Update: West Nile Virus Encephalitis—New York, 1999 FREE

MMWR. 1999;48:944-950

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The West Nile virus (WNV) encephalitis outbreak continues to wane in the Northeast with the onset of cooler temperatures and continued vector-control operations. This report updates the progress of the ongoing investigation. Since the last published update,¹ five additional domestic human cases and one international case have been identified. As of October 19, 56 (31 confirmed and 25 probable) cases of WNV infection have been identified, including seven deaths. The date of onset of the latest cases was September 22. The international case was a Canadian citizen who had visited the New York City (NYC) area in late August who had onset of fatal encephalitis on September 5. Active surveillance for human encephalitis cases in Connecticut and New Jersey has not detected any WNV cases.

Surveillance for WNV in mosquitoes and birds continues. As of October 19, 11 pools collected during September 12-October 4 of Culex spp. mosquitoes, positive for WNV, have been identified from NYC and Nassau and Suffolk counties. Pools of Culex and Aedes vexans mosquitoes collected during early to mid-September in Hudson County, New Jersey, tested positive for WNV by reverse transcriptase polymerase chain reaction (RT-PCR). Birds that tested positive for WNV now have been identified by RT-PCR on postmortem brain tissue from New York (NYC boroughs of Bronx, Brooklyn, Manhattan, Queens, and Staten Island; and Nassau, Orange, Rockland, Saratoga, Suffolk, and Westchester counties), New Jersey (Bergen, Burlington, Essex, Hudson, Hunterdon, Middlesex, Monmouth, Morris, Passaic, Somerset, Union, and Warren counties), and Connecticut (Fairfield County). In addition, postmortem brain tissue from birds from Fairfield and New Haven counties, Connecticut, have been reported as positive in culture for WNV by the Connecticut Department of Health. Although most WNV-positive birds have been American crows, infections also have been confirmed in other native species, including the ring-billed gull, yellow-billed cuckoo, rock dove, sandhill crane, fish crow, blue jay, bald eagle, laughing gull, black-crowned night heron, mallard, American robin, red-tailed hawk, and broad-winged hawk.

Laboratory studies conducted at CDC have identified the etiologic agent responsible for the human arboviral encephalitis outbreak in the NYC area as WNV. Confirmation of the genetic identity as WNV has been performed independently by collaborators at the United States Army Medical Research Institute for Infectious Diseases. WNV-specific gene sequences have been amplified by RT-PCR performed on RNA extracted from autopsy specimens (six case-patients). Sequences of genome fragments of WNV isolated from dead birds and mosquitoes are identical to gene sequences from the human autopsy specimens. Antigenic mapping of these isolates has been performed using a panel of monoclonal antibodies (Mabs) developed by CDC or provided by collaborators at the University of Queensland, Australia. These envelope (E)-glycoprotein specific Mabs, capable of distinguishing WN, Kunjin, and St. Louis encephalitis viruses, confirmed the sequence identification of these isolates as WNV.

A Fine, MD, M Layton, MD, J Miller, MD, D Cimini, MPH, MC Vargas, DVM, A Inglesby, MD, the New York City Outbreak Investigation Team, N Cohen, MD; I Weisfuse, MD; A Ramon, MD, I Poshni, PhD, H Stirling, MPH, New York City Dept of Health; T McNamara, DVM, Wildlife Conservation Society, New York City; A Huang, MD, A Rosenberg, MD, P Yang-Lewis, MPH, HN Adel, MD, Westchester County Health Dept, New Rochelle; M Sherman, G Terillion, B Smith, R Porter, A Greenberg, MD, KA Gaffney, MD, Nassau County Dept of Health and Public Works; A Novello, MD, D White, PhD, D Morse, MD, K Spitalny, MD, R Gallo, S Wong, MD, L Grady, MD, M Eidson, DVM, B Wallace, MD, P Smith, MD, State Epidemiologist, New York State Dept of Health. M Cartter, MD, R Nelson, DVM, J Hadler, MD, State Epidemiologist, Connecticut Dept of Public Health; T Andreadis, PhD, Connecticut Agricultural Experiment Station. J Blumenstock, J Degraaf, F Sorhage, DVM, C Campbell, DVM, J Brook, MD, M Gerwell, MD, D Adams, K Bruder, R Kent, R Eisner, DVM, N Halpern, DVM, New Jersey Dept of Agriculture; D Roscoe, DVM, New Jersey Dept of Environmental Protection; E Bresnitz, MD, State Epidemiologist, New Jersey Dept of Health and Senior Svcs. W Crans, PhD, Rutgers Univ, New Brunswick, New Jersey. J Mackenzie, PhD, R Hall, PhD, J Sherret, MSc, Univ of Queensland, Australia. H Artsob, PhD, Laboratory Centre for Disease Control, Health Canada. J Smith, PhD, M Parker, PhD, K Steele, DVM, United States Army Medical Research Institute for Infectious Diseases; National Veterinary Svcs Laboratories, Animal and Plant Health Inspection Svc, US Dept of Agriculture, Ames, Iowa. Infectious Disease Pathology Activity, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; Arbovirus Diseases Br, Div of Vector-Borne Infectious Diseases, National Center for Infections Diseases; and EIS officers, CDC.

The dates of onset of illness for laboratory-positive cases of WNV infection suggest that the outbreak peaked in late August. There have been no recognized cases of WNV infection with an onset date after September 22. WNV encephalitis has an incubation period of 5-15 days. The latest cases occurred outside NYC in Nassau and Westchester counties, which implemented mosquito-control measures later than NYC. Collectively, these data suggest that control measures, combined with cooler temperatures, have been effective in reducing the transmission cycle in nature and limiting further illnesses in humans. However, it is important to continue to recommend personal protective measures during outdoor activity at dusk and at night until the onset of cold weather in the affected areas.¹

The identification of WNV in birds from Orange and Saratoga counties, New York City, and Burlington County, New Jersey, may represent an extension northward and southward of the known area of natural transmission between birds and mosquitoes, but for this to be the case, either demonstration of WNV in vector mosquito populations or demonstration of neutralizing antibodies against WNV in resident birds is needed because these birds may have been infected elsewhere. The current known geographic distribution of infected dead birds is in counties surrounding the western half of Long Island Sound.

Serum samples collected from migrant and resident birds in several states will be analyzed for antibody to WNV. States included in this survey are New York, New Jersey, Maryland, Virginia, North Carolina, South Carolina, Georgia, and Florida. Collaborators in this survey include university ornithologists, state wildlife biologists, and state health departments. In addition, wildlife and health officials in all mid-Atlantic and southeastern states have been alerted to investigate reports of unusual clusters of dead birds.

All state epidemiologists have been informed of the characteristics of this outbreak and encouraged to enhance surveillance for cases of human encephalitis. Monitoring of mosquitoes and birds has been increased in several states with existing vector-control programs. Training to institute programs for arbovirus and mosquito vector surveillance will be offered to states without programs, beginning with Atlantic coast states. In addition, the emerging infections sentinel networks coordinated by the Infectious Diseases Society of America (IDSA EIN) and the International Society of Travel Medicine (GeoSentinel) are assisting case-finding efforts to define the extent of the outbreak in the United States.

A previous publication indicated that the New York virus was more closely related to Kunjin virus.² Data in this report based on phylogenetic analysis comparing published E-glycoprotein sequences from WNVs and other flaviviruses, including Kunjin, St. Louis encephalitis, and Japanese encephalitis indicate that the New York virus is WN. Complete genome sequencing of multiple WNV isolates is in progress.

MMWR. 1999;48:849-857

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At the beginning of the 20th century, for every 1000 live births, six to nine women in the United States died of pregnancy-related complications, and approximately 100 infants died before age 1 year.^1- 2 From 1915 through 1997, the infant mortality rate declined greater than 90% to 7.2 per 1000 live births, and from 1900 through 1997, the maternal mortality rate declined almost 99% to <0.1 reported death per 1000 live births (7.7 deaths per 100,000 live births in 1997).³ Environmental interventions, improvements in nutrition, advances in clinical medicine, improvements in access to health care, improvements in surveillance and monitoring of disease, increases in education levels, and improvements in standards of living contributed to this remarkable decline.¹ Despite these improvements in maternal and infant mortality rates, significant disparities by race and ethnicity persist. This report summarizes trends in reducing infant and maternal mortality in the United States, factors contributing to these trends, challenges in reducing infant and maternal mortality, and provides suggestions for public health action for the 21st century.

The decline in infant mortality is unparalleled by other mortality reduction this century. If turn-of-the-century infant death rates had continued, then an estimated 500,000 live-born infants during 1997 would have died before age 1 year; instead, 28,045 infants died.³

In 1900 in some U.S. cities, up to 30% of infants died before reaching their first birthday.¹ Efforts to reduce infant mortality focused on improving environmental and living conditions in urban areas.¹ Urban environmental interventions (e.g., sewage and refuse disposal and safe drinking water) played key roles in reducing infant mortality. Rising standards of living, including improvements in economic and education levels of families, helped to promote health. Declining fertility rates also contributed to reductions in infant mortality through longer spacing of children, smaller family size, and better nutritional status of mothers and infants.¹ Milk pasteurization, first adopted in Chicago in 1908, contributed to the control of milkborne diseases (e.g., gastrointestinal infections) from contaminated milk supplies.

During the first three decades of the century, public health, social welfare, and clinical medicine (pediatrics and obstetrics) collaborated to combat infant mortality.¹ This partnership began with milk hygiene but later included other public health issues. In 1912, the Children's Bureau was formed and became the primary government agency to work toward improving maternal and infant welfare until 1946, when its role in maternal and child health diminished; the bureau was eliminated in 1969.¹ A proponent of the Children's Bureau was Martha May Eliot. The Children's Bureau defined the problem of infant mortality and shaped the debate over programs to ameliorate the problem. The bureau also advocated comprehensive maternal and infant welfare services, including prenatal, natal, and postpartum home visits by health-care providers. By the 1920s, the integration of these services changed the approach to infant mortality from one that addressed infant health problems to an approach that included infant and mother and prenatal-care programs to educate, monitor, and care for pregnant women.

The discovery and widespread use of antimicrobial agents (e.g., sulfonamide in 1937 and penicillin in the 1940s) and the development of fluid and electrolyte replacement therapy and safe blood transfusions accelerated the declines in infant mortality; from 1930 through 1949, mortality rates declined 52%.⁴ The percentage decline in postneonatal (age 28-364 days) mortality (66%) was greater than the decline in neonatal (age 0-27 days) mortality (40%). From 1950 through 1964, infant mortality declined more slowly.¹ An increasing proportion of infant deaths were attributed to perinatal causes and occurred among high-risk neonates, especially low birth weight (LBW) and preterm babies. Although no reliable data exist, the rapid decline in infant mortality during earlier decades probably was not influenced by decreases in LBW rates because the decrease in mortality was primarily in postneonatal deaths that are less influenced by birthweight. Inadequate programs during the 1950s-1960s to reduce deaths among high-risk neonates led to renewed efforts to improve access to prenatal care, especially for the poor, and to a concentrated effort to establish neonatal intensive-care units and to promote research in maternal and infant health, including research into technologies to improve the survival of LBW and preterm babies.

During the late 1960s, after Medicaid and other federal programs were implemented, infant mortality (primarily postneonatal mortality) declined substantially.⁵ From 1970 to 1979, neonatal mortality plummeted 41% because of technologic advances in neonatal medicine and in the regionalization of perinatal services; postneonatal mortality declined 14%. During the early to mid-1980s, the downward trend in U.S. infant mortality slowed.⁶ However, during 1989-1991, infant mortality declined slightly faster, probably because of the use of artificial pulmonary surfactant to prevent and treat respiratory distress syndrome in premature infants.⁷ During 1991-1997, infant mortality continued to decline primarily because of decreases in sudden infant death syndrome (SIDS) and other causes.

Although improvements in medical care were the main force for declines in infant mortality during the second half of the century, public health actions played a role. During the 1990s, a greater than 50% decline in SIDS rates (attributed to the recommendation that infants be placed to sleep on their backs) has helped to reduce the overall infant mortality rate.⁸ The reduction in vaccine-preventable diseases (e.g., diphtheria, tetanus, measles, poliomyelitis, and Haemophilus influenzae type b meningitis) has reduced infant morbidity and has had a modest effect on infant mortality.⁹ Advances in prenatal diagnosis of severe central nervous system defects, selective termination of affected pregnancies, and improved surgical treatment and management of other structural anomalies have helped reduce infant mortality attributed to these birth defects.^10- 11 National efforts to encourage reproductive-aged women to consume foods or supplements containing folic acid could reduce the incidence of neural tube defects by half.¹²

Maternal mortality rates were highest in this century during 1900-1930.² Poor obstetric education and delivery practices were mainly responsible for the high numbers of maternal deaths, most of which were preventable.² Obstetrics as a speciality was shunned by many physicians, and obstetric care was provided by poorly trained or untrained medical practitioners. Most births occurred at home with the assistance of midwives or general practitioners. Inappropriate and excessive surgical and obstetric interventions (e.g., induction of labor, use of forceps, episiotomy, and cesarean deliveries) were common and increased during the 1920s. Deliveries, including some surgical interventions, were performed without following the principles of asepsis. As a result, 40% of maternal deaths were caused by sepsis (half following delivery and half associated with illegally induced abortion) with the remaining deaths primarily attributed to hemorrhage and toxemia.²

The 1933 White House Conference on Child Health Protection, Fetal, Newborn, and Maternal Mortality and Morbidity report¹³ demonstrated the link between poor aseptic practice, excessive operative deliveries, and high maternal mortality. This and earlier reports focused attention on the state of maternal health and led to calls for action by state medical associations.¹³ During the 1930s-1940s, hospital and state maternal mortality review committees were established. During the ensuing years, institutional practice guidelines and guidelines defining physician qualifications needed for hospital delivery privileges were developed. At the same time, a shift from home to hospital deliveries was occurring throughout the country; during 1938-1948, the proportion of infants born in hospitals increased from 55% to 90%.¹⁴ However, this shift was slow in rural areas and southern states. Safer deliveries in hospitals under aseptic conditions and improved provision of maternal care for the poor by states or voluntary organizations led to decreases in maternal mortality after 1930. Medical advances (including the use of antibiotics, oxytocin to induce labor, and safe blood transfusion and better management of hypertensive conditions during pregnancy) accelerated declines in maternal mortality. During 1939-1948, maternal mortality decreased by 71%.¹⁴ The legalization of induced abortion beginning in the 1960s contributed to an 89% decline in deaths from septic illegal abortions¹⁵ during 1950-1973.

Since 1982, maternal mortality has not declined.¹⁶ However, more than half of maternal deaths can be prevented with existing interventions.¹⁷ In 1997, 327 maternal deaths were reported based on information on death certificates; however, death certificate data underestimate these deaths, and the actual numbers are two to three times greater. The leading causes of maternal death are hemorrhage, including hemorrhage associated with ectopic pregnancy, pregnancy-induced hypertension (toxemia), and embolism.¹⁷

Despite the dramatic decline in infant and maternal mortality during the 20th century, challenges remain. Perhaps the greatest is the persistent difference in maternal and infant health among various racial/ethnic groups, particularly between black and white women and infants. Although overall rates have plummeted, black infants are more than twice as likely to die as white infants; this ratio has increased in recent decades. The higher risk for infant mortality among blacks compared with whites is attributed to higher LBW incidence and preterm births and to a higher risk for death among normal birthweight infants (greater than or equal to 5 lbs, 8 oz [≥2500 g]).¹⁸ American Indian/ Alaska Native infants have higher death rates than white infants because of higher SIDS rates. Hispanics of Puerto Rican origin have higher death rates than white infants because of higher LBW rates.¹⁹ The gap in maternal mortality between black and white women has increased since the early 1900s. During the first decades of the 20th century, black women were twice as likely to die of pregnancy-related complications as white women. Today, black women are more than three times as likely to die as white women.

During the last few decades, the key reason for the decline in neonatal mortality has been the improved rates of survival among LBW babies, not the reduction in the incidence of LBW. The long-term effects of LBW include neurologic disorders, learning disabilities, and delayed development.²⁰ During the 1990s, the increased use of assisted reproductive technology has led to an increase in multiple gestations and a concomitant increase in the preterm delivery and LBW rates.²¹ Therefore, in the coming decades, public health programs will need to address the two leading causes of infant mortality: deaths related to LBW and preterm births and congenital anomalies. Additional substantial decline in neonatal mortality will require effective strategies to reduce LBW and preterm births. This will be especially important in reducing racial/ethnic disparities in the health of infants.

Approximately half of all pregnancies in the United States are unintended, including approximately three quarters among women aged <20 years. Unintended pregnancy is associated with increased morbidity and mortality for the mother and infant. Lifestyle factors (e.g., smoking, drinking alcohol, unsafe sex practices, and poor nutrition) and inadequate intake of foods containing folic acid pose serious health hazards to the mother and fetus and are more common among women with unintended pregnancies. In addition, one fifth of all pregnant women and approximately half of women with unintended pregnancies do not start prenatal care during the first trimester. Effective strategies to reduce unintended pregnancy, to eliminate exposure to unhealthy lifestyle factors, and to ensure that all women begin prenatal care early are important challenges for the next century.

Compared with the 1970s, the 1980s and 1990s have seen a lack of decline in maternal mortality and a slower rate of decline in infant mortality. Some experts consider that the United States may be approaching an irreducible minimum in these areas. However, three factors indicate that this is unlikely. First, scientists have believed that infant and maternal mortality was as low as possible at other times during the century, when the rates were much higher than they are now. Second, the United States has higher maternal and infant mortality rates than other developed countries; it ranks 25th in infant mortality²² and 21st in maternal mortality.²³ Third, most of the U.S. population has infant and maternal mortality rates substantially lower than some racial/ethnic subgroups, and no definable biologic reason has been found to indicate that a minimum has been reached.

To develop effective strategies for the 21st century, studies of the underlying factors that contribute to morbidity and mortality should be conducted. These studies should include efforts to understand not only the biologic factors but also the social, economic, psychological, and environmental factors that contribute to maternal and infant deaths. Researchers are examining "fetal programming"—the effect of uterine environment (e.g., maternal stress, nutrition, and infection) on fetal development and its effect on health from childhood to adulthood. Because reproductive tract infections (e.g., bacterial vaginosis) are associated with preterm birth, development of effective screening and treatment strategies may reduce preterm births. Case reviews or audits are being used increasingly to investigate fetal, infant, and maternal deaths; they focus on identifying preventable deaths such as those resulting from health-care system failures and gaps in quality of care and in access to care. Another strategy is to study cases of severe morbidity in which the woman or infant did not die. More clinically focused than reviews or audits, such "near miss" studies may explain why one woman or infant with a serious problem died while another survived.

A thorough review of the quality of health care and access to care for all women and infants is needed to avoid preventable mortality and morbidity and to develop public health programs that can eliminate racial/ethnic disparities in health. Preconception health services for all women of childbearing age, including healthy women who intend to become pregnant, and quality care during pregnancy, delivery, and the postpartum period are critical elements needed to improve maternal and infant outcomes.

Before conception

During pregnancy

During postpartum period

Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, CDC.

MMWR. 1999;48:832

CDC'S National Immunization Program and the Public Health Training Network will cosponsor a live satellite broadcast, Surveillance of Vaccine-Preventable Diseases (VPDs), on December 2, 1999, from 12 noon to 3:30 p.m. eastern time. The broadcast is intended for physicians, infection control practitioners, epidemiologists, nurses, laboratorians, sanitarians, and others involved in surveillance of VPDs. The program will present guidelines for surveillance, case investigation, and outbreak control for diphtheria, Haemophilus influenzae type b, hepatitis A, influenza, measles, pertussis, rubella, and varicella, and will provide an in-depth discussion of several other issues related to VPD surveillance.

Continuing education credit for a variety of professions will be offered based on 3.5 hours of instruction. Additional information about the broadcast is available on the World-Wide Web at http://www.cdc.gov/phtn/surveillance/vpd.htm.