, particu- taminated human pituitary growth hor- lations) varied from 0/1,000,000 persons/ larly by immunohistochemistry or West- mone, human pituitary gonadotrophin, year to 2.47/1,000,000 persons/year (Fig- ern blot, is currently the most definitive dura mater grafts or corneal tissue, or ure 5). However, due to the very small method to diagnose human prion diseases. exposure to contaminated neurosurgi- numbers of cases of CJD that were re- In terms of treatment, although some cal equipment).4,9 However, all six of medications can help the cases linked to the use of contami- relieve jerking move- nated equipment occurred before the ments and unsteadi- implementation of sterilization proce- Figure 4. Creutzfeldt-Jakob disease deaths and death ness (e.g., clonaze- 4 dures currently used in health care fa- rates by age group, United States, 1979 through 1994. pam) and the pos- cilities. No such cases have been re- sible benefits of ported since 1976.9 quinacrine are un- The incubation period of CJD can range der evaluation, from one year to more than 30 years.10 there is no cure for Prodromal symptoms may include head- TSEs and they are in- ache, anorexia, behavioral changes, and variably fatal.6,8 depression.7 Initial neurologic signs can include progressive memory loss over US CJD weeks to months, as well as vertigo, Epidemiology blurred vision, visual field defects, or diplo- pia. Mental deficits rapidly lead to global In 1996, Holman dementia, as well as self-neglect, apathy, et al. examined or irritability. Some patients complain of trends in the inci- easy fatigability, somnolence, or insomnia. dence of CJD in the Other abnormalities of higher cortical func- United States. From

2 January 2005 ported, these rates are considered un- Table 1: Clinical and pathologic characteristics distinguishing stable. classic Creutzfeldt-Jakob disease (CJD) from variant CJD (vCJD) The average age at death of CJD cases in Virginia from 1986 through 2003 CDharacteristic CDJ vCJ was 70 years (range: 42-94 years). More Msedian age at death 6s8 yr 28 yr cases occurred in females (64%) than males. The disease predominantly oc- Msedian duration of illness 4s-5 month 13-14 month curred in whites (89%) with 8% of cases Clinical signs and Dementia; early Prominent psychiatric/behavioral in blacks and 1% of cases in Asians. symptoms neurologic signs symptoms; painful dysesthesias; Therefore, the overall pattern of CJD in delayed neurologic signs Virginia appears comparable to the US Periodic sharp waves on Otften present Absen pattern. electroencephalogram One limitation to our understanding of 'dPulvinar sign' on MRI* N%ot reporte Present in >75 CJD in Virginia and the US is that sur- veillance mainly uses death certificate Presence of 'florid plaques' Rsare or absent Present in large number on neuropathology data. However, it is very likely that some cases do not get recorded. CJD is an un- Immunohistochemical Variable Marked accumulation of PrPres** common disease and physicians who are analysis of brain tissue accumulation not familiar with the signs and symptoms Presence of agent in Ndot readily detected Readily detecte may mistake it for other conditions. Evi- lymphoid tissue dence of the under-reporting of cases Increased glycoform ratio on NPot reported Marked accumulation of Pr res comes from some European countries, immunoblot analysis of where enhanced surveillance has found PrPres higher than expected rates due to in- Genotype at codon 129 of Peolymorphic Methionine/methionin creased awareness and better diagno- prion protein sis.11 In addition, one small study reported Source: Adapted from Belay E, Schonberger L. 2002. Clin Lab Med. 22:849-62.14 that as many as 13% of patients diag- nosed with Alzheimer’s disease were *Symmetrical hyperintensity of the pulvinar (posterior) nuclei of the thalamus compared to the anterior putamen on brain magnetic resonance imaging (MRI); in the appropriate found upon autopsy to have actually had 15 CJD.12 Therefore, it seems likely that the clinical context, this signal is highly specific for vCJD. **Protease-resistant prion protein. current data underestimate the true inci- dence of CJD in Virginia and in the US. be increasing. This is partly explained by the epidemiology for the disease differs improved diagnosis and active surveillance, from “classic” CJD. For example, the Bovine Spongiform but new may also be occur- median age at death is much younger (28 Encephalopathy (BSE) and ring.13 years, versus 68 years for classic CJD).1,4 Variant CJD (vCJD) During the 10 years after the first cow In addition, the median duration of illness with BSE was identified, there was no before death is 13-14 months for vCJD Scrapie, an endemic spongiform en- change in clinical or neuropathologic fea- patients, compared to 4-5 months for clas- cephalopathy of sheep and goats, has tures of human cases of CJD in the UK. sic CJD (see Table 1).1 been recognized since the mid-18th cen- However, in 1994 a cluster of cases with Clinical differences also exist between 13 tury. The widespread epizootic of BSE a unique clinical picture began to appear. patients with vCJD and classic CJD. that was detected in 1986 in the United Termed “new variant of CJD” (vCJD), Patients with vCJD have prominent early Kingdom (UK) may have origi- behavioral or psychiatric mani- 4 nated from scrapie as a result festations and dysethesias of contaminated rendered sheep Figure 5. Creutzfeldt-Jakob Disease in Virginia 1986-2003 (painful sensory symptoms), carcasses that were fed to cattle. with neurologic signs such as Since then cases of BSE have myoclonus and extrapyramidal also been detected in many other dysfunction delayed for several countries as a result of imported months after illness onset. The contaminated live animals or live- characteristic electroenceph- stock food supplements. While alographic pattern of periodic the incidence of new cases is de- sharp waves observed in clas- creasing in some countries (in- sic CJD patients is absent in pa- cluding the UK) in other coun- tients with vCJD. In addition, tries (e.g., France, Portugal, Ger- Cases per million persons more than 75% of patients with many, Spain, and the Republic of 1.00-1.50 0 vCJD have a characteristic Ireland) the incidence appears to >0-0.50 1.51-2.00 0.51-1.00 2.01-2.50 symmetrical hyperintensity of

Epidemiology Bulletin 3 the pulvinar (posterior) nu- and the number of through direct animal-to-animal contact or clei of the thalamus com- cases of vCJD sug- indirect exposure, such as though contami- pared to the anterior puta- gests that the very nated feed and water sources.18 men on brain magnetic reso- small infectious Although the original CWD-endemic nance imaging (MRI) (the doses cannot readily areas were Colorado and Wyoming, the “pulvinar sign”); in the appro- surmount the com- geographic distribution seems to be chang- priate clinical context this is bined effects of a ing as a result of the natural movement of highly indicative of a vCJD di- “species barrier” deer and elk as well as commercial move- agnosis.1,15 Variant CJD cases and a comparatively ment of infected animals (Figure 6). For also have characteristic se- inefficient route of example, CWD in free-ranging cervids vere spongiform change, neu- infection.13 was first reported east of the Mississippi ronal loss, and astrocytosis in River in Wisconsin among white-tailed the basal ganglia and thala- Chronic deer harvested in the 2001 hunting sea- mus, and a distinctive florid or Wasting son.18 As a result, the Virginia Department “daisy” plaque (an amyloid Disease (CWD) of Game and Inland Fisheries is conduct- core surrounded by “petals” ing an extensive surveillance program. of spongiform change in the Chronic wasting From 2002-2004 over 1,200 animals were cerebrum and cerebellum and protease- disease (CWD) was tested from randomly selected hunter-har- resistant prion protein (PrPres) accumula- first identified as a syndrome of captive vested deer, target or suspect animal sur- tion in high density shown by immunocy- mule deer in the late 1960s and was rec- veillance, and all captive deer mortali- tochemistry).1,4,13 Prions are detected ognized as a TSE in 1978. Its only known ties. To date, CWD has not been detected readily by immunohistochemical analy- natural hosts are mule and white-tail deer in Virginia. In addition, measures to pre- sis in lymphoid tissues (e.g., appendix, (Odocoileus species) and Rocky Moun- vent the spread of CWD to Virginia in- lymph nodes, spleen, and tonsils) of vCJD tain elk (Cervus elaphus nelsoni).18 clude a ban on the importation or intrast- patients, but not in classic CJD patients. Clinical manifestations of CWD include ate movement of cervids, strict controls Finally, all persons with vCJD (tested as weight loss over weeks or months, behav- over the deer farming industry, euthanizing of January 2004) have had methionine ho- ioral changes, excessive salivation, diffi- and testing any illegal cervids, and a policy mozygosity at codon 129 of the prion pro- culty swallowing, polydipsia, and polyuria. decision not to reintroduce elk into Vir- tein gene, indicating that persons who do In some animals, ataxia and head tremors ginia.19 not carry this genotype (the majority of may occur. Most animals with the disease A major concern with CWD is the pos- the general population) may have in- die within several months of illness onset, sible transmission of the agent to domes- creased resistance to vCJD.1 sometimes from aspiration pneumonia. In tic animals, such as cattle and sheep, which Evidence to date indicates that there rare cases, illness may last for more than may come into contact with infected deer has never been a case of vCJD transmit- one year. In captive cervids, most cases and elk or CWD-contaminated environ- ted through direct contact of one person occur in animals 2 to 7 years of age; how- ments. If such transmissions were to oc- with another.16 The main association is ever, the disease has been reported in cur, it could increase the extent and fre- with the BSE epizootic in British cattle. cervids as young as 17 months and as old quency of human exposure to the CWD For example, the first and only (as of as 15 years of age. This disease can be agent. Passage of the agent through a sec- January 2005) probable vCJD case in a highly transmissible within captive deer ondary host could also alter its infectious US resident was diagnosed in 2002. This and elk populations, although the mode of properties, increasing its potential for be- patient had grown up in the UK when transmission is not fully understood. Evi- coming more pathogenic to humans.18 the risk for human exposure to the agent dence supports lateral transmission However, while CWD has been trans- of BSE was at its peak. Therefore, it mitted experimentally by intracerebral in- Figure 6. Positive CWD Areas in North America is likely that this patient was exposed jection to a number of animals, it does to the BSE agent one or more times not appear to occur naturally outside the during 1980-1992 before moving to the cervid family. Domestic cattle, sheep, and United States.17 goats residing in research facilities in Overall, the risk for acquiring vCJD close contact with infected cervids did from BSE-contaminated product appears not develop a prion disease. In addition, to be low. For example, in the UK more despite the decades-long endemicity of than one million cattle were probably in- CWD in Colorado and Wyoming, the in- fected with BSE.1 In contrast, the vCJD cidence of CJD and the age distribution outbreak has shown only a modest in- of CJD case-patients in these two states crease in cases (as of December 1, 2003, are similar to those seen in other parts of a total of 153 cases of vCJD had been the United States.18 Finally, laboratory in- reported worldwide).13,16 The disparity vestigations of case-patients diagnosed between the number of cases of BSE with CJD have not indicated a causal link

4 January 2005 18,20 to CWD. These findings suggest that the risk Index to Volume 104 (by Issue Number) of transmission of CWD to humans is very low.18 Unfortunately, the transmission of BSE to hu- Antibiotic Awareness Month ...... 9 mans and the resulting cases of vCJD indicate Antibiotic Resistance and Get Smart VA ...... 3 that, provided sufficient exposure, the species bar- rier may not completely protect humans from ani- CME: MMWR ...... 4 mal prion diseases. Because CWD has occurred Cover Your Cough Poster ...... 1 in a limited geographic area, an adequate number E. coli 0157:H7 Outbreak - CME ...... 8 of people may not have been exposed to the CWD agent to result in a clinically recognizable human Featured Website: NYNJ Public Health Training Center ..... 2 disease. However, the level and frequency of hu- Flu Corner ...... 3, 11, 12 man exposure to the CWD agent may increase Flu Corner (Avian Influenza) ...... 1 with the spread of CWD in the United States. More epidemiologic and laboratory studies need to be Harmful Algal Blooms (HABs) ...... 6 conducted to monitor the possibility of such trans- Influenza Antiviral Prioritization Recommendations ...... 10 18 missions. Influenza Outbreak Management in Institutions ...... 10 TSE Prevention Influenza Recommendations (Antivirals) ...... 9 Influenza Recommendations (Immunization) ...... 8 A wide range of efforts, from national to state to institutional level, have been developed in vari- Meningococcal Disease Prevention in Students ...... 8 ous countries to prevent the transmission of TSEs. MRSA in Special Populations ...... 1 In the US, these include: National Public Health Week Notice ...... 2 • Preventing importation—severe restrictions Norovirus Outbreak Investigation Summary ...... 11 are placed on the importation of live rumi- Norovirus Outbreaks Update ...... 12 nants (e.g., cattle, sheep, and goats) and certain ruminant products from countries Norovirus Review ...... 2 where BSE is/was known to exist;16 Outbreak Investigations Review ...... 2 • Surveillance in humans and animals; Pertussis in Virginia Update ...... 12 • Preventing amplification—the US Food and Pneumococcal (PCV7) Vaccine Temporary Suspension ..... 3 Drug Administration instituted a ruminant Pneumococcal (PCV7) Vaccine Update ...... 8 feed ban in June 1997 to prevent the trans- Pneumococcal Vaccine (PPV23) Reminder ...... 12 mission to other animals from infectious tissues;16 Rabies in Animals...... 4 • Preventing blood-borne human transmis- Rabies in Humans ...... 3 sion—a blood donor policy excludes dona- Rabies Vaccine Recall ...... 3 tions from anyone who has lived in or visited Reducing Public Health Disparities in VA ...... 4 European countries for a cumulative period of Regulations for Disease Control Changes ...... 7 13 six months or more since 1980. In addition, Regulations for Isolation and Quarantine Changes ...... 12 the American Red Cross will not accept blood RSV Update ...... 2 donations from people who have ever received a transplant of high-risk tissue (e.g., SARS Update ...... 1 dura mater) or from those who have a close Shiga Producing E. coli (STEC) ...... 6 blood relative who has had CJD;21 and, Summary of VA Reportable Diseases for 2003 ...... 5 • Infection control—since the standard meth- Syndromic Surveillance ...... 11 ods of sterilization are ineffective for prions, Thanks to Contributors ...... 4 the World Health Organization (WHO) has Thimerosal and Influenza Vaccine ...... 1 developed CJD infection control guidelines. Details are available from the WHO website VA Emergency Z-card ...... 3 at http://www.who.int/emc-documents/tse/ VA Medical Reserve Corps Recruitment ...... 10 whocdscsraph 2003c.html. Varicella Disease Reporting,...... 4 While not an exhaustive list of prevention mea- Virginia APIC Meeting Notice ...... 6 sures, this list suggests the wide scope of inter- Virginia Epidemiology Conference ...... 11 ventions that have been developed to monitor and prevent the spread of these diseases. Water-Related Skin Infections ...... 6 (continued on page 6) WNV Update ...... 9

Epidemiology Bulletin 5 (continued from page 5) for the presence of the 14-3-3 protein (a 6. BSE Inquiry Report. http://www.bseinquiry. marker for some prion diseases when gov.uk/ Conclusions 7. UCSF Memory and Aging Center. http:// other conditions have been excluded) in memory.ucsf.edu/Education/education_cjd.html. The need to better understand classic cerebrospinal fluid (CSF), detecting mu- 8. CDC Office of Health and Safety, BMBL CJD, the emergence of BSE and the tations in prion protein , and histo- Section VII, Agent Summary Statements: Section VII-D: Prions. http://www.cdc.gov/od/ohs/biosfty/ spread of CWD in the US all reinforce logical and immunohistochemical exami- bmbl4/bmbl4s7d.htm. the need to consider TSEs in patients, re- nation for the prion protein in specimens.1 9. CDC Fact Sheet: infection control. http:// gardless of age, who report with distin- Information about these services is avail- www.cdc.gov/ncidod/diseases/cjd/ guishing neurological signs and symptoms. cjd_inf_ctrl_qa.htm. able from NPDPSC at http://www.cjdsur 10. The Merck Manual. Section 13. Infectious Although reporting CJD cases in Virginia veillance.com or from the CDC (telephone Diseases. Chapter 162. http://www.merck.com/ is required only if the patient is less than 404-639-3091). Protocols for autopsy, bi- mrkshared/mmanual/section13/chapter162/ 55 years of age, healthcare providers are 162d.jsp. opsy and other specimens (e.g., blood, 11. Puopolo M, Ladogana A, Almonti S, et al. encouraged to report all cases of CJD to urine, CSF), forms and shipping/mailing in- 2003. J Clin Epi. 56:494-9. their local health departments as this may structions for specimens are also avail- 12. Manuelidis EE, Manuelidis L. 1989. help to identify cases of vCJD, as well as able on the NPDPSC website.1,3,17 Alzheimer Dis Assoc Disord. 3:100-9. 13. Brown P, Will RG, Bradley R, et al. 2001. improve the understanding of TSEs in Vir- EID. 7(1):6-16. ginia. Submitted by: Christopher Novak, MD, MPH and 14. Belay E, Schonberger L. 2002. Clin Lab Med. In addition, because testing brain tis- Aileen Buckler, MD, MPH 22:849-62. sue permits the most definitive diagnosis 15. Collie DA, Summers DM, Sellar RJ, et al. Acknowledgements: 2003. AJNR Am J Neuroradiol 24(8):1560-9. of all forms of CJD and identification of Special thanks to Dr. Michael Geschwind (UCSF 16. CDC Fact Sheet: vCJD. http://www.cdc.gov/ emerging forms of the disease, VDH en- Memory & Aging Center) for reviewing this ncidod/diseases/cjd/cjd_fact_sheet.htm courages physicians to arrange for brain article. 17. MMWR. 2002. 51(41):927-9. 18. Belay ED, Maddox RA, Williams ES, et al. autopsies in all decedents with known or References 2004. Emerg Infect Dis. 10(6):977-984. suspected CJD. The National Prion Dis- 1. MMWR. 2004. 52(53):1280-5. 19. Duncan B. VDGIF. Personal communications. ease Pathology Surveillance Center 2. USDA BSE Testing Results. www.aphis.usda.gov/ January 2005. lpa/issues/bse_testing/test_results.html. 20. MMWR. 2003. 52(07);125-127. (NPDPSC) provides neuropathologic and 3. MMWR. 2004. (Early Release):1-4. 21. Red Cross Blood Eligibility Guidelines (January biochemical diagnostic services free of 4. Holman RC, Khan AS, Belay ED, Schonberger 5, 2005). http://www.redcross.org/services/biomed/ charge to US physicians and state and lo- LB. 1996. EID. 2(4):333-7. 0,1082,0_557_,00.html#cjd. 5. Cohen JT, Duggar K, Gray GM, et al. 2003. cal health departments.This includes testing http://www.hcra.harvard.edu/pdf/madcow.pdf.

Office of the Chief Medical Examiner 2004 Annual Report

Under § 32.1-283 of the Code of • the sudden death of any infant less specific analyses Virginia, the Office of the Chief than eighteen months of age whose of deaths in Medical Examiner (OCME) has the death might be attributable to Sudden children, deaths responsibility for investigating: Infant Death Syndrome; and related to ethanol • any death from trauma, injury, • any other suspicious, unusual, or use, motor violence, or poisoning attributable to unnatural death. vehicle-related accident, suicide or homicide; The Virginia Department of Health deaths, and drug- • sudden deaths to persons in apparent Office of the Chief Medical Examiner related deaths good health or deaths unattended by 2004 Annual Report summarizes the have been a physician; findings from the 5,821 deaths (10.1% provided. Overall, this is the most • deaths of persons in jail, prison, or of the estimated total deaths in Virginia) detailed analysis of medical examiner another correctional institution, or in investigated by the OCME in 2003. The cases ever produced in Virginia. police custody; report includes detailed analyses of The full report from the OCME is • deaths of patients/residents of state overall deaths by temporal, geographic available on-line at: mental health or mental retardation and demographic factors, as well as www.vdh.virginia.gov/medexam/ facilities; manner of death. In addition, more OCMEAnRpt04.pdf.

Did you know? In Virginia in 2003, more deaths occurred on Saturdays than any other day of the week. The fewest number of deaths occurred on Tuesdays.

6 January 2005 Flu Corner

Influenza Activity For up-to-date information on vaccine available to health departments national influenza patterns go to: could be used for any non-VFC indi- Influenza activity was www.cdc.gov/flu/weekly/ viduals (child or adult) in localities where low in Virginia during fluactivity.htm. Information on the demand for influenza vaccine among October through early influenza surveillance in VFC eligible children has already been December 2004, but has Virginia is available on the met. Preservative-free pediatric 0.25ml increased steadily since VDH website at doses may be administered to adults if mid-December. During the www.vdh.virginia.gov/epi/ two doses are administered at separate week ending January 22, flu.htm. injection sites. This use of VFC vaccine 2005, influenza activity in Virginia is limited to health departments and non- was classified as Regional (activity Influenza Vaccine Update profit organizations, such as federally greater than threshold in two or more This season’s influenza vaccine qualified health centers and rural health regions AND either lab confirmed strains have been well matched antigeni- clinics, in accordance with policies influenza in the affected regions within cally to the influenza isolated to established by the district director, and the past 3 weeks OR recent detection date. Late-season vaccination can still only for the 2004-2005 influenza season. of a laboratory confirmed outbreak in offer protection against influenza this Private physicians may not adminis- two regions). Nationwide, fifteen states/ season. Therefore, the CDC continues ter VFC vaccine to non-VFC patients. territories reported widespread influenza to recommend aggressive efforts to Unused VFC influenza vaccine in activity, 17 reported regional activity, 10 vaccinate people in priority groups. private physicians’ offices may be reported local activity, and 11 reported On January 26, the State Health transferred to health departments. sporadic activity. The Centers for Commissioner authorized health direc- Only unopened vials may be accepted in Disease Control and Prevention (CDC) tors in Virginia to relax restrictions on the transfer. However, private physi- reported that during this same period the the use of influenza vaccine in their cians have the opportunity to purchase proportion of deaths attributed to respective districts if they feel the additional vaccine directly from sanofi pneumonia and influenza remained demand for vaccination within priority pasteur (formerly Aventis). A vaccine below the epidemic threshold. groups has been met. This will allow “return policy” has been developed (for By January 29, 2005, the Division of remaining doses of vaccine to be used to the current influenza season only) where Consolidated Laboratory Services provide protection against influenza for providers will be allowed to return (DCLS) reported 56 confirmed cases of as many people as possible. unused vaccine for a credit and will influenza (54 type A and 2 type B) by In addition, in January 2005 the have financial responsibility for direct fluorescent antibody (DFA) and/ demand for Vaccine for return shipping costs only. or culture. Twenty-nine cases were Children (VFC) influenza These strategies should from the central region, eleven were vaccine had decreased. To help ensure that as from the northwest region, nine were increase the availability of many people as from the eastern region, five were from the influenza vaccine to possible are pro- the southwest region and two were those who need it, on January tected from influ- from the northern region. 27, 2005, the CDC announced that enza. limited amounts of VFC influenza

Virginia Joins the National Electronic Disease Surveillance System (NEDSS)

The Virginia Department of Health (VDH) has begun to submit its weekly disease report data to the U.S. Centers for Disease Control and Prevention (CDC) using the National Electronic Disease Surveillance System (NEDSS). This makes Virginia the tenth state in the country to utilize this new system. While this is the first step in the process of implementing the system statewide, it represents the culmination of years of effort by VDH staff to prepare to imple- ment NEDSS in Virginia. For now, use of the system is limited to certain central office staff of the Office of Epidemiology. Use of the system will expand to district offices and other reportable disease program offices within VDH during 2005.

Epidemiology Bulletin 7 Cases of Selected Notifiable Diseases Reported in Virginia*

Total Cases Reported, December 2004

Total Cases Reported Statewide, Regions January through December

Disease State NW N SW C E This Year Last Year 5 Yr Avg AIDS 1464 1421148134727 797 82 Campylobacteriosis 408 17516013624 848 66 E. coli O157:H7 61032030 9 566 Giardiasis 48 987915562 3 472 42 Gonorrhea 6903 404387145 267 83,50 98,06 10,01 Hepatitis, Viral A 15 06333113 5 144 16 B, acute 33418 1317277 7 292 18 C, acute 11000015 7 19 HIV Infection 15404 24113030878 729 88 Lead in Children† 42 53941110890 776 70 Legionellosis 40202050 3 121 5 Lyme Disease 825001157 4 169 17 Measles 000000 0 0 4 Meningococcal Infection 00000028 0 244 Mumps 000000 3 1 7 Pertussis 397 17434293 3 221 17 Rabies in Animals 28 460126427 4 584 55 Rocky Mountain Spotted Fever 71202234 8 392 Rubella 000000 0 0 0 Salmonellosis 703 17112961613,14 17,18 1,22 Shigellosis 1162616 136 5 495 57 Syphilis, Early§ 3011 133416251 175 23 Tuberculosis 8844 4721319322 363 31 Localities Reporting Animal Rabies This Month: Accomack 1 raccoon; Appomattox 1 raccoon; Augusta 1 raccoon; Bedford 1 cow; Chesterfield 1 raccoon; Fairfax 2 foxes, 2 raccoons, 1 skunk; Floyd 1 raccoon; Goochland 1 raccoon; Hampton 1 raccoon; Highland 1 fox; King William 1 skunk; Loudoun 1 raccoon; Montgomery 1 cow; Northampton 1 cat; Patrick 1 raccoon, 1 skunk; Pittsylvania 1 skunk; Pulaski 1 raccoon; Rockbridge 1 skunk; Rockingham 1 skunk; Russell 1 skunk; Smyth 1 raccoon; York 2 raccoons. Toxic Substance-related Illnesses: Asbestosis 4; Adult Lead Exposure 15; Lung Cancer/Metal Exposure 1; Pneumoconiosis 6; Silicosis 1. *Data for 2004 are provisional. †Elevated blood lead levels >10µg/dL. §Includes primary, secondary, and early latent.

Published monthly by the VIRGINIA DEPARTMENT OF HEALTH PRESORTED Office of Epidemiology STANDARD P.O. Box 2448 U.S. POSTAGE Richmond, Virginia 23218 PAID http://www.vdh.virginia.gov Richmond, Va. Telephone: (804) 864-8141 Permit No. 591

8 January 2005