Incidence Of Human Disease Research Articles

Transmission Risk of Lyme Disease and Implications for Tick Management

Transmission risk of Lyme disease at a site can be estimated using the probability of exposure (P1 = probability of being bitten by at least one infected tick); P1 = 1 - (1 - kt)n, where n = number of tick bites per person and kt = spirochete prevalence in questing ticks. This probability is more directly related to the likelihood of acquiring Lyme disease than the standard measure of transmission risk (the number of infected ticks per sample) and allows for direct consideration of the level of tick/human contact (by varying n) in assessing exposure risk and designing management strategies. Projections predict that interventions that lower tick abundance or spirochete prevalence do not necessarily result in equivalent declines in human exposure risk. Management interventions are predicted to have greatest success at lowering disease incidence in humans when tick abundance and/or pathogen prevalence in questing ticks are initially low (e.g., for ticks in residential lawns or for low-prevalence diseases). These techniques are predicted to be less effective at lowering disease incidence in people engaged in high-risk activities at sites with high tick abundance and pathogen prevalence, such as wooded sites in highly endemic areas.

Incidence and clinical correlates of human papillomavirus disease in a pediatric population referred for evaluation of sexual abuse

Study Objective: To investigate the incidence of genital warts in a pediatric population at risk of sexual abuse.Design: Retrospective chart review of all files of the Child and Adolescent Sexual Abuse Referral Center at San Francisco General Hospital for identification of children with clinically evident genital warts.Results: The incidence of genital warts in this population was 0.3% (17 of 5506). The average age of children with evidence of genital warts was 3.4 years (range 13 months to 14 years 9 months), and of the 17 patients with warts, 6 had clinical evidence of sexual abuse.Conclusions: Genital warts are an uncommon finding in children referred for evaluation of sexual abuse. The majority of lesions occurred in children less than 4 years of age with no other evidence for sexual abuse. Perinatal transmission or other nonsexual routes of transmission may be important in this population.

Effect of breed on lipid metabolism in growing-fattening bulls 2. fatty acid composition in the carcasses

The incidence of human coronary heart disease has been correlated with the serum cholesterol level and a high consumption of saturated fat. Furthermore the cholesterol level can be raised by shorter chain fatty acids (Rose, 1990). It was therefore interesting to compare breeds extreme in terms of fatness. The adipose tissue proportion of the Belgian Blue double muscled type (BBDM) is low while that in Holstein is high, the Belgian Blue dual purpose (BBDP) type being intermediate. The present experiment was designed to investigate how large difference in degree of fatness can be associated with differences in fatty acid composition.Four bulls of the 3 breeds were used in a fattening trial. Their initial weight was 340 kg. Biopsy samples were taken from the Longitimus Dorsi (LD) at weeks 5 and 16 of the fattening period. They were slaughtered after 145 days. The 7-8-9 ribs and perirenal fat (PR) were removed at slaughter. Intramuscular (M) and intermuscular (IM) fats of the LD were obtained after dissection of the 7-8-9 ribs.

Fluoride: Benefits And Risks of Exposure

This summarizes current knowledge of the benefits and risks of fluoride ingestion. The preponderance of evidence indicates that fluoride can reduce the incidence of dental caries and that fluoridation of drinking water can provide such protection. Due to the ubiquitous nature of exposures to fluoride sources other than drinking water, it is currently impossible to draw firm conclusions regarding the independent effect of fluoride in drinking water on caries prevalence using an ecologic study design. Moderate dental fluorosis occurs in 1 to 2% of the population exposed to fluoride at 1 mg/l in drinking water and in about 10% of the population at 2 mg/l; moderate/severe fluorosis occurs in variable percentages ranging up to 33% of the population exposed to fluoride at 2.4 to 4.1 mg/l in drinking water. The issue of whether moderate or severe dental fluorosis represents an adverse health effect is still controversial. There is no evidence of skeletal fluorosis among the general U.S. population exposed to drinking water fluoride concentrations lower than 4 mg/l. Radiographically detected osteosclerosis after chronic exposure to fluoride in drinking water at 8 mg/l was not associated with clinical symptoms. Reports of crippling skeletal fluorosis associated with low concentrations of fluoride in drinking water in tropical countries have been attributed to other dietary factors. The available data suggest that some individuals may experience hypersensitivity to fluoride-containing agents. Further studies on hypersensitivity are required. There is no evidence of increased incidence of renal disease or renal dysfunction in humans exposed to up to 8 mg fluoride per liter in drinking water. Structural changes in kidneys of experimental animals have been detected at doses exceeding 1 to 5 mg fluoride per kilogram per day. Based on four case reports, individuals with renal insufficiency who consume large volumes of naturally fluoridated water at 2 to 8 mg/l are possibly at increased risk of developing skeletal fluorosis. Studies on the effects of fluoride in individuals with renal insufficiency are needed. There is no evidence that chronic exposure to concentrations of fluoride reported to be greater than 2 mg/l in drinking water increases human cancer mortality or incidence. A study of lifetime exposure to fluoride on cancer incidence in rats and mice has been completed, but assessment for cancer has not been completed. There is no evidence that fluoride is genotoxic except in some in vitro assays at cytotoxic concentrations. There is no in vivo evidence that fluoride affects human cellular enzyme activities.(ABSTRACT TRUNCATED AT 400 WORDS)

Cytosine methylation and the fate of CpG dinucleotides in vertebrate genomes.

The dinucleotide CpG is a "hotspot" for mutation in the human genome as a result of (1) the modification of the 5' cytosine by cellular DNA methyltransferases and (2) the consequent high frequency of spontaneous deamination of 5-methyl cytosine (5mC) to thymidine. DNA methylation thus contributes significantly, albeit indirectly, to the incidence of human genetic disease. We have attempted to estimate for the first time the in vivo rate of deamination of 5mC from the measured rate of 5mC deamination in vitro and the known error frequency of the cellular G/T mismatch-repair system. The accuracy and utility of this estimate (md) was then assessed by comparison with clinical data, and an improved estimate of md (1.66 X 10(-16) s-1) was derived. Comparison of the CpG mutation rates exhibited by globin gene and pseudogene sequences from human, chimpanzee and macaque provided further estimates of md, all of which were consistent with the first. Use of this value in a mathematical model then permitted the estimation of the length of time required to produce the level of "CpG suppression" currently found in the "bulk DNA" of vertebrate genomes. This time span, approximately 450 million years, corresponds closely to the estimated time since the emergence and adaptive radiation of the vertebrates and thus coincides with the probable advent of heavily methylated genomes. An accurate estimate of the 5mC deamination rate is important not only for clinical medicine but also for studies of gene evolution. Our data suggest both that patterns of vertebrate gene methylation may be comparatively stable over relatively long periods of evolutionary time, and that the rate of CpG deamination can, under certain limited conditions, serve as a "molecular clock".

Rift valley fever among domestic animals in the recent west African outbreak

Severe haemorrhagic disease among the human population of the Senegal River Basin brought the Rift Valley fever virus (RVFV) outbreak of 1987 to the attention of science. As in previous RVFV outbreaks, local herdsmen reported a high incidence of abortion and disease in their livestock. Serum samples were obtained from domestic animal populations from areas near Rosso, the best studied focus of human infection, as well as other areas distant from known human disease. Among animals from the area of high incidence of human disease, antibody prevalence was as high as 85%, with approximately 80% of the sera positive for both RVFV IgG- and viral-specific IgM antibodies. In contrast, human populations in the same area had lower RVFV antibody prevalences, 40% or less, with 90% also being IgM-positive. Sera from livestock in coastal areas 280 km south of the epidemic area were negative for RVFV antibodies. Thus, the detection of RVFV specific IgG and IgM antibodies provided evidence of recent disease activity without the requirement to establish pre-disease antibody levels in populations or individuals and without viral isolation. Subsequently, detection of modest levels of IgG and IgM in the Ferlo region, 130 km south of the Senegal River flood plain, established that RVFV transmission also occurred in another area of the basin. Similar serological testing of domestic ungulates in The Gambia, 340 km south of Rosso, demonstrated antibody prevalence consistent with a lower level of recent transmission of RVFV, i.e., 24% IgG-positive with 6% of the positive sera also having RVFV-specific IgM.

The CpG dinucleotide and human genetic disease

Reports of single base-pair mutations within gene coding regions causing human genetic disease were collated. Thirty-five per cent of mutations were found to have occurred within CpG dinucleotides. Over 90% of these mutations were C----T or G----A transitions, which thus occur within coding regions at a frequency 42-fold higher than that predicted from random mutations. These findings are consistent with methylation-induced deamination of 5-methyl cytosine and suggest that methylation of DNA within coding regions may contribute significantly to the incidence of human genetic disease.

Transfusion-Acquired Babesiosis and Failure of Antibiotic Treatment

HUMAN babesiosis is a zoonosis characterized by fever, malaise, and hemolytic anemia. In the United States, the disease is generally caused by the species Babesia microti , a protozoan parasite of rodents, and is transmitted by Ixodes dammini , the northern deer tick. 1 Most of the 200 known cases of human babesiosis in the United States followed exposure to I dammini on the coastal islands of the Northeast, particularly Nantucket Island, Massachusetts, and Shelter Island, New York. Asymptomatic infections occur frequently 2 and create potential for transmission of infection through blood donation. 3-6 Recently the range of I dammini , which is also the principal vector of Lyme disease, has increased dramatically, with a resulting increase in the incidence of human babesiosis and Lyme disease. 7 Herein we report the first case of babesiosis acquired in New Hampshire and cite evidence indicating that the infection was transfusion acquired. This case also documents

Resistance to bacterial and parasitic infections in the nutritionally compromised host.

Over the past few years the relationships and interactions of diet, disease, and immunology are becoming better defined with the development and understanding of host defenses. Nutritional state, immunity, and disease all influence each other in the hospitalized patient, the elderly, and the young. Disease can alter nutritional needs and immune responses to antigens. The roles of both dietary excesses and deficiencies on cellular, secretory, and humoral immune responses are related to diseases and disease incidence in humans and experimental animals. Malnutrition alters incidence and severity of fungal, bacterial, viral, and parasitic pathogens. The mechanisms of altered disease resistance in nutritionally stressed animal models occurs via changes in the lymphoreticular endothelial system. The effects of common nutritional deficiencies, low protein, and low carbohydrate diets on antibody production, macrophage function, secretory IgA synthesis, and T-cell functions. Nutritional supplementation can increase lymphocyte function and decrease growth of some pathogens and tumors. Alternatively, obesity and high fat have roles in infectious disease and immunity.

Socially Tolerable Cigarette Smoke?-Reply

The first issue raised by Dr Homburger on our recent article inThe Journalis the possible alteration in the proportion of toxic smoke constituents of today's cigarettes compared with pre-1960 cigarettes. The formulation of today's low tar and low nicotine cigarettes is carried out by processes that reduce quantitatively, and largely nonselectively, the amount of smoke produced in both the particulate phase (which contains tar, nicotine, and water) and the gas phase (which contains the other smoke constituents). Table 3 of our article suggests this overall quantitative reduction, in that the six constituents addressed are reduced for each of the cigarette brands listed. The constituents considered were chosen because these have been implicated in human disease incidence. These and other constituents have been addressed by the National Cancer Institute's Smoking and Health Program, where over 130 types of experimental cigarettes have been tested for potentially lower toxicity.

The Cholesterol Problem, the Egg and Lipid Metabolism in the Laying Hen

There is little doubt that high blood serum lipid levels are related to a higher incidence of atherosclerotic disease in humans. Experimental evidence to date suggests that dietary intervention can reduce blood lipid levels in most cases and that some small reduction in occurrence of cardiovascular disease will probably result. On the other hand no reduction in total mortality has been demonstrated in the well constructed dietary studies.It appears that there is considerable variation in the human population with regard to their patterns of lipid metabolism. Some apparently regulate body production of cholesterol in response to dietary changes, others do not. Some seem to excrete excess sterols efficiently, while some do not. It seems likely, therefore, that dietary manipulation would be useful for those disposed by heredity and other conditions to accumulation of excessive sterols in the body. On the other hand drug control of cholesterol biosynthesis and/or sterol excretion may be more effective solutions to the problem of sterol accumulation. Irrespective of whether diet or drugs prove to be the best answer to control of sterol balance, these should be applied only to that segment of the population known to require such treatment.The egg is an important dietary source of cholesterol and as a result is used sparingly in low cholesterol diets. On the other hand normal egg consumption of two eggs per day does not appear to overload cholesterol balance in the healthy human adult since depression in cholesterol biosynthesis and increased sterol excretion will result.Investigation of the lipid metabolism of the laying hen has shown that most of the cholesterol found in the egg is synthesized in the liver where it is under both dietary and drug control. Most of the cholesterol deposited in egg yolk may be essential for embryonic development. Drugs that severely limit cholesterol biosynthesis probably also limit synthesis of adrenal and sex hormones and hence limit reproduction. Moderate depressions in lipogenesis achieved without feeding of large amounts of dietary fat may offer a means for moderating cholesterol deposition in eggs. On the other hand, it also seems clear that genetic selection could be used to moderate egg cholesterol concentration. In any event, a great deal more evidence from well constructed human diet studies will be needed before low cholesterol diets can be recommended to the general population as an aid to control of cholesterol balance and heart disease.

Social Medicine at Oxford

THE Nuffield Provincial Hospitals Trust, with the approval of Lord Nuffield, is to devote £10,000 a year for ten years to the creation in the University of Oxford of a University professorship of social medicine, and the foundation of an institute in which the professor will work. The purposes of the institute are: “To investigate the influence of social, genetic, environmental, and domestic factors on the incidence of human disease and disability. To seek and promote measures, other than those usually employed in the practice of remedial medicine, for the protection of the individual and of the community against such forces as interfere with the full development and maintenance of man's mental and physical capacity. If required by the university to do so, to make provision in the institute for the instruction in Social Medicine of students and practitioners ol medicine approved by the Board of the Faculty oi Medicine in the University of Oxford”.

Relation of Incidence of Human and Animal Serum Disease

Relation of Incidence of Human and Animal Serum Disease