Childhood hepatitis B virus infections in the United States before hepatitis B immunization.

OBJECTIVE: To estimate the number of hepatitis B virus (HBV) infections among US children younger than 10 years before implementation of routine childhood hepatitis B immunization. METHODS: Incidence of HBV infection in children was modeled from existing prevalence data by means of regression analysis. Sources of data for the models included published and unpublished surveys that determined the prevalence of HBV infection in US-born children. The number of nonperinatal HBV infections in children younger than 10 years was estimated by applying these infection rates to 1991 population data according to maternal race, ethnicity, and birthplace. RESULTS: Estimated annual rates of infection ranged from 24 per 100 000 in non-Asian children to 2580 per 100 000 in children of Southeast Asian immigrant mothers. These rates indicate that by the early 1990s, HBV was infecting 16 000 children who were younger than 10 years (8700 non-Asian children and 7300 Asian-American children) annually. The total estimate, not including perinatal infections, ranged from 12 000 (95% confidence interval: 5500-27 700) to 24 900 (95% confidence interval: 16 700-42 300) infections and depended on how the estimated rates were applied to the population data. CONCLUSION: Thousands of US children were infected each year with HBV before routine infant hepatitis B immunization, placing them at high risk of death from cirrhosis or hepatocellular carcinoma later in life.

Incidence of herpes simplex virus type 2 infection in the United States.

Between the time that two large, national surveys were conducted, the Second National Health and Nutrition Examination Survey (1976-1980) and the Third National Health and Nutrition Examination Survey (1988-1994), prevalence of herpes simplex virus type 2 (HSV-2) infection in the United States increased by 30%. From these survey data, the authors estimated the incidence of HSV-2 infection in the civilian, noninstitutionalized population aged > or = 12 years by means of a mathematical model that allowed overall incidence to increase linearly with time but required the shape of the age-specific incidence curve to remain constant. From 1970 to 1985, annual incidence of HSV-2 infection in HSV-2-seronegative persons increased by 82%, from 4.6 per 1,000 (95% confidence interval: 4.2, 5.0) to 8.4 per 1,000 (95% confidence interval: 7.7, 9.1). Incidence in 1985 was higher in women than in men (9.9 vs. 6.9 per 1,000), higher in Blacks than in Whites (20.4 vs. 6.3 per 1,000), and highest in the group aged 20-29 years (14.6 and 22.5 per 1,000 in men and women, respectively). Thus, by 1985, approximately 1,640,000+/-150,000 persons (730,000 men and 910,000 women) were being infected annually with HSV-2.

Serotype distribution of Salmonella isolates from food animals after slaughter differs from that of isolates found in humans.

If raw meat and poultry are the primary point of entry for Salmonella species into human populations, a correlation might be expected between the serotype distribution of Salmonella species isolated from animals at the time of slaughter and that of isolates found in humans. For 1990-1996, sufficient national data were available to permit such a comparison. A mathematical model was developed to predict serotype distributions of Salmonella isolates among humans on the basis of animal data. There was a significant mismatch between the serotype distributions among humans predicted by the model and those actually observed. This mismatch raises questions about the validity of the "standard" assumptions about Salmonella transmission on which the model was based-namely, that raw animal products are the primary source for human salmonellosis, that the risk of transmission to humans is equal for all food product categories, and that all Salmonella serotypes have an equal ability to cause human illness.

The past incidence of hepatitis C virus infection: implications for the future burden of chronic liver disease in the United States.

Because chronic liver disease may develop many years after acute hepatitis C virus (HCV) infection, the past incidence of acute infections is a major determinant of the future burden of HCV-associated complications. We estimated past incidence of acute HCV infection using national seroprevalence data and relative age-specific incidence data from a sentinel counties surveillance system. Projections of the future prevalence of HCV-infected patients were derived from models that included an 85% drop in HCV infection incidence as observed for reported cases in the early 1990s. The models showed a large increase in the incidence of HCV infections from the late 1960s to the early 1980s. The degree of increase was dependent on the assumed rate of antibody loss; a model with 2.5% annual antibody loss showed annual incidence increasing from 45,000 infections (95% confidence interval [95% CI]: 0-110,000) in the early 1960s to 380,000 infections (95% CI: 250,000 to 500, 000) in the 1980s. Projections showed that although the prevalence of HCV infection may be declining currently because of the decline in incidence in the 1990s, the number of persons infected for >/=20 years could increase substantially before peaking in 2015. If the incidence of new HCV infections does not increase in the future, persons born between 1940 and 1965 will be at highest lifetime risk of acquiring the infection.

Outpatient visits for infectious diseases in the United States, 1980 through 1996.

BACKGROUND: Recent studies have documented increases in infectious disease mortality and in the proportion of hospitalizations attributable to infectious diseases. To further evaluate trends in the burden of infectious diseases in the United States, we analyzed data from the National Ambulatory Medical Care Survey from 1980 through 1996. OBJECTIVE: To examine the epidemiology of and recent trends in outpatient visits for infectious diseases. METHODS: Data were from a national probability sample of patient visits to office-based physicians. Diagnoses reported by the surveyed physicians were coded to indicate whether they were infectious or noninfectious. Infectious diseases were placed into 11 mutually exclusive categories. RESULTS: During the course of the survey, infectious diseases accounted for 19.0% of visits to physicians, or an average of 129 million visits per year. The infectious disease visit rate was higher in females than in males (587 vs 461 per 1000 persons per year) and higher in non-Hispanic whites than in non-Hispanic blacks or Hispanics (538 vs 407 vs 485 per 1000 persons per year). The visit rate for infectious diseases was greatest in 0- to 4-year-olds. Upper respiratory tract infections accounted for the largest proportion of visits (38.0% of infectious disease visits), followed by otitis (15.1%) and lower respiratory tract infections (14.1%). The age-adjusted visit rate for infectious diseases increased from 462 visits per 1000 persons (17.5% of all visits) in 1980 to 575 (20.2%) in 1990. From 1990 to 1996, this rate declined to 483 per 1000 (18.1%). CONCLUSIONS: Infectious diseases are responsible for a substantial proportion of outpatient visits to physicians in the United States. Upper respiratory tract infections account for the largest proportion of these visits.

Trends in infectious disease mortality in the United States during the 20th century.

CONTEXT: Recent increases in infectious disease mortality and concern about emerging infections warrant an examination of longer-term trends. OBJECTIVE: To describe trends in infectious disease mortality in the United States during the 20th century. DESIGN AND SETTING: Descriptive study of infectious disease mortality in the United States. Deaths due to infectious diseases from 1900 to 1996 were tallied by using mortality tables. Trends in age-specific infectious disease mortality were examined by using age-specific death rates for 9 common infectious causes of death. SUBJECTS: Persons who died in the United States between 1900 and 1996. MAIN OUTCOME MEASURES: Crude and age-adjusted mortality rates. RESULTS: Infectious disease mortality declined during the first 8 decades of the 20th century from 797 deaths per 100000 in 1900 to 36 deaths per 100000 in 1980. From 1981 to 1995, the mortality rate increased to a peak of 63 deaths per 100000 in 1995 and declined to 59 deaths per 100000 in 1996. The decline was interrupted by a sharp spike in mortality caused by the 1918 influenza epidemic. From 1938 to 1952, the decline was particularly rapid, with mortality decreasing 8.2% per year. Pneumonia and influenza were responsible for the largest number of infectious disease deaths throughout the century. Tuberculosis caused almost as many deaths as pneumonia and influenza early in the century, but tuberculosis mortality dropped off sharply after 1945. Infectious disease mortality increased in the 1980s and early 1990s in persons aged 25 years and older and was mainly due to the emergence of the acquired immunodeficiency syndrome (AIDS) in 25- to 64-year-olds and, to a lesser degree, to increases in pneumonia and influenza deaths among persons aged 65 years and older. There was considerable year-to-year variability in infectious disease mortality, especially for the youngest and oldest age groups. CONCLUSIONS: Although most of the 20th century has been marked by declining infectious disease mortality, substantial year-to-year variation as well as recent increases emphasize the dynamic nature of infectious diseases and the need for preparedness to address them.

Emerging foodborne pathogens: Escherichia coli O157:H7 as a model of entry of a new pathogen into the food supply of the developed world.

There would appear to be little argument that the large outbreaks of E. coli O157:H7 which have occurred since the early 1980s represent a distinct, new phenomenon. The number of reported cases have increased dramatically, starting from zero in 1981; however, it is also clear that this increase in reported cases is in part an artifact of improved surveillance and reporting. Available data suggest that E. coli O157:H7 infections were present prior to 1982, although numbers appear to have been small. At a molecular level, the organism shows evidence of clonal origin, but there is not the striking clonality, with virtually identical pulsed-field gel electrophoresis and ribotyping patterns, which has been seen in situations such as the emergence of Vibrio cholerae O139 Bengal in the Indian subcontinent in 1992 or the introduction of V. cholerae O1 into naïve populations in South America in 1991 (127-129). Findings are more consistent with the image of an organism which arose from a common ancestor, but which has had time to become distributed geographically and to show some evidence of genetic divergence. While this is an "emerging" infection, at least in terms of its distribution and public recognition, it is unlikely that it will be possible to identify the "first" O157:H7 case or to track the clonal spread of the organism through cattle or human populations.

Strain improvement of chymosin-producing strains of Aspergillus niger var. awamori using parasexual recombination.

Parasexual recombination was used to obtain improved chymosin-producing strains and to perform genetic analysis on existing strains. Chlorate resistance was used to select for a variety of spontaneous nitrate assimilation pathway mutations in strains previously improved for chymosin production using classical strain improvement methods including mutation and screening, and selection for 2-deoxyglucose resistance (dgr). Diploids of these improved strains were generated via parasexual recombination and were isolated on selective media by complementation of nitrate assimilation mutations. A preliminary genetic analysis of diploid and haploid segregants indicated that the dgr trait, resulting in overexpression of chymosin, was recessive. Also, mutations in two different dgr genes resulted in an increased level of chymosin production. When these mutations were combined via parasexual recombination, the resulting haploid segregants produced about 15% more chymosin than either parental strain. CHEF gel electrophoresis was used to determine the chromosomal location of the integrated chymosin DNA sequences, and to verify diploidy in one case where the chromosome composition of two haploid parents differed.