The following are pre-publication drafts of articles from the Morbidity and Mortality Weekly Report dated July 28, 1995. Late-breaking articles, and final editorial revisions are not included; therefore, these articles should be considered preliminary, and not to be released to the public. --CDC -------------------------------------------------------------- Progress Toward Elimination of Haemophilus influenzae Type b Disease Among Infants and Children -- United States, 1993-1994 Before effective vaccines were available, Haemophilus influenzae type b (Hib) was the most common cause of bacterial meningitis among children in the United States. Since the introduction of Hib conjugate vaccines in 1988, the incidence of invasive Hib infection has declined by at least 95% among infants and children (1,2). As part of the Childhood Immunization Initiative (CII), the Public Health Service has included Hib disease among children aged less than 5 years as one of the vaccine-preventable diseases targeted for elimination in the United States by 1996 (3). This report summarizes provisional data about invasive Hi disease during 1993-1994 based on information from three surveillance systems: the National Notifiable Diseases Surveillance System (NNDSS), the National Bacterial Meningitis and Bacteremia Reporting System (NBMBRS), and a multistate laboratory-based surveillance system. National Surveillance State health agencies reported weekly provisional notifiable disease data to NNDSS through the National Electronic Telecommunications System for Surveillance (NETSS) (4,5). Because the primary purpose of NNDSS is timely nationwide surveillance, the information transmitted included only basic demographic data about persons with invasive Hi disease. The capacity for the electronic transmission of critical supplemental information (e.g., the type of clinical illness, serotype causing disease, Hib vaccination status, and clinical outcome) for cases of Hi disease is available through NETSS and is used consistently by approximately half of the states. NBMBRS is a collaborative effort initiated in 1977 by CDC, state health departments, and the Council of State and Territorial Epidemiologists to collect information about invasive bacterial diseases in the United States. NBMBRS includes detailed information about each case identical to the supplemental information transmitted through NETSS. Approximately 20 states participate consistently in reporting through the NBMBRS. From 1993 to 1994, the incidence of invasive Hi disease among children aged less than 5 years reported to the NNDSS decreased 29% (from 2.4 cases per 100,000 to 1.7 cases per 100,000, respectively), a trend similar to that reported for 1992-1993 (Figure 1) (2). However, the total number of cases among children aged less than 5 years reported during the first 4 months of 1995 (105) is similar to that during the same period in 1994 (104). Supplemental case information was reported to CDC by 35 states and was obtained on request from the remaining states. Of the 340 cases of invasive Hi disease among children aged less than 5 years reported in 1994, supplemental information was available for 259 (76%). Of these, serotype data were available for 139 (54%)--41% of all reported cases. Hib accounted for 82 (59%) of the isolates for which serotype was known. Of the 60 (73%) cases of Hib disease for which information on age and vaccination status was available, none of the 12 children aged greater than 15 months had received four doses of Hib vaccine (Table 1). Two of the 19 children aged 7-15 months had received three vaccine doses, while most (17) had not completed the recommended primary series. Nearly half (29) were aged less than or equal to 6 months, below the age recommended for completion of the full three-dose primary series of the most commonly used Hib vaccines; of these, five had received two doses of vaccine. Laboratory-Based Surveillance The laboratory-based system coordinated by CDC includes surveillance projects with a total population of 10.4 million persons in four areas (three counties in the San Francisco Bay area, eight counties in metropolitan Atlanta, four counties in Tennessee, and the state of Oklahoma). Information routinely obtained for all cases of invasive Hi disease included serotype, clinical syndrome, outcome, vaccination status, and demographic information. Because blacks were overrepresented in the surveillance population, rates were race-adjusted to the 1990 age-specific U.S. population. The incidence of Hib disease among children aged less than 5 years declined from 1989 to 1993 but was stable from 1993 to 1994 (1.5 and 1.4 cases per 100,000, respectively) (Figure 2). Information about vaccination status was available for eight of the 10 children aged less than 5 years with invasive Hib disease reported in 1994. None of the infants had received two or more doses of vaccine, although three were aged 8 months and should have received three doses. The two children for whom vaccination information was not available were aged greater than 16 months. Based on a projection of these age-specific and race-adjusted incidence rates, an estimated 280 cases of Hib disease occurred among children aged less than 5 years in 1994 compared with an estimated 290 cases in 1993. During 1993 and 1994, Hib accounted for 37% of all the Hi isolates obtained from children aged less than 5 years. Reported by: G Rothbrock, Bur of Disease Control, Oakland, California. L Smithee, MS, Oklahoma State Dept of Health. M Rados, MS, Dept of Preventive Medicine, Vanderbilt Medical Center, Nashville, Tennessee. W Baughman, MSPH, Veterans' Administration Medical Svcs, Atlanta. National Immunization Program; National Center for Infectious Diseases; Epidemiology Program Office, CDC. Editorial Note: The goal to eliminate Hib disease among children aged less than 5 years is feasible because of the availability of Hib conjugate vaccines that are efficacious in children and reduce carriage of the organism, thereby interrupting transmission of infection. During 1988-1992, the incidence of invasive Hib disease declined rapidly among children; however, the findings in this report indicate that, since 1992, the rate of decline among children has slowed. This report also underscores two barriers to the elimination of invasive Hib disease among children: 1) the absence of accurate national surveillance for Hib incidence because of the lack of serotype information for most invasive Hi disease cases among children, and 2) the continued occurrence of disease among undervaccinated children and among infants too young to have completed the primary series of Hib vaccination. Serotype information for cases of invasive Hi disease is essential to evaluate the changing epidemiology of Hib disease during a period of low disease incidence. Surveillance data indicate that a decreasing proportion of Hi cases are caused by Hib--which in the past was responsible for greater than 90% of all Hi disease. Thus, the decline in the incidence of Hi disease among children observed in NNDSS data for 1994 may not have resulted from a reduction in Hib disease; data from laboratory-based surveillance suggests that, during 1993-1994, incidence of Hib disease remained stable. Because serotype information could be obtained for only 41% of cases reported to the NNDSS in 1994, the true incidence of Hib disease among children in the United States cannot be estimated from these data. In the national surveillance data, the higher proportion of Hib among Hi isolates of known serotype probably reflects incomplete serotyping information and preferential reporting of Hib cases in the national data. Both national and laboratory-based surveillance findings indicate that Hi disease now occurs primarily among undervaccinated children and among infants too young to have completed the primary series of vaccination. However, based on the findings from CDC's National Health Interview Survey, the quarterly levels of coverage with three or more doses of Hib vaccine among children aged 19-35 months increased significantly from the third quarter of 1993 (60%) to the second quarter of 1994 (76%) (6). Although overall Hib vaccination coverage may be increasing, population groups with low levels of vaccination coverage probably contribute to the ongoing occurrence of disease (7). The findings in this report indicate that no cases of vaccine failure were identified through laboratory-based surveillance in a population of 10.5 million. The small proportion of Hib cases reported through national surveillance among children who had received at least three doses of Hib vaccine suggests vaccine failure occurs infrequently, but is still consistent with previous reports showing extremely high efficacy of current vaccines (8-10). As a larger proportion of Hib cases is detected and investigated, more complete evaluations of cases among fully vaccinated persons will be possible. To meet the 1996 CII objectives to eliminate invasive Hib disease among children aged less than 5 years, CDC recommends two measures. First, national surveillance for Hi should be strengthened. To optimize surveillance efforts, case reports should satisfy four criteria: 1) because Hib vaccines protect against Hi serotype b organisms only, serotyping should be obtained for all cases of invasive Hi disease--state health departments are encouraged to identify laboratories to ensure that serotyping is available for all Hi isolates; 2) to improve characterization of groups at risk for undervaccination and Hib disease, vaccination status of all children with invasive Hib disease should be assessed; 3) to ensure continued high levels of vaccine effectiveness and to enable systematic evaluation of factors associated with vaccine failure in persons with Hib disease, the date, vaccine manufacturer, and lot number for each Hib vaccination should be reported; and 4) important indicators of the severity of Hi infections should be reported, including the type of clinical syndrome, specimen source (e.g., cerebrospinal fluid, blood, or joint fluid), and clinical outcome. Second, timely vaccination and vaccine coverage should be increased. Because conjugate vaccines reduce Hib carriage and interrupt transmission of the organism, timely vaccination of all children also should eliminate disease among infants who are too young to be completely vaccinated. References 1. Adams WG, Deaver KA, Cochi SL, et al. Decline of childhood Haemophilus influenzae type b (Hib) disease in the Hib vaccine era. JAMA 1993;269:221-6. 2. CDC. Progress toward elimination of Haemophilus influenzae type b disease among infants and children--United States, 1987-1993. MMWR 1994;43:144-8. 3. CDC. Reported vaccine-preventable diseases--United States, 1993, and the Childhood Immunization Initiative. MMWR 1994;43:57-60. 4. CDC. Mandatory reporting of infectious diseases by clinicians. MMWR 1990;39(no. RR-9):1-17. 5. CDC. National Electronic Telecommunications System for Surveillance--United States, 1990-91. MMWR 1991;40:502-3. 6. CDC. Vaccination coverage levels among children aged 19-35 months--United States, April-June 1994. MMWR 1995;44:396-8. 7. CDC. Vaccination coverage of 2-year-old children--United States, 1991-1992. MMWR 1994;42:985-8. 8. Black SB, Shinefield HR, Fireman B, et al. Efficacy in infancy of oligosaccharide conjugate Haemophilus influenzae type b (HbOC) vaccine in a United States population of 61080 children. Pediatr Infect Dis J 1991;10:97-104. 9. Santosham M, Wolff M, Reid R, et al. The efficacy in Navajo infants of a conjugate vaccine consisting of Haemophilus influenzae type b polysaccharide and Neisseria meningitidis outer-membrane protein complex. N Engl J Med 1991;324:1767-72. 10. Vadheim C, Greenberg D, Eriksen E, et al. Protection provided by Haemophilus influenzae type b conjugate vaccines in Los Angeles County: a case-control study. Pediatr Infect Dis J 1994;13:274-80. Community Outbreak of Hemolytic Uremic Syndrome Attributable to Escherichia coli O111:NM -- South Australia, 1995 Postdiarrheal hemolytic uremic syndrome (HUS) is characterized by microangiopathic hemolytic anemia, renal injury, and thrombocytopenia and is associated with infection with Shiga-like toxin-producing Escherichia coli (SLTEC). From January 4 through February 20, 1995, the South Australian Communicable Disease Control Unit of the Health Commission (SACDCU) received reports of 23 cases of HUS among children aged less than 16 years who resided in South Australia. In comparison, during 1994, a total of three cases of HUS was reported in South Australia (1991 population: 1.4 million). This report summarizes preliminary findings of the investigation of this outbreak by SACDCU, Women's and Children's Hospital, Institute of Medical and Veterinary Science, and the National Center for Epidemiology and Population Health of Australian National University. Three cases of HUS were reported to SACDCU during January 4-16. Subsequently, SACDCU requested that hospitals, commercial clinical laboratories, general practitioners, and--with the cooperation of the news media--the public throughout South Australia report persons with bloody diarrhea, HUS, or thrombotic thrombocytopenic purpura (TTP). The preliminary investigation suggested that HUS occurred as a complication of infection associated with consumption of uncooked, semi-dry fermented sausage product produced locally by a single manufacturer. On January 23, the South Australian Health Commission issued a press release noting the link to the sausage; the manufacturer subsequently initiated a recall (Figure 1) of products with a "use by" date of March 12, later extended to include products with dates during January 26-April 12. The median age of the 23 patients with HUS was 4 years (range: 4 months-12 years); 14 (61%) were male. Most (19 [83%]) patients resided in the city of Adelaide, and four resided in surrounding rural areas. Sixteen (70%) patients required dialysis; one 4-year-old girl died. Twenty-two of the patients had had onset of diarrhea during the 2 weeks preceding the diagnosis of HUS; of these, 16 had bloody diarrhea. During the 8 days preceding onset of illness, 16 patients had consumed uncooked, semi-dry fermented sausage produced locally by a single manufacturer; for three other patients, this product recently had been kept in the household, although consumption by the patients was not confirmed. Stool specimens obtained from all 23 patients during their illness were screened using polymerase chain reaction (PCR) for the genes encoding for Shiga-like toxins (SLTs) I and II (1); of these, 20 (87%) were positive for both SLTs I and II, one (4%) was positive for only SLT II, and two (9%) were negative. E. coli O111:NM (nonmotile) subsequently was isolated from stool specimens from 16 of these patients. Other E. coli strains positive by PCR for SLT also were detected in specimens from three patients. In addition to the 23 cases of HUS, physicians reported 30 persons with bloody diarrhea from whom no other bacterial pathogens had been isolated and three adults with TTP. Stool samples from eight (24%) of these 33 persons were PCR-positive for SLT genes, but E. coli O111:NM was isolated from only one. SACDCU also received 105 reports of persons with gastrointestinal illness other than bloody diarrhea; 32 (30%) had a history of consumption of the implicated sausage. Stool specimens from 20 of these persons were positive for SLT by PCR. SLTEC were isolated from all 20 of these PCR-positive specimens, and isolates from two persons were identified as E. coli O111:NM. Of 10 sausage samples taken during January 19-February 8 from the homes of nine patients (eight homes total), eight (all from the same manufacturer) were positive for SLTs I and II by PCR; E. coli O111:NM was isolated from four of these samples. Eighteen (39%) of 47 additional sausage samples produced by the same manufacturer obtained during January 19-March 9 from homes where diarrheal illness without HUS occurred and from retail stores were PCR positive; three yielded E. coli O111:NM. Sixty-three samples of sausage from other manufacturers were collected during the same period from retail outlets and from homes of persons with diarrheal illness but not HUS; E. coli O111:NM was not isolated from any of these specimens. Industry and food agencies in South Australia, in conjunction with the National Food Authority and the Department of Primary Industry and Energy, are investigating the implicated products and the quality controls employed by the manufacturer and its suppliers to determine the specific source of contamination. In addition, comparative epidemiologic studies are ongoing. Reported by: AS Cameron, MD, MY Beers, CC Walker, N Rose, E Anear, Z Manatakis, K Kirke, MBBS, I Calder, PhD, F Jenkins, PhD, Public and Environmental Health Svc, South Australian Health Commission; PN Goldwater, MBBS, A Paton, PhD, J Paton, PhD, K Jureidini, MBBS, A Hoffman, P Henning, MBBS, D Hansman, MBBS, A Lawrence, MSc, R Miller, Women's and Children's Hospital, Adelaide, South Australia; R Ratcliff, R Doyle, C Murray, D Davos, P Cameron, J Seymour-Murray, I Lim, MBBS, J Lanser, PhD, Institute of Medical and Veterinary Science, Adelaide, South Australia; L Selvey, PhD, S Beaton, National Center for Epidemiology and Population Health, Australian National Univ, Canberra, Australia. Foodborne and Diarrheal Diseases Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC. Editorial Note: SLTEC are now recognized as a cause of postdiarrheal HUS and TTP. Based on studies in North America and the United Kingdom, antecedent infection with one serogroup--E. coli O157--may account for greater than 75% of cases of postdiarrheal HUS in these locations (2,3). In addition, however, greater than 100 non-O157 SLTEC serotypes have been isolated from humans; most of these serotypes have been isolated from persons with HUS (3). This report documents the second outbreak of a non-O157 SLTEC with a probable link to a food product (4), and follows the recent report of an E. coli O157:H7 outbreak associated with a similar dry fermented sausage product in the United States (5). In Australia, E. coli O157 has not been isolated frequently; among non-O157 SLTEC, E. coli O111 is common. At one laboratory during 1987-1994, seven (50%) of 14 non-O157 SLTEC strains from persons with HUS in Australia identified were E. coli O111 (6). Outbreaks attributable to non-O157 SLTEC rarely have been reported. In an outbreak of SLTEC O111 infections in Italy during 1992, all nine patients had HUS, but a common source was not identified (7). In Australia, two cases of HUS attributable to O111 infection were reported in siblings residing in the same household (8). The outbreak described in this report is the largest reported community outbreak of HUS associated with E. coli O111 infection. In June 1994, HUS in persons aged less than 16 years became notifiable to the Australian Pediatric Surveillance Unit of the Australian College of Pediatrics. Reports of HUS are transmitted from participating pediatric microbiologists and nephrologists to the surveillance unit. Prompt reporting of HUS was important in recognizing this outbreak, determining the responsible pathogen, and removing the suspected source from the market to prevent additional cases. Based on an experimental inoculation study, E. coli O157:H7 survives the fermentation and drying process used in preparing products similar to those in this report (9). Isolation of E. coli O111 from dried sausage, in combination with the finding that non-O157 SLTEC commonly are isolated from the intestines of food animals (10), suggests that control measures for E. coli O157:H7 also can prevent E. coli O111 infections. These recommendations include the need to avoid eating raw or undercooked ground meats and prevent cross-contamination in the kitchen, and to wash hands, utensils, and preparation surfaces that have come in contact with raw meat. In general, children with any acute diarrheal illness should be excluded from child day care centers; children aged less than 5 years infected with SLTEC should not return to child day care centers until they are asymptomatic and have had two negative stool cultures. In addition, food handlers and health-care workers infected with SLTEC should not return to work until they are asymptomatic and have had two negative stool cultures. The E. coli O111 strain associated with the outbreak in this report ferments sorbitol--a characteristic that distinguishes this strain from E. coli O157:H7. In this outbreak, E. coli O111 would not have been detected by sorbitol-MacConkey medium, which is recommended for screening for E. coli O157:H7. Instead, screening by PCR coupled with serotyping of E. coli from PCR-positive specimens enabled detection of the pathogen in stool specimens and epidemiologically related food. Non-O157 SLTEC can be detected by screening stool specimens for SLTEC with PCR or genetic probes. However, such methods generally are not available for clinical laboratories. Therefore, in the United States, health-care providers who identify clusters of persons with bloody diarrhea or HUS from whom stool cultures do not yield E. coli O157:H7 should request that state health departments examine specimens for other SLTEC. In suspected cases, frozen stool specimens and isolates from routine culture plates can be saved for examination. References 1. Paton AW, Paton JC, Goldwater PN, Manning PA. Direct detection of Escherichia coli Shiga-like toxin genes in primary fecal cultures using polymerase chain reaction. J Clin Microbiol 1993;31:3063-7. 2. Rowe PC, Orrbine E, Lior H, Wells GA, McLaine PN, Canadian Pediatric Kidney Foundation Reference Center co-investigators. A prospective study of exposure to verotoxin-producing Escherichia coli among Canadian children with haemolytic uraemic syndrome. Epidemiol Infect 1993;110:1-7. 3. Griffin PM. Escherichia coli O157:H7 and other enterohemorrhagic Escherichia coli. In: Blaser MJ, Smith PD, Ravdin JI, Greenberg HB, Guerrant RI, eds. Infections of the gastrointestinal tract. New York: Raven Press, Ltd, 1995:739-61. 4. CDC. Outbreak of acute gastroenteritis attributable to Escherichia coli serotype O104:H21--Helena, Montana, 1994. MMWR 1995;44:501-3. 5. CDC. Escherichia coli O157:H7 outbreak linked to commercially distributed dry-cured salami--Washington and California, 1994. MMWR 1995;44:157-60. 6. Goldwater PN, Bettelheim KA. The role of enterohaemorrhagic Escherichia coli serotypes other than O157:H7 as causes of disease in Australia. Communicable Disease Intelligence 1995;19:2-4. 7. Caprioli A, Luzzi I, Rosmini F, et al. Communitywide outbreak of hemolytic-uraemic syndrome associated with non-O157 verocytotoxin-producing Escherichia coli. J Infect Dis 1994;169:208-11. 8. Gunzburg S, Gracey M, Forbes D, Hewitt I, Bettelheim K. Haemolytic-uremic syndrome and verocytotoxigenic Esch. coli. Med J Aust 1988;149:54-5. 9. Glass KA, Loeffelholz JM, Ford JP, Doyle MP. Fate of Escherichia coli O157:H7 as affected by pH or sodium chloride in fermented, dry sausage. Appl Environ Microbiol 1992;58:2513-6. 10. Wells JG, Shipman LD, Greene KD, et al. Isolation of Escherichia coli serotype O157:H7 and other Shiga-like-toxin-producing E. coli from dairy cattle. J Clin Microbiol 1991;29:985-9. Notice to Readers Licensure of Inactivated Hepatitis A Vaccine and Recommendations for Use Among International Travelers In February 1995, Havrix(R)*, an inactivated hepatitis A vaccine distributed by SmithKline Beecham Pharmaceuticals (Philadelphia, Pennsylvania) was licensed by the Food and Drug Administration for use in persons aged greater than or equal to 2 years to prevent hepatitis A virus (HAV) infection. The vaccine is licensed in adult and pediatric formulations, with different dosages and administration schedules (Table 1) and should be administered by intramuscular injection into the deltoid muscle. Immunogenicity studies have indicated that virtually 100% of children, adolescents, and adults develop protective levels of antibody to hepatitis A virus (anti-HAV) after completing the vaccine series (1,2). Based on a controlled clinical trial, the efficacy of two doses of vaccine (360 enzyme-linked immunosorbent assay units) administered 1 month apart in preventing hepatitis A in children was estimated to be 94% (95% confidence interval=79%-99%) (3). Vaccine recipients have been followed for as long as 4 years and still have protective levels of anti-HAV. Kinetic models of antibody decline suggest that protective levels of anti-HAV could persist for at least 20 years (1,4). Hepatitis A vaccine can be administered simultaneously with other vaccines and toxoids--including hepatitis B, diphtheria, tetanus, oral typhoid, cholera, Japanese encephalitis, rabies, and yellow fever--without affecting immunogenicity or increasing the frequency of adverse events (5,6). However, during simultaneous administration, the vaccines should be given at separate injection sites. When immune globulin (IG) is given concurrently with the first dose of vaccine, the proportion of persons who develop protective levels of anti-HAV is not affected, but antibody concentrations are lower. Because the final concentrations of anti-HAV are substantially higher than that considered to be protective, this reduced immunogenicity is not expected to be clinically important (7). Vaccination of an immune person is not contraindicated and does not increase the risk for adverse effects. Prevaccination serologic testing may be indicated for adult travelers who probably have had prior HAV infection if the cost of testing is less than the cost of vaccination and if testing will not interfere with completion of the vaccine series. Such persons may include those aged greater than 40 years and those born in areas of the world with a high endemicity of HAV infection (see recommendations). Postvaccination testing for serologic response is not indicated. The Advisory Committee on Immunization Practices (ACIP) offers the following interim recommendations for the use of inactivated hepatitis A vaccine among international travelers. 1. All susceptible persons traveling to or working in countries with intermediate or high HAV endemicity (countries other than Australia, Canada, Japan, New Zealand, and countries in Western Europe and Scandinavia) should be vaccinated with hepatitis A vaccine or receive IG before departure. Hepatitis A vaccine at the age-appropriate dose (Table 1) is preferred for persons who plan to travel repeatedly to or reside for long periods in these high-risk areas. IG is recommended for travelers aged less than 2 years. 2. After receiving the initial dose of hepatitis A vaccine, persons are considered to be protected by 4 weeks. For long-term protection, a second dose is needed 6-12 months later. For persons who will travel to high-risk areas less than 4 weeks after the initial vaccine dose, IG (0.02 mL per kg of body weight) should be administered simultaneously with the first dose of vaccine but at different injection sites. 3. Persons who are allergic to a vaccine component or otherwise elect not to receive vaccine should receive a single dose of IG (0.02 mL per kg of body weight), which provides effective protection against hepatitis A for up to 3 months. IG should be administered at 0.06 mL per kg of body weight and must be repeated if travel is greater than 5 months. The complete ACIP recommendations for the prevention of hepatitis A will be published. Additional information about hepatitis A vaccine is available from CDC's Hepatitis Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, telephone (404) 639-3048. Reported By: Advisory Committee on Immunization Practices. Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC. References 1. Clemens R, Safary A, Hepburn A, Roche C, Stanbury WJ, Andre FE. Clinical experience with an inactivated hepatitis A vaccine. J Infect Dis 1995;171(suppl 1):S44-S49. 2. Balcarek DB, Bagley MR, Pass RF, Schiff ER, Krause DS. Safety and immunogenicity of an inactivated hepatitis A vaccine in preschool children. J Infect Dis 1995;171(suppl 1):S70-S72. 3. Innis BL, Snitbhan R, Kunasol P, et al. Protection against hepatitis A by an inactivated vaccine. JAMA 1994;271:1328-34. 4. Ambrosch F, Widermann G, Andre FE, et al. Comparison of HAV antibodies induced by vaccination, passive immunization, and natural infection. In: Hollinger FB, Lemon SM, Margolis HS, eds. Viral hepatitis and liver disease. Baltimore: Williams and Wilkins, 1991:98-100. 5. Ambrosch F, Andre FE, Delem A, et al. Simultaneous vaccination against hepatitis A and B: results of a controlled study. Vaccine 1992;10(suppl 1):S142-S145. 6. Kruppenbacher J, Bienzle U, Bock HL, Clemens R. Co-administration of an inactivated hepatitis A vaccine with other travelers vaccines: interference with the immune response [Abstract]. In: Proceedings of the 34th Interscience Conference on Antimicrobial Agents and Chemotherapy. Washington, DC: American Society of Microbiologists, 1994:256. 7. Wagner G, Lavanchy D, Darioli R, et al. Simultaneous active and passive immunization against hepatitis A studied in a population of travelers. Vaccine 1993;11:1027-32. * Use of trade names and commercial sources is for identification only and does not imply endorsement by the Public Health Service or the U.S. Department of Health and Human Services. Notice to Readers Assessing Adult Vaccination Status at Age 50 Years In January 1994, the National Vaccine Advisory Committee (NVAC) reported on the status of adult vaccination in the United States (1) and concluded that vaccine-preventable infections among adults are a continuing cause of morbidity and mortality, particularly among older persons. Missed opportunities to vaccinate adults during health-care visits have markedly influenced adult vaccination levels (2). To improve vaccination levels, the NVAC recommended changes in clinical practice, including systems for regularly offering vaccines to patients at risk. Consistent with the NVAC recommendations, the American College of Physicians Task Force on Adult Immunization and the Infectious Diseases Society of America have recommended linking the assessment of vaccination status and the administration of vaccinations at age 50 years to other established prevention measures (3). At its meeting on October 19-20, 1994, the Advisory Committee on Immunization Practices (ACIP) adopted the recommendation that, for their patients aged 50 years, health-care providers 1) review adult vaccination status, 2) administer tetanus and diphtheria toxoids as indicated, and 3) determine whether a patient has one or more risk factors that indicate a need to receive one dose of pneumococcal vaccine and begin annual influenza vaccination. This recommendation is consistent with those of other groups that have recommended age 50 years as a time to assess important prevention measures, (e.g., screening for certain cancers that occur more commonly with advancing age or counseling of older women regarding estrogen replacement therapy) (4). Establishing a routine vaccination status assessment at age 50 years provides an opportunity to improve the delivery of vaccination services to adults. ACIP recommends that all primary-care physicians schedule a prevention visit for their patients at age 50 years to assess vaccination status, provide recommended vaccines, and offer other prevention services that may be indicated. In the United States, tetanus is primarily a problem among adults aged greater than 50 years (5) who never completed a primary vaccination series, never received appropriate treatment of a wound that could result in infection with Clostridium tetani, or both (5). Reviewing the need for either primary or booster tetanus toxoid administration at age 50 years would assure high levels of protection at an age when the incidence and the case-fatality rates of tetanus begin to increase. Although diphtheria has virtually disappeared from the United States, the re-emergence of diphtheria in the former Soviet Union (6) has heightened concerns regarding the low prevalence of protective antibody levels among adults in the United States. An age-based recommendation for tetanus and diphtheria toxoids (Td) vaccination should improve the use of Td among adults and decrease the risk for reoccurrence of widespread diphtheria in the United States. Many persons aged 50-64 years have either cardiovascular or pulmonary risk conditions and are, therefore, candidates to receive pneumococcal and influenza vaccines (CDC, unpublished data, 1994) (Table 1). The prevalence of these conditions is probably even higher among those who regularly seek medical care. Persons aged greater than or equal to 18 years for whom influenza and pneumococcal vaccines are recommended include all those aged greater than or equal to 65 years, those with chronic disorders of the pulmonary and cardiovascular systems, and those who have required regular medical follow-up or hospitalization during the preceding year because of chronic metabolic diseases (including diabetes mellitus), renal dysfunction, hemoglobinopathies, or immunosuppression (including immunosuppression caused by medications) (7,8). In addition, pneumococcal vaccine is recommended for persons with alcoholism, cirrhosis, cerebrospinal fluid leaks, and splenic dysfunction or anatomic asplenia (8). The rapid emergence of drug-resistant pneumococcal infections underscores the need for adherence to ACIP recommendations for pneumococcal vaccination (9). Physicians should review a patient's vaccination status at every visit to identify these conditions in patients and provide the appropriate vaccines whenever indicated. In 1991, 9% and 15% of persons with cardiovascular or pulmonary high-risk conditions, respectively, in the 50-64-year age group reported having ever received pneumococcal vaccine, and 21% and 28%, respectively, reported having received influenza vaccine during the previous year (CDC, unpublished data, 1994; Table 1). In contrast, although still below the national health objective for the year 2000 (60% vaccination levels for these vaccines; objective 20.11) (10), a substantially higher percentage of persons aged greater than or equal to 65 years with these conditions reported receiving these vaccines than did persons aged 50-64 years (Table 1). These data indicate that the recommendations to vaccinate persons aged less than 65 years based on the presence of certain chronic medical conditions have been inadequately implemented. A specific age-based standard should improve vaccination rates among those with high-risk conditions. Reported by: Advisory Committee on Immunization Practices. National Immunization Program, CDC. References 1. Fedson DS, for the National Vaccine Advisory Committee. Adult immunization: summary of the National Vaccine Advisory Committee Report. JAMA 1994;272:1133-7. 2. Williams WW, Hickson MA, Kane MA, Kendal AP, Spika JS, Hinman AR. Immunization policies and vaccine coverage among adults: the risk for missed opportunities. Ann Intern Med 1988;108:616-25. 3. American College of Physicians Task Force on Adult Immunization/Infectious Diseases Society of America. Guide for adult immunization. 3rd ed. Philadelphia, Pennsylvania: American College of Physicians, 1994. 4. US Preventive Services Task Force. Guide to clinical preventive services: an assessment of the effectiveness of 169 interventions. Baltimore, Maryland: Williams and Wilkins, 1989. 5. CDC. Diphtheria, tetanus, and pertussis: recommendations for vaccine use and other preventive measures: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 1991:40(no. RR-10). 6. CDC. Diphtheria epidemic--New Independent States of the former Soviet Union, 1990-1994. MMWR 1995;44:177-81. 7. CDC. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1995;44(no. RR-3). 8. CDC. Pneumococcal polysaccharide vaccine: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 1989;38:64-8,73-6. 9. Breiman RF, Butler JC, Tenover FC, Elliott JA, Facklam RR. Emergence of drug-resistant pneumococcal infections in the United States. JAMA 1994;271:1831-5. 10. Public Health Service. Healthy people 2000: national health promotion and disease prevention objectives. Washington, DC: US Department of Health and Human Services, Public Health Service, 1991:122-3; DHHS publication no. (PHS)91-50213.