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Other studies in Brazil showed a prevalence of less than 1% in 264 food handlers in the state of Minas Gerais; 10 discount 5mg prednisone amex allergy notes. In Argentina during 1989–1999 prednisone 20mg fast delivery allergy testing asthma, the prevalence rate was 2% in 207 children from Corrientes and 83. During that same period, the infection was found in 20% of 241 Sudanese refugees and in 33% of 275 children in southern Sudan; 4% of 70 children in Kenya; 6. The infection rate can reach as high as 85% in poor socioeconomic groups living in warm, humid regions of the tropics and in institutions such as hospitals for the men- tally ill, where there are frequent opportunities for fecal contamination. Strongyloidiasis in dogs appears to be distributed worldwide, but its prevalence is moderate. In a study conducted in a small town in the Democratic Republic of Congo, the prevalence was 34% in 76 children examined and 48% in 185 individuals from the general population (Brown and Girardeau, 1977). In another area, the infection rates were 7% and 2%, respectively, for the two species. The evidence suggests that, even though host immunity inhibits the development and pathogenicity of larvae, it does not terminate the infection. These hypobiotic larvae can remain in the patient’s tissues for years as an asymptomatic and overlooked infection, until a breakdown of immunity enables them to resume their development and become pathogenic once again. Mild infec- tions are usually well tolerated in immunocompetent individuals and produce no symptoms at all, or at most only vague and variable intestinal complaints. However, in persons with large parasite burdens or lowered immunity, the clinical picture can be cutaneous, pulmonary, or digestive, depending on the localization of the parasite, and the seriousness of the infection can range from mild to fatal (Liu and Weller, 1993). The cutaneous symptoms that develop when the larva penetrates the skin may be the only manifestation of the infection apart from peripheral eosinophilia. The first sign is a small erythematous papule at the invasion site, which may be associated with intense pruritus, urticaria, and petechiae in patients who have been sensitized by previous exposure. After that, a linear, serpiginous, urticarial inflammation appears, known as larva currens, which is virtually pathognomonic of the infection; a similar lesion can be caused by the larvae of nonhuman ancylostomids such as Ancylostoma braziliense and A. Some patients experience periodic urticaria, maculopapular exanthema, and pruritus, coinciding with attacks of diarrhea and the reappearance of larvae in feces. During the larvae’s pulmonary migration phase, symptoms may range from an irri- tating cough to full-blown pneumonitis or bronchopneumonia, sometimes with eosinophilic pleural effusion (Emad, 1999). A review of patients with severe pul- monary manifestations revealed that most of them had had some risk factor for strongyloidiasis, such as corticosteroid use, age over 65 years, chronic pulmonary disease, use of antihistamines, or some chronic debilitating disease. Almost all the patients were experiencing cough, dyspnea, panting, and hemoptysis; in addition, 90% had pulmonary infiltrates, 75% had peripheral eosinophilia, 60% were suffer- ing from secondary infections, 45% had adult respiratory distress syndrome, 15% had bacterial lung abscesses, and 30% of the patients died (Woodring et al. In most cases, the bronchopulmonary manifestations are discrete and disappear within a few days. The intestine of para- sitized individuals shows villous atrophy and cryptal hyperplasia (Coutinho et al. Depending on the severity of the lesions caused by the parasites in the intes- tinal mucosa, the symptoms may correspond to an edematous catarrhal enteritis with thickening of the intestinal wall or an ulcerative enteritis. Among the other symp- toms, epigastric pain, diarrhea, dyspepsia, nausea, and vomiting are common. Although 50% or more of infected individuals do not present symptoms, it should be kept in mind that asymptomatics can suddenly develop serious clinical disease if their immune resistance is lowered. This aggrava- tion of a preexisting infection may come from a rapid rise in the parasite burden due to an endogenous hyperinfection triggered by the renewed development of hypobi- otic larvae following the breakdown of immunity. A disruption of this kind in the equilibrium of the host-parasite relationship can occur in individuals weakened by concurrent illnesses, malnutrition, treatment with immunosuppressive drugs, or immunodeficiency diseases. Several fatal cases of strongyloidiases have occurred in patients treated with cor- ticosteroid or cytotoxic drugs. Most of these patients did not have symptoms of the infection and were not shedding larvae until the treatment was initiated. The clini- cal picture consists of ulcerative enteritis with abdominal pain, intense diarrhea, vomiting, malabsorption, dehydration, hypoproteinemia, and hypokalemia, and it can sometimes lead to death. In most of these cases, the predominant symptoms are respiratory and pulmonary (Celedón et al. Often, sec- ondary bacterial infections can develop, such as bacteremia, peritonitis, meningitis, endocarditis, and abscesses at various sites. It is believed that the filariform larvae spread bacteria from the intestine to different parts of the body (Ramos et al. The parasite does not seem to affect the organ recipient as long as he or she is receiving cyclosporin but can appear when the drug is suspended, perhaps because cyclosporin also has an inhibitory effect on the nematode (Palau and Pankey, 1997). Because simulta- neous parasitoses occur so frequently in the tropics, it is difficult to link a particular symptom to a specific parasite. The most common complaints associated with this agent are abdominal pain and occasional diarrhea, as was observed in patients in Zambia and also in an experimentally infected volunteer (Hira and Patel, 1977). Dogs and cats that have gotten rid of the parasite, either spontaneously or with treat- ment, are resistant to reinfection for more than six months. Unlike the human infec- tion, which generally lasts for a long time if left untreated, the parasitosis in animals is of limited duration. In sympto- matic cases, the first signs to appear in puppies are loss of appetite, purulent con- junctivitis, cough, and sometimes bronchopneumonia. The larval penetration phase can produce violent pruritus, erythema, and alopecia. The intestinal phase begins a week to 10 days later, with diarrhea, abdominal pain, and vomiting. Serious cases may include dehydration, emaciation, bloody diarrhea, and anemia, and they can even lead to death. In experimental infections, it has been observed that strongy- loidiasis can become chronic in some adult dogs, but in veterinary practice the dis- ease is limited to puppies. In mas- sive infections, the disease can be severe in weakened or very young animals. Source of Infection and Mode of Transmission: Man is the principal reservoir of S. For both man and animals, the main source of infection is feces that contaminate the soil. The parasite usually enters by the cutaneous—rarely the oral— route, when the host comes in contact with third-stage or filariform larvae. Warm, moist soil is propitious for exogenic development of the heterogonic (indirect) cycle, which produces the free-living nematodes, because it allows for rapid multiplication of the infective larvae. For this reason, the infection is more common in tropical than in subtropical regions. The role of dogs and cats in the epidemiology of strongyloidiasis has not yet been fully clarified. The susceptibility of dogs to certain biotypes or geographic strains would suggest that, at least in some parts of the world, these animals may contribute to human infection by contaminating the soil. However, the literature has recorded only one case (Georgi and Sprinkle, 1974) in which the source of human infection was attributed to canine feces. It is difficult to determine the frequency of human- animal cross-infections because there are no characteristics that distinguish the adults or larvae of S.

He holds bachelor’s and and Oxford universities buy 5 mg prednisone allergy forecast the woodlands tx, and he holds an adjunct appointment master’s degrees in engineering from McMaster and McGill at Harvard University as professor of population and interna- Universities and a Ph discount 40mg prednisone free shipping allergy treatment in vellore. Ezzati’s research interests center around understanding the causal determinants Colin D. Mathers is a senior scientist in the Evidence and of health and disease, especially as they change in the process of Information for Policy Cluster at the World Health social and economic development and as a result of technolog- Organization in Geneva. World Health Organization’s Epidemiology and Burden of xix His current research focuses on two main areas. Murray is the Richard Saltonstall professor of area is the relationship among energy, air pollution, and health public policy, professor of social medicine, and director of the in developing countries, on which he conducts field research Harvard Initiative for Global Health. This research has led to university, for five years he led the World Health Organization’s the identification and design of technological interventions for Evidence and Information for Policy Cluster, which was dedi- reducing exposure to indoor air pollution from household cated to building the evidence base and fostering a culture of evi- energy use. His second area of research is major health risk fac- dence to inform health decision making. The cluster was respon- tors and their role in the current and future disease burden sible for work on epidemiology and the burden of disease, the globally and in specific countries and regions. His research on World Health Survey,cost-effectiveness analysis,national health risk factors focuses on environmental risks, smoking, and accounts, catastrophic health spending, responsiveness, health nutritional risks. He was the lead scientist for the World Health financing policy, human resources for health systems, coverage Organization’s Comparative Risk Assessment Project, which of health interventions, quality of care and patient safety, stew- was reported in the World Health Report 2002: Reducing Health, ardship of health systems,assessment of health system perform- Promoting Healthy Life. He is currently studying the role of ance,health research policy,and a range of efforts to manage and major risk factors in health inequalities. Jamison is a professor of health economics in the School focused on tuberculosis control and the development with of Medicine at the University of California, San Francisco Alan D. Jamison concurrently serves as an Adjunct Professor in both metric for comparing deaths and disabilities caused by various the Peking University Guanghua School of Management and diseases and the contribution of risk factors to the overall bur- in the University of Queensland School of Population Health. Jamison was on the faculty of the neering effort has been hailed as a major landmark in public University of California, Los Angeles, and also spent a number health and an important foundation for policy formulation of years at the World Bank, where he was a senior economist and priority setting. Murray has contributed to in the research department, division chief for education the development of a range of new methods and empirical policy, and division chief for population, health, and nutri- studies for strengthening the basis for population health meas- tion. In 1992–93 he temporarily rejoined the World Bank to urement and cost-effectiveness analysis. A main thrust of his serve as Director of the World Development Report Office work has been the conceptualization, measurement, and appli- and as lead author for the Bank’s 1993 World Development cation of approaches to understanding the inputs, organiza- Report: Investing in Health. His publications are in the areas of tion, outputs, and outcomes of health systems. Jamison or edited eight books, many book chapters, and more than 90 studied at Stanford (B. National Academies, Gainesville, Florida, United States Perla Santos Ocampo President, National Academy of Science and Thechnology, San Guy de Thé, Co-chair Juan, Philippines Research Director and Professor Emeritus, Institut Pasteur, Paris, France G. Academy of Medical Sciences, Cambridge, Gates Foundation, Seattle, Washington, United States United Kingdom xxi Misael Uribe Witold Zatonski President, National Academy of Medicine of Mexico, Mexico Professor, Health Promotion Foundation, Warsaw, Poland City, Mexico Zhengguo Wang Professor, Chinese Academy of Engineering, Daping, China xxii | Advisory Committee to the Editors Contributors Stephen J. Murray World Bank Harvard University Initiative for Global Health; Harvard School of Public Health Goodarz Danaei Harvard School of Public Health; Harvard University Anthony Rodgers Initiative for Global Health University of Auckland Majid Ezzati Joshua Salomon Harvard School of Public Health; Harvard University Harvard School of Public Health Initiative for Global Health Sonbol A. Jamison Population Reference Bureau; Disease Control Priorities University of California, San Francisco; Disease Control Project Priorities Project Stephen Robert Vander Hoorn Julian Jamison University of Auckland University of California, Berkeley Jelka Zupan Joy E. Lopez University of Queensland; Harvard School of Public Health xxiii Disease Control Priorities Project Partners The Disease Control Priorities Project is a joint enterprise of billion to $22 billion each year in loans to its client countries, the Fogarty International Center of the National Institutes provided $1. The World Bank is working in more than 100 developing and the Population Reference Bureau. For 75 years, the The World Health Organization is the United Nations’ spe- bureau has analyzed complex data and research results to cialized agency for health. Its objective, as set out in its consti- provide objective and timely information in a format easily tution, is the attainment by all peoples of the highest possible understood by advocates, journalists, and decision makers; level of health, with health defined as a state of complete phys- conducted workshops around the world to give key audiences ical, mental, and social well-being and not merely the absence the tools they need to understand and communicate effec- of disease or infirmity. Breman, Mariam Claeson, tutions and individuals spanning a period of more than David B. Richard Suzman of the National Institute on from the contributions of those institutions and the efforts of Aging provided invaluable support and critical reactions. National medical academies or medical divisions of the scientific Institutes of Health. National Bank’s Health, Nutrition, and Population Department, Academy of Sciences, the U. Patrick Kelley and Dianne Stare of the Institute of involvement of Bank staff as coauthors and reviewers. Medicine managed this effort and provided critical, substan- • The World Health Organization. Evidence and Information for Policy Cluster, Christopher The Office of the Publisher at the World Bank provided Murray and Timothy Evans, coordinated the involvement of outstanding assistance, enthusiastic advice, and support dur- the World Health Organization. For much of the past eight ing every phase of production of this volume and helped years, the Evidence and Information for Policy Cluster has coordinate publicity and initial distribution. We particularly sponsored research and analysis central to this volume and wish to thank Dirk H. Rossel, Mary Fisk, Randi Park, Santiago Pombo-Bejarano, • The Bill & Melinda Gates Foundation. The book simply effort, and we are grateful for their contributions and hospital- could not have been completed without her efforts and we ity. University and Trish Sharkey and Kim Wicks at the University of Queensland for their valuable assistance. Murray In an era when most societies must cope with increasing changing, so that the information is more relevant for health demand for health resources, they will inevitably have to policy and planning purposes. Such planning must take into account of methods for assessing the reliability of data and imputing the needs that the health system must address; that is, policy missing data, and the use of a common metric to summarize makers must be aware of the comparative burden of diseases the disease burden from diagnostic categories of the and injuries and the risk factors that cause them, and how International Classification of Diseases and the major risk this burden is likely to change with the adoption of various factors that cause those health outcomes. Needs are, of course, not the a simplified version of this framework and indicates the only factors determining service provision, but should be a causal chain of events that matter for health outcomes, critical component of the decision-making and planning identifying the key components and determinants of health processes. What is needed accounting and for guiding the determination of health is a framework for integrating, validating, analyzing, and research priorities, for example, Australia (Mathers,Vos, and disseminating the fragmentary, and at times contradictory, Stevenson 1999); the state of Andra Pradesh, India information that is available on a population’s health, along (Mahapatra 2002); Mauritius (Vos and others 1995); Mexico with some understanding of how that population’s health is (Lozano and others 1995); South Africa (Bradshaw and 1 Distal Nonhealth socioeconomic Proximal Functional well-being and determinants Diseases and Impairments limitations environmental (risk factors) injuries (disability) causes Death Source: Mathers and others 2002. Note: This presentation is intended as a broad schema: for example, some exposures, such as environmental factors, can be proximate causes of disease, and injuries can lead directly to death. In order to recommend intervention den of disease analysis to the formulation of health policy. A concluding section takes stock of the (World Bank 1993; Jamison and Jardel 1994). Whereas work on disease burden since the early 1990s and suggests earlier attempts to quantify global cause of death patterns some key areas for further work. Chapter 3 reports on deaths and the disease and dataarelikelytocontainusefulinformationprovidedtheyare injury burden by age, sex, and 136 disease and injury cate- carefully screened for validity and completeness. Chapter 4 reports on the disease and injury burden priate methods, investigator commitment, and expert judg- resulting from 19 risk factors, specifically for a number of ment, obtaining internally consistent estimates of the global important conditions.

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Flinders University reserves the right to alter any information contained herein without prior notice. Introduction Ponemon Institute is pleased to present the findings of Medical Device Security: An Industry Under Attack and Unprepared to Defend, sponsored by Synopsys. The purpose of this research is to understand the risks to clinicians and patients because of insecure medical devices. To ensure a knowledgeable respondent participants in this research have a role or involvement in Figure 1. How likely is an attack on one or the assessment of and contribution to the more medical devices built or in use by your security of medical devices. Very likely and Likely responses combined In the context of this research, medical devices are any instrument, apparatus, appliance, or other article, whether used alone or in combination, including the software intended by its manufacturer to be used for diagnostic and/or therapeutic purposes. Examples range from simple devices such as medical thermometers to those that connect to the Internet to assist in the conduct of medical testing, implants, and prostheses. The following medical devices are manufactured or used by the organizations represented in this research: robots, implantable devices, radiation equipment, diagnostic & monitoring equipment, networking equipment designed specifically for medical devices and mobile medical apps. Despite the risks, few organizations are taking steps to prevent attacks on medical devices. Ponemon Institute: Private & Confidential Report 1 The research reveals the following risks to medical devices and why clinicians and patients are at risk. Both device makers and users have little confidence that patients and clinicians are protected. The use of mobile devices is affecting the security risk posture in healthcare organizations. Eighty percent of medical device manufacturers and users in this study say medical devices are very difficult to secure. Further, only 25 percent of respondents say security protocols or architecture built inside devices adequately protects clinicians and patients. In many cases, budget increases to improve the security of medical devices would occur only after a serious hacking incident occurred. Respondents believe their organizations would increase the budget only if a potentially life threatening attack took place. As a result, both manufacturers and users concur that medical devices contain vulnerable code due to lack of quality assurance and testing procedures and rush to release pressures on the product development team. Medical devices contain vulnerable code because of a lack of quality assurance and testing procedures as well as the rush to release. Device makers say another problem is the rush to release pressures on the product development team (50 percent). Only 9 percent of manufacturers and 5 percent of users say they test medical devices at least annually. Forty-three percent of manufacturers do not test (36 percent) or are unsure if testing takes place (7 percent). Accountability for the security of medical devices manufactured or used is lacking. Ponemon Institute: Private & Confidential Report 2 Manufacturers and users of medical devices are not in alignment about current risks to medical devices.

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For other leading diseases of this group order cheapest prednisone allergy shots effectiveness, such as diar- This illustrates the large order prednisone 40 mg with mastercard allergy symptoms medications, and at times neglected, disease rhea and lower respiratory infections, most epidemiological burden from risks that affect young adults, especially in low- studies have focused on children younger than five and do and-middle-income countries, with important conse- not provide estimates of hazardous effects for older children. The outcomes of these two risk factors were income may affect smoking, physical activity, and diet, mostly communicable, maternal, perinatal, and nutritional which are risk factors for cardiovascular diseases, both conditions, which dominate the disease burden in high- directly and through further layers of such intermediate mortality developing regions. In addition to their relative magnitude, the absolute loss Multicausality also means that a range of interventions can of healthy life years attributed to risk factors in low- and be used for disease prevention, with the specific choices middle-income regions is enormous. In these regions, which determined by factors such as cost, technology availability, account for 85 percent of the global population, childhood infrastructure, and preferences. Therefore, the second term in tiple determinants acting simultaneously (Rothman 1976; the right-hand-side of equation 4. One minus this term is the fraction ease due to multiple risk factors is theoretically unbounded. Although epidemiologically unavoidable and conceptu- Estimating the joint effects of multiple risk factors is, in ally acceptable, the lack of additivity adds to policy complex- practice, complex and does not follow the simple, inde- ity and implies the need for great care when interpreting and pendent, and uncorrelated relationship of equation 4. When estimating the total effects of individual distal factors on disease, both mediated and direct effects should be considered, because, in the presence of mediated effects, controlling for the intermediated factor would attenuate the effects of the more distal one (Greenland 1987). First, some of the effects of the more distal underweight, other micronutrient deficiencies, and unsafe factors, such as physical inactivity, are mediated through water and sanitation (third issue). For instance, a proportion of the haz- smoking may not only be correlated (third issue), but also ards of physical inactivity is mediated through overweight affect each other’s hazard for some diseases (second issue) and obesity, which is itself mediated through elevated blood (Rothman and Keller 1972). Estimating the joint effects of distal and intermediate factors requires knowledge of independ- Data Sources for Mediated Effects and Effect Modification ent hazards of the distal ones (versus individual risk factor effects, which are based on total hazard). Second, the hazard Despite the emphasis on removing or minimizing the effects due to a risk factor may depend on the presence of other risk of confounding in epidemiological research, mediated and factors (Koopman 1981; Rothman and Greenland 1998) stratified hazards have received disproportionately little (effect modification). We therefore reviewed the literature and exposures to multiple risk factors because they are affected reanalyzed cohort data to strengthen the empirical basis for by the same distal factors and policies. The sensitivity of estimates to nutrition, unsafe water and sanitation, and use of solid fuels these assumptions were negligible as described in detail else- are more common among poor rural households in devel- where (Ezzati, Vander Hoorn, and others 2004; Ezzati and oping countries and smokers generally have higher and others 2003). The epidemiological literature refers to the first and second Epidemiological studies of the effects of overweight and issues as biological interaction and the third issue as statistical obesity, physical inactivity, and low fruit and vegetable interaction (Miettinen 1974; Rothman and Greenland 1998; intake on cardiovascular diseases have illustrated some Rothman, Greenland, and Walker 1980). This distinction is, attenuation of the effects after adjustment for intermediate however, somewhat arbitrary, and the three scenarios may factors such as blood pressure or cholesterol (Berlin and occur simultaneously. For example, zinc deficiency affects Colditz 1990; Blair, Cheng, and Holder 2001; Eaton 1992; mortality from diarrhea directly as well as by reducing growth Gaziano and others 1995; Jarrett, Shipley, and Rose 1982; (first issue) (Brown and others 2002; Zinc Investigators’ Jousilahti and others 1999; Khaw and Barrett-Connor 1987; Collaborative Group 1999), and may also be correlated with Liu and others 2000, 2001; Manson and others 1990, 2002; Comparative Quantification of Mortality and Burden of Disease Attributable to Selected Risk Factors | 253 Rosengren, Wedel, and Wilhelmsen 1999; Tate, Manfreda, nutrition and previous infection (Pelletier, Frongillo, and and Cuddy 1998). The extent of attenuation has smoke from household use of solid fuels and unsafe water, varied from study to study, but has consistently been less sanitation, and hygiene, which result in lower respiratory than half of the excess risk of the distal factors. We used an infections and diarrhea respectively, may be mediated estimate of 50 percent as the proportion of the excess risk through underweight. In a review of the literature, Briend from these risk factors mediated through intermediate fac- (1990) concludes that attempts to disentangle direct tors that are themselves among the selected risks. To include and mediated contributions,especially over the long periods effect modification, we used deviations from the multiplica- needed to affect population-level anthropometry, have not tive model of 10 percent for ischemic heart disease and established diarrhea as a significant cause of underweight. To account for potential mediated effects, Joint Hazards of Smoking and Other Risk Factors. Liu we considered an upper bound of 50 percent on the pro- and others (1998, figures 4 and 6) find that in China, the portion of the excess risks from indoor smoke from house- relative risks of mortality from lung and other cancers, hold use of solid fuels and unsafe water, sanitation, and respiratory diseases, and vascular diseases are approximately hygiene mediated through underweight in regions where constant in different cities where mortality rates for these underweight was present. Studies that stratified hazards of smoking on serum choles- terol have confirmed this finding (Jee and others 1999). Risk Factor Correlation Joint Hazards of Childhood Undernutrition for To estimate the joint effects of risk factors with a continuous Infectious Diseases. Abel 1995; Ramakrishnan and Martorell 1998; West and Similarly, for categorical risk factors, positive correlation others 1991). Anthropometric (growth) be considerably smaller than the joint attributable indicators of childhood nutrition, such as weight-for-age, fraction, as described in detail elsewhere (Ezzati and are aggregate measures of multiple factors that include others 2003). This confirms that the joint actions of more than one of All Selected Risk Factors these risk factors acting simultaneously or through other Table 4. Globally, an estimated 45 percent of (96 percent), diarrhea (92 percent), ischemic heart disease mortality and 36 percent of the disease burden were attrib- (80 percent), lung cancer (74 percent), stroke (65 percent), utable to the joint effects of the 19 selected risk factors. Sub- chronic obstructive pulmonary disease (64 percent), and Saharan Africa (49 percent of the disease burden) and lower respiratory infections (53 percent) were attributable Europe and Central Asia (46 percent of the disease burden) to the joint effects of the 19 risk factors considered here. As the table shows, for most diseases the joint a number of other diseases were attributed to the risk factors effects of these risk factors were substantially less than the considered here. Comparative Quantification of Mortality and Burden of Disease Attributable to Selected Risk Factors | 255 Table 4. These factors also contribute to other diseases that are not among the leading 10. Affected by smoking in the category “other respiratory diseases” or “selected other medical causes” (Ezzati and Lopez 2003, 2004; Peto and others 1992). An important finding of this analysis is the key role of high cholesterol, smoking, overweight and obesity, alcohol nutrition in health worldwide. Approximately 11 percent of use, physical inactivity, low fruit and vegetable intake, and the global disease burden was attributable to the joint effects urban air pollution), and child mortality (childhood under- of underweight or micronutrient deficiencies. In addition, weight; vitamin A deficiency; zinc deficiency; iron deficiency almost 16 percent of the burden (28 percent for those aged anemia; unsafe water, sanitation, and hygiene; and indoor 30 years and older) can be attributed to risk factors that have smoke from household use of solid fuels). The joint effects of these risk factors were mitigation of many such conditions, including malaria, much lower than the crude sum of individual effects (64 per- tuberculosis, and injuries, may be better guided by analyses cent versus 126 percent for the disease burden), pointing to of the effects of interventions tailored to individual settings the extensive overlap in their hazards for cardiovascular dis- than by risk factor analysis. The overlap is partly because the hazardous effects of some risks are mediated through others and partly because multiple risk factors act in combination. Coupled with substantially risks that may be of particular interest to disease prevention more cardiovascular deaths and a larger disease burden in policies and programs. The risk factor clusters were those low- and middle-income countries, these risk factors result in affecting cancers (alcohol use, smoking, low fruit and veg- a much larger loss of healthy life in these nations. By considering the health consequences of past and current exposure, nearly all sexually transmitted diseases are attributable to unsafe sex. This is because, in the absence of sexual transmission in the past, current infections transmitted through other forms of contact would not occur if the infected hosts acquired their infection sexually (and so on in the sequence of past infected hosts). Practically all the mortality and disease burden from proximal exposures using multiple interventions. Examples childhood diseases attributable to major risk factors of such integrated strategies include using education and occurred in low- and middle-income countries (table 4. In such research, risk factor groups should be selected based on both biological relationships and socioeconomic factors that affect multiple diseases. Once risk exposure and hazard for different risks and the existing data factors are selected, the emphasis on reducing confounding gaps revealed the areas where data and monitoring need to should be matched by equally important inquiry into inde- be improved for better quantification of important risks and pendent and mediated hazard sizes that are stratified based for more effective intervention. Important examples regional levels, for example, rural and urban areas or differ- include detailed data on alcohol consumption volumes and ent geographical regions of individual countries, and should patterns, dietary and biological markers for micronutrients, include micro-level data and possibly a more comprehen- physical activity, and indoor smoke from household use of sive list of both distal and proximal risk factors, such as solid fuels, all of which were quantified using indirect meas- adverse life events and stress, risk factors for injuries, salt ures with limited resolution. These are coupled with hazards such as alcohol use, The limited evidence on the effects of multiple risk fac- smoking, high blood pressure, high cholesterol, and over- tors and risk factor interactions also points to important weight and obesity that are globally widespread and have gaps in research on multirisk and stratified hazards. Including multiple layers of causality in epidemiological The large remaining burden due to childhood mortality research and risk assessment would allow investigators to risks such as undernutrition; unsafe water, sanitation, and estimate the benefits of reducing combinations of distal and hygiene; and indoor smoke from household use of solid Comparative Quantification of Mortality and Burden of Disease Attributable to Selected Risk Factors | 267 fuels indicates the persistent need for developing and deliv- tions to the disease burden in policy debate. Finally, while ering effective interventions, including lowering the costs of the burden of disease due to a risk factor may be compara- pertinent technological interventions. At the same time, tively small, effective or cost-effective interventions may be four of the five leading causes of lost healthy life affect known.

The potential geographical distribution of the Old World screw-worm fly generic 5mg prednisone with mastercard allergy testing jersey channel islands, Chrysomya bezziana cheap 5 mg prednisone fast delivery allergy medicine on sale. Identification of screwworm species by polymerase chain reaction-restriction fragment length polymorphism. Partial sequencing of the cytochrome oxydase b sub- unit gene I: A tool for the identification of European species of blow flies for postmortem interval estimation. Studies on Rhinoestrus purpureus (Diptera: Oestridae) larvae infesting don- keys (Equus asinus) in Egypt. Etiology: There are two genera of pentastomids that are of medical interest: Linguatula and Armillifer, both of the family Porocephalidae. On rare occasions, Porocephalus (a snake parasite, with rodents as intermediate hosts), Leiperia (a croc- odile parasite, with fish as intermediate hosts), and Raillietiella (a lizard parasite, with cockroaches as intermediate hosts) have been mentioned as human parasites. Owing to the morphological and biological peculiarities of the pentastomids, their taxonomy and phylogenetic status are not yet well defined. On the basis of ultra- structural, embryologic, and genetic studies, they can be considered a class related to the arthropods (Self, 1982). Interestingly, almost all the adult parasites infest a host higher on the phylogenetic scale than the hosts of the larval forms, which sug- gests that the parasite evolved along with the host. The fact that the reverse is true in the case of certain pentastomids is difficult to explain, however. However, although their specific hosts seem to be limited, infections have been found in many animals. Except for a few epidemiological studies, human infection by pentastomids is infrequent: only eight cases had been reported in the United States up to 1991 (Guardia et al. Etiology: Linguatula serrata is a linguiform parasite with discreet transverse seg- mentation. The development cycle of the parasite requires herbivorous intermediate hosts, mainly sheep, goats, and lagomorphs. Bovines, deer, equines, swine, and various other mammals can also serve as intermediate hosts. Linguatula lays its eggs in the upper respiratory passages of the host, and they are then expelled into the environment by sneezing or splitting, or if swallowed, with the feces. The eggs ingested by the intermediate host with food or water release the first-stage larvae in the intestine; they possess four clawed feet and an apparatus that enables them to perforate the intestinal wall. The larvae migrate through the blood to the internal organs and encyst in the lymph glands, the liver, spleen, lungs, and other organs, where they form small pentastomid nodules that are discovered during the veterinary inspection of meat. Between 250 and 300 days after infection and after some 12 molts within the cyst, the larva reaches the nymph, or infective stage. The nymph can break the cystic envelope, migrate through the peritoneal cavity, and penetrate different tissues. If a carnivore consumes the tissues or organs of an infected intermediate host, the infective nymph migrates through the stomach and esophagus to the nasopharynx, where after several molts it reaches maturity and begins oviposition. Most cases have been reported in several countries of North Africa, Europe, and the Middle East. From 1989 to mid-2001, only one ocular case, in Ecuador, was reported worldwide (Lazo et al. The highest rates are seen in areas where dogs are fed raw viscera from sheep and goats. Data on the frequency of nymphal infection in domestic herbivores are not available. A study conducted in eight southeastern states found that 2% of 260 Sylvilagus floridanus rabbits had nymphs of L. When the infection occurs from the ingestion of eggs, the larvae become encapsulated in various organs, where they can survive up to two years. The larvae locate mainly in the liver, either below Glisson’s capsule or in the parenchyma and, to a lesser extent, in the mesentery and intestinal wall. The encysted nymphs do not produce clinical symptoms, and the infection is almost always discovered during surgery, radiologi- cal examination, or autopsy. Clinical cases of prostatitis, ocular infection (anterior chamber of the eye), and acute abdomen have been described; their origin is a par- asitized, inflamed lymph node adhering to the intestinal wall. The “halzoun” and “marrara” syndromes (infection of the human nasopharynx) are attributed to infec- tion caused by the nymph of L. The symptoms appear a few minutes to a half- hour after the infective food is eaten. The variation in the incubation period proba- bly depends on the place where the nymphs are released from their cysts, since the ones that are swallowed require more time to migrate to the tonsils and nasopha- ryngeal mucosa than the ones that become free in the mouth. Sometimes there is congestion and intense edema of the region, which may extend to the larynx, eustachian tube, conjunctiva, nose, and lips. At times, there is also dyspnea, dysphagia, vomiting, headaches, photophobia, and exophthalmia. The most serious symptomatology is believed to occur in persons sensitized by visceral infections with L. About half of the patients recover in less than one day; in others the illness may last one to two weeks. The Disease in Animals: The adult parasite causes a mucopurulent nasal catarrh, with sneezing, copious nasal discharge, and sometimes epistaxis in dogs. Larval infection in domes- tic herbivores and omnivores (intermediate hosts) is asymptomatic. Source of Infection and Mode of Transmission: The natural reservoirs are wild and domestic canids and, rarely, felids. Carnivores acquire the infection by ingest- ing viscera and tissues of infected intermediate hosts. In endemic areas, the cycles between dogs and goats and between dogs and sheep are of special interest. In the wild cycle, the infection circulates between wild herbivores and their carnivore predators. Herbivores become infected by ingesting pasture contaminated with feces or nasal secretions of the canids. Man contracts halzoun or marrara by consuming raw liver or lymph nodes from sheep, goats, or other infected domestic herbivores. Diagnosis: The visceral form (small pentastomid nodules) caused by nymphs is rarely diagnosed in living persons or domestic animals, except during surgery. Specific diagnosis is effected by identification of the nymph in a biopsy specimen. Histopathological examination reveals a granulomatous reaction with multiple eosinophilic abscesses, at the center of which degenerated nymphs are found. In very old cases, there may not be pathological findings around the calcified cysts. In dogs with suspicious nasal catarrh, diagnosis can be confirmed by detecting eggs in the nasal secretion or feces. Control: Visceral infection from ingestion of the eggs can be prevented by guard- ing against contamination of untreated water or raw food with carnivore depositions and washing hands carefully before eating. Halzoun and marrara or nasal infection with the adult parasite can be prevented by not consuming raw or undercooked vis- cera.

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Peppermint oil may benefit nonulcer dyspepsia discount prednisone 5mg with amex allergy symptoms tired, pro- vided a preexisting reflux problem is not worsened by relaxation of the car- diac sphincter quality 20mg prednisone allergy medicine 93. Raw crushed garlic18 and 386 Part Two / Disease Management goldenseal (500-mg tablet) can be taken for their antibacterial effects. Levenstein S: The very model of a modern etiology: a biopsychosocial view of peptic ulcer, Psychosom Med 62:176-85, 2000. Pignatelli B, Bancel B, Plummer M, et al: Helicobacter pylori eradication attenuates oxidative stress in human gastric mucosa, Am J Gastroenterol 96:1758-66, 2001. Elmstahl S, Svensson U, Berglund G: Fermented milk products are associated to ulcer disease. Pinn G: The herbal basis of some gastroenterology therapies, Aust Fam Phys 30:254-8, 2001. Zullo A, Rinaldi V, Hassan C, et al: Ascorbic acid and intestinal metaplasia in the stomach: a prospective, randomized study, Aliment Pharmacol Ther 14:1303- 9, 2000. Mills S, Bone K: Principles and practice of phytotherapy, Edinburgh, 2000, Churchill Livingstone. Furthermore, subjects with evidence of peripheral vascular or cardiac disease have, on average, a significant reduction in cognitive function equivalent to about 4 or 5 years of additional age. Despite consensus to treat risk factors for peripheral arterial disease and use exercise rehabilitation for patients with claudication, only antiplatelet ther- apy and possibly angiotensin-converting enzyme inhibitors for the preven- tion of ischemic events are conclusively supported by results of placebo-controlled trials that specifically investigated peripheral arterial disease. Intermittent claudication and absent distal pulses are indicative of impaired limb perfusion. The distance a patient can walk without needing to stop and rest is used as an indication of the severity of the disease. In chronic cases, nails are deformed and slow growing; muscles are atrophied; and the skin is shiny, atrophic, and hairless. Metabolic derangements, including impaired oxygen delivery and/or extraction, reduced nitric oxide synthesis, reduced glucose oxidation, accumulation of 389 390 Part Two / Disease Management toxic metabolites, and reduced carnitine availability all correlate with dis- ease severity. When successful, these measures substantially improve the patient’s quality of life by reducing the severity of claudication. Strong independent modifiable risk factors associated with the pathogen- esis of peripheral arterial disease are cigarette smoking, diabetes mellitus, an increased fibrinogen level, and/or increased systolic blood pressure. Nicotine and other products of cigarette smoke adversely affect lipids, blood coagulation, and vascular stability. Regular aerobic exercise stimulates vessel wall relaxation and develop- ment of a collateral circulation. Meta-analysis shows that patients with claudication who persisted with an exercise program for 6 or more months can increase their pain-free walking time by 180% and their maximal walk- ing time by 120%. Another study showed that 12 weeks of treadmill walking for 1 hour a day on 3 days of the week increased pain-free walking time and decreased the resting plasma short-chain acylcarnitine concentration. The reduced acylcarnitine levels correlated with improvement in peak walking time. Carnitine plays a major role in energy production at the mitochondrial level through stimulation of fatty acid metabolism. It improves glucose dis- posal, may reduce insulin resistance, and is important in energy production in muscle. Carnitine and its derivative, propionyl-L-carnitine, are endoge- nous cofactors that enhance carbohydrate metabolism and reduce the intra- cellular accumulation of toxic metabolites in hypoxic conditions. A randomized, double-blind, placebo-controlled trial demonstrated that pro- pionyl-L-carnitine, in doses of 2 g daily taken over a 6-month period, increased peak walking time and delayed the onset of pain. In addition to targeting energy production in an effort to limit anoxic damage, another therapeutic approach is to enhance perfusion. Interventions to reduce further vascular occlusion may represent attempts to dampen inflammation by using antioxidants and ω-3 fatty acids. Three months of administration of 40 g of extra-virgin olive oil and 16 g of fish oil daily favors a less atherogenic plasma-lipid profile in patients with periph- eral vascular disease. The vitamin C concentration is lower in patients with higher C-reactive protein levels and more severe peripheral arterial disease. A more effec- tive therapeutic choice may be α-tocopheryl nicotinate (200 mg three times daily). Niacin supplementation decreases low-density lipoprotein cholesterol and plasma fibrinogen levels in subjects with peripheral vascular disease. Significant improvement in patients with peripheral vascular disease has also been reported with administration of 2 g of inositol nicotinate twice daily for at least 3 months. Although arterial dila- tion may be a factor, it has been postulated that reduction in fibrinogen level, improvement in blood viscosity, and resultant improvement in oxygen transport all contribute to its therapeutic efficacy. Although high-dose niacin is reported to induce unwanted reactions including flushing, pruritus, gas- trointestinal complaints, and impaired glucose tolerance, no adverse effects have been reported in response to inositol hexaniacinate in doses of 4 g daily. L-Arginine has been found to be effective in a few patients with periph- eral vascular disease. In a meta-analysis of eight randomized, placebo-controlled, double-blind trials, Pittler and Ernst26 concluded that Ginkgo biloba extract was superior to placebo in the symptomatic treatment of intermittent claudication. Although ginkgo extracts are significantly more effective than placebo in increasing walking distance, the magnitude of the overall treatment effect is modest and of uncertain clinical relevance. The safety of garlic as a long-term treat- ment for intermittent claudication is uncertain. Arosio E, Cuzzolin L, De Marchi S, et al: Increased endogenous nitric oxide production induced by physical exercise in peripheral arterial occlusive disease patients, Life Sci 65:2815-22, 1999. Brevetti G, Diehm C, Lambert D: European multicenter study on propionyl- L-carnitine in intermittent claudication, J Am Coll Cardiol 34:1618-24, 1999. Langlois M, Duprez D, Delanghe J, et al: Serum vitamin C concentration is low in peripheral arterial disease and is associated with inflammation and severity of atherosclerosis, Circulation 103:1863-8, 2001. Linde K, ter Riet G, Hondras M, et al: Systematic reviews of complementary therapies—an annotated bibliography. Rahman K: Historical perspective on garlic and cardiovascular disease, J Nutr 131(3s):977S-979S, 2001. Ali M, Bordia T, Mustafa T: Effect of raw versus boiled aqueous extract of garlic and onion on platelet aggregation, Prostaglandins Leukot Essent Fatty Acids 60: 43-7, 1999. Anecdotal evidence suggests that women on a diet rich in fruits, vegetables, and soy products and low in dairy products and saturated fat before menstruation often experience fewer premenstrual symptoms. Despite inadequate scientific validation, nutritional modification has not been rejected as a therapeutic option, particularly for women with certain symptom patterns. A crossover study of women showed that a low-fat vegetarian diet was associated with an increased serum sex hormone binding globulin concen- tration and reductions in body weight, duration and intensity of dysmenor- rhea, and duration of premenstrual symptoms. Dietary avoidance of animal products in favor of plant products may modify gut bacteria and recirculation of glucuronide-linked estrogen.

The corresponding ratio is 3 in South Asia and more than 2 in East Asia order prednisone in india allergy gold, the Pacific buy line prednisone allergy treatment naet, Latin America, the Caribbean, the Middle East, and North Africa. But our interest lies not in the overall rate of transmission but in its reversal of male–female incidence. For example, it is possible that certain aspects of poverty can create “unintended” gender biases relative to the developed-country benchmark. A key finding is that heart disease accounts for a large fraction of excess female mortality. In developing countries, women simply die of cardiovascular disease at a rate closer to that of men. It could be genetic: for instance, the recently discovered “heart disease gene” so prevalent in South Asia (Dhandapany et al. Or it may truly be lack of “similar care”: women seek or receive medical care less often in developing countries, or may be subject to greater stress. Understanding why women appear to be at a particular disadvantage from cardiovascular disease is important work for future research. It is beyond the scope of this paper to disentangle the role of direct gender discrimination from other factors—biological, social, environmental, behavioural, or economic—in explaining the pervasive phenomenon of excess female mortality. By moving away from (while not abandoning) recent literature that highlights the importance of the sex ratio at birth as a key determinant of missing women, we have taken a preliminary step towards a unified study of a much broader set of issues. Schistosomiasis—infection by a parasitic worm—affects millions in sub-Saharan Africa. See Nikiforov and Mamaev (1998) for a historical perspective on gender imbalances in cardiovascular disease in now-developed countries. Even in rural areas of India, chronic diseases (primarily coronary) are now the leading cause of death (see Joshi et al. There is a large literature aimed at explaining differential mortality patterns by gender in developed countries; see, e. Stocks and flows Unlike several of the central papers we have cited, such as Sen (1990) and Coale (1991), our paper discusses annual “flows” of missing women, rather than the existing “stock” at any point of time. To understand the issues involved in converting flows to stocks, consider the difference between the actual female death rate and the corresponding reference rate: w w (a) ≡ d (a) − u (a). In computing the flow of missing women at age a, we multiply (a) by the female population at age a, as we have already done. However, the impact of (a) on the overall stock of missing women is more far-reaching: it affects every cohort of women currently older than a. M ore precisely, a cohort of age a is diminished at an earlier age a by an amount that depends on the value of (a) that prevailed a − a years ago. In general, we lack data on this value and this creates a serious difficulty in converting the flow numbers to stocks. We could make the “steady state” assumption that all age-specific death rates have remained constant over several years, but it would have to be defended, and that is beyond the scope of this paper. However, it is worth noting that, no matter how we resolve this issue, a given proportional flow at an earlier age must be more important than the same flow at a later age. It will simply affect more women, and must therefore translate into larger stocks. Simply as an example, we report our tentative estimates under the assumption of time-invariance of. W efind approximately 20 million missing women in India, 58 million missing women in China, and 8 million missing women in sub-Saharan Africa. Look at the enormous difference between China and the other two regions (in flows all three regions were about the same). This comes from the fact that excess female deaths in China are clustered at age 0. We reiterate, though, that these estimates must be treated with a great deal of caution. It is misleading because different countries have different fertility and death rates, and (in particular) different age distributions. They may also have different sex ratios at birth for genetic or environmental reasons that have nothing to do with missing females. The procedure is also uninformative: we cannot tell at what ages the missing women are clustered, or what diseases are responsible. Thus, we cannot begin to ask about the various channels: discrimination, biology, social norms, and so on. By unpacking missing women by age and disease, our paper takes a limited and preliminary step in this direction. First, once we control for natural variations in the sex ratio at birth, sub-Saharan Africa has as many missing women as India and China: significantly more as a percentage of the female population. Sub-Saharan Africa has no missing females at birth, while the corresponding proportion for India is under 11%. For instance, excess female mortality up to age 15 does not account for more than a third of the total in India or sub-Saharan Africa. Our study of excess female deaths by age and disease yields the following findings. For developing countries today, the epidemiological transition—the changing composition of dis- ease—explains very little of excess female mortality. Cardiovascular deaths are an overwhelmingly strong source of missing women at older ages in India and dominate all other sources of excess female mortality. Finally, congenital deaths at infancy, as well as Injuries, account for a suspiciously large total of excess female deaths in India. In sub-Saharan Africa, missing girls also die prematurely from preventable diseases: malaria is a primary killer. That said, there are excess female deaths in childhood which are due to respiratory and perinatal causes. To us, these are warning signs that active female discrimination in China possibly stretches beyond the prenatal. Indeed, a large chunk of missing women in China, as well as in India, are found after the age of 45. In China, these excess deaths from Group 2 diseases account for close to 40% of the flow of all missing women. These numbers point to the importance of studying the conditions of elderly women in India and China. As a final note, we observe some similarities between age-specific percentages of missing women in the historical United States (ca. Our exercise cannot disentangle the role of direct gender discrimination from other factors (biological, social, environmental, behavioural, or economic) in explaining “missing women”. But it allows us to seek out potential pathways of influence, and to assess the comparative contributions made by various categories to overall excess female mortality. In this context, observe that “category” need not be circumscribed by just age and disease.