From <@VMS.DC.LSOFT.COM:owner-mednews@ASUVM.INRE.ASU.EDU> Sun Sep 17 11:53:32 1995 (LSMTP for OpenVMS v0.1a) with SMTP id A00489AB ; Sun, 17 Sep 1995 11:38:51 - 0400 release 1.8b) with NJE id 1647 for MEDNEWS@ASUVM.INRE.ASU.EDU; Sun, 17 Sep 1995 08:36:31 -0700 (LMail V1.2a/1.8a) with BSMTP id 6435; Sun, 17 Sep 1995 08:36:30 - 0700 SMTP V2R3) with TCP; Sun, 17 Sep 95 08:36:27 MST (8.6.12/8.6.9) with UUCP id IAA19361 for mednews@asuvm.inre.asu.edu; Sun, 17 Sep 1995 08:07:31 -0700 mednews@asuvm.inre.asu.edu Comments: To: asumednews@stat.com HICNet Medical News Digest Sun, 17 Sep 1995 Volume 08 : Issue 32 Today's Topics: [MMWR 1-sep-95] Human Rabies --- Washington, 1995 [MMWR] Blood Lead Levels Among Children in a Managed-Care Organization [MMWR] "Immunization Update" Video Conference [MMWR] Hypertension Among Mexican Americans [MMWR Sep8] Arboviral Disease --- United States, 1994 [MMWR]NIOSH Alert: Request for Assistance in Preventing Deaths and [MMWR] Update: Influenza Activity --- Worldwide, 1995 +------------------------------------------------+ ! ! ! Health Info-Com Network ! ! Medical Newsletter ! +------------------------------------------------+ Editor: David Dodell, D.M.D. 10250 North 92nd Street, Suite 210, Scottsdale, Arizona 85258-4599 USA Telephone +1 (602) 860-1121 FAX +1 (602) 451-1165 Internet: mednews@stat.com Bitnet: ATW1H@ASUACAD Mosaic WWW *Asia/Pacific: http://biomed.nus.sg/MEDNEWS/welcome.html *Americas: http://outland.cardinal.com/hicn *Europe: http://www.dmu.ac.uk/ln/MEDNEWS/ Compilation Copyright 1995 by David Dodell, D.M.D. All rights Reserved. License is hereby granted to republish on electronic media for which no fees are charged, so long as the text of this copyright notice and license are attached intact to any and all republished portion or portions. The Health Info-Com Network Newsletter is distributed biweekly. Articles on a medical nature are welcomed. If you have an article, please contact the editor for information on how to submit it. If you are interested in joining the automated distribution system, please contact the editor. Associate Editors: E. Loren Buhle, Jr. Ph.D. Dept. of Radiation Oncology, Univ of Pennsylvania Tom Whalen, M.D., Robert Wood Johnson Medical School at Camden Douglas B. Hanson, Ph.D., Forsyth Dental Center, Boston, MA Lawrence Lee Miller, B.S. Biological Sciences, UCI Dr K C Lun, National University Hospital, Singapore W. Scott Erdley, MS, RN, SUNY@UB School of Nursing Jack E. Cross, B.S Health Care Admin, 882 Medical Trng Grp, USAF Albert Shar, Ph.D. CIO, Associate Prof, Univ of Penn School of Medicine Stephen Cristol, M.D. MPH, Dept of Ophthalmology, Emory Univ, Atlanta, GA Subscription Requests = mednews@stat.com anonymous ftp = vm1.nodak.edu; directory HICNEWS FAX Delivery = Contact Editor for information ---------------------------------------------------------------------- To: hicnews Human Rabies -- Washington, 1995 On March 15, 1995, a 4-year-old girl who resided in Lewis County, Washington, died from rabies. This report summarizes the clinical course, epidemiologic investigation, and probable exposure history of the case. On March 8, the child was transported to a local hospital after a 2-day history of drowsiness, listlessness, abdominal pain, anorexia, sore throat, and pain on the left side of her neck. During examination in the emergency department, she had nasal congestion and drooling. Rhinitis and bilateral conjunctivitis were diagnosed; antibiotics and symptomatic treatment were prescribed, and she was discharged. On the morning of March 9, she was transported to the same hospital because of an axillary temperature of 104.0 F (40.0 C) and behavioral changes. In addition, she had had hallucinations, difficulty standing, and insomnia and refused to drink fluids. On examination in the emergency department, findings included an axillary temperature of 101.2 F (38.4 C), pulse of 210 per minute, respiratory rate of 32 per minute, an enlarged reactive right pupil, and tremors. Laboratory test results included a white blood cell count of 20,800/mm3 (normal: 5000-10,000 mm3), blood urea nitrogen of 45 mg/dL (normal: 0-25 mg/dL), and sodium level of 151 mmol/L (normal: 135-145 mmol/L). Preliminary diagnoses included dehydration and possible drug intoxication, and intravenous fluids were administered. Screening of urine for drugs was negative, and computerized axial tomography of the brain was within normal limits. Later on the morning of March 9, her temperature increased, and she had a seizure. Cerebrospinal fluid findings were nonspecific. She was intubated for hypoventilation. In the emergency department and during air transport to the intensive-care unit of a regional hospital, she became bradycardic and required cardiopulmonary resuscitation. On arrival at the regional hospital, preliminary differential diagnoses included sepsis, viral encephalitis, and drug toxicity; ceftriaxone and acyclovir were administered. She became comatose, and an electroencephalogram (EEG) obtained on March 10 revealed generalized sharp and slow wave discharges. On March 13, an EEG revealed moderate to severe generalized slowing of cerebral activity. Based on information from family members about the child's possible exposure to a bat, diagnostic testing for rabies was initiated. A nuchal skin biopsy obtained on March 13 was positive for rabies by direct fluorescent antibody (DFA) testing at CDC on March 14. On March 15, the child died. On autopsy, gross examination revealed massive cerebral edema with uncal herniation and intracytoplasmic inclusions in the brain and spinal cord. At the Washington State Department of Health Public Health Laboratories a specimen of brain tissue obtained at autopsy also was positive by DFA, and rabies virus was isolated by mouse inoculation. Analysis at CDC also included viral isolation from sputum obtained on March 14 and a positive DFA and nucleotide sequence analysis result from brain tissue obtained at autopsy. During the child's hospitalization, family members reported that, on February 18, a bat had been found in her bedroom. Family members had examined the child but found no evidence of a bite. The bat was removed from the house, destroyed, and buried in the yard. On March 14, the local health department exhumed the bat. Despite trauma, decomposition, and partial consumption of the specimen by maggots, the bat brain was positive for rabies by DFA and nucleotide sequence analysis. Presumptive identification of the bat at CDC was either Myotis californicus or M. ciliolabrum. In addition, based on nucleotide sequence analysis, the rabies virus from the decedent and the bat were identical and was identified as a variant associated with small Myotis bats in the western United States. Based on possible percutaneous or mucous membrane exposure to tears or saliva from the patient, postexposure rabies immunoprophylaxis was administered to 72 persons: six registered nurses, six respiratory therapists, one laboratory technician, one diagnostic imaging technician, two physicians, six family members, and 50 children and adults who were contacts in a day care center. Reported by: A Paves, MD, P Gill, J Mckenzie, MN, Providence Hospital, Centralia; R Renbarger, RS, T Bell, MD, Lewis County Health Dept, Chehalis; A Movius, MD, H Baden, MD, PP O'Rourke, MD, A Melvin, MD, S Kuhl, MD, S Johnson, MD, J Bradshaw, MD, K Goodrich, L Spath, D Krous-Riggert, MPH, J Smith, MN, Children's Hospital and Medical Center, Seattle; M Goldoft, MD, J Kobayashi, MD, S LaCroix, MS, B Wieman, P Stehr-Green, DrPH, State Epidemiologist, Washington State Dept of Health. Viral and Rickettsial Zoonoses Br, Div of Viral and Rickettsial Disease, National Center for Infectious Diseases, Div of Field Epidemiology, Epidemiology Program Office, CDC. Editorial Note: The rabies case described in this report was the first to be documented in a human in the United States during 1995 and is consistent with a major epidemiologic pattern: since the 1950s, bats increasingly have been implicated as wildlife reservoirs for variants of rabies virus transmitted to humans. Variants of rabies virus associated with bats have been identified from 12 of the 25 cases of human rabies diagnosed in the United States since 1980. However, a clear history of animal bite exposure was documented for only six of these 25 cases. This finding suggests that even apparently limited contact with bats or other animals infected with a bat variant of rabies virus may be associated with transmission. The inability of health-care providers to elicit information from patients about potential exposures to bats may reflect circumstances that hinder recall or the limited injury inflicted by a bat bite. For example, the family members of the child described in this report had not witnessed contact between the child and the bat, and she denied a bite or any other contact on the night of the incident; however, both the epidemiologic findings and molecular data indicated that infection resulted from contact with the bat. The case in Washington and reports of similar cases (1,2), underscore that, in situations in which a bat is physically present and the person(s) cannot exclude the possibility of a bite, postexposure treatment should be considered unless prompt testing of the bat has ruled out rabies infection. This recommendation should be used in conjunction with guidelines of the Advisory Committee on Immunization Practices (3) to maximize a health-care provider's ability to respond to situations in which accurate exposure histories cannot be obtained and to ensure that inappropriate postexposure treatments are minimized. References 1. CDC. Human rabies--California, 1994. MMWR 1994;43:455-7. 2. CDC. Human rabies--New York, 1993. MMWR 1993;42:799,805-6. 3. ACIP. Rabies prevention--United States, 1991: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 1991;40(no. RR-3). ------------------------------ To: hicnews Organization Blood Lead Levels Among Children in a Managed-Care Organization -- California, October 1992-March 1993 Despite substantial progress in reducing exposures to lead among children, as recently as 1991, 9% of children in the United States had blood lead levels (BLLs) of greater than or equal to 10 ug/dL (1)--levels that can adversely affect intelligence and behavior. In 1991, CDC recommended screening all children for lead exposure except those residing in communities in which large numbers or percentages previously had been screened and determined not to have lead poisoning (2). Subsequently, the California Department of Health Services (CDHS) issued a directive to all California health-care providers participating in the Child Health and Disability Prevention Program to routinely screen children for lead poisoning in accordance with the 1991 CDC guidelines (3). This report presents findings of BLL testing during 1992-1993 from a managed-care organization that provides primary-care services to Medicaid beneficiaries in several locations in California (i.e., Los Angeles County, Orange County, San Bernardino County, Riverside County, Sacramento, and Placerville). From October 1992 through March 1993, BLLs were measured for 2864 consecutive children aged 1-6 years who received Medicaid benefits. Data were not collected about the number of children whose families did not consent to testing nor about those from whom blood could not be collected. Blood submitted by venipuncture was analyzed by a laboratory certified by the CDHS as proficient in blood lead analysis. Families completed a risk questionnaire (2) about exposures to older housing, home renovation or remodeling, adults with jobs or hobbies that involve lead, and industrial sources of lead, and answered a question about whether the child's playmates or siblings were known to have BLLs greater than or equal to 10 ug/dL. Children were categorized as "low risk" if all five questions were answered "no" or "high risk" if one or more questions were answered "yes." Overall, 2808 (98.0%) children had BLLs less than 10 ug/dL; 46 (1.7%) had BLLs 10-14 ug/dL, and 10 (0.3%) had BLLs greater than or equal to 15 ug/dL (Tables 1 and 2). The percentage of children with BLLs greater than or equal to 10 ug/dL was similar across age groups (Table 1). Although BLLs varied by clinic site (Table 2), no site had a prevalence of elevated BLLs exceeding 4.6%. The risk questionnaire had a sensitivity of 46%, specificity of 74%, and predictive values positive and negative of 3.4% and 98.6%, respectively. The prevalence of increased BLLs was greater among children identified as high risk (3.4%) than among other children (1.4%, prevalence ratio: 2.4; 95% confidence interval=1.4%-4.1%). Based on the CDHS reimbursement rate of $22.45 per test, the cost of screening tests per case identified was $1148 to identify a child with a BLL greater than or equal to 10 ug/dL and $9185 to identify a child with a BLL greater than or equal to 20 ug/dL. Reported by: CD Molina, MD, JM Molina, MD, Molina Medical Centers, Long Beach, California. Lead Poisoning Prevention Br, Div of Environmental Health and Hazard Evaluation, National Center for Environmental Health, CDC. Editorial Note: From 1991 through 1993, the number of California children identified with BLLs of at least 25 ug/dL increased from approximately 40 per year to approximately 500 per year (3). Universal screening also has substantially increased the number of lead-exposed children requiring individual management identified in some populations outside California (4). The burden of lead exposure varies among different U.S. communities and population subgroups. For example, prevalences of elevated BLLs have ranged from 37% among black children who reside in central cities to 5% among non-Hispanic white children who do not live in central cities (1). The prevalences of elevated BLLs in smaller jurisdictions or nonrepresentative clinic-based populations also varies widely, with lead-exposure prevalences ranging from less than 1% (5) to greater than 50% (6). Purposes of this study were to estimate lead-exposure prevalence in the population served by the managed-care organization, assess the performance of a questionnaire in identifying higher risk children, and help assess the usefulness of a universal screening policy in this population. The finding that prevalences of elevated BLLs were low among Medicaid recipients attending clinics at the managed-care organization was unexpected because previous population-based surveys in Compton and Sacramento had documented substantially higher prevalences of lead exposure (7). However, because the likelihood of lead exposure is greater in the summer and this assessment encompassed winter months (8), seasonal patterns may have accounted for some of the difference. The difference also may have reflected variations in the study design between this (clinic-based) and previous (population-based) assessments (9) and previously documented wide variations in prevalences of elevated BLLs among even apparently homogenous groups (10). Because characteristics of children receiving care at the managed-care organization probably differ from those of other groups of children in California, the findings in this report cannot be generalized. In this population, a standard risk questionnaire was of limited use in identifying children at higher risk for lead exposure: the prevalence of elevated BLLs was 3.4% in "high risk" children compared with 1.4% in lower risk children. Although this difference was statistically significant, the clinical utility of this finding is limited as a means for targeting blood lead testing. The usefulness of questionnaires to target BLL screening might be increased by adding locally important risk factors to such questionnaires (10). Questionnaires also may be useful in some settings to target education about potentially remediable risk factors for lead exposure regardless of children's current BLLs. The primary strategy for preventing lead poisoning is to reduce lead sources in the environment before children are exposed. However, because large environmental reservoirs of lead persist, especially in older housing, BLL screening and follow-up of children with elevated BLLs continues to be an important method for controlling lead exposure among children. The role of universal screening in relatively low-prevalence communities and practices has nonetheless been questioned (6). The purpose of screening is to identify children who require individual follow-up and medical or environmental management (i.e., children whose BLLs are persistently at least 15 ug/dL). In populations such as those served by the managed-care organization, in which small numbers of children who require individual management are identified by universal screening, alternative approaches to the prevention of childhood lead poisoning may include a combination of environmental controls, education, and more selective screening. References 1. Brody DJ, Pirkle JL, Kramer RA, et al. Blood lead levels in the U.S. population: phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III, 1988 to 1991). JAMA 1994;272:277-83. 2. CDC. Preventing lead poisoning in young children: a statement by the Centers for Disease Control. Atlanta: US Department of Health and Human Services, Public Health Service, 1991. 3. California Department of Health Services. Childhood lead poisoning in California: an update. In: California Morbidity. Berkeley, California: California Department of Health Services, June 1994:21-2. 4. Schlender TL, Fritz CJ, Murphy A, Shepeard S. Feasibility and effectiveness of screening for childhood lead poisoning in private medical practice. Archives of Pediatrics and Adolescent Medicine 1994;148:761-4. úÿ 5. Robin LF, Beller M, Middaugh JP. Childhood lead screening in Alaska, results of survey of blood lead levels among Medicaid-eligible children. Anchorage, Alaska: Alaska Department of Health Services, October 1994. 6. Wiley JF, Bell LM, Rosenblum LS, Nussbaum J, Tobin R, Henretig FM. Lead poisoning: low rates of screening and high prevalences among children seen in inner-city emergency departments. J Pediatr 1995;126:392-5. 7. CDC. Blood lead levels among children in high-risk areas--California, 1987-1990. MMWR 1992;41:291-4. 8. Baghurst PA, Tong Shi-Lu, McMichael AJ, Robertson EF, Wigg NR, Vimpani GV. Determinants of blood lead concentrations to age 5 years in a birth cohort study of children living in the lead smelting city of Port Pirie and surrounding areas. Archives of Environmental Health 1992;47:203-10. 9. Daniel K, Sedlis MH, Polk L, Dowuona-Hammond S, McCants B, Matte T. Childhood lead poisoning--New York City, 1988. MMWR 1990;39(no. SS-4). 10. Rooney Bl, Hayes EB, Allen BK, Strutt PJ. Development of a screening tool for prediction of children at risk for lead exposure in a midwestern clinical setting. Pediatrics 1994;93:183-7. ------------------------------ To: hicnews Notice to Readers "Immunization Update" Video Conference CDC's National Immunization Program will sponsor a live interactive satellite video conference, "Immunization Update," on September 7, 1995, from noon until 2:30 p.m. (eastern daylight time) to satellite downlink sites in 40 states. The course will provide updated information about varicella, hepatitis A, hepatitis B, and other vaccine-preventable diseases. Continuing Medical Education Credits and Continuing Education Units will be given to participants who complete the course. Physicians, physicians' assistants, nurse practitioners and their colleagues who give vaccinations or set policy for their offices, clinics, and communicable diseases/infection-control programs are invited to participate. Additional information is available through state immunization coordinators at state health departments. ------------------------------ To: hicnews Hypertension Among Mexican Americans -- United States, 1982-1984 and 1988-1991 Since 1960, data have been collected on measured blood pressure for non-Hispanic whites and blacks. However, few data have been available about measured blood pressure for Mexican Americans (1). Until the release of data from the National Health and Nutrition Examination III, Phase I (NHANES III), the only source of blood pressure data for most of the Mexican American population in the United States was the Hispanic Health and Nutrition Examination Survey (HHANES). Data on measured blood pressure for other Hispanic subgoups (i.e., Cuban Americans and Puerto Ricans) were available in HHANES but not in NHANES III. To identify trends in prevalence, awareness, treatment, and control of hypertension among Mexican Americans aged 18-74 years, HHANES (conducted during 1982-1984) and NHANES III (conducted during 1988-1991) were analyzed. This report summarizes the results of that analysis. CDC's HHANES and NHANES III are household interview and examination surveys of the U.S. civilian, noninstitutionalized population (2,3). HHANES sampled Mexican Americans* residing in Arizona, California, Colorado, New Mexico, and Texas; 84% of the total Mexican American population in 1980 resided in these states (2). NHANES III sampled Mexican Americans residing in the United States (3). All interviews were conducted by persons who were bilingual. Hypertension was defined as systolic blood pressure greater than or equal to 140 mm/Hg, and/or diastolic blood pressure greater than or equal to 90 mm/Hg, and/or taking antihypertensive medication (4). Analysis of characteristics of persons with hypertension included awareness status (being told by a health professional of having hypertension), treatment (taking antihypertensive medication), and control (taking antihypertensive medication and/or having blood pressure less than 140/90 mm/Hg). Information about awareness and treatment of hypertension was collected during the household interview. The protocol to measure blood pressure was similar in both surveys and included the use of four cuff sizes, standardized training for examiners, and the performance of quality-control visits during data collection (1). However, HHANES included two blood pressure measures by a physician (2) and NHANES III included three blood pressure measures by a trained interviewer during the home interview, and three blood pressure measures by a physician during the examination (3). To maximize comparability between both surveys, for this report blood pressure was calculated using the average of the two measures taken in HHANES and the first two measures taken by the physician during the examination in NHANES III. The prevalence of hypertension was calculated using a sample of 1552 men and 1952 women from HHANES and 1282 men and 1223 women from NHANES III. Data were weighted to provide estimates for the sampled populations (Mexican Americans residing in the Southwest [HHANES] and in the United States [NHANES III]). Standard errors were calculated using the Software for Survey Data Analysis. Prevalence estimates were age adjusted by the direct method to the 1980 U.S. population. The overall age-adjusted prevalence of hypertension among Mexican Americans was similar during 1982-1984 (21.1%) and 1988-1991 (18.0%) (Table 1). Estimates also were similar for the sex-specific and age-specific prevalence of hypertension (Table 1) and for hypertension awareness, treatment, and control (Table 2). Reported by: Office of Analysis, Epidemiology, and Health Promotion, and Div of Health Examination Statistics, National Center for Health Statistics, CDC. Editorial Note: Although the overall prevalence of hypertension among Mexican Americans was similar during 1982-1984 (HHANES) and 1988-1991 (NHANES III), age- and sex-specific prevalences suggest a slight downward trend (except among men aged 40-49 years)--a finding consistent with an overall decline in the prevalence of hypertension in the United States (1). In contrast, among Mexican Americans with hypertension (particularly women), levels of awareness, treatment, and control of hypertension did not increase as they did among whites and blacks (1). Low socioeconomic status and overweight are documented risk factors for hypertension (5). Despite the high prevalence of low socioeconomic status and overweight among Mexican Americans (5), the age-adjusted prevalence of hypertension among Mexican Americans is similar to the prevalence observed among whites (19.2%) and lower than that among blacks (30.2%) (6). Despite similarities in the age-adjusted prevalences of hypertension among whites and Mexican Americans during 1988-1991, Mexican Americans had lower levels of control of hypertension (21.3%) than whites and blacks (1). One of the national health objectives for the year 2000 is to attain control of hypertension in 50% of Mexican Americans with this condition (objective 15.4b) (7). The findings in this report are subject to at least two limitations. First, HHANES and NHANES used different sampling frames. However, the similarity of the prevalences of hypertension in both surveys supports the robustsness of the estimates despite the sampling variation. Second, the relatively short period between both surveys may have precluded detection of temporal changes in the prevalences of hypertension and hypertension awareness, treatment, and control. Although overall rates for Mexican Americans were similar in both surveys, some subgroups may have higher rates. Subsequent analysis of NHANES III, Phase II will provide information to further characterize trends in hypertension among Mexican Americans. The lack of improvement in awareness, treatment, and control among hypertensive Mexican Americans in combination with a high prevalence of overweight and low educational attainment (5) indicate an increased risk for cardiovascular diseases for persons of Mexican descent as the population ages. This finding underscores the need to improve the awareness and treatment of hypertension among Mexican Americans. References 1. Burt VL, Cutler JA, Higgins M, et al. Trends in the prevalence, awareness, treatment, and control of hypertension in the adult U.S. population: data from the health and examination surveys, 1960 to 1991. Hypertension 1995;26:60-9. 2. NCHS. Plan and operations of the Hispanic Health and Nutrition Examination Survey, 1982-84. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1985; DHHS publication no. (PHS)85-1321. (Vital and health statistics; series 1, no. 32). 3. NCHS. Plan and operation of the Third National Health and Nutrition Examination Survey, 1988-94. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1994; DHHS publication no. (PHS)94-1308. (Vital and health statistics; series 1, no. 32). 4. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). Arch Intern Med 1993;153:154-83. 5. Sorel JE, Ragland DR, Syme SL. Blood pressure in Mexican-Americans, whites and blacks: the Second National Health and Nutrition Examination Survey and the Hispanic Health and Nutrition Examination Survey. Am J Epidemiol 1991;134:370-8. 6. Burt VL, Whelton P, Roccella EJ, et al. Prevalence of hypertension in the U.S. adult population: results from the Third National Health and Nutrition Examination Survey, 1988-91. Hypertension 1995;25:305-13. 7. Public Health Service. Healthy people 2000: national health promotion and disease prevention objectives--midcourse review and 1995 revisions. Washington, DC: US Department of Health and Human Services, Public Health Service (in press). * For both surveys, Mexican Americans self-identified by responding to the question, "Which of those groups [specific groups listed] best represents your national origin or ancestry." ------------------------------ To: hicnews Arboviral Disease -- United States, 1994 Arboviruses are mosquitoborne and tickborne agents that persist in nature in complex cycles involving birds and mammals, including humans. Characteristics of arboviral infection include fever, headache, encephalitis, and sometimes death. In 1994, health departments in 20 states reported 100 presumptive or confirmed human cases of arboviral disease* to CDC. Of these, 76 were California (CAL) serogroup encephalitis; 20, St. Louis encephalitis (SLE); two, western equine encephalomyelitis (WEE); one, eastern equine encephalomyelitis (EEE); and one, Powassan encephalitis (POW). This report summarizes information about arboviral disease in the United States during 1994. Powassan Encephalitis POW was serologically confirmed in a 49-year-old female resident of Massachusetts who had onset of illness May 24. She reported removing an engorged tick from her abdomen approximately 2 weeks before onset of symptoms. She was admitted to the hospital on May 25 with a diagnosis of meningoencephalitis, which progressed during the following 72 hours to encephalitis involving the brain stem and basal ganglia. During hospitalization, the patient was comatose for 3 days and required mechanical ventilation. On June 16, she was discharged to a rehabilitation center and, on July 25, was transferred to a resident health-care facility. On examination in August 1995, she had residual weakness in her right leg requiring a brace. The patient's prolonged convalescence is consistent with that reported for POW encephalitis. California Serogroup Encephalitis During 1994, a total of 76 human CAL serogroup encephalitis cases were reported from 13 states: West Virginia (32 cases), Ohio (14), Wisconsin (seven), Illinois (six), Minnesota (four), Indiana and North Carolina (three each), Alabama (two), and Iowa, Kentucky, Michigan, Rhode Island, and Virginia (one each). Patients ranged in age from 6 months to 26 years (mean: 7 years). A total of 57 cases (75%) occurred among males. Onsets of illness occurred in May (one case), June (one), July (12), August (35), September (22), and October (five). St. Louis Encephalitis During 1994, a total of 20 human cases of SLE were reported from five states. Sixteen cases were reported in Louisiana; most (14) occurred in urban New Orleans (Orleans and Jefferson parishes). Three cases (in 44- and 60-year-old men and a 63-year-old woman) were fatal. Patients ranged in age from 12 to 78 years (mean: 46 years). Of the 16 cases, nine (56%) occurred among males. SLE cases also were reported in residents of Riverside County, California; Charlotte County, Florida; Forrest County, Mississippi; and Harris County, Texas (one each). For the 20 total cases, onsets of illness occurred in July (one case), August (nine), September (nine), and October (one). Western and Eastern Equine Encephalomyelitis During 1994, two human cases of WEE were reported from Goshen County in southeastern Wyoming; the cases occurred in a 40-year-old woman and a 42-year-old man. One human case of EEE in a 67-year-old man was reported from Iberville Parish, Louisiana. Western and Eastern Equine Encephalomyelitis in Animals Surveillance for arboviral disease includes cases in susceptible animals because, during previous outbreaks, animal cases preceded human cases by 2-3 weeks. During 1994, a total of five WEE cases among horses were reported from three states: Idaho (two cases), Wyoming (two), and Texas (one). WEE was isolated from emus in Boulder County, Colorado (one), and Lancaster County, Nebraska (one), and from a symptomatic pigeon in Stanislaus County, California. A total of 133 cases of EEE among horses were reported from 11 states: Florida (54 cases), South Carolina (20), North Carolina (15), Michigan (12), Georgia (nine), Alabama and New Jersey (seven each), Indiana and Louisiana (three each), Ohio (two), and Virginia (one). In addition, EEE virus was isolated from other species in five states. In Michigan, virus was isolated from two pheasant flocks. In Florida, EEE virus was isolated from specimens of viscera from a symptomatic duck and from 1-4-week-old piglets during an epizootic in the Florida panhandle in which 50 of 90 piglets observed had objective central nervous system signs; the number of deaths is unknown. In Georgia, EEE virus was recovered from a litter of 3-week-old boxer puppies; three of five puppies in the litter died. EEE cases in emus were reported from New Jersey (10 cases), Florida (three), Georgia (two), and North Carolina (one). Reported by: State health depts. D Jacoby, MD, Massachusetts General Hospital, Boston. M McGuilf, DVM, Epidemiology Div, J Fontana, MS, B Werner, PhD, Virology Div, Massachusetts Dept of Public Health State Laboratory. L McFarland, DrPH, S Wilson, M Kohn, MD, H Bradford, PhD, Louisiana Dept Health and Hospitals; E Bordes, New Orleans Mosquito Control Board, New Orleans. D Alstad, DVM, National Veterinary Svcs Laboratories, Animal Plant and Health Inspection Svc, US Dept of Agriculture, Ames, Iowa. H Rubin, DVM, Bur of Diagnostic Laboratories, Florida Dept of Agriculture and Consumer Svcs, Kissimmee. S Baldwin, DVM, Veterinary Diagnostic and Investigation Laboratory, Univ of Georgia, Tifton. Epidemiology and Ecology Section, Div of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, CDC. Editorial Note: The findings in this report indicate that CAL serogroup encephalitis remains the most frequently reported arbovirus infection in the United States. Although the number of CAL serogroup encephalitis cases has remained relatively constant since the 1970s and was reported primarily from the Midwest, the number of cases reported from the South has increased. For example, in 1994, Alabama for the first time reported CAL serogroup encephalitis cases, and Kentucky and Virginia--which previously had reported a total of only six cases since 1964--each reported one in 1994. In general, SLE occurs as periodic focal outbreaks followed by years of sporadic cases. In 1994, a small focal outbreak of SLE occurred in urban New Orleans. Evaluation of case-patients by date of illness onset and location suggests that the earliest cases occurred among persons living within or in proximity to urban public housing projects. Subsequent cases followed a pattern of radial spread from the central urban area, although the small number of cases preclude a definitive analysis. An investigation by New Orleans Mosquito Control Board personnel found large populations of immature and adult Culex pipiens quinquefasciatus mosquitoes under housing units. Leaking sewer lines located in the crawl space beneath these housing units provided an extensive and ideal habitat for the SLE virus vector mosquito. The POW case in Massachusetts in 1994 was the first reported from that state. Previously, the most recent POW case in the United States occurred in New York in 1978. POW virus is a tickborne flavivirus most closely related to Russian spring summer and Central European encephalitis viruses. Although understanding of the epidemiology of POW virus in the United States is limited, the virus appears to be widely distributed. In North America, Ixodes cookei has been implicated as the principal tick vector, and virus has been recovered from several rodent and carnivore species, including the red squirrel, woodchucks, striped and spotted skunks, foxes, short- and long-tailed weasels, and the white-footed deer mouse.** Human infections with POW virus occur infrequently, with seroprevalence rates of 0.5%-4.0% in areas where the virus is endemic (1). During 1958-1981, a total of 19 confirmed POW cases among humans were reported in North America, primarily from the northeastern United States and eastern Canada. Since 1981, five additional confirmed cases have been reported from Canada: Quebec (two, one fatal) (H. Artsob, Quebec Laboratory Center for Disease Control, personal communication, 1995); New Brunswick (one) (2); Ontario (one); and Nova Scotia (one) (M. Mahdy, Ontario Ministry of Health Laboratory Services, personal communication, 1995). Based on evaluation of the 24 total POW cases that occurred in North America during 1958-1994, risk for infection may be highest in wooded areas where potential contact with infected rodent or carnivore hosts or tick vectors is greatest. Of the 24 cases, 21 occurred in persons aged less than 20 years. Four of the acute infections were fatal, and two patients died 1 and 3 years after onset as a result of sequelae reported to be directly related to the disease. Health-care providers should consider arboviruses in the differential diagnosis of aseptic meningitis and encephalitis cases during the summer months. Early identification of arboviral cases is important to implement risk-reduction strategies (i.e., use of vector-control practices, repellents, and changes in human activity patterns). Serum (acute and convalescent) and cerebrospinal fluid samples should be obtained for serologic testing, and cases should be promptly reported to state health departments. New rapid úÿ diagnostic techniques, including detection of immunoglobulin M antibody in acute serum or cerebrospinal fluids, have facilitated confirmation of arbovirus infections. References 1. Artsob H. Powassan encephalitis. In: TP Monath, ed. The arboviruses: epidemiology and ecology. Vol IV. Boca Raton, Florida: CRC Press, Inc, 1988:29-49. 2. Fitch W, Artsob H. Powassan encephalitis in New Brunswick. Can Fam Physician 1990;33:1289-90. * At CDC, a confirmed case is defined as febrile illness with mild neurologic symptoms, aseptic meningitis, or encephalitis with onset during a period when arbovirus transmission is likely to occur, plus at least one of the following criteria: 1) fourfold or greater rise in serum antibody titer, 2) viral isolation from tissue, blood, or cerebrospinal fluid; or 3) specific immunoglobulin M (IgM) antibody in cerebrospinal fluid. A presumptive case is defined as compatible illness, plus either a stable elevated antibody titer to an arbovirus ( greater than or equal to 320 by hemagglutination inhibition, greater than or equal to 128 by complement fixation, greater than or equal to 256 by immunofluorescent assay, or greater than or equal to 160 by plaque-reduction neutralization test) or specific IgM antibody in serum by enzyme immunoassay. ** Tamiasciurus hudsonicus, Marmota monax and Mephitis mephitis, Spilogale putorius, Vulpes sp. Urocyon Cinereoargenteus (gray fox), Mustella erminea and Mustella frenata, and Peromyscus maniculatus, respectively. ------------------------------ To: hicnews and NIOSH Alert: Request for Assistance in Preventing Deaths and Injuries of Adolescent Workers CDC's National Institute for Occupational Safety and Health (NIOSH) periodically issues alerts about workplace hazards that have caused death, serious injury, or illness in workers. One such alert, Request for Assistance in Preventing Deaths and Injuries of Adolescent Workers (1), was recently published and is available to the public.* This alert summarizes information about work-related injuries and deaths among adolescents, identifies work that is especially hazardous, and offers recommendations for prevention. This information can help employers, parents, educators, and adolescent workers make informed decisions about safe work and recognize hazards in the workplace. Each year, approximately 70 adolescents die from injuries at work. Hundreds more are hospitalized, and tens of thousands require treatment in hospital emergency departments. For example, 68 adolescents aged less than 18 years died from work-related injuries in 1993 (2), and an estimated 64,000 adolescents had work-related injuries that required treatment in hospital emergency departments in 1992 (3). Compared with adults, adolescents have a higher risk for work-related injury (4) and a similar risk for fatal occupational injury (5). During 1980-1989, the risk for fatal injury among workers aged 16 and 17 years was 5.1 per 100,000 full-time equivalent workers, compared with 6.0 for adult workers--even though adolescents are employed less frequently in especially hazardous jobs. Agricultural businesses and retail trade accounted for the most work-related deaths among adolescents, and many deaths of workers aged less than 16 years occurred in family-owned businesses (1). Types of work associated with large numbers of deaths and serious injuries included the following: working in or around motor vehicles, operating tractors and other heavy equipment, working near electrical hazards, working in retail and service businesses with a risk for robbery-related homicide, working with fall hazards such as ladders and scaffolds, working around cooking appliances, and performing hazardous manual lifting. To reduce the potential for serious injuries and deaths of adolescent workers, NIOSH recommends: 1. Employers should know and comply with child labor laws and should evaluate workplace hazards for adolescent workers. 2. Parents should participate in their children's employment decisions and should discuss the types of work, training, and supervision provided by the employer. 3. Educators should know child labor laws, provide work experience programs with safe and healthful work environments, and incorporate occupational safety and health information in the general curriculum. 4. Adolescents should know their rights and responsibilities as workers and should seek training and information about safe work practices. References 1. NIOSH. Request for assistance in preventing deaths and injuries of adolescent workers. Cincinnati: US Department of Health and Human Services, Public Health Service, CDC, 1995; DHHS publication no. (NIOSH)95-125. 2. Toscano G, Windau J. The changing character of fatal work injuries. Monthly Labor Review 1994;118:17-28. 3. Layne LA, Castillo DN, Stout N, Cutlip P. Adolescent occupational injuries requiring hospital emergency department treatment: a nationally representative sample. Am J Public Health 1994;84:657-60. 4. CDC. Surveillance of occupational injuries treated in hospital emergency departments. MMWR 1983;32 (no. 2SS):31SS-37SS. 5. Castillo DN, Landen DD, Layne LA. Occupational injury deaths of 16- and 17-year-olds in the United States. Am J Public Health 1994;84:646-9. * Single copies of this document are available without charge from the Publications Office, NIOSH, CDC, Mailstop C-13, 4676 Columbia Parkway, Cincinnati, OH 45226-1998; telephone (800) 356-4674 ([513] 533-8328 for persons outside the United States); fax (513) 533-8573. ------------------------------ To: hicnews Update: Influenza Activity -- Worldwide, 1995 From October 1994 through August 1995, influenza activity occurred at low to moderate levels in most parts of the world. Influenza activity usually was associated with the cocirculation of influenza types A and B viruses. Overall, influenza A(H3N2) was the predominant influenza A subtype, but isolation of influenza A(H1N1) viruses increased during this period and was the most frequently isolated influenza virus in Australia from March through August. This report summarizes influenza activity worldwide from March through August 1995. Africa. In Madagascar, circulation of influenza A(H3N2) began during January and continued through April; during April, influenza A(H1N1) was isolated in Madagascar. In South Africa, influenza A(H1N1) and influenza A(H3N2) viruses were isolated from samples collected for respiratory virus isolation during May-July. Influenza B viruses also were detected in South Africa during July. Influenza A(H3N2) was isolated in Zambia during June. Asia. Influenza A(H1N1), A(H3N2), and influenza B viruses were isolated during every month from March through June in Asia. Influenza A(H1N1) viruses were isolated in Guam during May, in Hong Kong during March and April, and in Thailand during April, May, and July. Influenza A(H1N1) and influenza B viruses were isolated during outbreak-level activity in Taiwan during April-June. Other countries reporting influenza B activity associated with sporadic cases or outbreaks included China, Hong Kong, Japan, Korea, Singapore, and Thailand. Influenza A(H3N2) viruses were isolated in China in association with sporadic and outbreak activity during April and from sporadic cases during June. Influenza A(H3N2) viruses also were isolated in Korea and Thailand during March, in Guam during March and May, in Hong Kong during March and July, and in Japan during April. Singapore reported influenza A activity every month from March through June; influenza A (H3N2) isolates were subtyped during March, May, and June. Additional influenza A viruses, subtype unknown, were identified by antigen-detection methods in Malaysia during March. Europe. Activity in Europe began with an outbreak of influenza B virus in Portugal during October 1994 and continued from March through June. Influenza A(H3N2), A(H1N1), and influenza B viruses were isolated during this period. Outbreak activity was last reported from Romania and Bulgaria during May. Circulation of influenza A(H1N1) viruses increased from March through May and was associated with an outbreak in members of a military unit in Bulgaria. Detection of both influenza A and influenza B viruses continued in France during June. North America. Influenza A(H3N2) viruses predominated during the 1994-95 season, but influenza B and A(H1N1) viruses also were isolated. Following peak activity during February through early March in the United States, influenza A(H3N2), A(H1N1), and influenza B viruses continued to be isolated every month during March-June. Influenza A(H1N1) was isolated from one patient in Arizona during July. The number of influenza A(H1N1) isolates increased during February-May; most were collected during May. Late-season influenza activity also occurred in Canada. The most recent detection of influenza B virus was reported during the week ending June 3, and reports of influenza A virus isolation or detection continued during July and August. As in the United States, influenza A(H1N1) viruses were reported in Canada during the latter part of the influenza season. Central and South America. Influenza A and influenza B viruses were detected during the 1994-95 influenza season in South America with influenza A predominating. Brazil reported detection of influenza A from February through April. In Chile, outbreaks of influenza were detected during May-July; influenza A predominated, but influenza B also was detected. In Argentina, the first case of influenza A was diagnosed in late May and outbreaks were reported during June and July; influenza A predominated, but influenza B also was detected. Reports of influenza-like illness increased in Uruguay during May-July, and influenza A virus was identified by antigen-detection methods. Influenza A virus was detected in one patient in Panama during June, followed by a single detection of influenza B virus during July. All influenza A viruses from Argentina, Brazil, and Chile subtyped or further identified by serologic testing were influenza A(H3N2). No influenza A(H1N1) isolates were reported from Central or South America. Oceania. The influenza season began early in Australia with outbreaks in the Northern Territory at the end of March. Both influenza A(H1N1) and influenza B viruses were isolated during the outbreak, with influenza A(H1N1) viruses predominating. Influenza-like illness, as reported by general practitioners, increased through the beginning of July and remained stable during mid-July through the beginning of August. As the season progressed, the number of influenza B isolates increased; however, influenza A(H1N1) viruses remained more prevalent. Influenza A(H3N2) viruses were rarely isolated. In contrast, influenza B predominated in New Zealand through July, but the proportion of influenza A(H3N2) viruses isolated increased during July. Both influenza A(H3N2) and influenza B viruses were associated with outbreaks at the end of July. Characterization of influenza virus isolates. From October 1, 1994, through August 15, 1995, a total of 760 influenza isolates collected worldwide were antigenically characterized by the World Health Organization Collaborating Center for Surveillance, Epidemiology, and Control of Influenza at CDC. Of these, 535 (70%) were from North America, 76 (10%) from Europe, 130 (17%) from Asia, and 19 (3%) from South America and Oceania. Of the viruses subtyped, 396 (52%) were influenza A(H3N2), 91 (12%) A(H1N1), and 273 (36%) influenza B. Of the 396 influenza A(H3N2) isolates characterized, 227 (57%) were antigenically related to A/Shangdong/09/93, the 1994-95 vaccine strain, and 164 (41%) were more closely related to A/Johannesburg/33/94, the A(H3N2) component of the 1995-96 influenza vaccine. Of the 273 influenza B viruses, 66 (24%) were similar to B/Panama/45/90, the 1994-95 vaccine component, and 202 (74%) were similar to B/Beijing/184/93, the 1995-96 vaccine component. Of the 91 influenza A(H1N1) viruses, 12 (13%) were A/Texas/36/91-like, and 79 (87%) were more closely related to the antigenically similar A/Taiwan/01/86-like viruses (1,2). The influenza A(H1N1) component of the 1995-96 vaccine is A/Texas/36/91. Reported by: World Health Organization National Influenza Centers, Communicable Disease Div, World Health Organization, Geneva. World Health Organization Collaborating Center for Surveillance, Epidemiology, and Control of Influenza. Influenza Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC. Editorial Note: Based on recent patterns of worldwide influenza activity, the 1995-96 influenza season in the United States may be characterized by cocirculation of influenza type A(H3N2), type A(H1N1) and type B. However, because specific patterns of influenza activity cannot be predicted with certainty, the extent of virus circulation and the relative prevalence of the different influenza virus strains is unknown. Therefore, influenza vaccination should be offered each fall to persons at high risk for influenza-related complications and their close contacts and to health-care providers. The influenza vaccine is updated annually to include viruses that are antigenically similar to the strains of the three distinct groups of influenza viruses that have been in worldwide circulation. Most of the influenza viruses isolated since March 1995 are antigenically similar to the 1995-96 influenza vaccine strains (CDC, unpublished data, 1995). Vaccination against influenza is recommended by the Advisory Committee on Immunization Practices for 1) persons aged greater than or equal to 65 years; 2) persons who reside in nursing homes or chronic-care facilities; 3) persons with chronic cardiovascular or pulmonary disorders, including children with asthma; 4) persons who required medical follow-up or hospitalization during the previous year because of diabetes and other chronic metabolic diseases, renal dysfunction, hemoglobinopathies, or immunosuppression; and 5) children and adolescents who are receiving long-term aspirin therapy and who therefore may be at risk for developing Reye syndrome after influenza. Vaccination also is recommended for health-care workers and other persons who are in close contact with persons in high-risk groups, including household members. Women who will be in the third trimester of pregnancy during the influenza season may be at increased risk for medical complications following influenza infection and should consult with their health-care providers about receiving the vaccine. Influenza vaccine also can be administered to anyone who wants to reduce the likelihood of acquiring influenza. Beginning in September, persons at high risk who are seen by health-care providers for routine care or as a result of hospitalization should be offered influenza vaccine. The optimal time for organized vaccination campaigns is mid-October through mid-November. Health-care providers should continue to offer vaccine to high-risk persons up to and even after influenza activity is documented in a community. Information about influenza surveillance is available through the CDC Voice Information System (influenza update) by telephone ([404] 332-4555) or fax ([404] 332-4565) (document number 361100) or through the CDC Information Service on the Public Health Network electronic bulletin board. From October through May, the information is updated weekly. Periodic updates about influenza are published in MMWR, and information on local influenza activity is available through county and state health departments. References 1. CDC. Update: influenza activity--United States and worldwide, 1993-94 season, and composition of the 1994-95 vaccine. MMWR 1994;44:179-83. 2. CDC. Update: influenza activity--United States and worldwide, 1994-95 season, and composition of the 1995-96 vaccine. MMWR 1995;44:292-5. ------------------------------ End of HICNet Medical News Digest V08 Issue #32 *********************************************** --- Editor, HICNet Medical Newsletter Internet: david@stat.com FAX: +1 (602) 451-6135