In addition, the scientific literature implicates a variety of factors, including age, gender, diet, exercise, position of the food bowl, stress, and even weather conditions. Except for stress, much of the data is equivocal my working theory is that specific genetic factors shift the gut bacterial population (microbiome) to an unhealthy state (dysbiosis which predisposes the dog to bloat. Then some non-genetic trigger, such as stress, or an unusual meal can set off an episode of bloat in a genetically predisposed susceptible. The logic for this theory is complicated, but this is it in a nutshell. Certain genes of the immune system (dla genes in dogs) are responsible for detecting foreign invaders (like bacteria) and starting the process of destroying those invaders. These genes are highly variable, each having hundreds of variants (alleles) within the larger population of dogs. So each individual dog has a pretty unique array of these alleles, and a pretty unique ability to detect and destroy the thousands of potential invaders.
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1201 occurs at a 13 fold higher frequency in gdv dogs than in controls, preparing with a p value.0013. Allele 1101 appears to have a protective effect, being twice as frequent in control dogs with a p value.0089. We dont have enough data yet to see significant associations with dla88, and tlr5 shows no trend at all. Interestingly, the b allele of tlr5, which associated with risk for gdv in Great Danes, is completely missing from the german Shepherds. A new allele (C which has never been reported, has been seen 22 times in our gsd study, evenly distributed between gdv and control groups. The microbiome analysis is still at an early stage. We are just getting the last samples people in this week, and much of the processing for bacterial dna is done. But the high throughput sequencing and analysis are waiting for the last samples. They will all be sequenced together and the analysis should be fairly, the causes of bloat are poorly understood and may involve multiple triggers. Certainly, genetics plays a role.
So this sets up a possible mini hierarchy of tlr5 variants, with c as the most protective, b as the most risky and a as relatively neutral, with respect to bloat risk. The predominance of the risky b variant in Danes and the protective c in Shepherds correlates with the much higher risk of bloat in Great Danes. Harkey: we are just moving out of the collection phase and into the analysis phase of the study. So we do not yet have big enough numbers for strong statistical significance. But we do see one interesting number emerging for the drb1 gene. In Great Danes, the drb1: 1201 allele was associated with gdv. In the german Shepherds, this allele is already emerging as a significant risk factor.
Allele 1101 show a significant protective effect, associating with the healthy control group. In our previous study, this gene had only two variants in Great Danes, designated as a and. The b allele was found to be a risk allele, with a 4-fold higher frequency in the bloat group. The emerging data for tlr5 in German Shepherds also shows two variants. But, as with dla88, the risk variant found in Danes is not found in German Shepherds. Instead, we have observed a new variant, designated as c, which has not been previously reported in any breed. The c variant associates strongly with the control group, defining it as a protective variant. Since only 2 variants exist in the german Shepherds, a is a risk variant in this breed. But this same a variant was defined as the protective allele in Danes, because the other allele (B) associated with the gdv group.
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We will then analyze the gut microbiome profiles of 50 affected dogs and 50 controls to look for changes in the bacterial population that correlate with bloat. Early result of Genetic Analysis, with about 60 of the genetic data now in, we have preliminary analysis of the association of genetic variants with bloat. These results already show strong genetic associations with bloat that may lead to genetic tests for risk of this condition in German Shepherds. For the gene, dla88, dredging so far no variants associate with bloat. The risk variant of this gene, that associated with bloat in Great Danes, has not been seen in German Shepherds Since the frequency of gdv in German Shepherds is 4-5 fold lower than reviews in Great Danes, the 5101 allele may be correspondingly less frequent. Even by that logic, we should have seen this allele 3-4 times so far in the german Shepherd data set.
Alternatively, the dla88:05101 may play a breedspecific roll in bloat in Great Danes. Our data for the drb1 gene shows a strong association of variant 1201 with bloat. This is the same variant that was identified in Great Danes as a risk variant. So drb1:1201 may be a good genetic marker for bloat in a wide variety of breeds. Additionally, allele 1501 associates with the bloat group in German Shepherds. This allele was relatively rare in Danes (about 3 of all alleles) but is very frequent in Shepherds (30-50). The risk effect of 1501 is dose-dependent: that is, dogs with two copies of this variant are at higher risk of bloat than dogs with just one copy.
Chapter 31 (2.2 MB) responds to the request of the world health Assembly that the book should discuss "the principles and methods that are applicable to other programmes and assesses the costs and benefits of the sep. Title pages, table of Contents, foreword, Preface, acknowledgments, reviewers (0.5 MB) References (2.8 MB) Index of Names (0.4 MB) Subject Index (1.7 MB). Were fighting Bloat, the following is from. Harkey, chief investigator for the akc/chf research study entitled. The genetics of Bloat in German Shepherd Dogs: The roles of Immune system Genes and the gut Microbes.
The, american German Shepherd Dog Charitable foundation is proud to sponsor this research study., update From. Harkey (may 2018 we have proposed that genetic tendency to bloat may be caused largely by certain risk variants of genes of the immune system. These genes are responsible for distinguishing foreign cells from self, and as such, regulate which bacterial species in the gut will survive and which will be targeted for destruction. So these genes regulate the so-called gut microbiome. We hypothesized that dogs with a particular set of immune gene variants will maintain an unhealthy microbiome that predisposes them to bloat. Our recent research has supported this hypothesis in Great Danes. The purpose of the proposed research is to expand the genetic and microbiome analysis of bloat to german Shepherds. We proposed to repeat the genetic and microbiome analysis, described for Great Danes, in this group of German Shepherds. We plan to sequence the 3 immune genes, dla88, drb1, and tlr5, and determine if any variants associate with bloat.
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Chapter 12 (1.7 MB) south America, chapter 13 (1.6 MB) Indonesia chapter 14 (2.8 MB) Afghanistan and pakistan Chapter margaret 15 (5.2 MB) India and the himalayan Area chapter 16 (2.3 MB) Bangladesh Chapter 17 (3.6 MB) Western and Central Africa Chapter 18 (2.0 MB) zaire. Chapters 24-27 review the process of certification that smallpox had been eradicated Chapter 24 (2.4 MB) details the concepts, strategy and tactics used in certification. Chapter 25 (2.3 MB) describes certification by International Commissions from 1973-77. Chapter 26 (1.7 MB) describes the certification of 29 countries in Africa and Asia from 1978-79. Chapter 27 (2.1 MB) describes the completion of global certification in the horn of Africa and China. Chapter 28 (1.3 MB) describes the implementation, from 1980-88 of 19 recommendations made by the Global Commission book and adopted by Thirty-third World health Assembly for activities to be conducted in the post-eradication era. Chapter 29 (2.0 MB) details investigations into the nature and public health importance of human monkeypox, the smallpox-like disease discovered during the eradication campaign in Africa. Chapter 30 (1.3 MB) reviews the virology and epidemiology of smallpox to answer questions about its possible return.
Chapters 9-11 describe various aspects of the global eradication campaign. Chapter 9 (3.1 MB) explores the development and application of the concept of eradication; the events leading to the world health Assembly's 1959 resolution that global smallpox eradication be undertaken; progress from 1959-66; and the circumstances leading to the decision in 1966 to begin the. Chapter 10 (8.1 MB) summarizes major events and developments in the sep from 1967-80, providing a perspective for subsequent chapters. A year-by-year series of world maps, graphs, and text summarizes the accomplishments of this period. Chapter 11 (2.9 MB) is devoted to two topics of central importance to the sep: the provision of adequate amounts of a potent and stable vaccine and the development of better methods of vaccination. Chapters 12-22 describe the operations of the sep in different countries or parts of the world. The order of the chapters about corresponds, in large part, to the temporal sequence in which they were begun or strengthened.
3 (2.8 MB) describes the pathogenesis, pathology, and immunology of variola virus (the cause of smallpox) and vaccinia virus (used to produce the smallpox vaccine). Chapter 4 (2.2 MB) describes the epidemiology of smallpox—eradication could not have been achieved without understanding how the disease was transmitted or if an animal reservoir were present. Chapters 5-8 establish smallpox and its control in historical perspective. Chapter 5 (2.3 MB) addresses the history of smallpox from ancient times until the end of the 19th century. Chapter 6 (2.1 MB) describes early efforts at smallpox control: variolation, vaccination, and isolation and quarantine. Chapter 7 (2.2 MB) traces developments in smallpox vaccine production and vaccination techniques from 1900-66; complications of vaccination; and and an overview of vaccination programs from 1900-66. Chapter 8 (2.1 MB) is concerned with the extent, incidence, and control of smallpox from 1900-58, when global eradication was first proposed in who's World health Assembly.
This book, published by who, is the result. Each of the authors was deeply involved in word the execution of the Intensified Smallpox Eradication programme (SEP). Each reviewed and commented on multiple drafts of all chapters. In addition, 78 other persons, each an expert in an appropriate scientific field or who had personal knowledge of a national eradication or certification programme, commented on chapter drafts. The successful execution of the sep depended on activities ranging from field work to administration through laboratory studies and fund-raising. The authors believed that the book would be most instructive if it incorporated the whole spectrum of activities. The complete volume (83.9 MB) may be slow to open or download; individual chapters are available below. Chapters 1-4 are concerned with the basic sciences required in the sep.
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Please note the 'other details' displayed above are collected from a variety of public sources and are appended to this report for your convenience. As they are non-cro data, we can not vouch for their accuracy or timeliness. To update contact details on this company simply email. Smallpox and Its Eradication, fenner, frank; Henderson, donald A; Arita, isao; ježek, zdenek; Ladnyi, ivan Danilovich, world health Organization, geneva: pages; references:. Tables; 268 figures; 375 plates (84 color). In may 1980, who's Thirty-third World health Assembly plan accepted the report and recommendations of the Global Commission for the certification of Smallpox Eradication. One of these recommendations was that "the director-General. Of appropriate publications describing smallpox and its eradication, in order to preserve the unique historical experience of eradication and thereby contribute to the development of other health programmes".