",isbn:"978-1-83881-119-8",printIsbn:"978-1-83881-118-1",pdfIsbn:"978-1-83881-120-4",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"8bd4f03c89e63ef15984ee1b7f1485c4",bookSignature:"Prof. Andrew James Manning",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10407.jpg",keywords:"Hydrodynamics, Suspension/Saltation/Bedload, Numerical Modeling / CFD, Deposition, Flocculation, Sediment Types, Regional/Temporal Variability, Turbidity Currents, Dust Storms, Socio-Economic Effects, Contaminants, Storm / Severe Weather Effects",numberOfDownloads:205,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"May 27th 2020",dateEndSecondStepPublish:"September 11th 2020",dateEndThirdStepPublish:"November 10th 2020",dateEndFourthStepPublish:"January 29th 2021",dateEndFifthStepPublish:"March 30th 2021",remainingDaysToSecondStep:"6 months",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:"Dr. Manning is a highly published and world-renowned scientist in the field of depositional sedimentary flocculation processes.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"23008",title:"Prof.",name:"Andrew James",middleName:null,surname:"Manning",slug:"andrew-james-manning",fullName:"Andrew James Manning",profilePictureURL:"https://mts.intechopen.com/storage/users/23008/images/system/23008.jpeg",biography:"Professor Andrew J. 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1. Introduction
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For more than a decade, high blood pressure, arteriosclerosis, smoking, high blood sugar, and lack of movement have been dangerous factors leading to morbidity and mortality. Today, recent studies indicate that the first risk factor to rush to death is the lack of physical activity and time of daily sitting in addition to the poor selection of healthy food [1, 2, 3, 4, 5]. It may be the responsibility of everyone in us not to follow a healthy lifestyle that is inherited by generations, the most important factor that has led to a negative acceleration of human health. This would not have been possible without the negative use of technology for human life.
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The sedentary life experienced by most people has led to an increase in such risks and a marked increase in noncommunicable diseases. So, the most important issues that urge them to take the initiative in the marketing of sports and physical activity that the movement blessing and health crown on the heads of healthy cannot be achieved without beginning to modify the behavior and the adoption of a healthy lifestyle. This includes regular physical activity and stay away from pressure exercise relaxation and selection of appropriate food and early sleep with sufficient hours (quality of sleep) [5]. Therefore, in order to do so, school sports are a productive educational activity that is of great physical interest to the student [6]. Educational institutions and organizations have converged in recognition of the importance of school sports in maximizing the use of the time available to activate the lesson of physical education. This interest emphasizes the inclusion in many studies of its recommendations on the importance of school sports and its role in the development of students from the mental, psychological, and physical aspects [6, 7, 8, 9].
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Physical activity has much health, psychological, and social benefits. It helps to raise the level of fitness for better health and more active life. It also helps prevent many diseases or metabolic symptoms. It also reduces the risk of heart disease, diabetes, low back pain, and obesity, as well as the development of health and nutrition knowledge and the development of positive attitudes toward physical activity [2, 9, 10, 11].
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Metabolic syndrome is a combination of medical disorders that increase the risk of cardiovascular disease and diabetes, which refers to all the biochemical processes that occur in the body; it is a group of metabolic abnormality-related risk factors that greatly increase the risk of developing type 2 diabetes and health problems in the heart and blood vessels. Also, their biochemical processes in the body that leads to abdominal obesity and insulin resistance causing type 2 diabetes and Cardiovascular (hyperlipidemia) [12].
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2. Obesity facts
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While the prevalence of obesity appears to have plateau in the United States, emphasis is not only placed in treatment but also prevention as only 8% of normal weight children will become obese adults, while those who are obese during childhood tend to be obese adults. Also, a longitudinal change in percentages of obese children in Jordan, KSA, UAE, Kuwait, and Oman has similar trends. The increased rate of obesity in childhood and in the overall population is also present in the Arab world [13]. Data from this study done by students in Seeb, Muscat, demonstrate how the proportion of children who grew into adolescents that became overweight or obese increased from a single digit (about 7 percent) to more than 20% (so we are talking that in the same cohort of children when they were 6–7 years old only one in ten was classified as obese, but by the time they are late teens, one in five is classified as overweight). Participants were assessed at the beginning of the school year during the screening that took place before entering the different levels of education [14].
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Kilani et al. have also presented a similar prevalence of college students who are overweight at SQU, with a much higher proportion of students who present an unhealthy level of body fat [14]. In another survey, males and females had similar values for BMI and WC, and they maintained a normal BMI of <25 Kg/m2. The genetic predisposition might synergize with environmentally driven factors like physical activity and diet in the etiology of obesity and overweight among Omani and Jordanian adolescents [4, 15]. So, what are some differences between normal weight and obese people? Hormone research agenda is divided into two aspects: exercise endocrinology (hormonal responses to exercise) and the role of physical activity in promoting a healthy lifestyle.
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The main characteristics of the syndrome store excess fat in the abdomen as visceral fat (abdominal obesity) and “insulin resistance” [16, 17]. Firstly, obesity generally can be inherited or acquired, especially when an individual lives in an incubator environment to increase the number and size of fat cells. Prader-Willi syndrome (PWS) is rarely caused by a genetic defect that leads to physical, mental, and behavioral problems. One of the factors that contribute to childhood obesity great feeling of hunger and lack of control over eating which leads to chronic overeating (hyperphagia) and obesity [18].
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Defined etiology of obesity is accounted for (3-5%) with issues related to hormonal diseases, lesions in the hypothalamus, and altered genes (Early-onset hyperphagia caused the pathologic obesity) [18].
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The second is Multi-factorial obesity which results from an interaction between inherited predisposition and environment (epigenetic). PWS results from all alteration in the expression of the paternal chromosome 15, in the regions 11–13, and there are three main genetic alterations that result in the syndrome: paternal deletion, maternal uniparental disomy, and imprinting defect [19]. These causes that people with syndrome although share some common characteristics also present a wide range of abilities and disabilities. As babies, individuals with the syndrome are what we call floppy babies because of their decreased muscle tone, most of them have to be intubated as they fail to thrive, and somewhere between ages 4 and 8, an exacerbated seeking for food behavior begins which turns into hyperphagia that if it is uncontrolled it can turn into obesity [19]. Physically, they could be shorter than normal if not on growth hormone replacement therapy and have small hands and feet; some present intellectual disability, deficit in their sensorial systems and in their motor behavior [19]. Many researchers recommend to reduce weight by 10% of body weight in the first 6 months to a year and continued losing weight after reaching less than 25 in BMI. In general, recommendations include reducing calories including reducing 500–1000 calories per day [20, 21, 22].
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In some studies, 9007 men and 1491 women aged 44 +/−9 years free of metabolic syndrome took measurements of waist circumference and blood pressure and fat and sugar glucose as documented in the baseline and follow-up checks. Cardiorespiratory fitness was measured by maximal treadmill test duration. During the average follow-up of 5.7 years, 1346 men and 56 women developed metabolic syndrome. Inverse associations between fitness and metabolic syndrome incidence were found, suggesting that greater cardiorespiratory fitness levels may be beneficial in the primary prevention of metabolic syndrome [23]. The purpose of this paper was to review through scientific research published to respond on to the following question: Can the conditions during fetal development program the system to result in a survival advantage, yet increase vulnerability for adult diseases?
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3. Developmental plasticity
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The developmental plasticity is the ability of an organism to develop in various ways, depending on the particular environment or setting [24]. This can be based on the interaction of cellular cells, which refers to direct interactions between cell surfaces that play a crucial role in the development and functions of multicellular organisms, such as complex, structural humans. These interactions allow the cells to communicate with one another in response to changes in the microbial environment [25]. This ability to send and receive signals is essential for cell survival. For instance, normal embryonic and postnatal development requires a fine regulation of cell proliferation, differentiation, migration, and apoptosis. During organogenesis, cell–cell interactions trigger events such as epithelial-mesenchymal transition (thin protective layer) and tubulogenesis (kidney development) that describes tissue that forms a thin protective layer on exposed bodily surfaces and forms the lining of internal cavities, ducts, and organs. Another example is related to cystogenesis, tubulogenesis, and kidney development [26]. Cystogenesis and tubulogenesis are important for many complex biological processes such as organ development. Again, if we compare an epidermal keratinocyte and a pancreatic acinar cell, the same genome, yet their profound morphological, physiological, and biochemical differences are entirely the product of epigenetic modification. Keratinocyte cells are the building blocks of the skin. They are the most common type of skin cell and make keratin, a protein found in the skin, hair, and nails.
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One condition that causes the pancreas to stop producing adequate enzymes is pancreatic acinar atrophy. This occurs because the disease hurts slowly and without obvious symptoms. The ability of many animals is adaptability to environmental evolution. This can make small size and slow metabolism to live and survive, while the enlarged size and accelerated metabolism are advantages of reproductive success when resources are available. Often this occurs early in life or even through inheritance from parents and even grandparents. However, fetuses who are adjusting to one environment, such as the uterus, may be at risk when exposed to other environment when they become adults [27]. Effects of prenatal exposure to the Dutch famine on adult disease in later life. Bees determine the number of larvae within the appropriate age group and begin to place these larvae to become queens. The only difference between the honeybees and the queen is the food received during the process of maturity: the workers feed potential queens royal jelly throughout their lives, while the bees are working on royal jelly during the first 2 days of the larvae [28].
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4. Biological evidences
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Biological evidence may be relevant to understanding human development and susceptibility to disease. With the improved nutritional status of many mothers around the world, the characteristics of their offspring—such as body size and metabolism—also changed. Their mother’s prenatal response may generally respond to individuals so that they are more appropriate to the environment’s expectations through the signals available in early life. If the mother is a smoker during pregnancy, it is possible that the third generation of her offspring will be smokers. Ironically, however, rapid improvements in nutrition and other environmental conditions may have adverse effects on the health of those whose parents and grandparents lived in poor conditions, as happened in World War II in Europe [29] and the famine in India early in the last century [30]. The full understanding of the patterns of human plasticity in response to early nutrition and other environmental factors will have implications for public health management.
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5. Thrifty hypothesis
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The thrifty gene hypothesis indicates that certain populations may have genes that determine increased fat storage, which in times of famine represent a survival advantage, but in a modern environment result in obesity and type 2 diabetes. An example of the thrifty hypothesis showed by Dutch famine study which has shown that the offspring of mothers who were pregnant during the famine have more diabetes and those who were exposed in early gestation have more atherogenic lipid profile, altered clotting, more obesity, and a threefold increase in cardiovascular disease. Explanations for the heritability of these syndromes and the environmental contribution to disease susceptibility are addressed by the “thrifty genotype” and the “thrifty phenotype” hypotheses [27]. The underlying scientific hypothesis has been developed by epidemiology studies and emphasized by Dr. David Barker in the United Kingdom. During development fetuses respond to severe malnutrition by favoring the metabolic demands of the growing brain/CNS and heart at the expense of other tissues [31, 32]. In addition, the growing brain/CNS and heart tissue may not, however, escape entirely unscathed. The fetus is protected from death and is live-born but is more prone to diseases later in life [33]. Various studies have supported barker hypothesis.
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6. Epidemiology studies
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Epidemiology studies have shown that markers of malnutrition such as frank intrauterine growth retardation (IUGR), low birth weight, or small for gestation age (SGA) strongly predict the subsequent occurrence of hypertension, hyperlipidemia, insulin resistance, type 2 diabetes, and ischemic heart disease, in adult life.
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It has been shown that fetuses that are growth retarded during the first trimester of development are three times more likely to be obese as adults. In the case of premature infants, at the age of 4–10 years, these children who had been born prematurely had an increase in their acute insulin response, which compensated for insulin resistance. This decrease in insulin sensitivity may predispose premature infants to type 2 diabetes mellitus in adulthood, as already demonstrated among infants born at term who are SGA [33, 34], that compared with young people from the same region of Finland who are born after a pregnancy, and young people who ranged from 18 to 27 years of age who were preterm infants have become higher in chronic insulin resistance and more prone to glucose and high blood pressure [35]. Preterm births happen on their own early means that some of what would be the third trimester is lost. This is typically a sensitive period for programming and certainly a time during which the final aspects of organogenesis occur. This is explained by spending in the more difficult environment of a hospital setting in which there are many toxic substances as well as nutritional challenges. Now that many more extremely premature babies are surviving to adulthood, ensuring their health is crucial [36]. On the other hand excessive energy supply to the fetus or infant also has adverse consequences so a U shape works similarly at the tow ends of the malnutrition (Figure 1).
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Figure 1.
Excessive energy supply to the fetus or infant also has adverse consequences.
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Maternal hyperglycemia may lead to fetal hyperinsulinemia and fat deposition that influence the fetus. Offspring of obese women or women with diabetes are at greater risk for developing metabolic disorders themselves, even during childhood [37, 38, 39].
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As a consequences, an infant usually has about 5–6 billion fat cells during the third trimester when a mother is pregnant. This number increases during early childhood and puberty, resulting in a healthy adult body possessing 25–30 billion fat cells [40]. Meanwhile, excessive energy supply to the fetus or infant will increase the potential of becoming obese. Babies who depend on milk factory have the highest amount of energy, leading to an increase in body weight than children who were breastfed; it can affect the increase in obesity and its risks later in life [41]. This complicate the long-term effects due to Prenatal and postnatal nutrition during early infancy. In one study, carotid intima-media thickness at 9 years of age in 216 children of European ancestry whose mothers had energy intake in the lowest quartile during early or late pregnancy was higher than that of children whose mothers had intake in the highest quartile, implying that maternal nutrition during pregnancy can affect the subsequent risk of atherogenesis in the offspring [42].
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Thus, obesity comes from an increase in the numbers of fat cells, or adipocytes, and is hence due to a shift in the activity of certain genes during development. Because to maternal malnutrition during pregnancy, the offspring later suffering from obesity in the middle of the abdomen and lack of muscle mass, change the sensitivity of insulin, change in hepatic metabolism, decreased number of nephrons, high blood pressure, with a change in appetite regulation, activity level, and control of nerve endocrine glands [42]. There are critical periods in the differentiation and maturation of the tissues and cells involved in organogenesis throughout gestation and early postnatal life. The examples of the kidney, heart, and pancreas were obvious since their functional units are formed prenatally in the human fetus [43].
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7. Animal studies
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Embryos of pregnant rats fed with a low-protein diet during the preimplantation period (0–4.25 days) show altered development in multiple organ systems; the offspring had reduced birth weights, relatively increased postnatal growth, and adult-onset hypertension [44].
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Obviously, the preconception period is particularly sensitive, so that even the required nutrient deficiencies (B12 or folate or methionine) can have an effect on metabolism and blood pressure later in sheep [45]. It has recently been reported that the imbalance in B12 folic acid status and pain during pregnancy contributes to insulin resistance in childhood in humans [46].
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Glucocorticoid management to pregnant rats at specific times during pregnancy to cause high blood pressure [47], insulin resistance in offspring later in life [48], changes in gene expression in the developing brain of offspring, and increased sensitivity to stress after the birth have been reported. The administration of glucocorticoids to the pregnant rat at specific points during gestation has been reported to cause hypertension [47], insulin resistance in the offspring in later life [49], alterations in gene expression in the developing brain of the offspring, and increased sensitivity to postnatal stress [50].
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In mice, it may lack nutrition during pregnancy to breed showing later the following: visceral obesity, reduced lean body mass, changes in insulin sensitivity, different hepatic metabolism, decreased numbers of nephrons, high blood pressure, and altered endothelial function, together with altered appetite regulation, level of activity, and neuroendocrine control [51, 52, 53, 54].
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There are critical periods in the differentiation and maturation of the tissues and cells involved in organogenesis throughout gestation and early postnatal life. The examples are seen in the kidney, heart, and pancreas, since their functional units are formed prenatally in the human fetus.
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In the kidney, maternal dietary imbalance may lead to developmentally induced deviations from the optimal ratio of body mass to nephron number. This increased risk of inadequate renal function and hypertension in later life [54]. A predisposition to renal failure and a potentially reduced life span are predicted [55]. In the pancreas insulin secretion is also affected. Nutritional stress in pregnant rats reduces the growth of the endocrine pancreas during organogenesis and increases beta-cell apoptosis [55], leading to hyperglycemia and impaired insulin secretion when the offspring become adults. In the adult male rat offspring of mothers on a protein-restricted diet, low birth weight is associated with reduced expression of components of the insulin signal transduction pathway in the skeletal muscle [56]. Similar abnormalities have been reported in infants of low birth weight, and together with the developmentally induced reduction in skeletal muscle mass, these abnormalities might contribute to later insulin resistance.
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8. Programming
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Developmentally induced epigenetic modifications of DNA are generally stable during the mitotic cell divisions that continue throughout a lifetime. So, developmental plasticity of fetus through cell-cell interaction can be understood as a set of programs. “Programming” is the term used to describe lifelong changes in function that follow a particular event in an earlier period of the life span. Evolutionary plasticity requires a constant modification of genetic expression that appears to be mediated, at least in part, by genetic processes such as epigenetic mechanisms as cells use to control gene expression by virtue of DNA methylation. The role of DNA methylation in gene expression can be found in Phillips [57], and by a histone modification which is a histone protein includes methylation that can impact gene expression [58].
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Several studies show that skeletal muscle can be programmed, where early exposure to environmental stimuli leads to a constant change in the skeletal muscle phenotype in later life. This has been demonstrated in mammalian models where reduced nutrient availability during pregnancy weakens muscle fibers, muscle and skeletal formation (white/red fiber ratios), and birth size [59]. Epidemiological studies in human aging groups also suggest that low birth weight and gestational malnutrition are closely related to reduced muscle size, skeletal strength, and aging [59, 60].
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This refers to changes in gene expression due to nongenetic structural alterations of DNA and/or histones [58]. So, remember that cell-cell interaction can be transferable in the fetus so memory of active person eventually will be available later in life for the offspring babies [58]. Thus, developmental plasticity requires both the genome and the genetic variability of the environment interactively by the mature phenotype and determines the sensitivity and subsequent environmental factors and the subsequent risk of the disease affects [61]. The effects of maternal nutrition and behavior clearly target the promoter regions of specific genes rather than being associated with global changes in DNA methylation. DNA modulates the rate of transcription to messenger RNA. The phenotypic effects of epigenetic modifications during development may not manifest until later in life [62].
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9. Hormones
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It plays an important role in childhood growth and continues to have anabolic effects in adults. As the stress hormone, norepinephrine affects the brain’s amygdala, where attention and responses are controlled. It is also based on norepinephrine response to fight or flight, in addition to epinephrine, which raises the heart rate directly, leading to the release of glucose from energy stores and increasing blood flow to the skeletal muscles. It increases the supply of oxygen to the brain [63]. Glucagon is a peptide hormone, produced by alpha cells of the pancreas that raises blood glucose levels. Its main tasks are to increase blood sugar through protein conversion in the liver (gluconeogenesis). Suppress the immune system and help with fat, protein, and carbohydrate metabolism [64]. It also affects the density of the bones negatively, and it is possible to use cortisone in various forms to treat a variety of diseases.
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10. Conclusion
\n
The term used to describe lifelong changes in function that follow a particular event in an earlier period of the life span is called programming. Nevertheless, the previous information may have a significance of pediatric obesity endocrine abnormality. GH-IGF-1 axis is partially responsive for the signal to enhance muscle and bone development. Growth hormone (GH) response to exercise may be weak in obesity and may not appear until later in life, especially if they affect genes that are responding to subsequent environmental responses, such as high-fat diet. I do not know how the genetic change instigated development window in the main systems. Exercise is the best way to do this when you exercise regularly, and you build stronger muscles, even if you do not work out with weights. Muscles use more calories than fat throughout the day, even while you are resting. Fat cells of unhealthy obese were larger than those of any other group. It was swollen and full of inflammation. The collapse and filling of their fat stores were disabled and showed a closer look that their mitochondria were not functioning well causing loss of muscle power. This is due to fat cell accumulation which reduces its ability to burn fuel and produce adenosine triphosphate, or ATP, the body’s energy currency. It is natural that the behavior of the human being and his attitude of life inert to be aware of the importance of physical activity and live in the healthy lifestyle system in the prenatal stages. Thus, healthy genetic modification will be inherited for future generations.
\n
\n\n',keywords:"lifestyle, adult, metabolic syndrome",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/68874.pdf",chapterXML:"https://mts.intechopen.com/source/xml/68874.xml",downloadPdfUrl:"/chapter/pdf-download/68874",previewPdfUrl:"/chapter/pdf-preview/68874",totalDownloads:270,totalViews:0,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:1,dateSubmitted:"July 17th 2018",dateReviewed:"June 6th 2019",datePrePublished:"September 6th 2019",datePublished:"January 15th 2020",dateFinished:null,readingETA:"0",abstract:"Information on the health status in modern society and developed countries depicts an increase in noncommunicable diseases (NCDs) such as diabetes, overweight, obesity, and metabolic syndrome. An examination of factors related to this increase shows that there is a shift in the daily practices of the people, and especially children in all ages, as they grow older toward a more sedentary lifestyle. This chapter concentrated on the term used to describe lifelong changes in function that follow a particular event in an earlier period of the life span, which is called programming. These include the lifestyle in the fetus, pregnant woman, and parents; all of which affect pronounce metabolic syndrome in later life of adult. Therefore, regular physical activity and living systematic healthy lifestyle in the prenatal stages are of importance to genetic modification of inheritance for future generations.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/68874",risUrl:"/chapter/ris/68874",book:{slug:"cardiorespiratory-fitness"},signatures:"Hashem Kilani, Abdulsalam Al-Za’abi, Areej Kilani and Laila Kilani",authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Obesity facts",level:"1"},{id:"sec_3",title:"3. Developmental plasticity",level:"1"},{id:"sec_4",title:"4. Biological evidences",level:"1"},{id:"sec_5",title:"5. Thrifty hypothesis",level:"1"},{id:"sec_6",title:"6. Epidemiology studies",level:"1"},{id:"sec_7",title:"7. Animal studies",level:"1"},{id:"sec_8",title:"8. Programming",level:"1"},{id:"sec_9",title:"9. Hormones",level:"1"},{id:"sec_10",title:"10. Conclusion",level:"1"}],chapterReferences:[{id:"B1",body:'Kilani H, Al-Yarobi S, Zayed K, Alzakwani I, Bererhi H, Shukri A, et al. Physical fitness attributes, vitamin D, depression, and BMD in Omani’s children. European Scientific Journal. 2013;9(30):156-173\n'},{id:"B2",body:'Habsi A, Kilian H. Lifestyle of adult Omani women: A cross sectional study. Sultan Qaboos University Medical Journal. 2015;15(2):241-249\n'},{id:"B3",body:'Kilani H. Cardiovascular diseases risk, energy expenditure, and health fitness. Canadian Journal of Clinical Nutrition. 2015;3(2):1-4\n'},{id:"B4",body:'Kilani H, Alhazzaa H, Waly M, Musaiger A. Lifestyle habits: Diet, physical activity and sleep duration among Omani adolescents. Sultan Qaboos University Medical Journal. 2013;13(4):510-519\n'},{id:"B5",body:'Kilani H, Alfahdi B. What is the effect of the number of sleeping hours for military sports trainers in the Royal Air Force? European Journal of Sport Technology. 2018;20:2-19\n'},{id:"B6",body:'Al-Za’abi A, Kilani H, Bataineh M, Alnuaimi J. Perceived health benefits and barriers to physical activity among secondary school students. International Scientific Journal of Kinesiology-Sport Science Journal. 2018;2018:91-102\n'},{id:"B7",body:'Kilani H, Lala O. Fat mass percentage with hypertension and some variables of physical working capacity among students. In: Second International Scientific Conference about the latest Scientific Evidences of Physical Education. Irbid: Yarmouk University; 2007\n'},{id:"B8",body:'Mehana M, Kilani H. Enhancing physical education in Omani basic education curriculum: Rationale and implications. 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Proceedings of the National Academy of Sciences of the United States of America. 2010;107:16881-16886\n'},{id:"B35",body:'Hofman PL, Regan F, Jackson WE, et al. Premature birth and later insulin resistance. The New England Journal of Medicine. 2004;351:2179-2186\n'},{id:"B36",body:'Hovi P, Andersson S, Eriksson JG, et al. Glucose regulation in young adults with very low birth weight. The New England Journal of Medicine. 2007;356:2053-2063\n'},{id:"B37",body:'Boney CM, Verma A, Tucker R, Vohr BR. Metabolic syndrome in childhood: Association with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics. 2005;115(3):e290-e296\n'},{id:"B38",body:'Julie R. Ingelfinger, prematurity and the legacy of intrauterine stress. The New England Journal of Medicine. 2007;356:20\n'},{id:"B39",body:'Hillier TA, Pedula KL, Schmidt MM, Mullen JA, Charles MA, Pettitt DJ. Childhood obesity and metabolic imprinting: The ongoing effects of maternal hyperglycemia. Diabetes Care. 2007;30:2287-2292\n'},{id:"B40",body:'Kronemer C. Uncovering the Biology Behind Fat Cells. NFPT CEC. 2012. Available from: https://www.nfpt.com/blog/uncovering-the-biology-behind-fat-cells\n\n'},{id:"B41",body:'Reusens B, Remacle C. Programming of the endocrine pancreas by the early nutritional environment. The International Journal of Biochemistry and Cell Biology. 2006;38:913-922\n'},{id:"B42",body:'Harder T, Bergmann R, Kallischnigg G, Plagemann A. Duration of breastfeeding and risk of overweight: A meta-analysis. American Journal of Epidemiology. 2005;162:397-403\n'},{id:"B43",body:'Ozanne SE, Jensen CB, Tingey KJ, Storgaard H, Madsbad S, Vaag AA. Low birthweight is associated with specific changes in muscle insulin-signalling protein expression. Diabetologia. 2005;48:547-552\n'},{id:"B44",body:'Kwong WY, Wild A, Roberts P, Willis AC, Fleming TP. Maternal undernutrition during the preimplantation period of rat development causes blastocyst abnormalities and programming of postnatal hypertension. Development. 2000;127:4195-4202\n'},{id:"B45",body:'Sinclair KD, Allegrucci C, Singh R, Gardner DS, Sebastian S, Bispham J, et al. DNA methylation, insulin resistance, and blood pressure in offspring determined by maternal periconceptional B vitamin and methionine status. Proceedings of the National Academy of Sciences of the United States of America. 2007;104:19351-19356\n'},{id:"B46",body:'Yajnik CS, Deshpande SS, Jackson AA, Refsum H, Rao S, Fisher DJ, et al. Vitamin B12 and folate concentrations during pregnancy and insulin resistance in the offspring: The Pune maternal nutrition study. Diabetologia. 2008;51:29-38\n'},{id:"B47",body:'Levitt NS, Lindsay RS, Holmes MC, Seckl JR. Dexamethasone in the last week of pregnancy attenuates hippocampal glucocorticoid receptor gene expression and elevates blood pressure in the adult offspring in the rat. Neuroendocrinology. 1996;64:412-418\n'},{id:"B48",body:'Nyirenda MJ, Lindsay RS, Kenyon CJ, Burchell A, Seckl JR. Glucocorticoid exposure in late gestation permanently programs rat hepatic phosphoenolpyruvate carboxykinase and glucocorticoid receptor expression and causes glucose intolerance in adult offspring. The Journal of Clinical Investigation. 1998;101:2174-2181\n'},{id:"B49",body:'Welberg LA, Seckl JR, Holmes MC. Prenatal glucocorticoid programming of brain corticosteroid receptors and corticotrophin-releasing hormone: Possible implications for behaviour. Neuroscience. 2001;104:71-79\n'},{id:"B50",body:'Vickers MH, Breier BH, Cutfield WS, Hofman PL, Gluckman PD. Fetal origins of hyperphagia, obesity, and hypertension and postnatal amplification by hypercaloric nutrition. American Journal of Physiology. Endocrinology and Metabolism. 2000;279:E83-E87\n'},{id:"B51",body:'Langley-Evans SC, Welham SJ, Jackson AA. Fetal exposure to a maternal low protein diet impairs nephrogenesis and promotes hypertension in the rat. Life Sciences. 1999;64:965-974\n'},{id:"B52",body:'Brawley L, Itoh S, Torrens C, Barker A, Bertram C, Poston L, et al. Dietary protein restriction in pregnancy induces hypertension and vascular defects in rat male offspring. Pediatric Research. 2003;54:83-90\n'},{id:"B53",body:'Vickers MH, Breier BH, McCarthy D, Gluckman PD. Sedentary behavior during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 2003;285:R271-R273\n'},{id:"B54",body:'Aihie Sayer A, Dunn R, Langley-Evans S, Cooper C. Prenatal exposure to a maternal low protein diet shortens life span in rats. Gerontology. 2001;47:9-14\n'},{id:"B55",body:'Gale CR, Javaid MK, Robinson SM, Law CM, Godfrey KM, Cooper C. Maternal diet during pregnancy and carotid intimamedia thickness in children. Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1877-1882\n'},{id:"B56",body:'Ijuin T, Hatano N, Hosooka T, Takenawa T. Regulation of insulin signaling in skeletal muscle by PIP3 phosphatase, SKIP, and endoplasmic reticulum molecular chaperone glucose-regulated protein 78. Biochimica et Biophysica Acta. 2015;1853:3192-3201\n'},{id:"B57",body:'Phillips T. The role of methylation in gene expression. Nature Education. 2008;1(1):1-16\n'},{id:"B58",body:'Chen Z, Zang J, Whetstine J, Hong X, Davrazou F, Kutateladze TG, et al. Structural insights into histone demethylation by JMJD2 family members. Cell. 2006;125:691-702\n'},{id:"B59",body:'Sharples AP, Stewart CE, Seaborne RA. Does skeletal muscle have an ‘epi’-memory? The role of epigenetics in nutritional programming, metabolic disease, aging and exercise. Aging Cell. 2016;15:603-616\n'},{id:"B60",body:'Patel H, Jameson K, Syddall H. Developmental influences, muscle morphology, and sarcopenia in community-dwelling older men. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2012;67:82-87\n'},{id:"B61",body:'Patel HP, AlShanti N, Davies LC, Barton SJ, Grounds MD, Tellam RL, et al. Lean mass, muscle strength and gene expression in community dwelling older men: Findings from the Hertfordshire Sarcopenia Study (HSS). Calcified Tissue International. 2014;95:308-316\n'},{id:"B62",body:'Jaenisch R, Bird A. Epigenetic regulation of gene expression: How the genome integrates intrinsic and environmental signals. Nature Genetics. 2003;33(Suppl):245-254\n'},{id:"B63",body:'Bateson P, Barker D, Clutton-Brock T, et al. Developmental plasticity and human health. Nature. 2004;430:419-421\n'},{id:"B64",body:'Tanaka M, Yoshida M, Emoto H, Ishii H. Noradrenaline systems in the hypothalamus, amygdala and locus coeruleus are involved in the provocation of anxiety: Basic studies. European Journal of Pharmacology. 2000;405(1-3):397-406. DOI: 10.1016/S0014-2999(00)00569-0. PMID: 11033344\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Hashem Kilani",address:"hashemkilani@gmail.com",affiliation:'
School of PE, Health and Recreation Department, University of Jordan, Jordan
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\n
1. Introduction
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In dairy farms, biosecurity, surveillance, resilience/immunity, biocontainment, and control of disease spread within the herd are the pillars that need to be appropriately managed to ensure the healthy herd [1].
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Biosecurity is focused to reduce and prevent the introduction of diseases or pests of animals on a farm, and to minimize the spread of diseases or pests within a farm. Biosecurity action plans need to be implemented mainly in large dairy farms where the disease agents can be introduced by various sources such as labor, advisers, replacement cattle, supplies, feedstuffs, and vehicles [2].
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Surveillance programs are developed for early detection of emerging pathogens, to establish disease-free status or the prevalence of a specific disease in a herd [3].
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Relation resilience immunity is based on the individuals’ resistance to diseases that can be modulated by the ability of animals to adapt to adverse conditions (stress factor) and recover from them [4].
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Biocontainment and control programs are important backup systems for biosecurity plans that will prevent the emerging disease spreading within the herd or the endemic diseases spreading between animals into the farm [2, 5].
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The overall biosecurity of dairy farm uses different levels or shells of actions (national or supranational, regional, and local), linked with the epidemiological profile of the pathogen. For highly contagious infectious agent (e.g., foot-and-mouth disease), the most efficient biosecurity plan is at national or European Union level, while for infectious agents transmitted by close contact between animals (e.g., bovine tuberculosis), the regional biosecurity measures such as movement controls will protect the status of the region [1].
\n
Biosecurity practices on livestock farms have been described and prioritized in various ways [1, 2, 5, 6]. In this chapter, we grouped biosecurity measures in the following categories: dairy farm sanitation, facility biosecurity, animal biosecurity, feed biosecurity, and manure biosecurity.
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2. Dairy farm sanitation
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2.1 Employees and visitors
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Some infectious agents are specific for dairy cattle and others are zoonotic, affecting both bovine and human health. Employees and visitors can contribute to the spread of all these infectious agents on a dairy farm [7]. The transmission of pathogens by humans can be reduced or even stopped by providing on-farm laundry facilities for all protective clothing used on the farm, using only clean overalls during farm visits, providing disposable clean booties for visitors and cleaning of boots with disinfecting solution after scrubbing off any visible dirt at the end of the visit, and washing of hands before and after working with sick or young animals [7, 8, 9].
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Milking parlor personnel should wear latex gloves while milking to reduce the spreading potential of the contagious mastitis pathogens [9]. Sometimes, these hired personnel can take care of other animals outside the dairy farm and carry pathogens on the farm. Employees should be regularly trained in good practices to prevent the spread of disease (the principles of hygiene and disease security). They need to know that calves are susceptible to diseases carried by adult animals, and daily activities should be organized so that employees work with younger animals before working with older animals. Prevention of the infectious agent’s introduction and spreading from outside and inside sources should also be considered in the education of hired personnel in basic hygiene and disinfection [10]. The main actions included in the biosecurity plan for dairy farms should reduce the risk of infectious diseases to be introduced by employees and visitors (Table 1).
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\n\n
\n
Biosecurity measure
\n
Action
\n
\n\n\n
\n
Record in the logbook all farm visitors
\n
Place the visitor logbook at the farm entrance
\n
\n
\n
Restrict the access of visitors to the stable
\n
Locking the stable doors
\n
\n
\n
Inform unauthorized persons that they are not allowed to enter the stable
\n
Post-warning signs asking visitors not to pass inside stable and several directing signs to the farm offices
\n
\n
\n
The visitors can access the stable only with clean clothes and boots, which they have not used in other farms
\n
Provide clean boots and overalls for all visitors
\n
\n
\n
The visitors should use a footbath with disinfectant and clean their boots before entering the stable
\n
Place a disinfectant footbath and brushes outside the stable
\n
\n
\n
The dealer or transporter of the newly arrived animals is not allowed to enter in stable or in contact with the farm animals
\n
The access of the cars is made on a route that avoids contact with the farm animals, directly toward the quarantine area located at a distance from the herd
\n
\n
\n
The livestock renderer access in the stable or the contact with cattle is restricted
\n
Store dead animals away from the stable and main roads
\n
\n\n
Table 1.
Biosecurity measures designed to reduce the risk of the infectious disease’s introduction in dairy farms by employees and visitors.
\n
The access of visitors must be limited and recorded in a logbook; the farm touring must start from younger to older animal groups; barn doors are recommended to be locked and a warning sign must be posted to keep out unauthorized personnel [9].
\n
Also, along the access road of the farm must be displayed signs directing visitors to the administrative area and to the visitor parking, as well as warning signs to limit direct contact of visitors with farm feed and animals [11].
\n
\n
\n
2.2 Equipment biosecurity
\n
Equipment can be contaminated with infectious secretions, excretions, and blood and the movement of equipment between stalls and farms may also transport pathogens [12].
\n
All equipment used on the farm must be regularly cleaned and disinfected [11]. To prevent contamination of equipment, storage containers need to be used for all tools and feeding equipment. Also, all storage containers are regularly cleaned and disinfected. The storage containers must protect equipment from diseases, pests, or weeds [13]. Before use in healthy animals, equipment that has been used on sick animals must be cleaned and disinfected. However, it is better not to use clothing, shoes, and tools dedicated to the compartment of sick animals [14]. Dehorners, ear taggers, hoof knives, clippers, and all shared and hired equipment will be cleaned and disinfected between uses [11, 14].
\n
Nursing bottles and buckets must be sanitized before each feeding [14], calves kept indoors must have fresh clean dry bedding, and plastic calf hutches will be cleaned and disinfected after use [11].
\n
The equipment used for manure disposal will not be used for transporting or delivering feed [13].
\n
Disposable clothing and used veterinary equipment must be removed safely [11].
\n
\n
\n
2.3 Vehicle biosecurity
\n
Vehicles are considered fomites mainly for pathogenic robust organisms that can survive a long time in the environment [1]. Mainly external vehicles that collect milk, calves, and carcasses or deliver feedstuffs, pharmaceuticals, and semen can be involved in the transmission of infectious disease because they travel daily from farm to farm [2, 10]. A high biosecurity risk is associated with carcasses (dead stock) collectors because they are usually in contact with diseased animals [15, 16].
\n
To prevent the introduction of infectious agents, vehicles must be kept clean and should not have access to the zones where the animals are housed [10, 11, 17].
\n
External vehicles should not be allowed on the farm [18]. If vehicles are necessary on the farm, then ensure that vehicles and trailers are clean when entering the farm and disinfected before and after use [6, 11, 18, 19]. Cleaning and disinfection will cover both the exterior and the interior of the vehicles, with greater attention to areas where dirt may be hidden (e.g., wheel arches and tires) [11]. Because the transport by dealers may pose additional risks of infectious disease transmission between farms, it is recommended that the animal moving will use only farm-owned vehicles [20], with clean and ample bedding to prevent both injuries and disease [14].
\n
Guidance indicators and warning and restricting access signs to unauthorized vehicles must be placed at the entrance to the farm road and along the road. The farm must have a designated area for visitors’ vehicles that are at the entrance of the farm and away from the animal and animal stalls [6, 10, 14]. Also, service vehicles should not drive over the routes of feed delivery or manure handling [14].
\n
\n
\n
\n
3. Buildings biosecurity
\n
In a dairy farm, the building’s design can help prevent the spread of pathogens to sick cows, periparturient cows, and newborns [2]. Buildings should have a well-established destination, in correlation with the categories of animals present on the farm. Dairy farms can secure their premises against domestic and wild animals by installing various types of fences (e.g., electric fence) around the buildings. Disinfectant footbaths should be at the entry of livestock housing. All farms should have isolation building (the quarantine facility) where the health status of the newly purchased cows will be observed before they join the rest of the herd [21]. To prevent direct and indirect contact between residents and new animals, the quarantine facility should be located in the farthest possible place on the dairy farm [10]. The farm must have a biosecurity plan that includes building maintenance activities (e.g., check and maintain fences, replace bird netting, and repair holes in buildings), which will reduce the contact of cattle with wild animals and the feed contamination with birds droppings or badger feces [14, 21].
\n
\n
\n
4. Animal biosecurity
\n
\n
4.1 Live animal management
\n
The introduction of new cattle is one of the most important biosecurity risks for dairy farms [10]. In modern dairy farming, the sale and movement of cattle is an intrinsic part of the business as a consequence of the increased herd replacement rate of adult milking cows, the forced culling, and the need to increase the size of the herd [1]. Therefore, keeping a closed herd is the most effective biosecurity measure but is the least practical [6]. To reduce the risk of diseases spreading between farms, the new animals are purchased only from herds with known health status and known vaccination protocols [9, 10].
\n
The best solution to prevent the introduction of diseases through the acquisition of new animals is the hosting of the newly purchased cows in a quarantine facility with trained personnel to handle isolated animals [10, 21]. Quarantine is one of the most important biosecurity tools and consists of the separation of specific groups of animals to prevent the transmission of infectious diseases. Prophylactic quarantine is designed to separate the resident herd from newly acquired animals for 1 month or more. During the 30 days of isolation, the personnel from the quarantine facility will monitor cattle health status and prevent direct and indirect contact between new and resident animals [9, 10]. If the infections have short incubation times, then the animals will develop acute diseases during the quarantine period. In other cases, to prevent the diseases spreading from animals that might be hiding an infectious agent without exhibiting clinical signs to resident animals, the quarantined animals will be tested for various diseases such as bovine tuberculosis, Johne’s disease, brucellosis, leptospirosis, salmonellosis, campylobacteriosis, leucosis, bovine viral diarrhea (BVD), infectious bovine rhinotracheitis (IBR), trichomoniasis, neosporosis, ringworm, liver fluke, lungworm, digital dermatitis, and contagious mastitis pathogens (Streptococcus agalactiae and Staphylococcus aureus) [10, 14]. The testing of animals in the prophylactic quarantine is a valuable biosecurity tool when properly applied.
\n
To prevent the bovine tuberculosis introduction, the biosecurity plan should take into consideration all possibilities of Mycobacterium bovis transmission. Cattle are the main reservoir and spread microbes through aerosols (adults) or manure (calves) to many domestic and wild mammalian species. Sheep, goats, pigs, horses, and dogs are spillover hosts and spread M. bovis spread microbes in various ways (respiratory, digestive, by bites, or scratches). After infection, badgers, brush-tail opossums, wild boars, deer, and other wildlife species become wildlife reservoirs (maintenance host). Humans are susceptible and contract the infection mainly by drinking raw milk and raw milk products. People with pulmonary or urogenital tuberculosis can retransmit the infection to cattle [22].
\n
Calves are more susceptible and should be kept in a separate area to minimize their exposure to infectious agents [14]. Calves can carry many infectious diseases without clinical signs and positive results on the laboratory tests (e.g., Johne’s disease). This risk can be reduced by purchasing calves only from herds officially certified as disease-free [1].
\n
Because one of the most common ways of the BVD virus introduction in a free farm is via a pregnant heifer (“Trojan cow”) carrying a persistently infected fetus, all calves from purchased cattle should be tested at birth to detect persistently infected animals with BVD virus [1, 9, 10]. Persistently infected animals are the main route of the BVDV spreading between herds because they cannot be detected by serological tests (immunotolerant calves), but excrete massive amounts of virus [1, 23]. The risk of farm contamination can be reduced by purchasing animals only from herds officially certified as BVDV-free. If the BVDV status in the herd of origin is unknown, then pregnant females should be isolated on arrival (the contact with any animal of breeding age must be restricted), tested for BVD antibody and BVD antigen, and released from isolation only if they are negative results at both tests or antibody positive, antigen-negative, calved, and the calf was tested negative or removed from the herd [1]. To prevent BVDV introduction into a free farm, the following risk factors should be considered: trade with live animals, embryo transfer and semen recipients, return of animals from animal exhibitions, direct contacts between cattle on pasture or over fences, density and activity of arthropod vectors, vaccination, and employee and visitors contact with animals [9, 24].
\n
Sick and suspicious animals should be isolated in a specific area and always handled at the end. In the control of contagious mastitis, the latter are milked cows suspected of the disease [9].
\n
Implementing effective biosecurity programs will bring long-term economic benefits. Dutch studies have shown that the main benefits of a closed dairy herd with good biosecurity are better fertility and lower slaughter rates. The USA comparative studies in Johne’s disease-positive herds and Johne’s disease-negative herds revealed an economic loss of almost US$ 100 per cow in positive herds. Spread of an infectious disease onto a farm can lead to large economic losses. An outbreak of BVD in an Australian farm with 320 milking cows caused losses of $AUD 144,700 [25].
\n
Vaccination is another important biosecurity tool designed to protect resident cattle from infectious agents that could have been brought in by the newly purchased cows [26]. In dairy cattle, immunization mainly targets common infectious agents such as BVD virus, IBR virus, parainfluenza-3 (PI3) virus, bovine respiratory syncytial virus (BRSV), leptospirosis, and clostridial infections [27]. Vaccination programs should be established in collaboration with the herd veterinarian and adapted to the risk of the disease spreading on the farm, including infectious agents that evolve in the area [25, 28]. Vaccination should not be considered the primary or single biosecurity tool because no vaccine provides 100% immunity [26, 28].
\n
Dairy herd vaccination programs are affected by various factors such as age and category of production, disease history, housing, type of vaccine (killed or modified live), and costs [28]. Vaccination programs are designed by age categories and are applied continuously to maximize herd immunity and minimize the spread of the infectious agent [27, 28].
\n
Vaccination schedule for dairy heifers from birth to 6 months of age can be started with an oral modified live vaccine (MLV) for bovine rotavirus and bovine coronavirus given 30 minutes before the ingestion of colostrum to prevent the inactivation [28]. In the first hour of life, calves must receive 2.8 L of colostrum, and in the next 23 hours, the rest of 2.8 L [27]. Depending on the epidemiological situation, an intranasal vaccination of neonatal calves with respiratory vaccines (IBR/PI-3/BRSV) can be started at 3 days of age or older [28]. At 6 weeks old, dairy heifers can receive an injectable modified-live IBR/PI3/BRSV/BVD vaccine and a seven-way clostridial bacterin-toxoid [27]. The immunity of injectable vaccines is longer than the immunity of intranasal vaccines [28]. Following national and international regulations on brucellosis prophylaxis, at 4–6 months age replacement heifers should receive brucellosis RB51 vaccine. Also, depending on the epidemiological situation, calves can receive the appropriate vaccination for leptospirosis clostridial diseases and/or Histophilus somnus. At 6 months of age, heifers should be revaccinated with modified live IBR/PI3/BRSV/BVD virus vaccine, seven-way clostridial vaccine, and five-way leptospirosis bacterin [27, 28].
\n
Pre-breeding heifers (10–12 months of age) should be revaccinated with killed or modified live IBR/PI3/BRSV/BVD virus vaccine, five-way leptospirosis bacterin, and seven- or eight-way clostridial bacterin-toxoid [28]. Optionally, it can be done with vibriosis bacterin [27].
\n
Pre-calving heifers should be revaccinated 40–60 days before calving with killed IBR/PI3/BRSV/BVD virus vaccine, five-way leptospirosis bacterin, killed rotavirus and coronavirus vaccine, and Escherichia coli + Clostridium perfringens types C and D bacterin/toxoid. Three weeks before to calving, heifers should be revaccinated with killed rotavirus and coronavirus vaccine, and Escherichia coli + Clostridium perfringens types C and D bacterin/toxoid [27, 28]. Also, pre-calving heifers should be vaccinated with coliform mastitis bacterin [27].
\n
Adult cows should be annually vaccinated, 40–60 days before calving for IBR, PI3, BRSV, and BVDV [27]. Depending on the history of diseases in the region and the associated epidemiological risks, the farm veterinarian should choose vaccines that immunologically protect dairy cows during the lactation period and the dry period for leptospirosis, vibriosis, Rotavirus, Coronavirus, Clostridium perfringens types C and D, and Escherichia coli mastitis. Types of vaccines recommended are killed or bacterin/toxoid and modified-live vaccines (MLV) [27, 28]. Adult dairy cattle should receive a booster vaccination at 3 weeks before calving with killed rotavirus and coronavirus vaccine and Escherichia coli + Clostridium perfringens types C and D bacterin/toxoid vaccine [27]. MLV vaccines should be used with prudence in pregnant cows and only after consultation with the veterinarian [28]. The annual vaccination for vibriosis should be performed in dairy herds where the artificial insemination is not practiced [27].
\n
The annual vaccination of adult dairy cattle for calf scours (rotavirus and coronavirus, Escherichia coli, and Clostridium perfringens types C and D) should be considered in all herds with recent history as a part of the preventative management practices [27].
\n
Mastitis is one of the most important diseases in dairy cows that affects the welfare, production, and duration of the economic life of the animals [29]. Economic losses are due to direct milk production losses (reduction of quantity, unsalable, or poor quality), culling or removal from the herd of animals with unsatisfactory treatment results, cost of veterinary care, cost of excessive use of antimicrobials and other medicines, and the risk of antibiotic resistance [30].
\n
The main pathogens targeted by mastitis vaccines are Staphylococcus aureus, Streptococcus agalactiae, and Escherichia coli [29]. Reduction in the incidence and duration of intramammary infections can be obtained by applying the combination of vaccination with high milking hygiene procedures, treatment of clinical cases, segregation, and culling of known infected cows [29]. The following preventive measures were proved to have a positive result in the management of mastitis in dairy herds: the use of milkers’ gloves, blanket use of dry-cow therapy, washing unclean udders, maintaining cows upright after milking, back-flushing of the milking cluster after milking an animal with clinical mastitis, and application of a treatment protocol [30] Also, to maximize the success of immunization, within 5 days of mastitis vaccines, dairy cows must not receive any other Gram-negative bacterin vaccines (e.g., Escherichia coli, Salmonella spp., Pasteurella spp., Campylobacter sp., and Moraxella bovis) [27].
\n
To evaluate the effects of mastitis vaccines in dairy cows, the following monitoring parameters are most commonly used:
Clinical and subclinical mastitis incidence and severity
Somatic cell count
Serum and/or milk immunoglobulin G concentrations
Milk bacterial culture or Staphylococcus aureus count in milk
Newly acquired dairy herd bulls should be 30–60 days in prophylactic quarantine and tested with negative results for persistent BVDV infection, brucellosis, and tuberculosis. Recommended vaccination schedule for dairy herd bulls is an annual vaccination at the breeding soundness examination with IBR/PI3/BVD killed vaccine, five-way leptospirosis bacterin, and vibriosis bacterin [27].
\n
If there are animal species other than cattle, then the vaccination actions must take into account for these species as well. Farm dogs and cats should be vaccinated at least against rabies to protect humans and other animals [14].
\n
Antibiotic overuse can be reduced by using a proper mixture of natural antibacterial peptides, biological response modifiers, prebiotics, probiotics, and correct development of the gut microbiome [31].
\n
The limited use of bacterial culture and sensitivity testing by veterinarians are other causes of the persistence of the multidrug resistance (MDR) isolates in dairy farms. The findings of the last decades highlight the necessity of using antimicrobial susceptibility testing each time before prescribing an antibiotic [32].
\n
\n
\n
4.2 Dead animal management
\n
To reduce the risk of pathogens spreading in farm animals, dead animals should be disposed of in the shortest time. Depending on the national regulations and farm’s possibilities, the disposal of carcasses can be done by a licensed dead stock collector, burial, or composting [14].
\n
Studies designed to investigate what motivates and withholds farmers to implement biosecurity measures placed the carcass storage away from the stables on the second rank for feasibility, but with a lower score for efficacy [33].
\n
Rendering trucks have a particular risk for farm biosecurity because they are at high risk for carrying animals killed by infectious diseases [26]. To prevent farm contamination, mortality pick-up should be located away from the stable and feed storage bin and silo [34].
\n
\n
\n
\n
5. Feed and water biosecurity
\n
The biosecurity of feed and water must start from the source, respectively, from the fields where crops are grown and from the water capture source. Manure used as a natural fertilizer can contaminate the soil, crop, and water used for irrigation and groundwater sources [2]. The quality and potability of water should be tested regularly, and samples from each feedstuff batch or lot should be stored for possible laboratory analyses (e.g., bacteria, toxins, molds, and mycotoxins) until that batch is consumed without incidents [2, 10].
\n
To reduce the risk of the diseases being introduced by contaminated feed, the dairy producer should record and monitor the manure application on its pastures and fields cultivated with feedstuffs [2]. The risk of a feed-related disease outbreak is increased when feedstuffs are purchased from multiple locations or the crops were fertilized with manure from other dairy farms [2, 10].
\n
To prevent feedstuffs to be contaminated through fecal material and urine from rodents, birds, dogs, cats, and any wildlife, dairy farmers should design food storage areas in a way to be inaccessible (e.g., opened bags can be placed into containers with tight lids; barns can have welded wire fence) [2, 14].
\n
The biosecurity plan of the dairy farm should include the frequency of storage areas cleaning, the way of feed bags storage off the floor on pallets, removing and disposing of the not consumed feed within 24 hours, rotation of feed inventory for the purpose to reduce the possible presence of detrimental organisms or toxins in stored feeds, and periodically checking of silos, bins, and bunks to detect and remove as soon as possible moldy or spoiled feedstuff [14].
\n
Although not recommended, some cattle herds are still using surface water (e.g., lakes, ponds, and rivers) as a water source. Drinking water can be contaminated by animal carcasses (e.g., dead wild animals), manure from other livestock, bird droppings, urine and feces of wildlife, and human waste [2, 10, 14]. Water biosecurity programs should include several measures designed to prevent contamination with toxins and infectious agents such as restriction of the birds and wildlife access to farm water sources, filtration and chemical sterilization of water, and regular testing of water quality and potability [2]. Waterers should be cleaned once a week [14].
\n
\n
\n
6. Manure biosecurity
\n
In dairy farms, manure is the most problematic waste and should be treated as a biological risk material because it has a huge bacterial load [2]. Manure should be stored in an area inaccessible to cattle [14]. Contact with manure from infected cattle is the main means of spread for rotavirus, coronavirus, Escherichia coli, Salmonellosis, and Johne’s disease to other receptive animals. Manure handling should prevent environmental contamination and should not violate the legislation in force [14].
\n
Manure is rich in nutrients that could be recycled as fertilizer [35]. However, the use of this natural fertilizer should be done with caution to prevent contamination of crops, pastures, and groundwater sources [2]. Salmonella spp., Escherichia coli, Listeria spp., and Mycobacterium avium subsp. paratuberculosis can be killed by the process of manure composting but the process must be controlled before the use of compost in agriculture [2, 36, 37]. In the process of composting should not be used the manure from the hospital pen, where de infectious agents can be in a high concentration. Also, the temperature and microbial activity should be checked to confirm the complete sterilization [2, 14]. Also, manure can be recycled for bedding and to produce methane [2].
\n
Manure biosecurity programs should include measures to prevent the manure equipment used to handle feed, the environment infestation with files and intestinal parasites (manure must be removed frequently to prevent the pest life cycles completion), manure run-off or transfer from adults to calves, and feed contamination by manure-covered wheels of farm vehicles [14].
\n
Manure spreaders and slurry handling equipment are high-risk equipment and should be brought to the farm after proper cleaning or disinfection [1].
\n
The manure cleaning of vehicles and equipment must be done in areas specially designed for this purpose, where water or disinfectants would not splash onto feed or into drinking water. Throughout the entire cleaning and disinfection process, the equipment will be inspected visually to dispel any suspicion of cross-contamination [2].
\n
\n
\n
7. Conclusions
\n
The development and implementation of biosecurity programs in dairy farms improve cattle health, welfare, and productivity. These programs must be monitored and evaluated continuously to identify new methods of control and new effective critical control points and to further improve the program to prevent the introduction and spread of infectious agents on the farm. The biosecurity program should be focused on the decision and adapted to the specific situations of each dairy farm. Many of the problems encountered can be prevented or minimized with the support of veterinary services. Staff and visitors should be trained on biosecurity measures applied on the farm.
\n
\n
Conflict of interest
The authors declare no conflict of interest.
\n',keywords:"antibioresistance, biosecurity, dairy farm, cattle",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/72753.pdf",chapterXML:"https://mts.intechopen.com/source/xml/72753.xml",downloadPdfUrl:"/chapter/pdf-download/72753",previewPdfUrl:"/chapter/pdf-preview/72753",totalDownloads:174,totalViews:0,totalCrossrefCites:0,dateSubmitted:"January 30th 2020",dateReviewed:"June 16th 2020",datePrePublished:"July 8th 2020",datePublished:"March 3rd 2021",dateFinished:"July 8th 2020",readingETA:"0",abstract:"Biosecurity is a key element in the battle against antibiotic resistance. The goals of biosecurity are focused not only on the reduction or prevention of the introduction of new diseases from outside sources but also on the reduction or prevention of the movement of infectious diseases on the farm. In this regard, the use of antibiotics can be reduced by simple actions such as physically inspecting animals, testing for bovine diseases, vaccination, or quarantine for at least 3 weeks before mixing with the herd of all new additions. All these examples reduce the risk of diseases with germs from outside. This chapter attempts to synthesize the best biosecurity solutions that can be applied in modern dairy farms.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/72753",risUrl:"/chapter/ris/72753",signatures:"Stelian Baraitareanu and Livia Vidu",book:{id:"9521",title:"Antimicrobial Resistance",subtitle:"A One Health Perspective",fullTitle:"Antimicrobial Resistance - A One Health Perspective",slug:"antimicrobial-resistance-a-one-health-perspective",publishedDate:"March 3rd 2021",bookSignature:"Mihai Mareș, Swee Hua Erin Lim, Kok-Song Lai and Romeo-Teodor Cristina",coverURL:"https://cdn.intechopen.com/books/images_new/9521.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"88785",title:"Prof.",name:"Mihai",middleName:null,surname:"Mares",slug:"mihai-mares",fullName:"Mihai Mares"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"189099",title:"Dr.",name:"Stelian",middleName:null,surname:"Baraitareanu",fullName:"Stelian Baraitareanu",slug:"stelian-baraitareanu",email:"doruvet@yahoo.com",position:null,institution:{name:"University of Agronomic Sciences and Veterinary Medicine of Bucharest",institutionURL:null,country:{name:"Romania"}}},{id:"318163",title:"Prof.",name:"Livia",middleName:null,surname:"Vidu",fullName:"Livia Vidu",slug:"livia-vidu",email:"liviavidu@gmail.com",position:null,institution:{name:"University of Agronomic Sciences and Veterinary Medicine of Bucharest",institutionURL:null,country:{name:"Romania"}}}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Dairy farm sanitation",level:"1"},{id:"sec_2_2",title:"2.1 Employees and visitors",level:"2"},{id:"sec_3_2",title:"2.2 Equipment biosecurity",level:"2"},{id:"sec_4_2",title:"2.3 Vehicle biosecurity",level:"2"},{id:"sec_6",title:"3. Buildings biosecurity",level:"1"},{id:"sec_7",title:"4. Animal biosecurity",level:"1"},{id:"sec_7_2",title:"4.1 Live animal management",level:"2"},{id:"sec_8_2",title:"4.2 Dead animal management",level:"2"},{id:"sec_10",title:"5. Feed and water biosecurity",level:"1"},{id:"sec_11",title:"6. Manure biosecurity",level:"1"},{id:"sec_12",title:"7. Conclusions",level:"1"},{id:"sec_16",title:"Conflict of interest",level:"1"}],chapterReferences:[{id:"B1",body:'\nSibley RJ. Biosecurity in the dairy herd. In: WCDS Advances in Dairy Technology. Vol. 26. Alberta, Canada: University of Alberta; 11-14 March 2014. pp. 59-74\n'},{id:"B2",body:'\nVillarroel A, Dargatz DA, Lane VM, McCluskey BJ, Salman MD. Suggested outline of potential critical control points for biosecurity and biocontainment on large dairy farms. Journal of the American Veterinary Medical Association. 2007;230(6):808-819. DOI: 10.2460/javma.230.6.808\n'},{id:"B3",body:'\nHadorn DC, Stärk KD. Evaluation and optimization of surveillance systems for rare and emerging infectious diseases. Veterinary Research. 2008;39(6):57. DOI: 10.1051/vetres:2008033\n'},{id:"B4",body:'\nDantzer R, Cohen S, Russo SJ, Dinan TG. Resilience and immunity. Brain, Behavior, and Immunity. 2018;74:28-42. DOI: 10.1016/j.bbi.2018.08.010\n'},{id:"B5",body:'\nDargatz DA, Garry FB, Traub-Dargatz JL. An introduction to biosecurity of cattle operations. The Veterinary Clinics of North America. Food Animal Practice. 2002;18:1-5. DOI: 10.1016/s0749-0720(02)00002-6\n'},{id:"B6",body:'\nShortall O, Green M, Brennan M, Wapenaar W, Kaler J. Exploring expert opinion on the practicality and effectiveness of biosecurity measures on dairy farms in the United Kingdom using choice modeling. Journal of Dairy Science. 2017;100(3):2225-2239. DOI: 10.3168/jds.2016-11435\n'},{id:"B7",body:'\nNöremark M, Frössling J, Lewerin SS. A survey of visitors on Swedish livestock farms with reference to the spread of animal diseases. BMC Veterinary Research. 2013;9:184. DOI: 10.1186/1746-6148-9-184\n'},{id:"B8",body:'\nvan Schaik G, Schukken YH, Nielen M, Dijkhuizen AA, Barkema HW, Benedictus G. Probability of and risk factors for introduction of infectious diseases into Dutch SPF dairy farms: A cohort study. Preventive Veterinary Medicine. 2002;54(3):279-289. DOI: 10.1016/s0167-5877(02)00004-1\n'},{id:"B9",body:'\nWallace RL. Practical and sensible dairy farm biosecurity. In: Proceedings of the 6th Western Dairy Management Conference; 12-14 March 2003. Reno, NV: WDMC; 2003. pp. 201-206\n'},{id:"B10",body:'\nVillarroel A. Practical biosecurity on dairy farms. In: Oregon Veterinary Conference; 01 March 2007. Corvallis, OR: OVC; 2007. pp. 1-4. DOI: 10.13140/2.1.3657.7928\n'},{id:"B11",body:'\nGuidance. Disease Prevention for Livestock and Poultry Keepers. How to Prevent the Introduction and Spread of Animal and Bird Disease by Following Good Hygiene and Biosecurity Standards. 2015. Available from: https://www.gov.uk/guidance/disease-prevention-for-livestock-farmers#biosecurity-measures [Accessed: 02 May 2020]\n'},{id:"B12",body:'\nCaldow GL, Crawshaw M, Gunn GJ. Herd health security in the suckler herd. Cattle Practice. 1998;6:175-179\n'},{id:"B13",body:'\nFarm Biosecurity. Essentials. People, Vehicles & Equipment. Available from: https://www.farmbiosecurity.com.au/essentials-toolkit/people-vehicles-equipment/ [Accessed: 12 May 2020]\n'},{id:"B14",body:'\nLivestock Biosecurity. What Is it and Why Should I Care? Available from: https://dairy-cattle.extension.org/livestock-biosecurity/ [Accessed: 12 May 2020]\n'},{id:"B15",body:'\nHoe FG, Ruegg PL. Opinions and practices of Wisconsin dairy producers about biosecurity and animal well-being. Journal of Dairy Science. 2006;89(6):2297-2308. DOI: 10.3168/jds.S0022-0302(06)72301-3\n'},{id:"B16",body:'\nTroutt HF, Galland J, Hyatt D, Rossiter C, Lein D, Brewer RL, et al. Salmonella and the market dairy cow: Transport contamination—Risk for farm biosecurity. The Bovine Practitioner. 2008;42:56-62\n'},{id:"B17",body:'\nBAMN/APHIS. An Introduction to Infectious Disease Control on Farms (Biosecurity). 2001. Available from: http://www.aphis.usda.gov/animal_health/nahms/dairy/downloads/bamn/BAMN01_IntroBiosecurity.pdf [Accessed: 12 May 2020]\n'},{id:"B18",body:'\nPritchard G, Dennis I, Waddilove J. Biosecurity: Reducing disease risks to pig breeding herds. In Practice. 2005;27:230-237. DOI: 10.1136/inpract.27.5.230\n'},{id:"B19",body:'\nDEFRA Archive Website. Biosecurity Guidance to Prevent the Spread of Animal Diseases. 2003. Available from: https://webarchive.nationalarchives.gov.uk/20130402155521/http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/documents/biosecurity_guidance.pdf [Accessed: 16 April 2020]\n'},{id:"B20",body:'\nBrennan ML, Christley RM. Biosecurity on cattle farms: A study in north-west England. PLoS One. 2012;7(1):e28139. DOI: 10.1371/journal.pone.0028139\n'},{id:"B21",body:'\nTechnical Information. Buildings. Housing. Building Biosecurity. 2020. Available from: https://dairy.ahdb.org.uk/technical-information/buildings/housing/building-biosecurity/#.XsU6wkQzaHs [Accessed: 16 April 2020]\n'},{id:"B22",body:'\nBaraitareanu S. Infectious Diseases, Preventive Medicine and Clinical Lectures on Species 2. Course Manual. Printech: Bucharest; 2020. p. 180\n'},{id:"B23",body:'\nBaraitareanu S, Vidu L. The preventive medicine of bovine viral diarrhoea-mucosal disease in dairy farms: A review. Revista Romana de Medicina Veterinara. 2019;29(2):61-64\n'},{id:"B24",body:'\nLindberg AL, Alenius S. Principles for eradication of bovine viral diarrhoea virus (BVDV) infections in cattle populations. Veterinary Microbiology. 1999;64(2-3):197-222. DOI: 10.1016/s0378-1135(98)00270-3\n'},{id:"B25",body:'\nCockcroft PD, editor. Bovine Medicine. 3rd ed. Chichester: Wiley; 2015. p. 644\n'},{id:"B26",body:'\nSanderson M. Biosecurity for cow-calf enterprises. In: Anderson DE, Rings DM, editors. Food Animal Practice. 5th ed. Philadelphia: Saunders; 2009. pp. 594-599. DOI: 10.1016/b978-141603591-6.10113-7\n'},{id:"B27",body:'\nWaldner DN, Kirkpatrick J, Lehenbauer TW. Recommended Vaccination Schedules for a Comprehensive Dairy Herd Health Program. 2017. Available from: https://extension.okstate.edu/fact-sheets/recommended-vaccination-schedules-for-a-comprehensive-dairy-herd-health-program.html [Accessed: 16 April 2020]\n'},{id:"B28",body:'\nDewell G, Gorden P, Breuer R. Iowa State University Extension and Outreach. Dairy Cattle Vaccination Programs. 2016. Available from: https://store.extension.iastate.edu/Product/da3088-pdf [Accessed: 16 April 2020]\n'},{id:"B29",body:'\nIsmail ZB. Mastitis vaccines in dairy cows: Recent developments and recommendations of application. Veterinary World. 2017;10(9):1057-1062. DOI: 10.14202/vetworld.2017.1057-1062\n'},{id:"B30",body:'\nHogeveen H, Huijps K, Lam TJ. Economic aspects of mastitis: New developments. New Zealand Veterinary Journal. 2011;59(1):16-23. DOI: 10.1080/00480169.2011.547165\n'},{id:"B31",body:'\nTrevisi E, Zecconi A, Cogrossi S, Razzuoli E, Grossi P, Amadori M. Strategies for reduced antibiotic usage in dairy cattle farms. Research in Veterinary Science. 2014;96(2):229-233. DOI: 10.1016/j.rvsc.2014.01.001\n'},{id:"B32",body:'\nLawrence KE, Wakeford L, Toombs-Ruane LJ, MacLachlan C, Pfeffer H, Gibson IR, et al. Bacterial isolates, antimicrobial susceptibility and multidrug resistance in cultures from samples collected from beef and pre-production dairy cattle in New Zealand (2003-2016). New Zealand Veterinary Journal. 2019;67(4):180-187. DOI: 10.1080/00480169.2019.1605943\n'},{id:"B33",body:'\nDamiaans B, Sarrazin S, Heremans E, Dewulf J. Perception, motivators and obstacles of biosecurity in cattle production. Vlaams Diergeneeskundig Tijdschrift. 2018;87(3):150-163\n'},{id:"B34",body:'\nPayne M. CDQAP Ruminations: Dairy Biosecurity & Your Bottom Line. 2015. Available from: http://cdrf.org/2015/05/14/cdqap-ruminations-dairy-biosecurity-your-bottom-line/ [Accessed: 10 May 2020]\n'},{id:"B35",body:'\nHogan JS, Bogacz VL, Thompson LM, Romig S, Schoenberger PS, Weiss WP, et al. Bacterial counts associated with sawdust and recycled manure bedding treated with commercial conditioners. Journal of Dairy Science. 1999;82(8):1690-1695. DOI: 10.3168/jds.S0022-0302(99)75398-1\n'},{id:"B36",body:'\nLung AJ, Lin CM, Kim JM, Marshall MR, Nordstedt R, Thompson NP, et al. Destruction of Escherichia coli O157:H7 and Salmonella enteritidis in cow manure composting. Journal of Food Protection. 2001;64(9):1309-1314. DOI: 10.4315/0362-028x-64.9\n'},{id:"B37",body:'\nGrewal SK, Rajeev S, Sreevatsan S, Michel FC Jr. Persistence of Mycobacterium avium subsp. paratuberculosis and other zoonotic pathogens during simulated composting, manure packing, and liquid storage of dairy manure. Applied and Environmental Microbiology. 2006;72(1):565-574. DOI: 10.1128/AEM.72.1.565-574.2006\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Stelian Baraitareanu",address:"stelian.baraitareanu@gmail.com",affiliation:'
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