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The following are pre-publication drafts of articles from the
Morbidity and Mortality Weekly Report 44(05) dated Friday, February
10, 1995 .  Late- breaking articles, and final editorial revisions are
not included. Therefore, these articles should not be quoted without
consulting the official printed copy that is released to the public,
as received from the CDC.  Also, please refer to the printed copy for
any charts or graphically represented data.

       Table of Contents
       -----------------

       Update: AIDS Among Women -- United States, 1994
       Update: Influenza Activity -- United States, 1994-95 Season
       Human Rabies -- West Virginia, 1994
       Pregnancy-Related Mortality -- Georgia, 1990-1992
       Notice to Readers: Publication of Guidelines for the Prevention
            and Treatment of B Virus Infections in Exposed Persons
       Addendum: Vol. 43, Nos. 51 & 52
       Erratum: Vol. 44, No. 4
       Errata: Vol. 43, No. 50
       Monthly Immunization Table

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

Update: AIDS Among Women -- United States, 1994

     In 1993, human immunodeficiency virus (HIV)/acquired
immunodeficiency syndrome (AIDS) was the fourth leading cause of death
among women aged 25-44 years in the United States (1); in addition,
the incidence of AIDS is increasing more rapidly among women than men
(2). Women with AIDS reported in 1994 represented 13% of the
cumulative total of 58,448 cases among women. This report presents
characteristics of women and men reported with AIDS in 1994,
summarizes trends in cases reported during 1985-1994, and describes
findings of an HIV seroprevalence survey among childbearing women
during 1989-1993.* AIDS Surveillance

       In 1994, of the 79,674 persons aged greater than or equal to 13
years reported with AIDS, 14,081 (18%) occurred among women-- nearly
threefold greater than the proportion (534 [7%] of 8153) reported in
1985; in addition, the proportion of cases among women has increased
steadily since 1985 (Figure 1). The median age of women reported with
AIDS was 35 years, and women aged 15-44 years accounted for 84% of
cases. More than three fourths (77%) of cases among women occurred
among blacks and Hispanics, and rates for black and Hispanic women
were 16 and seven times higher, respectively, than those for white
women (Table 1).

       In 1994, the Northeast region accounted for the largest
percentage of AIDS cases reported among women (44%), followed by the
South (36%), West (9%), Midwest (7%), and Puerto Rico and U.S.
territories (4%). In the Northeast, most cases among women occurred in
urban areas; 1.4% of women with AIDS in the Northeast resided outside
metropolitan statistical areas (MSAs) compared with 10.2% of women who
resided outside MSAs in the South. Of all cases among women, 61% were
reported from five states: New York (26%), Florida (13%), New Jersey
(10%), California (7%), and Texas (5%).

       In 1994, 59% of AIDS cases among women were reported based on
criteria added in the 1993 expanded AIDS surveillance case definition
(3). This total included 7181 women with severe HIV-related
immunosuppression (CD4+ T-lymphocytes less than 200 cells/uL or
percentage of total lymphocytes less than 14), 557 with pulmonary
tuberculosis, 376 with recurrent pneumonia, and 164 with invasive
cervical cancer.

       In 1994, 41% of women with AIDS reported injecting-drug use;
38%, heterosexual contact with a partner at risk for or known to have
HIV infection or AIDS; and 2%, receipt of contaminated blood or blood
products; 19% had no specific HIV exposure reported. Of all women with
AIDS who were initially reported without risk but who were later
reclassified, most had heterosexual contact with an at-risk partner
(66%) or a history of injecting-drug use (27%) (4). In 1994, of the
5353 women reported with AIDS attributed to heterosexual contact, 38%
reported contact with a male partner who was an injecting-drug user;
7%, a bisexual male; 2%, a partner who had hemophilia or had received
HIV-contaminated blood or blood products; and 53%, a partner who had
documented HIV infection or AIDS but whose risk was unspecified. HIV
Seroprevalence in Childbearing Women

       Using findings from the HIV Survey in Childbearing Women (SCBW)
(5), an estimated 7000 HIV-infected women delivered infants in the
United States during 1993. Assuming a perinatal transmission rate of
15%-30%, approximately 1000-2000 infants were perinatally infected
with HIV during 1993. From 1989 through 1993, the annual prevalence of
HIV infection among childbearing women remained relatively stable
(1.6-1.7 per 1000), although prevalence varied regionally: in the
Northeast, prevalence decreased from 4.1 to 3.4 per 1000; in the
South, prevalence increased from 1.6 in 1989 to 2.0 in 1991 and
remained stable through 1993.

Reported by: Local, state, and territorial health depts. Div of
HIV/AIDS, National Center for Infectious Diseases; Office of Women's
Health, Office of the Director; Div of Reproductive Health, National
Center for Chronic Disease Prevention and Health Promotion, CDC.

Editorial Note: In 1994, as in previous years, the AIDS epidemic among
women continued to disproportionately affect racial/ethnic minorities,
primarily in the Northeast and South. AIDS among women was primarily
associated with two modes of HIV transmission: injecting-drug use and
heterosexual contact with an at-risk partner. The proportion of women
in 1994 with unreported risk will decrease substantially after
investigation by local and state health departments because, after
follow-up, most women are found to have a recognized risk for HIV.
Heterosexual contact is the most rapidly increasing transmission
category for women (6).

       The disproportionate impact of HIV/AIDS among women in
racial/ethnic minority groups reflects social and economic factors
that have not been completely defined. Despite the methodologic
limitations associated with use of race/ethnicity, these data have
assisted in the development and implementation of community-based
prevention efforts.

       The increase in the proportion of cases associated with
heterosexual transmission will complicate accurate ascertainment of
mode of transmission. In particular, women are more likely than men to
be reported initially without a risk for HIV because both women and
their care providers may not recognize or report the risk behaviors of
the woman or her partners (6). High rates of sexually transmitted
diseases are associated with the use of noninjecting drugs and with
the exchange of sex for drugs, money, or personal items that may
account for increased heterosexual transmission among some women (7).
In addition, some women who have sex with other women may be at risk
for HIV infection if they inject drugs or have partners with high-risk
behaviors (8).

       Findings from the SCBW indicate that approximately 7000 infants
are born to HIV-infected women in the United States each year. Recent
advances in the prevention of perinatal HIV transmission emphasize the
need for women to know their HIV-infection status. Zidovudine therapy
has been recommended for infected pregnant women and their newborns as
an effective means for reducing the risk for perinatal HIV
transmission (9). The Public Health Service is developing draft
recommendations to establish policy regarding HIV counseling and
testing of pregnant women to reduce vertical transmission and promote
referrals for on-going health care.

       Women at highest risk for heterosexually acquired HIV infection
include those whose heterosexual partners have high-risk behaviors
(e.g., injecting-drug use), adolescents and young adults with multiple
sex partners, and those with sexually transmitted diseases. To reduce
HIV transmission to women, prevention programs should emphasize
consistent condom use, the need for substance-abuse prevention and
treatment services, and counseling to support decisions by women and
their partners to reduce risk behaviors. Efforts to improve the
prevention of HIV transmission in women also should include the
development and evaluation of additional measures such as the female
condom and microbicides.

       References

       1. CDC. Annual summary of births, marriages, divorces, and
deaths: United States, 1993. Hyattsville, Maryland: US Department of
Health and Human Services, Public Health Service, CDC, 1994:18-20.
(Monthly vital statistics report; vol 42, no. 13).

       2. CDC. Update: acquired immunodeficiency syndrome--United
States, 1994. MMWR 1995;44:64-7.

       3. CDC. 1993 Revised classification system for HIV infection
and expanded surveillance case definition for AIDS among adolescents
and adults. MMWR 1992;41:(no. RR-17).

       4. CDC. HIV/AIDS surveillance report. Atlanta: US Department of
Health and Human Services, Public Health Service, 1994;6(no.
1):20,25-7.

       5. Gwinn M, Pappaioanou M, George JR, et al. Prevalence of HIV
infection in childbearing women in the United States. JAMA
1991;265:1704-8.

       6. CDC. Heterosexually acquired AIDS--United States, 1993. MMWR
1994;43:155-60.

       7. Edlin BR, Irwin KL, Faruque S, et al. Intersecting
epidemics: crack cocaine use and HIV infection among inner-city young
adults. N Engl J Med 1994;331:1422-7.

       8. Chu SY, Hammett TA, Buehler JW. Update: epidemiology of
reported cases of AIDS in women who report sex only with other women,
1980- 1991. AIDS 1992;6:518-9.

       9. CDC. Recommendations of the U.S. Public Health Service Task
Force on the Use of Zidovudine to Reduce Perinatal Transmission of
Human Immunodeficiency Virus. MMWR 1994;43(no. RR-11).

       * Single copies of this report will be available until Friday
         10, 1996, from the CDC National AIDS Clearinghouse, P.O. Box
         6005, Rockville, MD 20849-6003; telephone [phone].

       -----------------------------------------------------------
       Update: Influenza Activity -- United States, 1994-95 Season

       Influenza activity has increased throughout the United States
since late November 1994; however, the level of activity* has varied
widely in different parts of the country. This report summarizes
results of influenza surveillance in the United States from October 2,
1994, through January 28, 1995.

       From November 27, 1994, through January 21, 1995, most
influenza activity had been reported from the Northeast (Figure 1).
Regional influenza activity was first reported the week ending
December 3 in New York, and widespread activity was first reported the
week ending January 7 in Connecticut and Virginia. Regional or
widespread activity also was reported by Kentucky, Maryland, New
Jersey, and Pennsylvania during the first 3 weeks of January. All
other states reported either sporadic activity or no activity until
the week ending January 28, when regional activity was reported for
the first time in Arizona, Florida, and Wisconsin.

       From October 2, 1994, through January 28, 1995, a total of 686
influenza virus isolates were reported in the United States by the
World Health Organization collaborating laboratories. Of these, 487
(71%) were type A, and 199 (29%) were type B. Of the 216 influenza A
isolates that were subtyped, all have been type A(H3N2).
Laboratory-diagnosed influenza has been reported from all regions;
however, 84% of all isolates have been reported from the Mid-Atlantic
and South Atlantic regions. In the Mid-Atlantic region, influenza type
A accounted for 94% (259 of 276) of all isolates; in the South
Atlantic region, influenza type B accounted for 59% (176 of 297) of
isolates. As of January 27, influenza isolates were reported from 41
states; type A had been identified in 39 states and the District of
Columbia, and influenza type B had been identified in 22 states and
the District of Columbia (Figure 1).

       During the 17 weeks from October 2, 1994, through January 28,
the proportion of pneumonia and influenza deaths among total deaths
reported from 121 U.S. cities slightly exceeded the epidemic
threshold** during 5 weeks but has not exceeded the threshold for any
2 consecutive weeks.

Reported by: 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: The increase in influenza activity in regions of the
United States during December and January suggests the potential for
increased activity in other regions during this influenza season. The
timing of influenza activity can vary widely from one season to
another; in some previous seasons, substantial influenza activity has
occurred during April and May.

       Influenza vaccine can be administered after influenza activity
has begun in a community; however, in these circumstances, short-term
antiviral prophylaxis may be indicated because antibody may not
develop until up to 2 weeks after vaccination (1). Health-care
providers should be informed about findings of influenza surveillance,
particularly when influenza types A and B are cocirculating, because
of the availability of antiviral agents to treat and prevent influenza
type A (1).

       Reference

       1. 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).

         * Levels of activity are 1) sporadic--sporadically occurring
           influenza-like illness (ILI) or culture-confirmed
           influenza, with no outbreaks detected; 2)
           regional--outbreaks of ILI or culture-confirmed influenza
           in counties having a combined population of less than 50%
           of the state's total population; and 3)
           widespread--outbreaks of ILI or culture-confirmed influenza
           in counties having a combined population of greater than or
           equal to 50% of the state's total population.

        ** The epidemic threshold is 1.645 standard deviations above
           the seasonal baseline calculated using a periodic
           regression model applied to observed percentages since
           1983. This baseline was calculated using a robust
           regression procedure.

       -----------------------------------
       Human Rabies -- West Virginia, 1994

       On October 15, 1994, a 41-year-old male resident of Wirt
County, West Virginia, died from rabies. This report summarizes the
clinical course, epidemiologic investigation, and probable exposure
history of this case.

       On October 4, the man was examined at a local hospital with a
1-day history of shaking, speech difficulties, unwillingness to bring
liquids to his mouth, vomiting, and severe anxiety. During
examination, he had good long-term recall but a short attention span
and became extremely agitated when anyone approached him for
examination. A white blood cell count (WBC) was 13,600/mm superscript
3 (normal: 5000-10,000/mm superscript 3), and urinalysis indicated
greater than 80 mg/dL ketones (normal: absent), 100 mg/dL protein
(normal: absent), trace blood (normal: absent), and carboxy acid
tetrahydrocannabinol of 79 ng/mL (normal: absent). Preliminary
diagnosis was acute psychotic reaction associated with use of ethanol
or marijuana or ingestion of other drugs. The man declined further
examination and treatment and left the same day without being
admitted.

       On the evening of October 4, the man was examined at a regional
hospital with extreme agitation and muscle tremors; he was admitted to
the intensive-care unit for apparent encephalopathy. Findings on
admission included an oral temperature of 101.1 F (38.3 C) and pulse
of 64 beats per minute. Laboratory test results included a WBC of
18,100/mm superscript 3, creatinine phosphokinase of 1912 IU (normal:
5-50 IU), and a lactic dehydrogenase of 1000 U/L (normal: less than
300 U/L). Following evaluation, the preliminary differential diagnoses
included rabies, tetanus, viral encephalitis, acute hemorrhagic
encephalitis, and drug toxicities or withdrawal. Efforts to control
spastic movements included treatment with valium, librium, ativan,
phenobarbital, and morphine. Because of frequent expectoration of
frothy saliva from the mouth, he was placed in isolation. On October
6, he was paralyzed with pavulon/tracrium to control extreme agitation
and spastic muscle activity, mechanically ventilated, treated with
acyclovir for possible viral infection, and then transferred to a
tertiary-care facility.

       On October 6 and 7, serial computerized tomographies of the
brain revealed low attenuation in the left temporal lobe suggestive of
inflammation or neoplasm. On October 6 and 10, cerebrospinal fluid
specimens were obtained, but findings were nonspecific. Serologic
tests were negative for eastern equine, western equine, St. Louis, and
California group arboviral encephalitides. A serum sample and nuchal
biopsy specimen obtained on October 7 and a brain biopsy specimen
(left temporal lobe) obtained on October 10 were tested for rabies. On
October 12, the West Virginia Bureau of Public Health Laboratory
diagnosed rabies by both fluorescent antibody stain and demonstration
of Negri bodies in the brain tissue, and treatment with
paralytic/sedative drugs was terminated; the patient died on October
15.

       Subsequent confirmatory analysis at CDC included detection of
rabies neutralizing antibody in serum and the detection of rabies
antigen by direct fluorescent antibody staining of the nuchal biopsy
specimen. The specific viral RNA was identified as a variant
associated with the silver-haired bat (Lasionycteris noctivagans).

       Interviews with friends and family members on October 15
indicated that, in late June or early July 1994, the decedent and two
acquaintances had shot a bat from the front porch of his house and
that the decedent had examined the head of the bat by opening its
mouth and feeling the teeth. Descriptions of the bat were consistent
with the red bat (Lasiurus borealis).

       Postexposure rabies immunoprophylaxis was administered to 48
persons (15 medical technicians, 12 registered nurses, four
physicians, two licensed practical nurses [LPNs], one LPN student, one
physician assistant, one housekeeper, one secretary, and 11 family
members and friends).

Reported by: MS Hardman, MA Ballesca, MD, DM Senseng, MD, Roane
General Hospital, Spencer; S Spencer, SD Hanna, MD, BM Louden, MD, MA
Morehead, MD, P Anderson, St. Joseph's Hospital, Parkersburg; B
McTaggart, A Khan, MD, AA Marfin, MD, PJ Marks, MD, E Sang, MD, MA
Fisher, MD, RW Farr, MD, Robert C. Byrd Health Sciences Center of West
Virginia Univ, Morgantown; J Merrill, Mid-Ohio Valley Health Dept,
Elizabeth; C Slemp, MD, F Lambert, Jr, DrPH, D Dodd, L Haddy, MS,
State Epidemiologist, West Virginia Dept of Health and Human
Resources. Viral and Rickettsial Zoonoses Br, Div of Viral and
Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note: This report describes the 21st case of human rabies
reported in the United States since 1980 and the first from West
Virginia since 1979. Of the 21 cases, 11 are presumed to have been
acquired inside the United States, and nine have been attributed to
bat-associated virus. As a result of exposure to these 21 human rabies
cases, at least 880 persons have received postexposure rabies
immunoprophylaxis at an estimated direct cost of $900,000 (1).

       Although a specific exposure to rabies was not elicited before
this patient's death, a presumptive diagnosis of rabies had been
considered early during hospitalization. As a consequence, the
initiation of strict isolation practices reduced the number of persons
exposed and, therefore, eliminated the need for postexposure
prophylaxis for health-care workers involved with the patient's
transfer to and care at the tertiary-care facility. This case
emphasizes that prompt collection and analysis of antemortem specimens
in suspected cases of human rabies may expedite diagnosis and minimize
unnecessary exposures and treatments.

       Bat rabies is enzootic in the United States, and cases have
been reported from all 48 contiguous states. Although distinct
variants of rabies virus have been confirmed in red bats, this case is
the first in which the silver-haired bat variant has been potentially
linked with red bats. Because the natural history of rabies virus
circulation among bats is not completely understood, mammalogists
should collaborate with local health departments in the taxonomic
identification of bats submitted for rabies diagnosis. In addition,
CDC requests that brain tissue from rabid silver-haired and red bats
be forwarded from state diagnostic laboratories to CDC's Viral and
Rickettsial Zoonoses Branch, Division of Viral and Rickettsial
Diseases, National Center for Infectious Diseases, telephone (404)
639-1050.

       Exposure to potentially rabid animals (e.g., downed bats and
other wild animals) should be avoided. However, postexposure
prophylaxis is recommended for all persons bitten by such animals and
for nonbite exposures involving contamination of lesions or mucous
membranes with potentially infectious materials such as saliva (2).
Because some bat bites may be less severe--and therefore more
difficult to recognize--than bites inflicted by larger mammalian
carnivores, rabies postexposure treatment should be considered for any
physical contact with bats when bite or mucous membrane contact cannot
be excluded (3). Because reduction of bat populations is neither
feasible nor desirable as a means of controlling rabies in bats,
rabies-prevention programs should emphasize the exclusion of bats from
human dwellings to minimize direct contact with humans and companion
animals.

       References

       1. Fishbein DB, Robinson LE. Rabies. N Engl J Med
1993;329:1632-8.

       2. ACIP. Rabies prevention--United States, 1991:
recommendations of the Immunization Practices Advisory Committee
(ACIP). MMWR 1991;40(no. RR-3).

       3. CDC. Human rabies--California, 1994. MMWR 1994;43:455-7.

       -------------------------------------------------
       Pregnancy-Related Mortality -- Georgia, 1990-1992

       Many pregnancy-related deaths are preventable. State-based
surveillance is important for identifying such deaths and developing
prevention strategies. Surveillance for pregnancy-related deaths based
only on ascertainment through death certificates underestimates actual
deaths (1-7). However, when this surveillance method has been
supplemented by linking death certificates of reproductive-aged women
to birth and fetal death records, ascertainment has increased 1%-153%
(1,2,4,6,7). In 1994, the Division of Public Health, Georgia
Department of Human Resources, assessed the completeness of reporting
of pregnancy-related deaths during 1990-1992 by comparing current
death-certificate-based surveillance with a supplemental method of
linking women's death records and infants' birth records. This report
characterizes the increase in the total number of pregnancy-related
deaths identified and presents specific causes of pregnancy-related
deaths in Georgia.

       In this analysis, pregnancy-related deaths were defined as the
immediate result of complications of pregnancy, events initiated by
the pregnancy, or an exacerbation of an unrelated condition by the
physiologic or pharmacologic effects of the pregnancy that occurred up
to 1 year after giving birth or pregnancy termination (8). For both
surveillance methods, deaths among women during pregnancy or post
partum were first identified, then categorized by specific cause, and
coded as pregnancy-related using the American College of Obstetricians
and Gynecologists (ACOG) and CDC definitions. In Georgia, physicians,
medical examiners, and coroners are required to indicate on the death
certificate, regardless of cause of death, whether the decedent was
pregnant at the time of death or had given birth within the preceding
90 days. For the current surveillance method, deaths during pregnancy
or post partum were identified by manually reviewing each death
certificate for this notation or for a cause of death related to the
pregnancy or selected key words (e.g., cesarean delivery). For the
record-linkage method, females were identified who died within 1 year
of delivering a live-born infant by linking death certificates for
females aged 10-49 years who died during 1990-1992 to birth records
for 1989-1992. A probabalistic method was used to calculate the
likelihood of a correct linkage based on use of the mother's first and
last names and date of birth. All death and birth record matches
identified by the linkage were manually reviewed. The
pregnancy-related mortality ratio during 1990-1992 was calculated as
the number of pregnancy-related deaths divided by the number of live
births during the period.

       During 1990-1992, a total of 210 deaths among women during
pregnancy or post partum were identified by death-certificate review
and record linkage. Of these, 73 (35%) were pregnancy-related, 65
(31%) resulted from a medical problem unrelated to the pregnancy, and
72 (34%) resulted from injuries (Table 1). Of the 135 additional
deaths identified by record linkage, 118 (87%) were caused by injuries
and medical problems unrelated to pregnancy (Table 1). Although 35
(26%) of the 135 deaths occurred within 90 days of giving birth or
pregnancy termination (i.e., the specified time in Georgia for
indicating a recent pregnancy on the death certificate), this
information was not indicated on the death certificate.

       As a result of record linkage, the pregnancy-related maternal
mortality ratio during 1990-1992 increased 30%, from 16.8 deaths per
100,000 live births (based only on death-certificate review) to 21.9
per 100,000 (based on combined death-certificate review and record
linkage).

       The three leading causes of pregnancy-related death--
hemorrhage, embolism, and infection--were the same for deaths
identified by the current surveillance method and the combined methods
(Table 2). Compared with the current surveillance method, record
linkage resulted in increased case ascertainment for all but two
specific causes of death (pregnancy-induced hypertension and
anesthesia complications). The largest percentage increase in
pregnancy-related deaths (200%) was for cardiomyopathy.

Reported by: V Floyd, MD, C Hadley, MN, Family Health Br; M Lavoie,
MA, Center for Health Information; Office of Perinatal Epidemiology,
Epidemiology and Prevention Br; K Toomey, MD, State Epidemiologist,
Div of Public Health, Georgia Dept of Human Resources. Div of
Reproductive Health, National Center for Chronic Disease Prevention
and Health Promotion; Div of Field Epidemiology, Epidemiology Program
Office, CDC.

Editorial Note: In Georgia, ascertainment of pregnancy-related deaths
improved substantially when death certificates were linked to birth
records--a result also documented in other states (2,4,6). However,
compared with other states, the percentage increase in
pregnancy-related deaths in Georgia was lower. This finding may
reflect more complete death-certificate-based ascertainment in Georgia
and the linkage of live-birth records only instead of both fetal death
and live-birth records. The variation among states in the percentage
of additional pregnancy-related deaths identified by linked records
(1%-153%) also may be associated with such factors as differences in
definitions of maternal death, variables used to match records, and
methods used to link records.

       A year 2000 national health objective is to reduce the maternal
mortality rate to no more than 3.3 deaths per 100,000 live births
(objective 14.3). The findings in this report indicate that the
pregnancy-related mortality ratio in Georgia is higher than previously
estimated (9) and that efforts must be intensified to attain the
objective. State health departments should enhance ascertainment of
pregnancy-related deaths through linkage of birth and fetal death
records to death records of reproductive-aged women to more accurately
track pregnancy-related mortality.

       References

       1. Allen MH, Chavkin W, Marinoff J. Ascertainment of maternal
deaths in New York City. Am J Public Health 1991;81:380-2.

       2. CDC. Misclassification of maternal deaths--Washington state.
MMWR 1986;35:621-3.

       3. Speckhard ME, Comas-Urrutia AC, Rigau-Perez J, Adamsons K.
Intensive surveillance of pregnancy-related deaths, Puerto Rico,
1978-1979. Bol Asoc Med P R 1985;77:508-13.

       4. CDC. Enhanced maternal mortality surveillance--North
Carolina, 1988 and 1989. MMWR 1991; 40:469-71.

       5. Comas A, Navarro A, Conde J, Blasini I, Adamsons K.
Misreporting of maternal mortality in Puerto Rico. Bol Asoc Med P R
1990;82:343- 6.

       6. Dye TD, Gordon H, Held B, Tolliver NJ, Holmes AP.
Retrospective maternal mortality case ascertainment in West Virginia,
1985 to 1989. Am J Obstet Gynecol 1992;167:72-6.

       7. Rubin G, McCarthy B, Shelton J, Rochat RW, Terry J. The risk
of childbearing re-evaluated. Am J Public Health 1981;71:712-6.

       8. CDC. National pregnancy mortality surveillance coding
manual. Atlanta: US Department of Health and Human Services, Public
Health Service, CDC, 1992.

       9. Ledbetter JG, Galvin VG. Healthy Georgians 2000. Atlanta:
Georgia Department of Human Resources, Division of Public Health,
Center for Health Information, October 1993.

       -----------------
       Notice to Readers

       Publication of Guidelines for the Prevention and Treatment of B
       Virus Infections in Exposed Persons

       Cercopithecine herpesvirus 1 (B virus) infection is widespread
among Macaca genus primates; the virus is the biologic counterpart of
herpes simplex virus in humans. B virus infection in humans is
recognized as a rapidly ascending encephalomyelitis with a fatality
rate of approximately 70%. The need for guidelines in prevention and
treatment of human B virus infection was recognized in 1987 after a
cluster of four symptomatic infections occurred among persons in
Florida. CDC and the National Institutes of Health consulted primate
veterinarians and herpesvirus experts to develop guidelines for
preventing B virus infection in persons who work with macaques (1).
Recommendations intended to minimize the risk for infection of
laboratory workers exposed to B virus-contaminated primary rhesus
monkey cell cultures were published in 1989 (2). Guidelines for
primate handlers were expanded in 1990 in response to the recognition
of filovirus infection in quarantined primates (3).

       Human infections with B virus remain an uncommon result of
macaque-related injuries, and optimal diagnostic and therapeutic
approaches are unclear. However, the increase in the use of macaques
for research on simian retrovirus infection and hepatitis has expanded
the number of potential incidents of human exposure. In January 1990,
Emory University and CDC sponsored a B virus working group intended to
formulate a rational approach to the prevention, detection, and
management of human B virus infections. Written guidelines were
developed based on information from published and unpublished cases,
knowledge of the behavior of herpes simplex virus, and expert opinion.

       These guidelines (4) are intended to assist institutions in
which macaques are handled in developing and enforcing effective
standard operating procedures and quality-control interventions and to
enable local physician consultants identified by the institutions to
evaluate and treat persons with potential B virus exposure. Such
institutions should keep a copy of these guidelines in bite/wound kits
at the work site. Institutions also should provide copies of these
guidelines to injured employees referred for medical evaluation; to
the emergency rooms, clinics, or offices where injured employees will
seek care; and to employees to give to their personal physician. More
information on the guidelines is available from B Virus Guidelines,
Division of Viral and Rickettsial Diseases, National Center for
Infectious Diseases, CDC, Mailstop G-19, 1600 Clifton Road, NE,
Atlanta, GA 30333.

       References

       1. CDC. Guidelines for prevention of Herpesvirus simiae (B
virus) infection in monkey handlers. MMWR 1987;36:680-2,687-9.

       2. Wells DL, Lipper SL, Hilliard JK, et al. Herpesvirus simiae
contamination of primary rhesus monkey kidney cell cultures: CDC
recommendations to minimize risks to laboratory personnel. Diagn
Microbiol Infect Dis 1989;12:333-5.

       3. CDC. Update: Ebola-related filovirus infection in nonhuman
primates and interim guidelines for handling nonhuman primates during
transit and quarantine. MMWR 1990;39:22-4,29-30.

       4. Holmes GP, Chapman LE, Stewart JA, et al. Guidelines for the
prevention and treatment of B-virus infections in exposed persons.
Clin Infect Dis 1995;20:421-39.

       -------------------------------
       Addendum: Vol. 43, Nos. 51 & 52

       In the article "Hemorrhage and Shock Associated with Invasive
Pneumococcal Infection in Healthy Infants and Children--New Mexico,
1993-1994," the following person should be added to the credits
("reported by") on the fourth line on page 950: J McLaughlin, PhD,
Univ of New Mexico Hospital, Albuquerque.

       -----------------------
       Erratum: Vol. 44, No. 4

       In the article "Acute Pulmonary Hemorrhage Among Infants--
Chicago, April 1992-November 1994," on page 67, the sentence beginning
on the fifth line was incorrect. The sentence should read, "For six of
the infants who underwent bronchoscopy, the procedure was performed
within 2 weeks of the initial presentation with pulmonary hemorrhage."

       -----------------------
       Errata: Vol. 43, No. 50

       In the article "State-Specific Trends Among Women Who Did Not
Receive Prenatal Care--United States, 1980-1992," on page 939, in the
second sentence of the third paragraph, the maximum value in 1992
declined to 5.7%, rather than 4.8%. The fourth paragraph should read:
"For 1980-1981, the percentage of women who did not receive prenatal
care ranged from 0.18% (Vermont) to 3.64% (New York) (Table 1); for
1991-1992, the percentages ranged from 0.30% (Rhode Island) to 6.07%
(District of Columbia). When compared with 1980-1981, during 1991-1992
the percentage of women who did not receive prenatal care declined in
nine states (Florida, Kentucky, Minnesota, New Jersey, New York,
Oklahoma, Rhode Island, South Dakota, and Utah) and increased in 41
states and the District of Columbia; in eight states (Delaware,
Illinois, Indiana, Louisiana, Michigan, Pennsylvania, Vermont, and
Wisconsin) and the District of Columbia, the increase was greater than
100%."

       On page 940, the fourth sentence in the second paragraph should
read, "For example, the comparison of data for 1980-1981 with
1991-1992 demonstrated slight decreases in the percentage of women who
did not receive prenatal care in nine states and substantial increases
in eight states and the District of Columbia." On page 941, the
state-specific percentages were incorrect for several states. The
following table contains the corrected percentages and replaces Table
1.

       --------------------------
       Monthly Immunization Table

       To track progress toward achieving the goals of the Childhood
Immunization Initiative (CII), CDC publishes monthly a tabular summary
of the number of cases of all diseases preventable by routine
childhood vaccination reported during the previous month and
year-to-date (provisional data). In addition, the table compares
provisional data with final data for the previous year and highlights
the number of reported cases among children aged less than 5 years,
who are the primary focus of CII. Data in the table are derived from
CDC's National Notifiable Diseases Surveillance System.

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