------------------------------ Date: Mon, 02 Jan 95 22:25:26 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: [MMWR] Hantavirus Pulmonary Syndrome Message-ID: <4k8Byc3w165w@stat.com> Hantavirus Pulmonary Syndrome -- Virginia, 1993 Hantavirus pulmonary syndrome (HPS) was first recognized in June 1993 as a result of the investigation of a cluster of fatal cases of adult respiratory distress syndrome (ARDS) in the southwestern United States (1). During that month, a 61-year-old man was admitted to a hospital in southern Pennsylvania with ARDS; recent testing of all available specimens from this patient has confirmed the diagnosis of HPS. This report summarizes the case investigation. When hospitalized on June 28, 1993, the man reported a 4-day history of fever, chills, headache, myalgia, nausea, vomiting, and diarrhea. After admission, he became hypotensive and increasingly short of breath and was transferred to a tertiary-care medical center. Laboratory findings included leukocytosis (white blood cell count 25,300/mm3), hemoconcentration (hemoglobin of 20.0 g/L), thrombocytopenia (platelet count 65,000/mm3), and elevated blood urea nitrogen, creatinine (peak value 6.8 ug/dL), prothrombin time, activated partial thromboplastin time, aspartate aminotransferase (peak value 8500 U/L), lactic dehydrogenase, and lipase levels. A chest radiograph indicated bilateral diffuse infiltrates. During his prolonged hospital course, he required respiratory and circulatory support and hemodialysis. He was discharged on July 22, 1993. An enzyme-linked immunosorbent assay with heterologous antigens performed on serum samples obtained on July 2 and July 20 were highly suspect for hantavirus antibodies. Subsequent retesting of these samples, as well as of an additional sample obtained in September 1994, with Sin Nombre virus (SNV) antigens confirmed the diagnosis of HPS. In April 1993, the patient had started hiking on the Appalachian Trail northbound from Georgia through North Carolina, Tennessee, Virginia, and West Virginia. From May 13 through June 20, he hiked primarily along the Appalachian Trail in Virginia and reported evidence of mice, including excreta and rodent traps in shelters and bunkhouses. To further characterize the prevalence of hantavirus in local rodent populations, the offices of Epidemiology and Environmental Health of the Virginia Department of Health, local health departments, the National Park Service, and CDC are conducting rodent trapping. Reported by: BH Hamory, MD, C Zwillich, MD, T Bollard, MD, JO Ballard, MD, The Milton S Hershey Medical Center, Hershey; M Connor, DO, Chambersberg Hospital, Chambersberg; P Lurie, MD, M Moll, MD, J Rankin, DVM, State Epidemiologist, Pennsylvania Dept of Health. C Smith, MD, New River Health District, Radford; S Jenkins, VMD, E Barrett, DMD, GB Miller, Jr, MD, State Epidemiologist, Virginia Dept of Health. W Frampton, DVM, S Lanser MPH, CR Nichols, MPA, State Epidemiologist, Utah Dept of Health. DT King, Harpers Ferry, West Virginia; A Kingsbury, MS, Washington, DC, National Park Service, US Dept of the Interior. Special Pathogens Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC. Editorial Note: This report describes the first known case of HPS in the mid-Atlantic states. The patient's infection probably was acquired along the Appalachian Trail in Virginia, an area within the range of habitation of the primary rodent reservoir of SNV, Peromyscus maniculatus (deer mouse). The prodromal illness and respiratory failure are consistent with HPS (2); the renal involvement characteristic of Eurasian hemorrhagic fever with renal syndrome (HFRS) has not been typical of HPS. Moderate elevations ( greater than 2.5 ug/dL) in serum creatinine have occurred in only 10% of fatal cases of HPS; prominent renal involvement, such as that which occurred in this patient, has been documented only in two cases from the southeastern United States, both of which are believed to have been associated with hantaviruses other than SNV (provisionally named Black Creek Canal virus and Bayou virus) (3,4). Thus, the marked liver transaminase elevation in this patient has not been a prominent feature in other cases of HPS, although the prominent liver dysfunction has occurred with HFRS (5,6). However, because both renal and hepatic dysfunction can be caused by antecedent hypotension and other factors, additional case investigation is ongoing to clarify the relevance of these findings. Since June 1993, when HPS was first recognized in the United States, 98 cases have been identified in 21 states. The mean age of case- patients has been 35.1 years (range: 12-69 years), and the case-fatality rate is 52%; 52 (54%) cases have occurred in males. The earliest retrospectively identified case, inferred by a history of a compatible illness and elevated IgG titers detected for SNV, occurred in a 38-year-old man in Utah in 1959. The findings in this report extend the geographic area for risk of human infection with hantaviruses in the contiguous United States and emphasize the continued importance of minimizing exposure to rodents and their excreta. Persons engaged in outdoor activities such as camping or hiking should take precautions to reduce contact with rodents (7). National surveillance for HPS continues to characterize the spectrum of clinical illness associated with SNV and identify additional pathogenic hantaviruses and rodent hosts. Suspected cases of HPS should be reported through local and state health departments for evaluation and investigation. References 1. CDC. Outbreak of acute illness--southwestern United States, 1993. MMWR 1993;42:421-4. 2. Duchin JS, Koster FT, Peters CJ, et al. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. N Engl J Med 1994;330:949-55. 3. CDC. Newly identified hantavirus--Florida, 1994. MMWR 1994;43:99,105. 4. CDC. Hantavirus pulmonary syndrome--northeastern United States, 1994. MMWR 1994;43:548-9,555-6. 5. Chan YC, Wong TW, Yap EH, et al. Haemorrhagic fever with renal syndrome involving the liver. Med J Aust 1987;147:248-9. 6. Elisaf M, Stefanaki S, Repanti M, Korakis H, Tsianos E, Siamopoulos KC. Liver involvement in hemorrhagic fever with renal syndrome. J Clin Gastroenterology 1993;17:33-7. 7. CDC. Hantavirus infection--southwestern United States: interim recommendations for risk reduction. MMWR 1993;42(no. RR-11). ------------------------------ Date: Mon, 02 Jan 95 22:26:21 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: [MMWR] Alcohol Involvement in Fatal Traffic Accidents Message-ID: Alcohol Involvement in Fatal Motor-Vehicle Crashes -- United States, 1992-1993 The following figure compares alcohol involvement in fatal motor-vehicle crashes for 1992 and 1993 in the United States. A fatal crash is considered alcohol-related by the National Highway Traffic Safety Administration (NHTSA) if either a driver or nonoccupant (e.g., pedestrian) had a blood alcohol concentration (BAC) of greater than or equal to 0.01 g/dL in a police-reported traffic crash. Because BACs are not available for all persons in fatal crashes, NHTSA estimates the number of alcohol- related traffic fatalities based on a discriminant analysis (1) of information from all crashes for which driver or nonoccupant BAC data are available. The number of alcohol-involved fatalities decreased from 1992 to 1993 for most age groups. For BACs of 0.01 g/dL-0.09 g/dL, the overall decrease in alcohol-involved fatalities was 4%; at greater than or equal to 0.10 g/dL, the legal limit of intoxication in most states, the number of crash fatalities decreased 2%. The increase in fatalities for the nonalcohol-involved crashes probably resulted from a variety of factors, including an increase in the number and changes in the type of vehicle miles traveled (2). References 1. Klein TM. A method of estimating posterior BAC distributions for persons involved in fatal traffic accidents: final report. Washington, DC: US Department of Transportation, National Highway Traffic Safety Administration, 1986; report no. DOT-HS-807-094. 2. Wagenaar AC, Streff FM. Macroeconomic conditions and alcohol- impaired driving. J Stud Alcohol 1989;50:217-25. ------------------------------ Date: Mon, 02 Jan 95 22:27:30 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: [MMWR 9 Dec 94] Acute Pulmonary Hemorrage Among Infants Message-ID: Acute Pulmonary Hemorrhage/Hemosiderosis Among Infants -- Cleveland, January 1993-November 1994 Hemosiderosis is an uncommon childhood disease characterized by spontaneous pulmonary hemorrhage often associated with iron deficiency anemia. During January 1993-November 1994, eight cases of acute pulmonary hemorrhage/hemosiderosis were diagnosed among infants at a children's referral hospital in Cleveland. In comparison, during 1983-1993, a total of three cases of pulmonary hemosiderosis were diagnosed among infants and children at this hospital. This report summarizes the preliminary results of the ongoing epidemiologic, clinical, and laboratory investigations by pediatric pulmonologists in Cleveland, the Ohio Department of Health, the City of Cleveland Department of Public Health, the Cuyahoga County Board of Health, and CDC. In 1993, cases were diagnosed in January (one case) and October (one); in 1994, cases were diagnosed in March (one), June (one), July (two), September (one), and November (one). For each of the eight infants (mean age: 10.3 weeks; range: 4 weeks-16 weeks), onset of hemoptysis was associated with pallor and an abrupt cessation in crying; fever was not reported for any of the infants. Other reported symptoms on admission included limpness, lethargy, and grunting. At the time of initial evaluation at the hospital, seven infants required admission to the pediatric intensive-care unit because of hemoptysis and respiratory distress. All eight infants were black, and seven were male. The median age of their mothers was 20 years (range: 15-29 years). Seven of the pregnancies and deliveries occurred without complications; one infant born at 27 weeks' gestation and weighing 2 lbs, 2 oz (950 g) had complications of severe prematurity. All infants lived within a 6-mile radius of the hospital. No infants were breast fed; before admission, all were fed cow's-milk-based formula. Laboratory findings on admission included a normal white blood cell count (median=13.8 cells/mm3) and features consistent with a normocytic, normochromic anemia characteristic of acute blood loss with a mean hematocrit of 27.1% (normal: 36.0%-47.0%) and a mean hemoglobin of 9.1 g/dL (normal: 10.0-15.0 g/dL). Red blood cell morphology was suggestive of a microangiopathic process: microscopic examination indicated that five of the eight infants had mild to moderate (1+ to 2+) hemolysis characterized by the presence of microcytes, burr cells, spherocytes, and bizarre fragments. Based on guaiac testing, occult blood was present in the stool of three infants. Results of coagulation studies included normal prothrombin and partial thromboplastin time for all infants. Chest radiographs of all infants showed diffuse, bilateral infiltrates consistent with pulmonary hemorrhage. In six infants, the mean serum magnesium level was 2.1 mg/dL (normal: 1.4-1.9 mg/dL). Cultures of blood, urine, and bronchoalveolar lavage from seven infants were negative for bacterial, mycotic, and viral pathogens. Cultures of bronchoalveolar lavage from one infant grew Bacillus sp. Hemosiderin-laden macrophages--indicating continued pulmonary hemorrhage- -were detected in each of the seven infants who underwent bronchoscopy more than 2 weeks after the acute hemorrhage. No other source of bleeding (i.e., gastrointestinal or nasopharyngeal) was identified during endoscopic evaluation. Immunoglobulin G levels to cow's milk proteins were above normal (>20 U/mL) in five of seven infants. Five infants required mechanical ventilation for an average of 5 days. All infants survived the first hospitalization and were discharged in stable condition without evidence of hemoptysis after a median length of stay of 10 days (range: 2-35 days). In five infants, acute hemoptysis necessitating readmission recurred within 1 day to 6 months of discharge. One death--attributed to severe hypoxic encephalopathy secondary to recurring pulmonary hemorrhage--occurred in a 9-week-old full-term infant. Local surveillance measures and active case finding have not identified additional cases in the Cleveland area. A case-control study is under way to determine risk factors for acute pulmonary hemorrhage among infants. Reported by: DG Dearborn, MD, MD Infeld, MD, P Smith, DO, C Judge, MD, Rainbow Babies and Childrens Hospital; TE Horgan, MPH, T Allan, MPH, Cuyahoga County Board of Health; JA Zimomra, MPA, Cleveland Dept of Public Health, Cleveland; BK Mortensen, PhD, SA Burkett, MA, K Winpisinger-Slay, MS, S Wagner, MPH, Ohio Dept of Health. Div of Environmental Hazards and Health Effects, Div of Birth Defects and Developmental Disabilities, and Div of Environmental Health Laboratory Sciences, National Center for Environmental Health, CDC. Editorial Note: The eight cases of acute pulmonary hemorrhage/hemosiderosis described in this report exceed the number expected at this hospital during a 2-year period. Massive acute pulmonary hemorrhage occurs rarely in infants; it usually is attributed to cardiac or vascular malformations, infectious processes, immune vasculitides, trauma, or known milk protein allergies. Cases for which the etiology is undetermined, such as these eight reported from Cleveland, traditionally have been classified as idiopathic pulmonary hemosiderosis (IPH) and account for less than 5% of all cases of pulmonary hemorrhage during infancy. The pathologic mechanism for IPH in children is unknown. Recent histomorphologic techniques suggest that the initial histopathologic damage occurs at the alveolar epithelial surface (1). IPH has been associated with circulating antibodies to cow's milk protein; however, this association has not been consistently reproduced (1,2). In addition, some reports have described familial occurrences of pulmonary hemosiderosis, suggesting a possible genetic vulnerability to a toxicant (3,4). To identify additional cases of acute pulmonary hemorrhage/hemosiderosis, CDC has established the following provisional surveillance case definition: hemoptysis in an infant aged less than 1 year not attributed to cardiac or vascular malformations, infectious processes, or trauma. A case report form is available from CDC. Physicians should report possible cases through state health departments to CDC's Air Pollution and Respiratory Health Branch, Division of Environmental Hazards and Health Effects, National Center for Environmental Health; Internet: rae1@cehdeh1.em.cdc.gov; telephone (404) 488-7320; or fax (404) 488-7335. References 1. Levy J, Wilmott R. Pulmonary hemosiderosis. In: Hilman BC, ed. Pediatric respiratory disease: diagnosis and treatment. Philadelphia: WB Saunders, 1993:543-9. 2. Heiner DC, Sears JW, Kniker WT. Multiple precipitins to cow's milk in chronic respiratory disease. Am J Dis Child 1962;103:634-54. 3. Breckenridge RL, Ross JS. Idiopathic pulmonary hemosiderosis: a report of familial occurrence. Chest 1979;75:636-9. 4. Beckerman RC, Taussig LM, Pinnas JL. Familial idiopathic pulmonary hemosiderosis. Am J Dis Child 1979;133:609-11. ------------------------------ Date: Mon, 02 Jan 95 22:28:33 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: [MMWR] Injury Construction Workers Installing Frame Walls Message-ID: Injuries Among Construction Workers During the Raising of Wood-Framed Walls -- Colorado and California In Colorado, traumatic spinal cord injuries that produce documentable motor, sensory, bowel, and/or bladder impairments must be reported to the state or local health department. Persons with such injuries are interviewed by staff of the Colorado Department of Public Health and Environment (CDPHE) Spinal Cord Injury Early Notification System (ENS)*; injuries that occur in workplaces are investigated by staff of the CDPHE Sentinel Event Notification System for Occupational Risk (SENSOR) program**. This report describes the investigation of a construction-related spinal cord injury reported to the CDPHE SENSOR program on February 8, 1993, and summarizes information about a similar case in California. On February 1, 1993, the construction worker sustained a spinal cord injury--which resulted in permanent paraplegia--while attempting to raise a preconstructed wood-framed wall of a single-family house. A crew of three workers was using a standard procedure that consisted of laying the wall on the ground and "walking it up" to a vertical orientation. The wall was approximately 18 feet wide and 25 feet high at the center peak. During the procedure, two workers were positioned at the outer edges of the wall and one in the center. As the workers were raising the wall, they realized it was too heavy for them to control, possibly because it had become wet from snow that had accumulated on it during the previous evening. While the crew was attempting to lower the wall back to a horizontal orientation, the weight of the wall shifted; the crew lost control of the wall, and it fell to the ground. The worker in the center could not escape the falling wall and was trapped under it, sustaining a fracture dislocation of the seventh thoracic vertebra and spinal cord injury. During the investigation of this injury, Colorado SENSOR staff determined that the building technique used in this incident is common in the construction industry and that many companies employ similar practices for raising prefabricated walls. Colorado SENSOR staff learned of a similar incident that had occurred in California and resulted in a permanently disabling spinal cord injury. In that incident, an unspecified number of workers were raising a 19 x 17-1/2-foot rain- soaked wood-framed wall with an attached chimney chase. As the workers attempted to lift the wall, the base slipped forward, causing the wall to fall back toward the workers. Although most of the workers were able to clear the area before the wall collapsed, three were pinned beneath the wall as it fell. One of the three sustained fracture dislocations of the T12 and L1 vertebrae, spinal cord injury, and subsequent permanent paralysis. Reported by: K Gerhart, MS, Craig Hospital, Englewood; M Heinzman, R Johnson, M Cook, MS, RE Hoffman, MD, State Epidemiologist, Colorado Dept of Public Health and Environment. F Reinisch, MPH, AM Osorio, MD, GW Rutherford, III, MD, State Epidemiologist, California State Dept of úÿ (continued next message) ÿ@FROM :david@STAT.COM úÿ(Continued from last message) Health Svcs. Div of Safety Research, and Div of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, CDC. Editorial Note: The estimated annual incidence of acute traumatic spinal cord injury in the United States ranges from 28 to 50 injuries per million persons (1)***. During 1988 (the most recent year for which national published data are available), the estimated prevalence of spinal cord injuries that resulted in paraplegia and quadriplegia was approximately 177,000 (2). Most injuries (61%) occurred in persons aged 16-30 years (3). During 1988, the estimated total cost of spinal cord injuries in the United States was $5.6 billion: $3.4 billion in direct costs (i.e., hospitalization and other medical care, home modifications, equipment, and pharmaceuticals) and $2.2 billion in indirect costs (i.e., the value of productivity lost to society) (2). During January 1989-December 1992, the average annual rate for spinal cord injury in Colorado ranged from 34 to 43 cases per 1 million population (mean: 37) (4). Of the 506 spinal cord injury cases reported in Colorado during this period, 51 (10%) occurred on the job (4), including 14 (27%) among workers in the construction industry. The California Occupational Safety and Health Standards Board has promulgated regulations for the raising of wood-framed walls at construction sites. The regulation requires that temporary restraints (e.g., cleats on the foundation or floor, or straps on the wall bottom plate) be used when raising wood-framed walls measuring 10 or more feet to prevent inadvertent sliding or uplift of the bottom plate; anchor bolts cannot be used to brace such walls. Compliance with the procedures outlined in this standard--if it had been in effect--may have prevented the incidents in both California and Colorado. Securing the base of a wall being raised manually is an important measure for reducing some risks associated with raising wood-framed walls. Other measures include 1) establishing industry guidelines that classify size categories of walls according to linear feet of wood in the wall, specify the personnel or equipment required for raising each category of wall, and provide an upper limit beyond which cranes or boom trucks must be used to raise the wall; 2) using pulley systems or hydraulic jacks to raise walls; 3) developing a bracing system to arrest the fall of a wall; and 4) establishing and enforcing company and industry policies that prohibit raising of wet wood-framed walls unless additional employees or other raising techniques are used. To further characterize incidents similar to those described in this report and to assist in developing prevention measures, information about other injuries that have resulted from raising wood-framed walls in construction operations should be reported to Acting Chief, Injury Surveillance Section, Surveillance and Field Investigation Branch, Division of Safety Research, National Institute for Occupational Safety and Health; telephone (304) 285-5916. References 1. Kraus JF. Epidemiological aspects of acute spinal cord injury: a review of incidence, prevalence, causes, and outcome. In: Becker DP, Povlishock JT, eds. Central nervous system trauma status report, 1985. Bethesda, Maryland: US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Neurological and Communicative Disorders and Stroke, 1985:313-22. 2. Berkowitz M, Harvey C, Greene CG, Wilson SE. The economic consequences of traumatic spinal cord injury. New York: Demos Publications, 1992:1. 3. Stover SL, Fine PR, eds. Spinal cord injury: the facts and figures. Birmingham, Alabama: University of Alabama at Birmingham, 1986. 4. Colorado Department of Public Health and Environment. 1992 Annual report of the Spinal Cord Injury Early Notification System. Denver: Colorado Department of Transportation Printing Office, 1993. * Colorado is one of 21 states with spinal cord injury registries. Colorado's registry, the ENS, begun in January 1986, is a collaborative project between the Rocky Mountain Regional Spinal Injury System and the CDPHE and is funded through a National Institute on Disability, Rehabilitation, and Research grant and a cooperative agreement with CDC. ** During 1987-1992, CDC funded SENSOR projects in 10 states to develop state-based capacity for recognizing, reporting, investigating, and preventing selected occupational disorders. These 10 states and four additional states received renewed SENSOR funding in 1992. *** The range in estimated incidence rates reflects differences in case definitions. Some studies, for example, include hospital admissions only, which exclude acute fatal injuries. ------------------------------ Date: Mon, 02 Jan 95 22:29:55 MST From: mednews@stat.com (HICNet Medical News) To: hicnews Subject: [MMWR] Progress Towards Elimination of Neonatal Tetanus Message-ID: Progress Toward the Global Elimination of Neonatal Tetanus, 1989- 1993 Neonatal tetanus (NT) is a leading cause of neonatal mortality in many parts of the world. During the 1980s, NT accounted for half of all neonatal deaths and one fourth of all infant mortality in some countries (1). In addition, in 1993, an estimated 515,000 neonatal deaths were caused by NT* (2) for a global mortality rate of 4.1 per 1000 live births. In 1989, the World Health Organization (WHO) adopted a resolution to eliminate NT worldwide (3), and in 1990, the World Summit for Children issued a declaration for global elimination of NT by the end of 1995 (4). In 1993, WHO's goal was defined as the elimination of NT as a public health problem by reducing its incidence to less than one case per 1000 live births for each health district (2) (baseline: in 1988, a total of 32,454 NT cases were reported to WHO and an estimated 787,000 NT deaths occurred; the global NT mortality rate was 6.5 cases per 1000 live births [5])**. To achieve and maintain NT elimination, 80% or more of infants need to be protected at birth through vaccination of their mothers with at least two doses of tetanus toxoid (TT2+) or through clean delivery and cord-care practices (2). In addition, effective surveillance systems must be developed to detect NT cases and enable timely investigation of them. This report, which is based on data from WHO, presents reported coverage with TT2+ in developing countries*** only and reported number of NT cases and estimated number of NT deaths in all countries, and summarizes progress toward the global elimination of NT during 1989-1993 (WHO, unpublished data, 1994). Global. From 1989 to 1993, vaccination coverage with TT2+ among pregnant women increased from 27% to 45% (Figure 1). During the same period, the number of NT cases reported to WHO decreased from 29,494 in 1989 to 14,232 in 1993. However, only 2%-5% of all NT cases were reported (2). Of the estimated 515,000 deaths worldwide, approximately 80% occurred in 12 countries (Table 1). Most deaths (34.2%) occurred in the Southeast Asian Region (Table 2). Overall, an estimated 724,300 deaths attributable to NT were prevented**** in 1993 by vaccination with tetanus toxoid. Of the 156 countries reporting NT incidence to WHO in 1993, a total of 79 (51%) reported zero cases. In 1993, a total of 66% of live births occurred in areas with NT surveillance, compared with 39% in 1985 and 73% in 1989. African Region. Coverage with TT2+ increased from 25% in 1989 to 40% in 1993. In 1993, a total of 3461 cases (24% of the global total) were reported, compared with 7299 cases in 1989. Of the 47 countries in the region, 36 (77%) reported NT incidence to WHO for 1993; of these, four reported zero cases. Region of the Americas. From 1989 through 1993, TT2+ coverage increased from 29% to 40% in the Region of the Americas, where major efforts were undertaken to vaccinate women of childbearing age in high-risk areas. Reported cases decreased from 1430 in 1989 to 708 (5% of the global total) in 1993; Brazil reported 216 cases (31% of the regional total for 1993). Of the 47 countries in the region, 40 (85%) reported NT incidence to WHO for 1993; of these, 25 reported zero cases. Eastern Mediterranean Region. Coverage with TT2+ increased from 31% in 1989 to 50% in 1993. The number of reported cases decreased from 6314 in 1989 to 3350 (24% of the global total) in 1993. Of the 23 countries in the region, 21 (91%) reported NT incidence to WHO for 1993; of these, 10 reported zero cases. European Region. In 1993, TT2+ coverage levels of 16% were reported in the European Region, where only Turkey routinely reports tetanus toxoid coverage to WHO. During 1989-1992, 63-67 cases were reported annually. In 1993, a total of 48 NT cases were reported in the region-- 46 from Turkey. Of the 50 countries in the region, 30 (60%) reported NT incidence to WHO for 1993; of these, 27 reported zero cases. Southeast Asian Region. In 1993, TT2+ coverage was reported to be 74%. The number of reported cases decreased from 14,102 (48% of the global total) in 1989 to 5809 (40% of the global total) in 1993. Three countries accounted for 97% of all NT cases reported in the region: India (4339 [75%] cases), Bangladesh (720 [12%]), and Indonesia (566 [10%]). Of the 11 countries in the region, 10 (91%) reported NT incidence to WHO for 1993; of these, two reported zero cases. Western Pacific Region. In 1993, TT2+ coverage was 13% in the Western Pacific Region (including China, which began administering tetanus toxoid in selected areas in 1992). The number of cases reported to WHO increased from 282 in 1989 to 856 (6% of the global total) in 1993. Two countries reported 79% of the total cases for the region: Vietnam (333 cases) and the Philippines (343 cases). Of the 35 countries in the region, 18 (51%) reported NT incidence to WHO for 1993; of these, 11 reported zero cases. Reported by: Expanded Program on Immunization, Global Program for Vaccines and Immunization, World Health Organization, Geneva. International Health Program Office; National Immunization Program, CDC. Editorial Note: NT results from the effect of a neurotoxin elaborated by the anaerobic organism Clostridium tetani (6). Infection occurs when the umbilical cord becomes contaminated as a result of unclean childbirth or cord-care practices. Access to clean birth practices is ultimately the long-term goal for prevention; however, most infants in developing countries continue to be born at home under unsanitary conditions. Although global tetanus toxoid coverage levels nearly doubled to 45% during 1989-1993 in countries that administer the vaccine, reported coverage levels are underestimated because annual estimates do not include doses administered during previous years. In addition, many women do not maintain vaccination records, making verification of vaccination status difficult (7). WHO now recommends that women receive and maintain life-long vaccination records and that tetanus toxoid coverage be monitored nationally by determining the proportion of children protected at birth when they seek their first diphtheria and tetanus toxoids and pertussis vaccine dose. The findings in this report are subject to at least two limitations. First, because NT cases are grossly underreported, NT incidence is underestimated. Second, the numbers of NT deaths and prevented deaths are based on projections from national data (which often are estimated) or data extrapolated from other countries. As of August 1, 1994, the estimated NT case rate was less than one per 1000 live births nationwide (i.e., not by district) in 83 countries. In addition, in 57 countries, the estimated rate of NT was one to five cases per 1000 nationwide, while in 25 countries the estimated rate was higher than five cases per 1000. Although progress has been made toward eliminating NT as a public health problem, present resources and commitments must be increased and activities greatly accelerated if the 1995 goal is to be achieved by all countries (8). In 1993, the Global Advisory Group of WHO's Expanded Program on Immunization identified four constraints to NT elimination (2): 1) insufficient funds to purchase tetanus toxoid in selected high-risk countries; 2) lack of adequate health-care infrastructure in many countries, resulting in limited tetanus toxoid vaccination activities and poor access to clean birth practices; 3) civil unrest in some high-risk countries; and 4) high levels of NT underreporting. To reach the global elimination goal for NT, efforts must be accelerated, especially in the 12 countries from which 80% of NT cases were reported in 1993 and in countries where the incidence rate is higher than five per 1000 live births. Each country must identify areas where the incidence rate is higher than one per 1000 live births, coverage levels are low, or there is limited access to clean deliveries or trained birth attendants. These high-risk areas must be targeted for intensified vaccination efforts, including the use of mass vaccination campaigns. In addition, surveillance activities in all areas must be strengthened. Finally, because NT is not a communicable disease, and C. tetani cannot be eradicated from the environment, ensuring long-term elimination of NT will require the development of adequate health-care delivery systems to reach those at greatest risk--infants of poor women residing in rural areas in developing countries. References 1. World Health Organization. Neonatal tetanus elimination. Tokyo: World Health Organization, Expanded Program on Immunization, Global Advisory Group, October 16-20, 1989; publication no. WHO/EPI/GAG/89/WP.9. 2. Global Advisory Group, Expanded Program on Immunization, World Health Organization. Achieving the major disease control goals. Wkly Epidemiol Rec 1994;69:29-31,34-5. 3. World Health Assembly. Expanded Program on Immunization. Geneva: World Health Organization, May 19, 1989. (Resolution WHA42.32). 4. World Health Organization. Revised plan of action for neonatal tetanus elimination. Geneva: World Health Organization, Expanded Program on Immunization, 1993; publication no. WHO/EPI/GEN/93.13. 5. World Health Organization. The global elimination of neonatal tetanus: progress to date. Bull World Health Organ 1994;72:155-64. 6. Galazka AM. Tetanus: the immunologic basis for immunization. Geneva: World Health Organization, Expanded Program on Immunization, 1993; publication no. WHO/EPI/GEN/93.13. 7. Deming MS. Monitoring tetanus toxoid immunization coverage. Geneva: World Health Organization, Expanded Program on Immunization, 1990; document no. EPI/NNT/90/WP.3/Rev1. 8. World Health Organization. Global programme for vaccines and immunization: proceedings of the Meeting of the Scientific Advisory Group of Experts. Geneva: World Health Organization, October 17-19, 1994. * Estimates of NT deaths are derived from national mortality data, NT mortality rates from NT surveys, or in the absence of surveys, by assuming that rates are similar for countries with similar socioeconomic conditions and from tetanus toxoid coverage levels. ** Because the case-fatality rate for NT is high (100% in some countries), WHO estimates only the number of deaths for NT, not number of cases. *** Countries are categorized as developing based on criteria developed by the United Nations and used by WHO for analytic purposes only. **** The number of NT deaths prevented was calculated for each country using the number of live births, NT mortality rate, and tetanus toxoid coverage and efficacy. ------------------------------ End of HICNet Medical News Digest V08 Issue #01 *********************************************** --- Editor, HICNet Medical Newsletter Internet: david@stat.com FAX: +1 (602) 451-1165 Bitnet : ATW1H@ASUACAD