These books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\\n\\n
This collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\\n\\n
To celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
IntechOpen and Knowledge Unlatched formed a partnership to support researchers working in engineering sciences by enabling an easier approach to publishing Open Access content. Using the Knowledge Unlatched crowdfunding model to raise the publishing costs through libraries around the world, Open Access Publishing Fee (OAPF) was not required from the authors.
\n\n
Initially, the partnership supported engineering research, but it soon grew to include physical and life sciences, attracting more researchers to the advantages of Open Access publishing.
\n\n\n\n
These books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\n\n
This collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\n\n
To celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
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\r\n\tThe primary aim of this book is to integrate the knowledge of dairy product manufacturing with the chemistry of ingredients, along with the chemistry of several reactions which appear during the preparation of these products. Therefore, understanding the basic composition of milk and the chemistry of various constituents is of utmost importance. This will be the first topic that will be covered in this book, along with the advance and updated knowledge on the ingredients/ milk constituents. Over the years, the processing and manufacturing of several dairy products have witnessed upgraded processing equipment and hence the protocols of manufacturing. We also hope to cover the advanced processing methods for the production of dairy products. \r\n\tFurthermore, during the preparation of high-quality dairy products, several physical, chemical, enzymatic, and microbial transformations take place. We will consciously focus on this interaction of different constituents of milk under different processing conditions for the development of the products.
",isbn:"978-1-83768-093-1",printIsbn:"978-1-83768-092-4",pdfIsbn:"978-1-83768-094-8",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,isSalesforceBook:!1,isNomenclature:!1,hash:"420e687768b56ca7b3238d77f63f1302",bookSignature:"Dr. Neelam Upadhyay",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/12173.jpg",keywords:"Protein, Fat, Lactose, Carbohydrates, Milk Processing, Milk Products, Milk Constituents, Acid Coagulated, Enzyme Treated, Heat Treated, Dairy Products, Protocols of Manufacturing",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"May 18th 2022",dateEndSecondStepPublish:"July 19th 2022",dateEndThirdStepPublish:"September 17th 2022",dateEndFourthStepPublish:"December 6th 2022",dateEndFifthStepPublish:"February 4th 2023",dateConfirmationOfParticipation:null,remainingDaysToSecondStep:"24 days",secondStepPassed:!1,areRegistrationsClosed:!1,currentStepOfPublishingProcess:2,editedByType:null,kuFlag:!1,biosketch:"Dr. Upadhyay has received many awards most notable being the Young Woman Scientist Award 2020 from the Agro-Environmental Development Society and the Best Poster Award 2021 from the National Conference on Moringa Food Conclave 2021. She is a dedicated researcher in food and dairy processing and has published many research articles and papers in both national and international journals and publications.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"269538",title:"Dr.",name:"Neelam",middleName:null,surname:"Upadhyay",slug:"neelam-upadhyay",fullName:"Neelam Upadhyay",profilePictureURL:"https://mts.intechopen.com/storage/users/269538/images/system/269538.jpg",biography:"BRIEF BIODATA\n1.\tName in full: Neelam Upadhyay \n2.\tDate & Place of Birth: 29th December, 1987 at Delhi\n3.\tField of specialization: Food Technology\n4.\tPresent Position/ Designation: Scientist- Senior Scale\n5.\tAddress:\t(a)\tOfficial:\tTel. No.:0184-2259258\n\t\t\t\tE-mail: \ticar.neelam@gmail.com; neelam.upadhyay@icar.gov.in \n\t\t\t\tAddress: \tLaboratory No. 146, Dairy Technology Division, ICAR- \n\t\t\t\t\t\tNational Dairy Research Institute, Karnal \n\t\t\t(b)\tResidential: Tel. No.: +91-9255772587\n\tAddress (Permanent): 41-D, MIG DDA Flats, Shivam Enclave, Delhi-110032\n6.\t(a) Academic career and (b) professional attainments\n(a) Examination\tClass/ Percentage\tYear of Passing\tSubjects Taken\tName of University / Board\nXth \t1st/83\n(415/500)\t2003\tMathematics, Social Science, Science, English, Hindi\tK.V., Mumbai (CBSE)\nXIIth\t1st/78.2 \n(391/500)\t2005\tPhysics, Mathematics, Chemistry, Biology, English\tK.V., Delhi (CBSE)\nB.A.Sc. (Hons.)\t1st/83.43 (2044/2450)\n(3rd position)\t2008\tFood Technology\tSRCASW, University of Delhi, Delhi\nM.Sc.\t1st/8.62\n(1st position)\t2010\tFood Science & Technology\tCCS Har. Agri. Uni., Hisar, Haryana\nTitle of Research:\tDevelopment of flavoured whey-soya milk beverage\nMajor Advisor:\tDr. R. S. Dabur (Professor and Head)\nPh.D.\t1st/8.0\n(1st position)\t2014\tDairy Chemistry\tNational Dairy Research Institute, Karnal, Haryana\nTitle of Research: \tDetection of vegetable oil and animal body fat adulteration in ghee using solvent fractionation technique\nMajor Advisor:\tDr. Darshan Lal (Principal Scientist and Ex-Head)\nDistinctions during Academics\nDegree\tDistinctions\nBachelor of Applied Science (Hons.)\ti.\tY.K. Kapoor Memorial Scholarship 2006 by All India Food Processor’s Association \nii.\t3rd position in university\niii.\tReceived highest attendance award\niv.\tReceived trophy for ‘Most Disciplined Student’ for the graduation period 2005-2008\nv.\tCertificate of Honor from Honb’le Mr. Justice K.G. Balakrishnan, Chief Justice of India\nMaster of Science\ti.\t1st position in discipline and 2nd position in college\nii.\tReceived recognition for academic excellence from Jawaharlal Nehru Memorial Fund; \niii.\tQualified GATE\niv.\t2nd in inter-college yoga competition\nv.\tParticipated in various events of All India Youth Festival organized at UAS, Bangalore.\nDoctor of Philosophy\ti.\tReceived Merit Certificate for Academic Excellence in PhD course work\nii.\tReceived Certificate of Appreciation for outstanding work in the field of Dairy Processing during PhD\niii.\tQualified ICAR’s National Eligibility Test in 2010; Qualified the ICAR’s All India Examination, ICAR-SRF (PGS_-2011-2012 for award of ICAR-SRF (PGS) with 2nd rank (both in first attempt) \niv.\tQualified Agricultural Research Service Examination-2013 conducted by Agricultural Scientist Recruitment Board against the single vacancy (for UR) in the discipline of Food Technology\nv.\tStage Management Secretary of student’s council 2010-11\nvi.\tLiterary secretary of Student’s Council 2011-12\nvii.\tCompleted certificate e-course on “Publishing a Journal Manuscript - the Groundwork” directed by Springer in 2013\nviii.\tHave successfully completed certificate e-course – “Peer Review Academy” directed by Springer in 2013\nix.\tReceived a certificate on accomplishment IRIS 4-2 Information Literacy Plagiarism Quiz (on-line) in 2013 developed by Distance Learning Council of Washington, USA \n (b) Position Held\tInstitution \tPeriod of Appointment\tNature of Appointment\nScientist (Food Technology)\tICAR- National Academy of Agricultural Research Management, Hyderabad\t3 months\n(1st January, 2015 till 31st March, 2015)\tPermanent\n(Received ‘A’ grade for FOCARS)\nScientist \n(Food Technology)\tICAR- National Dairy Research Institute, Karnal\t10th March, 2015 till 31st December, 2018\n(after availing 10 days of transfer period)\tPermanent\nScientist-Senior Scale\n(Food Technology)\tICAR- National Dairy Research Institute, Karnal\t1st January, 2019 till date\tPermanent\n\n7. Special attainments in Research\n(https://scholar.google.co.in/citations?hl=en&user=PRz0Tz4AAAAJ&view_op=list_works&sortby=pubdate)\nPublications\tNumbers\tRemarks \nResearch Articles\t35\n(24 Intl, 9 National, 2 others)\tTotal Impact: 72.302\n\nBook Chapters\t7\t5 APA/CRC Press; 1 InTech Open; \n1 National\nReview Articles\t2\tTotal Impact:8.327\nTechnical Articles\t7\tCompendium of trainings, seminars, etc\nInstitute publication\t1\t\nPopular Article\t12\t6 in English; 5 in hindi\nCitations \t1066\t(as per googlescholar)\nH-index/ i10-index\t15/ 17\t\n.\n.\nJournal\tNumber of publications\tImpact factor\nResearch Articles\t35\t72.302\nInternational\t24 (15 as either corresponding or first author)\t72.302\nNational\t9 (3 as first or corresponding author)\tNAAS score\nOthers\t2\t\nReview article (International)\t2\t8.327\nInternational\t2\t8.327\n.\n \n\n\n\nRESEARCH ARTICLES\nInternational Journals \n1.\tTiwari, S., Upadhyay, N.*, Singh, A. K. (2022). Stability assessment of emulsion of carotenoids extracted from carrot bio-waste in flaxseed oil and its application in food model system. Food Bioscience, 47, 101631. https://doi.org/10.1016/j.fbio.2022.101631.\n2.\tPatil, A. T., Meena, G. S., Upadhyay, N., Khetra, Y., Singh, A. K., & Borad, S. G. (2021). Buffalo milk protein concentrate 60: Effect of skim milk heat treatment on its reconstitutability and functionality. Food Science & Technology – Lebensmittel -Wissenschaft & Tech, 148, 111638. \n3.\tUttamrao, H. J., Meena, G. S., Khetra, Y., Upadhyay, N., Singh, A. K., Arora, S., & Borad, S. G. (2022). Homogenization and sodium hydrogen phosphate induced effect on physical and rheological properties of ultrafilterd concentrated milk. Journal of Food Science and Technology, 59(3), 956-967. \n4.\tTiwari, S., Upadhyay, N.*, Malhotra, R. (2021). Three way ANOVA for emulsion of carotenoids extracted in flaxseed oil from carrot bio-waste. Waste Management, 121, 67-76. \n5.\tRanvir, S., Sharma, R., Gandhi, K., Upadhyay, N., Mann, B. (2020). Assessment of proteolysis in ultra-high temperature milk using attenuated total reflectance–Fourier transform infrared spectroscopy. International Journal of Dairy Technology. 73(2): 366-375. doi: 10.1111/1471-0307.12683. \n6.\tPonbhagavathi, T.R., Singh, A.K., Raju, P.N., Upadhyay, N. (2020). High performance liquid chromatographic (HPLC) determination of available lysine in milk protein-maize composite extrudates and its stability during storage. Journal of the Indian Chemical Society, 97(11a), 2344-2350\n7.\tTiwari, S., Upadhyay, N.*, Singh, A. K., Meena, G. S., & Arora, S. (2019). Organic solvent-free extraction of carotenoids from carrot bio-waste and its physico-chemical properties. Journal of Food Science and Technology, 1-10. 10.1007/s13197-019-03920-5\n8.\tBaria, B., Upadhyay, N.*, Singh, A. K., & Malhotra, R. K. (2019). Optimization of ‘green’extraction of carotenoids from mango pulp using split plot design and its characterization. Food Science & Technology – Lebensmittel -Wissenschaft & Tech, 104, 186-194. \n9.\tPatil, A. T., Meena, G. S., Upadhyay, N., Khetra, Y., Borad, S. G., & Singh, A. K. (2019). Effect of change in pH, heat treatment and diafiltration on properties of medium protein buffalo milk protein concentrate. Journal of Food Science and Technology, 56(3), 1462-1472. \n10.\tUttamrao, H. J., Meena, G. S., Borad, S. G., Punjaram, S. A., Khetra, Y., Upadhyay, N., & Singh, A. K. (2019). Effect of disodium phosphate and homogenization on physico-chemical and rheological properties of buffalo skim milk based ultrafiltered retentate. Journal of food science and technology, 56(5), 2426-2435. \n11.\tMeena, G.S., Dewan, A., Upadhyay, N., Barapatre, R., Kumar, N., Singh, A.K., & Rana, J.S. (2019). Fuzzy Analysis of Sensory Attributes of Gluten Free Pasta Prepared From Brown Rice, Amaranth, Flaxseed Flours and Whey Protein Concentrates. Journal of Food Science and Nutrition Research, 2(1), 022-037. DOI: 10.26502/jfsnr.2642-1100006\n12.\tPatil, A. T., Meena, G. S., Upadhyay, N.*, Khetra, Y., Borad, S., & Singh, A. K. (2018). Production and characterization of milk protein concentrates 60 (MPC60) from buffalo milk. Food Science & Technology – Lebensmittel -Wissenschaft & Tech, 91, 368-374. https://doi.org/10.1016/j.lwt.2018.01.028 \n13.\tUpadhyay, N.*, Jaiswal, P., & Jha, S. N. (2018). Application of attenuated total reflectance Fourier Transform Infrared spectroscopy (ATR–FTIR) in MIR range coupled with chemometrics for detection of pig body fat in pure ghee (heat clarified milk fat). Journal of Molecular Structure, 1153, 275-281. \n14.\tUpadhyay, N.*, Kumar A., Goyal A. and Lal, D. (2017). Complete liquification time test coupled with solvent fractionation technique to detect adulteration of foreign fats in ghee (heat-clarified milk fat). International Journal of Dairy Technology. 70(1): 110-118. doi: 10.1111/1471-0307.12323. \n15.\tUpadhyay, N.*, Goyal A., Kumar A. and Lal, D. (2017). Detection of adulteration of caprine body fat and mixture of caprine body fat and groundnut oil in bovine and buffalo ghee using Differential Scanning Calorimetry. International Journal of Dairy Technology. 70(2): 297-303. May 2017.doi:10.1111/1471-0307.12336. \n16.\tKumar, A., Upadhyay, N.*, Ghai, D.L., Kumar, A. Gandhi, K. and Sharma, V. (2016). Effect of preparation and storage of khoa on physico-chemical properties of milk fat. International Journal of Dairy Technology. 69(2): 294-300. doi: 10.1111/1471-0307.12266. \n17.\tUpadhyay, N.*, Jaiswal, P. & Jha, S.N. (2016). Detection of goat body fat adulteration in pure ghee using ATR-FTIR spectroscopy coupled with chemometric strategy. Journal of Food Science and Technology. 53 (10): 3752-3760. doi:10.1007/s13197-016-2353-2 ISSN 0022-1155\n18.\tRathi, M., Upadhyay, N.*, Dabur, R.S. and Goyal A. (2015). Formulation and physic-chemical analysis of whey –soymilk dahi. Journal of Food Science and Technology. 52(2): 968-975. doi 10.1007/s13197-013-1074-z. ISSN: 0022-1155. \n19.\tKanthale, P., Kumar, A. Upadhyay, N.*, Lal, D., Rathod G. and Sharma, V. (2015). Qualitative test for the detection of extraneous Thiocyanate in Milk. Journal of Food Science and Technology. 52(3): 1698-1704. DOI: 10.1007/s13197-013-1174-9. ISSN: 0022-1155.\n20.\tGoyal, A., Sharma, V., Upadhyay, N., Singh, A.K., Arora, S. and Ghai, D.L. (2015). Development of stable flaxseed oil emulsions as a potential delivery system of ω-3 fatty acids. Journal of Food Science and Technology. 52(7):4256-4265. \n21.\tUpadhyay, N.*, Kumar, A., Rathod, G., Goyal, A. and Lal, D. (2015). Development of a method employing reversed-phase thin-layer chromatography for establishing milk fat purity with respect to adulteration with vegetable oils. International Journal of Dairy Technology. 68(2): 207-217. doi. 10.1111/1471-0307.12178. \n22.\tGoyal, A., Siddiqui, S. Upadhyay, N., Soni, J. (2014). Effects of ultraviolet irradiation, pulsed electric field, hot water and ethanol vapours treatment on functional properties of mung bean sprouts. Journal of Food Science and Technology. 51(4): 708-714. doi 10.1007/s13197-011-0538-2. Publisher Springer. ISSN (electronic version): 0975-8402. \n23.\tKundu, H., Grewal, R.B., Goyal, A., Upadhyay, N.*, and Prakash S. (2014). Effect of incorporation of pumpkin (Cucurbita moshchata) powder and guar gum on the rheological properties of wheat flour. Journal of Food Science and Technology. 51(10):2600-2607. DOI: 10.1007/s13197-012-0777-x. ISSN: 0022-1155. \n24.\tUpadhyay, N.*, Kumar, A., Goyal, A. and Lal, D. (2014). A planar chromatographic method to detect adulteration of vegetable oils in ghee. JPC-Journal of Planar Chromatography-Modern TLC. 27 (6): 431-437. DOI: 10.1556/JPC.27.2014.6.5 \nNational Journals\n1.\tPonbhagavathi, T. R., Singh, A. K., Raju, P. N., Upadhyay, N. (2021). Textural and Sensory Characteristics of Milk Protein-Maize Flour-based Extrudates. Journal of Agricultural Engineering, 58(2), 124-136. 10.52151/jae2021581.1740\n2.\tPonbhagavathi, T.R., Singh, A.K., Raju, P.N., Upadhyay, N. (2020). Effect of Rennet Casein and Whey Protein Concentrate on Extrusion Behavior of Maize Flour. Current Journal of Applied Science and Technology. 39(33), 16-27, Article no.CJAST.57830.\n3.\tUpadhyay, N.*, Kumar, A., Lal, D., Kant, R., & Goyal, A. (2018). Detection of groundnut oil and goat body fat adulteration in ghee using principal component analysis on fatty acid profile. Indian Journal of Dairy Science. 71(5):464-472. \n4.\tUpadhyay, N.*, Kumar, A., Gandhi, K., Goyal, A. and Lal, D. (2014). Standardization of solvent fractionation technique for detection of adulteration in ghee by enriching animal body fat and vegetable oil in different fractions. Indian Journal of Dairy Science. 67 (4):323-327.\n5.\tGandhi. K., Upadhyay, N., Aghav, A.D., Sharma, V., and Lal, D. (2014). Detection of adulteration of ghee (clarified milk fat) with palmolein and sheep body fat using Reichert-Meissl (RM) value coupled with solvent fractionation technique. Indian Journal of Dairy Science. 67(5): 387-393. Received Second Best Paper Award during 44th Dairy Industry Conference organized by ICAR-NDRI, Karnal and Indian Dairy Association from 18-20, February 2016.\n6.\tAghav, A.D., Gandhi, K., Upadhyay, N., Kumar, A. and Lal, D. (2014). A study on the physico-chemical changes occurring in the milk fat during preparation of Paneer. Indian Journal of Dairy Science. 67 (5): 398-404.\n7.\tKumar, A., Upadhyay, N., Gandhi, K., Lal, D. and Sharma, V. (2013). Detection of soybean oil and buffalo depot fat in ghee using Normal-Phase Thin Layer Chromatography. Indian Journal of Dairy Science. 66(4): 294-99. ISSN: 0019-5146.\n8.\tKumar, A., Upadhyay, N., Gandhi, K., Kumar, A., Lal, D. and Sharma, V. (2013). Reverse-Phase Thin Layer Chromatography of Unsaponifiable Matter of ghee for detecting adulteration with soybean oil and buffalo depot fat. Indian Journal of Dairy Science. 66(6): 496-501. ISSN: 0019-5146.\n9.\tUpadhyay, N.*, Dabur R.S. and Rathi, M. (2011). Development and Shelf life Study of Flavoured Whey-soya milk beverage. Indian Journal of Dairy Science. 64(2): 92-101. ISSN: 0019-5146.\nOther Journals\n1.\tDewan, A., Meena, G.S., Upadhyay, N., Barapatre, R. Singh, A.K., Rana, J.S. (2017). Formulation of non-Gluten Pasta from the Optimized levels of Dairy and Non-Dairy ingredients. Madridge Journal of Food Technology. 2(2): 92–98. \n2.\tGalmessa, U., Prasad, S., Kumaresan, A., Oberoi, P. S., Baithalu, R. K., Upadhyay, N., and Dang, A. K. (2015). Modulation of Milk Fatty acid profile milk yield and composition through supplementation of omega-3 fatty acid in transition cow’s diet. Journal of Science and Sustainable Development. 3(1): 25-38. ISSN: 2070-1748\nREVIEW ARTICLES\n1.\tUpadhyay, N.*, Goyal, A. Kumar, A., Lal, D. and Singh, D. (2014). Preservation of milk and milk products for analytical purposes: A review. Food Reviews International. 30(3):203-224. DOI 10.1080/87559129.2014.913292. ISSN: 1525-6103\n2.\tGoyal, A., Sharma, V., Upadhyay, N., Gill, S. and Sihag, M. (2014). Flax and flaxseed oil: an ancient medicine & modern functional food. Journal of Food Science and Technology. 51(9): 1633-1653. DOI 10.1007/s13197-013-1247-9. ISSN: 0975-8402. \nBOOK CHAPTERS\n1.\tKumari, L., Sharma, M., & Upadhyay, N. (2021). Three-Dimensional Printing of Food Products: Printing Techniques, Novel Applications, and Printable Food Materials. Handbook of Research on Food Processing and Preservation Technologies: Volume 3: Computer-Aided Food Processing and Quality Evaluation Techniques, 55. Boca Raton, CRC Press\n2.\tUpadhyay, N.*, Harshitha, C. G., Pathak, N. K., & Sharma, R. (2021). Fourier Transform Infrared (FTIR) Spectroscopy with Chemometrics: Evaluation of Food Quality and Safety. Handbook of Research on Food Processing and Preservation Technologies: Volume 5: Emerging Techniques for Food Processing, Quality, and Safety Assurance, 271.\n3.\tNagarajappa, V., Upadhyay, N., Chawla, R., Mishra, S.K., & Nath, S. (2019). Functional Properties of Milk Proteins. In: Engineering Practices for milk products- Dairyceuticals, Novel Technologies, and Quality (pp 3-26). Apple Academic Press.\n4.\tUpadhyay, N., Kumar, M. C. T., Sharma, H., Borad, S., & Singh, A. K. (2019). Pulse Electric Field Processing of Milk and Milk Products. In: Non-thermal Processing of Foods (pp.129-144). Boca Raton, CRC Press\n5.\tUpadhyay, N., Nagaraj, V., & Singh, A. K. (2019). Advances in Fractionation of Milk Lipids: Analysis and Applications of fractions In: Recent Technologies in Dairy Science (pp. 325-344). Today and Tomorrow’s Printers and Publishers.\n6.\tNagaraj, V., Upadhyay, N.*, Nath, B. S., & Singh, A. K. (2018). Advances in Fractionation and Analysis of Milk Carbohydrates. In Technological Approaches for Novel Applications in Dairy Processing (pp. 127-147). IntechOpen. http://dx.doi.org/10.5772/intechopen.76312\n7.\tUpadhyay, N.*, Veena, N., Borad, S., & Singh, A. K. (2017). Application of Natural Antioxidants in Dairy Foods. In Natural Antioxidants (pp. 281-318). London: Apple Academic Press.\nINSTITUTE PUBLICATION\n1.\tDr. T. K. Datta, Dr. Meena Malik and Dr. Neelam Upadhyay (2017). Foundation Programme for Freshers at ICAR-NDRI 2017.\nPOPULAR AND LEAD ARTICLES\n1.\tPatil, A. T., Meena, G. S., Upadhyay, N., & Singh, A.K. (2017). Milk protein concentrates- Their Applications. Indian Dairyman, 69(9), 44-48.\n2.\tUpadhyay, N.* and R.K. Malik (2015). Nutritive Value of Milk. In: In Touch, Heinz Nutrition Foundation of India. Volume 17, Number 2&3, 2-11. (Lead Article). \n3.\tGoyal, A., Sharma, V., Upadhyay, N., Sihag, M. and Kaushik, R. (2013). High Pressure Processing and its impact on milk proteins: A Review. Research and Reviews: Journal of Dairy Science and Technology. 2 (1): 1-9. ISSN: 2319-3409.\n4.\tKumar, A., Upadhyay, N., and Naagar, S. (2012). Allergenicity of Milk Proteins, and its Management. Indian Food Industry. 31 (5&6): 45-50. ISSN: 0972-2610.\n5.\tGoyal, A. and Upadhyay, N. (2012). Nuclear Magnetic Resonance Spectroscopy in Dairy Science. Indian Food Industry. 31(1): 39-45. ISSN: 0972-2610.\n6.\tUpadhyay, N.*, Goyal, A. and Rathod, G. (2011). Microwave Spectroscopy and its applications in online processing. Indian Food Industry. 30(5&6): 63-73. ISSN: 0972-2610.\n7.\tउपाध्याय, नी*. (२०१८) भारत में कुपोषण: स्थिति और इससे निपटने के लिए रणनीतियाँ. दुग्ध—गंगा (आठवाँ अंक). अप्रैल-सितम्बर. २४-२९. \n8.\tउपाध्याय, नी.*, सिंह, आ.कु., गांगुली, स., सबिखी, ल. (२०१८) खाध्य और डेयरी क्षेत्र मे महिला उद्यमिता: कारण, समस्याए एवम उपलब्ध मंच. दुग्ध—गंगा (आठवाँ अंक). अप्रैल-सितम्बर. ६४-६९.\n9.\tउपाध्याय, नी*. (२०१९) ek¡ dk nw/k % f'k'kqvksa ds ekufld] 'kkjhfjd ,oa lkekftd mRFkku gsrq ve`r. दुग्ध—गंगा (नवाँ अंक). अकटूबर –मार्च १०२-१०४.\n10.\tउपाध्याय, नी*, fç;k ;koys (२०१९) [kk| inkFkksaZ esa —f=e ds cnys çk—frd jax o.kZd ds mi;ksx dh vko';drk दुग्ध—गंगा (दसवाँ अंक). अकटूबर –मार्च १०२-१०५.\n11.\tuhye mikè;k;, fuys'k dqekj ikBd (२०१९) d`f\"k] [kk| ,oa Ms;jh m|ksx ds Hkfo\"; eas lkSj ÅtkZ dk egRo दुग्ध—गंगा (दसवाँ अंक). अकटूबर –मार्च १२६-१३०. \n12.\tवैज्ञानिक और तकनीकी विषय के मूल हिंदी लेख जोकि गेहूँ एवम् जौ स्वर्णिमा में प्रकाशित हुए: उपाध्याय, नी*, राकेश कुमार (2020) महिला उद्यमिता के माध्यम से महिला सशक्तिकरण. गेहूँ एवम् जौ स्वर्णिमा (बारहवााँ अंक), पृष्ठ सं. 55-58; भाकृअनुप- भारतीय गेहूँ एवम् जौ अनुसंधान संस्थान, करनाल- १३२००१ द्वारा प्रकाशित\n\n8. Concepts/Processes/Products/Technologies/Patents/Others\n(i)\tConcepts \nCurrently, I am working on the integrated approach of application of green technology for the development of functional foods by utilizing under-utilized/ indigenous fruits and vegetables and/ or bio-waste. In the research projects, I am also keenly working on food chemistry and instrumental food analysis and applications of technologies/ products in dairy and non-dairy products. \nBesides this, I am working on development of functional food for addressing menopausal symptoms in osteopenic mice model. \n(ii)\tProducts/ Technologies ready for commercialization- 5\n1. Production of Milk Protein Concentrate 60 (MPC60), a high protein low lactose powder from buffalo milk (Co-Inventor)\n2. Technology for omega-3 rich mixed fat table spread (Inventor)\n3. Lipid and water soluble yellow natural colouring ingredient from bio-waste (Inventor)\n4. Technology for preparation of encapsulated flaxseed oil for its applications in foods (Inventor)\n5. Production of buffalo milk based Milk Protein Concentrate 60 (MPC60) powder with improved solubility (Co-Inventor)\n(iii) Expertise on\n1.Gas Liquid Chromatography\t5.Thin Layer Chromatography\n2.Fourier Transform Infra-red Spectroscopy\t6. Spectrophotometry\n3.Differential Scanning Calorimetry\t7.Chemical analysis including titration, distillation, etc.\n4.High Pressure Liquid Chromatography\t\n\n\n9. List of completed, on-going and submitted projects\nTitle of Project\tDuration\tRole\tFunding\tStatus\tRemarks\nEffect of storage on Baudouin test, sesamin test and RP-TLC test to detect adulteration of vanaspati and vegetable oils in ghee\t2015-2017\tCo-PI\tICAR-NDRI\n\tCompleted\tTwo research articles on RP-TLC\nPreparation and Characterization of Micro/nano delivery systems for “green” carotenoids\t2016-2019\tPI\t-Do-\t\t3 research articles+ 3 products/ technologies\nTechnology Development for the Production of Milk Protein Concentrate (MPC60) From Buffalo Milk\t2016-2019\tCo-PI\t-Do-\t\t4 research articles+ 2 products/ technologies\nTechnology of Goat Milk based Functional Beverage\t2017-2020\tCo-PI\t-Do-\t\tOne oral presentation\nTechnology for Moringa oleifera enriched cheese spread\t2020-2023\tPI\t-Do-\tOn-going\tCharacterization and incorporation of M. oleifera- pods in cheese spread is complete; shelf life study and animal trial is in progress\nDevelopment of flaxseed-rich probiotic dairy foods to address menopause symptoms\t2020-2023\tCo-PI\tDST\t\tDeveloped method -estimation of phytoestrogen; validation -in progress\nNutritional and therapeutic validation of chhachh and ghee prepared from indigenous cows by traditional method\tThree years (proposed)\tPI\tSEED Division, DST\tSubmitted \n \t\nCharacterization of Moringa oleifera leaves for functional bioactives and its application in table spread as model food system\tThree years (proposed)\tPI\tSYST, DST\t\t\nOther research work: \nDetection of adulteration of goat body fat and pig body fat in ghee using ATR-FTIR coupled with chemometrics; carried out during Professional Attachment Training at ICAR-CIPHET, Ludhiana\n\n\n\n10. Awards & honours \nName of Award\tYear\tAwarding Agency\nBest Paper Award\t2022\tGSAT (Gender Advancement for Transforming Institutions Self-Assessment Team), NDRI\nBest Poster Award\t2021\tNational Conference on Moringa Food Conclave-2021\nYoung Woman Scientist Award\t2020\tAgro Environmental Development Society during International Web-conference \nSecond Best Poster Award\t2020\tIndian Dairy Association\nCommendation certificate for Institute’s Magazine in which I am co-Editor\t2020\tTown Official Language Implementation Committee, Karnal\nLetter of Appreciation to editorial board of Institute’s magazine for receiving ICAR’s Second Prize and Trophy under Ganesh Shankar Vidyarthi Hindi Patrika Puraskar (2018-19)\t2020\tICAR- National Dairy Research Institute, Karnal\nAssociate Fellowship\t2019\tNational Academy of Dairy Science India\nFirst Prize in E-poster \t2018\tIndian Dairy Association\nOne Best oral Presentation\t2018\tHome Science Association of India\nBest Oral Presentation to my Master’s student\t2018\tICMR- National Institute of Nutrition\nBest Poster Award\t2016\tIndian Dairy Association\nSecond Best Paper Award\t2016\tIndian Dairy Association\nICAR-SRF (PGS) with 2nd rank\t2011-12\tICAR\nGATE (Engg Sciences: Food Tech; Thermodynamics)\t2010\tMHRD, GoI\nInstitution level awards\nThird prize in poster presentation \t2021\tICAR- National Dairy Research Institute, Karnal\nInstitute’s Rajbhasha Gaurav Certificate\t2020\t\nFirst prize in Scientific and Technical writing\t2019\t\nConsolation prize in Scientific and Technical writing \t2020, 2019 \t\nFirst prize in Poster Presentation- 2020, 2018, 2017\t\t\nThird prize in poster presentation\t2019\t\nFirst Prize in hindi extempore\t2017\t\nThird, first and second prize in hindi essay writing in consecutive years – 2020, 2019, 2018\t\t\n\n\n11. Teaching Assignments \n(a) Teaching: Actively involved either as course in-charge or associate \nClass\tB.Tech (DT)\tMSc/ MTech\n(FT) (till 2021)\tM.Tech (DT)\tPhD (DT/ DC/ FSQA)\nNo. of courses\t1-2\t2-3\t0-1\t2-3\nDT- Dairy Technology, DC- Dairy Chemistry, FT- Food Technology, FSQA- Food Safety Quality Assurance\n(b) Student’s guided\nDegree\tMajor Advisor \tCo-Advisory\tStatus/ Remarks\nM. Tech (DT)\t8\t2\tCompleted\n\t1\t0\tOn going\nM. Tech/ M Sc (FT/ FSN)\t2\t1\tCompleted\nM. Tech (DC)\t0\t3\tCompleted\nM. Tech (DM)\t0\t1\tCompleted\nPhD (DT)\t2 \t0\tOngoing \n\t0\t2\tCompleted\nPhD (DC)\t0\t1 \tCompleted\n\t\t1\tOn going\ni.\tThree students under my guidance as major advisor and one student as co-advisory member nominated for Best thesis award; \nii.\tOne represented NDRI at zonal-level student research convention ANVESHAN-2018\n\n12. Lectures/ member/convener of committees: \ni.\tLectures: \na.\tEntrepreneurship Development Programme (EDP) (conducted by SINED-TBI/BPD unit, ICAR-NDRI) and Online Training of Master Trainers on Fat and Oilseed processing conducted by SINED-TBI/BPD unit (ICAR-CIPHET); \nb.\tStudent’s Counselling session at SRCASW, University of Delhi, \nc.\tWorkshop conducted at DAV college, Karnal, etc\nd.\tDelivered talks at various villages on the importance of mother’s milk, nutrition in first 1000 days of an infant’s life, nutri-thali, etc\nii.\tTraining Organized: \na.\tTwenty one days Training at Centre for Advanced Faculty Training (DT Division) on ‘R & D strategies and interventions for effective agribusiness and entrepreneurship development in dairy and food sector’; \nb.\tone/two months or shorter duration trainings for students and others under BPD unit and KVK, NDRI, Karnal\nc.\tFive days training on the aspects of dairy processing to the farmers of Karnal district. \niii.\tGeneral Secretary, Staff Club, NDRI, Karnal\niv.\tMember: Student Empowerment Unit, Conferences organized from 2015 till 2018, convocation, credit seminar evaluation committees; Mera Gaon Mera Gaurav program, Farmer’s First Door programme, Swatchh Bharat Abhiyan, coordinator and mentor of different groups for organizing Foundation Program-2017, 2018, Nodal officer of Poshan Maah-2020 etc\nv.\tConvener/ Rapporteur of sessions: Conference, Dr. K. K. Iya Memorial oration; International conference of Proteomics Society of India\nvi.\tOther responsibilities: Management Representative of QMS-IS/ISO 9001:2008 and HACCP- IS 15000:2013 of Experimental Dairy (essential part of institute) until Jan 2019; one of the editors of Institute hindi magazine Dudgh Ganga which also received coveted award from ICAR (until 2019).\nvii.\tResource Generation on account of consultancy provided in field of dairy processing and by conducting sponsored trainings \nMore than ₹ 2 50 000/- (Two lakhs fifty thousand only)\nviii.\tBesides research, teaching and extension activities, I am also involved in promotion of Hindi language and have won several prizes during competitions (like extempore, essay, e-mail writing) organized by Official Language Units.\nix.\tLifetime Member of three scientific bodies: Indian Dairy Association- RE/NZ/LM/10852/HR; Association of Food Scientists & Technologists (INDIA)- AFST/LM/9-2018/KRN/2444; Lifetime member of Home Science Association of India; Membership number: HSAI-2017-HR-127-LF\nx.\tReviewed research papers of Journal of Ayurveda and Integrative Medicine (Elsevier), LWT, International Journal of Food Properties, Indian Journal of Dairy Science, Indian Journal of Natural Products and Resources, United Scientific Group, etc. \n\n\n\n\n\n\n\n\nDated: 12-04-2022\t \nNeelam Upadhyay",institutionString:"National Dairy Research Institute",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"National Dairy Research Institute",institutionURL:null,country:{name:"India"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"5",title:"Agricultural and Biological Sciences",slug:"agricultural-and-biological-sciences"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"444312",firstName:"Sara",lastName:"Tikel",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/444312/images/20015_n.jpg",email:"sara.t@intechopen.com",biography:"As an Author Service Manager, my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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1. Introduction
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Atherosclerotic cardiovascular disease (ASCVD), including its clinical manifestations, such as myocardial infarction (MI) and ischemic stroke (IS), is the leading morbidity and/or mortality cause worldwide. One of the most highly studied factors associated with ASCVD is low-density lipoprotein (LDL). Vast evidence has postulated that cholesterol-rich LDL and other apolipoprotein B (apoB)-containing lipoproteins (very low-density lipoproteins (VLDL), intermediate density lipoproteins (IDL), and lipoprotein(a) [Lp(a)]), are directly involved in the development of ASCVD [1].
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Statins are the first-line anti-lipemic pharmacotherapy, having been shown to reduce both LDL-C levels and cardiovascular (CV) events. However, a considerable number of statin-treated patients do not achieve target LDL-C levels, even after maximal statin dose-treatment, or are intolerant to intensive statin therapy [2].
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In the aforementioned situations patients can largely benefit from an additional LDL-C lowering agent. Ezetimibe is a non-statin drug that can additionally reduce ASCVD risk, when added to a statin, leading to a total of 34–61% LDL-C reduction [3]. Proprotein Convertase Subtilisin-Like/Kexin Type 9 (PCSK9) inhibitors, one of the newest anti-lipemic agents, can lower LDL-C by 45–65%, and are also proven to have ASCVD risk reduction properties [4].
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Therefore, the aim of this chapter is to address the question of therapeutic efficacy, as expressed through the lipid-lowering and anti-inflammatory effects, and atherosclerotic cardiovascular disease risk reduction when adding ezetimibe or PCSK9 inhibitors to statin therapy.
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1.1 HMG-CoA reductase inhibitors—statins
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3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, commonly known as statins, have been one of the most frequently prescribed medications worldwide, since their introduction 30 years ago. Currently, there are six statin drugs available on the market—pitavastatin, atorvastatin, rosuvastatin, pravastatin, simvastatin and fluvastatin [5].
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Statins are competitive, reversible inhibitors of HMG-CoA reductase, a rate-limiting step in the process of cholesterol biosynthesis. HMG-CoA is a microsomal enzyme—reductase which catalyzes the conversion of HMG-CoA to l-mevalonate and coenzyme A. Inhibiting the HMG-CoA reductase, statins ultimately prevent the endogenous cholesterol production. Cholesterol concentration reduction triggers an up-regulation of the expression of low-density lipoprotein (LDL)-receptors in the hepatocytes, promoting uptake of LDL and LDL-precursors from the systemic circulation. Therefore, a significant part of the statins’ cholesterol-lowering action is a result of an indirect increase in LDL clearance from plasma. Additional mechanisms of action include inhibition of the hepatic apolipoprotein B100 synthesis, and a reduction of the synthesis and secretion of triglyceride-rich lipoproteins [6].
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Statins are composed of two parts, the pharmacophore, a dihydroxyheptanoic acid segment, and a moiety composed of a ring system with various substituents. According to the chemical modification of the ring system and the nature of its substituents, different statin structures are generated. Ring substituents define the solubility of the statins, along with many of their pharmacological properties. Among the statins, lovastatin, simvastatin, atorvastatin, and fluvastatin are lipophilic, whereas pravastatin and rosuvastatin are more hydrophilic. Different chemical structures lead to different pharmacokinetic properties, pharmacological effects and pleiotropic actions [7].
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Statins can enter the systemic circulation passively, through the intestinal cells, and actively via the ATP-binding cassette (ABC) and solute carrier (SLC) transporters. Two enzyme groups are involved in statin metabolism, the cytochrome P450 (CYP450), and UDP-glucuronosyltransferase (UGT), mainly acting in the liver, and to a lesser extent, in the kidneys. Lipophilic statins are transported via passive diffusion, metabolized by the CYP450 enzymes, and mainly excreted through the biliary system. Hydrophilic statins enter the liver via active transport, and are actively excreted through the kidneys, mostly as unchanged drugs. Lipophilic statins have generally low bioavailability due to first pass metabolism. Absorption varies between 30 and 98%, and time to reach peak plasma concentration (Tmax) is within 4 h of administration. Statins are administrated orally as active hydroxy acids, except for lovastatin and simvastatin, which are administrated as lactone pro-drugs, and then hydrolyzed to the hydroxy acid form. Their bioavailability varies; pitavastatin has a bioavailability of 80%, whereas fluvastatin between 19 and 29%. The CYP3A4 isoenzyme is responsible for the metabolism of lovastatin, simvastatin and atorvastatin. Their active metabolites—2-hydroxy- and 4-hydroxy-atorvastatin acid from atorvastatin, and β-hydroxy simvastatin acid from simvastatin, carry a part of their inhibitory activity. Fluvastatin is mainly metabolized by the CYP2C9 isoenzyme. Pravastatin is eliminated by both the kidney and liver, mostly as an unchanged drug [6, 7, 8].
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1.2 Cholesterol absorption inhibitors—ezetimibe
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Ezetimibe, a cholesterol absorption blocker, has been the focus of many trials supporting its use in ASCVD risk reduction. For patients that cannot achieve target treatment goals with statin therapy alone, ezetimibe has proven to be a safe, well-tolerated medication which, combined with statins, leads to additional LDL-C reduction, thus resulting in a significant morbidity and/or mortality benefit [9].
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Serum cholesterol is derived from two major sources: cholesterol synthesized de novo in the liver and cholesterol that has been absorbed from the gastrointestinal tract. Statins reduce serum cholesterol by reducing its biosynthesis in the liver. Ezetimibe, on the other hand, targets gastrointestinal cholesterol absorption. Ezetimibe acts at the brush boarder of the small intestine, by selectively inhibiting the cholesterol transport protein Niemann Pick C1 like 1 protein (NPC1L1), thus preventing uptake of intestinal luminal cholesterol micelles into the enterocytes. The reduced cholesterol uptake leads to hepatic LDL-C stores depletion, resulting in upregulation of hepatic LDL receptors, causing LDL-C clearance from the blood. It is also suggested that ezetimibe inhibits the hepatic NPC1L1 as well, thus leading to reduced hepatic cholesterol absorption [3, 10, 11].
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Following ingestion, the drug is extensively (>80%) metabolized to its active form—ezetimibe-glucuronide. Glucuronidation of the 4-hydroxyphenyl group, by uridine 5′-diphosphate-glucuronosyltransferase isoenzymes, forms the major ezetimibe metabolite in the intestine and liver. Total ezetimibe (sum of ‘parent’ ezetimibe plus ezetimibe-glucuronide) concentrations reach a maximum 1–2 h after administration. Both the parent compound and the glucuronidated compound are absorbed, and recirculated via the hepatobiliary excretion, thus providing long-term cholesterol absorption inhibition. This cycle accounts for the long half-life of ezetimibe—about 22 h, allowing for once-a-day dosing. About 10–15% of the drug is excreted in the urine, and the rest in the feces, mainly as the parent drug. Ezetimibe does not appear to be metabolized or interact with the cytochrome P450 pathway, thus it does not affect bioavailability and kinetics of commonly used drugs that are affected by the CYP450 family [10, 12].
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1.3 Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors
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The discovery of PCSK9 in 2003 opened many new research directions in the cardiovascular field. Liver PCSK9 binds to the LDL receptor (LDL-R) and promotes its degradation in the endosomal/lysosomal pathway. Higher PCSK9 activity leads to lower liver LDL-R levels, resulting in reduced LDL-uptake from circulation, and thus in hypercholesterolemia [13].
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This led to a conclusion that the inhibition of PCSK9 would mean that more LDL receptors would be recycled to the surface of the cell, thus increasing the clearance of LDL cholesterol from the circulation. Since then various approaches to the pharmacological inhibition of PCSK9 have been investigated, and parenteral anti-PCSK9 monoclonal antibodies (MoAbs) have been the most successful strategy to date. MoAbs are now in late-stage (phase 3 clinical trials) testing [14].
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Anti-PCSK9 MoAbs are known to bind at or near PCSK9’s binding site for the LDL-R. This sterically inhibits the interaction of PCSK9 with the LDL-R, thus reducing the degradation of the receptor. This markedly increases the clearance of LDL and substantially lowers plasma LDL cholesterol, as well as apolipoprotein-B100 [15]. In 2015, the Food and Drug Administration (FDA) approved the PCSK9 inhibitors alirocumab and evolocumab for patients with clinical atherosclerotic cardiovascular disease on maximally tolerated statin therapy who “require additional lowering of LDL-C” [16].
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Evolocumab is a human monoclonal immunoglobulin G2 antibody directed against the circulating PCSK9 protein. Evolocumab is administered by subcutaneous injection to the abdomen, thigh, or upper arm. For patients with primary hyperlipidemia, who have clinical ASCVD, or heterozygous familial hypercholesterolemia, the recommended subcutaneous dose is 140 mg every 2 weeks or 420 mg once monthly. Maximum suppression of circulating unbound PCSK9 is seen after 4 h. Peak serum concentrations are obtained in 3–4 days, with an estimated bioavailability of 72%. The drug is estimated to have an effective half-life of 11–17 days [17].
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Alirocumab is a human monoclonal immunoglobulin G1 [IgG1] isotype antibody that binds to circulating PCSK9, thus inhibiting its action on LDL-R. Alirocumab reduces free PCSK9 in a concentration-dependent manner. Following a single subcutaneous administration of alirocumab 75 or 150 mg, maximal suppression of free PCSK9 occurs within 4–8 h. Within 4–8 weeks after initiating or titrating alirocumab therapy, LDL-C levels should be tested to determine the response and the need for (additional) dose adjustments. The drugs’ median apparent half-life at steady state is 17–20 days. Peak serum concentrations are obtained in 3–7 days, with an estimated bioavailability of 85%. At low concentrations, the elimination of alirocumab occurs predominately via saturable binding to PCSK9. At higher concentrations, elimination is through a nonsaturable proteolytic pathway [18].
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2. Effects of statins
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2.1 Effects of statin therapy on LDL-C concentrations
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During the past 20 years, the extensive use of statin therapy among patients known to have an occlusive vascular disease, or are considered to be at increased risk of cardiovascular events, has been associated with descending actions on LDL and total cholesterol concentrations [19].
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Different statins have different potencies, with the newer agents (e.g., atorvastatin and rosuvastatin) able to produce larger reductions in LDL cholesterol per mg of drug, compared to the older agents (e.g., simvastatin and pravastatin). Each dose doubling leads to an additional reduction of about 6 percentage points in LDL cholesterol (e.g., 43 vs. 49% reductions with atorvastatin 20 vs. 40 mg daily). The American College of Cardiology/American Heart Association (ACC/AHA) 2013 Blood Cholesterol Guideline classified statin regimens as being of low intensity (e.g., <30% LDL-C reduction with simvastatin 10 mg daily), moderate intensity (e.g., 30% to <50% reduction with simvastatin 20–40 mg, atorvastatin 10–20 mg, or rosuvastatin 5–10 mg daily), or high intensity (e.g., ≥50% reduction with atorvastatin 40–80 mg or rosuvastatin 20–40 mg daily) [20].
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High-intensity statin therapy would be expected to reduce LDL-C by at least 2 mmol/L in individuals with LDL-C concentrations of 4 mmol/L or more, but by only about 1 mmol/L in those presenting with concentrations of 2 mmol/L. Consequently, since vascular events rates reductions, in patients treated with statins, are related to the absolute reductions in LDL-C, intensive statin treatment should be used in individuals at higher risk of vascular events, rather than just on those with high cholesterol concentrations [21].
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The Cholesterol Treatment Trialists’ (CTT) Collaboration was settled to conduct meta-analyses of randomized controlled statin-oriented trials involving at least 2 years of treatment in at least 1000 patients. During the study treatment periods (on average 5 years), the average LDL-C reduction was about 1–1.5 mmol/L, comparing routine statin therapy vs. no routine statin therapy, with an additional LDL-C reduction of about 0.5 mmol/L in the trials comparing allocation to more vs. less intensive statin regimens. To summarize, an intensive statin regimen, compared to no statin therapy, reduced LDL-C concentrations by 1.5–2 mmol/L [22, 23].
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2.2 Reductions in major vascular event (MVE) rates
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Statins have been proven to be very effective in reducing ASCVD risk, with no apparent threshold at which LDL-C lowering is not associated with reduced risk. The Atherosclerosis Risk in Communities (ARIC) study, performed on 13,342 individuals, provided evidence that protection against ASCVD happens in a graded fashion with LDL-C level [24]. The CTT meta-analyses detected about 25,000 major vascular events (MVE) (composite of coronary deaths or non-fatal myocardial infarctions, strokes of any type, and coronary revascularisation procedures). Comparing routine vs. no routine statin treatment, there was a 20% proportional reduction in the MVE rate per mmol/L LDL-C reduction. Regarding the comparison of more vs. less intensive statin regimens, the average 0.5 mmol/L further LDL-C reduction lead to an additional 15% proportional reduction in the MVE rate [22, 23].
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By combining the findings from the two previously mentioned sets of trials, it can be concluded that a LDL-C concentration reduction by 2 mmol/L would reduce the MVE risk by about 45%. Given the aforementioned, larger LDL-C reductions should lead to larger risk reductions (e.g., 60–70% with 3–4 mmol/L LDL-C reductions); however, this is likely only to be clinically relevant in limited circumstances (such as for individuals with familial hypercholesterolemia who have very high LDL-C levels) [25].
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High-intensity statin treatment (atorvastatin 80 mg) in the Treating to New Targets (TNT), the Incremental Decrease in Endpoints Through Aggressive Lipid Lowering (IDEAL) trial and Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT) trial, demonstrated an additional 11–23% relative risk reduction of major CVD events, when compared to moderate-intensity statin therapy (atorvastatin 10 mg, simvastatin 20–40 mg, or pravastatin 40 mg). Nonetheless, the atorvastatin 80 mg treated patients still experienced a major CVD event during the trials (ranging from 4 to 11% per year). Mean LDL-C levels in the atorvastatin 80-mg groups ranged from 1.6 to 2.1 mmol/L [26, 27, 28, 29].
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The American College of Cardiology/American Heart Association 2013 Blood Cholesterol Guideline gives recommendations regarding statin therapy in terms of ASCVD prevention and risk reduction (Table 1) [20].
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ASCVD Statin Benefit Groups [20] Heart healthy lifestyle habits are the foundation of ASCVD prevention
The CTT meta-analyses showed a 12% proportional reduction in vascular mortality per mmol/L LDL-C reduction, attributable to an approximately 20% proportional reduction in coronary deaths, 8% reduction in other cardiac deaths, and little effect on death due to all types of stroke combined. No matter the cause of coronary death, the risk reduction per mmol/L LDL-C reduction appear to be similar in patients with and without pre-existing vascular disease, and in those who present at different levels of baseline vascular risk [22, 23].
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Regarding the effect of different statins, and different statin treatment intensities, on coronary mortality, the TNT trial showed no significant differences in the risk of death from cardiovascular or noncardiovascular causes between the patients treated with 10 mg or 80 mg atorvastatin per day [27]. The IDEAL study compared the effects of high-intensity statin therapy (atorvastatin 80 mg/d) vs. low-intensity statin therapy (usual-dose simvastatin, 20 mg/d), on occurrence rates of a major coronary event, defined as coronary death, confirmed nonfatal acute MI, or cardiac arrest with resuscitation. The results failed to show a statistically significant difference in all-cause or cardiovascular mortality between the two treatment regimens [28]. The PROVE-IT trial aimed to compare the effects of 40 mg of pravastatin daily (standard therapy) vs. 80 mg of atorvastatin daily (intensive therapy) in patients hospitalized for acute coronary syndrome. The risk of death due to coronary heart disease, myocardial infarction, or revascularization was reduced by 14% in the atorvastatin group, as compared with 22.3% in the pravastatin group [29].
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2.4 The question of residual risk
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Despite what was previously elaborated, a significant on-statin treatment residual risk of major CV events still exists. A meta-analysis of statin trials shows that there is residual CVD event risk even with LDL-C levels <2 mmol/L. The aforementioned TNT trial, conducted on patients with stable coronary artery disease (CAD), described an 8.7% incidence of a major event, over 5 years, in patients receiving 80 mg atorvastatin daily, with on-treatment LDL-C concentrations of 1.8–2.6 mmol/L [24]. Findings like these point to the unmet needs of the patients treated with statins. Several cholesterol treatment guidelines recommend a LDL-C treatment goal of <2.6 mmol/L or < 1.8 mmol/L, depending on the level of risk. However, in the everyday clinical practise many high-risk patients fail to reach the goal [26].
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The most resent Guidelines, the 2016 European Society of Cardiology and European Atherosclerosis Society (ESC/EAS) Guidelines for the management of Dyslipidemias and The 2017 Guidelines of the American Association of Clinical Endocrinologists (AACE) and the American College of Endocrinology (ACE) for Management of Dyslipidemia and Prevention of Cardiovascular Disease have recommended similar target LDL-C levels, and have suggested the use of combination therapy (ezetimibe and PCSK9 inhibitors) to achieve these targets in situations in which maximally tolerated statin monotherapy is insufficient (Table 2) [3, 26].
The AACE guidelines introduced an additional “extreme high-risk” category, which is not recognized by the ESC/EAS, and an additional treatment LDL-C target of <1.4 mmol/L. This “extreme high-risk” group represents patients with progressive disease, despite LDL-C levels of <1.8 mmol/L while on-statin therapy. The rationale of the aforementioned approach is in the individualization of the total CV risk reduction, which can be better done if goals are predefined. Treatment goals are defined and tailored to the total CV risk level of each individual patient. The “individualized approach “may possibly result with better patient adherence to the therapy. The growing number of evidence suggests that LDL-C lowering beyond the guidelines-set goals may lead to further reduction of CVD events, which can be especially beneficial in patients at very high CV risk [3, 30].
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Given what was previously discussed, in order to achieve this level of LDL-C reduction, combination therapy may be needed. The latest randomized clinical trials (RCTs), such as The LDL-C Assessment With Proprotein Convertase Subtilisin Kexin Type 9 Monoclonal Antibody Inhibition Combined With Statin Therapy 2 (LAPLACE-2) trial, The FOURIER (Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk) trial, and The Reductions in Atherogenic Lipids and Major Cardiovascular Events: A Pooled Analysis of 10 ODYSSEY Trials Comparing Alirocumab With Control, demonstrated that extremely low LDL-C levels (<0.5 mmol/L) appear to be safe. Furthermore, The IMPROVE-IT (Examining Outcomes in Subjects With Acute Coronary Syndrome: Vytorin vs. Simvastatin) and FOURIER trials demonstrated that not only such low levels are safe, but are also beneficial, in terms of additional CV risk reduction [30, 31, 32, 33, 34].
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3. Combination therapy
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3.1 Combination therapy: ezetimibe ad-on statin
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The unmet needs in terms of LDL-C targets and ASCVD protection raised the question of statin combination therapy. It only needed to be right positioned. Such positioning was done in the 2016 ESC/EAS Guidelines for the management of Dyslipidemias (Table 3) [3], and also in The 2016 ACC expert consensus decision pathway on the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk [35].
The FDA-approved ezetimibe indications are for treatment of primary hyperlipidemia, alone or in combination with a statin; mixed hyperlipidemia in combination with fenofibrates; in homozygote familiar hyperlipidemia (HoFH) in combination with atorvastatin or simvastatin; and in homozygous sitosterolemia (phytosterolemia) [3, 26, 35].
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In clinical studies, ezetimibe, as monotherapy, reduces LDL-C in hyper-cholesterolemic patients by 15–22%. Combined therapy with statins provides an incremental reduction in LDL-C levels of 15–20%, leading to a total LDL-C reduction by 34–61%, as previously mentioned [3].
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The most comprehensive data analysis for LDL-C lowering efficiency was performed by the group of Descamps, published in 2015. 27 differently designed trials (double-blind placebo and/or active controlled studies), in which statins (type of statin, statin brand, potency or dose difference) were compared with ezetimibe ad-on statin, were included, with over 21,671 patients, analyzing variables such as variances (standard deviation [SD], coefficient of variation [CV], and root mean squared error [RMSE] adjusted for various factors) for % change from baseline in LDL-C. In this very comprehensive data analysis, ezetimibe ad-on statin was found to lead to significantly more pronounced LDL-C lowering, as compared to statin monotherapy [36].
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Data from a large retrospective observational study (more than 27,000 patients), published in 2014 by Toth, demonstrated a more pronounced LDL-C lowering effect of ezetimibe ad-on statin therapy, and a higher percentage of goal attainment (with respect to the risk profile of the patients), with one third of the patients not being able to attain the recommended LDL-C goal of <1.8 mmol/L. However, it was realized that there is a low prescription frequency of high-dose statins. Half of the patients (50.9%) remained on the same statin monotherapy, irrespective of their treatment goal achievement [37]. The significance of this study is even bigger given that it is a real life situation, and not a randomized study with strictly predefined inclusion criteria, study population etc.
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The IMPROVE-IT study showed an on-trial average LDL-C level of 1.4 mmol/L in the simvastatin-ezetimibe group, as compared to 1.8 mmol/L in the simvastatin-monotherapy group (p < 0.001), leading to a total amount of LDL-C reduction of about 24% [38]. There are also a lot of small-scale studies that demonstrate superiority of ezetimibe ad-on statin therapy in terms of LDL-C lowering. For example, the Japanese study by Uemura, performed on 39 patients, compared two regimens: 10 mg atorvastatin + 10 mg ezetimibe vs. 20 mg atorvastatin in high risk patients with CAD and type 2 diabetes (T2DM). A significant improvement of the lipid profile was found in both groups in terms of total, LDL-C and high-density lipoprotein cholesterol (HDL-C), with a more pronounced improvement in the ezetimibe ad-on atorvastatin group (p = 0.005). A significant effect on the Apo B/Apo A-I ratio and remnant-like particle cholesterol was observed only in the atorvastatin ad-on ezetimibe treatment group. Probably the finding that gives as the most powerful information is the effect on oxidized LDL-C [malondialdehyde-modified LDL (MDA-LDL)], a form that is responsible for the proaterogenic effects of LDL-C, that was significantly more pronounced with the atorvastatin ad-on ezetimibe treatment (p = 0.0006) [39]. The existence of pleotropic effects, other than the hypo-lipemic effect that is widely recognized for statins, is evidentially true for ezetimibe as well. Evidence of anti-inflammatory and anti-oxidative effects is cumulating. Another Japanese study, by Tobaru, was performed on 35 CAD patients pre-treated with statins who remained above targeted LDL-C level. In terms of hypo-lipemic effect, significant additional decrease of total C, LDL-C, remnant lipoprotein C, LDL/HDL-C ratio was observed, and the percentage of patients who achieved target LDL-C level increased to 65.4% (p = 0.001) in the ezetimibe ad-on statin group. Although no significant effect was achieved on high-sensitive C-reactive protein (hsCRP) and oxidative stress markers, a significant reduction of tumor necrosis factor-α (TNF-α), 1.36 vs. 0.96 (p = 0.042) was observed [40]. On the other hand, given the IMPROVE-IT trial in which two laboratory targets were set: LDL-C (<1.8 mmol/L) and hsCRP (<2 mg/L), Bohula and colleagues summarized that ezetimibe ad-on statin treatment was far more successful in achieving both targets, or it was concluded: “Significantly more patients treated with ezetimibe/simvastatin met prespecified dual LDL-C and hsCRP targets, than patients treated with simvastatin alone (50% vs. 29%, p < 0.001)”. Reaching both LDL-C and hsCRP targets was associated with improved outcomes after multivariable adjustment (38.9% vs. 28.0%, adjusted hazard ratio, 0.73, 0.66–0.81; p < 0.001) [38].
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3.1.2 Effects of ezetimibe ad-on statins on ASCVD outcome
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The potential benefits of adding an additional lipid lowering agent—ezetimibe on statin therapy for CVD prevention and risk reduction have been confirmed in several clinical trials.
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The impact of dual lipid-lowering strategy with ezetimibe and atorvastatin on coronary plaque regression in patients with percutaneous coronary intervention: The Multicenter Randomized Controlled PRECISE-IVUS trial evaluated the effects of ezetimibe ad-on atorvastatin vs. atorvastatin monotherapy on the lipid profile and coronary atherosclerosis in Japanese patients who underwent percutaneous coronary intervention (PCI). The combination therapy resulted in lower levels of LDL-C, compared to atorvastatin monotherapy (1.6 mmol/L vs. 1.9 mmol/L; p < 0.001), and in the same time coronary plaque regression was observed in significantly higher percentage of patients who received atorvastatin ad-on ezetimibe (78% vs. 58%; p = 0.004) [41].
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The majority of studies addressing the efficacy of ezetimibe ad-on statin treatment are with simvastatin, including the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study, in patients with aortic stenosis, and the Study of Heart and Renal Protection (SHARP) (Simvastatin plus ezetimibe) trial, including 23% high risk patients with diabetes and chronic kidney disease (CKD) with or without requiring dialysis. The combination therapy demonstrated superiority over statin monotherapy in LDL-C reduction, translated in reduced primary endpoint of first major ASCVD event: nonfatal MI or CV death, non-hemorrhagic stroke, or any arterial revascularization procedure, over a median follow up of 4.9 years [3, 42].
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The landmark trial on ezetimibe-statin combination therapy, the largest and the longest one with ezetimibe, is the Improved Reduction of Outcomes: Vytorin Efficacy International Trial (IMPROVE-IT). A total of 18,144 patients with acute coronary syndrome (ACS) were randomized to ezetimibe (10 mg) or placebo, all receiving 40 mg simvastatin, which was increased to 80 mg if LDL-C on treatment was >2.04 mmol/L. The event rates for the primary end point at 7 years were 32.7% in the simvastatin-ezetimibe group and 34.7% in the simvastatin-monotherapy group, with an absolute risk reduction of 2% (HR 0.936; 95% CI 0.89–0.99; p = 0.016). Ischemic stroke was reduced by 21% (p < 0.008). Nevertheless, no benefit in reducing all-cause mortality or deaths from CV causes was observed, which was not unexpected, as prior trials of intensive vs. standard-dose statin therapy did not demonstrate a benefit in terms of mortality as well. There was no evidence of harm caused by the further LDL-C reduction. In this group of patients, already treated with statins to reach the goal, the absolute benefit from the added ezetimibe was small, although significant. However, the study supports the proposition that LDL-C lowering by means other than statins is beneficial and can be performed without adverse effects [38].
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The diabetic sub-group analysis in the IMPROVE-IT trial provided the outcomes in 4933 (27%) patients with diabetes, one of the pre-specified trial subgroups. In this patient subset, ezetimibe ad-on statin decreased LDL-C at 1 year by 1.1 mmol/L, as compared to 0.6 mmol/L with statin monotherapy. Diabetic patients on ezetimibe ad-on statin therapy had a 14% relative risk reduction, or 5.5% absolute reduction, compared with a 2% absolute risk reduction for non-diabetics. The most notorious reductions were seen regarding ischemic stroke (39%), MI (24%), and the composite of death due to CV causes, MI or stroke (20%). These CV effects of ezetimibe ad-on statin therapy are considered to be a result of the more prominent reduction of LDL-C (mean 0.5 mmol/L), compared to simvastatin monotherapy, with an average value of 1.4 mmol/L. This sub-study analysis demonstrated superiority of the statin-ezetimibe combination therapy in CV prevention in diabetic subsets especially [26, 34, 35, 38].
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Another significant effect of ezetimibe ad-on statin therapy is cerebrovascular protection. The 2013 ACC/AHA cholesterol guideline recommends the use of ezetimibe as an ad-on statin, additional LDL-C lowering agent in stroke patients [35]. The advantage of ezetimibe ad-on statin therapy in this patient subgroup was observed in the IMPROVE-IT study. The highest risk benefit was observed in the subgroup of patients with ischemic CVD with a 21% relative reduction of ischemic stroke (p < 0.008). The addition of ezetimibe as a non-statin type drug, to statin treatment contributed to further reduction of LDL-C, which translated into additional decrease in reoccurrence and mortality of/from cerebrovascular events. Achieving target values with ezetimibe ad-on statin combination allows administration of low to moderate-dose statin, which decreases the risks of adverse effects related to high-dose statin therapy [43].
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The current trial results make it obvious that the higher the risk profile of the patient is, the bigger is the benefit, in terms of risk reduction, when ezetimibe is ad-on statin treatment. Taken together, all these studies support the decision to propose ezetimibe as a second-line therapy, in association with statins, when the therapeutic goal is not achieved with the maximal tolerated statin dose or in patients intolerant or with contraindications to these drugs [3, 35].
The FDA approved the first PCSK9 inhibitor in 2015
There are currently two PCSK9 inhibitors on the market, alirocumab and evolocumab
There was a third PCSK9 inhibitor—bococizumab, but its’ development was discontinued by Pfizer in late 2016. The key reasons for this were a high level of immunogenicity and wide variability in the LDL-C lowering response. Immunogenicity: in statin-treated patients, PCSK9 inhibition with bococizumab led to a short-term LDL-C reduction of 55–60%. However, this effect was attenuated over time in 10–15% of patients due to the development of antidrug antibodies. This effect was specific to bococizumab, which is a partially humanized monoclonal antibody, characterized by substitution of rodent deoxyribonucleic acid (DNA) sequences for <5% of human DNA sequences. It is thought that this substitution may have directly affected the immunogenicity of the antibody. This effect has not been reported for either evolocumab or alirocumab, which are fully human monoclonal antibodies. This immunogenicity may also explain the higher rate of injection site reactions (~10%) observed with bococizumab, compared with either alirocumab or evolocumab (<5%). Variability in LDL-C lowering response: Irrespective of the presence or absence of antidrug antibodies, there was wide individual variability in the LDL-C lowering response with bococizumab; about 1 in 10 showed no reduction in LDL-C levels
Patients with familial hyperlipidemia and those with clinical ASCVD, not reaching lipid-reducing goals, including those with statin intolerance, are at greatest need of PCSK9 inhibitors, because no adequate alternative treatment exists
Multiple guidelines with different approaches to lipid treatment have created confusion among clinicians; thus, defining the patients with ASCVD, or at high CV risk, who have not met LDL-C treatment goals is complicated
Although PCSK9 inhibitors seem to support the LDL-C hypothesis (the lower the LDL-C level, the lower the CV risk), results of ongoing long-term outcome studies are yet to be presented
Prescribing PCSK9 inhibitors will likely be limited by economics rather than by clinicians’ judgment about the best interest of their patients [44].
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Many believe that proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are the pharmacotherapeutic innovation of the past 2 decades in terms of CV events prevention.
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The 2017 Update of ESC/EAS Task Force on practical clinical guidance for proprotein convertase subtilisin/kexin type 9 inhibition in patients with atherosclerotic cardiovascular disease or in familial hypercholesterolemia defined:
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Patients with clinical ASCVD and substantially elevated LDL-C levels (patients already on maximally tolerated statin therapy (ideally with concomitant ezetimibe), or unable to tolerate three or more statins), and,
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Familial hypercholesterolemia (FH) patients without clinical ASCVD but with substantially elevated LDL-C levels (patients on maximally tolerated statin therapy plus ezetimibe), as priority patient groups for PCSK9 inhibitors (Figure 1) [45].
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Figure 1.
Appropriate use of PCSK9 inhibitor, as recommended in 2017 update of ESC/ESC task force on practical clinical guidance for proprotein convertase subtilisin/kexin type 9 inhibition in patients with atherosclerotic cardiovascular disease or in familial hypercholesterolemia. ASCVD, atherosclerotic cardiovascular disease; LDL-C, low-density lipoprotein-cholesterol; 1Including: familial hypercholesterolemia; diabetes mellitus with target organ damage, or a major risk factor; severe and/or extensive ASCVD; rapid progression of ASCVD (i.e. repeated ACS, unplanned coronary revascularizations). 2Including: diabetes mellitus with target organ damage, or a major risk factor; Lipoprotein(a) > 50 mg/dL; major risk factors: smoking, marked hypertension; >40 years of age without treatment; premature ASCVD (<55 years in males and <60 years in females) in first-degree relatives; imaging indicators.
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3.2.2 LDL-C lowering and PCSK9 inhibitors: what have we learned?
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The Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk (FOURIER) trial, aimed to evaluate the efficacy of evolocumab, compared to placebo, in patients with clinically evident CVD. 69% of the patients were on a high-intensity statin, while 30% were on a moderate-intensity statin therapy, randomized to evolocumab 140 mg subcutaneous every 2 weeks or 420 mg monthly (n = 13,784) vs. placebo every 2 weeks (n = 13,780). Evolocumab led to a 59% LDL-C level reduction (from 2.4 mmol/L to 0.78 mmol/ L), with an absolute LDL-C reduction of 1.4 mmol/L [46].
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The Goal Achievement After Utilizing an Anti-PCSK9 Antibody in Statin Intolerant Subjects-3 (GAUSS-3) trial aimed to evaluate the effect of 24 weeks of evolocumab administered subcutaneously (SC) every month, compared with ezetimibe, on LDL-C levels in adults with high cholesterol, who are unable to tolerate an effective dose of a statin due to muscle-related side effects (MRSE). Evolocumab produced significantly larger reductions in LDL-C levels, compared to ezetimibe (16.7% reduction with ezetimibe and a more than 50% reduction with evolocumab). Despite very high baseline values, the LDL-C goal of less than 1.8 mmol/L was achieved in nearly 30% of evolocumab-treated patients and 1.4% of ezetimibe-treated patients. The LDL-C reduction for both drugs was stable for 4 weeks and sustained during the course of the 24 weeks of treatment [47].
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The effect of evolocumab or ezetimibe added to moderate- or high-intensity statin therapy on LDL-C lowering in patients with hypercholesterolemia—the LAPLACE-2 randomized clinical trial evaluated the efficacy and tolerability of evolocumab when used in combination with a moderate- vs. high-intensity statin. 2067 patients with primary hypercholesterolemia and mixed dyslipidemia were randomized to 24 treatment groups. Patients were initially randomized to a daily, moderate-intensity (atorvastatin 10 mg, simvastatin 40 mg, or rosuvastatin 5 mg) or high-intensity (atorvastatin 80 mg, or rosuvastatin 40 mg) statin. After a 4-week lipid-stabilization period, patients were randomized to compare evolocumab (140 mg every 2 weeks) vs. placebo (every 2 weeks) or ezetimibe (10 mg daily; atorvastatin patients only) when added to statin therapies. In patients treated with atorvastatin (10 mg or 80 mg), the addition of ezetimibe resulted in LDL-C reductions by 17–24% from baseline, compared with the addition of evolocumab, administered every 2 weeks, which reduced LDL-C values by 61–62% (treatment differences vs. placebo and ezetimibe both significant [p < 0 .001]. For patients receiving a moderate-intensity statin, evolocumab reduced LDL-C values from a baseline mean of 3.1 mmol/L to an on-treatment mean of 1.2 mmol/L, and 88–94% of the patients achieved target LDL-C levels, less than 1.8 mmol/L. For patients receiving a high-intensity statin, evolocumab reduced LDL-C values from a baseline mean of 2.4 mmol/L to an on-treatment mean of 0.9 mmol/L, and 94% achieved the target LDL-C value. In the atorvastatin-treated patients, addition of ezetimibe resulted in achievement of an LDL-C level less than 1.8 mmol/L in 17–20% of patients receiving moderate-intensity statins and 51–62% of those receiving high-intensity statins, vs. 86–94% of patients achieving target LDL-C values in the evolocumab-atorvastatin group [31].
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The efficacy and safety of alirocumab in high cardiovascular risk patients with inadequately controlled hypercholesterolemia on maximally tolerated doses of statins: the ODYSSEY COMBO II randomized controlled trial aimed to compare efficacy, in terms of LDL-C lowering, and safety of alirocumab vs. ezetimibe as ad-on therapy to maximally tolerated statin treatment in high CV risk patients with inadequately controlled hypercholesterolemia. Patients were randomized to subcutaneous alirocumab 75 mg every 2 weeks (plus oral placebo) or oral ezetimibe 10 mg daily (plus subcutaneous placebo) on a background of statin therapy. At week 24, mean ± SE reductions in LDL-C from baseline were 50.6 ± 1.4% for alirocumab vs. 20.7 ± 1.9% for ezetimibe (p < 0.0001). 77.0% of alirocumab and 45.6% of ezetimibe patients achieved target LDL-C values of <1.8 mmol/L (p < 0.0001). Mean achieved LDL-C levels, by week 24, were 1.3 mmol/L with alirocumab and 2.1 mmol/L with ezetimibe [32].
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3.2.3 Cardiovascular outcome studies with PCSK9 inhibitors: what have we learned?
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The FOURIER trial, evaluating the effect of evolocumab on the risk of CV death, MI, stroke, hospitalization for unstable angina, or coronary revascularization, in 27,564 patients with clinically evident CVD, is the first randomized study to be completed, regarding PCSK9 inhibitors long-term efficacy and safety. The primary outcome, incidence of CV death, MI, stroke, hospitalization for unstable angina, or coronary revascularization, occurred in 12.6% of the evolocumab group vs. 14.6% of the placebo group (p < 0.0001). There was a 9.8% absolute MACE rate reduction, compared to 11.3% with placebo, over 2.2 years, with a relative risk reduction of 15%. This finding was consistent among all tested subgroups. Benefit was enhanced among higher-risk subgroups (those with recent MI, multiple prior MIs, and residual multivessel coronary artery disease), compared to those without such characteristics. There was a linear relationship between LDL-C and adverse CV events, such that adverse events continued to decline to the lowest levels of LDL-C (p = 0.0012). Among those with baseline LDL-C < 1.8 mmol/L, evolocumab reduced the primary endpoint (hazard ratio [HR] 0.80, 95% confidence interval [CI] 0.60–1.07) to a similar degree as those with baseline LDL-C ≥ 1.8 mmol/L (HR 0.86, 95% CI 0.79–0.92; p = 0.65 for interaction).
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There was a greater absolute reduction in major adverse events for evolocumab vs. placebo among those with the highest baseline inflammatory risk (among those with high-sensitivity C-reactive protein <1 mg/dl, 1–3 mg/dl, and >3 mg/dl, there was an absolute reduction in the primary outcome of 1.6, 1.8, and 2.7%, respectively). PCSK9 inhibition represents a novel approach to lower LDL-C levels and improves cardiovascular outcomes. However, for the duration of follow-up, there was no benefit on cardiovascular or all-cause mortality, and cost remains an issue [46].
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Regarding alirocumab, cardiovascular outcomes and safety will be assessed in an ongoing study, the ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab trial. 18,600 patients, who have experienced an acute coronary syndrome (ACS), are allocated to alirocumab or placebo, for a maximum duration of 64 months. The primary objective of the trial is to compare the effect of alirocumab with placebo on the occurrence of cardiovascular events (composite endpoint of coronary heart disease (CHD) death, non-fatal MI, fatal and non-fatal IS, unstable angina requiring hospitalization). No results are reported yet [32].
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4. Safety profiles of statin monotherapy and statin combination therapy
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4.1 Adverse effects of statin therapy
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The only excesses of adverse events that have been reliably demonstrated to be caused by statin therapy are myopathy and diabetes mellitus, along with a probable excess of hemorrhagic stroke. However, the absolute risks of these adverse effects remain small, by comparison with the absolute benefits [25].
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4.1.1 Increases in myopathy rates
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Approved statin regimens have been associated, both in observational studies and in randomized trials, with large relative risks for myopathy, but typically with small absolute excesses (about 1 case per 10,000 people treated per year), and even smaller excesses in the incidence of rhabdomyolysis (about 2–3 cases per 100,000 treated per year). It usually resolves rapidly when statin therapy is . [48]. The risk of myopathy is dose related and it appears to depend on the statin circulation levels. In the Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) randomized trial, simvastatin 80 mg daily produced a more than ten-fold higher rate (at least 1 case of myopathy per 1000 patients treated yearly), compared to 20 mg daily (about 1 case per 10,000 yearly), so the high-dose regimen is no longer recommended routinely [49].
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4.1.2 Increases in diabetes rates
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In the Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) randomized trial, among 17,802 patients without a history of vascular disease, concentrations of glycated hemoglobin, after 2 years, were slightly higher among the patients allocated to rosuvastatin 20 mg daily compared to those allocated to placebo (5.9 vs. 5.8%; p = 0.001). There was also a small excess of newly diagnosed diabetes (3.0 vs. 2.4%; p = 0.01), which corresponds to a 25% proportional increase. In subsequent meta-analyses, standard statin dose regimens were associated with a proportional increase of about 10% in reported diabetes, and more intensive statin regimens (as used in JUPITER) with about a 10% further increase. This excess of diabetes diagnoses appeared soon after the start of statin therapy, mainly among patients who had previous risk factors for diabetes [50].
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4.1.3 Probable increases in hemorrhagic stroke rates
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In The Stroke Prevention by Aggressive Reduction of Cholesterol Levels (SPARCL) trial, among 4731 patients with prior cerebrovascular disease, allocation to atorvastatin 80 mg daily produced a definite reduction in ischemic stroke (218 [9.2%] vs. 274 [11.6%]; p = 0.008), but there was also a possible increase in hemorrhagic stroke (55 [2.3%] vs. 33 [1.4%]; p = 0.02). When these results were combined with those from the other trials included in the CTT meta-analysis, there was a 21% (95% CI 5–41; p = 0.01) proportional increase in the incidence of hemorrhagic stroke per mmol/L reduction in LDL-C [51].
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4.2 Safety profile of ezetimibe ad-on statins combination therapy
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The relationship between lipid-lowering medications, glycemic control, insulin resistance and new-onset diabetes has been studied since the introduction of hipo-lipemic medications. We know that glycemic control is impaired not only by statin treatment but also with niacin. At the opposite, bile-acid sequestrates demonstrate moderate lipid and glucose lowering effects, and fibrates (particularly bezafibrate) may produce beneficial effects on glucose metabolism and insulin sensitivity. Considering statins, as the most widely used hypo-lipemic drugs, this is an important issue. Statins lead to a mild elevation of hemoglobin A1c (HgbA1c) and fasting plasma glycose (FPG), and increase the incidence of new-onset diabetes, an effect known to be dose and agent dependent (Pravastatin and Pitavastatin have less diabetogenic effect and positive impact on insulin sensitivity). The aforementioned is most pronounced in patients with baseline impaired fasting blood glucose (FBG), at older age and with metabolic syndrome. However, it has been demonstrated that the risk of new-onset diabetes is overweight by the benefit of CV risk reduction [3].
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For a long period of time there was a lack of clinical trials addressing the same question in ezetimibe treatment, but data was gathered from experimental animal studies that described how ezetimibe ameliorates metabolic markers, such as hepatic steatosis and insulin resistance. The process is via inhibition of the intestinal cholesterol absorption, and inhibition of the hepatic NPC1L1, leading to decreased hepatic insulin resistance, improved glycemic control and insulin sensitivity, especially in patients with metabolic disorders (obesity and hepatic steatosis). This was harder to prove in humans, as ezetimibe is usually used as statin co-therapy and individual impact of ezetimibe cannot be evaluated. In a recently published systematic review of randomized clinical trials, performed by Wu and co-authors on 2440 patients, experimental data was confirmed. Ezetimibe did not cause any adverse effects in terms of increased levels of FBG and HbA1c. Compared with high-dose statin therapy, ezetimibe ad-on low-dose statin for more than 3 months may even have beneficial effects on glycemic control [52].
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Statin associated muscle symptoms are a very common side effect, also known to be dose-dependent. It seems that ezetimibe ad-on low dose statin therapy is one of the possibilities to achieve good LDL-C control and CV risk reduction with lesser side effects, as demonstrated with myalgia [53]. The 2016 ESC/EAS Guidelines for the management of dyslipidemias recommend ezetimibe to be considered in combination with a low-dose statin or second- or third-line statin in order to manage statin-attributed muscle symptoms [3].
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4.3 Safety profile of PCSK9 inhibitors ad-on statins combination therapy
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Despite this new evidence from the FOURIER trial, gaps remain in our knowledge regarding the use of PCSK9 inhibition in clinical practice. The ODYSSEY Outcomes trial will provide additional information in patients treated with a PCSK9 inhibitor within 1–12 months [45].
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As with all novel treatments, long-term safety remains to be established. To date there are exposure data for up to 4 years’ treatment with a PCSK9 inhibitor, involving a background of concomitant statin therapy. Potential injection site reactions occurred in <5% of patients, and were mainly of very mild intensity with no evidence of a cumulative effect. When the PCSK9 inhibitor was compared to the previous standard of care (statin with or without ezetimibe), annualized event rates for muscle symptoms (4.7% vs. 8.5% with standard of care), and new-onset diabetes (2.8% vs. 4.0%, respectively) appeared similar [45].
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The safety of very low LDL-C levels merits special consideration, given that one in four patients treated with evolocumab in FOURIER attained LDL-C levels less than 0.5 mmol/L. Evidence to date suggests no detrimental impact on steroid hormone production, enterohepatic circulation of bile acids, or neuronal cell function. Indeed, these LDL-C levels are also consistent with the very low levels observed in newborns which, despite the physiological and developmental demands of infancy, are compatible with normal development [54].
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Additionally, data from the ODYSSEY program, the FOURIER and 6-year follow-up from the IMPROVE-IT trial showed no increase in adverse events including severe muscle symptoms, liver enzyme elevation, cognitive adverse events, or hemorrhagic stroke with very low LDL-C levels [45].
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5. The war of today
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We now know the battle is going to be very hard. The “old ones” are not ready to go to history, while the “young ones” are still to be proven. What does the newest published data say? In January 2018 Khan and co-authors published a meta-analysis of statins, PCSK9 inhibitors and ezetimibe, the later two with or without statins, regarding ASCVD reduction benefit. The most comprehensive meta-analysis included 189,116 patients from 39 randomized control trials. PCSK9 inhibitors were ranked as the best treatment for prevention of major adverse cardiovascular events: myocardial infarction and stroke. Statins were ranked as the most effective therapy for reducing all-cause and CV mortality. In terms of reduction of CV mortality PCSK9 inhibitors were ranked as the second best treatment followed by ezetimibe ad-on statin [55].
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6. Conclusion
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Statins remain the cornerstone anti-lipemic treatment, proven to be very effective in reducing ASCVD risk. Ezetimibe ad-on statin combination therapy is an effective treatment that leads to additional LDL-C lowering, recommended in situations where with maximal or maximally tolerated statin monotherapy treatment LDL-C target goals cannot be achieved. It leads to an additional CVD risk reduction, and in the same time is safe, with a possible beneficial effect over the statin adverse influence on glycemic metabolism. Having in mind the evidence from the first of the cardiovascular outcomes studies with PCSK9 inhibitors, the addition of a PCSK9 inhibitor should be considered in patients with ASCVD, and in FH patients without a prior clinical event, who have substantially elevated LDL-C levels despite maximally tolerated statin with or without ezetimibe therapy, or inability to tolerate appropriate doses of at least three statins. Prioritizing the use of combination therapy in these specific patient groups may help reduce cardiovascular outcomes and the impact of the associated physical and/or psychological disability.
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Acknowledgments
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Both authors equally contributed to this chapter.
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Conflict of interest
We declare no conflict of interest. This chapter was written independently. No company or institution supported it financially.
Abbreviations
AACE
American Association of Clinical Endocrinologists
ABC
ATP-binding cassette
ACC/AHA
American College of Cardiology/American Heart Association
ACE
American College of Endocrinology
ACS
acute coronary syndrome
ApoB
apolipoprotein B
ARIC study
the Atherosclerosis Risk in Communities study
ASCVD
atherosclerotic cardiovascular disease
CAD
coronary artery disease
CHD
coronary heart disease
CKD
chronic kidney disease
CTT
Cholesterol Treatment Trialists’ Collaboration
CV
cardiovascular
CV
coefficient of variation
CVD
cardiovascular disease
CYP450
cytochrome P450
DNA
deoxyribonucleic acid
ESC/EAS
European Society of Cardiology/European Atherosclerosis Society
FBG
fasting blood glucose
FDA
Food and Drug Administration
FH
familial hypercholesterolemia
FOURIER trial
Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk trial
FPG
fasting plasma glycose
GAUSS-3 trial
the Goal Achievement After Utilizing an Anti-PCSK9 Antibody in Statin Intolerant Subjects-3 trial
HDL-C
high-density lipoprotein cholesterol
HgBA1C
hemoglobin A1c
HMG-CoA
3-hydroxy-3-methylglutaryl coenzyme A
HoFH
homozygote familiar hyperlipidemia
hsCRP
high-sensitive C-reactive protein
IDEAL trial
the Incremental Decrease in Endpoints Through Aggressive Lipid Lowering trial
IDL
intermediate density lipoproteins
IgG1
immunoglobulin G1
IMPROVE-IT study
Examining Outcomes in Subjects With Acute Coronary Syndrome: Vytorin vs. Simvastatin
IS
ischemic stroke
JUPITER trial
in the Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin randomized trial
LAPLACE-2 trial
the LDL-C Assessment With Proprotein Convertase Subtilisin Kexin Type 9 Monoclonal Antibody Inhibition Combined With Statin Therapy 2 trial
LDL
low-density lipoprotein
LDL-C
low-density lipoprotein cholesterol
LDL-R
LDL receptor
Lp(a)
lipoprotein(a)
MDA-LDL
malondialdehyde-modified LDL
MI
myocardial infarction
MoAbs
monoclonal antibodies
MRSE
muscle-related side effects
MVE
major vascular events
NPC1L1
Niemann Pick C1 like 1 protein
ODDYSSEY trial
the Reductions in Atherogenic Lipids and Major Cardiovascular Events: A Pooled Analysis of 10 ODYSSEY Trials Comparing Alirocumab With Control
PCI
percutaneous coronary intervention
PCSK9
Proprotein Convertase Subtilisin/Kexin Type 9
PRECISE-IVUS trial
the Impact of Dual Lipid-Lowering Strategy With Ezetimibe and Atorvastatin on Coronary Plaque Regression in Patients With Percutaneous Coronary Intervention: The Multicenter Randomized Controlled trial
PROVE-IT trial
Pravastatin or Atorvastatin Evaluation and Infection Therapy trial
RCTs
randomized clinical trials
RMSE
root mean squared error
SC
subcutaneously
SD
standard deviation
SEARCH trial
in the Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine randomized trial
SEASE study
Simvastatin and Ezetimibe in Aortic Stenosis study
SHARP trial
the Study of Heart and Renal Protection (Simvastatin plus ezetimibe) trial
SLC
solute carrier
SPARCL trial
in The Stroke Prevention by Aggressive Reduction of Cholesterol Levels trial
T2DM
type 2 diabetes mellitus
TNF-α
tumor necrosis factor-α
TNT trial
treating to New Targets trial
UGT
UDP-glucuronosyltransferase
VLDL
very low-density lipoproteins
\n',keywords:"hyperlipidemia, statins, ezetimibe, PCSK9 inhibitors, cardiovascular diseases, cerebrovascular disease, prevention, adverse effects, diabetes, residual risk",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/65211.pdf",chapterXML:"https://mts.intechopen.com/source/xml/65211.xml",downloadPdfUrl:"/chapter/pdf-download/65211",previewPdfUrl:"/chapter/pdf-preview/65211",totalDownloads:1306,totalViews:0,totalCrossrefCites:0,totalDimensionsCites:1,totalAltmetricsMentions:0,impactScore:0,impactScorePercentile:41,impactScoreQuartile:2,hasAltmetrics:0,dateSubmitted:"June 17th 2018",dateReviewed:"November 13th 2018",datePrePublished:"January 24th 2019",datePublished:"January 22nd 2020",dateFinished:"January 17th 2019",readingETA:"0",abstract:"Statins have proved to be very effective in reducing atherosclerotic cardiovascular disease (ASCVD) risk, with no apparent threshold at which low-density lipoprotein cholesterol (LDL-C) lowering is not associated with a reduced risk. Yet, several meta-analyses of statin trials show significant on-treatment residual risk of major cardiovascular (CV) events. This finding points to the unmet needs, in terms of LDL-C targets and ASCVD protection, of statin-treated patients, raising the question of statin combination therapy. Ezetimibe is a cholesterol absorption inhibitor, with the potency to decrease LDL-C for about 10–18%, apolipoprotein B (apoB) for 11–16%, while, in combination therapy with statins, leads to an additional LDL-C lowering of 25%, with a total LDL-C lowering of 34–61%. It is also estimated that 10–20% of patients on statin treatment cannot tolerate them. As a result, adequate doses to achieve treatment target, or as recommended for the patient-specific risk profile, cannot be prescribed. Proprotein convertase subtilisin/kexin type 9 (PCSK9) Inhibitors are monoclonal antibodies that inhibit the binding of PCSK9 to LDL-C receptors. Besides a very potent lipid-lowering effect, PCSK9 inhibitors have added ASCVD risk reduction benefit due to a very aggressive LDL-C lowering action, especially beneficial in patients who are intolerant to statins.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/65211",risUrl:"/chapter/ris/65211",book:{id:"6966",slug:"lipid-peroxidation-research"},signatures:"Marija Vavlukis and Ana Vavlukis",authors:[{id:"221486",title:"Prof.",name:"Marija",middleName:null,surname:"Vavlukis",fullName:"Marija Vavlukis",slug:"marija-vavlukis",email:"marija.vavlukis@gmail.com",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:null},{id:"264541",title:"MSc.",name:"Ana",middleName:null,surname:"Vavlukis",fullName:"Ana Vavlukis",slug:"ana-vavlukis",email:"ana.vavlukis@gmail.com",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_1_2",title:"1.1 HMG-CoA reductase inhibitors—statins",level:"2"},{id:"sec_2_2",title:"1.2 Cholesterol absorption inhibitors—ezetimibe",level:"2"},{id:"sec_3_2",title:"1.3 Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors",level:"2"},{id:"sec_5",title:"2. Effects of statins",level:"1"},{id:"sec_5_2",title:"2.1 Effects of statin therapy on LDL-C concentrations",level:"2"},{id:"sec_6_2",title:"2.2 Reductions in major vascular event (MVE) rates",level:"2"},{id:"sec_7_2",title:"2.3 Reductions in coronary mortality",level:"2"},{id:"sec_8_2",title:"2.4 The question of residual risk",level:"2"},{id:"sec_10",title:"3. Combination therapy",level:"1"},{id:"sec_10_2",title:"3.1 Combination therapy: ezetimibe ad-on statin",level:"2"},{id:"sec_10_3",title:"3.1.1 Effects of ezetimibe ad-on statins on LDL-C",level:"3"},{id:"sec_11_3",title:"3.1.2 Effects of ezetimibe ad-on statins on ASCVD outcome",level:"3"},{id:"sec_13_2",title:"3.2 Combination therapy: PCSK9 inhibitors ad-on statin",level:"2"},{id:"sec_13_3",title:"3.2.1 Key points",level:"3"},{id:"sec_14_3",title:"3.2.2 LDL-C lowering and PCSK9 inhibitors: what have we learned?",level:"3"},{id:"sec_15_3",title:"3.2.3 Cardiovascular outcome studies with PCSK9 inhibitors: what have we learned?",level:"3"},{id:"sec_18",title:"4. Safety profiles of statin monotherapy and statin combination therapy",level:"1"},{id:"sec_18_2",title:"4.1 Adverse effects of statin therapy",level:"2"},{id:"sec_18_3",title:"4.1.1 Increases in myopathy rates",level:"3"},{id:"sec_19_3",title:"4.1.2 Increases in diabetes rates",level:"3"},{id:"sec_20_3",title:"4.1.3 Probable increases in hemorrhagic stroke rates",level:"3"},{id:"sec_22_2",title:"4.2 Safety profile of ezetimibe ad-on statins combination therapy",level:"2"},{id:"sec_23_2",title:"4.3 Safety profile of PCSK9 inhibitors ad-on statins combination therapy",level:"2"},{id:"sec_25",title:"5. The war of today",level:"1"},{id:"sec_26",title:"6. Conclusion",level:"1"},{id:"sec_27",title:"Acknowledgments",level:"1"},{id:"sec_30",title:"Conflict of interest",level:"1"},{id:"sec_29",title:"Abbreviations",level:"1"}],chapterReferences:[{id:"B1",body:'Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. European Heart Journal. 2017;38(32):2459-2472. DOI: 10.1093/eurheartj/ehx144\n'},{id:"B2",body:'Nozue T. Lipid lowering therapy and circulating PCSK9 concentration. Journal of Atherosclerosis and Thrombosis. 2017;24(9):895-907. DOI: 10.5551/jat.RV17012\n'},{id:"B3",body:'Catapano AL, Graham I, De Backer G, et al. The Task Force for the Management of Dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) developed with the special contribution of the European Assocciation for Cardiovascular Prevention & Rehabilitation (EACPR). 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. European Heart Journal. 2016;37:2999-3058. DOI: 10.1093/eurheartj/ehw272\n'},{id:"B4",body:'Robinson JG. 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Journal of the American Medical Association. 2012;308:1545-1554\n'},{id:"B20",body:'Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(suppl 2):S1-S45\n'},{id:"B21",body:'Soran H, Schofield JD, Durrington PN. Cholesterol, not just cardiovascular risk, is important in deciding who should receive statin treatment. European Heart Journal. 2015;36:2975-2983\n'},{id:"B22",body:'Cholesterol Treatment Trialists’ (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: A meta-analysis of data from 170 000 participants in 26 randomised trials. Lancet. 2010;376:1670-1681\n'},{id:"B23",body:'Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: Meta-analysis of individual data from 27 randomised trials. Lancet. 2012;380:581-590\n'},{id:"B24",body:'Soran H, Dent R, Durrington P. Evidence-based goals in LDL-C reduction. Clinical Research in Cardiology. 2017;106:237-248. DOI: 10.1007/s00392-016-1069-7\n'},{id:"B25",body:'Collins R, Reith C, Emberson J, et al. Interpretation of the evidence for the efficacy and safety of statin therapy. Lancet. 2016;388:2532-2561. DOI: 10.1016/ S0140-6736(16)31357-5\n'},{id:"B26",body:'Jellinger PS, Handelsman Y, Rosenblit PD, et al. AACE 2017 Guidelines, American Association of Clinical Endocrinologists and American College of Endocrinology Guidelines for Management of Dyslipidemia and Prevention of Cardiovascular Disease. Endocrine Practice. 2017;23(Suppl 2):1-63\n'},{id:"B27",body:'LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. The New England Journal of Medicine. 2005;352:1425-1435. DOI: 10.1056/NEJMoa050461\n'},{id:"B28",body:'Pedersen TR, Faergeman O, Kastelein JJ, et al. High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction the IDEAL study: A randomized controlled trial. Journal of the American Medical Association. 2005;294(19):2437-2445. DOI: 10.1001/jama.294.19.2437\n'},{id:"B29",body:'Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. The New England Journal of Medicine. 2004;350:1495-1504. DOI: 10.1056/NEJMoa040583\n'},{id:"B30",body:'Baer J. AACE and EAS lipid guidelines. Expert analysis. AACE and EAS lipid guidelines—American College of Cardiology [internet]. http://www.acc.org/latest-in-cardiology/articles/2017/08/11/08/35/aace-and-eas-lipid-guidelines. [Accessed: 2018-10-05]\n'},{id:"B31",body:'Robinson JG, Rogers WJ, Nedergaard BS, et al. Rationale and design of LAPLACE-2: A phase 3, randomized, double-blind, placebo- and Ezetimibe-controlled trial evaluating the efficacy and safety of Evolocumab in subjects with hypercholesterolemia on background statin therapy. Clinical Cardiology. 2014;37(4):195-203. DOI: 10.1002/clc.22252\n'},{id:"B32",body:'Ray KK, Ginsberg HN, Davidson MH, et al. Reductions in atherogenic lipids and major cardiovascular events: A pooled analysis of 10 ODYSSEY trials comparing alirocumab with control. Circulation. 2016;134(24):1931-1943. DOI: 10.1161/CIRCULATIONAHA.116.024604\n'},{id:"B33",body:'Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. The New England Journal of Medicine. 2017;376(1713):1722. DOI: 10.1056/NEJMoa1615664\n'},{id:"B34",body:'Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe added to statin therapy after acute coronary syndromes. The New England Journal of Medicine. 2015;372(2387):2397. DOI: 10.1056/NEJMoa1410489\n'},{id:"B35",body:'Lloyd-Jones D, Morris P, Ballantyne C, et al. 2016 ACC expert consensus decision pathway on the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk: A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. Journal of the American College of Cardiology. 2016;68:92-125. DOI: 10.1016/j.jacc.2016.03.519\n'},{id:"B36",body:'Descamps O, Tomassini JE, Lin J, et al. Variability of the LDL-C lowering response to ezetimibe and ezetimibe + statin therapy in hypercholesterolemic patients. Atherosclerosis. 2015;240(2):482-489. DOI: 10.1016/j.atherosclerosis.2015.03.004\n'},{id:"B37",body:'Toth PP, Foody JM, Tomassini JE, et al. Therapeutic practice patterns related to statin potency and ezetimibe/simvastatin combination therapies in lowering LDL-C in patients with high-risk cardiovascular disease. Journal of Clinical Lipidology. 2014;8(1):107-116. DOI: 10.1016/j.jacl.2013.09.009\n'},{id:"B38",body:'Bohula E, Giugliano R, Cannon C, et al. Achievement of dual low-density lipoprotein cholesterol and high-sensitivity C-reactive protein targets more frequent with the addition of ezetimibe to simvastatin and associated with better outcomes in IMPROVE-IT. Circulation. 2015;132:1224-1233. DOI: 10.1161/CIRCULATIONAHA.115.018381\n'},{id:"B39",body:'Uemura Y, Watarai M, Ishii H, et al. Atorvastatin 10 mg plus ezetimibe 10 mg compared with atorvastatin 20 mg: Impact on the lipid profile in Japanese patients with abnormal glucose tolerance and coronary artery disease. Journal of Cardiology. 2012;59(1):50-56. DOI: 10.1016/j.jjcc.2011.09.001\n'},{id:"B40",body:'Tobaru T, Seki A, Asano R, et al. Lipid-lowering and anti-inflammatory effect of ezetimibe in hyperlipidemic patients with coronary artery disease. Heart and Vessels. 2013;28(1):39-45. DOI: 10.1007/s00380-012-0243-8\n'},{id:"B41",body:'Tsujita K, Sugiyama S, Sumida H, et al. Impact of dual lipid-lowering strategy with Ezetimibe and atorvastatin on coronary plaque regression in patients with percutaneous coronary intervention: The multicenter randomized controlled PRECISE-IVUS trial. Journal of the American College of Cardiology. 2015;66(5):495-507. DOI: 10.1016/j.jacc.2015.05.065\n'},{id:"B42",body:'Mancini J, Hegele R, Leiter L. Dyslipidemia. Canadian Diabetes Association clinical practice guidelines expert committee. Canadian Journal of Diabetes. 2013;37(Suppl 1):S110-S116. DOI: 10.1016/j.jcjd.2013.01.032\n'},{id:"B43",body:'Lovadi E, Csécsei P, Lovig C, et al. Lipids and cerebrovascular disease—New therapeutic options in lowering LDL-cholesterol. Orvosi Hetilap. 2016;157(52):2059-2065. DOI: 10.1556/650.2016.30643\n'},{id:"B44",body:'Lepor NE, Kereiakes DJ. The PCSK9 inhibitors: A novel therapeutic target enters clinical practice. American Health & Drug Benefits. 2015;8(9):483-489\n'},{id:"B45",body:'Landmesser U, Chapman MJ, Stock JK, et al. 2017 update of ESC/EAS task force on practical clinical guidance for proprotein convertase subtilisin/kexin type 9 inhibition in patients with atherosclerotic cardiovascular disease or in familial hypercholesterolaemia. European Heart Journal. 2017;0:1-13\n'},{id:"B46",body:'Sabatine MS, Giugliano RP, Keech AC, et al. FOURIER steering committee and investigators. Evolocumab and clinical outcomes in patients with cardiovascular disease. The New England Journal of Medicine. 2017;376:1713-1722\n'},{id:"B47",body:'Nissen SE, Stroes E, Dent-Acosta R, et al. Efficacy and tolerability of Evolocumab vs Ezetimibe in patients with muscle-related statin IntoleranceThe GAUSS-3 randomized clinical trial. Journal of the American Medical Association. 2016;315(15):1580-1590. DOI: 10.1001/jama.2016.3608\n'},{id:"B48",body:'Macedo AF, Taylor FC, Casas JP, et al. Unintended eff ects of statins from observational studies in the general population: Systematic review and meta-analysis. BMC Medicine. 2014;12:51\n'},{id:"B49",body:'SEARCH Collaborative Group. Intensive lowering of LDL cholesterol with 80 mg versus 20 mg simvastatin daily in 12 064 survivors of myocardial infarction: A double-blind randomised trial. Lancet. 2010;376:1658-1669\n'},{id:"B50",body:'Ridker PM. The JUPITER Trial-results, controversies, and implications for prevention. Circulation: Cardiovascular Quality and Outcomes. 2009;2:279-285\n'},{id:"B51",body:'Huisa BN, Stemer AB, Zivin JA. Atorvastatin in stroke: A review of SPARCL and subgroup analysis. Vascular Health and Risk Management. 2010;6:229-236\n'},{id:"B52",body:'Wu H, Shang H, Wu J. Effect of ezetimibe on glycemic control: A systematic review and meta-analysis of randomized controlled trials. Endocrine. 2018;60(2):229-239. DOI: 10.1007/s12020-018-1541-4\n'},{id:"B53",body:'Saxon DR, Eckel RH. Statin intolerance: A literature review and management strategies. Progress in Cardiovascular Diseases. 2016;59(2):153-164. DOI: 10.1016/j.pcad.2016.07.009\n'},{id:"B54",body:'Olsson AG, Angelin B, Assmann G, et al. Can LDL cholesterol be too low? Possible risks of extremely low levels. Journal of Internal Medicine. 2017;281:534-553\n'},{id:"B55",body:'Khan SU, Talluri S, Riaz H, et al. A Bayesian network meta-analysis of PCSK9 inhibitors, statins and ezetimibe with or without statins for cardiovascular outcomes. European Journal of Preventive Cardiology. 2018;25(8):844-853. DOI: 10.1177/2047487318766612\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Marija Vavlukis",address:"marija.vavlukis@gmail.com",affiliation:'
University Clinic of Cardiology, Medical Faculty, Ss’ Cyril and Methodius University, Republic of Macedonia
Faculty of Pharmacy, Ss’ Cyril and Methodius University, Republic of Macedonia
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1. Introduction
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Due to intensification of small ruminant farming, there is increase in the number of disease outbreaks in the recent years. Among the various infectious diseases, diseases caused by bacterial pathogens contribute to severe economic loss to the goat farmers. Various factors like increase in herd size, reduced ventilation in farm and poor husbandry practices can predispose to diseases. Bacterial diseases like anthrax, enterotoxaemia, tetanus, gas gangrene, caseous lymphadenitis, listeriosis, tuberculosis, Johne’s disease, dermatophilosis, pasteurellosis/mannheimiosis, brucellosis, foot rot, contagious caprine pleuropneumonia, colibacillosis, salmonellosis, etc., affect goats and can cause various ailments and some diseases can cause heavy mortality leading to huge economic loss to the farmer [1]. Different bacterial pathogens affect different organs of goat thereby eliciting various clinical signs based on which a tentative diagnosis can be made (Figure 1).
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Figure 1.
Different bacterial diseases of goat and the organ/ tissues affected. Brucellosis affects reproductive tract, dermatophilosis affect the skin, johne’s disease causes corrugation of intestine, pasteurellosis/ mannheimiosis, tuberculosis, contagious caprine pleuropneumonia affects the respiratory system, caseous lymphadenitis affects the lymph nodes and tetanus affects the nervous system. This figure is propriety of the authors.
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Antibacterial agents can be used to treat various bacterial diseases but these drugs should be used judiciously due to the risk of development of antimicrobial resistance. Vaccination is the best way to prevent infectious diseases and based on the pattern of the disease annual vaccination should be practiced to prevent disease outbreaks. Diseases like anthrax, brucellosis and tuberculosis pose threat to human since these diseases can be transmitted to human through direct or indirect route of transmission [2]. Due care should be taken while handling infected goats or dead goats in farm as the zoonotic diseases can cause severe aliments in human.
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2. Methods
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This chapter is a comprehensive summary of important bacterial diseases of goats and this can be a guide to veterinary students, field veterinarians and goat farmers regarding the impact of these bacterial diseases. This chapter also highlights the preventive measures and zoonotic potential associated with the bacterial diseases of goats. Important bacterial diseases that are zoonotic and economically important like anthrax, brucellosis, tetanus, enterotoxaemia, Johne’s disease, Pasteurellosis/ Mannheimiosis, caseous lymphadenitis, contagious caprine pleuropneumonia, dermatophilosis and foot rot are discussed. Each disease is delt with various subsections like definition of the diseases, etiology, epizootiology, transmission clinical signs, diagnosis, treatment, preventive measures and public health significance, if any.
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3. Anthrax
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Anthrax is a peracute, acute or subacute, often fatal disease of animals including goats. In goats the disease is mainly characterized by septicaemia, splenomegaly and gelatinous infiltration of subcutaneous or subserosal tissues. The disease is commonly known as woolsorter’s disease, splenic fever, charbon, and milzbrand.
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3.1 Etiology
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The disease is caused by Bacillus anthracis, a gram positive, capsulated, non-motile, aerobic, spore-forming, rod shaped bacterium [3].
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3.2 Epizootiology
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The disease is worldwide in distribution and is endemic in some countries, while occurs in defined regions of other countries. It was reported to be associated with heavy mortalities in goats and sheep of sub-saharan region in 1960–70s and in other countries. In recent days, through strict vaccination procedures the incidence reduced in most countries, however, sporadic cases are still being reported. B. anthracis is widely distributed in the environment, as they produce highly resistant endospores. They can tolerate extremely adverse conditions such as desiccation, high temperatures and chemical disinfectants. When the vegetative bacteria are exposed to atmospheric oxygen under favorable temperature (20–40°C) and relative humidity (>60%), the spores are formed. Further, the calcium plays a role in spore formation and in combination with dipicolinic acid, enhances the spore survival. Hence, its survival is more in alkaline soil that is rich in calcium and nitrogen and with high moisture content, the endospores can survive for more than 50 years. Further, recurrent cycles of flooding and evaporation may concentrate spores in particular low-lying regions [3].
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3.3 Transmission
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Goats are infected by ingestion of food, water or soil contaminated with spores. The infection can also occur through inhalation or abraded skin and oral mucosa. Mechanical transmission by biting insects is also reported. Wild animals acting as carriers makes the control programme challenging as it is least possible to vaccinate all wild animals.
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3.4 Clinical signs
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The incubation period ranges from hours to days. The disease is usually fatal, especially in sheep and goats, after 1–3 days. The peracute case is characterized by sudden death without any premonitory signs. However, there may be fever, dysponea, congestion of mucous membranes, muscular tremors and terminal convulsions in few animals. In acute cases, fever, anorexia, labored breathing, increased heart rate, ruminal stasis and reduce milk production may be observed. There may be bloody discharges from orifices like mouth, nostrils, anus and/or vulva. Diarrhea or dysentery and oedema and swelling of the tongue, throat, flank and perineum (anus, vulva) may be seen. Pregnant animal abort and blood-tinged milk is produced. Animals then collapse with terminal convulsions and die [4].
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Necropsy of suspected carcass is not recommended, as the vegetative bacteria may get transformed into spore and hence contaminate the environment. The pathological features such as absence of rigor mortis and rapid putrefaction and bloating of the carcass are common clinical features. Oozing of unclotted dark, tarry colored blood from orifices, soft and enlarged spleen, blood-stained fluid in body cavities and widespread ecchymotic hemorrhages are frequently observed post mortem findings.
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3.5 Diagnosis
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Though clinical signs are highly suggestive, the diagnosis based on clinical signs alone is difficult. Thin smears of blood from ear tip can be stained with polychrome methylene blue stain to reveal short chains of truncated blue color rods, surrounded by pink capsules (McFadyean reaction). The organism can be cultured on Sheep or Ox blood agar which shows flat, dry grayish colonies with ‘ground glass’ appearance after 24–48 hours of incubation (Figure 2). The selective media for the organism is PLET (Polymyxin-lysozyme-EDTA thallous acetate) medium. The Ascoli’s thermo-precipitation test is also commonly used test to detect antigens of B. anthracis. Agar gel immunodiffusion, complement fixation test, ELISA and immunofluorescence tests though available are insensitive and not routinely used [4]. The PCR test can be used for direct detection of the organism from decomposed samples and can also be employed for targeting the pXO1 and pXO2 plasmids to confirm the virulence of isolates from the culture.
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Figure 2.
Ground glass appearance Bacillus anthracis colonies on sheep blood agar. This figure is propriety of the authors.
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3.6 Treatment
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Ailing animals in early stages of infection can be treated with penicillin or oxytetracycline or other long-acting antibiotics. An anthrax antiserum may result in recovery if used in early stages. Vaccination should follow 7–10 days after the conclusion of antibiotic therapy [4].
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3.7 Preventive measures
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In endemic areas, annual vaccination is advisable. The goat should be vaccinated with ‘Sterne strain’ live spore vaccine one month before the anticipated outbreaks. In non-endemic areas, movement of animals and their products should be restricted; feed and bedding materials etc., should not be transferred from affected herds. Disinfection of the premises with 5% formalin, 5% sodium hydroxide or 3% peracetic acid and placing foot-baths containing these sporicidal disinfectants at the entrances of the affected farms will help to control the spread of infection. Contaminated building should be fumigated with formaldehyde before removing the bedding materials [5]. Proper disposal of carcasses and the infected materials should be done either by deep burial or incineration.
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3.8 Public health significance
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\nB. anthracis is considered a bioterrorism agent. Three forms of disease occur in human beings. When endospores enter through abraded skin, the cutaneous form of anthrax (malignant pustule) develops. While, the pulmonary form (woolsorters’ disease) follows inhalation route and intestinal form results from ingestion of infective material. The disease usually fatal if not treated early [6].
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4. Brucellosis
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Caprine brucellosis is an infectious zoonotic disease having substantial economic impact on both livestock and human. Caprine brucellosis is reported since ancient days; Hippocrates II first described the human brucellosis in 400 B.C. which was most likely to be associated with consumption of raw milk or derivatives of infected sheep or goats.
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4.1 Etiology
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The causative agent is Brucella species mainly B. melitensis that are small, non-motile, non-spore forming, gram-negative coccobacilli. Goats are also susceptible to infection by B. abortus, particularly when housed in close proximity with infected cattle; however, they do not sustain the infection in the herd [7].
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4.2 Epizootiology
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The disease is prevalent worldwide and it remains a major burden in parts of Mediterranean region, the Middle East, Central and Southeast Asia (including India and China), sub-Saharan Africa, and parts of Latin America [8]. Goat herds from USA, Canada, Colombia, Chile, and Uruguay are reported to be free from B. melitensis infection.
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4.3 Transmission
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Infection occurs primarily through ingestion of the organisms. Goats acquire infection by licking the aborted fetuses, placentas, newborn kids, vaginal discharges, or by consumption of feed contaminated with these infectious materials [9]. Milkers can also spread the infection through unsanitary milking practices.
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4.4 Clinical signs
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The disease is more severe in goats and is protracted than in sheep. Clinical manifestations include high abortion rates particularly during the fourth month of pregnancy and retained placentas, orchitis in bucks, arthritis and hygromas. In goats, mastitis and lameness may also be seen. The abortion rate can be high when this bacterium first enters a naive flock or herd [10]. The abortion rates are usually much lower once B. melitensis has become established in a herd and only a few animals abort repeatedly but affected animals shed bacteria during parturition. Healthy asymptomatic carriers become a potential source of infection. Other clinical signs include death of weak offspring, low weaning weight, decreased milk production, and epididymitis, and reduced fertility which is more common in sheep. In case of abortions, fetus might reveal excess of blood-stained fluids in the body cavities, with enlarged spleen and liver. Moreover, infected foetal membranes can show thickened and dull-gray color necrotic cotyledons [11].
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4.5 Diagnosis
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Diagnosis is made based on clinical signs, direct examination of MZN-stained smears of fluids or tissues, isolation and identification of B. melitensis from milk or an aborted fetus or by serum agglutination tests. The Rose-Bengal agglutination test and the complement fixation test are the most widely used methods for detecting B. melitensis infection and are approved for international trade. Indirect enzyme-linked immunosorbent assays (ELISA) have been developed and are also approved tests for the purposes of international trade [12]. Isolation and identification of B. melitensis from aborted foetal stomach contents, placenta and uterine fluids can be attempted and isolation is the gold standard technique for confirmation of brucellosis (Figure 3). Isolation should be carried out in biosafety cabinet class III as the organism is zoonotic.
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Figure 3.
\nBrucella melitensis colonies on sheep blood agar. This figure is propriety of the authors.
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4.6 Preventive measures
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Test and slaughter policy of the infected herd is generally implemented in countries where the disease is considered exotic. This can also reduce the prevalence of disease in endemic areas. In most countries where B. melitensis is endemic, vaccination with the Rev. 1 strain is commonly employed [13]. It is a live attenuated strain of B. melitensis; administered by the subcutaneous or conjunctival routes and is used for vaccination of kids and lambs up to 6 months of age.
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4.7 Public health significance
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\nB. melitensis is highly pathogenic than other species of Brucella for human beings. The infection in human is characterized by fever, chills, headache, malaise, back pain, myalgia and lymphadenopathy, which may be accompanied by splenomegaly and/ or hepatomegaly. The patients may experience drenching sweats at night and nonspecific gastrointestinal signs such as vomition, diarrhea and/or constipation [14]. Localized manifestations such as arthritis, spondylitis, sacroiliitis, osteomyelitis, bursitis and tenosynovitis may be observed. Epididymo-orchitis, prostatitis and seminal vesiculitis can be seen in males, whereas abortion or premature births are seen in pregnant women. Deaths are usually uncommon except in infants caused by endocarditis or infections of the brain.
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5. Tetanus
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Tetanus (Lockjaw) is an acute, highly fatal intoxication of all domestic animals and humans caused by neurotoxin produced by the bacteria Clostridium tetani [15]. Though all species of livestock are susceptible, sheep and goats are more susceptible than cattle and horses being the most susceptible. It is characterized by hyperasethesia, tetany and convulsions.
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5.1 Etiology
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The etiological agent, Clostridium tetani is a strictly anaerobic, motile, slender, straight, spore forming (‘drumstick appearance’), Gram-positive rod. Based on flagellar antigens, so far 10 serotypes of C. tetani have been described and all produce antigenically a similar neurotoxin called tetanospasmin. Though endospores are resistant to chemicals and boiling, they are destroyed by autoclaving.
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5.2 Epizootiology
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Tetanus is worldwide in distribution and occurs sporadically. The organism is normal inhabitant of intestinal tract of animals and persists as resistant spores in soil, manure [16].
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5.3 Transmission
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The toxemia in tetanus is caused by a specific neurotoxin produced by C. tetani in necrotic tissue. Spores are introduced into the tissue through wounds, specifically deep puncture wounds that provide the favorable anaerobic environment. Most outbreaks occur following mass contamination of animals during castration, vaccination, ear tagging, docking and other surgical procedures [17]. Grazing on rough and spiky pastures may injure the oral mucosa and hence may facilitate the invasion of the bacteria. The spores remain dormant in tissues and proliferate to liberate toxins under favorable conditions.
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5.4 Clinical signs
\n
The incubation period is usually of 4 days to 3 weeks. The initial signs include muscle stiffness, tremors and prolapse of the third eyelid. This is followed by rigidity and extension of the limbs leading to a stiff gait and abnormal flexion of the joints. Tetany of masseter muscles causes drooling of saliva (lock jaw) and regurgitation through nostrils [17]. The animals may exhibit bloat, an inability to chew, and hyperthermia. Retracted lips, hypersensitivity to external stimuli, and a ‘saw-horse’ stance are frequent signs. The spasms of alimentary and urinary tract muscle may cause constipation and retention of urine [17]. The abnormal muscular contracture may result in opisthotonus, curvature of the spine and bending of the tail. The disease is highly fatal and death occurs within 3–10 days with mortality nearing 100%, primarily as a result of respiratory failure. Necropsy features usually are nonspecific except for the inflammatory reaction associated with the wound.
\n
\n
\n
5.5 Diagnosis
\n
Diagnosis can be made based on clinical features such as muscular spasms, prolapse of third eyelid and based on history of trauma or surgery. The Gram-positive rods with terminal spores can be demonstrated in the smears prepared from necrotic tissue or wound [18]. Anaerobic culture of the bacteria from necrotic tissue may be attempted but is often unsuccessful. PCR and real-time PCR techniques can be employed for the detection of neurotoxin genes of the organism. Mouse inoculation test can be performed to demonstrate circulating neurotoxin from the serum of affected animals.
\n
\n
\n
5.6 Treatment
\n
Treatment mainly aimed at wound management, antibiotic therapy, antitoxin administration and vaccination. Wound management consists of surgical debridement of infected wounds and removal of debris, flushing with hydrogen peroxide to produce aerobic condition that helps to inhibit replication of the bacteria at the site of infection. The antibiotics (large doses of Penicillin) can be given both parenterally and flushed into the cleaned wound to prevent further replication of the bacteria and production of toxin [19]. Affected animals must be kept in a quiet and dark environment. Fluid replacement therapy, sedatives and muscle relaxants can minimize clinical discomfort and maintain vital functions. To neutralize unbound toxin, the tetanus antitoxin must be administered on time, either intravenously or into the subarachnoid space for three consecutive days. Vaccination with tetanus toxoid may be given subcutaneously to promote an active immune response even in those animals that are treated with antitoxin.
\n
\n
\n
5.7 Preventive measures
\n
Tetanus can be controlled by following good sanitation measures, aseptic surgical and management procedures and vaccination. Goats in a herd must be vaccinated routinely with tetanus toxoid which is very effective for stimulating long-term immunity. They can be vaccinated 2–3 times during the first year of life followed by booster vaccination before parturition to ensure colostral antibodies [20]. Further, a booster dose may be advisable if a vaccinated animal sustains a deep wound.
\n
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6. Enterotoxemia
\n
\n
6.1 Etiology
\n
Enterotoxaemia in goats is caused by Clostridium perfringens, a gram-positive, non-motile, spore-forming bacilli that grows well in anaerobic or micro-aerophilic conditions. This disease condition tends to be associated mainly with sheep and is of less importance in goats and cattle. C. perfringens Type D primarily produce enterotoxamia and Type C sometimes causes sudden death in goats. Grain-fed kids (3–12 weeks old) on a high-concentrate diet are most susceptible, but adult goats may also be affected. Goats are commonly affected with a hemorrhagic form of enterotoxemia.
\n
\n
\n
6.2 Epizootiology
\n
\nC. perfringens is worldwide in distribution and is found in soil, feces, and in the intestinal tracts of animals and humans. C. perfringens types B, C and D may survive in soil as spores for several months. C. perfringens type A constitutes a part of the normal intestinal flora and is widely dispersed in soil. Overcrowding and prolonged confinement may increase the spread and severity of the condition.
\n
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6.3 Transmission
\n
The C. perfringens type D is found as obligate parasite in the intestinal tract of animals [21]. The animals on a high grain diet or on succulent pasture are predisposed to this condition (hence described as ‘over-eating disease’). Thus, the disease is more common in well-fed animals in intensive feedlots.
\n
\n
\n
6.4 Clinical signs
\n
The peracute condition is characterized by sudden death of younger and healthy kids. This is occasionally preceded by other signs such as loss of appetite, lack of rumen activity and rumination, bloat, depression and a drunken appearance; the animals may show neurological signs such as incoordination, inability to stand, and convulsions. There may be watery diarrhea and glucosuria. In goat’s acute disease is mainly characterized by dysentery, abdominal discomfort and convulsions.
\n
In acute cases of goats, the necropsy findings include pulmonary edema, necrosis of intestinal walls and scattered hyperaemic areas of intestine. Intestinal contents may be green, blood-stained or mucoid, and fibrinous casts may be present in the lumen of the large intestine [22]. Mesentric lymph nodes may be edematous. Fluid accumulation in the pericardial sac, extremely necrotic, soft kidneys (‘pulpy kidneys’), focal encephalomalacia, and petechiae of serosa of the brain, diaphragm, gastrointestinal tract and heart are common findings.
\n
\n
\n
6.5 Diagnosis
\n
Diagnosis of enterotoxaemia depends on epidemiological features, type of diet, clinical and pathological features. Gram positive rods can be demonstrated in the smears of intestinal contents or in the lesions of intestine. The culture of bacteria from fecal samples in cooked meat media may be suggestive of the disease (Figure 4). Organism on blood agar plates show double zone of hemolysis which is suggestive of C. perfringens. Demonstration of the epsilon toxin in the intestinal content is highly reliable method. Protection of mice injected with infiltrates of toxin from intestinal contents against specific antisera is diagnostic. Genotyping by PCR can be used to type isolates of C. perfringens as an alternative to in vivo toxin neutralization tests. Though ELISA tests can be performed, misdiagnosis may occxur as this test detects low levels of toxin in the intestinal contents of normal animals [23].
\n
Figure 4.
Double zone hemolytic colonies of Clostridium perfringens on sheep blood agar. This figure is propriety of the authors.
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\n
\n
6.6 Treatment
\n
Treatment generally is ineffective as most cases are acute in nature. A hyperimmune serum, if available, can be used and a combination of hyperimmune serum along with sulphadimidine has been found useful in goats. Chelating agents can be used to neutralize toxins [21].
\n
\n
\n
6.7 Preventive measures
\n
Vaccination before the anticipated outbreaks is the primary method of control. Alum precipitated formalin killed whole culture toxoid vaccines are commercially available. In ruminants, maternal antibodies last about 5–6 weeks postpartum and hence, the young animals must be vaccinated at this time. Kids are usually vaccinated twice at 4 weeks interval and then re-vaccinated at once in 6 months. However, several anaphylactic reactions have been reported in Sannen kids re-vaccinated with toxoids [24]. Sudden dietary changes and other predisposing factors to enterotoxaemias must be managed. Feeding regimens and feeding of concentrates even to adult goats should be monitored carefully.
\n
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\n
7. Johne’s disease (JD)
\n
A chronic, contagious, granulomatous disease affecting small intestine of adult ruminants and the affected animals show weight loss and intermittent diarrhea [25].
\n
\n
7.1 Etiology
\n
JD is caused by Mycobacterium avium subspecies paratuberculosis, a fastidious, acid-fast, gram-positive rod [25].
\n
\n
\n
7.2 Transmission
\n
The organism is present in the environment and animals at young are affected either through ingestion of contaminated milk or direct contact. Infected goats may excrete the bacteria in the feces thereby contaminating the environment [26].
\n
\n
\n
7.3 Clinical signs
\n
The incubation period is usually months to years. Chronic wasting is a characteristic sign in goat and at times pasty feces or diarrhea (in advanced cases) can be witnessed. In advanced cases the animals may lose weight rapidly and will have a hide and bone condition. During PM examination intestine of the affected animals have a corrugated appearance [27].
\n
\n
\n
7.4 Diagnosis
\n
Affected animals can be identified in the herd by intradermal skin testing using Johnin purified protein derivative (PPD). Alternatively, Interferon gamma assay (IGRA) can also be used to assess the cellular immunity. Lymph nodes (Ileal and ileocecal) aspirates, intestinal scrapping can show acid fast bacilli in staining (Figure 5). Organism my shed intermittently in feces and hence, bacilli can be found by acid fast staining [27]. Organism can be detected intestinal tissues, lymph node and feces by culture and PCR. Detection of antibody in the later or final stages of the disease can also be attempted for diagnosis.
\n
Figure 5.
Acid fast bacilli in intestinal scrapping. This figure is propriety of the authors.
\n
\n
\n
7.5 Treatment
\n
Treating animals with antimycobacterial agents are not fruitful.
\n
\n
\n
7.6 Preventive measures
\n
Due to its chronic nature, it is difficult to identify the disease early hence, it is advised to test a newly purchased animal before letting into the farm. Test and cull policy is better to break the chain of infection. Suspected animals should be separated from the herd and affected animals milk should not be fed to neonates [25]. The organism may survive longer in the pasture hence, once an animal is found positive it is best to change the pasture land.
\n
\n
\n
7.7 Public health significance
\n
A similar condition in human named as Crohn’s disease has been suspected to be caused by Mycobacterium avium subspecies paratuberculosis still there is no clear evidence for zoonotic transmission of the pathogen [28].
\n
\n
\n
\n
8. Pasteurellosis and Mannheimiosis
\n
Pasteurellosis and Mannheimiosis is an acute fatal disease characterized by pneumonia and septicemia.
\n
\n
8.1 Etiology
\n
\nPasteurella multocida and Mannheimia haemolytica are aerobic, bipolar, nonmotile, non-spore forming gram-negative rods [29].
\n
\n
\n
8.2 Epizootiology and transmission
\n
\nP. multocida and M. haemolytica are ubiquitous and even present in respiratory tract of healthy animals. Young animals are prone to infection than adults. Stress including weaning, transportation (hence termed as shipping fever), change in diet/weather and overcrowding are the predisposing factors for the condition. Viral diseases can also predispose Pasteurellosis and Mannheimiosis and the organism can be transmitted directly or indirectly through inhalation or ingestion [30].
\n
\n
\n
8.3 Clinical signs
\n
Acute rhinitis or pharyngitis is the common sign noticed in animals. Animals may have high fever, anorexia, and rapid breathing along with profuse mucopurulent nasal/ ocular discharges. Kids are more susceptible than adult goats and death may occur without any clinical signs [30]. PM changes include marbling of lungs, pleural adhesion, sero-fibrinous fluid in the thorax, frothy exudate in trachea and also in bronchi.
\n
\n
\n
8.4 Diagnosis
\n
Bipolar organisms of P. multocida can be noticed in the impression smears from dead animals (Figure 6). Isolation of the organism on selective media and biochemical confirmation is the standard diagnostic procedure. M. haemolytica produces hemolytic colonies on blood agar and it can grow on MacConkey agar which are the differentiating features from P. multocida. Molecular diagnosis can be carried out by PCR [31].
\n
Figure 6.
Bipolar organism in lung impression smear. This figure is propriety of the authors.
\n
\n
\n
8.5 Treatment
\n
Use of antibiotics based on antimicrobial susceptibility testing can be used to control the bacterial propagation and anti-inflammatory agents can be used to control fever [30].
\n
\n
\n
8.6 Preventive measures
\n
\nM. haemolytica and P. multocida bacterins can be used as vaccines to prevent the occurrence of the disease [32]. Other measures like reducing overcrowding thereby improving the ventilation in enclosures and also reducing the stress during transportation can prevent the occurrence of the disease.
\n
\n
\n
\n
9. Caseous lymphadenitis
\n
Caseous lymphadenitis (CLA) is contagious, subclinical and chronic suppurative condition of sheep and goats, occasionally in cattle and is characterized by the formation of abscesses in lymph nodes and visceral organs [33].
\n
\n
9.1 Etiology
\n
CLA is caused by Corynebacterium pseudotuberculosis, small, non-motile, non-spore forming, pleomorphic, Gram-positive bacteria which may occur in curved, coccoid, club and rod forms (coryneform morphology) [33]. Two biotypes of C. pseudotuberculosis are recognized; ovine/caprine biotypes that lack nitrate-reducing capacity mainly affect sheep and goats, causing superficial and visceral abscesses. The second equine/bovine biotype usually reduce nitrate and mainly affects horses and cattle, causing ulcerative lymphangitis.
\n
\n
\n
9.2 Epizootiology
\n
CLA is worldwide in distribution and the probable dissemination of the disease throughout the world occurred through importation of infected animal [34]. This disease is found in parts of North and South America, Australia, New Zealand, the Middle East, Asia and Africa and is being reported more often in Britain and other European countries.
\n
\n
\n
9.3 Transmission
\n
The bacteria can survive in the environment for about 6 months or more. Transmission can occur either through direct or indirect contact or through wounds contaminated with pus from the abscesses of infected animals. The organism enters through contamination of skin wounds arising from castration, ear tagging or tattooing, docking or shearing operations. Arthropod bites or contaminated dips can also be the source of infection [34]. Goats having traumatized buccal mucosa have more chances of taking the bacterium from contaminated feed. The organism has also been isolated from the milk of affected goats.
\n
\n
\n
9.4 Clinical signs
\n
The incubation period varies from weeks to months; usually is about 3 months. CLA may be manifested in two forms: in its superficial form it is characterized by infection of peripheral lymph nodes, such as the submandibular, parotid, pre-scapular and supramammary lymph nodes (Figure 7). These peripheral lymph nodes enlarge, may erode and eventually leads to formation of abscess in chronic cases. Visceral form is characterized by abscessation of internal organs, such as lungs, liver, kidneys, uterus, spleen and internal lymph nodes (mainly mediastinal and bronchial lymph nodes) that may not be detectable antemortem [35]. These two forms can co-exist; however, the visceral form is more common among sheep, while superficial form is more frequent among goats with external abscesses in the lymph nodes particularly of the head and neck regions.
\n
Figure 7.
Lymph node enlargement in goats noted in caseous lymphadenitis. This figure is propriety of the authors.
\n
Eventually, the affected animal become exercise-intolerant, anorectic, ill-thrift and debilitated (often known as thin-ewe syndrome in sheep). Fever, increased respiratory rates, and pneumonia may also be noticed. Morbidity up to 15% is common, and morbid animals will often eventually succumb to the disease. The infection can also lead to abortion in doe and orchitis and/or epididymitis in bucks. Though less common, orchitis can be acute in which the buck develops fever, reduced appetite, lack of walking ability and loss of libido. The infected testes appear swollen, hot and painful to touch.
\n
\n
\n
9.5 Diagnosis
\n
Diagnosis is based on clinical signs and lesions and abscessation of both superficial and visceral lymph nodes is typical. Radiographs may be useful in identifying affected central nodes which also must be confirmed by culture of tracheal washings. Gram and Giemsa staining can be used for identification of the bacteria. Isolation of organism from purulent material from abscessed lymph nodes in case of live animals and /or from abscesses of internal organs from dead animals. ELISA tests which detect antibodies directed against either cell wall antigens or the exotoxin (Phospholipase D - PLD) are available [34]. Further, the detection of INF-γ by ELISA, an indicator of cell-mediated immunity, has also been potentially used for demonstration of CLA in eradication programs. Molecular techniques such as PCRs targeting 16S rDNA, rpo and pld genes have also been used in the recent years for the diagnosis of caseous lymphadenitis.
\n
\n
\n
9.6 Treatment
\n
Though C. pseudotuberculosis, in vitro is susceptible to antibiotics, the antibiotic therapy is usually not much effective in animals. The chronic nature of infection, the intracellular location of the bacteria and the formation of biofilm in natural infections reduce the antibiotic efficacy, making them useless. Draining of abscesses, followed by cleansing and chemical cauterization with 10% iodine may be helpful or the localized abscesses may be removed entirely from valuable animals [34].
\n
\n
\n
9.7 Preventive measures
\n
As CLA is contagious in nature, the animals with draining and punctured lesions should be kept isolated until healed. Reducing the environmental contamination, proper sanitation and biosecurity of facilities and instruments and safety measures to prevent injuries are all important in control. The causative agent is sensitive to common disinfectants such as hypochlorite, formalin and cresol; however, the surfaces should be cleaned before disinfection, as organic matter usually interferes with the action of these agents. The control measures vary with the prevalence of infection. In countries with a high incidence, rigorous sanitary procedures must be implemented, along with vaccination. Disease eradication can be achieved in endemically-infected herds by test and disposal policy [36].
\n
Most of the commercially available vaccines contain inactivated PLD of either C. pseudotuberculosis or of other pathogens, such as Clostridium species. Glanvac vaccine (Vetrepharm, Inc. London) is licensed for use in sheep and goats in Canada, Australia and New Zealand. However, the use of PLD toxoid in goats may result in some adverse consequences such as reduction in milk, fever, ventral edema, ataxia and convulsions; therefore, its use is restricted [34]. On the other hand, live vaccines targeting the attenuation of PLD gene, confers the best and longest-lasting immune response, due to its similarity to natural infection.
\n
\n
\n
9.8 Public health significance
\n
Human beings are rarely affected, some cases of human infections have been documented as occupational infection in veterinary doctors and assistant as well as farm experts.
\n
\n
\n
\n
10. Contagious caprine pleuropneumonia
\n
Contagious caprine pleuropneumonia (CCPP) is a highly contagious and rapidly spreading mycoplasmal disease of goat, occasionally sheep and wild ruminants. CCPP is characterized by severe sero-fibrinous pleuropneumonia, very high morbidity (100%), and mortality (80–100%) and results in heavy economic losses.
\n
\n
10.1 Etiology
\n
CCPP is caused by Mycoplasma capricolum subspecies capripneumoniae (Mccp), which was earlier known as Mycoplasma biotype F38. It belongs to the class Mollicutes that lack cell wall. M. ovipneumoniae, M. mycoides subspecies capri, and M. mycoides subspecies mycoides (Large Colony Type) are also considered as etiological agents of caprine pneumonia in the United States [1].
\n
\n
\n
10.2 Epizootiology
\n
CCPP is becoming a novel emerging and rapidly spreading disease in most parts of the world and at present, goat populations in more than 40 countries are affected with CCPP and sporadic cases of CCPP are also being reported from many more countries [37]. It mostly occurs in countries of Africa, Middle East and Asia.
\n
\n
\n
10.3 Transmission
\n
The disease is highly contagious and main mode of transmission is through inhalation of infected aerosols. The direct contact with affected animals is the main source of transmission. Airborne transmission can result in distant spread of about 50 m distance. However, the shorter survival time (3–14 days) of the organisms in external environment limits transmission of Mccp [38]. Yet under cold, moist and overcrowded environment these bacteria can persists for longer durations and may lead to severe outbreaks mostly in winter.
\n
\n
\n
10.4 Clinical signs
\n
CCPP is strictly a respiratory illness and is characterized by severe dyspnea, nasal discharge, cough, and fever. This can occur in peracute, acute and/or chronic forms in endemic areas. In peracute form, affected goats may die within 1–3 days without premonitory clinical signs. In acute infection, the initial signs are high fever (41–43°C), lethargy and anorexia, followed within 2–3 days by coughing and laboured breathing. The cough is frequent, violent and productive. In the final stages of infection, the goat may not be able to move and stands with its front legs wide apart and its neck stiff and extended [37]. Saliva can drip continuously from the mouth, and the animal may exhibit grunt or bleat in pain. Frothy nasal discharge and stringy saliva may be seen terminally. Pregnant goats may abort. Acutely affected goats generally die within seven to 10 days. In the chronic cases, there is chronic cough, nasal discharge and debilitation. These forms with resembling clinical signs in goats were also reported from captive wild goats.
\n
Pathological features during necropsy are also limited to respiratory system. Acute form is characterized by unilateral pneumonia and sero-fibrinous pleuritis with straw colored fluid in the thorax. The lung is granular with copious straw-colored exudates oozing out on cut section. Pea-sized, yellow-colored nodules may be noticed in lungs and these nodules are surrounded by areas of congestion. Varying degrees of lung consolidation or necrosis may also be noticed [37]. The regional lymph nodes mainly bronchial lymph nodes are enlarged. Some long-term survivors reveal chronic pleuropneumoniae or chronic pleuritis, with encapsulation of acute lesions and numerous adhesions to the chest wall. The interlobular septa are not usually thickened in domesticated goats.
\n
\n
\n
10.5 Diagnosis
\n
CCPP can be diagnosed based on cultural, biochemical, serological, and molecular methods following a tentative clinical diagnosis. Ultrasonography and X-rays may help in diagnosis and CCPP-associated changes may be evident in lungs, pleura, thorax, and associated structures. Cultural isolation and identification (‘fried egg-like appearance’ of the colonies under microscope), though is conventional but is still considered as standard method for detection of Mccp from lung tissue and/or pleural fluid at necropsy. Due to the difficulty in isolation, PCR is the technique of choice for the diagnosis of CCPP. The agglutination tests, ELISA, FAT, CFT (most widely used), passive or indirect haemagglutination tests (IHT) are the immunological methods employed for diagnosis of CCPP [38]. Latex agglutination test is being increasingly used in diagnostic laboratories as a pen side test. It can used to test whole blood as well as serum.
\n
\n
\n
10.6 Treatment
\n
Tylosin is considered the drug of choice against Mccp. Further, oxytetracycline is also found effective when administered in early stages of infection. However, some infections are slow to resolve.
\n
\n
\n
10.7 Preventive measures
\n
In endemic areas, proper care should be taken while introducing new goats into the flock. Flock testing, slaughter, and on-site quarantine may be helpful in controlling the spread of disease. Vaccines available in some areas may help in prevention of the disease. The commercially available CCPP vaccine containing inactivated Mccp suspended in saponin provides protection for over 1 year [37].
\n
\n
\n
\n
11. Dermatophilosis
\n
Dermatophilosis is a chronic, exudative and sometimes proliferative dermatitis occurs in domestic ruminants, wild animals and occasionally in human beings. Also known as Cutaneous streptothricosis, Strawberry foot rot or Lumpy wool.
\n
\n
11.1 Etiology
\n
Dermatophilosis is caused by Dermatophilus congolensis, which is a gram positive, nonacid-fast, facultative anaerobic actinomycete that produces motile zoospores.
\n
\n
\n
11.2 Epizootiology
\n
The disease occurs worldwide and is more common in tropics and subtropics. The organism is believed to be a saprophyte of soil and persists in dry scabs and crusts, to survive for up to 42 months. It has been reported from many countries, but occurs particularly in humid climates and areas where ticks of the genus Amblyomma are endemic [39].
\n
\n
\n
11.3 Transmission
\n
Transmission occurs by direct contact with infected animals. The infection can be transmitted indirectly by mechanical vectors (ectoparasites) and also through intradermal inoculation by contaminated thorny bushes. The pathogenesis may be influenced by factors such as mechanical injury to the skin, rainfall, tick infestation, concurrent diseases and/or stresses that compromise the host’s immune system.
\n
\n
\n
11.4 Clinical signs
\n
The disease is painful but non-pruritic, and is characterized by exudative, proliferative or hyperkeratotic dermatitis, accompanied by the production of crusts and folliculitis. In sheep, it may be seen in two forms: mycotic dermatitis (lumpy wool) and strawberry foot rot. While in goats and cattle, similar signs of crusty, suppurative dermatitis are seen and are often referred as cutaneous streptothricoses. The skin lesions appear raised, thick, yellow-brown colored discrete or confluents crusts containing matted hair. Sometimes may be seen in nodular form also with discrete encrustation of scab. The whole body may be affected but less hairy parts such as ears, axilla, scrotum, prepuce, ventral abdomen, limbs etc., show severe lesions [40]. Lesions in younger goats are mostly seen along the tips of the ears and under the tail. Most affected animals will recover within 3–4 weeks and lesions have little effect on overall health. In severe generalized infections, the animals often loose condition. If there are lesions at the feet, lips and muzzle, the movement of animals and eating become difficult.
\n
\n
\n
11.5 Diagnosis
\n
Diagnosis of dermatophilosis is mainly based clinical signs particularly based on the appearance of the characteristic skin lesions. The same can be confirmed by the demonstration of the organism from the lesions beneath the scabs. The softened scab materials stained by the Giemsa method, reveal the characteristic branching filaments containing zoospores. The organism can be cultured on blood agar at 37°C under 2.5–10% CO2 for up to 5 days and Haalstra technique based on chemotaxis of the zoospores to CO2 can be employed for efficient recovery of the organism.
\n
\n
\n
11.6 Treatment
\n
Animals can be treated with antibiotics such as high doses of penicillin or long acting tetracyclines. Topical applications alone are ineffective. Antibiotic therapy is augmented by topical treatment with lime sulfur as well as control of ectoparasites and biting flies. Povidone iodine shampoos or chlorhexidine solutions also help in clearing the disease.
\n
\n
\n
11.7 Preventive measures
\n
Control measures are based on minimizing the effects of predisposing factors and prompt treatment of affected goats. Animals with skin lesions must be isolated and treated at the earliest. Minimizing moist conditions (such as providing shelter during rainfall) is helpful in control and prevention. Grazing management especially removal of thorny bushes in pasture land that damages skin will also help. Prophylactic antibiotic therapy can also be given.
\n
\n
\n
11.8 Public health significance
\n
\nD. congolensis is a zoonotic organism and rare human infections have occurred from handling diseased animals.
\n
\n
\n
\n
12. Foot rot
\n
A contagious, either acute or chronic dermatitis of the hoof and its underlying tissues leading to lameness [41].
\n
\n
12.1 Etiology
\n
Foot rot is caused by Dichelobacter nodosus and Fusobacterium necrophorum, anaerobic, non-spore forming, gram negative rods.
\n
\n
\n
12.2 Epizootiology
\n
The organism F. necrophorum is ubiquitous in nature while D. nodosus is obligate pathogen, can be present in skin and hoof of animals and cannot survive much longer in environment. Moist environment, humid condition, wet grounds and overcrowding are the predisposing factors for foot rot [42].
\n
\n
\n
12.3 Clinical signs
\n
Interdigital region will be moist and will have a foul odor due to necrosis (Figure 8). Lameness is the common sign of foot rot. Based on the severity of the infection animals may lose weight due to anorexia and there will be decrease in production [43].
\n
Figure 8.
Moist, necrotic interdigital region seen in foot rot condition. This figure is propriety of the authors.
\n
\n
\n
12.4 Diagnosis
\n
Diagnosis is based on clinical signs and isolation of organism from the foot lesions. Since the organisms are anaerobic isolation is tricky and hence molecular diagnosis like PCR can be used for diagnosis.
\n
\n
\n
12.5 Treatment
\n
Hooves of the animals should be trimmed so as to remove the necrotic material thereby eliminating the anaerobic environment. Local antibiotics may be applied to the affected hoof after trimming. 10% zinc or copper sulfate or 10% formalin can be used for footbath [44].
\n
\n
\n
12.6 Preventive measures
\n
\nD. nodosus, though present in epidermal tissues of the hoof, survives for less than 7 days in the environment and hence, affected animals should be separated from the herd to prevent spread to other animals. Regular hoof trimming and cleaning should be practiced. Bacterins can be used as vaccines to prevent the infection.
\n
\n
\n
\n
13. Conclusions
\n
Goat is called as poor man’s cow but there are various bacterial diseases that cause economic loss to the goat farmers. Serval bacterial diseases cause acute infection hence there will be sudden onset of infection leading to huge mortality. Measures like use of vaccines before onset of disease, good management practices, etc., are essential to prevent the disease outbreaks. Animals with infection or clinical signs should be separated from rest of the animals so that infectious pathogens do not transmit to naïve animals and it is also recommended to quarantine newly purchased animals before admitting them into the farm. These practices can curtail the spread of infectious agents. It is also advisable to screen for diseases before purchasing the animals to the farm. Diseases like TB, JD and brucellosis should be screened before the purchase since these diseases are chronic in nature hence can remain undiagnosed. Animals infected with diseases that can affect human like anthrax, brucellosis, etc., should be handled carefully and better bio-security measures should be followed to prevent spread of disease within herd and also to human beings. Most of the bacterial infection can be treated with antimicrobial agents but these agents should be used judiciously because in the recent times antimicrobial resistance is a major problem.
\n
\n
Conflict of interest
The authors declare no conflict of interest.
\n',keywords:"Goat, Bacterial disease, Brucella, Anthrax, Preventive measures",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/76276.pdf",chapterXML:"https://mts.intechopen.com/source/xml/76276.xml",downloadPdfUrl:"/chapter/pdf-download/76276",previewPdfUrl:"/chapter/pdf-preview/76276",totalDownloads:593,totalViews:0,totalCrossrefCites:0,dateSubmitted:"November 9th 2020",dateReviewed:"March 26th 2021",datePrePublished:"April 13th 2021",datePublished:null,dateFinished:"April 13th 2021",readingETA:"0",abstract:"Bacterial diseases of goats can cause huge economical loss to the farmers. Due to intensification of goat farming and poor hygienic practices there is increase in the number of bacterial diseases that affect the goats. Diseases like tuberculosis, Johne’s disease and Brucellosis are chronic diseases that may be identified in the initial stages of infection during which they spread to other animals. Similarly, brucellosis, tuberculosis and also anthrax are zoonotic diseases hence due consideration has to be provided while handling animals suspected for these diseases. Use of vaccine before onset of the disease in endemic areas can prevent the disease outbreak and spread to other naïve population. Good hygienic practices and biosecurity measures at farm are essential to prevent disease spread. The present chapter deals with various bacterial diseases affecting goats and its preventive measures. This chapter can be a guide to field veterinarians, students and farmers as it highlights the important bacterial diseases of goats.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/76276",risUrl:"/chapter/ris/76276",signatures:"Kumaragurubaran Karthik and Manimuthu Prabhu",book:{id:"9706",type:"book",title:"Goat Science - Environment, Health and Economy",subtitle:null,fullTitle:"Goat Science - Environment, Health and Economy",slug:null,publishedDate:null,bookSignature:"Prof. Sándor Kukovics",coverURL:"https://cdn.intechopen.com/books/images_new/9706.jpg",licenceType:"CC BY 3.0",editedByType:null,isbn:"978-1-78984-709-3",printIsbn:"978-1-78984-708-6",pdfIsbn:"978-1-78985-193-9",isAvailableForWebshopOrdering:!0,editors:[{id:"25894",title:"Prof.",name:"Sándor",middleName:null,surname:"Kukovics",slug:"sandor-kukovics",fullName:"Sándor Kukovics"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Methods",level:"1"},{id:"sec_3",title:"3. Anthrax",level:"1"},{id:"sec_3_2",title:"3.1 Etiology",level:"2"},{id:"sec_4_2",title:"3.2 Epizootiology",level:"2"},{id:"sec_5_2",title:"3.3 Transmission",level:"2"},{id:"sec_6_2",title:"3.4 Clinical signs",level:"2"},{id:"sec_7_2",title:"3.5 Diagnosis",level:"2"},{id:"sec_8_2",title:"3.6 Treatment",level:"2"},{id:"sec_9_2",title:"3.7 Preventive measures",level:"2"},{id:"sec_10_2",title:"3.8 Public health significance",level:"2"},{id:"sec_12",title:"4. Brucellosis",level:"1"},{id:"sec_12_2",title:"4.1 Etiology",level:"2"},{id:"sec_13_2",title:"4.2 Epizootiology",level:"2"},{id:"sec_14_2",title:"4.3 Transmission",level:"2"},{id:"sec_15_2",title:"4.4 Clinical signs",level:"2"},{id:"sec_16_2",title:"4.5 Diagnosis",level:"2"},{id:"sec_17_2",title:"4.6 Preventive measures",level:"2"},{id:"sec_18_2",title:"4.7 Public health significance",level:"2"},{id:"sec_20",title:"5. Tetanus",level:"1"},{id:"sec_20_2",title:"5.1 Etiology",level:"2"},{id:"sec_21_2",title:"5.2 Epizootiology",level:"2"},{id:"sec_22_2",title:"5.3 Transmission",level:"2"},{id:"sec_23_2",title:"5.4 Clinical signs",level:"2"},{id:"sec_24_2",title:"5.5 Diagnosis",level:"2"},{id:"sec_25_2",title:"5.6 Treatment",level:"2"},{id:"sec_26_2",title:"5.7 Preventive measures",level:"2"},{id:"sec_28",title:"6. Enterotoxemia",level:"1"},{id:"sec_28_2",title:"6.1 Etiology",level:"2"},{id:"sec_29_2",title:"6.2 Epizootiology",level:"2"},{id:"sec_30_2",title:"6.3 Transmission",level:"2"},{id:"sec_31_2",title:"6.4 Clinical signs",level:"2"},{id:"sec_32_2",title:"6.5 Diagnosis",level:"2"},{id:"sec_33_2",title:"6.6 Treatment",level:"2"},{id:"sec_34_2",title:"6.7 Preventive measures",level:"2"},{id:"sec_36",title:"7. Johne’s disease (JD)",level:"1"},{id:"sec_36_2",title:"7.1 Etiology",level:"2"},{id:"sec_37_2",title:"7.2 Transmission",level:"2"},{id:"sec_38_2",title:"7.3 Clinical signs",level:"2"},{id:"sec_39_2",title:"7.4 Diagnosis",level:"2"},{id:"sec_40_2",title:"7.5 Treatment",level:"2"},{id:"sec_41_2",title:"7.6 Preventive measures",level:"2"},{id:"sec_42_2",title:"7.7 Public health significance",level:"2"},{id:"sec_44",title:"8. Pasteurellosis and Mannheimiosis",level:"1"},{id:"sec_44_2",title:"8.1 Etiology",level:"2"},{id:"sec_45_2",title:"8.2 Epizootiology and transmission",level:"2"},{id:"sec_46_2",title:"8.3 Clinical signs",level:"2"},{id:"sec_47_2",title:"8.4 Diagnosis",level:"2"},{id:"sec_48_2",title:"8.5 Treatment",level:"2"},{id:"sec_49_2",title:"8.6 Preventive measures",level:"2"},{id:"sec_51",title:"9. Caseous lymphadenitis",level:"1"},{id:"sec_51_2",title:"9.1 Etiology",level:"2"},{id:"sec_52_2",title:"9.2 Epizootiology",level:"2"},{id:"sec_53_2",title:"9.3 Transmission",level:"2"},{id:"sec_54_2",title:"9.4 Clinical signs",level:"2"},{id:"sec_55_2",title:"9.5 Diagnosis",level:"2"},{id:"sec_56_2",title:"9.6 Treatment",level:"2"},{id:"sec_57_2",title:"9.7 Preventive measures",level:"2"},{id:"sec_58_2",title:"9.8 Public health significance",level:"2"},{id:"sec_60",title:"10. Contagious caprine pleuropneumonia",level:"1"},{id:"sec_60_2",title:"10.1 Etiology",level:"2"},{id:"sec_61_2",title:"10.2 Epizootiology",level:"2"},{id:"sec_62_2",title:"10.3 Transmission",level:"2"},{id:"sec_63_2",title:"10.4 Clinical signs",level:"2"},{id:"sec_64_2",title:"10.5 Diagnosis",level:"2"},{id:"sec_65_2",title:"10.6 Treatment",level:"2"},{id:"sec_66_2",title:"10.7 Preventive measures",level:"2"},{id:"sec_68",title:"11. Dermatophilosis",level:"1"},{id:"sec_68_2",title:"11.1 Etiology",level:"2"},{id:"sec_69_2",title:"11.2 Epizootiology",level:"2"},{id:"sec_70_2",title:"11.3 Transmission",level:"2"},{id:"sec_71_2",title:"11.4 Clinical signs",level:"2"},{id:"sec_72_2",title:"11.5 Diagnosis",level:"2"},{id:"sec_73_2",title:"11.6 Treatment",level:"2"},{id:"sec_74_2",title:"11.7 Preventive measures",level:"2"},{id:"sec_75_2",title:"11.8 Public health significance",level:"2"},{id:"sec_77",title:"12. Foot rot",level:"1"},{id:"sec_77_2",title:"12.1 Etiology",level:"2"},{id:"sec_78_2",title:"12.2 Epizootiology",level:"2"},{id:"sec_79_2",title:"12.3 Clinical signs",level:"2"},{id:"sec_80_2",title:"12.4 Diagnosis",level:"2"},{id:"sec_81_2",title:"12.5 Treatment",level:"2"},{id:"sec_82_2",title:"12.6 Preventive measures",level:"2"},{id:"sec_84",title:"13. Conclusions",level:"1"},{id:"sec_88",title:"Conflict of interest",level:"1"}],chapterReferences:[{id:"B1",body:'\nUnderwood WJ, Blauwiekel R, Delano ML, Gillesby R, Scott A, Mischler SA, Schoell, A. Biology and Diseases of Ruminants (Sheep, Goats, and Cattle). Editor(s): Fox JG, Anderson LC, Otto GM, Pritchett-Corning KR, Whary MT, In American College of Laboratory Animal Medicine, Laboratory Animal Medicine (Third Edition): Academic Press; 2015. p. 623-694, https://doi.org/10.1016/B978-0-12-409527-4.00015-8.\n'},{id:"B2",body:'\nRahman MT, Sobur MA, Islam MS, Ievy S, Hossain MJ, El Zowalaty ME, Rahman AT, Ashour HM. Zoonotic Diseases: Etiology, Impact, and Control. Microorganisms. 2020;8(9):1405.\n'},{id:"B3",body:'\nShafazand S, Doyle R, Ruoss S, Weinacker A, Raffin TA. Inhalational Anthrax: Epidemiology, Diagnosis and Management. Chest. 2001; 116: 1369-1376.\n'},{id:"B4",body:'\nMisgie F, Atnaf A, Surafel K. A Review on Anthrax and its Public Health and Economic Importance. 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PLoS ONE. 2008; 3(7): e2760. doi:10.1371/journal.pone.0002760.\n'},{id:"B14",body:'\nKochar DK, Gupta BK, Gupta A, Kalla A, Nayak KC, Purohit SK. Hospital-based case series of 175 cases of serologically confirmed brucellosis in Bikaner. J Assoc Physicians India. 2007; 55:271-275.\n'},{id:"B15",body:'\nMuralidharan J, Ramesh V, Saravanan S. Tetanus in sheep of an organized livestock farm- a case report. Indian Journal of Field Veterinarians 2010; 5:43-44.\n'},{id:"B16",body:'\nHarish BR, Chandranaik BM, Bhanuprakash RA, Jayakumar SR, Renukaprasad C, Krishnappa G. Clostridium tetani infection in goats. Intas Polivet. 2006; 7: 72-74.\n'},{id:"B17",body:'\nPugh DG, Baird AN. Sheep and Goat Medicine,2nd edn. Saunders, an imprint of Elsevier Inc:Philadel-phia, PA; 2012. p. 621\n'},{id:"B18",body:'\nPopoff MR. Tetanus in animals. J Vet Diagn Invest. 2020;32(2):184-191. doi: 10.1177/1040638720906814.\n'},{id:"B19",body:'\nLotfollahzadeh S, Heydari M, Mohebbi MR, Hashemian M. Tetanus outbreak in a sheep flock due to ear tagging. Vet Med Sci. 2019;5(2):146-150. doi: 10.1002/vms3.139. Epub 2018 Dec 13. PMID: 30549234; PMCID: PMC6498517.\n'},{id:"B20",body:'\nCenters for Disease Control and Prevention. Epidemiology and Prevention of Vaccine Preventable Diseases. Hamborsky J, Kroger A, Wolfe S, eds. 13th ed. Washington DC: 348 Public Health Foundation, 2015.\n'},{id:"B21",body:'\nBlackwell TE, Butler DG. Clinical signs, treatment, and postmortem lesions in dairy goats with enterotoxemia: 13 cases (1979-1982). J Am Vet Med Assoc. 1992;200(2):214-217. PMID: 1559880.\n'},{id:"B22",body:'\nKarthik K, Manimaran K, Bharathi R, Shoba K. Report of enterotoxaemia in goat kids. Adv. Anim. Vet. Sci. 2017; 5(7): 289-292.\n'},{id:"B23",body:'\nUzal FA, Songer JG. Diagnosis of Clostridium perfringens intestinal infections in sheep and goats. Journal of Veterinary Diagnostic Investigation. 2008; 20: 253-265.\n'},{id:"B24",body:'\nKusiluka L, Kambarage D. Diseases of small ruminants in Sub-Saharan Africa - A handbook. 1996. p. 25-62\n'},{id:"B25",body:'\nSweeney RW, Collins MT, Koets AP, McGuirk SM, Roussel AJ. Paratuberculosis (Johne\'s disease) in cattle and other susceptible species. J Vet Intern Med. 2012;26(6):1239-1250. doi: 10.1111/j.1939-1676.2012.01019.x. Epub 2012 Oct 28. PMID: 23106497.\n'},{id:"B26",body:'\nMcGregor H, Dhand NK, Dhungyel OP, Whittington RJ. Transmission of Mycobacterium avium subsp. paratuberculosis: dose–response and age-based susceptibility in a sheep model. Prev Vet Med. 2012;107(1-2):76-84.\n'},{id:"B27",body:'\nWhittington R, Donat K, Weber MF, Kelton D, Nielsen SS, Eisenberg S, Arrigoni N, Juste R, Sáez JL, Dhand N, Santi A, Michel A, Barkema H, Kralik P, Kostoulas P, Citer L, Griffin F, Barwell R, Moreira MAS, Slana I, Koehler H, Singh SV, Yoo HS, Chávez-Gris G, Goodridge A, Ocepek M, Garrido J, Stevenson K, Collins M, Alonso B, Cirone K, Paolicchi F, Gavey L, Rahman MT, de Marchin E, Van Praet W, Bauman C, Fecteau G, McKenna S, Salgado M, Fernández-Silva J, Dziedzinska R, Echeverría G, Seppänen J, Thibault V, Fridriksdottir V, Derakhshandeh A, Haghkhah M, Ruocco L, Kawaji S, Momotani E, Heuer C, Norton S, Cadmus S, Agdestein A, Kampen A, Szteyn J, Frössling J, Schwan E, Caldow G, Strain S, Carter M, Wells S, Munyeme M, Wolf R, Gurung R, Verdugo C, Fourichon C, Yamamoto T, Thapaliya S, Di Labio E, Ekgatat M, Gil A, Alesandre AN, Piaggio J, Suanes A, de Waard JH. Control of paratuberculosis: who, why and how. A review of 48 countries. BMC Vet Res. 2019;15(1):198. doi: 10.1186/s12917-019-1943-4. PMID: 31196162; PMCID: PMC6567393.\n'},{id:"B28",body:'\nMcNees AL, Markesich D, Zayyani NR, Graham DY. Mycobacterium paratuberculosis as a cause of Crohn\'s disease. Expert Rev Gastroenterol Hepatol. 2015;9(12):1523-1534. doi:10.1586/17474124.2015.1093931.\n'},{id:"B29",body:'\nMohamed RA, Abdelsalam EB. A review on pneumonic pasteurellosis (respiratory mannheimiosis) with emphasis on pathogenesis, virulence mechanism and predisposing factors. Bulg. J. Vet. Med. 2008;11(3):139-160.\n'},{id:"B30",body:'\nLaishevtsev AI. IOP Conf. Ser. Earth Environ. Sci. 2020: 548 072038.\n'},{id:"B31",body:'\nHussain R, Mahmood F, Ali HM, Siddique AB. Bacterial, PCR and clinico-pathological diagnosis of naturally occurring pneumonic pasturellosis (mannheimiosis) during subtropical climate in sheep. Microb Pathog. 2017;112:176-181. doi: 10.1016/j.micpath.2017.09.061. Epub 2017 Sep 29. PMID: 28970175.\n'},{id:"B32",body:'\nSrinand S, Hsuan SL, Yoo HS, Maheswaran SK, Ames TR, Werdin RE. Comparative evaluation of antibodies induced by commercial Pasteurella haemolytica vaccines using solid phase immunoassays Veterinary Microbiology. 1996; 49:181-195.\n'},{id:"B33",body:'\nKuria JK, Mbuthia PG, Kang\'ethe EK, Wahome RG. Caseous lymphadenitis in goats: the pathogenesis, incubation period and serological response after experimental infection. Vet Res Commun. 2001; 25(2):89-97. doi: 10.1023/a:1006400617235. PMID: 11243659.\n'},{id:"B34",body:'\nOsman AY, Nordin ML, Kadir AA, Saharee AA. The Epidemiology and Pathophysiology of Caseous Lymphadenitis: A Review. J. Vet. Med. Res. 2018; 5: 1129.\n'},{id:"B35",body:'\nFontaine MC, Baird GJ. Caseous lymphadenitis. Small Rumin. Res. 2008; 76: 42-48.\n'},{id:"B36",body:'\nGuimarães AS, Carmo FB, Heinemann MB, Portela RWD, Meyer R, Lage AP, Seyffert N, Miyoshi A. Azevedo V, Gouveia AM. High sero-prevalence of caseous lymphadenitis identified in slaughterhouse samples as a consequence of deficiencies in sheep farm management in the state of Minas Gerais, Brazil. BMC Vet Res. 2011; 7:68. doi: 10.1186/1746-6148-7-68.\n'},{id:"B37",body:'\nYatoo MI, Parraya OR, Bashir ST, Muheet RA, Bhat, Gopalakrishnan A, Karthik K, Dhama, K, Singh SV. Contagious caprine pleuropneumonia – a comprehensive review. Veterinary Quarterly, 2019; 39 (1): 1-25\n'},{id:"B38",body:'\nOIE. World Organisation for Animal Health – contagious caprine pleuropneumonia. In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals, Chapter 2.7.5. Paris; 2014.\n'},{id:"B39",body:'\nLoria GR, La Barbera E, Monteverde V, Sparagano OAE, Caracappa S. Dermatophilosis in goats in Sicily. Veterinary Record. 2005; 156: 120-121\n'},{id:"B40",body:'\nMsami HM, Khaschabi D, Schöpf K, Kapaga AM, Shibahara T. Dermatophilus congolensis infection in goats in Tanzania. Trop Anim Health Prod. 2001 Oct;33(5):367-377. doi: 10.1023/a:1010587621843. PMID: 11556616.\n'},{id:"B41",body:'\nKaler J, Green LE. Naming and recognition of six foot lesions of sheep using written and pictorial information: A study of 809 English sheep farmers. Prev. Vet. Med. 2008; 83(1):52-64.\n'},{id:"B42",body:'\nGreen LE, George TRN. Assessment of current knowledge of foot rot in sheep with particular reference to Dichelobacter nodosus and implications for elimination or control estrategies for sheep in Great Britain. Vet. Journal 2008; 175:173-180.\n'},{id:"B43",body:'\nBennett G, Hickford J, Sedcole R, Zhou H. Dichelobacter nodosus, Fusobacterium necrophorum and the epidemiology of footrot. Anaerobe. 2009; 15: 173-176\n'},{id:"B44",body:'\nAbbott KA, Lewis CJ. Current approaches to the management of ovine footrot. The Veterinary Journal. 2005; 169: 28-41\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Kumaragurubaran Karthik",address:"karthik_2bvsc@yahoo.co.in",affiliation:'
Tamil Nadu Veterinary and Animal Sciences University, Chennai, Tamil Nadu, India
Tamil Nadu Veterinary and Animal Sciences University, Chennai, Tamil Nadu, India
'}],corrections:null},book:{id:"9706",type:"book",title:"Goat Science - Environment, Health and Economy",subtitle:null,fullTitle:"Goat Science - Environment, Health and Economy",slug:null,publishedDate:null,bookSignature:"Prof. Sándor Kukovics",coverURL:"https://cdn.intechopen.com/books/images_new/9706.jpg",licenceType:"CC BY 3.0",editedByType:null,isbn:"978-1-78984-709-3",printIsbn:"978-1-78984-708-6",pdfIsbn:"978-1-78985-193-9",isAvailableForWebshopOrdering:!0,editors:[{id:"25894",title:"Prof.",name:"Sándor",middleName:null,surname:"Kukovics",slug:"sandor-kukovics",fullName:"Sándor Kukovics"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},profile:{item:{id:"328576",title:"Prof.",name:"Zainalabidin",middleName:null,surname:"Mohamed",email:"zainal.mohamed@gmail.com",fullName:"Zainalabidin Mohamed",slug:"zainalabidin-mohamed",position:null,biography:null,institutionString:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",totalCites:0,totalChapterViews:"0",outsideEditionCount:0,totalAuthoredChapters:"1",totalEditedBooks:"0",personalWebsiteURL:null,twitterURL:null,linkedinURL:null,institution:{name:"Universiti Putra Malaysia",institutionURL:null,country:{name:"Malaysia"}}},booksEdited:[],chaptersAuthored:[{id:"73311",title:"Organizational Support and Sustainable Entrepreneurship Performance of SMEs, the Moderating Role of Strategic Sustainability Orientation",slug:"organizational-support-and-sustainable-entrepreneurship-performance-of-smes-the-moderating-role-of-s",abstract:"Small and medium sized enterprises’ (SMEs) activities have contributed significantly to environmental degradation that causes a disastrous effect on us and our future generation. Considering this, sustainable entrepreneurship has been promoted as a resolution of ecological problems capable of addressing climate change issues, public health, and safety concerns, and has become critical for competing in international markets. SMEs activities increased pollution exclusively causing environmental degradation. In response, the world is focusing on ensuring that SMEs produce products through safe and environmentally friendly practices. Literature suggests that organizational support provide SMEs with the impetus to achieve competitive advantage regarding turnover, customer attraction and market share opportunities to achieve business performance. Nonetheless, the implementation of sustainable entrepreneurship among them is still low due to numerous challenges. This paper intends to investigate the influence of organizational support on sustainable entrepreneurship towards performance among SMEs. A case study involving 300 herbal-based SMEs were surveyed using structured questionnaire. Data was analyzed using descriptive statistics, exploratory factor analysis, confirmatory factor analysis, and structural equation model. The results show that organizational support have a positive effect on sustainable entrepreneurship and performance among the SMEs, accounting for 52% and 47% variance respectively. This finding reveals that organizational support is significantly related to entrepreneurship performance, thus substantiates previous findings on the crucial roles of organizational support in enabling organizations to achieve sustainable entrepreneurship performance. This study contributes to triple bottom line literature based on incorporation of strategic choice theory, strategic sustainability orientation and resource-based view theory in entrepreneurship framework.",signatures:"Muhammad Auwal Abdullahi, Zainalabidin Mohamed, Mad Nasir Shamsudin, Juwaidah Sharifuddin and Fazlin Ali",authors:[{id:"321678",title:"Dr.",name:"Muhammad Auwal",surname:"Abdullahi",fullName:"Muhammad Auwal Abdullahi",slug:"muhammad-auwal-abdullahi",email:"muhammad.auwal@fud.edu.ng"},{id:"328576",title:"Prof.",name:"Zainalabidin",surname:"Mohamed",fullName:"Zainalabidin Mohamed",slug:"zainalabidin-mohamed",email:"zainal.mohamed@gmail.com"},{id:"328577",title:"Prof.",name:"Mad Nasir",surname:"Shamsudin",fullName:"Mad Nasir Shamsudin",slug:"mad-nasir-shamsudin",email:"mns@upm.edu.my"},{id:"328578",title:"Dr.",name:"Juwaidah",surname:"Sharifuddin",fullName:"Juwaidah Sharifuddin",slug:"juwaidah-sharifuddin",email:"juwaidah@upm.edu.my"},{id:"328579",title:"Dr.",name:"Fazlin",surname:"Ali",fullName:"Fazlin Ali",slug:"fazlin-ali",email:"fazlin_ali@upm.edu.my"}],book:{id:"10421",title:"Sustainable Organizations",slug:"sustainable-organizations-models-applications-and-new-perspectives",productType:{id:"1",title:"Edited Volume"}}}],collaborators:[{id:"292841",title:"Ph.D.",name:"Kassu",surname:"Jilcha Sileyew",slug:"kassu-jilcha-sileyew",fullName:"Kassu Jilcha Sileyew",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Addis Ababa University",institutionURL:null,country:{name:"Ethiopia"}}},{id:"321678",title:"Dr.",name:"Muhammad Auwal",surname:"Abdullahi",slug:"muhammad-auwal-abdullahi",fullName:"Muhammad Auwal Abdullahi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"322184",title:"Dr.",name:"Nkemdilim",surname:"Iheanachor",slug:"nkemdilim-iheanachor",fullName:"Nkemdilim Iheanachor",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"322642",title:"Mrs.",name:"Ngunan M.",surname:"Ikpaya",slug:"ngunan-m.-ikpaya",fullName:"Ngunan M. 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UK Research and Innovation (former Research Councils UK (RCUK) - including AHRC, BBSRC, ESRC, EPSRC, MRC, NERC, STFC.) Processing charges for books/book chapters can be covered through RCUK block grants which are allocated to most universities in the UK, which then handle the OA publication funding requests. It is at the discretion of the university whether it will approve the request.)
UK Research and Innovation (former Research Councils UK (RCUK) - including AHRC, BBSRC, ESRC, EPSRC, MRC, NERC, STFC.) Processing charges for books/book chapters can be covered through RCUK block grants which are allocated to most universities in the UK, which then handle the OA publication funding requests. It is at the discretion of the university whether it will approve the request.)
Wellcome Trust (Funding available only to Wellcome-funded researchers/grantees)
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The equipment required to perform the distillation process is known as distillation column. Since initial investment and maintenance costs for distillation columns are very high it is necessary to have an appropriate mathematical model that allows improving the comprehension of the column dynamics, especially its thermal behaviour, in order to enhance the control and safety of the process. This chapter presents a general panorama of the mathematical modelling of distillation columns, having as a specific case of study the comparison of a space-state non-linear model and a Takagi-Sugeno fuzzy model for a batch distillation column using a binary mixture (Ethanol-Water).",book:{id:"5452",slug:"distillation-innovative-applications-and-modeling",title:"Distillation",fullTitle:"Distillation - Innovative Applications and Modeling"},signatures:"Adriana del Carmen Téllez-Anguiano, Mario Heras-Cervantes, Juan\nAnzurez-Marín, Gerardo Marx Chávez-Campos and José Antonio\nGutiérrez Gnecchi",authors:[{id:"12387",title:"Dr.",name:"Jose Antonio",middleName:null,surname:"Gutierrez Gnecchi",slug:"jose-antonio-gutierrez-gnecchi",fullName:"Jose Antonio Gutierrez Gnecchi"},{id:"189166",title:"Dr.",name:"Adriana",middleName:null,surname:"Téllez-Anguiano",slug:"adriana-tellez-anguiano",fullName:"Adriana Téllez-Anguiano"},{id:"194844",title:"MSc.",name:"Mario",middleName:null,surname:"Heras-Cervantes",slug:"mario-heras-cervantes",fullName:"Mario Heras-Cervantes"},{id:"194845",title:"Dr.",name:"Juan",middleName:null,surname:"Anzurez-Marín",slug:"juan-anzurez-marin",fullName:"Juan Anzurez-Marín"},{id:"194846",title:"Dr.",name:"Gerardo",middleName:"Marx",surname:"Chávez-Campos",slug:"gerardo-chavez-campos",fullName:"Gerardo Chávez-Campos"}]},{id:"54078",title:"Distillation Techniques in the Fruit Spirits Production",slug:"distillation-techniques-in-the-fruit-spirits-production",totalDownloads:4985,totalCrossrefCites:15,totalDimensionsCites:26,abstract:"During the distillation of the fermented fruit mash or juice, ethanol and water are the carriers of a huge number of the other volatile aroma compounds. Unique and distinctive flavour of the final spirits depends on their quantity and quality. Fruit spirits have higher concentration of almost all types of volatile compounds with comparing to other types of distilled spirits. The art of distillation run is to obtain the best balance between congeners present. Two different types of distillation equipment are used for the production of fruit spirits: copper Charentais alembic and batch distillation columns. Although both distillation methods are based on the same theoretical principles, a different quantity of the flavour compounds of the final spirits is produced by using different distillation equipment. The main difference was shown in different distributions of the methanol, n-propanol, higher alcohols and fatty acid esters. Distillation methods need to be adjusted for each fruit spirits regardless to distillation equipment employed because fermented mash of different fruit varieties has a different requirement for distilling. Alembic stills yield better aroma and more characteristic fruit distillates but are slow and require more labour. Column still cleans the distillate giving a decent aroma and higher concentration of alcohol.",book:{id:"5452",slug:"distillation-innovative-applications-and-modeling",title:"Distillation",fullTitle:"Distillation - Innovative Applications and Modeling"},signatures:"Nermina Spaho",authors:[{id:"189124",title:"Associate Prof.",name:"Nermina",middleName:null,surname:"Spaho",slug:"nermina-spaho",fullName:"Nermina Spaho"}]},{id:"54676",title:"Fractional Distillation of Organic Liquid Compounds Produced by Catalytic Cracking of Fats, Oils, and Grease",slug:"fractional-distillation-of-organic-liquid-compounds-produced-by-catalytic-cracking-of-fats-oils-and-",totalDownloads:1749,totalCrossrefCites:0,totalDimensionsCites:2,abstract:"This work aims to investigate the fractional distillation of organic liquid products (OLP) obtained by catalytic cracking of palm oil (Elaeis guineensis Jacq.) at 450°C, 1.0 atm, with 5, 10, and 15% (wt) Na2CO3, using a stirred tank reactor of 143 L. The fractional distillations of OLP were carried out in laboratory scale with and without reflux using columns of different heights, and a pilot‐packed distillation column with internal reflux. OLP and distillation fractions (gasoline, kerosene, light diesel, and heavy diesel) were physicochemically characterized for density, kinematic viscosity, acid value, saponification value, refractive index, flash point, and copper strip corrosion. The OLP and light diesel fractions were analyzed by Fourier transform infrared spectroscopy (FT‐IR) and gas chromatography‐mass spectrometry (GC‐MS). For the experiments in laboratory scale, the yields of distillates decrease along with column height, with and without reflux, while those of bottoms products increase. The yields of distillates and gas increase with increasing Na2CO3 content, while those of bottoms products decrease. The densities of gasoline, kerosene, and light diesel produced in laboratory scale with reflux superpose exactly those of kerosene, light diesel, and heavy diesel produced in laboratory scale without reflux. The kinematic viscosity decreases with increasing column height for the experiments in laboratory scale. The acid values of distillation fractions decrease along with the column height for the experiments with and without reflux. The FT‐IR of distillation fractions in pilot and laboratory scales identified the presence of aliphatic hydrocarbons and oxygenates. The GC‐MS analysis identified OLP composition of 92.84% (area) hydrocarbons and 7.16% (area) oxygenates. The light diesel fraction contains 100% hydrocarbons with an acid value of 0.34 mg KOH/g, proving the technical feasibility of OLP de‐acidification by the fractional distillation process.",book:{id:"5452",slug:"distillation-innovative-applications-and-modeling",title:"Distillation",fullTitle:"Distillation - Innovative Applications and Modeling"},signatures:"C. C. Fereira, E. C. Costa, D. A. R. de Castro, M. S. Pereira, A. A.\nMâncio, M. C. Santos, D. E. L. Lhamas, S. A. P. da Mota, M. E. Araújo,\nLuiz E. P. Borges and N. T. 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He also obtained an MSc in Molecular and Genetic Medicine, and a Ph.D. in Clinical Immunology and Human Genetics from the University of Sheffield, UK. He also completed a short-term fellowship in Pediatric Clinical Immunology and Bone Marrow Transplantation at Newcastle General Hospital, England. Dr. Rezaei is a Full Professor of Immunology and Vice Dean of International Affairs and Research, at the School of Medicine, Tehran University of Medical Sciences, and the co-founder and head of the Research Center for Immunodeficiencies. He is also the founding president of the Universal Scientific Education and Research Network (USERN). Dr. Rezaei has directed more than 100 research projects and has designed and participated in several international collaborative projects. He is an editor, editorial assistant, or editorial board member of more than forty international journals. He has edited more than 50 international books, presented more than 500 lectures/posters in congresses/meetings, and published more than 1,100 scientific papers in international journals.",institutionString:"Tehran University of Medical Sciences",institution:{name:"Tehran University of Medical Sciences",country:{name:"Iran"}}},{id:"180733",title:"Dr.",name:"Jean",middleName:null,surname:"Engohang-Ndong",slug:"jean-engohang-ndong",fullName:"Jean Engohang-Ndong",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/180733/images/system/180733.png",biography:"Dr. Jean Engohang-Ndong was born and raised in Gabon. After obtaining his Associate Degree of Science at the University of Science and Technology of Masuku, Gabon, he continued his education in France where he obtained his BS, MS, and Ph.D. in Medical Microbiology. He worked as a post-doctoral fellow at the Public Health Research Institute (PHRI), Newark, NJ for four years before accepting a three-year faculty position at Brigham Young University-Hawaii. Dr. Engohang-Ndong is a tenured faculty member with the academic rank of Full Professor at Kent State University, Ohio, where he teaches a wide range of biological science courses and pursues his research in medical and environmental microbiology. Recently, he expanded his research interest to epidemiology and biostatistics of chronic diseases in Gabon.",institutionString:"Kent State University",institution:{name:"Kent State University",country:{name:"United States of America"}}},{id:"188773",title:"Prof.",name:"Emmanuel",middleName:null,surname:"Drouet",slug:"emmanuel-drouet",fullName:"Emmanuel Drouet",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/188773/images/system/188773.png",biography:"Emmanuel Drouet, PharmD, is a Professor of Virology at the Faculty of Pharmacy, the University Grenoble-Alpes, France. As a head scientist at the Institute of Structural Biology in Grenoble, Dr. Drouet’s research investigates persisting viruses in humans (RNA and DNA viruses) and the balance with our host immune system. He focuses on these viruses’ effects on humans (both their impact on pathology and their symbiotic relationships in humans). He has an excellent track record in the herpesvirus field, and his group is engaged in clinical research in the field of Epstein-Barr virus diseases. He is the editor of the online Encyclopedia of Environment and he coordinates the Universal Health Coverage education program for the BioHealth Computing Schools of the European Institute of Science.",institutionString:null,institution:{name:"Grenoble Alpes University",country:{name:"France"}}},{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},{id:"332819",title:"Dr.",name:"Chukwudi Michael",middleName:"Michael",surname:"Egbuche",slug:"chukwudi-michael-egbuche",fullName:"Chukwudi Michael Egbuche",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/332819/images/14624_n.jpg",biography:"I an Dr. Chukwudi Michael Egbuche. I am a Senior Lecturer in the Department of Parasitology and Entomology, Nnamdi Azikiwe University, Awka.",institutionString:null,institution:{name:"Nnamdi Azikiwe University",country:{name:"Nigeria"}}},{id:"284232",title:"Mr.",name:"Nikunj",middleName:"U",surname:"Tandel",slug:"nikunj-tandel",fullName:"Nikunj Tandel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/284232/images/8275_n.jpg",biography:'Mr. Nikunj Tandel has completed his Master\'s degree in Biotechnology from VIT University, India in the year of 2012. He is having 8 years of research experience especially in the field of malaria epidemiology, immunology, and nanoparticle-based drug delivery system against the infectious diseases, autoimmune disorders and cancer. He has worked for the NIH funded-International Center of Excellence in Malaria Research project "Center for the study of complex malaria in India (CSCMi)" in collaboration with New York University. The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. Received the CSIR-SRF (Senior Research Fellow) award-2018, FIMSA (Federation of Immunological Societies of Asia-Oceania) Travel Bursary award to attend the IUIS-IIS-FIMSA Immunology course-2019',institutionString:"Nirma University",institution:{name:"Nirma University",country:{name:"India"}}},{id:"334383",title:"Ph.D.",name:"Simone",middleName:"Ulrich",surname:"Ulrich Picoli",slug:"simone-ulrich-picoli",fullName:"Simone Ulrich Picoli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334383/images/15919_n.jpg",biography:"Graduated in Pharmacy from Universidade Luterana do Brasil (1999), Master in Agricultural and Environmental Microbiology from Federal University of Rio Grande do Sul (2002), Specialization in Clinical Microbiology from Universidade de São Paulo, USP (2007) and PhD in Sciences in Gastroenterology and Hepatology (2012). She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. Dr. Aqib joined the Department of Clinical Medicine and Surgery at UAF for one year as an assistant professor where he developed a research laboratory designated for pathogenic bacteria. Since 2018, he has been Assistant Professor/Officer in-charge, Department of Medicine, Manager Research Operations and Development-ORIC, and President One Health Club at Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan. He has nearly 100 publications to his credit. His research interests include epidemiological patterns and molecular analysis of antimicrobial resistance and modulation and vaccine development against animal pathogens of public health concern.",institutionString:"Cholistan University of Veterinary and Animal Sciences",institution:null},{id:"62900",title:"Prof.",name:"Fethi",middleName:null,surname:"Derbel",slug:"fethi-derbel",fullName:"Fethi Derbel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62900/images/system/62900.jpeg",biography:"Professor Fethi Derbel was born in 1960 in Tunisia. He received his medical degree from the Sousse Faculty of Medicine at Sousse, University of Sousse, Tunisia. He completed his surgical residency in General Surgery at the University Hospital Farhat Hached of Sousse and was a member of the Unit of Liver Transplantation in the University of Rennes, France. He then worked in the Department of Surgery at the Sahloul University Hospital in Sousse. Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). He was also awarded 'Outstanding Clinician in General Medicine” by Venus International Foundation for his extensive research expertise and services, perform over and above the standard expected in the advancement of healthcare, patient safety and quality of care.",institutionString:"Interfaith Medical Center",institution:{name:"Interfaith Medical Center",country:{name:"United States of America"}}},{id:"93517",title:"Dr.",name:"Clement",middleName:"Adebajo",surname:"Meseko",slug:"clement-meseko",fullName:"Clement Meseko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/93517/images/system/93517.jpg",biography:"Dr. Clement Meseko obtained DVM and PhD degree in Veterinary Medicine and Virology respectively. He has worked for over 20 years in both private and public sectors including the academia, contributing to knowledge and control of infectious disease. Through the application of epidemiological skill, classical and molecular virological skills, he investigates viruses of economic and public health importance for the mitigation of the negative impact on people, animal and the environment in the context of Onehealth. \r\nDr. Meseko’s field experience on animal and zoonotic diseases and pathogen dynamics at the human-animal interface over the years shaped his carrier in research and scientific inquiries. He has been part of the investigation of Highly Pathogenic Avian Influenza incursions in sub Saharan Africa and monitors swine Influenza (Pandemic influenza Virus) agro-ecology and potential for interspecies transmission. He has authored and reviewed a number of journal articles and book chapters.",institutionString:"National Veterinary Research Institute",institution:{name:"National Veterinary Research Institute",country:{name:"Nigeria"}}},{id:"158026",title:"Prof.",name:"Shailendra K.",middleName:null,surname:"Saxena",slug:"shailendra-k.-saxena",fullName:"Shailendra K. Saxena",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRET3QAO/Profile_Picture_2022-05-10T10:10:26.jpeg",biography:"Professor Dr. Shailendra K. Saxena is a vice dean and professor at King George's Medical University, Lucknow, India. His research interests involve understanding the molecular mechanisms of host defense during human viral infections and developing new predictive, preventive, and therapeutic strategies for them using Japanese encephalitis virus (JEV), HIV, and emerging viruses as a model via stem cell and cell culture technologies. His research work has been published in various high-impact factor journals (Science, PNAS, Nature Medicine) with a high number of citations. He has received many awards and honors in India and abroad including various Young Scientist Awards, BBSRC India Partnering Award, and Dr. JC Bose National Award of Department of Biotechnology, Min. of Science and Technology, Govt. of India. Dr. Saxena is a fellow of various international societies/academies including the Royal College of Pathologists, United Kingdom; Royal Society of Medicine, London; Royal Society of Biology, United Kingdom; Royal Society of Chemistry, London; and Academy of Translational Medicine Professionals, Austria. He was named a Global Leader in Science by The Scientist. 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