Following is the final electronic text from the Morbidity and Mortality
Weekly Report (MMWR), vol. 44, no. 7, dated February 24, 1995.  The MMWR
is published by the U.S. Department of Health and Human Services, Public
Health Service, Centers for Disease Control and Prevention (CDC), Atlanta,
Georgia.
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CONTENTS OF THIS ISSUE:
Pages/Title
    121-124
        Serogroup B Meningococcal Disease -- Oregon, 1994
    124-125, 131-132
        Trends in Sexual Risk Behavior Among High School Students --
        United States, 1990, 1991, and 1993
    132-134
        Update: Influenza Activity -- New York and United States,
        1994-95 Season
    135
        Notice to Readers
        -- Availability of Draft Recommendations
           for HIV Counseling and Testing
        Erratum: Vol. 44, No. 5
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Serogroup B Meningococcal Disease -- Oregon, 1994

     In Oregon, the incidence of meningococcal disease has increased
substantially, more than doubling from 2.2 cases per 100,000 persons in
1992 to 4.6 per 100,000 in 1994--the highest incidence in Oregon since
1943. This incidence was almost fivefold higher than recent estimates for
the United States during 1989-1991 (approximately one case per 100,000
persons annually) (1). This report describes meningococcal disease
surveillance data from 1994 and summarizes epidemiologic and laboratory
data on serogroup B meningococcal disease in Oregon during 1987-1994.
     During 1994, a total of 143 cases of meningococcal disease was
reported to the State Health Division. In 124 cases, Neisseria meningitidis
was isolated from a normally sterile site (confirmed cases); in four cases,
gram-negative diplococci were detected in specimens obtained from a
normally sterile site or in persons who had classic symptoms after contact
with a confirmed case (presumed cases). Characteristic symptoms (including
petechial rash and hypotension) occurred in 14 cases; however, these cases
were not culture confirmed (suspected cases). Of 115 isolates for which
serogroup was known, 70 (61%) were serogroup B, 40 (35%) were serogroup C,
four were serogroup Y, and one was serogroup W-135. When compared with 1992
and 1993, the serogroup-specific incidence in 1994 was higher for both
serogroups B and C.
     Of the 70 culture-confirmed cases of serogroup B infection, 34 (49%)
occurred in females. Seven (10%) cases were fatal; of these, one occurred
in a child aged 2 years, and four deaths occurred in persons aged 55-88
years.
     During 1987-1992, 63% (84 of 133) of cases of serogroup B occurred in
children aged less than 5 years; in comparison, in 1994, 27% (19 of 70)
occurred in this age group. When compared with 1987-1992, the incidence of
reported serogroup B disease in 1994 increased modestly among those aged
less than 5 years (from 6.9 to 8.4), approximately 14-fold among those aged
15-19 years (from 0.4 to 5.4), and approximately fourfold among those aged
greater than or equal to 60 years (from 0.3 to 1.1) (Figure 1).
     In 1994, serogroup B cases occurred in 17 of the 36 counties in
Oregon; these counties account for 83% of the total population of Oregon.
The risk for disease was highest in counties in the Willamette Valley in
the northwestern part of the state. Based on investigation of serogroup B
cases, six (9%) were linked to other cases. Two co-primary cases (disease
in a close contact within 24 hours of disease onset in a primary case) were
linked to a single primary case. Four secondary cases (disease in a close
contact greater than 24 hours after disease onset in a primary case) were
identified; at least two occurred in patients for whom appropriate
chemoprophylaxis had been prescribed but who were noncompliant with
therapy.
     Of the 114 N. meningitidis serogroup B strains isolated in Oregon
during 1993-1994, a total of 64 (56%) has been characterized at CDC by
multilocus enzyme electrophoresis. Of these, 55 (86%) belong to the enzyme
type-5 (ET-5) complex, a group of genetically related serogroup B
meningococcal strains associated with epidemic meningococcal disease in
other countries (2). Twelve of these isolates also have been serotyped,
serosubtyped, and immunotyped; all are serotype 4 or 15, serosubtype
P1.7,16, and immunotype L3,7,9,8,10.

Reported by: K Hedberg, MD, F Hoesly, MD, D Fleming, MD, State
Epidemiologist, State Health Div, Oregon Dept of Human Resources. K
Steingart, MD, Southwest Washington Health District; M Goldoft, MD, P
Stehr-Green, DrPH, State Epidemiologist, Washington Dept of Health. Div of
Field Epidemiology, Epidemiology Program Office; Childhood and Respiratory
Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for
Infectious Diseases, CDC.

Editorial Note: The recent increased occurrence of serogroup B
meningococcal disease in Oregon has been associated with a group of closely
related strains belonging to the ET-5 clonal complex. These strains were
first identified as the cause of a serogroup B meningococcal epidemic in
Norway that began in 1974 and persisted through 1991 (3). After its
identification in 1974, serogroup B meningococci belonging to the ET-5
complex subsequently caused epidemics in Europe, Cuba, and South America
(2). Endemic meningococcal disease typically is caused by a heterogeneous
mix of strains. In comparison, the predominance of closely related strains,
or clones, in Oregon is characteristic of epidemic disease, as is the
disproportionate increase in age-specific incidence among young adults. The
latter pattern has been suggested as a reliable predictor of the transition
from endemic to epidemic meningococcal disease (4,5).
     Although serogroup C meningococcal outbreaks have occurred with
increasing frequency nationwide since 1991 (6), Oregon is the only state
to report substantially increased rates of serogroup B meningococcal
disease. While Washington state had only a slight increase in the overall
rate of meningococcal disease in 1994, rates of serogroup B meningococcal
disease in Clark County, Washington (1994 population: 280,800) (across the
Columbia River from metropolitan Portland, Oregon), have increased almost
fivefold (from 1.5 per 100,000 in 1987 to 7.1 per 100,000 in 1994). These
increasing rates underscore the need for determining the serogroup of all
isolates to assist in assessing trends in the occurrence of meningococcal
disease and serogroup distribution of invasive N. meningitidis in other
states.
     The primary means for the control and prevention of serogroup B
meningococcal disease is chemoprophylaxis of close contacts. The
meningococcal vaccine licensed in the United States provides protection
against serogroups A, C, Y, and W-135 but does not provide protection
against serogroup B meningococcal disease. Meningococcal capsular
polysaccharides determine serogroup and are used in purified form to
produce the A/C/Y/W-135 vaccine. Unlike the other major meningococcal
serogroups, however, serogroup B capsular polysaccharide is poorly
immunogenic in humans. Alternate approaches to the development of a
serogroup B meningococcal vaccine have focused on use of outer-membrane
proteins from specific epidemic serogroup B meningococcal strains.
     Three outer-membrane protein-based serogroup B meningococcal vaccines
employing two-dose regimens have been effective among older children and
young adults in large clinical trials outside the United States (7-9);
estimated efficacies ranged from 57% to 83%. The only vaccine available
commercially is not licensed for use in the United States but has been used
in some South American countries to control serogroup B meningococcal
epidemics. In Sao Paulo, Brazil, approximately 2.4 million children aged
3 months to 6 years were vaccinated during 1989 and 1990, and the vaccine
was estimated to be 74% effective in children aged 4-6 years (10). Efforts
to initiate studies in the United States to evaluate available vaccines
under an investigational new drug application are in progress.
     Oregon and three other states (California, Connecticut, and Minnesota)
are participating in a cooperative agreement with CDC to study emerging
infectious diseases. One focus of this program in Oregon is disease caused
by N. meningitidis serogroup B; a study of potentially modifiable risk
factors for meningococcal disease is under way.

References
1. Jackson LA, Wenger JD, Meningococcal Disease Study Group.
Laboratory-based surveillance for meningococcal disease in selected areas,
United States--1989-1991. In: CDC surveillance summaries (June). MMWR
1993;42(no. SS-2):21-30.
2. Caugant DA, Froholm LO, Bovre K, et al. Intercontinental spread of a
genetically distinctive complex of clones of Neisseria meningitidis causing
epidemic disease. Proc Natl Acad Sci U S A 1986;83:4927-31.
3. Lystad A, Aasen S. The epidemiology of meningococcal disease in Norway,
1975-91. NIPH Ann 1991;14:57-66.
4. Peltola H, Kataja JM, Makela PH. Shift in the age-distribution of
meningococcal disease as predictor of an epidemic? Lancet 1982;2:595-7.
5. Jones DM, Mallard RH. Age incidence of meningococcal infection England
and Wales, 1984-1991. J Infect 1993;27:83-8.
6. Jackson LA, Schuchat A, Reeves MW, Wenger JD. Serogroup C meningococcal
outbreaks in the United States: an emerging threat. JAMA 1995;273:383-94.
7. Sierra GVG, Campa HC, Varcacel NM, et al. Vaccine against group B
Neisseria meningitidis: protection trial and mass vaccination results in
Cuba. NIPH Ann 1991;14:195-207.
8. Bjune G, Hoiby EA, Gronnesby JK, et al. Effect of outer membrane vesicle
vaccine against group B meningococcal disease in Norway. Lancet
1991;338:1093-6.
9. Boslego JB, Garcia J, Cruz C, et al. Efficacy, safety, and
immunogenicity of a meningococcal group B (15:P1.3) outer membrane protein
vaccine in Iquique, Chile. Vaccine 1995 (in press).
10. de Moraes JC, Perkins BA, Camargo MCC, et al. Protective efficacy of
a serogroup B meningococcal vaccine in Sao Paulo, Brazil. Lancet
1992;340:1074-8.


Trends in Sexual Risk Behavior Among High School Students --
United States, 1990, 1991, and 1993

     Since the early 1980s, adolescents in the United States have
experienced high rates of unintended pregnancies (1) and sexually
transmitted diseases (STDs) (2), including HIV infection (3). Since 1990,
CDC's Youth Risk Behavior Surveillance System has enabled measurement of
priority health-risk behaviors among high school students at the national,
state, and local levels (4). This report examines data from the 1990, 1991,
and 1993 national Youth Risk Behavior Survey (YRBS)* to describe trends in
selected self-reported sexual risk behaviors among U.S. high school
students.
     The YRBS employed a cross-sectional, three-stage, cluster sample of
students in grades 9-12 in public and private schools in all 50 states and
the District of Columbia. For 1990, 1991, and 1993, sample sizes were
11,631, 12,272, and 16,296, respectively, and the overall response rates
were 64%, 68%, and 70%, respectively. To enable separate analysis of black
and Hispanic students, schools with high proportions of these students were
oversampled; numbers of students in other racial groups were too small for
meaningful analysis. A weighting factor was applied to each student record
to adjust for nonresponse and oversampling. Trends were assessed only for
sexual risk behaviors measured by questions identically worded in each
survey year. To determine temporal differences, 95% confidence intervals
were calculated for each estimate by using SUDAAN (5).
     From 1990 to 1993, the percentages of high school students remained
constant for those who reported ever having had sexual intercourse (i.e.,
sexually experienced), ever having had sexual intercourse with four or more
partners, having had sexual intercourse during the 3 months preceding the
survey (i.e., sexually active), having used alcohol or drugs before last
sexual intercourse, and having used birth control pills at last sexual
intercourse (Table 1). In contrast, the percentage of those who reported
condom use at last sexual intercourse increased significantly, from 46.2%
in 1991 to 52.8% in 1993 (Table 1); however, subgroup analyses indicated
a significant increase in condom use only among females (from 38.0% to
46.0%) and blacks (from 48.0% to 56.5%) (Table 2).

Reported by: Div of Adolescent and School Health, National Center for
Chronic Disease Prevention and Health Promotion, CDC.

Editorial Note: During the 1980s, the proportion of adolescents who
reported being sexually experienced increased substantially in the United
States (6). The findings in this report indicate that, from 1990 through
1993, the proportion of high school students who reported being sexually
experienced remained stable, while an increasing percentage of sexually
active students used condoms, thereby reducing their risk for unintended
pregnancy and STDs, including HIV infection.
     The sex, grade, and race/ethnicity findings in this report may assist
in identifying groups with higher prevalences of sexual risk behaviors.
However, the underlying causes (e.g., education levels, economic factors,
or cultural influences) for within-subgroup differences could not be
addressed in this study.
     In 1991 and 1992, two health outcomes associated with sexual risk
behaviors--live births and gonorrhea--also declined. Live-birth rates among
15-19-year-olds decreased in 40 states and the District of Columbia,
increased in eight states, and were stable in two states. In addition,
rates of gonorrhea decreased among 15-19-year-old males in 45 states and
the District of Columbia and among 15-19-year-old females in 41 states and
the District of Columbia. Of the 41 areas reporting declines in live-birth
rates, 34 also reported declines in gonorrhea rates for both males and
females; six other states reported declines for either males or females.
Overall, live-birth rates for adolescents decreased significantly (2%) (7),
and gonorrhea rates decreased significantly among both adolescent males and
adolescent females (20% and 13%, respectively) (8).
     The plateau in the proportion of high school students who reported
being sexually experienced, the increasing rates of condom use among high
school students, and the decreasing rates of live births and gonorrhea
among adolescents may reflect, in part, efforts to reduce risks for HIV
infection and other STDs among adolescents. For example, since 1986, CDC
has collaborated with local, state, and national health and education
agencies, national and community-based organizations, and the media to
increase development, implementation, and awareness of HIV-prevention
education programs for youth.
     Despite the decreases in live-birth rates and gonorrhea rates and the
increases in condom use, the findings in this report document that many
adolescents continue to be at risk for HIV infection, other STDs, and
unintended pregnancy because they engage in unprotected sexual intercourse.
Efforts to assist all adolescents in delaying first sexual intercourse and
increasing condom use among those who do engage in sexual intercourse must
be emphasized by health, education, and social service agencies and
providers.
     The data presented in this report and other data describing changes
in rates of pregnancy, abortion, live birth, and gonorrhea among
adolescents during the 1980s and 1990s have been summarized by state and
for the nation in a new CDC monograph**, Adolescent Health: State of the
Nation--Pregnancy, Sexually Transmitted Diseases, and Related Risk
Behaviors Among U.S. Adolescents (8).

References
1. Ventura SJ, Taffel SM, Mosher WD, Henshaw S. Trends in pregnancies and
pregnancy rates, United States, 1980-88. Hyattsville, Maryland: US
Department of Health and Human Services, Public Health Service, CDC, 1992.
(Monthly vital statistics report; vol 41, no. 6, suppl).
2. Wasserheit J. Effect of changes in human ecology and behavior on
patterns of sexually transmitted diseases, including human immunodeficiency
virus infection. Proc Natl Acad Sci U S A 1994;91:2430-5.
3. Lindegren ML, Hanson C, Miller K, Byers RH Jr, Onorato I. Epidemiology
of human immunodeficiency virus infection in adolescents, United States.
Pediatr Infect Dis J 1994;13:525-35.
4. Kolbe LJ, Kann L, Collins JL. Overview of the Youth Risk Behavior
Surveillance System. Public Health Rep 1993;108(suppl 1):2-10.
5. Shah BV, Barnwell BG, Hunt PN, LaVange LM. SUDAAN user's manual, release
5.50. Research Triangle Park, North Carolina: Research Triangle Institute,
1991.
6. CDC. Premarital sexual experience among adolescent women--United States,
1970-1988. MMWR 1991;39:929-32.
7. NCHS. Advance report of final natality statistics, 1992. Hyattsville,
Maryland: US Department of Health and Human Services, Public Health
Service, CDC, 1994. (Monthly vital statistics report; vol 43, no. 5,
suppl).
8. CDC. Adolescent health: state of the nation--pregnancy, sexually
transmitted diseases, and related risk behaviors among U.S. adolescents.
Atlanta: US Department of Health and Human Services, Public Health Service,
1995; DHHS publication no. (CDC)099-4630.

* The YRBS was not conducted in 1992.
** Single copies of this document are available from CDC's Division of
Adolescent and School Health, National Center for Chronic Disease
Prevention and Health Promotion, Mailstop K-33, 4770 Buford Highway, NE,
Atlanta, GA 30341-3724; telephone (404) 488-5330.


Update: Influenza Activity --
New York and United States, 1994-95 Season

     Influenza activity in the United States during the current influenza
season began in the Northeast, and during late January, spread to other
regions of the country. This report describes influenza outbreaks in
nursing homes in New York and summarizes national influenza surveillance
data from October 2, 1994, through February 11, 1995.

New York
     The first influenza outbreak reported to CDC during the 1994-95 season
occurred in a 300-bed skilled-nursing facility in Long Island, New York.
On November 30, 1994, eight residents on one 20-bed corridor developed
influenza-like illness (ILI) (i.e., fever greater than or equal to 100 F
[greater than or equal to 38 C] and cough). On December 1, nasopharyngeal
swab specimens from these eight residents were submitted for rapid antigen
testing; within 5 hours after transport to the laboratory, influenza type
A was detected by enzyme immunoassay in six specimens. On the evening of
December 1, 293 of the 299 residents in the facility each received 100 mg
of amantadine hydrochloride as treatment for the eight ill residents and
as prophylaxis against influenza A infection for the other 285 residents.
Most (285 [95%]) residents had received influenza vaccine before the
outbreak. On December 2, as part of the nursing home's contingency plan for
influenza outbreaks, amantadine dosages were modified for individual
residents based on estimated creatinine clearance (1,2), and prophylaxis
was continued for 14 days. Other outbreak-control measures included
confining ill residents to their rooms for at least 72 hours after the
initiation of amantadine treatment and prophylaxis, confining all residents
to their individual units, suspending group activities, and minimizing the
assignment of nursing staff to multiple units. The amantadine dosage
subsequently was discontinued for five residents and reduced for 13
residents because of side effects (primarily confusion and agitation); for
most patients, side effects resolved within 48 hours of dosage adjustment.
     During the first 48 hours of amantadine prophylaxis and treatment, six
additional residents developed ILI. Of the 14 residents who developed
outbreak-associated ILI, five subsequently developed clinical pneumonia.
During the 2-week period of amantadine prophylaxis, sporadic cases of
febrile respiratory illness occurred in other units of the facility;
however, there was no clustering of cases.
     Tissue culture of all eight nasopharyngeal specimens yielded influenza
type A(H3N2). These isolates were further characterized at CDC; all were
antigenically similar to the A/Shangdong/09/93 strain included in the 1994-
95 influenza vaccine.
     Influenza surveillance in New York state indicated increasing activity
beginning in late November 1994. From December 1, 1994, through February
11, 1995, outbreaks associated with influenza type A(H3N2) in 46 other
nursing homes were reported to the New York State Department of Health
(NYSDOH); of these, 16 were reported from nursing homes in Long Island. For
all 16 facilities, influenza type A infection was documented by rapid
antigen detection; in 13 facilities, amantadine was administered as an
outbreak-control measure. Outbreaks in five other nursing homes were caused
by influenza type B and, in two nursing homes, by influenza types A and B.
Based on findings of virologic surveillance in New York, influenza has
occurred in persons in all age groups during the 1994-95 season. Of the 385
influenza virus isolates reported by laboratories in New York this season,
332 (86%) have been type A.

United States
     From November 27, 1994, through January 21, 1995, most influenza
activity was reported from the Northeast (3). However, during January 22-
February 11, regional or widespread activity was reported from states in
every region.
     Through February 11, World Health Organization collaborating
laboratories reported 1282 influenza virus isolates; of these, 923 (72%)
isolates have been type A and 359 (28%) have been type B. Of the influenza
A isolates that have been subtyped, all have been type A(H3N2).
     The proportion of deaths attributable to pneumonia and influenza
reported from 121 U.S. cities slightly exceeded the epidemic threshold
during six of the 19 weeks from October 2, 1994, through February 11, 1995,
but has not exceeded the threshold for any 2 consecutive weeks.

Reported by: IH Gomolin, MD, Gurwin Jewish Geriatric Center, Commack, New
York; HB Leib, MS, RJ Gallo, S Kondracki, G Brady, G Birkhead, MD, DL
Morse, MD, State Epidemiologist, New York State Dept of Health.
Participating state and territorial epidemiologists and state public health
laboratory directors. World Health Organization collaborating laboratories.
Sentinel Physicians Influenza Surveillance System of the American Academy
of Family Physicians. WHO Collaborating Center for Surveillance,
Epidemiology, and Control of Influenza, Div of Viral and Rickettsial
Diseases, National Center for Infectious Diseases, CDC.

Editorial Note: Influenza vaccination is 70%-90% effective in preventing
ILI in young, healthy adults when the vaccine antigens closely match the
circulating influenza virus strains. Because of the decreased immunologic
response among the elderly, the vaccine is less effective in preventing the
occurrence of ILI in nursing home residents (i.e., 30%-40% effective) (4).
However, vaccination of nursing home residents is associated with a
substantial (i.e., 50%-60% effectiveness) reduction in the occurrence of
serious complications and hospitalization and with preventing death (up to
80% effective); in addition, vaccination reduces the risk for outbreaks in
nursing home settings (4,5). Antiviral agents are recommended as an adjunct
to vaccination in controlling influenza type A. To control influenza A
outbreaks in the nursing home setting, antiviral drugs should be
administered to all residents, regardless of influenza vaccination status.
     Influenza outbreak-control measures used in the New York nursing home
(e.g., rapid influenza A antigen detection and prompt initiation of
antiviral treatment and prophylaxis to all residents) were based on
recommendations of the Advisory Committee on Immunization Practices (ACIP)
(3,6) and CDC and are actively promoted by NYSDOH. Although annual
influenza vaccination of nursing home residents is considered a standard
of care, use of antiviral agents as an adjunct to vaccination is less
common, reflecting, in part, concern about side effects and, until
recently, the protracted time required for laboratory confirmation of
influenza type A.
     The use of amantadine as an adjunct for the control of influenza type
A outbreaks in New York during the current season illustrates the
usefulness of education about and promotion of the use of antiviral agents
and rapid influenza diagnostic methods. In September 1994, NYSDOH mailed
information to all health-care facilities in New York urging health-care
providers to administer vaccine in accordance with the recommendations of
the ACIP, to use rapid antigen-detection testing and viral culture when
institutional outbreaks of ILI are initially recognized, and to use
amantadine when appropriate. On December 20, the NYSDOH sent an electronic
mail message to these institutions to report the rapid identification of
influenza type A in the first nursing home outbreak and to reinforce the
recommendations for influenza control measures in health-care facilities.
     Recommendations of the ACIP for use of amantadine and rimantadine, the
two antiviral drugs currently available for treatment and prophylaxis of
influenza type A, were published in MMWR on December 30, 1994 (4). These
recommendations also provide information for assisting health-care
providers in selecting the appropriate drug for specific patient groups but
do not recommend preferential use of either drug.
     As influenza activity continues to increase in the United States,
health-care providers should be informed about findings of local, state,
and national influenza surveillance and be familiar with methods for rapid
viral diagnosis. Updated information about national influenza surveillance
is available through the CDC Information System by voice or fax (404)
332-4551. In addition, providers should develop contingency plans to
control influenza outbreaks that include the use of rapid diagnosis. When
possible, policy decisions regarding use of amantadine and rimantadine
should be made before outbreaks occur.

References
1. Gomolin IH, Leib HB, Arden NH, Sherman FT. Control of influenza
outbreaks in the nursing home: guidelines for diagnosis and management. J
Am Geriatr Soc 1995;43:71-4.
2. ACIP. Prevention and control of influenza: part II, antiviral agents--
recommendations of the Advisory Committee on Immunization Practices (ACIP).
MMWR 1994;43(no. RR-15).
3. CDC. Update: influenza activity--United States, 1994-95 season. MMWR
1995;44:84-6.
4. Arden NH, Patriarca PA, Kendal AP. Experiences in the use and efficacy
of inactivated influenza vaccine in nursing homes. In: Kendal AP, Patriarca
PA, eds. Options for the control of influenza. New York: Alan R. Liss,
1986:155-68.
5. Patriarca PA, Weber JA, Parker RA, et al. Efficacy of influenza vaccine
in nursing homes: reduction in illness and complications during an
influenza A(H3N2) epidemic. JAMA 1985;253: 1136-9.
6. ACIP. Prevention and control of influenza: part I, vaccines--
recommendations of the Advisory Committee on Immunization Practices (ACIP).
MMWR 1994;43(no. RR-9).


Notice to Readers
Availability of Draft Recommendations
for HIV Counseling and Testing for Pregnant Women

     CDC is requesting public review and comment on the draft document U.S.
Public Health Service Recommendations for HIV Counseling and Testing for
Pregnant Women. This document is available from the CDC National AIDS
Clearinghouse, P.O. Box 6003, Rockville, MD 20849-6003; telephone (800)
458-5231 or (301) 217-0023. Written comments must be received by April 10,
1995, and should be mailed to CDC's Technical Information Activity,
Division of HIV/AIDS, Mailstop E-49, 1600 Clifton Road, NE, Atlanta, GA
30333; fax (404) 639-2007.


Erratum: Vol. 44, No. 5
     In the article "Update: AIDS Among Women--United States, 1994," on
page 81, the sentence beginning on the fourth line was incorrect. The
sentence should read, "Women with AIDS reported in 1994 represented 24% of
the cumulative total of 58,428 cases among women."
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                              * * *
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Inquiries about the MMWR Series, including material to be considered for
publication, should be directed to: Editor, MMWR Series, Mailstop C-08,
Centers for Disease Control and Prevention, Atlanta, GA 30333; telephone
(404) 332-4555.

All material in the MMWR Series is in the public domain and may be used and
reprinted without special permission; citation as to source, however, is
appreciated.
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Director, Centers for Disease Control and Prevention
     David Satcher, M.D., Ph.D.
Deputy Director, Centers for Disease Control and Prevention
     Claire V. Broome, M.D.
Director, Epidemiology Program Office
     Stephen B. Thacker, M.D., M.Sc.
Editor, MMWR Series
     Richard A. Goodman, M.D., M.P.H.
Managing Editor, MMWR (weekly)
     Karen L. Foster, M.A.
Writers-Editors, MMWR (weekly)
     David C. Johnson         Darlene D. Rumph-Person
     Patricia A. McGee        Caran R. Wilbanks
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

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