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Query: UMLS:C0009450 (infectious diseases)
 83,438 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The long-range prognosis of viral diseases must be assessed differently according to their geographical occurrence. The genetic disposition, environmental factors and additional infectious diseases play a decisive part here. Vaccinations are the most important measures in the prevention of these infections. The spectrum of possible chemotherapeutic intervention for viral infectious diseases is very small, which usually makes specific treatment impossible. The most important infective viruses epidemiologically, which lead to persistent complications, are discussed in detail as follows: influenza virus, measles virus, human T-cell leukaemia virus, human immuno-deficiency virus, hepatitis B and C virus. In a discussion conclusions are drawn from the virologist's point of view for a possible long-range prognosis, which depends on the one hand on the infective agent and on the other on individual reactivity. The last chapter talks about insurance medical aspects of the most important infective viruses, which have already been discussed virologically. Some scientific developments are shown which could be future solutions of problems in diagnosis and prognosis. Such new developments could help insurance medical officers to important decision parameters for long-range prognosis, which are still largely missing at present.
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PMID:[Possible long-term prognosis in epidemiologically significant virus infections]. 167 99

Researchers analyzed data from the National Child Development Study--a cohort of every child born in England, Scotland, and Wales during the 1st week of March 1953 with follow up studies in 1965, 1969, 1973, and 1980-1981 to examine the relationship between health status and birth order and whether children with low birth orders were less likely to experience illness than those with older siblings. 1st born children tended to have received the needed number of immunizations, but children of higher birth order did not tend to have received them. Further they were more likely to have attended infant welfare and toddler clinics for health care than children of higher birth order. The only childhood contagious disease which demonstrated a social class effect was pertussis. It tended to afflict children from nonmanual homes regardless of birth order. Absences from school lasting between 1 week-1 month of 1st born children were less frequent than for other children. The leading reasons for 1st, 3rd, and later born 11 year old children who experienced such long absences included infectious diseases; bronchitis; ear, nose, and throat complaints; pneumonia; tonsillitis, or viral influenza. After age 15, 1st and 2nd born children were less likely to be absent and, if absent, they tended to only miss 1 week of school. Significantly more 3rd and 4th born children were absent from school for 1 week-3 months. 1st and 2nd born children from more affluent families tended to have early childhood asthma. In conclusion, the health experiences of the later birth orders were different than those of the 1st born. This did not mean, however, that later birth order children were in poorer health than 1st born children.
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PMID:Birth order and health status in a British national sample. 173 12

A stochastic infectious disease model was developed by Ball (1986, Advances in Applied Probability 18, 289-310) in which the distribution of the length of the infectious period is allowed to have any distribution that can be described by its Laplace transform. We extend this model such that the infection can be transmitted within the population or from an unspecified source outside the population. Also, discrete heterogeneity in the population can be modeled to incorporate variable susceptibility, variable infectivity, and/or mixing behaviors. The model is fitted to serologic data from two influenza epidemics in Tecumseh, Michigan, using maximum likelihood estimation procedures. The estimates show a clustering pattern by age groups.
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PMID:A generalized stochastic model for the analysis of infectious disease final size data. 174 49

Infection by influenza virus is initiated by a cellular adhesion event that is mediated by the viral protein, hemagglutinin, which is exposed on the surface of the virion. Hemagglutinin recognizes and binds to cell surface sialic acid residues. Although each individual ligand binding interaction is weak, the high affinity of influenza virus for cells that bear sialic acid residues is thought to result from a multivalent attachment process involving many similar recognition events. To evaluate such binding we have synthesized three series of compounds, each containing two sialic acid residues separated by spacers of different length, and have tested them as ligands for influenza hemagglutinin. No increased binding to the bromelain-released hemagglutinin ectodomain was seen for any of the bivalent compounds as determined by 1H NMR titration. In contrast, however, a spacer length between sialic acid residues of approximately 55 A sharply increases the binding of these bidentate species to whole virus as determined by hemagglutination inhibition assays. The most effective compound containing glycines in the linking chain displayed 100-fold increased affinity for whole virus over the paradigm monovalent ligand, Neu5Ac alpha 2Me.
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PMID:Ligand recognition by influenza virus. The binding of bivalent sialosides. 174 43

The discussion of communicable disease mortality highlights the problems of utilizing leading cause of death reporting, where the definition and characteristics of a short list influence the relative of all structural components, and thus the sequence of ranking. Leading cause structure is truncated and definitions and frequencies of nonleading causes are usually not made available. However, cause specific is all inclusive and can be easily visualized. Mortality analyses need to become more public health oriented and explanatory, to assist in the evaluation of the health status of the population, and be useful in delineating priorities and resource allocation. The importance of the issue is that developing countries appear to be similar to developed countries in their leading causes of death; communicable diseases are obscured as a leading cause. The broadness of the cause group gives a better chance of qualifying as a leading cause, i.e., diseases of the heart, cerebrovascular disease, malignant neoplasms, and accidents. Another problem is the use of a short list of causes when there has been a shift in the mortality pattern. When leading cause analysis is combined with infectious disease surveillance, infectious diseases are listed singly along with broad categories such as diseases of the heart. There is no one single best cause list of mortality. A given causal category may not qualify for all countries as a leading cause. Cause groups should be need determined. In consideration of these problems, a progressive structural approach and a new ICD--9 was recommended by PAHO in 1988. 6 principles were identified: hierarchy, comparability, expandability, consistency, suitability for identification of leading causes of death, and responsiveness to public health needs. The new short list is comprised of 61 all-inclusive categories in 6 broad cause groups (communicable diseases, neoplasms, diseases of the circulatory system, certain conditions originating in the neonatal period, external causes of injury and poisoning, and all other diseases, as well as symptoms, signs, and ill-defined conditions (SSI). The provision for SSI means data can be limited to defined causes only and if SSI becomes too large, a reappraisal is in order. This 6-group causal structure has been helpful in epidemiologic mortality patterns in the Americas, where communicable diseases (including influenza and pneumonia) rank in t he 5 leading causes of death. This was possible because of the modification of the communicable disease list to include all infectious and parasitic diseases, meningitis, and acute respiratory infections.
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PMID:Communicable disease mortality: now you see it, now you don't. 180 90

Background. Herd immunity describes the collective immunocompetence of a population and its ability to resist disease. The diseases of mycobacteria, salmonella, hepatitis A, cryptosporidia, syphilis, measles, influenza, and numerous others recently have been seen in epidemic proportions in the United States. An association between these superimposed secondary infections and the human immunodeficiency virus (HIV) epidemic can be made since the HIV's imposition on individual immunity has ramifications on a population level through a decline in herd immunity. Conclusion. Exploring these epidemic phenomena as consequential to a reduction in herd immunity can provide a unifying hypothesis to explain existing and predict future infectious disease epidemic dynamics. The benefits of acting upon these implications has advantages for both the HIV infected and the uninfected.
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PMID:Herd immunity and the HIV epidemic. 186 55

Hyaluronidase and hyaluronic acid activities are markedly changed in influenza, these changes directly depending on the severity of the inflammatory process that depends on the presence of bacterial complications in influenza. The authors' findings correlate with the literature data on the blood mucolytic system status in various infectious diseases. The results recommend measurements of hyaluronidase and hyaluronic acid activities as an additional test for the early diagnosis of influenza complications.
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PMID:[Hyaluronic acid and hyaluronidase in influenza]. 186 70

The clinical picture of influenza A virus infections indicates that release of tumor necrosis factor-alpha (TNF-alpha) may be involved. In the present study we exposed the murine macrophage line PU5-1.8 to influenza A virus and observed a productive infection which was followed by subsequent cell death. Infection of macrophages was accompanied by TNF-alpha mRNA accumulation and TNF-alpha release. TNF-alpha production could only be induced by live virus whereas interferon release was also stimulated by inactivated virus. When virus-infected macrophages were exposed to low amounts of lipopolysaccharide (LPS; 1-10 ng/ml) TNF-alpha production was strongly potentiated. These data show that low LPS concentrations could readily trigger a high TNF-alpha release from influenza-A-virus-infected macrophages which could, at least partially, explain the serious complications of combined influenza A virus and bacterial infections.
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PMID:Influenza A virus infects macrophages and stimulates release of tumor necrosis factor-alpha. 188 18

Medical science has made tremendous strides in overcoming infectious diseases in the 20th century. Despite this, several epidemics of previously unrecognized diseases have occurred during the last 15 years. These diseases include Lyme disease, Legionnaires' disease, toxic shock syndrome, and AIDS. Examination of past epidemics, including the plague of Athens, the black death, syphilis, and influenza, suggests that the sudden occurrence of diseases that were previously unrecognized is not unusual. Analysis of the new infectious disease indicates that while all four appeared suddenly, isolated cases of the disease occurred before the actual epidemic. Further, all four new diseases were found to be due to agents or toxins that were not previously recognized. Epidemics due to new infectious diseases may arise by several mechanisms, including mutation of the pathogen to a virulent form and introduction of an infectious agent into a nonimmune population. Environmental and behavioral factors may play an important role, as illustrated by toxic shock syndrome, Legionnaires' disease, and AIDS. On the other hand, epidemic diseases tend to abate over time because of changes in the infecting pathogen and in the host. Hence, epidemics can be seen as cycles; new diseases will arise periodically, occasionally with a devastating outcome. With time the effects of these diseases on the population will ameliorate. The cycle will begin again when a new disease emerges.
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PMID:Plagues--what's past is present: thoughts on the origin and history of new infectious diseases. 192 88

In a previous paper we defined the efficacy of a vaccine as 1-beta 1/beta 0, where beta 0 is the instantaneous probability of transmission of infection to an unvaccinated person exposed to a single infectious person, and beta 1 is similarly defined for a vaccinated person. We showed that under the conditions of an outbreak of an acute, directly transmitted infectious disease in a homogeneous and randomly mixing population, an estimate of this measure of vaccine efficacy is 1-[1n(1-A1)/1n(1-A0)], where A0 and A1 are the observed final attack rates among unvaccinated and vaccinated persons, respectively. In the present work we present an approximation for the standard error of this estimator, accounting for both the sampling and process variation. We extend the results of our previous paper to a stratified population, where the strata correspond to different levels of susceptibility and may have different vaccination coverage. We also consider populations that consist of small units (for example, households) where individuals mix primarily in these units. In this case, definition of vaccine efficacy is in terms of the within-unit transmission probabilities and is estimable by using transmission models for infectious diseases. We apply the estimation methods described above to data from influenza and measles outbreaks. We also examine, via a stochastic simulation study, the robustness of the vaccine efficacy estimators under various population structures and mixing patterns.
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PMID:Estimation of vaccine efficacy in outbreaks of acute infectious diseases. 194 13


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