The following are pre-publication drafts of articles from the Morbidity and Mortality Weekly Report dated September 1, 1995. Late-breaking articles, and final editorial revisions are not included; therefore, these articles should be considered preliminary, and not to be released to the public. --CDC -------------------------------------------------------------- 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). 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. 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. 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." 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.