Illustrated veterinary pathology (General & systemic pathology)

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Illustrated veterinary pathology (General & systemic pathology)

  1. 1. IllustratedVeterinary Pathology(General & SystemicPathology)Prof. R.S. ChauhanMVSc., PhD. (Path.), FNAVS, FSIIP,FIAVPInternational Book Distributing Co.
  2. 2. ILLUSTRATEDVETERINARY PATHOLOGY(General & Systemic Pathology)A widely preferred text book of Veterinary Pathology for second yearBVSc & AH students under Veterinary Council of India (VCI) SyllabusProf. R.S. ChauhanMVSc., PhD. (Path.), FNAVS, FSIIP, FIAVPJoint Director (CADRAD)Centre for Animal Disease Research and DiagnosisIndian Veterinary Research InstituteIzatnagar - 243 122 Bareilly, U.P. IndiaE-mail: rs_chauhan123@rediffmail.comInternational Book Distributing Company(Publishing Division)
  3. 3. Published byInternational Book Distributing Co.(Publishing Division)Khushnuma Complex Basement7, Meerabai Marg (Behind Jawahar Bhawan)Lucknow 226 001 U.P. (INDIA)Tel. :91-522-2209542,2209543,2209544,2209545Fax: 0522-4045308E-Mail: ibdco@airtelbroadband.inFirst Edition 2002Second Revised and Enlarged Edition 2007ISBN 978-81-8189-137-2©PublisherNo part ofthis publication may be reproduced, stored in a retrieval system,or transmitted, in any form or by any means, electronic, mechanical,photocopying, recording or otherwise, without the prior written permissionofthe publisher.Composed & Designed at :Panacea Computers3rd Floor, Agrawal Sabha BhawanSubhash Mohal, Sadar Cantt. Lucknow-226 002Phone: 0522-2483312,9335927082E-mail: prasgupt@rediffmail.comPrinted at:Salasar Imaging SystemsC-7/5, Lawrence Road Industrial AreaDelhi - 110035Tel. : 011-27185653, 9810064311
  4. 4. FOREWORD TO THE FIRST EDITIONThe past few decades have seen a tremendous change in concepts of livestockand poultry diseases, many new diseases being added up. The large quantity ofinformation unearthed, most coming in small analytical bits, undigested and unrelated,needed to be properly categorized, and incorporated in books in updated form.The book, "Illustrated Veterinary Pathology" written by Dr. R.S. Chauhan,NatIonal FellowlProfes~or, Department ofPathology, College ofVeterinary Sciences,G.B. Pant University of Agriculture and Technology, Pantnagar, is an appropriateattempt to fill the gap in the study ofVeterinary Pathology. The syllabi ofVeterinarySciences has been changed as per modem requirements and has been in vogue inalmost all the Veterinary Colleges of the country. The book prepared as per therequirement of the new syllabus of Veterinary Council of India, has been dividedinto two sections.The General Pathology section covers topics including introductory part,historical milestones, general concepts ofpathology such as degenerative and vascularchanges, healing, concretions, calcification, growth disturbances and inflammationand their etiological factors. Each pathological condition has been described with rel-evant photographs and diagrams to make it more understandable. Similarly, sectiontwo has been divided in ten chapters covering systemic pathology of animals andpoultry. Pathology of each organ and system has been nicely presented withmacroscopic and microscopic features supported by photographs and diagrams. Thepractical aspect has been covered in appendices containing post-mortem techniques,VIscera examination, collection and preservation ofmaterial, necropsy of veterolegalcases and dispatch of material to forensic laboratory for diagnosis. Steps of post-mortem examination are suitably presented with photographs and diagrams. In theend of each chapter, model questions are given for self assessment of the studentsand is one of the unique feature of the book.I am sure the book will prove of immense value to the students, teachers andveterinarians for better understanding ofVeterinary Pathology and disease processes.N.P. SingbFormer Prof. Path. and DeanFaculty of Veterinary Sciences, PantnagarInternational Consultant I1CA,Fed. Mini. Agri. (Nigeria)/World Bank
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  6. 6. PREFACE TO THE SECOND EDITIONSince the first edition ofthis book "Illustrated Veterinary Pathology" exhausted,I received messages in the form of letters, phones, SMSs, etc. from the students ofBVSc&AH, from different parts of the country to bring out its second edition andmake it available to the students. During last 4 years various suggestions and appre-ciations were also received about the book. Illustrated Veterinary Pathology book hasbeen revised as per the need of its readers. Differential features ofvarious Pathologi-cal conditions are given to present in an easily understandable form. Various chaptersare updated with some new photographs. The latest classification ofviruses has beenincorporated in the chapter Etiology. Students ofVeterinary Pathology will find it suit-able for their study and to prepare for competitive examinations like ICAR, NET,ASRB, etc. Feedback received from the readers is given due care while preparingsecond edition of the book and most of the suggestions are incorporated.In my opinion, it will become were useful to not only the students but also to theteachers, field veterinarians and diagnosticians. I must extend thanks to all those whohelped me in this meticulous task.Centre for Animal Disease Research and Diagnosis (CADRAD),Indian Veterinary Research Institute, Izatnagar-243 122, Bareilly (UP) IndiaEmail: rs_chauhan123@rediffmail.comRS Chauhan
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  8. 8. PREFACE TO THE FIRST EDITIONEver since the VCI course curriculum was implemented, need ofsuitable literaturefor students was felt at many fora. In the busy curriculum of veterinary sciences, thesubject ofpathology forms a vital link between basic subjects ofanatomy, biochemistryand physiology on one hand, and the clinical subjects of surgery, gynaecology andmedicine, on the other. The students face difficulty in understanding pathology sincethey are confronted with the dilemma ofchoosing between exhaustive and voluminousbooks ofVeterinary Pathology, most ofthem without photographs/illustrations. Majorityof available textbooks on Veterinary Pathology are written by western authors andEnglish being a foreign language in this country, most of our students find it hard tounderstand and reproduce the highly technical subject from these books. Most of theavailable textbooks were written a decade or more than that back,and are out datedin present scenario. Needless to say that some ofthe books written by Indian authorsare also too exhaustive and without illustrations, thu!>, creating confusion in the mindof students.In preparing this textbook, I have kept these problems in mind and recalled thedifficulties I faced as a student. How far have I succeeded in my endeavour is for thestudents and my professional colleagues to judge.The very purpose of the Illustrated Veterinary Pathology is to provide theundergraduate Veterinary students a textbook with diagrams and photographs to makethe text comprehensive. To broaden the scope further, laboratory methods, includingpost-mortem examination, histopathological procedures and clinicopathologicalprocedures are also included in the appendices.Physically, the book is of the standard textboo~ size, each chapter being wellillustrated and provided with salient features of macroscopic and microscopicobservations. The book is divided into two sections ofGeneral Pathology and SystemicPathology. The text provides a complete, uptodate and concise coverage of thetraditionally difficult subject in simple, lucid and clear language. Wherever newterms/unfamiliar words appear in the text, they are first defined and explained. Thematerial has been organized meticulously in such a way that the student can easilyunderstand, retain and reproduce it. Various levels of headings, sub-headings, boldtype set and italics given in the text are meant to aid the student for quick revision ofthe subject. Another major point ofthis book is inclusion oforiginal and high standardquestions including fill in the gaps, true/false, definitions, short notes and multiplechoice questions (MCQ), which are not only helpful in their self-assessment but also
  9. 9. in preparation for competitive examinations like ICARjunior research fellowship (JRF)etc.In a work of this magnitude, it is natural for the sole author of a book to solicithelp and cooperation from others. The most overwhelming enthusiasm, good will,love and affection have generously come from my students for which I shall remainalways indebted to them. I wish to express gratitude to the Vice-Chancellor, Dr. J.B.Chowdhary, who always encouraged me to produce such a useful textbook forundergraduate students. The SUppOlt and encouragement from Dr. Harpal Singh, Dean,PGS & former Dean, V.Sc., Dr. Amresh Kumar, Dean, V.Sc. and Dr. S.P. Singh,Head, Pathology in accomplishing this academic work is thankfully acknowledged. Iwish to thank my colleagues who helped me a lot during preparation ofthe text book,including Dr. G.K. Singh, Prof. & Head, Anatomy, Dr. D.K. Agrawal, Assoc. Prof.,Pathology and Dr. Avadhesh Kumar, SMS. The valuable suggestions and criticismfrom Dr. Lokesh Kumar, Dr. B.P. Singh, Dr. Rajesh Kumar and Dr. Sumeet Bagga isthankfully acknowledged. My teacher, Dr. Nagendra P. Singh, Ex-professor Pathologyand Dean, Veterinary Sciences, has been a source of constant inspiration andencouragement to me for successful completion ofthis work. Some ofthe illustrationsprovided by Dr. Ramesh Somvanshi, IVRI, Dr. Arup Das, Dr. Stayendra Kumar, Dr.Avadhesh Kumar, Dr. R. Sharma, Dr. G.K. Singh and others are duly acknowledged.I am thankful to Agricultural Research Service, United States, Department ofAgriculture (ARS/USDA) for the photographs of various unusual and rare diseaseconditions and consent to produce them in this text book for the benefit of students.The meticulous type setting and photograph setting by Sri. Navin Joshi and TasabberKhan are thankfully acknowledged.Finally, I would be failing in my duties, if I fail to mention the contributions ofmy family. The cooperation and help provided by my wife, Mrs. Vandana, and thechildren, Ms. Mahima and Master Yatishwar cannot be overlooked because it wastheir time that I used to spend in preparation of this book.Lastly, in spite of my best efforts at perfection, element ofhuman error is stilllikely to creep in which the readers are welcome to point out since that would helpme in improving the text book further.College of Veterinary SciencesG.B. Pant University of Agri. & Tech.Pantnagar- 263145. Uttaranchal, INDIAE-mail: rs_chauhan123@rediffmail.comAugust, 2001R.S. CHAUHANM.V.Sc. Ph.D. FNAVSNational FellowDepartment of Pathology
  10. 10. CONTENTSPart A: General Veterinary Pathology1. Introduction ............................................................................................ 12. Etiology ................................................................................................ 133. Genetic disorders developmental anomalies and monsters ....................... 354. Disturbances in growth .,........................................................................ 435. Disturbancesincirculation ..................................................................... 496. Disturbances incell metabolism .............................................................. 587. Necrosis, gangrene and post-mortem changes ........................................ 658. Disturbances incalcificationandpigment metabolism .............................. 769. Inflammationandhealing ........................................................................ 8410. Concretions........................................................................................ 11311. ImmunityandImmunopathology .......................................................... 118Part B: ,Systemic Pathology12. Pathologyofcutaneous system ............................................................ 13713. Pathologyofmusculoskeletal system .................................................... 14714. Pathologyofcardiovascularsystem ...................................................... 15615. Pathologyofrespiratorysystem ........................................................... 16816. Pathologyofdigestive system .......................................................,...... 18317. Pathologyofhemopoietic and immune system ....................................... 20418. Pathologyofurinarysystem ................................................................. 21519. Pathologyofgenital system .................................................................. 22620. Pathologyofnervous system ................................................................ 23721. Pathologyofendocrine system, eyes and ear........................................ 24422. Appendix ............................................................................................ 25123. Index .................................................................................................. 294
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  12. 12. Part AGeneral Veterinary Pathology
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  14. 14. 1INTRODUCTION• Definitions• Historical Milestones• Model Questions
  15. 15. General Veterinary PathologyDEFINITIONSPathologyPathology is the study of the anatomical, chemicaland physiological alterations from normal as aresult of disease in animals. It is a key subjectbecause it forms a vital bridge between preclinicalsciences (Anatomy, Physioiogy, Biochemistry) andclinical branches of medicine and surgery.Pathology is derived from the Greek word pathos= disease, logos = study. It has many branches,which are defmed as under:General PathologyGeneral Pathology concerns with basic alterationsof tissues as a result of disease. e.g. fatty changes,thrombosis, amyloidosis, embolism, necrosis (Fig.1.1 ).Systemic PathologySystemic Pathology deals with alterations intissues/organs of a particular system. e.g.respiratory system, genital system etc. (Fig. 1.2).Specific PathologySpecific Pathology is the application of the basicalterations learned in general pathology to variousspecific diseases. It involves whole body or a partofbody. e.g. tuberculosis, rinderpest.Experimental PathologyExperimental Pathology concerns with theproduction of lesion through experimental methods.e.g. Rotavirus 7 calves 7 enteritis/ diarrhoea incalves (Fig. 1.3).Clinical PathologyClinical Pathology includes certain laboratorymethods which help in making the diagnosis usinganimal excretions/secretions/blood/skin scrapingslbiopsy etc. e.g. urine examination, bloodexamination (Fig. 1.4).Post-mortem PathologyPost-mortem Pathology is examination of ananimal after death. Also known as Necropsy orAutopsy. It forms the base for study of pathology(Fig. 1.5).2Microscopic PathologyMicroscopic Pathology deals with examination ofcells/tissues/organs using microscope. It is alsoknown as histopathology/cellular pathology. e.g.microscopy, electronmicroscopy (Figs. 1.6 & 1.7).Humoral PathologyHumoral Pathology is the study of alterations influids like antibodies in serum (Fig. 1.8).Chemical PathologyChemical Pathology ·is the study of chemicalalterations of body fluids/tissues. e.g. enzymes intissue.Physiological PathologyPhysiological Pathology deals with alteration in thefunctions of organ/system. It is also known asPathophysiology. e.g. indigestion, diarrhoea,miscarriage (Fig. 1.9).Nutritional PathologyNutritional Pathology is the study of diseases dueto deficiency or excess of nutrients. e.g. Vit.-Adeficiency induced nutritional roup, rickets due tocalcium deficiency (Fig. 1.10).Comparative PathologyComparative Pathology is the study of diseases ofanimals with a comparative study in human beingsand other animals. e.g. zoonotic diseases such astuberculosis (Fig. 1.11).OncologyOncology is the study of cancer/tumor/neoplasms.ImmunopathologyImmunopathology deals with the study of diseasesmediated by immune reactions. It includesImmunodeficiency diseases, autoinununity andhypersensitivity reactions (Fig. 1.12).CytopathologyCytopathology is the study of cells shed off fromthe lesions for diagnosis.
  16. 16. /IltroductiollFig. 1.1 Necrosis in liverFig. 1.2. Female genital system ofpoulayFig. 1.3. ExperimentalPathologyFig. 1.4. Examination ofblood for protozoan parasites3Fig. 1.5. Post-mortem examination ofpoulayFig. 1.6. Histopathological examination ofsldn sectionshowinj? inclusions ofpoxvirus infection.Fig. 1.7. Electronmicrophotograph showingpoxvirus in cytoplasm ofa cellFig. I.B. Detection ofantibodies in serumusinj? EL/SA
  17. 17. General Veterinary PathologyHealthHealth is a state of an individual Iiving in completeharmony with his environment/surroundings (Fig.1.13). .DiseaseDisease is a condition in which an individual showsan anatomical, chemical or physiological deviationfrom the normal. (Discomfort with environment &body) (Fig. 1.14).IllnessIllness is the reaction of an individual to disease inthe form of illness.Forensic PathologyForensic Pathology includes careful examinationand recording of pathological lesions in case ofveterolegal cases.HomeostasisHomeostasis is the mechanism by which bodykeeps equilibrium between health and disease. e.g.Adaptation to an altered environment.ToxopathologyToxopathology or Toxic Pathology deals with thestudy of tissue/organ alterations due totoxins/poisons (Fig.I.15).EtiologyEtiology is the study of causation of disease (Fig.1.16).DiagnosisDiagnosis is an art of precisely knowing the causeof a particular disease (Dia= thorough, gnosis=knowledge) (Fig 1.17).SymptomsAny subjective evidence of disease of animalcharacterized by an indication of altered bodily ormental state as told by owner (complaints of thepatients).SignsIndication of the existence of something, anyobjective evidence of disease, perceptible to4veterinarian (observations ofthe clinicians).SyndromeA combination of symptoms caused by alteredphysiological process.LesionLesion is a pathological alteration in structure/function that can be detectable (Fig. 1.18).PathogenesisPathogenesis is the progressive development of adisease process. It starts with the entry of causalagent in body and ends either with recovery ordeath. It is the mechanism by which the lesions areproduced in body.Incubation periodIncubation period is the time that elapses betweenthe action of a cause and manifestation ofdisease.Course of diseaseCourse of disease is the duration for which thedisease process remains till fate either in the formofrecovery or death.PrognosisPrognosis is an estimate by a clinician of probableseverity/outcome of disease.Morbidity rateMorbidity rate is the percentage/proportion ofaffected animals out of total population in aparticular disease outbreak. e.g. out of 100 animals20 are suffering from diarrhoea, the morbidity rateof diarrhoea will be 20%.Mortality rateMortality rate is the percentage/proportion ofanimals out of total population died due to diseasein a particular disease outbreak. e.g. if in apopulation of 100 animals, 20 fall sick and 5 died,the mortality rate will be 5%.Case fatality rateCase fatality rate is the percentage/proportions of
  18. 18. Fig.1.9. A calfshowing diarrhoeaFig. 1.10. Calcium deficiency causing ricketsin calfFig. 1.11. Transmission ofdisease fromanimals to man.FIg. J.12. Lamb showing DTH reaction on neckIntroductionFig. 1.13. A healthy calfFig. 1.14. Lamb suffering from pneumoniaFig. 1.16. Rotavirus - A cause ofdiarrhoea5
  19. 19. General Veterinary PathologyFig. 1.17. Diagnosis ofdiseases in animals.animals died among the affected animals. If in apopulation of 100 animals, 20 fall sick and 5 die,.the case fatality rate will be 25%.BiopsyBiopsy is the examination of tissues received fromliving animals.InfectionInfection is the invasion of the tissues of the bodyby pathogenic organisms resulting in thedevelopment of a disease process.Fig. 1.lB. Haemorrhagic lesion in heartInfestationInfestation is the superficial attack of anyparasite/organism on the surface ofbody.PathogenicityPathogenicity is the capability of an organism forproducing a disease.VirulenceVirulence is the degree of invasiveness ofpathogenic organism.HISTORICAL MILESTONES2500·1500 BC2100 BCShalihotra(Indian)Muni Palkapya(Indian)Hammurabi• First known veterinarian ofthe world• Wrote Haya Ayurvedl Ashwa- Ayurved in Sanskrit, 8volumes on equine medicine with diagnosis, treatment,effect of planetary forces and evils on health• Wrote a treatise on elephants - Gaj AyurvedConduct of Veterinary Practitioners, "Laws of Hammurabi"6
  20. 20. 1000 BC800 BC500 BC460-375 BC384-323 BC300 BC53 BC-37 AD131-206 AD450-500 AD600 ADKrishna(Indian)Nakul (4thPandav)(Indian)Sahdev(5thPandav)(Indian)Charak(Indian)leevak (Indian)Hippocrates(Greece)Aristotle(Greece)Chandra GuptaMaurya periodSarnrat AshokCornelius Celsus(Rome)Claudius Galen(Rome)Renatus Vegetius(Rome)MadhavIntroduction• Mathura is known for best cattle production/milkproduction• Wrote Ashwa- Chikitsa, a book on equine medicine.• He is considered as an expert of equine management• Expert in cattle rearing and disease management.• Wrote Charak Sanhita with details of cause of diseasesand impact ofenvironment.• Described the pathology ofbrain.• Physician, studied malaria, pneumonia , also known as"Father of Medicine"• Humoral theory of disease• Father ofZoology• Originator ofModern Anatomy & Physiology• In Kautilya, Arthshashtra description on "AnimalHusbandry and Veterinary Sciences", rules on animalethics and jurisprudence• First Veterinary Hospital established for treatment ofanimal diseases• Prevention of cruelity on animals advertised throughwritings on walls.• Wrote 8 volumes ofpathology (IsI special pathology)Cardinal signs of inflammation (redness, swelling, heatand pain)• Meat inspection• 5thcardinal sign of inflammation "Loss of function"• Father ofVeterinary Medicine• Disregard divine pleasure• Disease of animals influence on man• Described pathology ofdiarrhoea, dysentery, icterus,tuberculosis and various toxic conditions.7
  21. 21. 980-1037 AD1497 AD-1558 AD1564 AD-1642 AD1578-1657 AD1617 AD-1619 AD1617-1680 AD1632 AD-1723 AD1682-1771 AD1712-1779 AD1728- 1793 AD1753-1793 AD1762 AD1771-1802 AD1801-1858 AD1804-1878 AD1818-1865 ADGeneral Veterinary PathologyAvicennaJean FemelGalileo GalileiWilliam HarveyDrebbelSolleysel(French)Antony vanLeeuwen-hoekG.B. Morgagni(Italian)Bourgelat, C(French)John Hunter(English)Saint Bel(French)Bourgelat, C(French)Bichat(French)Mueller. J.(German)Carl Rokitan-Skey (German)Semmelwiss(Hungarian)• Cause of disease are minute organism• Spreads through air, food, water.• Compiled the information ofhis time First to attempt tocodify the knowledge ofPathology.• Developed single microscope• Blood vascular system and its impact on pathology• Developed double lens microscope• Book on Le Parfact Marechal• Saw microbes fIrst• Book - Little animals• Conducted 700 autopsies• Began modem pathology• Book The seats and causes ofdisease• New knowledge of equine medicine• First experimental pathologist• Teacher at Alfort established Vet School in England 1791and in 1793 died due to glanders.• 1st Veterinary school established - Ecole VeterinaireNationaled Alfort• Father ofpathological anatomy• Foundation for the study of histology• Father of histology• Cellular pathologist, known for his work "The fInestructure and form ofmorbid tumors"• Supreme descriptive pathologist• Surgery/autopsy• Started hospital sanitation8
  22. 22. 1821-1902 AD1822-1895 AD1839-1884 AD1843-1890 AD1850-1934 AD1869 AD1883-1962 AD1884 AD1884-1955 AD1885-1979 AD1889 AD1905-1993 AD1913 AD1924 AD1926 AD1931 ADR. Virchow(German)Louis Pasteur(French)J. Colmheim(German)R. Koch(German)W.H. Welch(U.S.A)Bruck Muller(USA)G.N. PapanicolaouE. MetchnikoffRobert Feulgen(German)WilliamBo.Yci(Canadian)L. Ackerman(American)IndiaIndiaE. JoestIndiaIntroduction• Journal Virchows Archives• Great work on cellular pathology, "Father of modernPathology"• Bacteria cause of disease• Originator of modern experimental pathology• Detected 1eucocytes at the site of inflammation• His work forms the basis for the pathology ofinflammation• Introduced frozen sections• Kochs postulates• Identified Tuberculosis, Staphylococcus and Vibrio ascause of disease• Professor Pathology• Started pathology in USA.• Textbook ofpathological anatomy of domestic and zooanimals.• Father of exfoliative cytology• Phagocytosis (microphages/macrophages)• Founder ofHistochemistry.• Aftthot ofTextbook ofPathology• Establishment of Imperial Bacteriological Laboratory atMukteshwar (Now IVRI)• Authority on interpretation of frozen sections.• Imperial Bacteriological Laboratory (now IVRI)established at new campus at Izatnagar- Bareilly• The Publication of Indian Veterinary Journal started• Wrote 5 volumes of Veterinary Pathology• The publication ofIndian Journal of Veterinary Sciencesand Animal Husbandry (Presently Indian Journal ofAnimal Sciences) started9
  23. 23. 1933 AD1936 AD1938 AD1953 AD1968 AD1973 AD1976 AD1983 AD1989 AD1998 ADGeneral Veterinary PathologyRuska and Lorries • First developed electronrnicroscope.Bittner • Milk transmission ofcancerR.A. Runnels • Wrote book on "Animal Pathology".Watson and Crick • Structure of DNAG.A. Sastry (India) • Author of Veterinary Pathology textbook.• The Publication ofIndian Veterinary Medical Journalstarted from Lucknow• The publication ofIndian Journal ofVeterinary Pathologystarted from Izatnagar• Indian Association ofVeterinary Pathologist established.• Veterinary Council ofIndia established• Dr. C.M. Singh became 1st President ofVCI• 1stVeterinary and Animal Sciences University establishedin Madras (now Chennai).• Establishment of" Society for Immunology andImmunopathology" at Pantnagar.• Publication of "Journal ofImmunology andImmunopathology" started from PantnagarFrom left to right: Dr. Ramesh Kumar, Professor. Microbiology, AIIMS;Dr. N.K. Ganguly, Director General Indian Council of Medical Research;Dr. C.M. Singh, Former Director, IVRI and President VCI; Dr. R.S. Chauhan, NatIonal Fellow,at inaugural function of Society for Immunology and Immunopathology.10
  24. 24. IntroductionMODEL QUESTIONSQ.1. In a dairy farm a total of 1000 cows are kept for milk purpose. On 3.1.2001,80 animals were foundsick and were suffering from nasal discharge, fever and diarrhoea. Out of these 30 animals died till18.1.2001 and rest recovered. The blood and serum samples were collected from affected animalsfor laboratory examination. The dead animals were necropsied and their tissue samples were alsocollected for microscopic examination. Based on this describe the followings:1. Morbidity rate2. Mortality rate3. Case fatality rate4. Course ofdisease5. State the branch ofpathology under which following activity falls:(a) Examination ofblood .................... .(b) Examination ofdead animals .................... .(c) Examination of serum for Ca, P, enzymes .................... .(d) Microscopic examination oftissues .................... .(e) Examination of serum for antibodies .................... .(t) Examination of urine and faeces of affected animals..................... .Q. 2. Fill in the blanks with suitable word(s).Q.3.1. ..........is the father of Veterinary Medicine.2. .. ........gave 4 cardinal signs of inflammation which included ............., ...................,............. and .......... while the fifth cardinal sign ............... was given by .............. .3. .........deals with study ofdiseases ofanimals and man.4. Immunopathology deals with the study ofdiseases mediated by ...... and it includes .........,................ and ...........5. Symptoms are any ............... evidence of disease of animals while signs are the existenceof any ................ evidence that is the observations of the clinicians.6. .. ................is the progressive development of a disease process; it starts with the............. of causal agent in body and ends either with ................ or .............. .7. ............. is the examination oftissues received from living animals.Define thefollowing.1. Health2. Disease3. Experimental Pathology4. Oncology5. Homeostasis6. Diagnosis7. Syndrome8. Prognosis9. Lesion10. InfectionQ. 4. Justify the statement "Pathology is a key subject in Veterinary Sciences, which is quite helpfulin prevention and control ofdiseases in animals".Q. 5. Select most appropriate word(s) from thefour options given with each question.1. The process of phagocytosis by macrophages was first described by.............. .(a) B. Muller (b) E. Metchnikoff (c) Bittner (d) Bichat11
  25. 25. General Veterinary Pathology2. First Veterinary School was established in the year ..........(a) 1762 (b) 1884 (c) 1889 (d) 17733. The originator ofmodem Experimental Pathology is .............. .(a) R. Koch (b) J. Cohnheim (c) John Hunter (d) R. Virchow4. Study oftumors is known as ...........(a) Cytopathology (b) Clinical Pathology (c) Chemical Pathology (d) Oncology5. Study of zoonotic diseases fall under the branch of ............. Pathology.(a) Nutritional (b) Comparative (c) Experimental (d) Systemic6. Humoral Pathology is the study of alterations in.............. .in animals.(a) Antibodies (b) Fibrin (c) Urine (d) Faeces7. Immunodeficiency disorders of animals fall under the branch of ...........(a) Cytopathology (b) Humoral Pathology (c) Microscopic Pathology(d) Immunopathology8. General Pathology does not include one ofthe following activity(a) Fatty changes (b) Embolism (c) Inflammation (d) Digestive systemdisorders.9. Examination of dead animals is known as .................(a) Necropsy (b) Autopsy (c) Lethopsy (d) Microscopy10. Nutritional roup is an example of ...............Pathology(a) Chemical (b) Nutritional (c) Humoral (d) Post-mortem12
  26. 26. •••2ETIOLOGYIntrinsic CausesExtrinsic Causes• Physical Causes• Biological Causes• Chemical Causes• Nutritional CausesModel Questions
  27. 27. General Veterinary PathologyETIOLOGYEtiology is the study of cause of disease. It givesprecise causal diagnosis of any disease. Broadly,the cause ofdiseases can be divided into two:a. Intrinsic causes.b. Extrinsic causes.INTRINSIC CAUSESThose causes which determine the type of diseasepresent within an individual over which he has nocontrol. These causes are further divided intofollowing subgroups:GenusSpecific diseases occur in a particular genus orspecies ofanimals. e.g. Hog cholera in pigs, Caninedistemper in dogsBreed/RaceDiseases do occur in particular breed of animalssuch as: dairy cattle are more prone for mastitis.Brain tumors are common in Bull dog/ Boxer.FamilyGenetic relationship plays a role in occurrence ofdiseases in animals. e.g. some chickens haveresistance to leucosis; hernia in pigs due to weakabdominal wall.AgeAge of animal may also influence the occurrence ofdiseases such as:• At young age diarrhoea/pneumonia (Fig. 2.1).• Old age tumor• Canine distemper - Young dogs• Strangles - Young horse• Prostatic hyperplasia - Old dogs• Coccidiosis - Young chickensSexReproductive disorders are more common infemales• Milk fever, mastitis and metritis in females.14• Nephritis is more common in male dogs thanfemale, but Bovine nephritis is more commonin females.ColourColour may also play role in occurrence ofdiseases. e.g. squamous cell carcinoma in whitecoat colour cattle, melanosarcoma in grey andwhite horsesIdiosyncracyAn unusual reaction of body to some substancessuch as:• Drug reaction: Small dose of drug mayproduce reaction.• Individual variations.EXTRINSIC CAUSESSome etiological factors which are present in theoutside environment may cause/influence theoccurrence of disease. These are also known asexciting cause/acquired cause. Majority of causesof diseases fall under this group which are furtherclassified as physical, chemical, biological andnutritional causes.PHYSICAL CAUSESTRAUMATraumatic injury occurs due to any force or energyapplied on body of animal e.g. during control /restraining, shipping or transport ofanimal.ContusionslBruisesContusions or bruises arise from rupture of bloodvessel with disintegration of extravassated blood(Fig. 2.2).AbrasionsAbrasions are circumscribed areas whereepithelium has been removed by injury and it mayindicate the direction offorce (Fig. 2.3).ErosionsPartial loss of surface epithelium on skin ormucosal surface is termed as erosion (Fig. 2.4).
  28. 28. Etiology,rsl--V.,~.b.ll.·f:III....~II~~;, . ,t ,}"-- - --- - - - -----Fig. 2.5. Diagram showing incised woundFig. 2.1. Rotaviral diarrhoea in young calfFig. 2.6. Diagram showing lacerationFig. 2.2. Diagram showing contusionFig. 2.7. Photomicrograph ofthIrd degree bum in skinFig. 2.3. Diagram showing abrasionFig. 2.4. Diagram showing erosion Fig. 2.B. Electronmicrophotograph ofpoxvirus in CAM15
  29. 29. General Veterinary PathologyIncised wounds/cutsIncised wounds are produced by sharp-edgedinstrument. They are longer than deep (Fig. 2.5).Stab woundStab wounds are deeper than longer produced bysharp edged instrument.LacerationSeverance of tissue by excessive stretching and iscommon over bony surfaces or are produced by cutthrough a dull instrument (Fig. 2.6).CompressionCompression injury is produced as a result of forceapplied slowly e.g. during parturition.Blast injuryForce of compression waves against surfacesfollowed by a wave of reduced pressure. It canrupture muscles/viscera.Bullet woundHitting at 90° by flrearms to produce uniformmargins of abrasion. Exit wounds are irregular andlacerated.ELECTRICAL INJURYHigh voltage current induces tetanic spasms ofrespiratory muscles and hits the respiratory centreof brain. It also produces flash burns. Lightningcauses cyanotic carcass, post-mortem bloat,congestion of viscera, tiny haemorrhage and skindamage.TEMPERATUREBurnsI degree burnsThere is only congestion and injury to thesuperflcial layers of epidermis e.g. sun burn onhairless parts or white skinned animal.11 degree burnsEpidermis is destroyed; hair follicles remain intactand provide a nidus for healing ofepithelium.16III degree burnsEpidermis and dermis both are destroyed leading tofluid loss, local tissue destruction, laryngeal andpulmonary oedema, renal failure, shock and sepsis.Till 20 hrs of burn, the burn surface remains sterilethen bacterial contamination occurs. After 72 hrsmillions of bacteria enter in the affected tissue.Bacteria such as Staphylococci, Streptococci andPseudomonas aeruginosa invade the deeper layersof skin and cause sepsis. There is a state ofimmunosuppression in severe burns leading toimpaired phagocytosis by neutrophils (Fig. 2.7).HyperthermiaHyperthermia means increased body temperaturedue to high environmental temperature e.g. pets inhot environment without water. Hyperthermia leadsto increased respiration (hyperpnoea), rapid heartbeat (tachycardia), and degeneration inmyocardium, renal tubules and brain.HypothermiaHypothermia means decreased body temperatureand includes freeze induced necrosis of tissues atextremitiesRADIATION INJURYRadiation as a result ofexposure to X-rays, Gammarays or ultra violet (UV) rays leads to cell swelling,vacuolation of endoplasmic reticulum, swelling ofmitochondria, nuclear swelling and chromosomaldamage resulting in mutation. The impact ofradiation is more on dividing cells of ovary, sperm,lymphocytes, bone marrow tissue and intestinalepithelium. It is characterized by vomiting,leucopenia, bone marrow atrophy, anemia, oedema,lymphoid tissue and epithelial necrosis.BIOLOGICAL CAUSESVirusViruses are smallest organisms, which have onlyone type of nucleic acid DNA or RNA in their corecovered by protein capsid.
  30. 30. Fig. 2.9. Electron microphotograph ofreovirus in CAMFig. 2 10. Electronmicrophotograph ofrotaVIruSFig. 2.11. Diagram ofLeptospira.-., A::1, .........:•••••• •" "."••.... ~(; C..... --, ,I, - ......."",.:-B.....,.......•......"" It"#, .t.~. ...Fig. 2.12. Diagram ofbacteria (a) Staphylococci,(b) Streptococci (c) BacilliEtiology17Fig. 2.13. Photomicrograph ofTrichophyton sp. acause ofringworm~i~ 2.14. Photomic;ograph ofAspergillusflavus.~I ~ ••J"", "~tA • 11• g . --t!.i, !f,.~ l.cv . .,1-., ..,~.~ &. .1 -_ .1Fig. 2.15. Photomicrograph ofTrypanosomaevanSl infectIOnA11ri.~~I :I ; :! I" .;.!/Fig. 2.16. Diagram ofEchinococcus and Taenia spp.
  31. 31. General Veterinary PathologyViruses of Veterinary Importance with their classification(International Committee on taxonomy ofviruses, 2005)DNA Viruses (Fig. 2.8)S.No. Family Genus Virus species DiseaseGroup I - ds DNA viruses ( Double stranded DNA virus)I. Adenoviridae Aviadenovirus Fowl adenovirus IBH, EDS, HPS in birdsAtadenovirus Ovine adenovirus A Pneumonia in SheepMastadenovirus Canine adenovirus I ICH in Dog2. Herpesviridae Alphaherpes virus Herpes suis Pseudorabies in pigsBovine herpes virus - I (BHV-I) IBR, IPV in cattleEquine herpes virus - I (EHV-I ) Equine viral abortionEquine herpes virus - 4 (EHV-4) Rhinopneumonitis in equinesEquine herpes virus - 3 (EHV-3) Coital exanthemaAvian herpes virus type-I (AHV- ILT in birdsI)Betaherpes virus Porcine cytomegalo virus Inclusion body rhinitis in pigsGammaherpes Malignant catarrhal fever virus MCF in cattlevirusMareks disease virus Mareks disease in birds3. Papillomaviridae Papillomavirus Bovine papillomavirus Cutaneous papilloma in cattleOral papilloma in dogsCanine oral papillomavirus Cutaneous papilloma inRabbit papillomavirus rabbits4. Poxviridae Orthopox virus Vaccinia virus, Cowpox virus, Pox in animalsBuffalopox virus, Monkeypoxvirus, Rabbitpox virusCamelpox virusAvipox virus Fowlpox virus, Pigeonpox virus, Fowl pox, Pigeon pox,Turkeypox virus, Canarypox virus Turkeypox, CanarypoxCapripox virus Sheeppox virus, Goatpox virus Sheep pox, Goat poxLeporipox virus Myxoma virus Myxomatosis in RabbitsSuipox virus Swinepox virus Swine poxParapox virus Orfpox virus Orfin sheepGroup II - ss DNA viruses (Single stranded DNA virus)I. Circoviridae Circovirus Porcine circovirus -Gyrovirus Chicken anemia virus Chicken infectious anemia2. Parvoviridae Parvovirus Murine minute virusBocavirus Bovine parvovirus Diarrhoea in cattleCanine parvovirus Enteritis, myocarditis in dogsPorcine parvovirus Infertility, fetal death in pigs18
  32. 32. EtiologyRNAVIruses (F 29 & 2 IQ)IgS.S.No. Family Genus Virus species DiseaseGroup 111- ds RNA virus ( Double stranded RNA virus)1. Birnaviridae Avibimavirus IBD virus IBD in birdsAquabimavirus Infectious pancreatic Infectious pancreaticnecrotic virus necrosis2. Reoviridae Orthoreovirus Mammalian orthoreo virus Pneumoenteritis in calvesOrbivirus Blue tongue virus Blue tongue in sheepRotavirus Rotavirus Diarrhoea in neonatesGroup IV - (+ve) ss RNA virus (Positive single stranded RNA or M RNA Iike~1. Arteriviridae Arterivirus Equine arteritis virus Equine viral arteritis2. Coronaviridae Coronavirus Infectious bronchitis virus Infectious bronchitis inbirdsBovine coronavirus Diarrhoea in calves3. Astroviridae Avastrovirus Turkey astrovirus -4. Calciviridae Vesivirus Swine vesicular exanthema Vesicular exanthema invirus pigsLagovirus Rabbit haemorrhagic Haemmorhagic disease indisease virus rabbitNorovirus Norwalk virus -5. Flaviviridae Flavirus Yellow fever virus Yellow fever in manHepacivirus Hepatitis C virus Hepatitis in manPestivirus BVD virus, CSF virus BVD, CSF6. Picomaviridae Enterovirus Poliovirus Polio in manRhinovirus Rhinovirus RhinitisHepatovirus Hepatitis A virus HepatitisCardiovirus Encephalomyocarditis EncephalomyocarditisvirusAphthovirus FMD virus FMDErbovirus Equine rhinitis B virus Respiratory disease inequines7. Togaviridae Alphavirus Equine Encephalomyelitis Equine encephalomyelitisvirusRubivirus RubellavirusGroup V - (-ve) ss RNA virus (Negative single stranded RNA)I. Paramyxoviridae Paramyxovirus Parainfluenza virus 1 (PI- Respiratory diseases in1)- Pigs, pigsParainfluenza virus 2 (PI- Kennel cough in dogs2)- Dogs,Parainfluenza virus 3 (PI- Respiratory disease in3)- Cattle cattleAvulavirus Ranikhet disease virus Ranikhet disease in birdsMorbillivirus Canine Distemper virus CD in dogsRinderpest virus RP- in animalsPPR virus PPR - sheep, goat19
  33. 33. General Veterinary PathologyS.No. Family Genus Virus species Disease2. Bomaviridae Boma disease virus Boma disease virus Boma disease in sheep3. Filoviridae Ebolavirus - -Filovirus - -4. Rhabdoviridae Vesiculovirus Vesicular stomatitis virus Vesicular stomatitis inbovinesLyssavirus Rabies virus RabiesEphemerovirus Ephemeral fever virus Ephemeral fever inanimals5. Bunyaviridae Hantavirus Hantaanvirus Hantavirus pulmonarysyndrome, Koreanhaemorragic feverPhlebovirus Nairobi sheep disease Nairobi Sheep disease,virus, Rift valley fever RVFvirus, Akabana disease Akabana diseasevirus6. Orthomyxoviridae Influenza virus A Influenza virus A Influenza in animalsInfluenza virus B Influenza virus BInfluenza virus C Influenza virus CGroup VI ss RNA-RT virus (Single stranded RNA virus with reverse transcriptase)1. Retroviridae Alpharetrovirus Avian leucosis virus ALC in birdsBetaretrovirus Mouse mammary tumour Cancer in micevirusGammaretrovirus Murine leukemia virus Leukemia in miceFeline leukemia virus Leukemia in catsDeltaretrovirus Bovine leukemia virus Bovine leukemiaLentivirus Bovine immunodeficiency Bovinevirus immunodeficiencysyndromeFeline immunodeficiency Feline immunodeficiencyvirus syndromeGroup VII ds DNA-RT virus (Double stranded DNA virus with reverse transcriptase)1. Hepadnaviridae Orthohepadnavirus Hepatitis B virus HepatitisAvihepadna virus Duck hepatitis B virus Duck hepatitis20
  34. 34. Eti%gySubviral agents• Prion proteins are infectious proteins withoutany nucleic acid. e.g. Bovine spongiformencephalopathy.• Viroids have only nucleic acid withoutproteins. They do not cause any disease inanimals. However, They are associated withplant diseases.RickettsiaCoxiella burnetti causes Q-feverMycoplasmaMycoplasma mycoides is responsible forpneumonia, joint ailments and genital disordersChlamydiaChlamydia trachomatis, C. psittaci cause abortions,pneumonia, and eye ailments.SpirochaeteLeptospira sp. causes abortion, icterus.Borrelia ansernia causes fowl spirochetosis lDchickens (Fig. 2.11).BacteriaBacteria are classified as Gram positive and Gramnegative on the basis of Grams staining. GramposItive bacteria include Staphylococci,Streptococci, Corynebacterium, Listeria, BacillusClostridia. Gram negative bacteria are Escherichiacoli, Salmonella, Proteus, Klebsiella, Pasteurella,Pseudomonas, Brucella, Yersinia, Campylobactoretc. Besides, there are certain organisms stainedwith Zeihl Neelson stain and are known as acid fastbacilli e.g.Mycobacterium tuberculosis and M.paratuberculosis (Fig. 2.12).FungiFungi pathogenic for animals mostly belong tofungi imperfecti. e.g. Histoplasmosis.21Fungi cause three type of disease - Mycosis e.g.Actinomycosis; Allergic disease e.g. Ringworm;Mycotoxicosis e.g. Aflatoxicosis (Figs. 2.13, 2.14).ParasitesParasites are classified mainly in 3 groups:Protozoan parasitesTrypanosoma evansi, Theileria annulata, Babesiabigemina, Toxoplasma gondii, Eimeria Spp. (Fig.2.15).HelminthsNematodes - Roundworms e.g. Ascaris.Trematod - Flat worms e.g. Liverfluke.Cestodes - Tapeworms e.g Taenia spp. (Fig. 2.16).ArthropodsTicks, Mites, Flies, Lice (Figs. 2.17, 2.18, 2.19,2.20).TRANSMISSIONBiological agents are transmitted from one animalto another through horizontal or verticaltransmission.Horizontal TransmissionHorizontal transmission ofbiological causes occursthrough direct contact or indirectly via animal orinanimate (fomites) objects. It is also known aslateral transmission as it occurs in a populationfrom one to another. Various methods of horizontaltransmission are as under:
  35. 35. General Veterinary PathologyI Fig. 2.21. Photograph ofcalves with strychnine poisoningFig. 2.17. Diagram ofa tickFig. 2.22. Photograph ofcalves with strychnine poisoningFig. 2.18 Photograph ofbullock with tick infestationFig. 2.19. Diagram ofa MiteFig. 2.23. Pesticide spray in cropsFig. 2.20. Photomicrograph ofSarcoptes scabei Fig. 2.24. Pesticide cycle in environment22
  36. 36. EtiologyIngestionFood, water, faecal-oral route e.g. Salmonellosis,Johnes disease, Rotavirus infection.InhalationAir-borne infections, droplet infection e.g. R.P.,FMD, Tuberculosis.ContactFungal infection, Bacterial dermatitis, Flu,Brucellosis, Rabies through bite.InoculationIntroduction of infection in body through punctureeither mechanically through needles or byarthropods such as by ticks. Ticks transmit diseasesthrough transovarian (one generation to nextgeneration) or transstadial (through developmentalstages) transmission.IatrogenicTransmission of infection during surgicalprocedures or caused by doctor, through dirtyinstrument and contaminated preparations.CoitusThrough sexual contact of animals, biologicalagents spread from one to another animals. e.g.Campylobacteriosis, Trichomonosis.Vertical TransmissionVertical transmission occurs from one generation toanother generation in ova/in utero or through milk.These include:HereditaryInfection/disease carried in the genome of eitherparent e.g. RetrovirusCongenitalDiseases acquired either in utero/in ova• Infection in ovary/ ovum (Germinativetransmission) e.g. ALC in chickens, lymphoidleukemia in mice, Salmonellosis in poultry.• Infection through placenta. e.g. Felinepanleukopenia virus (Transmission to embryo)23• Ascending infection from lower genital canalto amnion / placenta e.g. Staphylococci.• Infection at parturition: Infection from lowergenital tract during birth. e.g. Herpex simplexvirus.MAINTENANCE OF INFECTIONBiological agents face difficulty of survival at bothplaces - in environment and in host. Two types ofhazards which create problem to agent are:Internal hazards e.g. Hosts immune systemExternal hazards e.g. Desiccation, DV lightAgents try to maintain themselves by adoptingfollowing maintenance strategies:• Avoidance of a stage in the externalenvironment.• Resistant forms e.g. Anthrax spores.• Rapidly in-rapidly out strategy e.g. Viruses ofrespiratory tract.• Persistence within the host e.g. Mycobacteriumtuberculosis, Slow viral diseases.• Extension of host range.• Infection in .more than one host e.g. Foot andmouth disease.CHEMICAL CAUSESBiological ToxinsSnake venomSnake venom has phospholipase A2 which causeslytic action on membranes of RBC and platelets.The presence of hyaluronidase, phosphodiesteraseand peptidase in snake venom are responsible foroedema, erythema, haemolytic anemia, swelling offacial/laryngeal tissues, haemoglobinurea, cardiacirregularities, fall in blood pressure, shock andneurotoxicity.Microbial toxinsMicrobial toxins are those toxins/poisons that areproduced by microbial agents particularly bybacteria and fungi.Bacterial toxinsBacterial toxins include structural proteins(endotoxins) and soluble peptides/ secretary toxins(exotoxins). Endotoxins are present in cell wall of
  37. 37. General Veterinary PathologyGram-negative bacteria and are found to beresponsible for septicemia and shock. Exotoxinsare secreted by bacteria outside their cell wall andare responsible for protein lysis and damage to cellmembrane. e.g. Clostridium toxins suppressmetabolism of cell. Most potent clostridial toxinsare botulinum and tetanus, which are the cause ofhemolysis and are powerful neurotoxin. Besides,Clostridium chauvei toxins are responsible forblack leg disease in cattle.Fungal Toxins (Mycotoxins)There are several fungi known for production oftoxins. Such toxins are known as mycotoxins andthey are mostly found in food! feed items, whichcause disease in animals through ingestion.AflatoxinsAflatoxins are produced by several species of fungiincluding mainly Aspergillus flavus, A. parasiticusand Penicillium puberlum. These aflatoxins areclassified as Bh B2, Gh G2, Mh M2, B2a, G2a andaspertoxin. Aflatoxins are produced in moistenvironment in grounded animaVpoultry feed onoptimum temperature and are more common intropical countries where storage conditions are poorand provide suitable environment for the growth offungi. These toxins are known to causeimmunosuppression, formation of malignantneoplasms and hepatopathy.ErgotErgot is produced by Claviceps purpura in grainswhich causes blackish discoloration. It producesgangrene by chronic vasoconstriction, ischemia andcapillary endothelium degeneration. It is alsoassociated with summer syndrome in cattlecharacterized by gangrene of extremities.Fusarium toxinsFusarium toxins are produced by Fusariumtricinctum in paddy straw, which are found to causegangrene in extremities. Zearalenone toxin is thecause ofovarian abnormality in sow.24OchratoxinsOchratoxins are produced by Aspergillusochraceous and A. viridicatum fungi in groundedfeed on optimum temperature and moisture and arefound to cause renal tubular necrosis in chickensand pigs.Plant toxinsOver 700 plants are known to produce toxin. e.g.Braken fern which causes haematuria andencephalomalacia. Strychnine from Strychnosnuxvomica is highly toxic and causes death inanimals with nervous signs. It is used for dogkilling in public health operations to control rabies(Figs. 2.21 & 2.22). HCN is found in sorghumwhich is known to cause clonic convulsions anddeath in animals characterized by haemorrhage inmucous membranes.Drug toxicity• Antibiotics: Cause direct toxicity by destroyinggut microflora. Oxytetracyline, sulfonamidesare nephrotoxic. Neomycin and Lincomycincause Malabsorption diarrhoea andimmunosuppression.• Anti-inflammatory drugs, like acetaminophencauses hepatic necrosis, icterus and hemolyticanemia.• Anticoccidiostate drug: Monensin isresponsible for necrosis of cardiac and skeletalmuscles.• Trace elements: There are various traceelements, excess of which may causepoisoning in animals. e.g. Selenium poisoning"Blind staggers" or "Alkali Disease" in cattlecharacterized by chronic debilitating disease. Italso causes encephalomalacia in pigs.EnvironmentalpollutantsEnvironment is polluted due to presence ofunwanted materials in food, water, air andsurroundings of animals, particularly byagrochemicals including pesticides and fertilizers.The environmental pollutants exert their direct orindirect effect on the animal health and production.The main pollutants are:
  38. 38. Etiology• Heavy metals such as mercury, lead, cadmiumare found in industrial waste, automobile andgenerator smoke, soil, water and also ascontaminants ofpesticides and fertilizers. Theyare responsible for damage in kidneys, immunesystem and neuropathy. They are alsoassociated with immune complex mediatedglomerulonephritis.• Sulphur dioxide is produced by automobiles,industries and generators. It is responsible forloss of cilia in bronchiolar epithelium.• Hydrogen sulphide is produced by animalsdecay and in various industries. It inhibitsmitochondrial cytochrome oxidase leading todeath.• Pesticides are agrochemicals used in variousagricultural, animal husbandry and publichealth operations. They are classified asinsecticides, herbicides, weedicides androdenticides. Chemically, insecticides aregrouped mainly as organochlorineorganophosphates, carbamates and syntheticpyrethroids. Acute poisoning of pesticidescauses death in animals after nervous clinicalsigns of short duration. Chronic toxicity ischaracterized by immunosuppression,nephropathy, neuropathy, hypersensitivity andautoimmunity in animals (Figs. 2.23 & 2.24).NUTRITIONAL CAUSESMalnutrition causes disease in animals either due todeficiency or excess of nutrients. It is very difficultto diagnose the nutritional causes and sometimes itis not possible to fmd a precise cause as in case ofinfectious disease because functions of one nutrientcan be compensated by another in cell metabolism.Experimental production of nutritional deficiencyis not identical to natural disease. When tissueconcentration of nutrient falls down to the criticallevel, it leads to abnormal metabolism and theabnormal metabolites present in tissues can bedetected in urine and faeces. First changes ofnutritional deficiency are recorded in rapidlymetabolizing tissues e.g. skeletal muscle,myocardium and brain. Immature animals are more25susceptible to nutritional disease. e.g. calves,chicks, piglets etc.Types of deficiency• Acute/chronic e.g. thiamine deficiency in pigs.• Multiple deficiencies: e.g. poor quality food.• Nutritional imbalance: e.g. imbalance incalcium: phosphorus (2:1) ratio.• Protein malnutrition: e.g. malabsorption.• Calorie deficiency: e.g. Loss of fat/ musclewasting.Factors responsible for nutritional deficiency• Interference with intake e.g. anorexia, G.!.tract disorders.• Interference with absorption e.g. intestinalhypermotility, Insoluble complexes in food(Fat/Calcium)• Interference with storage e.g. hepatic diseaseleads to deficiency of vit. A.• Increased excretion e.g. polyuria, sweating andlactation• Increased requirement e.g. fever,hyperthyroidism and pregnancy• Natural inhibitors e.g. presence of thiaminasesin feed, leads to thiamine deficiency.Calorie deficiencyCalorie deficiency in animals occurs due to fooddeprivation or starvation.Food deprivationDietary deficiency of food in terms ofquantity/quality leads to emaciation, loss ofmusculature, atrophy of fat, subcutaneous oedema,cardiac muscle degeneration and atrophy of visceraincluding liver and pancreas. The volume ofhepatocytes reduced by 50% and mitochondrialtotal volume also reduced by 50%.StarvationStarvation is the long continued deprivation offood. It is characterized by fatty degeneration ofliver, anemia and skin diseases. Young and veryold animals are more susceptible to starvationwhile in pregnant animals it causes retarded growth
  39. 39. General Veterinary Pathologyof foetus. In animals, following changes can beseen due to starvation.Intestinal involutionAbsorptive surface is reduced with shrunken cellsand pyknotic nuclei. Villi become shorter and showatrophy.Atrophy ofmusclesThere is decrease in muscle mass.LipolysisIncreased cortisol leads to increased lipolysisresulting in formation of fatty acids in liver whichin turn converts into ketones used by brain.GluconeogenesisIn early fasting blood glucose level drops down.The insulin level becomes low while glucagon goeshigh in starvation. The glucose comes from skeletalmuscle, adipose tissue and lymphoid tissue duringstarvation. Twenty-four hours of food deprivationcauses reduction in liver glycogen and bloodglucose. Fatty acid from adipose tissue formsglucose and in mitochondria after oxidation itforms acetoacetate, hydroxybutyrate and acetone.These are also known as ketone bodies and arepresent in blood stream during starvatibn. This stateis also known as ketosis e.g. ketosis/acetonemia inbovines. Lack of glucose in blood leads tooxidation of fatty acids which form ketone bodiesas an alternate source of energy. They are normal!physiological at certain level but may becomepathological when their level is high.Clinically it is characterized by anorexia,depression, coma, sweet smell in urine.Concentration of acetone increases in milk, bloodand urine along with hyperlipimia and acidosis. Asimilar condition also occurs in sheep known aspregnancy toxaemia which is characterized bydepression, coma and paralysis. This situationoccurs when many foetus are present in uterus.There are fatty changes in liver, kidneys, and heart,with subepicardial petechiae or echymosis.26Protein deficiencyGenerally, protein deficiency does not occur.However, the deficiency of essential amino acidshas been reported in animals when certainingredients are deficient in certain amino acids. e.g.maize is deficient in lysine and tryptophan thatleads to slow growth; peanuts and soybean aredeficient in methioine. Protein deficiency ischaracterized by hypoproteinemia, anemia, poorgrowth, delayed healing, decreased or cesation ofcell proliferation, failure of collagen formation,atrophy of testicles and ovary, atrophy of thymusand lymphoid tissue.Deficiency ofLipidsGenerally, there is no deficiency of fat in animals.However, essential fatty acids, including linolenicacid, linoleic acid and arachdonic acid, deficiencymay occur which causes dermatoses in animals. Fathas high calorie value and it is required in bodybecause there are certain vitamins soluble in fatonly.Deficiency of WaterDeficiency of water may lead to dehydration andslight wrinkling in skin. Deficiency may occur dueto fever, vomiting, diarrhoea, haemorrhage andpolyuria, which can be corrected through adequateoral water supply or through intravenous fluidtherapy.Deficiency of VitaminsVitamin deficiency may occur due to starvation.There are two types of vitamins viz., fat solubleand water soluble. Fat soluble vitamins are vit. A,D, E and K and water soluble are vit B complexandC.Vitamin AIt is also known as retinol. It is derived from itsprecursor carotene. It is found in abndance in plantshaving yellow pigment, animal fat, liver, cod liveroil, shark liver oil. ~-carotene is cleaved in gutmucosa into two molecules of retinol (Vit. Aaldehyde) which, after absorption, is stored in liver.Bile salts and pancreatic juice are responsible for
  40. 40. Etiologyabsorption of vit. A from gut. Deficiency of vit. Aoccurs due to damage in liver.Vit. A deficiency may lead to following diseaseconditions:Squamous metaplasia of epithelial surfaces inesophagus, pancreas, bladder and parotid duct,which is considered pathognomonic in calves.Destruction of epithelium! goblet cell in respiratorymucosa is generally replaced by keratinsynthesizing squamous cells in vit. A deficientanimals. There are abnormal teeth in animals dueto hypoplasia of enamel and its poormineralization. Vitamin A deficiency is alsoassociated with still birth and miscarriages in pigs.It causes night blindness (Nyctalopia) in animals.Due to deficiency of Vit. A there are recurrentepisodes of conjunctivitis/ keratitis: In poultry,there is distention of mucous glands, which opensin pharynx and esophagus because of metaplasia ofduct epithelium leading to enlargement ofesophageal glands due to accumulation of itssecretions. The glands become spherical, 1-2 mmdia. over mucosa. It is considered pathognomonicfor hypovitaminosis A. and is known as Nutritionalroup (Fig. 2.25a&b). Inflammation of upperrespiratory tract lead to coryza. Urinary tract ofcattle, sheep and goat suffers due to formation ofcalculi, which may cause obstruction in sigmoidflexure of urethra in males. Such calculi are madeup of desquamated epithelial cells and salts and thecondition is known as urolithiasis. Deficiency ofvit. A may also lead to in abnormal growth ofcranial bones and there may be failure of foramenovale to grow leading to constriction of opticnerves which results in blindness in calves,increased CSF pressure, blindness at birth andfoetal malformations. In sows, piglets are bornwithout eyes (Anophthalmos) or with smaller eyes-(Microphthalmos).Vitamin DVitamin D occurs in three forms viz. vitamin D2 orcalciferol, Vit. D3 or cholecaliciferol and Vit D, orimpure mixture of sterols. About 80% Vit. D issynthesized in body skin through UV rays on 7-hydrocholesterol. In diet containing egg, butter, it is27found in abundant quantity in milk, plants, grainsetc. Active forms of vit. Dare 25-hydroxy vit. Dand 1,25 dihydroxy vit D. (Calcitriol) which is 5 to10 times more potent than former. Vit D is storedin adipose tissue in body. The main functions of vitD are absorption of Ca and P from intestines andkidneys, mineralization of bones, maintenance ofblood levels of Ca and P and immune regulation asit activates lymphocytes and macrophages.• The deficiency of vitamin D is associated withrickets in young animals (Fig. 2.26),osteomalacia in adult animals andhypocalcemic tetany.• Excess of vitamin D leads to the formation ofrenal calculi, metastatic calcification andosteoporosis in animals.Vitamin E (a- tocopherol)Source of vitamin E is grains, oils, nuts, vegetables,and in body it is stored in adipose tissue, liver andmuscles. It has antioxidant activity and preventsoxidative degradation of cell membrane.• Deficiency of vit E causes degeneration ofneurons in peripheral nerves. There isdenervation of muscles leading to muscledystrophy e.g. White muscle disease in cattleand Stiff lamb disease in sheep andMyoglobinuria in horses. Deficiency of vit. Ecauses degeneration of pigments in retina andreduces life span of RBC, leading to anemiaand sterility in animals. Crazy chick disease(Encephalomalacia) is also caused by vit Edeficiency; the chicks become sleepy withtwisting of head and neck. There is musculardystrophy in chickens due to vit. E deficiency(Fig. 2.27).VitaminKVit. K occurs in two forms namely vit. K, orphylloquinone found in green leaf and vegetablesand Vit- K2 or menadione which is produced by gutmicroflora. Its main function is coagulation ofblood. Deficiency of vit K may leads tohypoprothrombinemia and haemorrhages.
  41. 41. General Veterinary Pathology(a)(b)Fig. 2.25.(a) Diagram of squamous metaplasia in esophagealglands due to vitamin A deficiency (b) Photograph ofeosophagus ofpoultry showing nutritional roup.Fig. 2.26. Photograph ofa calf showing rickets28Fig 2.27. Muscular dystrophy due to vitamin EdeficiencyFig. 2.28. Curled toe paralysis in a chick due toRiboflavin deficiencyFig. 2.29. Silpped tendon or perosis In chicks
  42. 42. EtiologyVitamin BVitamin B is a water soluble vitamin which has atleast 9 sub types including B or thiamine, B2 orriboflavin, B6 or pyridoxine, B2 orcyanocobalamin, niacin or nicotinic acid, folate orfolic acid, choline, biotine and pantothenic acid.ThiamineIn ruminants, synthesis of thiamine occurs inrumen. Sources of vit. B are pea, beans, pulses,green vegetables, roots, fruits, rice, wheat bran etc.Strong tea, coffee have antithiamine action. It isstored in muscles, liver, heart, kidneys and bones ofanimals. Thiamine plays active role in carbohydratemetabolism• Deficiency of thiamine may lead to Beriberidisease characterized by Ataxia andneuraVlesions. Chastek paralysis in cats, foxand mink and stargazing attitude of chicks dueto thiaminase (thiamine deficiency) in mealmay be observed. Bracken fern poisoning incattle and horses may cause deficiency ofthiamine due to presence of thiaminaseenzyme in bracken fern. Toxicity of thiaminesplitting drugs like amprolium, a coccidiostate,may cause polioencephalomalcia in cattle andsheep. Cardiac dialation in pigs has also beenobserved due to vit. B deficiency.RiboflavinRiboflavin is a component of several enzymes andis found in plants, meat, eggs and vegetables.• Deficiency of riboflavin may cause CurledToe Paralysis in chicks and swelling of sciaticand brachial nerves (Fig. 2.28).NiacinRole of niacin (NADINADP, nicotinamide adeninedinucleotide) is in electron transport inmitochondria of cells. It is found in grains, cereals,meat, liver, kidneys, vegetables and plants.• Deficiency of niacin is associated with skindisorders in man Pellegra; anorexia, diarrhoea,anemia in pigs and mucous hyperplasia,haemorrhage in gastrointestinal tract and black29tongue in dogs which is also known as Caninepellegra.PyridoxineIt is found in egg, green vegetables, meat, liver etc.• Deficiency of pyridoxine causes uremia,convulsions, dermatitis and glossitisPantothenic acid• Pantothenic acid deficiency is associated withstunted growth of chicks.Folate• Folic acid is required in formation oferythrocytes and hence its deficiency leads toanemia.CyanocobalaminDeficiency of cyanocobalamin may also lead toanemia, as it is also needed in RBC formation.BiotinBiotin deficiency causes paralysis of hind legs incalves and perosis in chicks.CholineCholine deficiency is associated with fatty changesin liver and perosis.Vitamin C (Ascorbic acid)It is found in green plants and citrus fruits.Deficiency of vit. C may cause retardation offibroplasia, scurvy in G. pigs, haemorrhage,swelling, ulcers and delayed wound healing inanimals.MINERALSVarious minerals are also necessary for survival ofanimals. Deficiency of anyone of them or incombination may cause serious disease in animals.Some ofthe important minerals are:• Sodium chloride • Cobalt• Calcium • Manganese• Phosphorus • Potassium• Magnesium • Fluorine• Iodine • Sulphur• Iron • Selenium• Copper • Zinc
  43. 43. General Veterinary PathologySodium chlorideSodium chloride is an essential salt whichmaintains osmotic pressure in blood, interstitialtissue and the cells because 65% of osmoticpressure is due to sodium chloride. Chloride ions ofhydrochloric acid present in stomach also comefrom sodium chloride.• The excess of sodium chloride causesgastroenteritis in cattle, gastroenteritis andeosinophilic meningoencephalitis in pigs andascites in poultry.• Deficiency of sodium chloride is characterizedby anorexia, constipation, loss of weight insows and pica, weight loss, decreased milkproduction and polyurea in cattle. Deficiencyof salt occurs due to diarrhoea, dehydrationand vomiting.CalciumNormal range ofcalcium is 10-11 mg/lOO rnl bloodin body of animals. If it increases above 12 mg/IOOrnl blood, metastatic calcification occurs, while itslevel less than 8 mg/IOO rnl blood may show signsofdeficiency characterized by tetany.Absorption of calcium from gut is facilitated by vit.D. Paratharmone stimulates to raise blood Ca levelfrom bones while calcitonin from thyroidstimulates its deposition in bones and thus reducesblood Ca levels.• In pregnant cows, calcium deficiency occursjust after parturition. During gestation calciumgoes to foetus from skeleton ofcows, resultingin weak skeleton of dam. If calcium is notprovided in diet, it may cause disease in damcharacterized by locomotor disturbances,abnormal curvature of back, distortion ofpelvis, tetany, incoordination, muscle spasms,unconsciousness and death. Such symptomsoccur in animals when their blood calciumlevel falls below 6 mg/lOO ml of blood and ifit is less than 3 mg/lOOrnl blood, death occursinstantly.• Milk fever is a disease of cattle that occursdue to deficiency of calcium just afterparturition. Cow suddenly becomes recumbentand sits on sternum with head bending30towards flank and is unable of get up. Nogross/ microscopic lesion is reported in thisdisorder. The calcium therapy recovers theanimal immediately.• The excess of calcium may cause metastaticcalcification leading to its deposition in softtissue ofkidney, lungs and stomach.MagnesiumIt acts as activator of many enzymes e.g. alkalinephosphatase. It is required for activation ofmembrane transport synthesis of protein, fat andnucleic acid and for generation! transmission ofnerve impulses. The normal blood levels are 2mg/IOO rnl ofblood.• Dietary deficiency leads to hypomagnesaemiaand a level below 0.7 mg/IOO rnl causessymptoms in calves characterized by nervoushyperirritability, tonic and clonic convulsions,depression, coma and death.• The post-mortem lesions of magnesiumdeficiency includes haemorrhage in heart,intestines, mesentery and congestion ofviscera.• Microscopic lesions include calcification ofintimal layer~ of heart blood vessels(metastatic) muscles and kidneys. Grass tetanyand Grass staggers occurs due to hypomagne-saemia and are characterized by hyper-irritability, abnormal gait, coma and death.PhosphorusNormal level of phosphorus is 4-8 mg/IOO rnl ofblood. In bones, it is in the form of calciumphosphate. Deficiency of phosphorus qlay lead tohypophosphatemia and is characterized by pica,rheumatism and hemoglobinurea.• Pica is licking/eating of objects other thanfood. It mainly occurs in cattle, buffaloes andcamels, who eat bones, mud and other eartbernmaterials. Such animals have heavy parasiticload in their gut.• Rheumatism like syndrome is characterized bylameness in hind legs particularly in camelsand buffaloes.• Hemoglobinurea is characterized by thepresence of coffee colour urine of animal dueto extensive intravascular hemolysis Hemo-
  44. 44. Etiologyglobin urea is thus known as postparturienthemoglobin urea.SeleniumDeficiency of selenium causes hemolysis as itprotects cell membrane of RBC and thus itsdeficiency leads to anemia. Blind Staggers occursdue to excess of selenium.IronDeficiency of iron leads to anemia, which ishypochromic and microcytic but rarely occurs inanimals.CopperDeficiency of copper results in anemia and steelwool disease in sheep, which is characterized byloss of crimp in wool. Enzootic ataxia withincoordination of posterior limb has been observedin goats.CobaltVit. Bl2 is synthesized by ruminal bacteria fromcobalt in ruminants. Cobalt also stimulateserythropoiesis. Its deficiency may cause wastingdisease, cachexia and emaciation in animals. Thepathological lesions are comprised of anemia,hemosiderosis in liver, spleen and kidneys.ManganeseDeficiency of manganese causes slipped tendon inchicken or perosis characterized by shortening oflong bones in chickens. It occurs as the epiphysealcartilage fails to ossify at 12 week of age andepiphysis becomes loose and thus gastrocnemioustendon slips medially. This condition is known asSlipped Tendon or Perosis (Fig. 2.29).ZincDeficiency of zinc may cause parakeratosis in pigsat 10-20 weeks age. Calcium in diet with phytateor phosphate forms a complex with zinc making itunavailable for absorption leading to its deficiency,which is characterized by rough skin of abdomen,medial surface of thigh, which becomes homy. Italso causes fascial eczema in cattle, thymichypoplasia in calves and immunodeficiency inanimals.IodineDeficiency of iodine causes goiter in newborn pigscharacterized by absence of hair on their skin.Other signs ofiodine deficiencies include abnormalspermatozoa, decreased spermatogenesis, loss oflibido, reduced fertility, suboestrus, anoestrus,miscarriages, dystocia and hydrocephalus. Excessofiodine may lead to lacrimation and exfoliation ofdandruff like epidermal scales from skin.FluorineExcess of fluorine causes mottling in teeth andbones. The teeth become shorter, broader withopaque areas.MODEL QUESTIONSQ. 1. Fill in the blanks with suitable word(s) to answer thefollowings.1. .. .. .. .. .. .. ... in severe burns leads to impaired phagocytosis by .............. .2. Radiation mainly affects the...............cells ofbody in........., ........., ......... and.........3. Viruses are classified into two major groups viz................ and ............... on the basis ofpresence of .............. .4. Acid fast bacilli causing disease in animals are ..............., ............... and .............. .5. The transmission ofinfection created by man / doctor is known as ........ .6. Snake venom contains ............, ..............., ............... and ............ causing lysis oferythrocytes and platelets leading to ................ and........... .31
  45. 45. General Veterinary Pathology7. The gangrene on extremities produced by feeding of............... to the animals and is alsoknown as............... disease.8. Fungal toxins like. .... ...... .... cause immunosuppression and hepatotoxicity while............... causes renal damage in chickens.9. Pesticides are classified into four major groups..............., ..............., ............. and,............... of which a major group is .............. .10. Heavy metals such as ..............., ............... and............... are immunotoxic as well asnephrotoxic in animals.11. The first changes of nutritional deficiency are recorded in rapidly metabolizing tissues such as............, ............ and .......... ..12............. animals are more susceptible to nutritional disorders.13. Starvation is the ............ of food and is characterized by ............ , ............ and .......... ..14. Ketone bodies are ............, ............ and .......... ..15. Protein deficiency may lead to failure of collagen formation resulting in atrophy of...............,.....................,........................and................. .16. Maize is deficient in................... and ..............amino acids.17. Essential fatty acids are ................., ..................... and...................18. The deficiency ofVit. A is the cause ofrecurrent episodes of ......... and ......... in animals.19. Encephalomalacia is caused by deficiency ofvitamin ....................20. Perosis is caused by...................., ...................... and .................. deficiency in birds.Q. 2. Write true orfalse against each statement and correct thefalse statement.1. .........Hog cholera occurs only in pigs.2. .. .......Beefcattle are more prone to mastitis.3. .........Nephritis is more common in male in comparison to female bovines.4. .........Canine distemper occurs in old dogs.5. .........Burns and surgery may lead to immunosuppression.6. .........Rabies is caused by lyssavirus which belongs to retroviridae family.7. .........Pathogenic fungi belong to fungi imperfecti.8. .........Trypanosomasis may be transmitted through inoculation.9. .........Ochratoxin causes bile duct hyperplasia and hepatcarcinoma in birds.10. .........Most ofthe antibiotics show their deleterious effect on gut microflora, which maylead to gastrointestinal tract problems.11. .........Newly born piglets are less prone to deficiency diseases.12..........Starvation may cause stunted growth offoetus in pregnant animals.13..........Presence of ketone bodies in blood should always be suspected for ketosis in cows.14..........Soybean is deficient in lysine amino acid.15. .........Vitamin B complex and Care water-soluble.16..........Nyctalopia is caused by vitamin E deficiency.17. .........Microphthalmos is defmed as newborn with smaller eyes.18..........Vitamin D regulates the immune system of animals and activates the lymphocytes andmacrophages.19..........Vitamin K2 is produced by gastrointestinal flora and is known as phylloquinone.20..........Slipped tendon is caused by manganeese deficiency is birds.32
  46. 46. EtiologyQ.3. Define thefollowings.1. Multiple deficiency 11. Microphthalmos2. Lipolysis 12. Parakeratosis3. Dehydration 13. Perosis4. Urolithiasis 14. Hemoglobinurea5. Anophthalmos 15. Myoglobinurea6. Idiosyncracy 16. Drug toxicity7. Bums 17. Immunotoxicity of environmental pollutants8. Mode of transmission 18. Microbial toxins9. Maintenance of infection 19. Electrical injury10. Aflatoxin 20. Radiation injuryQ.4. Write short notes on.1. Erosions 11. Convulsions2. Laceration 12. Neuropathy3. Latency 13. Exotoxins4. Septicemia 14. Hematuria5. Blind staggers 15. Bacteriostate6. Osteomalacia 16. Factors responsible for nutritional deficiency7. Gluconeogenesis 17. Milk fever8. Ketosis 18. Goiter9. Pregnancytoxemia 19. White muscle disease10. Nutritionalroup 20. Salt poisoningQ. 5. Select one appropriate word from the four options provided with each question.1. Hog cholera occurs in........................(a) Pig (b) Dog (c) Horse (d) Cow2. Partial loss ofepithelium on skin or mucous membrane is known as................(a) Abrasion (b) Erosion (c) Laceration (d) Contusion3. Bum area ofskin and tissues remains sterile till..........(a) 12 hrs (b) 16 hrs (c) 20 hrs (d) 24 hrs4. Epidermis and dermis are destroyed leading to shock in ...............bum.(a) I degree (b) 11 degree (c) III degree (d) IV degree5. Radiation affects the dividing cells of.......(a) Ovary (b) Testes (c) Lymphocytes (d)All ofthe above6. Leptospira is a......... which causes miscarriages in cattle.(a) Bacteria (b) Virus (c) Chlamydia (d) Spirochaete7. Coxiella burnetti is a...... which causes Q-fever in animals.(a) Mycoplasma (b) Bacteria (c) Rickettsia (d) Chlamydia8. Ringworm is caused by a.......(a) Bacteria (b) Virus (c) Fungi (d) Parasite9. Transmission ofdiseases from one generation to another is known as.......(a) Vertical (b) Horizontal (c) Triangular (d)All of the above10. Aflatoxins are produced by..........(a) Aspergillusflavus (b) Asperfillus parasiticus (c) Penicillium puberlum (d)All of the above33
  47. 47. General Veterinary Pathology11. Pesticide includes..... .(a) Insecticide (b) Rodenticide (c) Weedicide (d)All ofthe above12. Acetone, ~-hydroxybutyrate and acetoacetic acid are known as.......(a) Ochratoxins (b) Ketone bodies (c) Heinze bodies (d)Pyknotic bodies13. Prolonged starvation leads to................... ofmuscles(a) Hypertrophy (b) Hyperplasia (c) Atrophy (d) Metaplasia14. Deficiency ofvitamin A causes....................(a) Nutritional roup (b) Nyctalopia (c) Calculi in urethra (d)All ofthe above15. Vitamin D regulates the activity of......................(a) Lymphocytes (b) Macrophages (c) All ofthe above (d) None ofthe above16. Star grazing in chicks in caused by ....... deficiency(a) Vitamin BJ (b) Vitamin B2 (c) Vitamin B6 (d) Vitamin BJ217. Curled toe paralysis is caused by ....... deficiency(a) Thiamine (b) Riboflavin (c) Choline (d) Biotin18. Crazy chick disease is caused by ....... deficiency(a) Vitamin A (b) Vitamin C (c) Vitamin D (d) Vitamin E19. Perosis is caused by ....... deficiency.(a) Biotin (b) Choline (c) Manganese (d)All ofthe above20. Rheumatism like syndrome is caused by deficiency of .......(a) Calcium (b) Phosphorous (c) Copper (d) Zinc34
  48. 48. 3GENETIC DISORDERS,DEVELOPMENTALANOMALIES AND MONSTERS• Genetics• Chromosomes• Genetic disorders• Aberrations in chromosomes• Anomalies• Monsters• Model Questions
  49. 49. General Veterinary PathologyGENETICSGenetics is the branch of science that deals withstudy of genes, chromosomes and transmittance ofcharacters from one to generation another.CHROMOSOMESChromosomes are thread-like structures present inthe form of short pieces in nucleus of a cell. Theyare in pairs; of which one pair is sex chromosomeand others are autosomes.Table 3.1 Number of chromosomes in differentspecies of animalsSI.No.1.2.3.4.5.6.7.8.••••AnimalChromosomesMale FemalePairs TotalCattle 30 60 XY XXSheep 27 54 XY XXGoat 30 60 XY XXPig 19 38 XY XXDog 39 78 XY XXCat 19 38 XY XXHorse 32 64 XY XXPoultry 39 78 ZZ ZWEach chromosome is composed of twochromatids connected at centromere.x__ChromathiFig. 3.1 Diagram o/ChromosomesChromosomes are grouped together on thebasis of their length, location of centromereand this procedure is known as karyotyping.The study of karyotyping is known ascytogenetics.Chromosomes are composed of 3 components:• DNA-20%• RNA -10%• Nuclear proteins - 70%36Deoxyribo nucleic acid (DNA)• Double helix structure of polynucleotidechain.• A nucleotide consists of phosphate, sugar andbase of either purine (Adenine, Guanine) orpyrimidine (Thymine, Cytosine).Fig. 3.2. Double helix DNA structure• A sequence of 3 nucleotide determines thesynthesis of an amino acid and is known asgenetic code/codon.• During cell division, one half of DNAmolecule acts as template for the synthesis ofother half by an enzyme DNA polymerase totransmit the genetic information which mayalso transit some disorders to next progeny.Gene• Sequence of nucleotides which controls thesynthesis of one specific protein is known asgene. It is a unit of function. Study of genes istermed as Genetics. In higher animals about1.0 million genes are present.• Genes located on X or Y chromosomes aretermed as sex linked and all other genes areautosomal genes.• When the genes at one locus are same fromboth parents they are termed as homo(,Ygousbut when they are different at one locus theyare known as hetero(,Ygous.• In heterozygous, characters of one gene aremanifested in phenotype and such gene isknown as dominant while unexpressed gene iscalled as recessive.
  50. 50. Genetic Disorders, Developmental Anomalies and MonstersKaryotyping• Karyotyping is the study of chromosomes incell.• Collection of blood, separation oflymphocytesusing Histopaque-l077 gradient.• The lymphocytes are cultured with mitogenconcanavalin A (ConA) or phytohemagglutinin- M (PHA-M) for 72 hrs.• Colchicine is used after 72 hrs to arrest the celldivision at metaphase stage.• Hypotonic solution is added to allow cells toswell which causes separation ofchromosomes.• Prepare glass slides and stain with Giemsa orother special stain.• Identify the chromosomes and photographthem.• Cut photographs having homologous chromo-somes and make pairs.GENETIC DISORDERSABERRATION IN CHROMOSOMES• A large number of chromosomal aberrationsare removed due to death of gamete or zygotewhich is termed as "species cleansing effect".However, some aberrations persist and areexpressed in phenotype leading to illness.1. Aberration in number• Chromosomes are in pairs (2n). When numberof chromosomes are other than (n) or (2n). Itis known as heteroploidy.(a) Heteroploidy• The number of chromosomes are other than(n) or (2n).• When abnormal number is exact multiplies ofthe haploid set due to errors in mitosis. Thepolar body may fail to be extruded from ovumleaving diplod set to be fertilized by sperm (n)i.e. 2n + n = 3n (Triploid zygote).• When abnormal number is not the exactmultiplies of haploid set. It may have specificchromosome in triple number (trisomy) or in,single number (monosomy).37(b) Duplication and deficiencies• Duplication or deficiency may occur in asection of chromosome and total number ofchromosomes remains same.• Translocation is the rearrangement ofa part ofchromosome in two non-homologouschromosomes. It may be reciprocal or non-reciprocal. Absence of a piece of chromosomeis known as deletion.(c) Mosaicism• In mosaicism, there is more than onepopulation of cells in body; each populationdiffers in their chromosomes/ genes due toerror during development.• May be due to chromosomal non-disjunctionthere is, e.g. XXY in some cells, XY in othercells.(d) Chimerism• In this, one type of cells are acquired in uterofrom a twin e.g. Bovine twin, 1 male and 1female, with~oint placenta. The blood cells ofmale may go in female counterpart. Then thefemale will have two types of cell population,one of its own and another acquired from twin.Similarly, male may also have XX leucocytesin its blood. Such chimeric bulls are sterile.2. Abnormalities in sex chromosomes(a) Klinefelters syndrome• Males have sex chromatin i.e. XXY = 47(2n)in man.• In some cells, different number ofchromosomes i.e. XX, XXY, XXXY, XXYY• It is recognized in adolscence by small testes,tall body, and low sexual characters, mostlyinfertile.• May occur in sheep, cattle and horse.(b) Tortoiseshell male cat• Male cat has small testes, lack of libido andabsence of spermatozoa in testes with 3nchromosomes (XXY).
  51. 51. General Veterinary Pathology(c) Turners syndrome• Mare are with XO karyotype having gonadaldysgenesis and such animals are sterile and donot have sex chromatin.• In mice XO karyotype is normal.(d) Intersexes• In this condition ambiguity occurs in genitaliaor the secondary sex characters are present forboth the sexes including male and female.• Hermaphrodites have male and femalegenitalia while pseudohermaphrodites haeexternal genitalia of one sex and gonads ofopposite sex.(e) Freemartinism• In bovine twins, one male with (XY) and onefemale (XX) karyotype but they shareplacental circulation so cells of embryoestablish in other co-twin.(j) Testicularjeminization• The animal has female genitalia as externaland internal organs but in place of ovaries,there are testes. It occurs due to single genedefect and makes tissues unresponsive toandrogenic hormones.3. Abnormalities in autosomal chromosomes(a) Downs syndrome!Mongolism• It occurs as a result of trisomy, number of aparticular chromosome increases leaving 2n, as61 in bovines, 77 in dogs and 47 in man e.g.bovine lymphosarcoma occurs in animals with2n=61. Male dog with 2n= 77 are prone tolymphoma.(b) Sterility in hybrids• Donkey has 2n=62 and horse has 2n=64. Theircross mule has 2n=63.• Cause of sterility in mules is not known, maybe due to uneven number ofchromosomes.4. Abnormalities in genes• Lethal genes are those genes which areresponsible for death ofzygote.38• Sublethal genes• X-linked or sex linked: Diseases transmittedby heterozygous carrier females only to maleoffsprings who are homozygous for X-chromosome.ANOMALIESAnomaly is a developmental abnormality thatoccurs in any organ/tissue. It may be due to geneticdisorder and may affect the zygote itself within afew days after fertilization or may occur during anystage ofpregnancy. It may be classified as under:1. Imperfect development(a) AgenesisAgenesis is incomplete development of an organ ormostly it is associated with absence ofany organ.• Acrania is absence ofcranium.• Anencephalia is absence ofbrain.• Hemicrania is absence ofhalf ofhead.• Agnathia is absence oflower jaw.• Anophthalmia is absence ofone or both eyes.• Abrachia is absence offore limbs.• Abrachiocephalia is absence of forelimbs andhead.••Adactylia is absence ofdigits.Atresia is absence of normal opening e.g.Atresia ani is absence ofanus opening.(b) FissuresFissures are a cleft or narrow opening in an organon the median line ofhead, thorax and abdomen.• Cranioschisis is a cleft in skull.• Chelioschisis is a cleft in lips also known asharelip.• Palatoschisis is a cleft in palates; also knownas cleftpalate.• Rachischisis is a cleft in spinal column.• Schistothorax is a fissure in thorax.• Schistosomus is a fissure in abdomen.(c) FusionFusion is joining ofpaired organs.• Cyclopia is fusion ofeyes.
  52. 52. Genetic Disorders, DevelopmentalAnomalies and Monsters• Renarcuatus is fusion of kidneys; also knownas horseshoe kidneys.2. Excess of development• Congenital hypertrophy ofany organ.• Increase in the number of any organ or part/tissue.• Polyotia is increased number ofears.• Polyodontia is increased number ofteeth.• Polymelia is increased number oflimbs.• Polydactylia is increased number ofdigits.• Polymastia is increased number ofmammary gland.• Polythelia is increased number ofteats.3. Displacement during development(a) Displacement oforgan• Dextrocardia is the transposition of heart intoright side instead of left side ofthoracic cavity.• Ectopia cordis is the displacement of heartinto neck.(b) Displacement oftissues• Teratoma is a tumor ansmg due to someembryonic defect and composed of two ormore types of tissues. In this at least twotissues should be oforigin.• Dermoid cyst is a mass containing skin, hair,feathers or teeth depending on the species andoften arranged as cyst. It mostly occurs in thesubcutaneous tissues.MONSTERSMonster is a disturbance of development in severalorgans and causes distortion of the foetus e.g.Duplication of all or most of the organs (Fig. 3.3).• Monsters develop from a single ovum; theseare the product of incomplete twinning.• Monsters are classified as under:1. Separate twinsOne twin is well developed while another ismalformed and lacks the heart, lungs or trunk,head, limbs.39Fig.3.3. Photograph showing monster calf.2. United twinsThese twins are united with symmetricaldevelopment and are further classified as:(a) Anterior twinningAnterior portion of foetus is having doublestructures while posterior remains as single.• Pyopagus is a monster twin united in thepelvic region with the bodies side by side.• Ischiopagus is a monster twin united in thepelvic region with the bodies at more than aright angle.• Dicephalus is a monster having two separateheads, neck, thorax, and trunk.• Diprosopus is a monster having double organsin cephalic region without complete separationof heads and with double face.(b) Posterior twinningWhen in monsters, the anterior portion remainssingle and posterior parts become double.• Craniopagus is a monster having separatebrain with separate bodies arranged at an acuteangle.• Cephalothoracopagus is the monster havingunited head and thorax.• Dipygus is the monster having doubleposterior extremities and posterior parts ofbody.(c) Almost complete twiningIn some monster, twins have complete develop-ment with joining in thorax and abdomen.
  53. 53. General Veterinary Pathology• Thoracopagus is a monsters united in thoraxregion.• Rachipagus is the monster in which thoracicand lumber portion of vertebral column areunited in twin.• Prosopothoracopagus is the monster twinunited at thorax, head, neck and abdomen.MODEL QUESTIONSQ.1. Fill in the blanks with suitable word(s).1. Chromosomes are grouped together on the basis of ................ and ................... and thisprocedure is known as .....................2. .. ................. is the rearrangement of a part of chromosome in two non-homologouschromosomes and it may be ................... or ................... .3. Acrania is absence of ................... while ................... is absence offorelimbs.4. .. ........... is absence of normal opening; for example................ is absence ofanus opening.S. .. ................, is a fissure in lips which is also known as ....................6. Palatoschisis is a ................... in palates and is also known as...................7. ................... is transposition ofheart into ................... ofthoracic cavity.8. Monsters develop from ................... and are the products of ................... twinning.9. ................... is a monstor united in the pelvic region with the bodies side by side.10. .. ................. is fusion of kidneys and is also known as .................. ..Q. 2. Write true orfalse against each statement. Correct the false statement.Q.3.1. ............Hemicrania is absence ofhead.2. ............Polyotia is decreased number of ears.3. ............Each chromosome contains about 70% DNA.4. .. ..........Monsters develop from a single ovum.5. .............Abrachiocephalia is a absence of forelimbs and head.6. ............ Chromosomes are thread-like structures, composed to two chromatids connectedwith a centromere.7. ............Dipygus is a monster having double anterior extremities and other parts ofbody.8. .. ...........Schistosomus is a fissure in spinal column.9. .............Dicephalus is a monster having two separate head, neck, thorax and trunk.10..............Prosopothoracopagus is a monster, which is not united at head.Write short notes on the following.1. Draw a diagram of DNA structure2. Karyotyping3. Freemartinism4. Anomalies5. Monsters6. Dermoid cyst7. Teratoma8. Aberration in chromosomes9. Testicular feminization10. MosaicismQ. 4. Define the following with suitable examples.1. Cytogenetics 11. Thoracopagus2. Heteroploidy 12. Abrachia3. Agnathia 13. Renarcuatus40
  54. 54. Genetic Disorders, Developmental Anomalies and Monsters4. Anophthalmia5. Cyclopia6. Polythelia7. Ischiopagus8. Ectopia cordis9. Craniopagus10. Polymelia14. Pseudohermaphrodite15. Rachischisis16. Hemicrania17. Chimerism18. Rachipagus19. Deletion20. CephalothoracopagusQ. 5. Each question is provided with four options. Select most appropriate option to fill in or answerthe question.1. Each chromosome contains the DNA content as...................(a) 20% (b) 10% (c) 70% (d) 30%2. The study ofkaryotyping of chromosomes falls under .............. .(a) Immunogenetics (b) Cytogenetics (c) Moleculer genetics (d) Nucleargenetics.3. In heterozygous, one gene character is manifested in phenotype and such gene is known as...(a) Autosomal (b) Recessive (c) Dominant (d) Sex linked4. In karyotyping, colchicine is added in culture ofperipheral blood lymphocytes for arresting thecell division in .......... ..(a) Telophase (b) Meiosis (c) Anaphase (d) Metaphase5. In heteroploidy, the chromosome number will be ...............in cells.(a) n (b) 2n (c) 3n (d) All ofthem6. Intersexes is the condition in animals which occurs due to ambiguity in..............(a) Genitalia (b) Bones (c) Ears (d) Eyes7. In Turners syndrome, mare have karyotype as.................... .(a) XX (b) XXX (c) XXXX (d) XO8. Mules have chromosome number as...........(a) 61 (b) 62 (c) 63 (d) 649. Bovine lymphosarcoma occurs in animals having chromosome number.......(a) 60 (b) 61 (c) 62 (d) 64.10. Dogs with chromosome number......... are more prone to lymphoma(a) 76 (b) 78 (c) 77 (d) 7511. Absence oflower jaw in foetus is known as.......... ..(a) Acrania (b) Adactylia (c) Agnathia (d) Abrachia12. Rachischisis is a cleft in .............. .(a) Spinal column (b) Abdomen (c) Skull (d) Lips13. Harelip is due to fissure in lips and is also known as.............(a) Palatoschisis (b) Cranioschisis (c) Schistosomus (d) Chelioschisis14. Fusion of eyes occurs in monsters and is known as................. .(a) Renarcuatus (b) Columbia (c) Cyclopia (d) Anophthalmia15. Increased number of limbs in monsters is known as .............. .(a) Polythelia (b) Polymastia (c) Polymelia (d) Polydactylia16. Dextrocardia is transposition ofheart in........... ..(a) Right thorax (b) Left thorax (c) Neck (d) Abdomen17. Tumor arising from embryonic defect and composed of more than two tissue.....(a) Dermatoma (b) Hematoma (c) Papilloma (d) Teratoma41
  55. 55. General Veterinary Pathology18. A monster having two separate brains with bodies separately arranged at an acute angle......(a) Cephalothoracopagus (b) Dicephalus (c) Craniopagus (d) Cranioschisis19. A monster united at thorax region and with complete development as twin is known as........ .(a) Prosopothoracopagus (b) Thoracopagus (c) Dipygus (d) Cephalothoracopagus20. A monster having thorax and lumber portion ofvertebral column united in twin is known as.....(a) Rachipagus (b) Craniopagus (c) Thoracopagus (d) Dipygus42
  56. 56. 4DISTURBANCES IN GROWTH• Aplasia• Hypoplasia• Atrophy• Hypertrophy• Hyperplasia• Metaplasia• Anaplasia• Dysplasia• Model Questions

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