HICNet Medical News Digest Wed, 15 Dec 1993 Volume 06 : Issue 55 Today's Topics: [MMWR 10 Dec 93] Absence of Reported Measles [MMWR] Infant Mortality [MMWR] Outbreaks of Mycoplasma pneumoniae Respiratory Infection [MMWR] Driver Safety-Belt Use [MMWR] Flood-Related Mortality New Treatment Prevent Respiratory Infection in High Rish Infants +------------------------------------------------+ ! ! ! Health Info-Com Network ! ! Medical Newsletter ! +------------------------------------------------+ Editor: David Dodell, D.M.D. 10250 North 92nd Street, Suite 210, Scottsdale, Arizona 85258-4599 USA Telephone +1 (602) 860-1121 FAX +1 (602) 451-6135 Compilation Copyright 1993 by David Dodell, D.M.D. All rights Reserved. License is hereby granted to republish on electronic media for which no fees are charged, so long as the text of this copyright notice and license are attached intact to any and all republished portion or portions. The Health Info-Com Network Newsletter is distributed biweekly. Articles on a medical nature are welcomed. If you have an article, please contact the editor for information on how to submit it. If you are interested in joining the automated distribution system, please contact the editor. E-Mail Address: Editor: Internet: david@stat.com FidoNet = 1:114/15 Bitnet = ATW1H@ASUACAD LISTSERV = MEDNEWS@ASUACAD.BITNET (or internet: mednews@asuvm.inre.asu.edu) anonymous ftp = vm1.nodak.edu Notification List = hicn-notify-request@stat.com FAX Delivery = Contact Editor for information ---------------------------------------------------------------------- Date: Wed, 15 Dec 93 22:56:40 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR 10 Dec 93] Absence of Reported Measles Message-ID: <6oZmec1w165w@stat.com> Current Trends Absence of Reported Measles -- United States, November 1993 For the first time since measles reporting began in 1912, no measles cases have been reported in the United States for 3 consecutive weeks (November 7-November 27 [weeks 45-47], 1993). In addition, no cases have been reported with onset since September 22 that were not directly linked with importations. Of the provisional total of 277 measles cases reported in 1993 through November 27, a total of 57 persons had onsets of illness since July 4. Of these, 29 (51%) were imported or linked through a continuous chain of transmission to an imported case. Twelve (21%) cases resulted from continued transmission from measles outbreaks that began before July 4. Fourteen (25%) cases could not be linked to an existing outbreak, an international importation, or another reported case and were classified as sporadic index cases. Two cases were epidemiologically linked to these cases. Twelve of the 14 sporadic index cases were laboratory confirmed. Reported by: State and local health depts. National Immunization Program, CDC. Editorial Note: The 3-week period without reported measles cases reflects at least four factors: 1) major increases in measles vaccination coverage levels among preschool-aged children; 2) increased use of a second dose of measles vaccine among school-aged children and young adults attending college; 3) an overall increase in efforts to control measles throughout the Western Hemisphere; and 4) the usual seasonally low incidence of measles during the fall (1,2). Furthermore, the absence of any reported persons with sporadic index cases of measles who had onset after September 22 may reflect a cessation of endemic measles transmission in the United States during this period. The absence of reported endemic foci of measles transmission does not indicate that measles has been eliminated in the United States. In the past, substantial numbers of measles cases were not reported to public health authorities (3). Therefore, surveillance must be intensified to permit the identification and elimination of any remaining foci of transmission. Any case of rash illness suspected to be measles should be reported promptly to public health authorities to enable immediate investigation and vigorous control measures to minimize spread of infection. For each case, laboratory confirmation should be obtained, vaccination status determined, and source of exposure ascertained. Although current measles activity is at its lowest level ever in the United States, previous periods of low activity have been followed by resurgences (4,5). High vaccination coverage levels among preschool- and school-aged children need to be achieved and sustained in all communities to ensure the elimination of endemic measles transmission. References 1. CDC. Measles--United States, first 26 weeks, 1993. MMWR 1993;42:813-6. 2. Pan American Health Organization. Central America: defeating measles. EPI Newsletter 1993;XV(5):2-3. 3. Davis SF, Strebel PM, Atkinson WL, et al. Reporting efficiency during a measles outbreak in New York City, 1991. Am J Public Health 1993;83: 1011-5. 4. CDC. Measles--United States, 1982. MMWR 1983;32:49-51. 5. Atkinson WL, Orenstein WA, Krugman S. The resurgence of measles in the United States, 1989-90. Annu Rev Med 1992;43:451-63. ------------------------------ Date: Wed, 15 Dec 93 22:57:11 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Infant Mortality Message-ID: <1PZmec2w165w@stat.com> Current Trends Infant Mortality -- United States, 1991 The final infant (less than 1 year of age) mortality rate for the United States for 1991--8.9 infant deaths per 1000 live births--was the lowest rate ever recorded and represented a decrease of 3% from the rate of 9.2 for 1990 (Figure 1). Based on provisional data, the trend of declining infant mortality continued through 1992 (rate: 8.5) (1). Infant mortality rates varied by race; race reflected differing distributions of several risk factors for infant death (e.g., low birthweight [LBW] [less than 2500 g (5 lbs 9 oz) at birth]) and is useful for identifying groups at greatest risk for infant death. This report uses race-specific information from birth and death certificates compiled by CDC's National Center for Health Statistics' Vital Statistics System (2) to characterize infant mortality in 1991 and compares findings with those for 1990. In this report, cause-of-death statistics are based on the underlying cause of death* reported on the death certificate by the attending physician, medical examiner, or coroner in a manner specified by the World Health Organization. Race for infants who died was tabulated by race of infant; race for live births (which comprise the denominator of infant mortality rates) was tabulated by race of mother. Rates are presented only for black and white infants because the Linked Birth/Infant Death Data Set (used to more accurately estimate infant mortality rates for other racial groups) was not available for 1990 and 1991. A total of 36,766 infants died during 1991, compared with 38,351 during 1990. The mortality rate for white** infants in 1991 (7.3 per 1000) decreased 4% from the rate in 1990 (7.6); for black** infants, the difference between the rates for 1990 and 1991 was not statistically significant (18.0 and 17.6, respectively). From 1990 to 1991, the neonatal (less than 28 days of age) mortality rate decreased 3% (5.8 to 5.6 per 1000). For white infants, the rate decreased from 4.8 to 4.5 and for black infants, from 11.6 to 11.2. The postneonatal (28 days-11 months of age) mortality rate remained constant at 3.4 in 1990 and 1991. From 1990 to 1991, the infant mortality rate decreased for six of the 10 leading causes of infant death and increased for three causes (Table 1). The largest decreases were for intrauterine hypoxia and birth asphyxia (International Classification of Diseases, Ninth Revision [ICD-9], code 768) (20%), respiratory distress syndrome (RDS) (ICD-9 code 769) (9%), and congenital anomalies (ICD-9 codes 740-759) and newborn affected by maternal complications of pregnancy (ICD-9 code 761) (6% each). The increases were for disorders relating to short gestation and unspecified LBW (ICD-9 code 765) (4%), accidents*** and adverse effects (ICD-9 codes E800-E949) (4%), and infections specific to the perinatal period (ICD-9 code 771) (2%). The rank order of the 10 leading causes of infant death differed by race (Table 1). Although the first four leading causes of death were the same for white and black infants, their rank ordering differed; these same four causes accounted for 56% and 50% of all deaths among white and black infants, respectively. For white infants, the leading cause of death was congenital anomalies, which accounted for 25% of all deaths among white infants; for black infants, the leading cause of death was disorders relating to short gestation and unspecified LBW, which accounted for 16% of all deaths among black infants. In 1991, the risk for dying during the first year of life was 2.4 times greater for black than for white infants. For each of the leading causes of death, the risk for death was higher for black than for white infants, although there were large variations in the magnitude of the excess by cause. The cause-specific ratios were highest for disorders relating to short gestation and unspecified LBW (4.4:1), pneumonia and influenza (ICD-9 codes 480-487) (3.2:1), RDS (2.6:1), infections specific to the perinatal period (2.6:1), and newborn affected by maternal complications of pregnancy (2.5:1). The ratios were lowest for sudden infant death syndrome (SIDS) (ICD-9 code 798.0); newborn affected by complications of placenta, cord, and membranes (ICD-9 code 762); and accidents and adverse effects (2.1:1 each) and congenital anomalies (1.2:1). Three of the 10 leading causes of infant death accounted for 42% of the difference in infant mortality between black and white infants: disorders relating to short gestation and unspecified LBW (22%), SIDS (12%), and RDS (8%). Reported by: Mortality Statistics Br, Div of Vital Statistics, National Center for Health Statistics, CDC. Editorial Note: The infant mortality rate--a standard index of health--is higher in the United States than in many other developed countries. In 1989 (the most recent year for which comparative data are available), the U.S. infant mortality rate ranked 24th among countries or geographic areas with a population of at least 1 million (3), a decline in rank from 1980 (20th) (4). The U.S. infant mortality rate declined by approximately 5% per year during the 1970s, but slowed to an annual average decrease of 3% during the 1980s. The decline of 6% from 1989 to 1990 primarily reflected a 24% decrease in mortality from RDS. From 1990 to 1991, the infant mortality rate declined by 3%; more than half of this decrease represented declines in mortality from congenital anomalies (35%) and RDS (19%). The decline in mortality from congenital anomalies (6% overall) was primarily among whites; mortality from congenital anomalies remained constant among blacks. Shifts in the age distribution of mothers between 1990 and 1991 may account for some of the decline in mortality from congenital anomalies (5). The decline in mortality from 1990 to 1991 from RDS may reflect improvements in medical management of this condition (6). Differences in infant mortality rates by race may reflect differences in factors such as socioeconomic status, access to medical care, and the prevalence of specific risks. For example, the mortality rate is substantially higher for infants born to mothers of low socioeconomic status (7). In 1990, nearly three times as many black as white infants (56% versus 20%) were members of families with incomes below the poverty level (Bureau of the Census, unpublished data, 1992). In addition, because of income differentials, a lower proportion of black women have health insurance that covers the costs of adequate care for pregnancy and childbirth (6,8). LBW is an important intermediate variable between some risk factors and infant mortality. In 1987 (the most recent year for which such data were available), 6.9% of infants were born with LBW; however, 61% of all infant deaths occurred among these infants. In 1991, 13.6% of black infants were born with LBW, compared with 5.8% of white infants (6). Most of the causes of death for which black infants are at substantially elevated risk for death are closely associated with LBW. For three of the four causes of infant death characterized by the highest ratios of black-to-white mortality rates (i.e., disorders relating to short gestation and unspecified LBW, RDS, and newborn affected by maternal complications of pregnancy), approximately 95% of the deaths in 1987 occurred among LBW infants (CDC, unpublished data, 1992). The 1990 national health objective to reduce the overall infant mortality rate to 9.0 deaths per 1000 live births (9) was achieved in 1991 (recorded rate: 8.9). A year 2000 national health objective is to reduce the overall infant mortality rate to no more than 7.0 per 1000 live births (objective 14.1) (9). This objective can be achieved by sustaining an average annual decrease of at least 2.4% for the total population. Strategies to achieve the national health objective for reducing infant mortality should consider the heterogeneity of factors accounting for infant mortality in the United States. For example, reducing mortality from disorders related to short gestation and unspecified LBW will require both improved access to adequate prenatal care and understanding of etiologic risk factors for preterm delivery; reduction of deaths related to maternal complications of pregnancy will require both expansion of access to prenatal care and assessment of the adequacy of the content of care (10). Efforts to address these and other heterogenous risk factors may increase the likelihood of achieving the year 2000 national health objective to reduce infant mortality. References 1. NCHS. Annual summary of births, marriages, divorces, and deaths: United States, 1992. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1993. (Monthly vital statistics report; vol 41, no. 13). 2. NCHS. Advance report of final mortality statistics, 1991. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1993. (Monthly vital statistics report; vol 42, no. 2, suppl). 3. NCHS. Health, United States, 1992. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1993; DHHS publication no. (PHS)93-1232. 4. NCHS. Health, United States, 1988. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1989; DHHS publication no. (PHS)89-1232. 5. NCHS. Advance report of final natality statistics, 1991. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1993. (Monthly vital statistics report; vol 42, no. 3, suppl). 6. Long W, Corbet A, Cotton R, et al. A controlled trial of synthetic surfactant in infants weighing 1250 g or more with respiratory distress syndrome. N Engl J Med 1991;325:1696-703. 7. Gould JB, Davey B, LeRoy S. Socioeconomic differentials and neonatal mortality: racial comparison of California singletons. Pediatrics 1989;83:181- 6. 8. Alan Guttmacher Institute. Blessed events and the bottom line: financing maternity care in the United States. New York: Alan Guttmacher Institute, 1987. 9. Public Health Service. Healthy people 2000: national health promotion and disease prevention objectives--full report, with commentary. Washington, DC: US Department of Health and Human Services, Public Health Service, 1991; DHHS publication no. (PHS)91-50212. 10. Public Health Service. Caring for our future: the content of prenatal care--a report of the Public Health Service Expert Panel on the Content of Prenatal Care. Washington, DC: US Department of Health and Human Services, Public Health Service, 1989. *Defined by the World Health Organization's International Classification of Diseases, Ninth Revision (ICD-9), as "(a) the disease or injury which initiated the train of morbid events leading directly to death, or (b) the circumstances of the accident or violence which produced the fatal injury." **Includes Hispanic and non-Hispanic infants. ***When a death occurs under "accidental" circumstances, the preferred term within the public health community is "unintentional injury." ------------------------------ Date: Wed, 15 Dec 93 22:58:01 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Outbreaks of Mycoplasma pneumoniae Respiratory Infection Message-ID: Epidemiologic Notes and Reports Outbreaks of Mycoplasma pneumoniae Respiratory Infection -- Ohio, Texas, and New York, 1993 From June through November 1993, three outbreaks of acute respiratory illness (ARI) occurred in institutional settings in Ohio, Texas, and New York. This report summarizes investigations by state and local public health officials, military personnel, and CDC, which indicate that Mycoplasma pneumoniae was the cause of these outbreaks. Ohio From June 15 through September 5, ARI characterized by acute onset of cough and fever occurred among 47 (12%) of 403 staff members and clients of a sheltered workshop for developmentally disabled adults in Ohio (Figure 1). The median age of patients was 35 years (range: 20-60 years); seven (15%) required hospitalization, and 31 (66%) had radiographic evidence of pneumonia. Thirty-eight persons had laboratory evidence of Mycoplasma infection: all had convalescent-phase serum antibody titers for Mycoplasma greater than or equal to 32 by complement fixation (CF), 22 (58%) had CF titers of greater than or equal to 128, and four (11%) had a fourfold rise in CF titers. M. pneumoniae was isolated from nasopharyngeal secretions of two of eight patients with available specimens. Serologic and microbiologic studies were negative for acute viral and non-Mycoplasma bacterial infections. Although no deaths occurred among persons with laboratory-confirmed cases, one workshop participant who had not been evaluated for Mycoplasma infection died on June 30 from complications of pneumonia. Beginning August 6, persons with ARI were excluded from work until completion of at least 3 days of antimicrobial therapy. No cases of M. pneumoniae have been identified since September 5. Texas From August 1 through November 14, a total of 215 cases of ARI occurred among staff members at a 4500-employee tertiary-care center in southern Texas. Illnesses were characterized by abrupt onset of headache, shaking chills, and severe myalgias, followed by fever and cough. The median age of patients was 32 years (range: 19-70 years); 43 (20%) had radiographic evidence of pneumonia, and five (2%) required hospitalization. Of 58 patients for whom paired serum specimens were available, convalescent-phase antibody titers by CF for Mycoplasma were greater than or equal to 32 for 47 (81%); fourfold rises in CF antibody titers occurred in 12 (21%). Immunoblot studies in five patients demonstrated antibody to M. pneumoniae in convalescent-phase serum specimens. Serologic and microbiologic tests were negative for acute viral and non-Mycoplasma bacterial infections. The most recent radiographically confirmed case of pneumonia occurred on November 8. Laboratory confirmation of other ARI cases is pending. New York On October 6, the New York State Department of Health initiated an investigation of ARI among clients and employees of an autism program in a residential developmental center in upstate New York. From August 1 through October 26, 48 cases (25%) of ARI or acute otitis media were identified among the 189 employees and clients of the program. The median age of affected persons was 33 years (range: 12-61 years). Three patients (6%) were hospitalized, 11 (23%) had radiographic evidence of pneumonia, and two (4%) had bullous myringitis. M. pneumoniae was isolated from oropharyngeal secretions of two of five patients with available specimens. Of six patients with serum specimens available, CF convalescent-phase antibody titers were greater than or equal to 64 in two. Serologic and microbiologic tests were negative for acute viral and non-Mycoplasma bacterial infections. From October 7 through November 10, contact between clients and employees of the autism program and the other sections of the center was restricted. The most recent patient had onset of illness on October 26. Reported by: L Smyth, S Swope, DO, L Wiser, GT Reed, DVM, Warren County Combined Health District, Lebanon; ED Peterson, RA French, MPA, FW Smith, MD, TJ Halpin, MD, State Epidemiologist, PJ Somani, MD, Director of Health, Ohio Dept of Health. M Emig, MD, RR Liu, MD, K Storms, GP Melcher, MD, MJ Dolan, MD, United States Air Force; J Schuermann, DM Simpson, MD, State Epidemiologist, Texas Dept of Health. SF Kondracki, CK Csiza, PhD, RA Duncan, MS, GS Birkhead, MD, DL Morse, MD, State Epidemiologist, New York State 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: M. pneumoniae is a common cause of acute upper and lower respiratory infection in children and young adults. Infections with M. pneumoniae occur sporadically throughout the year, and outbreaks are most common during the fall, typically in 4-7-year cycles (1). However, the findings in this report suggest a potential increase in the occurrence of M. pneumoniae infections this winter. Transmission of M. pneumoniae infections probably occurs through close contact with contaminated respiratory droplets (2). The investigations in Ohio, Texas, and New York indicate that epidemics spanning several months may occur in institutional settings where prolonged contact is common (2,3). The incubation period for this pathogen (16-32 days) (4) may contribute to protracted duration of epidemics and may limit the effectiveness of cohorting as a measure for controlling outbreaks. The precise incidence of Mycoplasma infection is unknown because surveillance is not conducted, and laboratory confirmation is usually not obtained. However, prospective studies suggest that M. pneumoniae accounts for 15%-20% of community-acquired lower respiratory infection in adults (1,5). Approximately 20% of infections are asymptomatic; symptomatic disease is typically mild and is characterized by nonproductive cough, fever, malaise, and pharyngitis (6). Other features include myalgias (45%) and otalgia (31%); 3%-13% of patients infected with M. pneumoniae develop pneumonia (4,6). Less common complications include adult respiratory distress syndrome, pericarditis, myocarditis, hemolytic anemia, and encephalitis (1). Macrolides or tetracycline are the antimicrobials of choice for M. pneumoniae infections; however, treatment does not eradicate carriage of the organism (7). The efficacy of prophylactic antimicrobial use in outbreak settings is undetermined. Distinguishing M. pneumoniae from other causes of acute respiratory infection is difficult because of a lack of reliable, widely available, rapid diagnostic tests. Definitive diagnosis requires isolation of Mycoplasma or a fourfold rise in CF antibody titers between acute- and convalescent-phase serum specimens, ideally obtained 2-3 weeks apart (8). Isolation of this organism can be difficult and may require up to 6 weeks (9). Although single, elevated CF titers can be useful in identifying cases in epidemiologic investigations, they are of limited usefulness for clinical diagnosis. Cold agglutinins may be present in the acute serum of 30%-60% of patients; however, this finding is nonspecific and is not useful for diagnostic purposes (8). Rapid, direct assays of respiratory secretions are being evaluated but are not widely available commercially (9). M. pneumoniae should be considered in patients with acute respiratory illnesses, especially if associated with failure to improve when patients are treated with beta-lactam antibiotics. Persistence of the organism in respiratory secretions, despite appropriate antimicrobial therapy, may limit the usefulness of short-term cohorting during outbreaks. Prompt recognition of outbreaks in institutional settings, combined with cohorting of symptomatic patients when feasible, may avert morbidity. References 1. Foy HM. Infections caused by Mycoplasma pneumoniae and possible carrier state in a different population of patients. Clin Infect Dis 1993;17(suppl):S37-S46. 2. Steinberg P, White RJ, Fuld SL, Gutekunst RR, Chanock RM, Senterfit LB. Ecology of Mycoplasma pneumoniae infections in Marine recruits at Parris Island, South Carolina. Am J Epidemiol 1969;89:62-73. 3. Fernald GW, Clyde WA Jr. Epidemic pneumonia in university students. J Adolesc Health Care 1989;10:520-6. 4. Foy HM, Grayston JT, Kenny G, et al. Epidemiology of Mycoplasma pneumoniae infection in families. JAMA 1966;197:859-66. 5. Marston BJ, Plouffe JF, Breiman RF, et al. Preliminary findings of a community-based pneumonia incidence study. In: Barbaree JM, Breiman RF, Dufour AP, eds. Legionella: current status and emerging perspectives. Washington, DC: American Society for Microbiology, 1993:36-7. 6. Clyde WA Jr. Clinical overview of typical Mycoplasma pneumoniae infections. Clin Infect Dis 1993;17(suppl):S32-S36. 7. McCormick WM. Susceptibility of Mycoplasmas to antimicrobial agents: clinical implications. Clin Infect Dis 1993;17(suppl):S200-S201. 8. Jacobs E. Serological diagnosis of Mycoplasma pneumoniae infections: a critical review of current procedures. Clin Infect Dis 1993;17(suppl):S79-S82. 9. Marmion BP, Williamson J, Worswick DA, Kok T-W, Harris RJ. Experience with newer techniques for the laboratory detection of Mycoplasma pneumoniae infection: Adelaide 1978-1992. Clin Infect Dis 1993;17(suppl):S90-S99. ------------------------------ Date: Wed, 15 Dec 93 22:58:35 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Driver Safety-Belt Use Message-ID: International Notes Driver Safety-Belt Use -- Budapest, Hungary, 1993 An estimated 300,000 persons die and 10-15 million persons are injured each year in traffic crashes throughout the world (1). Safety-belt use is one of the most effective means of reducing the number and severity of injuries in motor-vehicle crashes (2). In Hungary, front-seat occupants of all motor vehicles have been required to use safety belts since 1976. Since March 1993, rear-seat passengers have been required to wear safety belts in nonurban areas. Drivers in violation of the law are subject to fines and potential suspension of driving privileges. To evaluate driver compliance with the safety-belt use law, on May 10, 1993, CDC conducted an observational prevalence survey of safety-belt use in Budapest in conjunction with the U.S. Department of State and the American International School of Budapest; this survey was performed in collaboration with the Hungarian Ministry of Transport, Communication, and Water Management and the Budapest Police Department. This report presents findings of the study. Driver lap/shoulder safety-belt use was observed at seven moderate-to high-volume traffic sites in Budapest (1993 estimated population: 2,009,000). Sites were selected to reduce repetitive counting of observed vehicles. Pairs of pretrained high school students from the American International School collected information between 4:30 p.m. and 6 p.m. by observing vehicles at intersections convenient and safe for the students and by using a standardized form to record driver's safety-belt use, sex, and the type of vehicle (Eastern European or non-Eastern European [i.e., any cars not manufactured in the former Warsaw Pact countries]). Drivers of taxis (who are not required to wear safety belts) were included; drivers of buses, trucks, farm machinery, and motorcycles were excluded. Data differentiating taxis from other vehicles were not systematically recorded. A total of 4894 eligible vehicles were included in the survey. Of the drivers, 3850 (79%) were male. The overall belt-use rate was 61%; however, the percentage of drivers using safety belts varied by observation site (range: 58%-65%). The prevalence of safety-belt use was higher among female (64%) than male (60%) drivers (prevalence ratio [PR]=1.03; 95% confidence interval [CI]=1.00-1.06). Fifty percent of the vehicles were non-Eastern European models; drivers of Eastern European vehicles were more likely to use safety belts than drivers of non-Eastern European vehicles (65% versus 57%) (PR=1.2; 95% CI=1.1-1.3). Safety-belt use was higher among both female and male drivers of Eastern European vehicles (68% [95% CI=64%-72%] and 64% [95% CI=62%-66%], respectively) than among female and male drivers of non-Eastern European vehicles (59% [95% CI=55%-63%] and 56% [95% CI=54%-58%], respectively). Reported by: LE Cohen, Environment, Science, and Technology Attache, MD Laude, Fascell Fellow, US Embassy, Dept of State, Budapest; G Csaszar, Div of Roads and Road Transport, Ministry of Transport, Communication, and Water Management; E Komaromi, Dept of Prevention, Budapest Police Dept; FL Wassersug, Student Services, American International School of Budapest. Air Pollution and Respiratory Health Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health; National Center for Injury Prevention and Control, CDC. Editorial Note: Safety-belt use legislation, first introduced in Australia in 1970, is the most effective means of increasing safety-belt use in many countries (3). At least 35 countries require safety-belt use (4). In the United States, safety-belt use is mandatory in 44 states. The only U.S. jurisdictions that have enacted legislation similar to that in Hungary-- allowing primary enforcement of safety-belt use in all seating positions--are Oregon, California, American Samoa, and the Mariana Islands. When compared with secondary enforcement laws, implementation of primary enforcement laws appears to result in greater and more rapid and sustained increases in safety- belt use (5). Observations in this study indicate that by May 1993, the prevalence of safety-belt use by drivers had increased from that documented by the Ministry of Transport, Communication, and Water Management in October 1992 (6). In that study, 31% of front-seat occupants (both drivers and passengers) were belted (6); however, only 40% of cars had a front-seat passenger. Although recent changes in the safety-belt use law in Hungary have targeted persons in rear- seat positions, increased use of safety belts among drivers may reflect three factors: 1) recent increases in fines, 2) stricter police enforcement of the law since April 1, 1993, and 3) increased public awareness generated by the media, which during April 1993 routinely broadcast information about the changes in the law. The findings in this report are subject to at least three limitations. First, because many Eastern European vehicles have nonretractable lap/shoulder belts, some drivers of these vehicles may have been categorized as belted when they may have placed the belts across their shoulders and laps without buckling them. Second, this survey also included taxi drivers, who are not required to wear safety belts, and data differentiating taxis from other vehicles were not systematically gathered. Therefore, the percentage of drivers subject to the law who were in compliance was greater than 61%. Third, other potential sources of bias in the interpretation of the data from this study include lack of random selection of observation sites, restriction of observations to the commuting hour on a single day, and the highly urbanized environment in which the observations were made. In Hungary, traffic crashes were the second leading cause of violent deaths (after suicide) in 1992, resulting in 2346 deaths (7). Although the number of deaths that could have been prevented by safety-belt use has not been determined, the crude mortality rate for motor-vehicle crashes decreased 9% in the month after the safety-belt use law was expanded (Ministry of Transport, Communication, and Water Management, unpublished data, 1993). To increase safety-belt use, law enforcement officials in Budapest plan to widely disseminate the results of this study on television and are considering a campaign of expanded and long-term enforcement of the safety-belt law, with initial emphasis on low safety-belt use locations identified by this study. References 1. Ross A, Baguley C, Hills B, McDonald M, Silcock D. Towards safer roads in developing countries: a guide for planners and engineers. Crowthorne, England: Transport and Road Research Laboratory, 1991. 2. Chorba TL. Assessing technology for preventing injuries in motor vehicle crashes. Int J Technol Assess Health Care 1991;7:296-314. 3. Vaaje T. Safety belt usage laws in various countries. In: Effectiveness of safety belt use laws: a multinational examination. Washington, DC: US Department of Transportation, National Highway Traffic Safety Administration, 1986:13-23; publication no. DOT-HS-807-018. 4. El-Nour S, Mufti MH. Seat belt legislation and the experience of the world. Journal of Traffic Medicine 1992;20:83-90. 5. Escobedo LG, Chorba TL, Remington PL, Anda RF, Sanderson L, Zaidi AA. The influence of safety belt laws on self-reported safety belt use in the United States. Accid Anal Prev 1992;24:643-53. 6. Kozlekedesi Hirkozlesi es Vizugyi Miniszterium [Ministry of Transport, Communication, and Water Management]. Szemelygepkocsik biztonsagi oveinek viselesi aranyai [Frequency of safety belt use in passenger cars]. Budapest: Technischer Uberwachungs Verein Hannover Kft., 1992. 7. Kozponti Statisztikai Hivatal [Central Statistical Office]. Kozlekedesi balesetek [Transport accidents]. Budapest: Agria Kiado Kft., 1991. ------------------------------ Date: Wed, 15 Dec 93 22:59:13 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Flood-Related Mortality Message-ID: Epidemiologic Notes and Reports Flood-Related Mortality -- Missouri, 1993 Public health surveillance documented the impact of flood-related morbidity following the floods in the midwestern United States during the summer of 1993 (1,2). Because of extensive flooding of the Missouri and Mississippi rivers and their tributaries, the Missouri Department of Health (MDH) initiated surveillance to monitor flood-related mortality. This report summarizes epidemiologic information about deaths in Missouri that resulted from riverine flooding and flash flooding during the summer and fall of 1993. To identify flood-related deaths, CDC and MDH telephoned and obtained epidemiologic information from medical examiners and coroners (ME/Cs) in the 71 disaster-declared counties and in St. Louis (1990 combined population: 4,166,122) and contacted coroners of 24 counties adjacent to disaster-affected areas (1990 combined population: 435,127). A flood-related death was defined as a death resulting from an event that occurred after June 28 (when flash floods began to occur and the potential threat of riverine flooding was recognized by the State Emergency Management Agency) and would not have happened--given the information provided by ME/Cs--had the floods not occurred. Summer Flood-Related Mortality From July 1 through August 31, ME/Cs from disaster-declared counties classified 27 deaths as flood-related. Decedents' ages ranged from 9 years to 88 years (mean: 37.8 years); 18 (67%) were male. No flood-related deaths were reported in adjacent counties. Of the 27 deaths, 21 were directly related to the floods and resulted from drowning; six were indirectly related to the floods (i.e., flood-related activity with no direct physical contact with flood water). Thirteen of the 27 deaths were motor-vehicle-related (i.e., associated with operating or riding in a motor vehicle). Of the 16 (59%) deaths directly related to flash flooding, 14 resulted from drowning; of these, eight deaths occurred in four separate motor-vehicle-related incidents. Of the 11 (41%) deaths directly related to riverine flooding, seven resulted from drowning; of these, three deaths occurred in separate motor-vehicle-related incidents. Of the six deaths indirectly related to the floods, two each were attributed to electrocutions that occurred during cleaning efforts in or while reentering a flooded residence or business, stress-induced cardiac arrests, and trauma from motor- vehicle crashes in which usual traffic patterns were diverted because of rising water. Of the 21 drownings, 10 were associated with recreational activities. Six drownings occurred in one incident when a flash flood inundated a cave in which the victims were exploring, and four drownings occurred in separate incidents associated with riverine flooding. Fall Flood-Related Mortality Flooding from heavy rains that occurred periodically from late September through early November contributed to 16 additional deaths: 14 were motor- vehicle-related, and two occurred when rising waters from the Missouri River flooded homes. Four deaths were associated with the Missouri River and 12 with smaller rivers or creeks. Reported by: HD Donnell, Jr, MD, State Epidemiologist, R Hamm, MD, Office of Epidemiology, Missouri Dept of Health. Emergency Response and Coordination Group, and Disaster Assessment and Epidemiology Section, Health Studies Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health, CDC. Editorial Note: Patterns of flood-related mortality vary according to flood type as determined by hydrologic characteristics (3). Flash floods, characterized by high-velocity streamflow and short warning and response times, have the greatest potential for causing death. In contrast, because riverine floods usually are caused by gradual accumulation of heavy rainfall, warning times are sufficient to allow safe evacuation of nearby communities. In Missouri, both flash flooding and riverine flooding occurred almost simultaneously on two major rivers and on other smaller rivers and creeks. During the summer and fall floods of 1993 in Missouri, drowning was the leading cause of flood-related deaths--similar to other hydrologic disasters (3-6). Furthermore, a large proportion of flood-related drownings have been attributed to operating or occupying motor vehicles, particularly during flash floods. This may reflect motorists' misconception that motor vehicles can provide adequate protection from rising or swiftly moving flood waters. In this report, 75% (27/36) of the drownings that occurred during the summer and fall floods in Missouri were motor-vehicle-related. The findings in this report underscore the importance of two strategies for preventing flood-related injuries and death. First, information about flood and post-flood hazards must be disseminated rapidly and widely to groups at increased risk for injury. For example, motorists should be warned not to drive through areas inundated by flash floods, not to enter swiftly moving water, and that only 2 feet of water can carry away most automobiles (7). In addition, recreational activities, such as wading or bicycling, in flooded areas should be discouraged. Second, hydrologic studies and hazard analyses should address potentially flood-prone tributaries. The hazard potential of such areas during flash floods should be identified, and appropriate warning signs should be posted. MDH is continuing surveillance of flood-related mortality to monitor circumstances of death. References 1. CDC. Public health consequences of a flood disaster--Iowa, 1993. MMWR 1993;42:653-6. 2. CDC. Morbidity surveillance following the Midwest flood--Missouri, 1993. MMWR 1993; 42:797-8. 3. French JG. Floods. In: Gregg MB, ed. The public health consequences of disasters. Atlanta: US Department of Health and Human Services, Public Health Service, CDC, 1989:39-49. 4. French JG, Ing R, Von Allmen S, Wood R. Mortality from flash floods: a review of National Weather Service reports, 1969-81. Public Health Rep 1983;98:584-8. 5. Duclos P, Vidonne O, Beuf P, Perray P, Stoebner A. Flash flood disaster --Nimes, France, 1988. Eur J Epidemiol 1991;7:365-71. 6. Wintemute GJ, Kraus JF, Teret SP, Wright MA. Death resulting from motor vehicle immersions: the nature of the injuries, personal and environmental contributing factors, and potential interventions. Am J Public Health 1990;80:1068-70. 7. National Weather Service/American Red Cross/Federal Emergency Management Agency. Flash floods and floods...the awesome power!: a preparedness guide. Washington, DC: US Department of Commerce, National Oceanic and Atmospheric Administration, National Weather Service/American Red Cross, 1992; report no. NOAA/PA 92050, ARC 4493. ------------------------------ Date: Wed, 15 Dec 93 22:59:57 MST From: mednews (HICNet Medical News) To: hicnews Subject: New Treatment Prevent Respiratory Infection in High Rish Infants Message-ID: NATIONAL INSTITUTES OF HEALTH National Institute of Allergy and Infectious Diseases November 17, 1993 Hope for High-Risk Infants: New Treatment Safe, Effective in Preventing Dangerous Respiratory Infection An experimental therapy can safely protect high-risk infants from the severe and sometimes fatal complications of a common viral infection of the respiratory tract, according to a study supported by the National Institute of Allergy and Infectious Diseases (NIAID), the National Center for Research Resources' General Clinical Research Centers at the University of Colorado and the University of Rochester, and MedImmune, Inc. The study findings suggest that babies born prematurely or with certain heart or lung problems can be protected against severe symptoms of respiratory syncytial virus (RSV) infection and associated hospital care by receiving a solution rich in RSV-fighting antibodies. RSV is the leading cause of early childhood pneumonia and bronchiolitis (wheezy bronchitis) in the United States. "Although almost everyone gets infected with RSV, the disease's real impact is on the most vulnerable of babies," says Anthony S. Fauci, M.D., NIAID director. "These new findings and their promise of keeping high-risk infants healthy and out of the hospital are an important advance in our ongoing effort to improve the health of all children." Jessie R. Groothuis, M.D., of the University of Colorado School of Medicine and The Children's Hospital in Denver directed the study, which appears in the Nov. 18 The New England Journal of Medicine. Of all U.S.-born infants, five to 10 of every 1,000 require hospitalization for the most severe forms of RSV illness -- pneumonia or bronchiolitis. Infants at high risk for long-term RSV-related illness or death include those with certain forms of congenital heart disease or bronchopulmonary dysplasia (BPD), a chronic disease of the airways seen most often in premature infants previously on ventilators. Annually, RSV causes an estimated 2,000 to 5,000 deaths and 90,000 hospitalizations as well as causing long-term lung complications. The new treatment, called RSV-enriched intravenous immunoglobulin (RSVIG), uses antibodies extracted from the blood of volunteers, such as pediatric nurses, who have been exposed to RSV and have high RSV antibody levels. In a process known as passive immunization, infants are infused with these antibodies during a two-hour period. In contrast, conventional or active immunization uses a vaccine to stimulate a patient's own immune system to produce antibodies. For the study, Dr. Groothuis and her colleagues enrolled 249 children born prematurely with or without BPD or congenital heart disease at high-risk baby clinics in Denver, Boston, Washington D.C., Rochester and Buffalo. Children received monthly treatments of RSVIG in one of two doses, 750 or 150 milligrams (mg.) per kilogram (kg.) of body weight, or no drug. The investigators did not know what a child received until the study ended. Each child received treatments over one RSV season, which runs from December to April in the United States, and was monitored closely in a second season. Children treated with 750 mg./kg. of RSVIG experienced a 63 percent reduction in lower respiratory tract infections, a 63 percent reduction in days in the hospital and a 97 percent reduction in days in intensive care units, as compared with children who did not receive RSVIG. Although they spent fewer days in intensive care units, children receiving the 150 mg./kg. of RSVIG otherwise did little better in terms of RSV-related symptoms and outcomes than those receiving no RSVIG treatment. The children tolerated RSVIG well during the study: adverse reactions occurred in only 3 percent of patients. Side effects included a transient accumulation of fluid in the lungs, a mild decrease in blood oxygen levels and fever. Six deaths occurred during the three-year study period, none of which were linked to the treatment. "Because there is no vaccine for RSV and treatment options for this disease are limited, RSVIG therapy currently offers the only opportunity to protect high-risk babies against serious RSV illness," says Dr. Groothuis. "This study suggests that RSVIG offers safe and effective protection for infants and children at risk for serious RSV infections. RSVIG therapy also may help reduce the financial burden of managing RSV infections by reducing the number and length of hospital stays and time spent in intensive care units by these medically fragile infants." RSV spreads readily through the air in tiny droplets when an infected person exhales, coughs or sneezes. RSV can live on surfaces up to 45 minutes, and individuals can become infected if they touch their eyes or nose after touching a contaminated surface, such as table tops, doorknobs, tissues or toys. The ease of transmission of RSV means that in settings such as large families, day-care centers and pediatric wards virtually everyone becomes infected during an RSV outbreak. Adults and older children usually suffer only mild symptoms akin to those of the common cold: sniffling, coughing and sore throat. But for babies younger than 1 year, especially those born close to or during RSV season, RSV infection can cause serious and sometimes deadly consequences. RSV's initial cold-like symptoms, with or without low-grade fever, may progress to severe coughing and wheezing. Such symptoms can quickly exhaust a baby, particularly premature and other high-risk infants, says Dr. Groothuis. Ear infections may develop as a secondary complication, and sometimes babies will refuse feeding, adding to their weakness. Also, a child's airways can become obstructed, and the sickest of these babies may be unable to breathe on their own. Within two to three days of the onset of symptoms, some children may require mechanical ventilators to assist them in breathing. One previous study found that 37 percent of babies with congenital heart disease and serious RSV infection died compared with 1.5 percent of healthy children with RSV. However, even babies who recover from RSV illness in the lower respiratory tract may suffer a long-term reduction of lung function. Researchers have found that children who have serious RSV infections as infants can develop persistent lung abnormalities as well as a greater tendency toward coughing, wheezing and asthma as long as seven to 10 years later. ------------------------------ End of HICNet Medical News Digest V06 Issue #55 ***********************************************