Case definitions for public health surveillance.
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Biomedical subjects
Publications and source records attributed to T L Chorba.
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An outbreak of epidemic hysteria, in which 210 students at a North Carolina elementary school became ill and 102 were evaluated in hospital emergency departments, is described in terms of an outbreak of infectious disease. The outbreak began when a radiator boiler was fired for the first time in the 1985-1986 school year. The most common symptoms were headache, light-headedness, abdominal pain, and nausea; anxiety was later proposed to be the agent of illness. The outbreak appeared to have propagated by friend-to-friend transmission of anxiety within social (grade, race, and sex) cohorts, and by other audiovisual cues in the absence of person-to-person contact. An environmental survey found no plausible toxic or infectious cause of the outbreak. Separation of vectors and susceptible hosts preceded recovery from the outbreak, and reassurance and discussion of the findings of the investigating team with students, teachers, and parents may have prevented the recurrence of symptoms by alleviating anxiety.
In this paper we present the leading causes of fatal childhood injury in the United States. We examine three types of explanations for why injury rates are so high in the United States compared with what they could be and actually are in a number of industrialized European countries. Our conclusions are based on what we learn when we look at specific injury problems and apply that knowledge to the field of childhood-injury prevention as a whole. To decrease the number of fatal injuries to children, we should: 1. Recognize injuries as a major public health problem. Injuries have been perceived not as problems to be solved but as "accidents" which are determined by fate, not understandable, and consequently not preventable. In addition, injuries have not been addressed in the multidisciplinary fashion that typifies the successful public health approach to other problems. 2. Address intentional injury as part of the problem. Intentional injury has been treated as a separate field entirely and not addressed scientifically as a public health problem. One consequence of this is that injuries due to firearms have been addressed most frequently as a problem of "unintentional injury." As a result, 93% of all firearm injuries, ie, those which are intentional, have not been studied or addressed adequately. This situation is like studying motor vehicle injuries but excluding drunk driving and speeding as contributing factors, or like studying acquired immunodeficiency syndrome but ignoring anal intercourse or intravenous drug use. 3. Develop and support organizations that can plan and coordinate effectively a national approach to injury control.(ABSTRACT TRUNCATED AT 250 WORDS)
Reporting of cases of communicable disease is important in the planning and evaluation of disease prevention and control programs, in the assurance of appropriate medical therapy, and in the detection of common-source outbreaks. In the United States, the authority to require notification of cases of disease resides in the respective state legislatures. We examined the laws and regulations of health departments of all US jurisdictions to ascertain diseases and conditions currently required to be reported in each state or territory. We present herein the state reporting requirements for infectious diseases and infectious disease-related conditions. To obtain additional information regarding time frames for reporting, agencies to which reports are required, persons required to report, and specific conditions under which reports are required, the reader is referred to the statutes and health department regulations of the respective states.
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Because of the T-cell abnormalities observed in Hodgkin's disease and the growing number of Hodgkin's disease cases observed in association with the acquired immunodeficiency syndrome (AIDS), concern has been expressed that a retrovirus may be the primary cause of Hodgkin's disease. We examined plasma specimens from 17 patients with Hodgkin's disease that were drawn in 1979. Because serum containing antibodies to either human T-lymphotropic virus type I (HTLV-I) or HTLV-II precipitate the major core protein, p24, of HTLV-I, lack of reactivity to HTLV-I p24 in all the specimens demonstrated absence of antibodies to HTLV-I or -II. None of the specimens was reactive to human immunodeficiency virus type 1 (HIV-1) by ELISA. None of the specimens were reactive on Western blot assays for HTLV-I or -II or HIV-1. Lack of evidence of cross-reacting antibodies to prototype strains of those retroviruses in specimens drawn before the AIDS epidemic suggests that classic Hodgkin's disease is not the result of infection with one of the known human lymphocytotropic retroviruses or a closely related agent.
The Patient Knowledge Assessment Study (PKAS) was conducted among 107 male hemophilic patients, aged 15 to 67 years, at 19 hemophilia treatment centers (HTC). Participants were given a 30-item questionnaire concerning the cause of acquired immunodeficiency syndrome (AIDS), the groups at risk, and modes of transmission. The questionnaire included questions on the participant's status in regard to antibody to human T-lymphotropic retrovirus, type III/lymphadenopathy-associated virus (HTLV-III/LAV), and the meaning of this test result. HTC health-care providers were asked to complete a separate questionnaire containing 17 questions about information given patients concerning their HTLV-III/LAV antibody status and its meaning. Overall, patients had a good base of knowledge about AIDS; however, there were gaps in this knowledge. Twenty-nine percent of patients did not know that spouses of AIDS patients were at risk for AIDS; 47% did not know that sexual partners of persons with hemophilia were at risk; and 32% did not know that hemophilic children were at risk. Further, only 69% understood that antibody-positive individuals had had contact with the AIDS virus. Identifying these and other areas of misunderstanding will provide the information needed to design educational strategies and psychosocial support programs appropriate for the hemophilic population, and which may serve as a model for other populations.
We report an outbreak of Salmonella typhimurium in the infant room of a day care center. Time between onset dates, clustering of cases in the room, lack of a common food exposure, lack of illness among other children and staff, and lack of community-wide infection suggested person-to-person or continuing-common-source transmission. Successful preventive measures included instruction of personnel in proper handwashing and diaper-changing procedures and cohorting of infected and non-infected children. This is the second description of a non-foodborne outbreak of salmonellosis in a day care center, and the first involving S. typhimurium.
We compared recipients of eight lots of factors VIII and IX voluntarily withdrawn from distribution because one donor was known to have subsequently developed the acquired immunodeficiency syndrome with a nonexposed cohort matched by age, sex, and factor use. The factor VIII recipient cohorts did not differ in prevalence of antibody to human immunodeficiency virus (HIV) (exposed, 75%; nonexposed, 86%), T-cell subset numbers (median: exposed, 619 T-helper cells per cubic millimeter; nonexposed, 659 T-helper cells per cubic millimeter), T-helper to T-suppressor ratios, or immunoglobulin levels. Exposed individuals had higher levels of immune complexes by C1q binding and staphylococcal binding assays and lower responses to phytohemagglutinin and concanavalin A. However, only the staphylococcal binding assay values were outside the normal range for our laboratory. Factor IX recipient cohorts did not differ in HIV antibody prevalence (exposed, 30%; nonexposed, 40%) or any immune tests. Although exposed and nonexposed individuals did not differ from each other in a clinically meaningful fashion at initial testing, both the exposed and nonexposed cohorts had high rates of HIV seroprevalence. Market withdrawals were clearly insufficient means of limiting the spread of HIV in hemophilic patients; however, the currently available methods of donor screening and viral inactivation of blood products will prevent continued exposure within this population.
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Acute-phase serum from a patient with aplastic crisis provided sufficient human parvovirus B19 to make a monoclonal antibody against B19 and to develop antigen and immunoglobulin M (IgM) and IgG antibody detection enzyme-linked immunosorbent assays (ELISAs). The indirect capture antibody method was used for all three assays. Antigen was detected in 8 of 29 sera drawn within 2 days of onset of illness from patients with aplastic crisis. These sera had high titers of virus by electron microscopy and DNA hybridization and had no detectable B19 antibody. Antigen was not detected in serum specimens that had low titers of B19 DNA and had B19 antibody. With the IgM ELISA, we detected B19 IgM in over 85% of clinical cases of aplastic crisis and fifth disease and less than 2% of controls. The prevalence of B19 IgG antibodies increased with age. Approximately 2% of children less than 5 years of age and 49% of adults greater than 20 years of age had B19 IgG antibodies. The B19 antibody ELISAs are sensitive and specific tests to detect B19 infections.
From March to August 1984, 26 patients with hereditary hemolytic anemia in northeastern Ohio developed acute, profound red cell aplasia. The patients included 14 males and 12 females 2 to 23 years old, with sickle cell anemia (20 cases), hemoglobin SC-disease (4 cases), sickle-beta-thalassemia (1 case), or hereditary spherocytosis (1 case). All had an acute onset of severe reticulocytopenia and anemia and prodromal symptoms of illness including fever, abdominal symptoms, headache, and arthralgias. Twenty-two received transfusions. Reticulocytosis occurred spontaneously within 2 to 14 days of presentation. In five acute-phase sera, 10(8) to 10(12) viral particles/mL were detected by electron microscopy. Human parvovirus B19 DNA was demonstrated in high concentration by hybridization in the same five acute-phase sera and in low concentration in sera of eight additional patients. The five highly viremic sera inhibited erythroid colony formation in vitro. B19-specific IgM was detected in sera of 24/26 patients, and B19-specific IgG in 21 of 22 patients tested. Our results indicate that human parvovirus B19 was the etiologic agent in this large epidemic of life-threatening acute red cell aplasia in patients with hereditary hemolytic anemia.
Serum samples from 85 Austrian hemophilia patients treated with lyophilized factor concentrates prepared from U.S. plasma sources, 24 hemophilia patients from Georgia on a home therapy program with factor concentrates, and 10 U.S. hemophilia patients with acquired immunodeficiency syndrome (AIDS) were analyzed by two different methods for the presence of antibodies to the major internal antigen of human T-cell leukemia virus I (HTLV-I) p24. All but one, a Georgia sample, were negative. The absence of antibody to HTLV-I p24 in the serum of European hemophilia patients, of U.S. hemophilia patients with no symptoms of AIDS, and of U.S. hemophilia patients with AIDS is interpreted as an indication of the lack of ready transmissibility of HTLV-I in lyophilized factor concentrates.
The effects of mediastinal irradiation (RT) on the numbers and functions of purified peripheral blood T-lymphocytes from patients with locally advanced non-small cell lung cancer were evaluated. The patients were candidates for a randomized trial to evaluate the immunorestorative properties of synthetic thymosin alpha-1. Twenty-one patients studied before RT did not exhibit any significant difference in T-cell numbers or function compared to age-matched healthy subjects. However, 41 patients studied within 1 week after completing RT exhibited significant depressions of E-rosette-forming cells at 4 degrees C (E4 degrees-RFC)/mm3, E-rosette-forming cells at 29 degrees C (E29 degrees-RFC)/mm3, OKT3/mm3, OKT4/mm3, and OKT8/mm3 (P = 0.0001); total T-cell percentages (%OKT3, P = 0.01); and T-cell proliferative responses in mixed lymphocyte cultures (MLR) (P = 0.01) and to the mitogen phytohemagglutinin under suboptimal conditions (P less than or equal to 0.03). Nine patients studied before and after RT showed a significant increase in OKT4/OKT8 (P = 0.01) following RT. A short-term in vitro incubation with thymosin alpha-1 could enhance MLR of T-cells in 12 of 27 patients with post-RT abnormalities. In 13 patients who were treated with placebo, the RT-induced depression of T-cell numbers and function persisted for at least 3 to 4 months. In addition, in 12 patients progressive decreases developed in %E4 degrees-RFC, %OKT3, %OKT4, and OKT4/OKT8, which always preceded clinical relapse. This study indicates that mediastinal RT results in prolonged depletion of circulating T-cells, alterations of T-cell subset proportions, and intrinsic T-cell functional deficiencies. This patient population provides a uniformly immunosuppressed group of subjects with which to evaluate the immunorestorative effects of thymosin alpha-1 or other biologic response modifiers.
The phenotypic and ultrastructural characterization of the blast cells from a T-cell acute lymphoblastic leukemia (T-ALL) that was associated with disseminated intravascular coagulation (DIC) is described. The bone marrow blasts were considered to represent neoplastic medullary thymocytes and were acid phosphatase (+), terminal deoxynucleotidyl transferase (-), acid alpha-naphthyl acetate esterase (-), E-rosette (+) at 4 degrees C and 37 degrees C, Fc- and C3-receptor (-), and cALLA-, Ia-, 9.6+, OKT3+, OKT4+, OKT6+/-, OKT8+, OKT10+. On transmission electron microscopic study, the predominant cell was 6 micron in diameter and possessed an irregular nucleus, moderate-sized nucleolus, marginated heterochromatin, abundant Golgi elements and granules, and prominent intermediate filaments. The cells were analyzed with normal and factor-deficient human plasmas and contained significant amounts of tissue factor-like procoagulant activity. This is the first report of a well-characterized medullary thymocyte T-ALL in which DIC was an accompanying feature, and the first demonstration of tissue factor-like procoagulant activity in acute lymphoblastic leukemia. In view of thrombohemorrhagic phenomena observed in association with other medullary thymocyte leukemias, these findings suggest that tissue factor-like procoagulant activity may be a characteristic of medullary thymocyte-derived lymphoid leukemias.
During the period of 1979 to 1983, 38 patients with cystic fibrosis (CF) at the CF center of St. Christopher's Hospital for Children in Pennsylvania developed respiratory tract colonization with Pseudomonas cepacia. Seventeen (45%) of the patients with colonization died. Yearly incidence rates of P. cepacia colonization fluctuated between 1.3% and 6.1%, suggesting an endemic phenomenon. Case-control studies showed that severe underlying CF, use of aminoglycosides, and having a sibling with CF and P. cepacia colonization were significant risk factors for P. cepacia colonization. Once colonized with P. cepacia, patients with CF were likely to be hospitalized longer (P = 0.008) and to die sooner (P = 0.0001) than control patients with CF. Environmental and microbiologic studies did not identify a common source or mode of transmission of P. cepacia among patients. The results of this investigation suggest that P. cepacia colonization of patients with CF was endemic in the hospital, occurred more frequently in those with severe disease, and was associated with adverse clinical outcome.