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
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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.