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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

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----------------------------------------------------------------------

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.


                                                                                                                

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.



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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."



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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


                                                                    

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.


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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.


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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.



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End of HICNet Medical News Digest V08 Issue #32
***********************************************


---
Editor, HICNet Medical Newsletter
Internet: david@stat.com                 FAX: +1 (602) 451-6135

                                       
