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This document provides a table of contents for a veterinary infectious diseases textbook. The table of contents lists 16 sections that will cover viral diseases, bacterial and mycotic diseases, parasitic and rickettsial diseases, and appendices. Some key sections include Section 2 on viral diseases of various livestock species, Section 3 on bacterial and mycotic diseases, and Section 4 on parasitic and rickettsial diseases. The document also provides brief descriptions of what each section will include.

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Table of Contents Section (l)_Introduction Section(2) Viral Diseases 29 16
Table of Contents Untitled 15
Veterinary Infectious Diseases Dr. Ahmed A.A. EL- Sawalhy Professor ofInfectious Diseases Department of Internal Medicine & Infectious and Fish Diseases Faculty ofVeterinary Medicine Mansoura University SECOND EDITION U^RACTITIONER'S and students guide ---- - , ———
Veterinary Infectious Diseases A PRACTITIONER’S AND STUDENTS GUIDE Ahmed A. EL- Sawalhy First Edition, July 22,1997 Second Edition, July 22,1999 All rights reserved Cover design and plates color separation by EL-Araby Graphics in Zagazig 5 Mohamed Saad St., from Nadi EL- Moalemieen St., phone No. 055/331724 and printed in Mansoura Printed and bound in Zagazig by ZAFER OFFICE El-Montazh, Phone No. Q55/.2328163 Distributed in Egypt by AL AHRAM DISTRIBUTION AGENCY I.S.B.N. 977 -19 -8617-1 Corresponding address and request Dr. Ahmed ELSawalhy Department ofInternal Medicine & Infectious and Fish Diseases Faculty ofVeterinary Medicine - Mansoura University Mansoura, Egypt. Phone 050-2030906 / 2236063 / 2214906 Fax 0500 2236041 Home 055-2344220
The Second Edition of Veterinary Infectious Diseases A PRACTITIONER’S AND STUDENTS GUIDE Is Dedicated To ♦ My Family for their constant and loving support during my hard work to advance this book to new levels, ♦ The veterinarians and veterinary students who will use this book in helping to provide the best care for the patients, and ♦Finally to my Colleagues, may you continue to strive foi excellence in our field.
PREFACE Maintenance of animal health and protection of humans against zoonoses are considered to be of the most important tasks ofveterinarians. So, the objective of this book is to provide the field veterinarians and veterinary students with a concise summary of the important infectious diseases in domestic animals with especial emphasis upon to those endemic in Egypt. The book is presented in five sections: 1. Section (1). provides as introduction to infectious diseases, including the definition ofsome terms which are commonly used; 2. Section (2), includes some viral diseases of cattle, buffaloes, sheep, goats, camels, equines, dogs and cats: 3. Section (3), includes bacterial and mycotic diseases; 4. Section (4). includes parasitic and some rickettsial diseases; 5. Section (5). includes 16 appendices for quick reference to commonly used data. This book is supported with many color clinical photos (about 240 photos distributed in 24 color plates) or figures and tables whenever possible. I hope that this book will be a useful guide for field veterinarians and veterinary students in Egypt. The author would like to thank Ms. Jennifer Brown of Prudue University, School of Veterinary' Medicine for her reading and suggestions. Finally 1 am gratefully indebted to my family for their constant and loving support. Ahmed EL- Sawalhy
CONTENTS (v) CONTENTS Section (l)_Introduct»on ................................................................. ... 1 Section!?) Viral Diseases .............................................................................. 13 1. Rinderpest ... ... ... ... ... ... ... ... 15 2. Foot and mouth disease ... ... ... ... ... ... 23 3. Bovine viral diarrhea-Mucosal disease complex ... ... ............... 32 4. Infectious bovine rhinotracheitis ... ... ... ... ... 41 5. Malignant catarrhal fever ... ... ... ... ... ... 49 6. Vesicular stomatitis ... ... ... ... ... ... ... 53 7. Bovine ephemeral fever ... ... ... ... ... ... 57 8. Bovine spongiform encephalopathy ... ... ... ... ... 63 9. Akabane disease ... ... ... ... ... ... ... ... 69 10.Lumpy skin disease ... ... ... ... ... ... ... 73 11 .Enzootic bovine leukosis ... ... ... ... ... ... ... 80 12.Sporadic bovine leukosis ... ... ... ... ... ... ... 86 13.Sheep and goat pox ... ... ... ... ... ... ... 88 14.Cow and buffalo pox ... ... ... ... ... ... ... 94 15.Pseudocowpox ... ... ... ... ... ... ... 97 16.Camel pox ... ... ... ... ... ... ... ... 99 17.Rift valley fever ... ... ... ... ... ... ... ... 102 18.Bluetongue... ... ... ... ... ... ... ... — HI 19.Contagious ecthyma ... ... ... ... ... ... ... 116 20.Peste des petits ruminants... ... ... ... ... ... ... 1-0 21.African horse sickness ... ... ... ... ... — — 1-5 22.Equine influenza ... ... ... ... ... — — 1-9 23.Equine viral arteritis ... ... ... ... ... ... — 134 24.Equine viral rhinopneumonitis ... ............... ... ... — 138 25.Equine infectious anemia ... ........................... . ............... I4- 26.Equine encephalomyelities ................................................................... I45 27.Rabies ................................................................................ ............... 149 28.Pseudorabies ... ... ... ... — — ••• 1^4 29.Canine distemper ... ... ... ............... — ............... 1?'
CONTENTS (vi) _____________________ ~~~~-------—— 30Jnfectious canine hepatitis...................................................................... ... 160 31. Canine parvovirus enteritis ............... — ••• ••• ... 163 32.Viral puppy mortality ...................................................................... - 166 33.Feline panleukopenia ... ............... ... — ••• ••• 169 34.Feline viral rliinotracheitis... ... ... — — ••• ••• 174 35.Feline infectious peritonitis ... ... — ••• — 177 36.Feline immunodeficiency syndrome ... ... — ••• — 181 Section (3) Bacterial and Mycotic Diseases ... ••• ••• ••• 187 37.Anthrax ..................................................................... ••• ••• — 189 38.Clostridial diseases ... ................ ... ••• — — 197 39.Lamb dsentery ... ... ... ... ... — ••• ••• 198 40.Struck ... ............... ... ... ... — ••• — 205 41.Pulpy kidney ............... ... ... ... ... ••• — 207 42.Malignant edema............... ... ... ... ... ••• 210 43.Braxy ................................................................................... — ••• 214 44.Blackleg ... — — 215 45.Bighead ........................................... — - 220 46. Black disease ....................................................... ... ... 221 47.Bacillary hemoglobinuria.......................................... ... ... ••• 225 48.Tetanus ... ... — 229 49.BrucelIosis.................................................................................. ... — 50.Listeriosis ..................................................................... ... — z 51 .Leptospirosis ....................................................... ... ... ••• 258 52.Contagious bovine pleuropneumonia ............................. ... —265 53.Haemorrhagic septicaemia.......................................... ... ... ...270 54.Tuberculosis ............................. ... - 276 55.Skin tuberculosis..................................................................... ... - 284 56 Johne’s disease ..................................................................... ... - 285 291 57.Actinomycosis ..................................................................... ... - 5g.Actinobacillosis ..................................................................... ... - 294 • • 997 59.Dermatophilosis ..................................................................... 60.Bovine farcy ............... ... ... •••
CONTENTS (vii) 61.Contagious skin necrosis ... ... ... ... ... ... .. 304 62.Infectious bovine keratoconjunctivitis ... ... ... ... ... 306 63.Mastitis ... ... ... ... ... ... ... ... ... 310 64.Infectious calf diarrhea ... ... ... ... ... ... ... 329 65.Salmonellosis ... ... ... ... ... ... ... ... 341 66.Respiratory disease complex in calves ... ... ... ... ... 351 67.Navel ill ... ... ... ... ... — — — ••• 358 68.Calf diphtheria ... ... ... ... ... ... — 360 69.Contagious foot rot ... ... ... ... ... ... — 363 70.Caseous lymphadenitis ... ... ... ... ... --- 367 71.Ulcerative lymphangitis ... ... ... ... — ... — 371 72.Strangles ... ... — ••• — — ••• — — 377 73.Glanders ... ... ... ••• ... — ••• — — 381 74.Epizootic lymphangitis ... ... ... ... — — 385 75.Sporotrichosis ... ... ... ... ••• ••• ••• 388 76.Ringworm ... ... ... ... ••• — ••• — ••• 391 Section (4) Parasitic and Some Rickettsial Diseases ... ... ... 399 77.Bovine Babesiosis ... ... ... ... ... — — — 401 78.Ovine and Caprine Babesiosis ... ... ... ... ••• — 408 79.Equine Babesiosis ... ... ... ... ... — — 409 80.Canine Babesiosis ... ... ... ... ... — — — 412 81.Theileriosis... ... ... ... ... ... — — ••• 414 82.Tropical Theileriosis ... ... ... ... ••• — ••• 415 83.Malignant ovine theileriosis ... ... ... ••• — — 419 84.Anaplasmosis ... ... ... ... — — ••• ••• 421 85.Trypanosomiasis ... ... ... ... ... — ••• — 425 86.Surra ......................................................................................................................426 87.Dourine ... ... ... ... ... ••• ••• ••• ••• 432 88.Toxoplasmosis ... ... ... — — ••• ••• — 436 89.Coccidiosis ... ... ... ... ••• — — 440 90.Cryptosporidiosis ... ... ... ... — ••• ••• 444 91.Mange ... ... ... ... ... ... ••• ••• 448
CONTENTS (viii),_________________________ 92. Warble ... ••• ••• ••• ... ... ... . 453 93. Screw worm myiasis .......................................... ... _ 455 94. Nasal Myiasis .................................................................... ... 462 95. Botfly ................................................................................. ... ... 464 96. Fascioliasis .................................................................... ... 466 97. Paramphistomiasis ................ ... ... ... ... _ 473 98. Schistosomiasis................................................................................... ... 475 99. Habronemiasis ............................ • ............................................ ... 480 100.Verminous pneumonia ............... ... ................. 433 101.Ascariasis .................................................................... ... ... 487 102.Strongylosis of horses .....................................................................................490 103.Parasitic gastroenteritis.....................................................................................493 104.Filariasis......................................... — ... ... ... ... 504 105 .Tapeworm infestation .....................................................................................509 106.Coenurosis ....................................................... ... ... ... 511 107.Echinococcosis ............... ... ... ... ... ... ... 513 Section (5) Appendices ...................................................................... ... 515 108.Appendix (1) Clinical normality of domestic farm animals ... ... 517 109.Appendix (2) Normal hematology values of domestic farm animals ... 518 110.Appendix (3) Normal Clinical chemistry values of domestic farm animals 519 111 .Appendix (4) Topographical anatomy of a cow ... ... ................. 520 112.Appendix (5) Differential diagnosis of cattle and buffalo diseases ... 522 113.Appendix (6) Differential diagnosis of sheep diseases ... ... ... 525 114.Appendix (7) Differential diagnosis of goat diseases ... ... ... 528 115.Appendix (8) Differential diagnosis of horse diseases ... ... ... 531 116.Appendix (9) Differential diagnosis of dog diseases ... ... ... 534 117.Appendix (10) Differential diagnosis of cat diseases ... ... ... 536 118.Appendix (11) Drug dosage list in domestic farm animals ... ... 539 119.Appendix (12) Some common veterinary drugs in Egypt.............. ... 542 120.Appendix (13) Suggested vaccination programs for farm animals in Egypt 555 121.Appendix (14) Susceptibility of farm animals to infectious diseases 557 122.Appendix (15) Patterns ofmammalian reproduction in different animals 560
LIST OF COLORED PLA TES (ix) LIST OF COLORED PLATES 1. Plate 1 A ... ... ... 2. Plate 1 B ... ... ... ................ 40 3. Plate 1 C ... ... ... ... 51 4. Plate ID ... ... ... ... ... ... . 52 5. Plate 2 A ... ... ... ... ... ................ ... 89 6. Plate 2 B ... ... ... ... ... ... ... ... 90 7. Plate 2 C ................................................................................................... 107 8. Plate 2 D ... ... ... ... ... ... .... ... 108 9. Plate 3 A ....................................................................................................185 10.Plate3B 11.Plate3C 12.Plate 3 D 13.Plate4A 14.Plate 4 B 15.Plate 4 C 16.Plate 4 D 17.Plate5A 18.Plate 5 B 19.Plate 5 C 20.Plate 5 D 21.Plate6A ............................. .............................. .............................. 457 ... 458 22.Plate 6 B ... 459 23.Plate 6 C .............................................. - ................. ... 460 24.Plate 6 D
LIST OF TABLES (x)__________________ ________________________ __ ________________ LIST OF TABLES 1. Differential diagnosis of Rinderpest and in cattle and sheep ................. 20 2. Differential diagnosis of Foot and mouth disease and vesicular stomatitis 29 3. Specimens for laboratory use in Bovine viral diarrhea-Mucosal disease ... 36 4. Susceptibility of animals to Brucella organisms ... ... ... ... 238 5. Differential diagnosis of Brucellosis ... ... ... ... ... 248 6. Types ofvaccines available to use for control of Brucellosis ... ... 250 7. The pathogenicity of Mycobacteria spp to domestic and laboratory animals 276 8. The relationship between the stages in the pathogenesis of Johne’s disease, the presence of clinical disease and results of diagnostic tests ... 287 9. The relationship between the number of leukocytes in the milk and results of California mastitis test ... ... ... ... ... ... 320 10.The relationship between the number of bacteria in the milk and degree of clinical manifestation of udder ... ... ... ... ... ... 321 11.Bacteriological cure rates of mastitis for selected gram positive intramammary infections using Cloxicillin............ ... ... ... ... ... 323 12.Guide to estimate the degree of dehydration and the corresponding ' base deficit in diarrheic calves.......... ... ... ... ... ••• 337 13.The different types of organisms incriminated in the etiology of Respiratory disease complex....... ... ... ... ... ... 351 14.Antimicrobials commonly used in calves ... ... ... ... ... 356 15. Different species of Babesia in cattle and buffaloes in relationship to vectors, distribution and climatic reference......... ... ... ... 402 16.Different species ofTheileria in domestic animals in relationship to vectors, disease produced, distribution and pathognomonic clinical signs 414 17.Different species ofTrypanosomes in domestic animals and humans in - relation to vector transmission, disease produced, distribution and pathognomonic clinical signs ... ... ... ... ... 425 18.Chemotherapy of trypanosomiasis in livestock ... ... ... ... 431 19.Different species of mites in domestic animals, in relationship to - disease produced, and pathogenomic clinical signs ... ... ... 448 20.Difference between Fasciola and Paramphistomum eggs ... ... ... 470 21.Some common drugs used for treatment of Fasciolasis ... ... ... 472 22.Some common drugs used for treatment of Paramphistomiasis ... ... 476 23.Different species of Schistosoma in relation to intermediate host snails, definitive hosts, and distribution ... ... ... ... ... 477 24.The different species of gastrointestinal parasites in domestic animal species in relation to diseases produced and pathognomonic clinical signs 495
LIST OF TABLESAND FIGURES (xi) 25.The different species of filaria in different domestic animal species in relationship to disease produced and pathognomonic clinical signs............. 505 26.Clinical normality of domestic Farm animals ... ... ... ... 517 27.Normal hematological values in domestic farm animals ... ... ... 518 28.Normal clinical chemistry values in domestic farm animals ... ... 519 29.Drug dosage list of some drugs in domestic farm animals ... ... 539 30.Common broad spectrum anthelmintic drugs used in Egypt ... ... 542 31.Common drugs used for blood parasites in Egypt... ... ... ... 547 32.Common broad spectrum antibiotic drugs used in Egypt ... ... ... 549 33.Common drugs used for treatment of mastitis in Egypt ... ... ... 552 34.Common drugs for general use in Egypt.............................................................554 35.Suggested vaccination program for cattle and buffaloes in Egypt... ... 555 36.Suggested vaccination program for sheep, horses and dogs in Egypt ... 556 37.Susceptibility of domestic animals to various infectious diseases 557 38.Pattern of mammalian reproduction in different animals ... ... ... 560 LIST OF FIGURES 1. Pathogenesis of Enzootic bovine leukosis ... ... ... ... ... 82 2. Transmission of RVF............ ... ... ... ... ... ... 102 3. Pathogenesis of enteric Salmonellosis ... ... ... ... ... 343 4. Pathogenesis of septicemic Salmonellosis... ... ... ... ... 344 5. Life cycle of the liver fluke ... ... ... ... ... ... 467 6. Lung worm life cycle ... ... ... ... ... ... ... 484 7. Diagramatic representation of the life cycle of haemonchus species ... 494 8. Topographical anatomy of a cow ... ... ... ... ... ... 520
LIST OFABBREVIATIONS (xii) LIST OF ABBREVIATIONS IP Incubation period pl Microliter AGID Agar gel immunodiffusion pm Micrometer CIEP Counter immunoelectrophoresis iu International unit PAA Passive haemagglutination test Vs viruses ELISA Enzyme linked immunosorbent assay i/p intraperitoneal MDBK Madin Darby bovine kidney i/m intramuscular IIFT Indirect immunofluorscent test i/v intravenous DIFT Direct immunofluorscent test s/c subcutaneously BHV Bovine herpes virus i/n intranasally MLV Modified live virus vaccine kg kilogram HI Haemagglutination inhibition B.W. Body weight EM Electron microscope PCV Packed cell volume CAM Chorioallantoic membranes of Hb Hemoglobin embryonated eggs epg eggs per gram of feces RIA Radioimunoassay USA United state of America CNS Central nervous system UK United kingdom EDTA Ethylene diamine tetra acetic acid USSR Former Soviet union SNT Serum neutralization test CPE Cytopathic effect VNT virus neutralization test PCR Polymerasechain reaction CFT Complement fixation test ml milliliter BHK Baby hamster kidney cell line i.e. that is TCID50 Tissue culture infective dose 50 e-g- for example VIA Virus infection associated antigen °C Celcius degree RNA Ribonucleic acid PH negative logarithm of DNA Deoxyribonucleic acid hydrogen ion activity % percent sp/spp species a alpha / per P beta Q sigma 8 delta > greater than £ epsilon greater than or equal Y gamma < less than K kappa C less than or equal ± plus or minus equal
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_ __________________________________________________INTRODUCTION (1) INTRODUCTION Disease can be defined as an inability to perform physiological functions at normal levels, provided that nutrition and other environmental requirements are present with adequate levels; or, it may be defined as any deviation in the general state ofthe normal body. In general, the diseases can be classified according to:- I. The infectiousness A. Infectious disease, is that disease caused by entrance, multiplication and activities of any infectious agents (bacteria, viruses, fungi and parasites), which cause pathological changes in tissues, manifested by the development of signs of illness (symptoms). According to their spread from one host to another, they can be typed into contagious diseases and non contagious diseases. B. Non infectious disease, is that disease caused by to any disturbances in '■ normal metabolism, environmental conditions, trauma, physical and chemical agents. IL The transmissibility The transmissibility of the pathogen involves its ability to grow profusely and to be shed in large numbers in body fluids or excretions in order to infect or to be transmitted to a new host; also, the highly virulent pathogenic strains must survive in adverse environmental conditions, through which they reach a new host; or it may be defined as the case with which a disease agent is spared within populations. The diseases can be typed according to their transmissibility into:- A. Contagious disease, is one in which the specific infectious agent or its toxic products are transmitted from an infected animal, person or inanimate reservoir to a susceptible host, cither by direct and indirect contact. The spread of the disease depends mainly on the way of the elimination of tire organism from the host. In general examples for contagious bacterial diseases include Brucellosis and Contagious bovine pleuropneumonia; examples for viral diseases include foot and mouth disease. Cattle plague. Cow pox. Contagious ecthyma in sheep,
INTRODUCTION (2)___________________________________________________________________ - and Epizootic lymphangitis in equine; and finally, examples for parasitic diseases include Coccidiosis in calves and Mange in sheep. B. Non contagious infectious disease, is one that is not communicable to others, such as wound. bift and insect borne infections, include Tetanus, Black disease, Rabies, Bluetongue and African horse sickness. III. The etiology A. Bacterial disease, is one that induced by bacteria. Examples include Brucellosis, Leptospirosis, Tuberculosis. Anthrax and Clostridial diseases. B. Viral disease, is one that is induced by viruses. Examples includ Cattle plague, Foot and mouth disease, Rift valley fever and Contagious ecthyma. C. Fungal disease, is one that is induced by molds and fungi. Example include Mycotic dermatitis. D. Parasitic disease, is one that is induced by parasites which may be due to protozoa (examples Babesiosis, Theileriasis, Anaplasmosis, Trypanosomiasis); it may be due to arthropods (as Hypoderma bovis, Oestrus ovis or Nasal myiasis); it may be due to trematode (as Fascioliasis, Paramphistomiasis); it may be due to nematodes (as Verminous pneumonia or parasitic gastroenteritis); or it may be due to cestode (as Tape worm infestation). E. Multifactorial disease, is one that is induced by several infectious agents, as Infectious calfdiarrhea and Mastitis. The course (duration), means the time from appearance of signs until the end result of the disease (either recovery or death). A. Pcraciite disease (fonn), is one that causes very rapid death within a few hours or days, usually due to septicemia, as in Anthrax and Clostridial diseases. B. Acute disease (form), is one that causes severe infection and takes a relatively longer course (a few days to one or two weeks) as in Cattle plague, Foot and mouth disease and Salmonellosis. C. Subacute disease (form), is one that takes a longer course (extended to few e---— ...................................... •'«— weeks).
INTRODUCTION (3) D. Chronic disease (form), is one that takes a very long course (prolonged for several months to few years) due to the slow growth of the organism, as in Bovine tuberculosis, Caseous lymphadentitis in sheep and Glanders in horses. VTThe occurrence^) A. Sporadic disease, is one that occurs rarely and without regularity in a population. One explanation might be that infection exists in the population inapparently, and only in occasional few animals do signs ofdisease appear, as in Blackleg, Bovine viral diarrhea-Mucosal disease complex and Malignant catarrhal fever. B. Endemic disease, is one that is characterized by a usual frequency of occurrence in a population and the constant presence in a population (confined to a certain district or locality), as in Fascioliasis or soil borne infections in Egypt. C. Epidemic disease (Epizootic), is one in which the frequency within the population during a given time interval is clearly in excess of the expected frequency, usually such diseases are characterized by a rapid spread as in Cattle plague and Foot and mouth disease. A pandemic is a ven large scale epidemic, usually involving several countries or continents. — - . - . ■■ ------ I' — • D. Exotic disease, is one that is introduced into a certain area or country’ that was previously free from it; animals are usually highly susceptible to the disease agent; the main sources ofdisease producing agents are importation of living animals, animal products, semen, embryos and biological materials; lack of quarantine facilities, free animal movement and deficiency of laboratory skill, diagnostic materials and modem technical facilities facilitate the introduction of exotic diseases in developing countries. In Egypt, exotic diseases of European origin are Bovine viral diarrhea-Mucosal disease complex. Infectious bovine rhinotracheitis (IBR) and Infectious bovine pustular vulvovaginitis (IPV) in 1976, and Para influenza 3 (PI3); exotic diseases of African origin as Lumpy skin disease introduced in 1988, Equine influenza in 1989, Rift valley fever in 1977, Bluetongue in 1970, Peste des petits ruminants in 1989, Contagious ecthyma, African horse sickness, and Contagious bovine pleuropnumonia in 1969, In general the exotic diseases in one country may be endemic in another country.
INTRODUCTION (4)________________________________________________ ______ There are a general rules for recent exotic diseases in a country, as: no treatment, no vaccination by live attenuated vaccine, and the animals must be slaughtered under strict hygienic conditions. Some common terms may be used in infectious diseascs:- A. Notifiable disease, means the owner or field veterinarians must immediately report any suspicions of some infectious diseases to local authorities for protection of both human and animal health to take all the required measures to confirm the diagnosis, quarantine and other control measures; such diseases cause high economic loss or are characterized by public health importance, as in Anthrax, Brucellosis, Tuberculosis, Glanders, Cattle plague, Foot and mouth disease and Rabies. B. Epidemiology, may be defined as the study of health and disease of populations and involves ♦ The observational study of naturally occurring versus experimentally induced disease; ♦ The study of disease in the population versus the individual; ♦ The detection of associations by inferential methods versus the study of pathologic methods. Epidemiology also can be defined as the study and interpretation of the mass phenomena of health and disease. It is the counterpart of clinical medicine, taking the population group or the herd as the unit of study rather than the individual paitents. The term epidemiology derives from the Greek words Epi = upon or about; demos = people; and logo = science. The term epizootology is sometimes used in reference to studies of animal population; but now the term epidemiology is understood to refer to all animal populations, human and other wise. C. Morbidity rate or attack rate:- It can be defined as the amount of disease in a population, it is useful for identifying risk factors for a specific disease. No. ofaffected animals during outbreak Morbidity rate = —-------------------------------------------------------- X 100 Population at risk at the beginning of outbreak
INTRODUCTION (5) D. Mortality rate or fatality rate:- It can be defined as the number of deaths in a population, it is used for determining the prognosis for a specific disease. No. of deaths from a specific cause Mortality rate =------------------------------------------------ X 100 Total No. of cases of the same disease E. Incidence rate:- It can be defined as the number ofnew cases that occur in a known population over a period of time. It measures the flow of individuals from the disease free to the diseased state. No. of new cases of a disease over a time interval Incidence rate - --------------------------------------------------------------------- X 100 Average population at risk during same time interval F. Prevalence rate (P):- It can be defined as the amount of disease in a known population at a designated time, without distinction between old and new cases. No. of individuals having a disease at a particular point in time p - ------------------------------------------------------------------------------------ X100 No. of individuals in the population at risk at that point of time For example, if 20 cows in a herd of 200 cows were lame on a particular day, the prevalence of lameness in the herd on that day would be 20/200 XI00 = 10 %, that means the probability of an animal having a specified disease at a given time. The prevalence (p) depends on the duration (D) and incidence (I) of a disease. P oc I x D . This means change in prevalence can be due to change in incidence, a change in the average duration of the disease, or a change in both. G. Inapparent infection:- Can be defined as infection of a susceptible animal without clinical signs. The infection usually runs a similar course to that which produces a clinical case, with replication and shedding of agent; this causes a considerable problem for disease control. H. The carrier state:- May be defined as any animal that sheds an infectious agent without demonstrating clinical signs. Thus, an apparently or subclinically infected animal may be a carrier, and shed the agent either continuously or intermittently .
INTRODUCTION (6)_________________________________________________ I. Latent infection:- A latent infection is one that persists in an animal without producing clinical signs. J. Incubation period:- Is the period oftime between infection and the development of clinical signs. K. Routes of infection (Mode of infection):- The site(s) by which an infectious agent gains entry to the body of a susceptible individual and by which it leaves the host (exit); the agents routes of infection include: alimentary, respiratory, urogenital, anal, skin and conjunctiva: L. Mode of transmission (Mode of spread):- Refers to the way(s) in which an infectious agent is transmitted from affected to susceptible individuals; it may be classified as horizontal or vertical and within horizontal as direct, indirect or air borne. M. Horizontal transmission:- Means the transmission of an infectious agent from any segment of a population to another, either directly or indirectly. N. Direct transmission:- Occurs when a susceptible host contracts an infection, either by direct contact with an infected host or through touch, a scratch, lick, bite or intercourse or by contact with the latter’s infected discharges as feces, urine or droplet spread onto the conjunctiva or mucous membranes of the eyes, nose, or mouth, during coughing or sneezing. O. Indirect transmission:- Involves an intermediate vehicle, living or inanimate vector, that transmits infection between infected and susceptible hosts. f Vehicle borne transmission, occurs through exposure to contaminated inanimate objects (fomites) such as bedding, surgical instruments, soil, water, food, or milk and biological products as blood, serum. The agent may or may not have multiplied or developed in or on the vehicle before being transmitted. / Vector borne transmission, is generally understood to mean transmission by invertebrate vectors, such as flies, mosquitoes or ticks. In some cases vertebrate hosts such as dogs, foxes or bats may serve as vectors as in case of Rabies transmission. Transmission may be through infection of salivary gland fluid during biting, or by regurgitation or deposition of feces on the skin, or other body fluids that contaminate host tissues through the bite wound or through an area of trauma.
INTRODUCTION (7) • induced by scratching or rubbing. Vector borne transmission may be either mechanical or biological. Mechanical transmission results from simple mechanical carriage ofthe disease agent between hosts by the vector. It does not require multiplication or development of the disease agent in the vector. The disease agent is transmitted between hosts on soiled appendages or the proboscis, or by passage of organisms through the gastrointestinal tract. Biological transmission requires a period ofmultiplication, cyclic development or both before the vector can transmit the infective form ofthe agent (RVF), the disease agent may be transmitted vertically (transovarially) between generations of vectors or from one stage to another within a single generation (Babesiosis). P. Air borne transmission involves the dissemination of microbial aerosols. Microbial aerosols are suspensions of particles in the air, consisting partially or wholly of microorganisms; they may remain suspended in the air for long periods of time and usually infect the host via the respirator}' tracts; particles diameters range 1-100 pm (FMD). Q. Vertical transmission describes the transmission of a disease agent from animals of one generation to subsequent generations (Akabane disease and BVD-MD complex). Vertical transmission may be transovarial (example: between generations of invertebrate vectors via the egg), in utero or transplacental, (example: from parent to offspring within the uterus), or colostral, (from parent to offspring at parturition via colostrum or milk). Vertical transmission provides an important reservoir for certain vector borne viruses and protozoa. R. Symptom is any subjective evidence of disease or of a patient's condition (i.e., such evidence as perceived by the patient); a change in a patient's condition indicative of some bodily or mental state. S. 'fhe Officer International des Epizooties (OIE), an organization in France, was established in 1924 in order to promote world animal health, and its main activities are as follows:-
INTRODUCTION (8)___________________________________________ ♦ To collect and disseminate to its Member Countries, information (including emergency information) on the occurrence, course and treatment of animal diseases. ♦ To provide guidelines and standards for health regulations applicable in the international trade of animals. ♦ To promote and co-ordinate research on the pathology, treatment and prevention of animal diseases when international collaboration in such research is desirable. According to the OIE numbering system the diseases are listed in three lists:- ♦ List A includes those diseases which spread rapidly, the scope of which extends beyond national borders, these diseases have particularly serious socio-economic or public health consequences and are ofmajor importance in the international trade of animal products. (Example: Foot and Mouth disease, Rinderpest, Peste des petits ruminants. Contagious bovine pleuropneumonia, Lumpy skin disease, Rift Valley fever, Bluetongue, Sheep and Goat pox and African horse sickness). ♦ List B includes those diseases which are considered of socio-economic and I or public health importance within countries, and which are also of course, significant in the international trade of animals and animal products such as Anthrax, Bovine brucellosis, Bovine tuberculosis, Haemorrhagic septicaemia, Leptospirosis, Glanders, Rabies, Bovine leukosis, Equine influenza, Babesiosis, Theilcriosis, Trypanosomiasis, Dourine and Mange. ♦ List C includes those diseases with important socio-economic and /or sanitary influence at the local level, such as Listeriosis, Toxoplasmosis, Blackleg and Fasciolasis T. Koch’s postulates:- In 1882 Koch set forth the following postulates for determining that an infectious agent is the cause of a disease:- ♦ The organism must be present in every case of the disease; ♦ The organism must be isolated and grown in pure culture; ♦ The organism must, when inoculated into a susceptible animal, cause the specific disease; ♦ The organism must then be recovered from the animal and identified.
________________________________________ ______ ____________ INTRODUCTION (9) u. Sensitivity of a test, means the proportion ofdiseased animals that are detected by a test; and the ability of a test to detect amount of antigen, enzyme, and so on; a sensitive test will detect small amounts, example as in Rose Bengal plate test (RBPT) for detection ofBrucellosis in animals. True positive Absolute sensitivity (%) =--------------------------------- X 100 Total animals examined True positive Relative sensitivity (%) = ---------------------------------- X 100 True positive + False positive V. Specificity of a test, means the proportion of non diseased animals that are detected by a test; degree of refinement; the greater the specificity, the greater the degree, example as in Rose Bengal plate test (RBPT) for detection of Brucellosis in animals. True negative Absolute specificity (%) =---------------------------------- X 100 Total animals examined True negative Relative specificity (%) = ---------------------------------- X 100 True negative + False negative W.Antigen, a substance (usually protein) that induces a specific immune response (as circulating antibody production) such substance is of high molecular weight. X. Antibody, a protein produced by an animal's immunological system in response to exposure to a foreign substance (antigen). Y. Vaccine is a suspension of attenuated or killed micro-organisms or its products, administered for the prevention and control of infectious diseases; they are used routinely to prevent diseases, and may be used during epidemics to decrease the number of susceptible animals (emergency vaccination), thus assisting in the termination of an epidemic.
INTRODUCTION (10)____________________________________ There are various types ofvaccine. Attenuated vaccines are prepared from live micro-organisms that have lost their virulence but retained their ability to induce protective immunity, as in Sheep pox vaccine, Rift valley fever vaccine and Bj9 for Brucellosis; killed vaccines are prepared from killed micro­ organisms that have lost their virulence completely but retained their ability to induce protection as in Foot and mouth disease vaccine, Rift valley fever vaccine and hemorrhagic septicemia vaccine. Killed vaccines are safer than live vaccines and can be produced more quickly when new agents are discovered. An autogenous vaccine is a vaccine prepared from cultures ofmaterial derived from a lesion of the animal to be vaccinated; toxoid is a toxin that has been treated by heat or chemical agents (such as fonnalin) to destroy its deleterious properties without destroying its abilities to stimulate the formation of antibodies^-as in bivalent or polyvalent clostridial vaccine; serovaccine is a combination of an antisera with a vaccine to produce passive and active immunity. Z. Vaccination is the introduction ofa vaccine into the body to produce immunity to a specific disease. The vaccine may be administered by subcutaneous, intramuscular, intradermal injection, scarification, or by mouth and inhalation. ♦ Quarantine, this is a period of time during which an animal’s movement is restricted, and it is tested and observed for evidence of disease. Quarantine is used to prevent the interherd transmission ofthe disease especially during the incubation period. ♦ Dry cow, A cow that is not producing milk. ♦ Dry off, the act of causing a cow to cease lactation in preparation for her next lactation. ♦ Dry period, non lactating days between lactation. ♦ Colostrum, the first milk produced by the female immediately after giving birth to young. It is highly nutritious and a rich source of antibodies. ♦ California mastitis test, a cow side test for determining whether or not a cow is afflicted by mastitis. A stream of milk is placed in a small cup containing a chemical reagent. The reaction observed indicates the absence or presence and I or severity of mastitis.
INTRODUCTION (11) ♦ Somatic cell count, the number of leukocytes and other body cells found in 1 ml of milk. A high count indicates problems with mastitis in a cow or a herd of cows. ♦ Immunity, a condition in which the animal becomes resistant to disease either through the use of vaccines or sera, or through the production of antibodies resulting from having had the disease. ♦ Pathogen, any microorganism (bacteria, viruses, yeasts, molds, protozoa, helminths) that produces disease. ♦ Bacteriostatic, a substance that prevents the growth of bacteria but does not kill them. ♦ Broad spectrum antibiotic, an antibiotic that is active against a large number of microbial species. Each disease, with few exceptions in this book is described according to the following outline:- I. Introduction 1.1. Synonyms:- Includes the other synonyms and the Arabic name I. 2. Definition:- Short description of the disease, including clinical forms, etiology, hosts, transmission, pathognomonic clinical signs and postmortem lesions. I. 3. History:- With special reference to the history of the disease in Egypt whenever possible II, Etiology The science or study of the causes ofdisease, both direct and predisposing and the mode oftheir operation with especial reference to II. 1. Morphology and staining II. 2. Growth requirements and characteristics II. 3. Resistance III. Epidemiology In studying the epidemiology of any infectious disease, special emphasis is gives to the following points: III. 1. Distribution:- Geographical distribution of the disease all over the world.
INTRODUCTION (12)___________________ III. 2. Transmission:- Includes source of infections and mode of infections, as by ingestion, inhalation, inoculation or injection through skin or mucous membrane by biting insect, contaminated syringe or needle, or wound infection, through the vagina during coitus, contaminated instruments as catheters or semen, and finally may be transplacental infection III. 3. Host susceptibility:- Animals susceptibility in descending order. III. 4. Factors influencing susceptibility:- As in age, sex, breed, condition and season III. 5. The economic importance ofthe disease. IV. Pathogenesis V. Clinical signs Includes the incubation period, morbidity rate, mortality rate and the course, clinical signs and forms of the disease in different animal species. VI. Postmortem lesions VII. Diagnosis VII. 1. Field diagnosis:- Based on the epidemiology, the pathognomonic clinical signs and the postmortem lesions VII. 2. Laboratory diagnosis includes specimensfor laboratory use VII, 3. Differential diagnosis VIII, Prognosis It’s the end results of the disease, which is usually described by favorable, unfavorable or bad prognosis. IX, Treatment Whenever possible includes general and hygienic treatment, supportive treatment, specific treatment and symptomatic treatment. X, Prevention and control With special interest to control measures in enzootic areas and vaccination programs. References
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WRAL DISEASES (15) RINDERPEST JnJC!1dii£iifln j. synonym- Rinderpest (RP), cattle plague, pestis bovina, peste bovine, ordinc to OIE list (A) jjcUaJl ! 2. Defn,i,i0":'RP 1S an acUte hlghly conlagious viral disease primarily of cattle 'nd buffaloes, secondarily of sheep, goat and swine, characterized clinically by fever- erosion- ulceration and necrosis of the alimentary mucosa and severe jfurhea. serous or mucopurulent ocular and nasal discharges. History:- RP was diagnosed for the first time after a severe epidemic spread all over Europe with heavy losses in cattle in 1711-1714. In Egypt, the first epidemic was recorded in Rashid, with very high mortalities in 1827 followed by ^sequent outbreaks in 1841-1843,1927, 1953, 1958,1982 until 1986. fLXlisilesx RP virus is an RNA virus belonging to the genus Morbillivirus of the Family Paramyxoviridae. Strains of RP virus vary in their degree of p’dwaenicity, but all of them are antigenically identical and immunization protects aaainst all strains. RP virus has some antigenic relationship to the viruses of canine distemper, measles of humans and peste des petits ruminants (PPR) which causes a rinderpest like disease (pseudorinderpest) in sheep and goats. II. I. Growth in tissue culture:- RP virus grows well in various tissue culture systems (as in calf kidney cell culture). It produces cytopathic changes, characterized by syncytium formation, intracytoplasmic and sometimes intranuclear inclusion bodies. II. 2. Resistance:- RP virus is very fragile and sensitive to ordinary' environmental conditions, it does not survive outside the host for many hours, also the virus is inactivated by putrefaction, the virus is inactivated in sunlight within 2 hours, in strong acid or alkaline conditions within 10 minutes, and chemical agents as 5 % chloroform, 2 % phenol and 2 % formalin. IIL Epidemiology III. 1. Distribution:- RP is confined to Africa, Middle East, and pans of Asia •tee enzootic foci exist, while Europe. North and South America. Austraha and New Zealand are free from the disease.
RINDERPEST (16) __ ____________________________________________________________ III. 2. Transmission:- A. Source of infection, the RP virus is present in the blood, tissue secretions and excretions of infected animals, such as conjunctival, nasal, vaginal discharge, feces, urine and milk, they contain large quantities of the virus during early stages of the infection. The vims reaches its peak ofconcentration at the peak of temperature reaction and subsides gradually to disappear about a week after the temperature returns to normal. B. Mode of infection, in nature the disease is transmitted by direct contact between infected and susceptible cattle and buffaloes via the major route inhalation, and ingestion of food and water contaminated by the discharge of clinical cases. Animals in the incubation stage may also be an important source of infection, especially in pigs, also the vims can be isolated from a variety of insects, but their role in transmission is not clear, experimentally successful infection occurred by instillation of the vims intranasal, conjunctival, vaginal and orally. On rare occasions, transmission has occurred through indirect contact with contaminated bedding, equipment and clothing. III. 3. Host susceptibility:- Most domestic and wild ruminants are susceptible, but natural infection is most commonly observed in(cattle, buffaloes^ and sporadically in sheep, goats, pigs and camels; wild ruminants are a common source ofinfection and play an important role in eradication programs. III. 4. Factors influencing susceptibility:- Susceptible cattle and buffaloes of all ages, sexes, and breeds are equally susceptible and can be infected and develop serious clinical disease. III. 5. The economic importance ofthe disease:- RP is one of the epizootics in cattle and buffaloes will] the highest losses, it also impairs animal production and activates latent infections such as Babesiasis. lyjPalhegencsis The RP virus has an affinity for lymphoid tissues and the epithelium of the upper respiratory and alimentary tracts. Animals are infected by inhalation of infectious aerosols, after absorption through the mucosa, the virus multiplies in the local draining lymph nodes and then throughout the lymphoid system causing
VIRAL DISEASES (17) destruction to lymphocytes in the tissues, the direct cause for leukopenia. Furthermore viremia occurs which is manifested clinically by fever and at the same time transports the vims to various epithelia, especially in the alimentary tract where its cytopathic growth causes the characteristic lesions. During early stages of the disease, the vims replicates rapidly in the host with production of easily detectable specific antigen which induces high titers of antibody that usually persist for life in recovered animals. Strains of RP vims van’ in their degree of pathogenicity but there is only one main serotype and immunization protects against all strains. Most RP deaths are due to cardiogenic shock in peracute cases, fluid and electrolyte imbalance in later stages. V. Clinical signs ~) V. 1. Cattle and Buffalo:^ A. Incubation period (IP) 3-9 days, with course 6-17 days, the morbidity rate is high approximately 100 % and the mortality rate is 25-90 % (Plate IA photo 1). There is a variety of clinical forms which may be peracute, acute and subacute. B. The(^eracyteform is characterized by sudden onset, inappetence, high fever, depression, deep congestion of visible mucosa, severe panting and racing pulse, death within 2-3 days even before mucosal erosions develop, occurring most frequently in young calves and exotic animals. CfAcujg) form or the classical syndrome is characterized by 4 phases, the feverish or the prodromal phase, the phase of lesions at mucous membranes (Plate 1A photos 2-6), the phase of gasirointestipa[ symptoms and diarrhea (Plate IA photo 8 and Plate 1 B photo I), and the convalescence^phase in surviving animals. The onset of the prodromal fever is sudden, the animal is restless and depressed with shallow rapid respiration, the muzzle is dry, appetite is impaired, rumination is retarded, constipation, lacrimation and serous nasal discharge, visible mucous membranes are congested, the first suggestive sign of RP occurs 2-5 days after the onset of fever, raised pin point gray or white <focb) of necrotic epithelium appear on the mucous membrane lining the mouth, nasal passages and urogenital tracts during the next 2-4 days, these lesions increase in size and number and coalesce into caseous plaques that easily detach leaving
RINDERPEST (18)_______________________________________________ raw red erosions, profuse salivation, the ocular and nasal discharges_become <------- - 1 ■ ■-—«. — purulent. The diarrhea begins as the fever falls 2-3 days after the first appearance ofmucosal erosions, the dark fluid feces contain excess mucus and shreds of epithelium and necrotic debris streaked with blood. D. IifjataT cases progressive dehydration, sunken eyes, collapse and death occurs 6-12 days after the onset of the prodromal fever. In surviving cases the diarrhea stops within a week of its onset, pregnant animals may abort during convalescence which is prolonged and the return to full health will take many weeks. E. Generally subacute forms or milder cases may have all or some of these signs to a lesser degree and a variable proportion ofthe affected animals recover, mouth lesions heal rapidly. In convalescent animals full recovery isprolonged. F. In endemic areas, the disease is generally mild and restricted to calves and yearlings. Epidemic RP particularly in areas where animals have not been infected or vaccinated is characterized by high mortality rates and occurs in all age groups ofaffected animals. G./l common sequel:- RP virus destroys T- and B- lymphocytes, but not memory cells, thus latent pathogens are commonly activated after 4-7 days from the beginning ofthe fever, as in Babesiasis both processes induce clinical signs which create the greatest diagnostic confusion. K 2. Camel:- Can develop subclinical rinderpest especially through contact with infected cattle, but their role in the epidemology ofRP is not clear. 3. Goat and sheep:- The course of the disease is shorter and pneumonic symptoms are more prominent, fever, erosive stomatitis, serous nasal and lacrimal secretion, diarrhea, acute cases die 6-7 days after the onset of illness. 4. Pigs:- Fever, inappetence, depression and the affected pig shivering, vomiting and bleeding from the nose, shallow erosions in the oral mucosa, diarrhea, dehydration and emaciation and pregnant animals may abort. VI. Postmortem lesions The carcass is dehydrated and solid with diarrhea and discharges, erosions and congestion are found throughout the alimentary tract, especially the mouth, pharynx, pillars ofthe rumen, abomasum (Plate 1A photo 8) and large intestine.
VIRAL DISEASES (19) Congestion of capillaries along the crests of the longitudinal folds in the rectal mucosa create the characteristic lesion of "Zebra Striping" (Plate IB photo 1). Other organs have less specific signs, the lungs and the heart may be congested. Lymphoid tissues, the primary target of the virus may have edema and congestion and may be enlarged. VII. Diagnosis VII. 1. Field diagnosis:- RP should be suspected from history of recent animal movement, the epidemiological patterns; as high morbidity and mortality rates, rapid spread, affect all ages; also from clinical signs especially fever, erosions of oral mucosa and diarrhea; and finally from pathognomonic postmortem lesions especially "Zebra Striping" in the colon and rectum . VII. 2. Laboratory diagnosis Specimens for laboratory use are A. In early stage of the fever until the beginning of the erosions collect two blood samples, one with heparin or EDTA (buffy coat), and one without to separate serum and both forward on ice for virus isolation. B. Collect gum scrapings, tears and biopsies of superficial lymph nodes on ice for virus isolation and viral antigen detection tests C. Paired sera are collected from infected animals, one during the acute phase and the second during convalescence. D. Collect slices of lymph nodes, spleen, tonsils and mucosal lesions in 10% formalin saline for histopathology. Three main keys to establish RP virus infection, one is to detect the viral antigen; the second is to isolate the virus; and the third is to detect the specific antibodies Demonstration of the presence of specific viral antigens:- In the tissue, excretions, and secretions of suspected cases using hyperimmune RP antisera via the following tests A. Agar gel immunodiffusion (AGID), it is a rapid field test, commonly used, the positive lines are clearly visible within 2 hours. B. Counter immunoelectrophoresis (CIEP), it is slightly quicker and more sensitive. C. Immunofluorescence, it is useful on frozen sections.
RINDERPEST (20) D. Passive haemagglutination test (PHA) and latex bead agglutination test are more sensitive. E. Indirect enzyme linked immunosorbent assay (ELISA), in which specimens as ocular secretions are simply absorbed onto microtiter plates and then detected by RP hyperimmune sera. Isolation and identification of RP virus:- From the tissues, excretions and secretions by dilution 1:10 in transport medium plus buffy coats and then 10 % suspensions of tissues are inoculated onto young monolayers of primary or secondary bovine kidney or Vero cells growing tubes. A typical CPE of cell rounding, syncytia and strand formation develops 3 days post inoculation of cells. The specificity of CPE can be confirmed by indirect fluorescent test (IF) and histological stains which show intracytoplasmic and sometimes intranuclear inclusions bodies. The detection ofa rise in specific antibodies:- In the sera of suspected cases, the paired sera were examined for antibodies using serum neutralization test (SNT), or ELISA. Histopathological examination:- Of lymphoid organs and mucosal epithelium reveals early formation of multinucleated giant cells containing intracytoplasmic and intranuclear inclusions and later necrosis of lymphocytes and epithelial cells. VII. 3. Differential diagnosis:- RP should be differentiated clinically from A. Diseases with oral lesions and diarrhea, as Malignant catarrhal fever, Bovine viral diarrhea-Mucosal disease complex and alimentary form of Infectious bovine rhinotracheitis. B. Diseases with oral lesions and without diarrhea, as Foot and mouth disease, Bluetongue more common in sheep and goat clinically not affect cattle challenge with virulent strains is indicated, in addition these viruses are antigenically distinct
VIRAL DISEASES (21) and can be distinguished by comparing the reactions of antibodies, antigen or virus with reference reagents, homologous reactions give higher titers than heterologous reactions. Recently cDNA probes have become available that distinguish between the two viruses. VIII. Prognosis The prognosis is very bad due to high mortality rate. IX. Treatment There is no specific treatment and the disease is notifiable X. Prevention and control measures X. 1. In free countries:- Control measures should be directed to prevent introduction of infection by application of all quarantine measures for susceptible livestock, all unprocessed animal products and imported livestock should be antibody negative. X. 2. In enzootic areas:- Control measures depend on the periodic vaccination of all susceptible livestock especially yearling cattle, when outbreaks occur all affected and incontact animals are emergency vaccinated, restricting the movement of both living animals and fresh animal products, all susceptible infected animals and incontact groups must be slaughtered and disposed under strict hygienic measures or keeping the animals in strict isolation for at least one month after clinical recovery with emergency vaccination and infected premises should be disinfected. Attenuated vaccines used to control RP are:- Caprinized vaccine, Lapinized vaccine, Avianized vaccine, and recently tissue culture adapted vaccine is produced in calf kidney cells after upto 100 passages of the virus, these give a high level of attenuation for cattle and advantage its failure to spread by contact, the vaccine does not activate latent infections, it is safe for use in pregnant animals. The vaccine is produced in lyophilized form after reconstitution in normal saline s/c injection of 100 TCID5Q of virus induces high level of protection and life long immunity up to 8-11 years. This type of vaccine produced in Egypt from "Kabete 0 strain" in lyophilized form in vials of 200 and 100 doses which reconstituted in 200 and 100 ml cooled saline respectively and 1 ml injected s/c, branding ear tagging or ear punching help to identify vaccinated animals. Animals recovered
RINDERPEST (22) from natural infection as well as vaccinated animals have life long immunity, this acquired immunity is transmitted to their offspring via colostrum which persist for 5-6 months and prevent the development of active immunity by vaccination during this period, therefore the minimum age for vaccination in calves 5-6 months, but if no colostral antibodies, is indicated to vaccinate the calves in the first week and revaccination again after 6-8 months. Plate 1 A 1. RP causes a high mortality. 2. Excessive salivation follows appearance of oral lesions. 3. Erosions produced by RP on the dental pad and the hard palate resemble FMD lesions. 4. Erosions on the gums caused by RP. 5. Lesions on the buccal mucosa and gums RP. 6. Erosions at the base ofthe tongue. 7. Before dying from RP. cattle frequently assume the classical “Milk fever” position. 8. Fundic portion ofthe abomasum with congestion and hemorrhage RP. Plate 1 B 1. “Zebra striping” in the distal colon and rectum RP References 1. Callis, J. J.; Dardiri, A. H.; Ferris, D. H.; Gay, J. G.; Mason, J. and Wilder, F. W. (1982) "Illustrated manual for the recognition and diagnosis of certain animal diseases" Mexico- United, Commission for the prevention ofFoot and mouth disease. 2. FAO/OIE/WHO (1995) "Animal Health Year Book" 36 Rome, Roma 3. Hungerford. T. G. (1990) "Rinderpest In: Hungerford's diseases of livestock" 9 Edit., McGraw - Hill Book Company Sydney, NewYork, London, Tokyo, toronte, PP 386 - 387 4. Kahrs, R. F.(l 981) "Rinderpest In: Viral diseases of cattle" The Lowa State University Press /Ames, Iowa (32): 275 - 281 5. Radostits, 0. M.; Blood, D. C.; and Gay, C. C. (1994) "Veterinary Medicine A textbook of the diseases of cattle, sheep, pigs, goats, and horses ".8& Edit. Baillier Tindall, England 6. Reid, H.W. (1981) Rinderpest, In: " Diseases of cattle in the tropics" (Ristic, M. and MCIntyreJ., eds) Martinus NijhoffPublishers, The Hague, Boston / London (11): 133 -152 7. Rossiter, P. B. (1992) Rinderpest, In: "Veterinary Diagnostic Virology" (Castro,A.E.,and Heuschele, W. P., eds) Mosby Year Book St. Louis, Baltimore, Boston, London, Toronto (40): 123 - 126 8. Rossiter, P. B. and Wamwayi, H. M. (1989) "Surveillance and monitoring programs in the Rinderpest" A review Tropical Anim. Hith. Prod. 21, 89 - 99 9. Scott, G. R. (1990) Cattle plague, in "Handbook on Animal Diseases in the tropics" (Sewell, M. H., and Brocklesby, D. W., eds) 4 & Edit. Bailliere Tindall, London, Philadelphia, Tokyo PP 287 - 292. 10. Scott, G. R.; Taylor, W. P. and Rossiter, P. B. (1986) "Manual on the diagnosis of Rinderpest" FAO Animal Production and Health Series No. 23 Rome. 11. Uirich Werneiy, and Oskar - Rueger Kaaden (1995) "Infectious diseases ofcamelides" 1 Si Edit. Blackwell Wissenschafts-Verlage, Berlin, Oxford, Edinbuurg, Boston, London.
VIRAL DISEASES (23) FOOT AND MOUTH DISEASE I, Introduction I. 1. Synonyms:- Foot and mouth disease (FMD), Aphthous fever, Aftosa, according to OIE list (A) or ja I. 2. Definition:- FMD is a highly contagious, viral disease of cloven hoofed animals, characterized clinically by fever, vesicular eruptions on the buccal mucosa, the skin ofthe interdigital space and the coronary band. I. 3. History:- FMD was the first animal infection proved to be caused by a virus and the first published data was in Italyl514. In Egypt the first outbreak was detected in 1953, and later outbreaks occurred. II. Etiology FMD viruses belong to the genus Aphthovirus, of the family Picomaviridae, single stranded RNA molecule, ether and chloroform resistant, there are 7 immunologically and serologically, distinct serotypes with different degrees of virulence, within these serotypes there are more than 65 subtypes which are antigenically different based on genomic analysis {A (32), O (11), C (5), SAT} (7), SAT2 (3), SAT3 (4), and Asiai(3)}. There are biotypical strains which become adapted to a particular animal species and virulent to others. In Egypt type A was identified during outbreaks in 1953, 1956, 1958, and type SATj was isolated and identified in 1960, but type Oj substrain wras identified and the most prevalent since 1972 and during the different outbreaks later until now. II. 1. Growth in tissue culture:- FMD Vs grow well in calf kidney or bovine thyroid cell cultures, piglet kidney cell cultures and produce cytopathic changes and the virus is most stable between pH 7.4-7.6 II. 2. Resistance:- FMD Vs are acid and alkali labile, sunlight quickly inactivates the viruses, the vinises can survive after drying in and upon inanimate material from one week to months, they also can remain viable at - 20 °C for 2 years, and in frozen meat for up to 80 days especially in the lymph nodes. The virus may persist for a year or more in infected premises, for 10-12 weeks on clothing and feed. FMD Vs are inactivated by 2 % sodium hydroxide and it is considered the best disinfectant especially after cleaning with 5 % sodium carbonate, also 2 % formalin kills the viruses within a few hours. The virus is destroyed by boiling or autoclaving.
FOOTAND MOUTH DISEASE (24) III. Epidemiology III. 1. Distribution:- FMD is world wide distributed, it occurs enzootically in Africa, the Middle East, Asia and most countries of South America. In contrast only a few countries all over the world are free from infection such as the USA, Canada, Australia, New Zealand, Japan and Great Britain, with a few sporadic outbreaks, the disease is eradicated in most European countries. III. 2. Transtnission:- A. Sources of infections are clinically active animals, carriers and those in the incubation period. Such animals shed the virus in all body secretions and excretions such as saliva due to discharging the vesicular fluids which contain high concentrations ofthe virus, milk, feces, urine and semen. All meat tissues and meat products especially bone, bone marrow, viscera, blood vessels and lymph nodes, remain infective and act as a source of infection for long periods, especially if quick frozen used and to a lesser extent meat chilled or frozen by a slow process due to the development of acidic pH. B. Infection with FMD virus occurs by both inhalation (air borne disease) and ingestion, aerosols of infective droplets generated by infected cattle and pigs under suitable environmental conditions may spread the virus indirectly downwind (wind borne) over a distance of 100 km. C. FMD virus is transmitted and spread either directly by the movement of diseased animals, humans or apparently healthy carrier ones, or transmitted indirectly by transportation of the virus on inanimate objects, vehicles for animal transport, packing material, stable utensils, clothing, feed stuffs, uncooked and unprocessed meat and meat products, milk and its products, and semen. FMD virus can be spread via unsusceptible domestic animals as dogs, cats, migrant birds, poultry, rats and maybe insects such as ticks. III. 3. Host susceptibility:- A. All cloven hoofed animals are susceptible to FMD virus, among the domestic animals cattle and buffaloes, have the highest morbidity rates, followed by pigs, sheep and goats. In Egypt buffaloes are equally susceptible as cows to FMD. B. Many rodents, birds and wild ruminants such as elephants, ungulates and capybara are susceptible and may provide reservoirs of infection for domestic animals.
___________________________________________________ VIRAL DISEASES (25) C. Clinical disease in humans occurs especially in children but is usually rare, infection occurs by drinking infected milk, accidental infection of laboratory workers with the virus, people handling infected animals may become carriers and have the virus in their nasopharynx for more than 24 hours. D. Some sheep, goats and cattle may remain carriers ofthe disease to susceptible animals for up to 6 months after recovery due to continuous low multiplication of the virus in the pharyngeal tissues and mammary glands. 4. Factors influencing susceptibility:- A. In susceptible populations, all ages, sexes, and breeds are infected and develop clinical signs. B. Fatality rates in neonates (calves, lambs and kids) are higher than adults. III. 5. The economic importance ofthe disease:- A. Production of meat and milk is seriously impaired due to the severity of the acute stage ofthe disease and prolonged convalescence period. B. Impairment of the international trade and transit due to restriction ofthe movement of livestock and animal products between countries. C. Occasionally high mortality up to 50 % in calves. D. Mild form of the disease in humans may occur. IV. Pathogenesis The FMD virus gains access to the blood stream after infection either by inhalation or by ingestion, multiplication and transitory viremia occurs for 4-6 days, followed by localization and multiplication ofthe virus in the predilection tissues such as the epithelium of the buccal cavity, pharynx, esophagus, stomachs, feet, teats and occasionally muscles especially cardiac muscles and skeletal muscles, multiplication of the virus results in continuous irritation and / or degenerative changes with formation of the vesicles at these sites which rupture, producing . . secondary bacterial infections and ulcers. V. _Clinical signs K 1. Cattle and buffaloes:- A. The IP in natural infection is 3-8 days, high morbidity rate up to 100 %, but usually low in enzootic areas with mild clinical signs, mortality rate in adults 0.2-5 %, except the malignant form of the disease, in calves it is high upto 50 - 70 % (Plate 1 C photo 4).
FOOTAND MOUTHDISEASE (26)__________________________________________ The course of the disease is usually 2-3 weeks without complications and 6 weeks ifcomplications occur. B. High fever (40-41 °C), for the first 1-4 days, associated with depression, anorexia, cessation ofrumination, increased thirst, and a marked drop in milk production. C. Acute painful stomatitis due to vesicle formation, the body temperature returns to normal after rupture ofthe vesicles, serous nasal discharge, severe ropy salivation and smacking ofthe lips (Plate IB photos 2-3). D. The characteristic vesicles (1-2 cm in diameter) appear on the mucous membranes ofthe mouth, tongue, dental pad, muzzle, udder, teats, on the feet especially in the interdigital space and the coronary band, these vesicles are thin walled contain straw colored fluid and rupture within 24 hours, leaving a painful raw eroded surface, which heals within a week, unless complicated by secondary bacterial infection (Plate 1 B photos 4-8 and Plate 1 C photos 1-3). E. Severe lameness may be complicated by the loss ofthe horny covering ofthe foot and sometimes complete recumbence (Plate 1 C photos 1-2). F. Lactating cows develop vesicles and ulcers on the udder and teats which predispose to mastitis (Plate 1 C photo 3). G. Loss ofcondition, abortion and infertility troubles may occur. Common sequel io FMD in cattle:- A. A chronic syndrome of dyspnea, anemia, diabetes mellitus, over growth of hair, loss ofthermal regulation "Panting" probably due to pituitary lesion. B. Mastitis and abortion may occur during the acute stage or during convalescence with subsequent infertility trouble. C. Myocardial degeneration and deaths in calves (Plate 1 C photos 4-5). D. Sloughing ofthe claws (Plate 1 C photo 2). V. 2. Camels:- There is agreement that camels play an important role as viral reservoirs in the epidemiology of FMD. However FMD in camels creates an especially difficult situation since camels excrete the virus over a certain period oftime, yet produce no antibodies. V. 3. Adult sheep and goats:- Mainly lameness at first, followed by vesicle formation in the buccal cavity and salivation.
VIRAL DISEASES (27) V. 4. Young animals:- Calves, lambs, kids and piglets, sometimes deaths without previous clinical signs due to myocardial necrosis and degeneration, some surrviving animals after FMD attacks exhibit severe dyspnea when exercised and are known as " Panters". V. 5. Pigs:- salivation, vesicles on the snout, rupture leaving shallow ulcers, foot lesions are more easily detected on the coronary band, lameness and the pigs walk on the tips of their toes, sometimes sloughing ofthe hooves. V. 6. Human:- FMD in human inapparent infection, rarely development of vesicles on the hands, feet, oral mucosa, headache and nausea. VI. Postmortem lesions A. Vesicles, erosions and ulcers are found in the buccal cavity, esophagus, stomachs, feet, udder, sometimes trachea and bronchi. B. The pericardium may contain serous fluid. C. In the malignant form of the disease or the newly bom animals, acute degeneration of the cell fibres and necrosis, manifested by the appearance of a small grayish foci in the myocardium (myocarditis) produce a striped appearance known as "Tiger heart" (Plate 1C photo 5) similar lesion may be found in the skeletal muscle. VII. Diagnosis VII. 1. Field diagnosis:- FMD should be suspected from the epidemiological pattern of the disease, rapid spread, high morbidity, low mortality, except the malignant form, high mortality in neonates, clinical signs as salivation, lameness, vesicles, and erosions. VII. 2. Laboratory diagnosis:- Specimens for laboratory use A. For virus isolation or viral antigen detection fresh vesicular fluid and epithelium from ruptured vesicles suspended in equal amounts of glycerol and 0.04 M phosphate buffer pH 7.2-7.6, whole blood sample (huffy coat) in early stage of the disease on heparin from feverish or suspected diseased animals is indicated, esophageal pharyngeal fluid from acute, convalescent and recovered animals, and lymph nodes, kidney, adrenal glands, heart tissues, thyroid or other tissues collected at necropsy are also indicated, and should be frozen. B. For serological examination paired sera should be collected from suspected diseased animals immediately and 3 weeks later to detect antibody titer.
FOOTAND MOUTH DISEASE (28) Isolation and identification ofFMD virus by:- A. Inoculation of vesicular fluid or epithelium in primary or secondary calf kidney or bovine thyroid cell cultures, piglet kidney cell cultures or in susceptible permanent cell lines such as BHKo], baby mice (2-7 days old) and the diagnosis ofvirus by using known antiserum is highly efficient. B. The direct complement fixation test (CFT) on the original epithelial suspension is a rapid method to detect the positive infection within few hours, type specific and strain specific complement fixing antisera used for typing. C. Recently polyacrylamide gel electrophoresis, and polymerase chain reaction (PCR) are used in diagnosis of FMD in Egypt. Serological examination:- Neutralization test, ELISA and fluorescent antibody technique is also indicated for detection of virus or viral antigen as well as its antibodies. ELISA tests for antibody to virus - infection - associated (VIA) antigen may be employed to differentiate between humoral responses to vaccination and natural infection. Experimental transmission in:- A. Unweaned white mice used to detect the virus in suspected material by intraperitoneal (i/p) inoculation, paralysis in the hind legs and death within 7 days, the infection is confirmed by CFT. B. Guinea pig inoculation used to detect FMD virus in suspected material by the intradermoplantar injection offresh vesicular fluid into one foot pad, vesicles appear on all the pads in 1 -7 days and in the mouth 1-2 days later. C. Large animal inoculation test may be used. VII. 3. Differential diagnosis:- A. FMD should be differentiated from diseases with vesicular syndrome, based on the different species susceptibilities to their viruses as in Table 1. Also cross immunity test in guinea pigs may be used to differentiate FMD from VS. B. FMD should be differentiated from mucosal disease complex as Mucosal disease, RP, Malignant catarrhal fever and Bovine infectious rhinotracheitis. C. FMD should be differentiated from pox herpes complex as Papular stomatitis, Cow pox, Bovine mammalitis. D. FMD should also be differentiated from diseases causing lameness as Contagious footrol and Bovine ephemeral fever.
VIRAL DISEASES (29) Items Cattle Swine Sheep & goat Horse guinea pigs and unweaned mice FMD 4“4- + 4- - 4- Vesicular stomatitis (VS) 4-4- 4- 4-4- 4“ Vesicular exanthema y ? - - - VITL Prognosis A. Favorable in adult animals without complications. B. Unfavorable or bad in neonates due to the high fatality of the disease. TX, Treatment FMD is a notifiable disease, isolation and slaughter to control outbreaks in epizootics, but usually in endemic areas as in Egypt, symptomatic treatment as broad spectrum antibiotics, mild disinfectant and protective dressings io inflamed area in mouth and feet to prevent secondary infection, systemic antivirals may be indicated, supportive treatment as glucose solution intravenously in acute cases. X. Prevention and control measures X. 1. FMD Free countries:- A. Prevent the importation of live animals from FMD infected areas and all imported animals should be quarantined for 21 days and tested for the presence of FMD virus in the pharyngeal tissues and for the presence of the antibodies, if possible importation should be directed towards the young stock, which have not been previously vaccinated, so if positive for the antibodies, there is evidence of exposure to infection. B. Importation of frozen meat or meat products and all biological products as semen from FMD infected areas should be prohibited. X. 2. FMD occasionally epizootics occurs infree areas:- A. As soon as the diagnosis of the disease is established all cloven hoofed animals in the exposed groups should be immediately slaughtered and burned or buried. B. Proper disinfection of all materials in infected premises as motor vehicles, farm feeding utensils, machine, bedding, animal products and water proof clothing using 1-2 % sodium hydroxide, fonnalin or 4 % sodium carbonate.
FOOTAND MOUTH DISEASE (30) C. When all possible sources of infection are destroyed the farm should be left unstocked for 6 months and restocking permitted only when "sentinel test" animals are introduced and remain uninfected. D. Human movement to and from infected premises must be reduced to a minimum; persons working and their clothing must be disinfected by spraying or boiling E. Strict quarantine measures on the infected focus within a 16-24 km diameter, no animal movement can be permitted, human and motor traffic must be reduced to a minimum, ring vaccination using killed vaccine around the infected focus may be indicated < X. 3. FMD endemic areas:- During outbreaks, strict quarantine measures, 1 restriction of animal and human movements, closing of markets, destruction of all { sources of infection and vaccination. Vaccination is the basis of most control ( measures and the vaccines must be type specific, but production of the vaccines i from locally isolated virus is becoming a more common practice. Two types of ] vaccine are used: (1) Inactivated vaccines may be monovalent, bivalent and trivalent vaccines, inactivating agent as formalin or recently betapropiolactone or acetylethylenimine (Aziridine), modern vaccines contain aluminum hydroxide or saponin, the antibodies appear and reach a peak 3 weeks post vaccination, the duration of immunity in cattle is 6-8 months and vaccination every 6 months is required. The duration of immunity after natural infection in cattle ranges from 1/2-4 years, and calves receive antibodies via the colostrum of immune cows which are protective for 1-2 months. ) FMD vaccines in Egypt A. Aziridine inactivated tissue culture Oj vaccine is used now and it gives immunity for 8 months, booster dose after 6 months and requires 2 vaccination per year, the dose in cattle and buffaloes is 2 ml and in calves, and sheep 1 ml s/c in dewlap and if the calves were born to vaccinated dams it should be vaccinated at 6 months of age with booster dose at 10 months and if the calves were born to non vaccinated dams it should be vaccinated at 4 months of age with a booster dose at 8 months. B.Formalin inactivated tissue culture 0] vaccine. C. Oil adjuvent 0] vaccine (2) Living attenuated vaccines may be used but it is not safe because the virus is attenuated for one animal species it can remain virulent for others.
VIRAL DISEASES (31) Plate 1 B 2. Excessive salivation cow with FMD. 3. Buffalo with ropy salivation due to FMD. 4. Intact vesicle on the tongue of a bovine. 5. Extensive area denuded of epithelium on the tongue of a cow. 6. A recent ruptured vesicles on the mucosa above dental pad in a cow. 7. Irregular ulcers on the mucosa above dental pad in a buffalo. 8. Ruptured vesicle on the upper lip and buccal surface of a cow. Plate 1 C 1. Ulcer in the interdigital space of a buffalo 2. Sloughing ofthe claw of a buffalo as a common complication 3. Vesicle at the end of the teats in a cow 4. Calf mortality in FMD. 5. Necrotic streaks in the myocardium (Tiger heart) occasionally seen in FMD. References 1. Abd El-Samea, M. M.; El-Sawalhy, A. A.; Hamouda, F. K.; Selim, A. M. and Metwally, N. (1994) "The duration of maternal derived antibodies in buffalo calves borne from FMD vaccinated dams" 2 Vet. Med. Congress Zagazig: 569-575 2. Blaha, T. (1989) "Foot and mouth disease. In: Applied Veterinary Epidemiology" 121 Edition Elsevier Science Publishers, Amsterdam, oxford, New York, Tokyo, PP 17-26 3. Brooksby, J. B. (1981) "Foot and mouth disease. In: Diseases of cattle in the tropics" (Ristic, M. and MCIntyreJ., eds) Martinus NijhoffPublishers, The Hague, Boston /London (10): 123 -132 4. Brown, F. (1986) "Foot and mouth disease one of remaining great plagues " A review Proc. Roy. Sco. Lond. B, 229,215-226 5. Callis, J. J. and Gregg, D. A. (1992) "Foot and mouth disease. In : Veterinary Diagnostic Virology " (Castro, A. E., and Heuschele, W. P., eds ) Mosby Year Book St. Louis, Baltimore, Boston, London, Sydney, Toronto (32): 100 - 103 6. Callis, J. J.; Dardiri, A. H.; Ferris, D. H.; Gay, J. G.; Mason, J. and Wilder, F. W. (1982) "Illustrated manual for the recognition and diagnosis of certain animal diseases" Mexico- United, Commission for the prevention of Foot and mouth disease. 7. Donaldson, A. I. and Doel, T. R. (1992) "Foot and mouth disease: The risk for great Britain after 1992 " A review Vet. Rec., 131,114-120 8. FAO/OIE/WHO (1995) "Animal Health Year Book" 36 Rome, Roma. 9. Genral Veterinary Services (1994) "Foot and mouth disease (in Arabic). TTc, NARP, Ministry of Agriculture, Egypt 10. Hamoda, F. K. 1.(1988) "Interference with locomotion in relation to infectious diseases of cattle" M.V.Sc. Thesis, Dept, of Animal Medicine, Fac. of Vet. Med. Zagazig University 1 l.Kahrs, R. F.(1981) " Viral diseases ofcattle" The Lowa State University Press/Ames, Iowa (29) :255 - 262. 12. Radostits, 0. M.; Blood, D. C.; and Gay, C. C. (1994) "Veterinary'Medicine A textbook of the diseases of cattle, sheep, pigs, goats and horses".8^ Edit. Baiilier Tindall, England 13.Scott, G. R. . (1990) Foot and mouth disease, In: "Handbook on Animal Diseases in the tropics" (Sewell, M. M. H.. and Brocklesby, D. W„ eds) 4 & Edit. Bailliere Tindall, London, Philadelphia, Tokyo PP 309 - 312, 14.Uirich Werncry, and Oskar - Rueger Kaaden (1995) "Infectious diseases of camelides" 1 21 Edit. Blackwell Wissenschafts-Verlage, Berlin, Oxford, Edinbuurg, Boston, London.
BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (32) BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX L Introduction I. 1. Synonyms:- Bovine viral diarrhea-Mucosal disease (BVD-MD), Bovine viral diarrhea (BVD), Mucosal disease (MD), according to OIE list (B) or I. 2. Definition:- BVD-MD is an acute or chronic infectious viral disease of cattle, characterized clinically by fever, diarrhea, ulceration and erosion of the alimentary mucosa, salivation, respiratory signs, leukopenia, abortion and congenital anomalies. I. 3. History:- BVD-MD was diagnosed for the first time in the world in USA 1946 from a herd outbreak of an acute fatal rinderpest like syndrome with ulceration of the alimentarv mucosa and diarrhea. Later the disease was detected «/ in different countries of tlie world and confirmed in Egypt for the first time in 1975. H, Etiology BVD-MD virus is classified as a small RNA virus of genus Pestivirus, it is antigenically closely related to the viruses causing Border disease in sheep and Hog cholera in pigs. There is a wide range of strains that produce cytopathic and non cytopathic effects in tissue culture, and many ofthem infect cattle and sheep. II. 1. Growth in tissue culture:- BVD-MD virus grows well in a primary bovine kidney cell culture (BK) producing cytopathic effects after 96 hours from inoculation. II. 3. Resistance:- BVD-MD virus is stable at temperatures below 10 °C and at a pH range of 3-9. The virus is unstable in the environment, the virus is killed by lysol, iodophors and aldehydes. HI. I. Distribution:- BVD-MD is widely distributed in Africa, Europe, North America and the Middle East including Egypt. III. 2. Transmission:- A. Source of infection, the virus isolated from nasal discharge, saliva, semen, feces, urine, tears, milk, placental fluid, fetal tissues and animals with persistent BVD virus infection are the major source of infection to susceptible I non immune cattle.
_______________ VIRAL DISEASES (33) The virus is a common contaminant of biological materials such as fetal calf serum and cell culture lines which plays an important role in transmission of the virus. B. The disease is transmitted by direct contact between susceptible animals via ingestion or inhalation of materials contaminated by infected oculonasal discharges, saliva, urine, also transplacental transmission occurs, as well as venereal infection of susceptible female cattle through service or by insemination with semen from a persistently infected bull usually resulting in early embryo loss and repeat breeding. III. 3. Host siisceptibility:- A. BVD-MD virus and related pestiviruses infect cattle, buffalo, sheep, goats, pigs and deer naturally. B. Cattle and buffaloes are the only species which develop clinical forms ofthe disease C. The importance ofsheep, goats and pigs sources ofinfection for cattle is still unknown. III. 4. Factors influencing susceptibility:- A. Cattle of all ages, sexes, and breeds are equally susceptible, but the majority of acute and chronic cases occur at 6-24 months ofage. B. Calves usually show congenital anomalies. III. 5. The economic importance ofthe disease:- A. Abortion, stillbirths, reproductive failure and congenital defects. B. Increased neonatal mortality. C. Prenatal and postnatal growth retardation. D. BVD-MD virus infection in calves may enhance diseases due to other pathogens especially respiratory diseases in calves such as IBR, Parainfluenza 3, pasteurellosis as a result of immune dysfunction (biological immunosuppression). 1Y> Pathogenesis A. In general it is not completely understood, but after natural infection ofnon immune susceptible cattle, the BVD-MD virus spreads via the blood stream and produces erosions and ulcers on the epithelium of the muzzle, nostrils, and alimentary tract.
BO’INE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (34)------------------------------- B The virus has an affinity for lymphocytes causing leukopenia and lymphoid depiction in lymph nodes and peyers patches, the virus has immunosuppressive or immunodepleting effect, so BVD-MD vims infection in calves may enhance diseases due to other pathogens especially IBR, parainfluenza 3, pasteurellosis as a result of immune dysfunction. C. The virus can cross the placental barrier and invade the fetus and the results depend only on the stage of pregnancy, in early stage up to 100 days, abortion or mummification of the fetus occurs resulting in infertility and repeat breeding; in the middle and late stages, congenital defects and or persistent lifelong infection without clinical signs is a common sequel, as a result of these congenital anomalies, abortion and stillbirths may occur and calves may be born weak with a low body weight, incoordination, varying degrees of blindness due to cerebellar hypoplasia (Plate 1C photo 8) or degeneration, microphthalmia, cataracts, optic nerve injury', and other CNS lesions such as musculoskeletal malformations, and a variety' of skin lesions such as alopecia. Fetuses infected in early stage up to 125 days will be positive for the virus and persistent lifelong infection later and negative for antibodies, (immune tolerance), in contrast the fetuses infected in the late stage 180 days or later the calves will be positive for neutralization antibody' (active immunity) even before colostrum intake and such calves will be negative for virus. V. Clinical signs There is a variety of clinical forms ofthe disease, which may all occur in the same herd or appear separately, those clinical forms vary in severity from inapparent, subclinical infection or mild febrile disease to an acute fatal syndrome, a chronic debilitating infection can also occur. V. 1. Acute fatal syndrome (acute MD):- IP varies from 2-3 weeks, morbidity rate is low 5-10 %, mortality rate is high up to 90 %, the course of the disease is 1-3 weeks, this form usually occurs at age 6-24 months, it is sporadic in nature, it is characterized by fever 40-41 °C and depression, anorexia, weakness, cessation of rumination, increased heart rate and respiration, severe leukopenia, salivation profuse watery diarrhea occur 2-4 days from the onset ofthe clinical signs the feces are foul smelling and may contain mucus or blood, erosions and ulcers on the oral, alimentary tract mucosa, muzzle, nostrils and pharynx.
VIRAL DISEASES (35) mucopurulent nasal discharge, lameness due to laminitis, coronitis and erosive lesions of the skin in the interdigital cleft, corneal opacity begins in the center and extends outwards (in contrast to Malignant catarrhal fever), pregnant females may abort, dehydration and death occurs after 5-8 days from the onset of signs. V. 2. Chronic form:- Develops as a sequel to either subclinical infection or non fatal clinical cases, and is characterized by progressive emaciation and weakness, inappetence, continuous or intermittent diarrhea, ocular and nasal discharge, chronic bloat, chronic erosions in the oral mucosa (Plate 1C photo 7) and skin over the perineum, around vulva, scrotum, prepuce, in the interdigital cleft and around coronary band, if in a pregnant female a variety of fetal abnormalities, abortion and fetal mummification, the chronic form is difficult to distinguish from the "unthrifty poor doers" with a persistent viremia in calves as a result of in utero infection, which is characterized by retardation of growth until development of a fatal form or other infections as pneumonia. V. 3. Inapparent, subclinical or mild infection:- This form is more common, and characterized by high morbidity 80-100 % and low' fatality 0-20 %, mild fever, leukopenia, inappetence and mild diarrhea V. 4. Congenital defects in calves:- These include cerebellar - ocular agenesis, ocular defects, musculoskeletal deformities (Plate 1C photo 6), alopecia, and intrauterine growth retardation. VI. Postmortem lesions The carcass is dehydrated, the gross abnormalities are confined to the alimentary tract, and characterized by shallow erosions with very little inflammation around them on the mouth, pharynx, esophagus, forestomachs, also in the muzzle, larynx and congenital defects in calves may be observed. VII. Diagnosis VII. I. Field diagnosis:- Clinical diagnosis is based on the history, the epidemiological patterns, clinical signs especially fever, diarrhea, oral lesions, abortion and congenital anomalies in newdybom calves. VII. 2. Laboratory diagnosis:- Specimens for laborator}7 use as shown in Table 1. There are two main keys to establish BVD-MD virus infection, one is to isolate the virus and the second is to detect the specific antibodies.
BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (36) Isolation and identification ofBVD-MD virus by:~ | Purpose BVD-MD 1 diagnosis in I live animals Samples_______ __ Paired sera (with 3 weeks in between Single sera, with heparinized blood, (buffy coat) and nasal, oropharyngeal secretion, tears, urine and feces_______ Tissues samples from spleen, lung, kidney, lymph nodes as mesenteric Laboratory test Serology as SN Serology as SN and virus isolation Comments SingR sera are of no value Both tests are essential Diagnosis in dead animals Antigen detection tests and virus isolation Select alimentary tract tissues with macro scopic lesions I Detection of persistent Single serum sample SNT and virus isolation Both tests are essential I J111ccnon_______ Abortion inquiries, Fetus Tissue samples, thyroid, spleen, salivary' gland, fetal fluid______________ ______ Antigen det­ ection tests, virus isolation, SNT Preferred samples Dam Paired sera with 3 weeks in between SNT Serological response often completed at abortion time Investigation of congenital | abnormality Single serum sample SNT and virus isolation Precolostral serum is essential A. Isolation of the virus by inoculation of the specimens into a variety of cell cultures as primary bovine kidney cell culture (BK) and incubation, if vacuolation and or degeneration with detachment of cells will be noticed after 2-7 days indicates presence of cytopathic strains, but if no changes in cultures, non cytopathic strains are suspected and the virus is confirmed by indirect methods as IFT, SNT, using specific known antisera; indirect ELISA may be used to detect extra cellular virus in samples such as serum or cell cultures, also a sensitive and specific PCR may be used for detection of the virus, as well as the immunoperoxidase procedure.
VIRAL DISEASES (37) B.The diagnosis of primary postnatal BVD-MD vinis infection, detection of its specific antibodies are required using virus neutralization (VNT), IIF, ELISA, immunodiffusion and CFT, precolostral serum samples from neonatal calves may be also tested for the virus antibodies to confirm the cause of teratogenesis, abortions, mummification, stillbirths or weak calves. VII. 3. Differential diagnosis:- BVD-MD should be differentiated clinically from A. Diseases with oral lesions and diarrhea as Malignant catarrhal fever, RP, alimentary form of Infectious bovine rhinotracheitis (IBR). B. Diseases with oral lesions and without diarrhea, as Foot and mouth disease, Vesicular stomatitis, Bluetongue, Necrotic stomatitis, Bovine papular stomatitis. C. Disease with diarrhea and without oral lesion as parasitic scours, Salmonellosis, Johne's disease, Tuberculosis, Enterotoxaemia and non infectious as copper, cobalt, selenium, vitamin A deficiency. VIII. Prognosis The prognosis for acute form with profuse watery diarrhea and oral lesions is unfavorable, most acute clinical cases will die in spite oftrials for treatment, but animals with subclinical, mild or chronic infections are favorable, such animals should be destroyed to prevent dissemination of the virus in the herd. IX. Treatment There is no specific treatment but in general symptomatic treatment is recommended as a course of antibiotics to control secondary infections, electrolyte fluid therapy to prevent dehydration, antidiarrhea drugs and supportive treatment. X. Prevention and control measures Control measures should be directed to limiting the spread of the disease via application of all hygienic precautions and clinical cases should be isolated and slaughtered; limiting the risk of transplacental infection via detection and identification ofpersistently infected animals and vaccination of susceptible cattle and buffaloes by:- A. Killed or inactivated virus vaccine usually safe, used in pregnant females, no post vaccinal complications but generally considered less immunogenic, its
1 BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (38) A recommended as early as 2-4 weeks ofage in calves and should be followed by booster dose annually at 6-8 months and its used in pregnant animals in late stage of pregnancy in two doses with 2-3 weeks intervals, this type of vaccine may be used singly or in combination with others viruses as IBR, PI - 3, this type ofvaccine is produced in Egypt. B. Modified live virus vaccine (MLV) may be used but it may be immunosuppressive, sometimes post vaccination BVD-MD appears within 3 weeks of vaccination, should not be given to pregnant cattle, should be given to the calves after 6 months, sometimes MLV contaminated with a virulent BVD virus strain, this type ofvaccine not recommended in Egypt. Plate 1C 6. Cerebellar ataxia in a calf infected in utero; teratogenic effect (BVD). 7. Erosions on the dorsal surface ofthe tongue (BVD). 8. Cerebellar hypoplasia shown in BVD compared with a normal cerebellum on the left. References 1. Callis, J. J.; Dardiri, A. H.; Ferris, D. H.; Gay, J. G.; Mason, J. and Wilder, F. W. (1982) "Illustrated manual for the recognition and diagnosis of certain animal diseases" Mexico- United, Commission for the prevention of Foot and mouth disease. 2. Duffell, S. J. and Harknen, J. W. (1985) "Bovine virus diarrhea-Mucosal disease infection in cattle " A review Veterinary Record 117,240 - 245. 3. El Sawalhy, A. A.; El Bagoury; Salem, S. A. and Youssef, M. A. (1995) "Bovine viral diarrhea complicated with Rota virus infection among foreign breed herd in Sharkia Governorate" 3 Sci. Cong. Egyptian Society for cattle diseases 66-77 4. FAO/O1E/WHO (1995) "Animal Health Year Book" 36 Rome, Roma 5. Hungerford, T. G. (1990) "Hungerford's diseases of livestock" 9 — Edit., McGraw - Hill Book Company Sydney, NewYork, London, Tokyo, toronte, PP 378 - 384 6. Kahrs, R. F.(l 981)" Viral diseases of cattle" The Lowa State University Press / Ames, Iowa 89-106 7. Kahrs, R. F (1981) "Bovine viral diarrhea, In: Diseases of cattle in the tropics" (Ristic, M. and MClntyreJ., eds) Martinus NijhoffPublishers, The Hague, Boston/London (15): 189- 195 8. Potgieter, L. N. D. (1992) "Bovine viral diarrhea In: Veterinary Diagnostic Virology " (Castro, A. E., and Heuschele, W. P., eds) Mosby Year Book St. Louis, Baltimore, Boston, London, Sydney, Toronto 88-92 9. Radostits, 0. M.; Blood, D. C.; and Gay, C. C. (1994) "Veterinary Medicine A textbook of the diseases of cattle, sheep, pigs, goats and horses".8& Edit. Baillier Tindall, England, London lO.Scott, G. R. (1990) "Bovine viral diarrhea-Mucosal disease, In: Handbook on Animal Diseases in the tropics" (Sewell, M. H., and Brocklesby, D. W., eds) 4 & Edit. Bailliere Tindall, London, Philadelphia, Tokyo PP 278 - 281
__________________________________________________________VIRAL DISEASES (41) BOVINE HERPES VIRUSES 1. Bovine herpes virus 1 (BHV-1) infection causes a variety of syndromes in the bovine with the same virus as Infectious bovine rhinotracheitis (IBR) or Infectious pustular vulvovaginitis (IPV) in females, Infectious pustular balanoposthitis (IPB) in bulls, alimentary tract (enteritis), ocular (conjunctivitis and keratoconjunctivitis), abortion and encephalitis forms of herpes virus infection, encephalitis and enteritis is restricted to newborn animals and is often lethal; ocular and respiratory infections commonly occur simultaneously; but it is uncommon to see the respiratory and genital involvement in the same animal. 2. Bovine herpes virus 2 (BHV-2) infection is characterized by skin lesions including Bovine herpes mammilitis (BHM) and Allerton virus infection. 3. Also herpes virus infection causes Malignant catarrhal fever (MCF) and Pseudorabies which are immunologically distinct from (BHV-1) and (BHV-2) INFECTIOUS BOVINE RHINOTRACHEITIS I. Introduction I. 1. Synonyms:- Infectious bovine rhinotracheitis (IBR), Infectious pustular vulvovaginitis (IPV), IBR/IPV, Red nose, bovine herpes virus 1 infection, according to OIE list (B) or J5jjuAi uiy>i j UuS'i I. 2. Definition:- IBR is a highly infectious disease of cattle and buffaloes caused by bovine herpes virus 1 and characterized clinically by rhinotracheitis, conjunctivitis, fever, short course and high recovery’ rate. I. 3. History:- IBR/IPV virus was firstly isolated in Germany, Western United States, and Egypt in 1928,1955 and 1976 respectively. IL Etiology. IBR/IPV virus is an alphaherpesvirus (BHV-1), all these strains have different tissues affinities but arc immunologicaly the same and cause IBR, IPV, IPB, one of the characteristics of (BHV-1) is its ability to become latent following primary infection with a mild strain of the virus or following vaccination with an attenuated strain.
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veterinary infectious diseases 2nd edition.pdf

  • 1. Table of Contents Section (l)_Introduction Section(2) Viral Diseases 29 16
  • 3.
  • 4. Veterinary Infectious Diseases Dr. Ahmed A.A. EL- Sawalhy Professor ofInfectious Diseases Department of Internal Medicine & Infectious and Fish Diseases Faculty ofVeterinary Medicine Mansoura University SECOND EDITION U^RACTITIONER'S and students guide ---- - , ———
  • 5. Veterinary Infectious Diseases A PRACTITIONER’S AND STUDENTS GUIDE Ahmed A. EL- Sawalhy First Edition, July 22,1997 Second Edition, July 22,1999 All rights reserved Cover design and plates color separation by EL-Araby Graphics in Zagazig 5 Mohamed Saad St., from Nadi EL- Moalemieen St., phone No. 055/331724 and printed in Mansoura Printed and bound in Zagazig by ZAFER OFFICE El-Montazh, Phone No. Q55/.2328163 Distributed in Egypt by AL AHRAM DISTRIBUTION AGENCY I.S.B.N. 977 -19 -8617-1 Corresponding address and request Dr. Ahmed ELSawalhy Department ofInternal Medicine & Infectious and Fish Diseases Faculty ofVeterinary Medicine - Mansoura University Mansoura, Egypt. Phone 050-2030906 / 2236063 / 2214906 Fax 0500 2236041 Home 055-2344220
  • 6. The Second Edition of Veterinary Infectious Diseases A PRACTITIONER’S AND STUDENTS GUIDE Is Dedicated To ♦ My Family for their constant and loving support during my hard work to advance this book to new levels, ♦ The veterinarians and veterinary students who will use this book in helping to provide the best care for the patients, and ♦Finally to my Colleagues, may you continue to strive foi excellence in our field.
  • 7. PREFACE Maintenance of animal health and protection of humans against zoonoses are considered to be of the most important tasks ofveterinarians. So, the objective of this book is to provide the field veterinarians and veterinary students with a concise summary of the important infectious diseases in domestic animals with especial emphasis upon to those endemic in Egypt. The book is presented in five sections: 1. Section (1). provides as introduction to infectious diseases, including the definition ofsome terms which are commonly used; 2. Section (2), includes some viral diseases of cattle, buffaloes, sheep, goats, camels, equines, dogs and cats: 3. Section (3), includes bacterial and mycotic diseases; 4. Section (4). includes parasitic and some rickettsial diseases; 5. Section (5). includes 16 appendices for quick reference to commonly used data. This book is supported with many color clinical photos (about 240 photos distributed in 24 color plates) or figures and tables whenever possible. I hope that this book will be a useful guide for field veterinarians and veterinary students in Egypt. The author would like to thank Ms. Jennifer Brown of Prudue University, School of Veterinary' Medicine for her reading and suggestions. Finally 1 am gratefully indebted to my family for their constant and loving support. Ahmed EL- Sawalhy
  • 8. CONTENTS (v) CONTENTS Section (l)_Introduct»on ................................................................. ... 1 Section!?) Viral Diseases .............................................................................. 13 1. Rinderpest ... ... ... ... ... ... ... ... 15 2. Foot and mouth disease ... ... ... ... ... ... 23 3. Bovine viral diarrhea-Mucosal disease complex ... ... ............... 32 4. Infectious bovine rhinotracheitis ... ... ... ... ... 41 5. Malignant catarrhal fever ... ... ... ... ... ... 49 6. Vesicular stomatitis ... ... ... ... ... ... ... 53 7. Bovine ephemeral fever ... ... ... ... ... ... 57 8. Bovine spongiform encephalopathy ... ... ... ... ... 63 9. Akabane disease ... ... ... ... ... ... ... ... 69 10.Lumpy skin disease ... ... ... ... ... ... ... 73 11 .Enzootic bovine leukosis ... ... ... ... ... ... ... 80 12.Sporadic bovine leukosis ... ... ... ... ... ... ... 86 13.Sheep and goat pox ... ... ... ... ... ... ... 88 14.Cow and buffalo pox ... ... ... ... ... ... ... 94 15.Pseudocowpox ... ... ... ... ... ... ... 97 16.Camel pox ... ... ... ... ... ... ... ... 99 17.Rift valley fever ... ... ... ... ... ... ... ... 102 18.Bluetongue... ... ... ... ... ... ... ... — HI 19.Contagious ecthyma ... ... ... ... ... ... ... 116 20.Peste des petits ruminants... ... ... ... ... ... ... 1-0 21.African horse sickness ... ... ... ... ... — — 1-5 22.Equine influenza ... ... ... ... ... — — 1-9 23.Equine viral arteritis ... ... ... ... ... ... — 134 24.Equine viral rhinopneumonitis ... ............... ... ... — 138 25.Equine infectious anemia ... ........................... . ............... I4- 26.Equine encephalomyelities ................................................................... I45 27.Rabies ................................................................................ ............... 149 28.Pseudorabies ... ... ... ... — — ••• 1^4 29.Canine distemper ... ... ... ............... — ............... 1?'
  • 9. CONTENTS (vi) _____________________ ~~~~-------—— 30Jnfectious canine hepatitis...................................................................... ... 160 31. Canine parvovirus enteritis ............... — ••• ••• ... 163 32.Viral puppy mortality ...................................................................... - 166 33.Feline panleukopenia ... ............... ... — ••• ••• 169 34.Feline viral rliinotracheitis... ... ... — — ••• ••• 174 35.Feline infectious peritonitis ... ... — ••• — 177 36.Feline immunodeficiency syndrome ... ... — ••• — 181 Section (3) Bacterial and Mycotic Diseases ... ••• ••• ••• 187 37.Anthrax ..................................................................... ••• ••• — 189 38.Clostridial diseases ... ................ ... ••• — — 197 39.Lamb dsentery ... ... ... ... ... — ••• ••• 198 40.Struck ... ............... ... ... ... — ••• — 205 41.Pulpy kidney ............... ... ... ... ... ••• — 207 42.Malignant edema............... ... ... ... ... ••• 210 43.Braxy ................................................................................... — ••• 214 44.Blackleg ... — — 215 45.Bighead ........................................... — - 220 46. Black disease ....................................................... ... ... 221 47.Bacillary hemoglobinuria.......................................... ... ... ••• 225 48.Tetanus ... ... — 229 49.BrucelIosis.................................................................................. ... — 50.Listeriosis ..................................................................... ... — z 51 .Leptospirosis ....................................................... ... ... ••• 258 52.Contagious bovine pleuropneumonia ............................. ... —265 53.Haemorrhagic septicaemia.......................................... ... ... ...270 54.Tuberculosis ............................. ... - 276 55.Skin tuberculosis..................................................................... ... - 284 56 Johne’s disease ..................................................................... ... - 285 291 57.Actinomycosis ..................................................................... ... - 5g.Actinobacillosis ..................................................................... ... - 294 • • 997 59.Dermatophilosis ..................................................................... 60.Bovine farcy ............... ... ... •••
  • 10. CONTENTS (vii) 61.Contagious skin necrosis ... ... ... ... ... ... .. 304 62.Infectious bovine keratoconjunctivitis ... ... ... ... ... 306 63.Mastitis ... ... ... ... ... ... ... ... ... 310 64.Infectious calf diarrhea ... ... ... ... ... ... ... 329 65.Salmonellosis ... ... ... ... ... ... ... ... 341 66.Respiratory disease complex in calves ... ... ... ... ... 351 67.Navel ill ... ... ... ... ... — — — ••• 358 68.Calf diphtheria ... ... ... ... ... ... — 360 69.Contagious foot rot ... ... ... ... ... ... — 363 70.Caseous lymphadenitis ... ... ... ... ... --- 367 71.Ulcerative lymphangitis ... ... ... ... — ... — 371 72.Strangles ... ... — ••• — — ••• — — 377 73.Glanders ... ... ... ••• ... — ••• — — 381 74.Epizootic lymphangitis ... ... ... ... — — 385 75.Sporotrichosis ... ... ... ... ••• ••• ••• 388 76.Ringworm ... ... ... ... ••• — ••• — ••• 391 Section (4) Parasitic and Some Rickettsial Diseases ... ... ... 399 77.Bovine Babesiosis ... ... ... ... ... — — — 401 78.Ovine and Caprine Babesiosis ... ... ... ... ••• — 408 79.Equine Babesiosis ... ... ... ... ... — — 409 80.Canine Babesiosis ... ... ... ... ... — — — 412 81.Theileriosis... ... ... ... ... ... — — ••• 414 82.Tropical Theileriosis ... ... ... ... ••• — ••• 415 83.Malignant ovine theileriosis ... ... ... ••• — — 419 84.Anaplasmosis ... ... ... ... — — ••• ••• 421 85.Trypanosomiasis ... ... ... ... ... — ••• — 425 86.Surra ......................................................................................................................426 87.Dourine ... ... ... ... ... ••• ••• ••• ••• 432 88.Toxoplasmosis ... ... ... — — ••• ••• — 436 89.Coccidiosis ... ... ... ... ••• — — 440 90.Cryptosporidiosis ... ... ... ... — ••• ••• 444 91.Mange ... ... ... ... ... ... ••• ••• 448
  • 11. CONTENTS (viii),_________________________ 92. Warble ... ••• ••• ••• ... ... ... . 453 93. Screw worm myiasis .......................................... ... _ 455 94. Nasal Myiasis .................................................................... ... 462 95. Botfly ................................................................................. ... ... 464 96. Fascioliasis .................................................................... ... 466 97. Paramphistomiasis ................ ... ... ... ... _ 473 98. Schistosomiasis................................................................................... ... 475 99. Habronemiasis ............................ • ............................................ ... 480 100.Verminous pneumonia ............... ... ................. 433 101.Ascariasis .................................................................... ... ... 487 102.Strongylosis of horses .....................................................................................490 103.Parasitic gastroenteritis.....................................................................................493 104.Filariasis......................................... — ... ... ... ... 504 105 .Tapeworm infestation .....................................................................................509 106.Coenurosis ....................................................... ... ... ... 511 107.Echinococcosis ............... ... ... ... ... ... ... 513 Section (5) Appendices ...................................................................... ... 515 108.Appendix (1) Clinical normality of domestic farm animals ... ... 517 109.Appendix (2) Normal hematology values of domestic farm animals ... 518 110.Appendix (3) Normal Clinical chemistry values of domestic farm animals 519 111 .Appendix (4) Topographical anatomy of a cow ... ... ................. 520 112.Appendix (5) Differential diagnosis of cattle and buffalo diseases ... 522 113.Appendix (6) Differential diagnosis of sheep diseases ... ... ... 525 114.Appendix (7) Differential diagnosis of goat diseases ... ... ... 528 115.Appendix (8) Differential diagnosis of horse diseases ... ... ... 531 116.Appendix (9) Differential diagnosis of dog diseases ... ... ... 534 117.Appendix (10) Differential diagnosis of cat diseases ... ... ... 536 118.Appendix (11) Drug dosage list in domestic farm animals ... ... 539 119.Appendix (12) Some common veterinary drugs in Egypt.............. ... 542 120.Appendix (13) Suggested vaccination programs for farm animals in Egypt 555 121.Appendix (14) Susceptibility of farm animals to infectious diseases 557 122.Appendix (15) Patterns ofmammalian reproduction in different animals 560
  • 12. LIST OF COLORED PLA TES (ix) LIST OF COLORED PLATES 1. Plate 1 A ... ... ... 2. Plate 1 B ... ... ... ................ 40 3. Plate 1 C ... ... ... ... 51 4. Plate ID ... ... ... ... ... ... . 52 5. Plate 2 A ... ... ... ... ... ................ ... 89 6. Plate 2 B ... ... ... ... ... ... ... ... 90 7. Plate 2 C ................................................................................................... 107 8. Plate 2 D ... ... ... ... ... ... .... ... 108 9. Plate 3 A ....................................................................................................185 10.Plate3B 11.Plate3C 12.Plate 3 D 13.Plate4A 14.Plate 4 B 15.Plate 4 C 16.Plate 4 D 17.Plate5A 18.Plate 5 B 19.Plate 5 C 20.Plate 5 D 21.Plate6A ............................. .............................. .............................. 457 ... 458 22.Plate 6 B ... 459 23.Plate 6 C .............................................. - ................. ... 460 24.Plate 6 D
  • 13. LIST OF TABLES (x)__________________ ________________________ __ ________________ LIST OF TABLES 1. Differential diagnosis of Rinderpest and in cattle and sheep ................. 20 2. Differential diagnosis of Foot and mouth disease and vesicular stomatitis 29 3. Specimens for laboratory use in Bovine viral diarrhea-Mucosal disease ... 36 4. Susceptibility of animals to Brucella organisms ... ... ... ... 238 5. Differential diagnosis of Brucellosis ... ... ... ... ... 248 6. Types ofvaccines available to use for control of Brucellosis ... ... 250 7. The pathogenicity of Mycobacteria spp to domestic and laboratory animals 276 8. The relationship between the stages in the pathogenesis of Johne’s disease, the presence of clinical disease and results of diagnostic tests ... 287 9. The relationship between the number of leukocytes in the milk and results of California mastitis test ... ... ... ... ... ... 320 10.The relationship between the number of bacteria in the milk and degree of clinical manifestation of udder ... ... ... ... ... ... 321 11.Bacteriological cure rates of mastitis for selected gram positive intramammary infections using Cloxicillin............ ... ... ... ... ... 323 12.Guide to estimate the degree of dehydration and the corresponding ' base deficit in diarrheic calves.......... ... ... ... ... ••• 337 13.The different types of organisms incriminated in the etiology of Respiratory disease complex....... ... ... ... ... ... 351 14.Antimicrobials commonly used in calves ... ... ... ... ... 356 15. Different species of Babesia in cattle and buffaloes in relationship to vectors, distribution and climatic reference......... ... ... ... 402 16.Different species ofTheileria in domestic animals in relationship to vectors, disease produced, distribution and pathognomonic clinical signs 414 17.Different species ofTrypanosomes in domestic animals and humans in - relation to vector transmission, disease produced, distribution and pathognomonic clinical signs ... ... ... ... ... 425 18.Chemotherapy of trypanosomiasis in livestock ... ... ... ... 431 19.Different species of mites in domestic animals, in relationship to - disease produced, and pathogenomic clinical signs ... ... ... 448 20.Difference between Fasciola and Paramphistomum eggs ... ... ... 470 21.Some common drugs used for treatment of Fasciolasis ... ... ... 472 22.Some common drugs used for treatment of Paramphistomiasis ... ... 476 23.Different species of Schistosoma in relation to intermediate host snails, definitive hosts, and distribution ... ... ... ... ... 477 24.The different species of gastrointestinal parasites in domestic animal species in relation to diseases produced and pathognomonic clinical signs 495
  • 14. LIST OF TABLESAND FIGURES (xi) 25.The different species of filaria in different domestic animal species in relationship to disease produced and pathognomonic clinical signs............. 505 26.Clinical normality of domestic Farm animals ... ... ... ... 517 27.Normal hematological values in domestic farm animals ... ... ... 518 28.Normal clinical chemistry values in domestic farm animals ... ... 519 29.Drug dosage list of some drugs in domestic farm animals ... ... 539 30.Common broad spectrum anthelmintic drugs used in Egypt ... ... 542 31.Common drugs used for blood parasites in Egypt... ... ... ... 547 32.Common broad spectrum antibiotic drugs used in Egypt ... ... ... 549 33.Common drugs used for treatment of mastitis in Egypt ... ... ... 552 34.Common drugs for general use in Egypt.............................................................554 35.Suggested vaccination program for cattle and buffaloes in Egypt... ... 555 36.Suggested vaccination program for sheep, horses and dogs in Egypt ... 556 37.Susceptibility of domestic animals to various infectious diseases 557 38.Pattern of mammalian reproduction in different animals ... ... ... 560 LIST OF FIGURES 1. Pathogenesis of Enzootic bovine leukosis ... ... ... ... ... 82 2. Transmission of RVF............ ... ... ... ... ... ... 102 3. Pathogenesis of enteric Salmonellosis ... ... ... ... ... 343 4. Pathogenesis of septicemic Salmonellosis... ... ... ... ... 344 5. Life cycle of the liver fluke ... ... ... ... ... ... 467 6. Lung worm life cycle ... ... ... ... ... ... ... 484 7. Diagramatic representation of the life cycle of haemonchus species ... 494 8. Topographical anatomy of a cow ... ... ... ... ... ... 520
  • 15. LIST OFABBREVIATIONS (xii) LIST OF ABBREVIATIONS IP Incubation period pl Microliter AGID Agar gel immunodiffusion pm Micrometer CIEP Counter immunoelectrophoresis iu International unit PAA Passive haemagglutination test Vs viruses ELISA Enzyme linked immunosorbent assay i/p intraperitoneal MDBK Madin Darby bovine kidney i/m intramuscular IIFT Indirect immunofluorscent test i/v intravenous DIFT Direct immunofluorscent test s/c subcutaneously BHV Bovine herpes virus i/n intranasally MLV Modified live virus vaccine kg kilogram HI Haemagglutination inhibition B.W. Body weight EM Electron microscope PCV Packed cell volume CAM Chorioallantoic membranes of Hb Hemoglobin embryonated eggs epg eggs per gram of feces RIA Radioimunoassay USA United state of America CNS Central nervous system UK United kingdom EDTA Ethylene diamine tetra acetic acid USSR Former Soviet union SNT Serum neutralization test CPE Cytopathic effect VNT virus neutralization test PCR Polymerasechain reaction CFT Complement fixation test ml milliliter BHK Baby hamster kidney cell line i.e. that is TCID50 Tissue culture infective dose 50 e-g- for example VIA Virus infection associated antigen °C Celcius degree RNA Ribonucleic acid PH negative logarithm of DNA Deoxyribonucleic acid hydrogen ion activity % percent sp/spp species a alpha / per P beta Q sigma 8 delta > greater than £ epsilon greater than or equal Y gamma < less than K kappa C less than or equal ± plus or minus equal
  • 17. _ __________________________________________________INTRODUCTION (1) INTRODUCTION Disease can be defined as an inability to perform physiological functions at normal levels, provided that nutrition and other environmental requirements are present with adequate levels; or, it may be defined as any deviation in the general state ofthe normal body. In general, the diseases can be classified according to:- I. The infectiousness A. Infectious disease, is that disease caused by entrance, multiplication and activities of any infectious agents (bacteria, viruses, fungi and parasites), which cause pathological changes in tissues, manifested by the development of signs of illness (symptoms). According to their spread from one host to another, they can be typed into contagious diseases and non contagious diseases. B. Non infectious disease, is that disease caused by to any disturbances in '■ normal metabolism, environmental conditions, trauma, physical and chemical agents. IL The transmissibility The transmissibility of the pathogen involves its ability to grow profusely and to be shed in large numbers in body fluids or excretions in order to infect or to be transmitted to a new host; also, the highly virulent pathogenic strains must survive in adverse environmental conditions, through which they reach a new host; or it may be defined as the case with which a disease agent is spared within populations. The diseases can be typed according to their transmissibility into:- A. Contagious disease, is one in which the specific infectious agent or its toxic products are transmitted from an infected animal, person or inanimate reservoir to a susceptible host, cither by direct and indirect contact. The spread of the disease depends mainly on the way of the elimination of tire organism from the host. In general examples for contagious bacterial diseases include Brucellosis and Contagious bovine pleuropneumonia; examples for viral diseases include foot and mouth disease. Cattle plague. Cow pox. Contagious ecthyma in sheep,
  • 18. INTRODUCTION (2)___________________________________________________________________ - and Epizootic lymphangitis in equine; and finally, examples for parasitic diseases include Coccidiosis in calves and Mange in sheep. B. Non contagious infectious disease, is one that is not communicable to others, such as wound. bift and insect borne infections, include Tetanus, Black disease, Rabies, Bluetongue and African horse sickness. III. The etiology A. Bacterial disease, is one that induced by bacteria. Examples include Brucellosis, Leptospirosis, Tuberculosis. Anthrax and Clostridial diseases. B. Viral disease, is one that is induced by viruses. Examples includ Cattle plague, Foot and mouth disease, Rift valley fever and Contagious ecthyma. C. Fungal disease, is one that is induced by molds and fungi. Example include Mycotic dermatitis. D. Parasitic disease, is one that is induced by parasites which may be due to protozoa (examples Babesiosis, Theileriasis, Anaplasmosis, Trypanosomiasis); it may be due to arthropods (as Hypoderma bovis, Oestrus ovis or Nasal myiasis); it may be due to trematode (as Fascioliasis, Paramphistomiasis); it may be due to nematodes (as Verminous pneumonia or parasitic gastroenteritis); or it may be due to cestode (as Tape worm infestation). E. Multifactorial disease, is one that is induced by several infectious agents, as Infectious calfdiarrhea and Mastitis. The course (duration), means the time from appearance of signs until the end result of the disease (either recovery or death). A. Pcraciite disease (fonn), is one that causes very rapid death within a few hours or days, usually due to septicemia, as in Anthrax and Clostridial diseases. B. Acute disease (form), is one that causes severe infection and takes a relatively longer course (a few days to one or two weeks) as in Cattle plague, Foot and mouth disease and Salmonellosis. C. Subacute disease (form), is one that takes a longer course (extended to few e---— ...................................... •'«— weeks).
  • 19. INTRODUCTION (3) D. Chronic disease (form), is one that takes a very long course (prolonged for several months to few years) due to the slow growth of the organism, as in Bovine tuberculosis, Caseous lymphadentitis in sheep and Glanders in horses. VTThe occurrence^) A. Sporadic disease, is one that occurs rarely and without regularity in a population. One explanation might be that infection exists in the population inapparently, and only in occasional few animals do signs ofdisease appear, as in Blackleg, Bovine viral diarrhea-Mucosal disease complex and Malignant catarrhal fever. B. Endemic disease, is one that is characterized by a usual frequency of occurrence in a population and the constant presence in a population (confined to a certain district or locality), as in Fascioliasis or soil borne infections in Egypt. C. Epidemic disease (Epizootic), is one in which the frequency within the population during a given time interval is clearly in excess of the expected frequency, usually such diseases are characterized by a rapid spread as in Cattle plague and Foot and mouth disease. A pandemic is a ven large scale epidemic, usually involving several countries or continents. — - . - . ■■ ------ I' — • D. Exotic disease, is one that is introduced into a certain area or country’ that was previously free from it; animals are usually highly susceptible to the disease agent; the main sources ofdisease producing agents are importation of living animals, animal products, semen, embryos and biological materials; lack of quarantine facilities, free animal movement and deficiency of laboratory skill, diagnostic materials and modem technical facilities facilitate the introduction of exotic diseases in developing countries. In Egypt, exotic diseases of European origin are Bovine viral diarrhea-Mucosal disease complex. Infectious bovine rhinotracheitis (IBR) and Infectious bovine pustular vulvovaginitis (IPV) in 1976, and Para influenza 3 (PI3); exotic diseases of African origin as Lumpy skin disease introduced in 1988, Equine influenza in 1989, Rift valley fever in 1977, Bluetongue in 1970, Peste des petits ruminants in 1989, Contagious ecthyma, African horse sickness, and Contagious bovine pleuropnumonia in 1969, In general the exotic diseases in one country may be endemic in another country.
  • 20. INTRODUCTION (4)________________________________________________ ______ There are a general rules for recent exotic diseases in a country, as: no treatment, no vaccination by live attenuated vaccine, and the animals must be slaughtered under strict hygienic conditions. Some common terms may be used in infectious diseascs:- A. Notifiable disease, means the owner or field veterinarians must immediately report any suspicions of some infectious diseases to local authorities for protection of both human and animal health to take all the required measures to confirm the diagnosis, quarantine and other control measures; such diseases cause high economic loss or are characterized by public health importance, as in Anthrax, Brucellosis, Tuberculosis, Glanders, Cattle plague, Foot and mouth disease and Rabies. B. Epidemiology, may be defined as the study of health and disease of populations and involves ♦ The observational study of naturally occurring versus experimentally induced disease; ♦ The study of disease in the population versus the individual; ♦ The detection of associations by inferential methods versus the study of pathologic methods. Epidemiology also can be defined as the study and interpretation of the mass phenomena of health and disease. It is the counterpart of clinical medicine, taking the population group or the herd as the unit of study rather than the individual paitents. The term epidemiology derives from the Greek words Epi = upon or about; demos = people; and logo = science. The term epizootology is sometimes used in reference to studies of animal population; but now the term epidemiology is understood to refer to all animal populations, human and other wise. C. Morbidity rate or attack rate:- It can be defined as the amount of disease in a population, it is useful for identifying risk factors for a specific disease. No. ofaffected animals during outbreak Morbidity rate = —-------------------------------------------------------- X 100 Population at risk at the beginning of outbreak
  • 21. INTRODUCTION (5) D. Mortality rate or fatality rate:- It can be defined as the number of deaths in a population, it is used for determining the prognosis for a specific disease. No. of deaths from a specific cause Mortality rate =------------------------------------------------ X 100 Total No. of cases of the same disease E. Incidence rate:- It can be defined as the number ofnew cases that occur in a known population over a period of time. It measures the flow of individuals from the disease free to the diseased state. No. of new cases of a disease over a time interval Incidence rate - --------------------------------------------------------------------- X 100 Average population at risk during same time interval F. Prevalence rate (P):- It can be defined as the amount of disease in a known population at a designated time, without distinction between old and new cases. No. of individuals having a disease at a particular point in time p - ------------------------------------------------------------------------------------ X100 No. of individuals in the population at risk at that point of time For example, if 20 cows in a herd of 200 cows were lame on a particular day, the prevalence of lameness in the herd on that day would be 20/200 XI00 = 10 %, that means the probability of an animal having a specified disease at a given time. The prevalence (p) depends on the duration (D) and incidence (I) of a disease. P oc I x D . This means change in prevalence can be due to change in incidence, a change in the average duration of the disease, or a change in both. G. Inapparent infection:- Can be defined as infection of a susceptible animal without clinical signs. The infection usually runs a similar course to that which produces a clinical case, with replication and shedding of agent; this causes a considerable problem for disease control. H. The carrier state:- May be defined as any animal that sheds an infectious agent without demonstrating clinical signs. Thus, an apparently or subclinically infected animal may be a carrier, and shed the agent either continuously or intermittently .
  • 22. INTRODUCTION (6)_________________________________________________ I. Latent infection:- A latent infection is one that persists in an animal without producing clinical signs. J. Incubation period:- Is the period oftime between infection and the development of clinical signs. K. Routes of infection (Mode of infection):- The site(s) by which an infectious agent gains entry to the body of a susceptible individual and by which it leaves the host (exit); the agents routes of infection include: alimentary, respiratory, urogenital, anal, skin and conjunctiva: L. Mode of transmission (Mode of spread):- Refers to the way(s) in which an infectious agent is transmitted from affected to susceptible individuals; it may be classified as horizontal or vertical and within horizontal as direct, indirect or air borne. M. Horizontal transmission:- Means the transmission of an infectious agent from any segment of a population to another, either directly or indirectly. N. Direct transmission:- Occurs when a susceptible host contracts an infection, either by direct contact with an infected host or through touch, a scratch, lick, bite or intercourse or by contact with the latter’s infected discharges as feces, urine or droplet spread onto the conjunctiva or mucous membranes of the eyes, nose, or mouth, during coughing or sneezing. O. Indirect transmission:- Involves an intermediate vehicle, living or inanimate vector, that transmits infection between infected and susceptible hosts. f Vehicle borne transmission, occurs through exposure to contaminated inanimate objects (fomites) such as bedding, surgical instruments, soil, water, food, or milk and biological products as blood, serum. The agent may or may not have multiplied or developed in or on the vehicle before being transmitted. / Vector borne transmission, is generally understood to mean transmission by invertebrate vectors, such as flies, mosquitoes or ticks. In some cases vertebrate hosts such as dogs, foxes or bats may serve as vectors as in case of Rabies transmission. Transmission may be through infection of salivary gland fluid during biting, or by regurgitation or deposition of feces on the skin, or other body fluids that contaminate host tissues through the bite wound or through an area of trauma.
  • 23. INTRODUCTION (7) • induced by scratching or rubbing. Vector borne transmission may be either mechanical or biological. Mechanical transmission results from simple mechanical carriage ofthe disease agent between hosts by the vector. It does not require multiplication or development of the disease agent in the vector. The disease agent is transmitted between hosts on soiled appendages or the proboscis, or by passage of organisms through the gastrointestinal tract. Biological transmission requires a period ofmultiplication, cyclic development or both before the vector can transmit the infective form ofthe agent (RVF), the disease agent may be transmitted vertically (transovarially) between generations of vectors or from one stage to another within a single generation (Babesiosis). P. Air borne transmission involves the dissemination of microbial aerosols. Microbial aerosols are suspensions of particles in the air, consisting partially or wholly of microorganisms; they may remain suspended in the air for long periods of time and usually infect the host via the respirator}' tracts; particles diameters range 1-100 pm (FMD). Q. Vertical transmission describes the transmission of a disease agent from animals of one generation to subsequent generations (Akabane disease and BVD-MD complex). Vertical transmission may be transovarial (example: between generations of invertebrate vectors via the egg), in utero or transplacental, (example: from parent to offspring within the uterus), or colostral, (from parent to offspring at parturition via colostrum or milk). Vertical transmission provides an important reservoir for certain vector borne viruses and protozoa. R. Symptom is any subjective evidence of disease or of a patient's condition (i.e., such evidence as perceived by the patient); a change in a patient's condition indicative of some bodily or mental state. S. 'fhe Officer International des Epizooties (OIE), an organization in France, was established in 1924 in order to promote world animal health, and its main activities are as follows:-
  • 24. INTRODUCTION (8)___________________________________________ ♦ To collect and disseminate to its Member Countries, information (including emergency information) on the occurrence, course and treatment of animal diseases. ♦ To provide guidelines and standards for health regulations applicable in the international trade of animals. ♦ To promote and co-ordinate research on the pathology, treatment and prevention of animal diseases when international collaboration in such research is desirable. According to the OIE numbering system the diseases are listed in three lists:- ♦ List A includes those diseases which spread rapidly, the scope of which extends beyond national borders, these diseases have particularly serious socio-economic or public health consequences and are ofmajor importance in the international trade of animal products. (Example: Foot and Mouth disease, Rinderpest, Peste des petits ruminants. Contagious bovine pleuropneumonia, Lumpy skin disease, Rift Valley fever, Bluetongue, Sheep and Goat pox and African horse sickness). ♦ List B includes those diseases which are considered of socio-economic and I or public health importance within countries, and which are also of course, significant in the international trade of animals and animal products such as Anthrax, Bovine brucellosis, Bovine tuberculosis, Haemorrhagic septicaemia, Leptospirosis, Glanders, Rabies, Bovine leukosis, Equine influenza, Babesiosis, Theilcriosis, Trypanosomiasis, Dourine and Mange. ♦ List C includes those diseases with important socio-economic and /or sanitary influence at the local level, such as Listeriosis, Toxoplasmosis, Blackleg and Fasciolasis T. Koch’s postulates:- In 1882 Koch set forth the following postulates for determining that an infectious agent is the cause of a disease:- ♦ The organism must be present in every case of the disease; ♦ The organism must be isolated and grown in pure culture; ♦ The organism must, when inoculated into a susceptible animal, cause the specific disease; ♦ The organism must then be recovered from the animal and identified.
  • 25. ________________________________________ ______ ____________ INTRODUCTION (9) u. Sensitivity of a test, means the proportion ofdiseased animals that are detected by a test; and the ability of a test to detect amount of antigen, enzyme, and so on; a sensitive test will detect small amounts, example as in Rose Bengal plate test (RBPT) for detection ofBrucellosis in animals. True positive Absolute sensitivity (%) =--------------------------------- X 100 Total animals examined True positive Relative sensitivity (%) = ---------------------------------- X 100 True positive + False positive V. Specificity of a test, means the proportion of non diseased animals that are detected by a test; degree of refinement; the greater the specificity, the greater the degree, example as in Rose Bengal plate test (RBPT) for detection of Brucellosis in animals. True negative Absolute specificity (%) =---------------------------------- X 100 Total animals examined True negative Relative specificity (%) = ---------------------------------- X 100 True negative + False negative W.Antigen, a substance (usually protein) that induces a specific immune response (as circulating antibody production) such substance is of high molecular weight. X. Antibody, a protein produced by an animal's immunological system in response to exposure to a foreign substance (antigen). Y. Vaccine is a suspension of attenuated or killed micro-organisms or its products, administered for the prevention and control of infectious diseases; they are used routinely to prevent diseases, and may be used during epidemics to decrease the number of susceptible animals (emergency vaccination), thus assisting in the termination of an epidemic.
  • 26. INTRODUCTION (10)____________________________________ There are various types ofvaccine. Attenuated vaccines are prepared from live micro-organisms that have lost their virulence but retained their ability to induce protective immunity, as in Sheep pox vaccine, Rift valley fever vaccine and Bj9 for Brucellosis; killed vaccines are prepared from killed micro­ organisms that have lost their virulence completely but retained their ability to induce protection as in Foot and mouth disease vaccine, Rift valley fever vaccine and hemorrhagic septicemia vaccine. Killed vaccines are safer than live vaccines and can be produced more quickly when new agents are discovered. An autogenous vaccine is a vaccine prepared from cultures ofmaterial derived from a lesion of the animal to be vaccinated; toxoid is a toxin that has been treated by heat or chemical agents (such as fonnalin) to destroy its deleterious properties without destroying its abilities to stimulate the formation of antibodies^-as in bivalent or polyvalent clostridial vaccine; serovaccine is a combination of an antisera with a vaccine to produce passive and active immunity. Z. Vaccination is the introduction ofa vaccine into the body to produce immunity to a specific disease. The vaccine may be administered by subcutaneous, intramuscular, intradermal injection, scarification, or by mouth and inhalation. ♦ Quarantine, this is a period of time during which an animal’s movement is restricted, and it is tested and observed for evidence of disease. Quarantine is used to prevent the interherd transmission ofthe disease especially during the incubation period. ♦ Dry cow, A cow that is not producing milk. ♦ Dry off, the act of causing a cow to cease lactation in preparation for her next lactation. ♦ Dry period, non lactating days between lactation. ♦ Colostrum, the first milk produced by the female immediately after giving birth to young. It is highly nutritious and a rich source of antibodies. ♦ California mastitis test, a cow side test for determining whether or not a cow is afflicted by mastitis. A stream of milk is placed in a small cup containing a chemical reagent. The reaction observed indicates the absence or presence and I or severity of mastitis.
  • 27. INTRODUCTION (11) ♦ Somatic cell count, the number of leukocytes and other body cells found in 1 ml of milk. A high count indicates problems with mastitis in a cow or a herd of cows. ♦ Immunity, a condition in which the animal becomes resistant to disease either through the use of vaccines or sera, or through the production of antibodies resulting from having had the disease. ♦ Pathogen, any microorganism (bacteria, viruses, yeasts, molds, protozoa, helminths) that produces disease. ♦ Bacteriostatic, a substance that prevents the growth of bacteria but does not kill them. ♦ Broad spectrum antibiotic, an antibiotic that is active against a large number of microbial species. Each disease, with few exceptions in this book is described according to the following outline:- I. Introduction 1.1. Synonyms:- Includes the other synonyms and the Arabic name I. 2. Definition:- Short description of the disease, including clinical forms, etiology, hosts, transmission, pathognomonic clinical signs and postmortem lesions. I. 3. History:- With special reference to the history of the disease in Egypt whenever possible II, Etiology The science or study of the causes ofdisease, both direct and predisposing and the mode oftheir operation with especial reference to II. 1. Morphology and staining II. 2. Growth requirements and characteristics II. 3. Resistance III. Epidemiology In studying the epidemiology of any infectious disease, special emphasis is gives to the following points: III. 1. Distribution:- Geographical distribution of the disease all over the world.
  • 28. INTRODUCTION (12)___________________ III. 2. Transmission:- Includes source of infections and mode of infections, as by ingestion, inhalation, inoculation or injection through skin or mucous membrane by biting insect, contaminated syringe or needle, or wound infection, through the vagina during coitus, contaminated instruments as catheters or semen, and finally may be transplacental infection III. 3. Host susceptibility:- Animals susceptibility in descending order. III. 4. Factors influencing susceptibility:- As in age, sex, breed, condition and season III. 5. The economic importance ofthe disease. IV. Pathogenesis V. Clinical signs Includes the incubation period, morbidity rate, mortality rate and the course, clinical signs and forms of the disease in different animal species. VI. Postmortem lesions VII. Diagnosis VII. 1. Field diagnosis:- Based on the epidemiology, the pathognomonic clinical signs and the postmortem lesions VII. 2. Laboratory diagnosis includes specimensfor laboratory use VII, 3. Differential diagnosis VIII, Prognosis It’s the end results of the disease, which is usually described by favorable, unfavorable or bad prognosis. IX, Treatment Whenever possible includes general and hygienic treatment, supportive treatment, specific treatment and symptomatic treatment. X, Prevention and control With special interest to control measures in enzootic areas and vaccination programs. References
  • 30. WRAL DISEASES (15) RINDERPEST JnJC!1dii£iifln j. synonym- Rinderpest (RP), cattle plague, pestis bovina, peste bovine, ordinc to OIE list (A) jjcUaJl ! 2. Defn,i,i0":'RP 1S an acUte hlghly conlagious viral disease primarily of cattle 'nd buffaloes, secondarily of sheep, goat and swine, characterized clinically by fever- erosion- ulceration and necrosis of the alimentary mucosa and severe jfurhea. serous or mucopurulent ocular and nasal discharges. History:- RP was diagnosed for the first time after a severe epidemic spread all over Europe with heavy losses in cattle in 1711-1714. In Egypt, the first epidemic was recorded in Rashid, with very high mortalities in 1827 followed by ^sequent outbreaks in 1841-1843,1927, 1953, 1958,1982 until 1986. fLXlisilesx RP virus is an RNA virus belonging to the genus Morbillivirus of the Family Paramyxoviridae. Strains of RP virus vary in their degree of p’dwaenicity, but all of them are antigenically identical and immunization protects aaainst all strains. RP virus has some antigenic relationship to the viruses of canine distemper, measles of humans and peste des petits ruminants (PPR) which causes a rinderpest like disease (pseudorinderpest) in sheep and goats. II. I. Growth in tissue culture:- RP virus grows well in various tissue culture systems (as in calf kidney cell culture). It produces cytopathic changes, characterized by syncytium formation, intracytoplasmic and sometimes intranuclear inclusion bodies. II. 2. Resistance:- RP virus is very fragile and sensitive to ordinary' environmental conditions, it does not survive outside the host for many hours, also the virus is inactivated by putrefaction, the virus is inactivated in sunlight within 2 hours, in strong acid or alkaline conditions within 10 minutes, and chemical agents as 5 % chloroform, 2 % phenol and 2 % formalin. IIL Epidemiology III. 1. Distribution:- RP is confined to Africa, Middle East, and pans of Asia •tee enzootic foci exist, while Europe. North and South America. Austraha and New Zealand are free from the disease.
  • 31. RINDERPEST (16) __ ____________________________________________________________ III. 2. Transmission:- A. Source of infection, the RP virus is present in the blood, tissue secretions and excretions of infected animals, such as conjunctival, nasal, vaginal discharge, feces, urine and milk, they contain large quantities of the virus during early stages of the infection. The vims reaches its peak ofconcentration at the peak of temperature reaction and subsides gradually to disappear about a week after the temperature returns to normal. B. Mode of infection, in nature the disease is transmitted by direct contact between infected and susceptible cattle and buffaloes via the major route inhalation, and ingestion of food and water contaminated by the discharge of clinical cases. Animals in the incubation stage may also be an important source of infection, especially in pigs, also the vims can be isolated from a variety of insects, but their role in transmission is not clear, experimentally successful infection occurred by instillation of the vims intranasal, conjunctival, vaginal and orally. On rare occasions, transmission has occurred through indirect contact with contaminated bedding, equipment and clothing. III. 3. Host susceptibility:- Most domestic and wild ruminants are susceptible, but natural infection is most commonly observed in(cattle, buffaloes^ and sporadically in sheep, goats, pigs and camels; wild ruminants are a common source ofinfection and play an important role in eradication programs. III. 4. Factors influencing susceptibility:- Susceptible cattle and buffaloes of all ages, sexes, and breeds are equally susceptible and can be infected and develop serious clinical disease. III. 5. The economic importance ofthe disease:- RP is one of the epizootics in cattle and buffaloes will] the highest losses, it also impairs animal production and activates latent infections such as Babesiasis. lyjPalhegencsis The RP virus has an affinity for lymphoid tissues and the epithelium of the upper respiratory and alimentary tracts. Animals are infected by inhalation of infectious aerosols, after absorption through the mucosa, the virus multiplies in the local draining lymph nodes and then throughout the lymphoid system causing
  • 32. VIRAL DISEASES (17) destruction to lymphocytes in the tissues, the direct cause for leukopenia. Furthermore viremia occurs which is manifested clinically by fever and at the same time transports the vims to various epithelia, especially in the alimentary tract where its cytopathic growth causes the characteristic lesions. During early stages of the disease, the vims replicates rapidly in the host with production of easily detectable specific antigen which induces high titers of antibody that usually persist for life in recovered animals. Strains of RP vims van’ in their degree of pathogenicity but there is only one main serotype and immunization protects against all strains. Most RP deaths are due to cardiogenic shock in peracute cases, fluid and electrolyte imbalance in later stages. V. Clinical signs ~) V. 1. Cattle and Buffalo:^ A. Incubation period (IP) 3-9 days, with course 6-17 days, the morbidity rate is high approximately 100 % and the mortality rate is 25-90 % (Plate IA photo 1). There is a variety of clinical forms which may be peracute, acute and subacute. B. The(^eracyteform is characterized by sudden onset, inappetence, high fever, depression, deep congestion of visible mucosa, severe panting and racing pulse, death within 2-3 days even before mucosal erosions develop, occurring most frequently in young calves and exotic animals. CfAcujg) form or the classical syndrome is characterized by 4 phases, the feverish or the prodromal phase, the phase of lesions at mucous membranes (Plate 1A photos 2-6), the phase of gasirointestipa[ symptoms and diarrhea (Plate IA photo 8 and Plate 1 B photo I), and the convalescence^phase in surviving animals. The onset of the prodromal fever is sudden, the animal is restless and depressed with shallow rapid respiration, the muzzle is dry, appetite is impaired, rumination is retarded, constipation, lacrimation and serous nasal discharge, visible mucous membranes are congested, the first suggestive sign of RP occurs 2-5 days after the onset of fever, raised pin point gray or white <focb) of necrotic epithelium appear on the mucous membrane lining the mouth, nasal passages and urogenital tracts during the next 2-4 days, these lesions increase in size and number and coalesce into caseous plaques that easily detach leaving
  • 33. RINDERPEST (18)_______________________________________________ raw red erosions, profuse salivation, the ocular and nasal discharges_become <------- - 1 ■ ■-—«. — purulent. The diarrhea begins as the fever falls 2-3 days after the first appearance ofmucosal erosions, the dark fluid feces contain excess mucus and shreds of epithelium and necrotic debris streaked with blood. D. IifjataT cases progressive dehydration, sunken eyes, collapse and death occurs 6-12 days after the onset of the prodromal fever. In surviving cases the diarrhea stops within a week of its onset, pregnant animals may abort during convalescence which is prolonged and the return to full health will take many weeks. E. Generally subacute forms or milder cases may have all or some of these signs to a lesser degree and a variable proportion ofthe affected animals recover, mouth lesions heal rapidly. In convalescent animals full recovery isprolonged. F. In endemic areas, the disease is generally mild and restricted to calves and yearlings. Epidemic RP particularly in areas where animals have not been infected or vaccinated is characterized by high mortality rates and occurs in all age groups ofaffected animals. G./l common sequel:- RP virus destroys T- and B- lymphocytes, but not memory cells, thus latent pathogens are commonly activated after 4-7 days from the beginning ofthe fever, as in Babesiasis both processes induce clinical signs which create the greatest diagnostic confusion. K 2. Camel:- Can develop subclinical rinderpest especially through contact with infected cattle, but their role in the epidemology ofRP is not clear. 3. Goat and sheep:- The course of the disease is shorter and pneumonic symptoms are more prominent, fever, erosive stomatitis, serous nasal and lacrimal secretion, diarrhea, acute cases die 6-7 days after the onset of illness. 4. Pigs:- Fever, inappetence, depression and the affected pig shivering, vomiting and bleeding from the nose, shallow erosions in the oral mucosa, diarrhea, dehydration and emaciation and pregnant animals may abort. VI. Postmortem lesions The carcass is dehydrated and solid with diarrhea and discharges, erosions and congestion are found throughout the alimentary tract, especially the mouth, pharynx, pillars ofthe rumen, abomasum (Plate 1A photo 8) and large intestine.
  • 34. VIRAL DISEASES (19) Congestion of capillaries along the crests of the longitudinal folds in the rectal mucosa create the characteristic lesion of "Zebra Striping" (Plate IB photo 1). Other organs have less specific signs, the lungs and the heart may be congested. Lymphoid tissues, the primary target of the virus may have edema and congestion and may be enlarged. VII. Diagnosis VII. 1. Field diagnosis:- RP should be suspected from history of recent animal movement, the epidemiological patterns; as high morbidity and mortality rates, rapid spread, affect all ages; also from clinical signs especially fever, erosions of oral mucosa and diarrhea; and finally from pathognomonic postmortem lesions especially "Zebra Striping" in the colon and rectum . VII. 2. Laboratory diagnosis Specimens for laboratory use are A. In early stage of the fever until the beginning of the erosions collect two blood samples, one with heparin or EDTA (buffy coat), and one without to separate serum and both forward on ice for virus isolation. B. Collect gum scrapings, tears and biopsies of superficial lymph nodes on ice for virus isolation and viral antigen detection tests C. Paired sera are collected from infected animals, one during the acute phase and the second during convalescence. D. Collect slices of lymph nodes, spleen, tonsils and mucosal lesions in 10% formalin saline for histopathology. Three main keys to establish RP virus infection, one is to detect the viral antigen; the second is to isolate the virus; and the third is to detect the specific antibodies Demonstration of the presence of specific viral antigens:- In the tissue, excretions, and secretions of suspected cases using hyperimmune RP antisera via the following tests A. Agar gel immunodiffusion (AGID), it is a rapid field test, commonly used, the positive lines are clearly visible within 2 hours. B. Counter immunoelectrophoresis (CIEP), it is slightly quicker and more sensitive. C. Immunofluorescence, it is useful on frozen sections.
  • 35. RINDERPEST (20) D. Passive haemagglutination test (PHA) and latex bead agglutination test are more sensitive. E. Indirect enzyme linked immunosorbent assay (ELISA), in which specimens as ocular secretions are simply absorbed onto microtiter plates and then detected by RP hyperimmune sera. Isolation and identification of RP virus:- From the tissues, excretions and secretions by dilution 1:10 in transport medium plus buffy coats and then 10 % suspensions of tissues are inoculated onto young monolayers of primary or secondary bovine kidney or Vero cells growing tubes. A typical CPE of cell rounding, syncytia and strand formation develops 3 days post inoculation of cells. The specificity of CPE can be confirmed by indirect fluorescent test (IF) and histological stains which show intracytoplasmic and sometimes intranuclear inclusions bodies. The detection ofa rise in specific antibodies:- In the sera of suspected cases, the paired sera were examined for antibodies using serum neutralization test (SNT), or ELISA. Histopathological examination:- Of lymphoid organs and mucosal epithelium reveals early formation of multinucleated giant cells containing intracytoplasmic and intranuclear inclusions and later necrosis of lymphocytes and epithelial cells. VII. 3. Differential diagnosis:- RP should be differentiated clinically from A. Diseases with oral lesions and diarrhea, as Malignant catarrhal fever, Bovine viral diarrhea-Mucosal disease complex and alimentary form of Infectious bovine rhinotracheitis. B. Diseases with oral lesions and without diarrhea, as Foot and mouth disease, Bluetongue more common in sheep and goat clinically not affect cattle challenge with virulent strains is indicated, in addition these viruses are antigenically distinct
  • 36. VIRAL DISEASES (21) and can be distinguished by comparing the reactions of antibodies, antigen or virus with reference reagents, homologous reactions give higher titers than heterologous reactions. Recently cDNA probes have become available that distinguish between the two viruses. VIII. Prognosis The prognosis is very bad due to high mortality rate. IX. Treatment There is no specific treatment and the disease is notifiable X. Prevention and control measures X. 1. In free countries:- Control measures should be directed to prevent introduction of infection by application of all quarantine measures for susceptible livestock, all unprocessed animal products and imported livestock should be antibody negative. X. 2. In enzootic areas:- Control measures depend on the periodic vaccination of all susceptible livestock especially yearling cattle, when outbreaks occur all affected and incontact animals are emergency vaccinated, restricting the movement of both living animals and fresh animal products, all susceptible infected animals and incontact groups must be slaughtered and disposed under strict hygienic measures or keeping the animals in strict isolation for at least one month after clinical recovery with emergency vaccination and infected premises should be disinfected. Attenuated vaccines used to control RP are:- Caprinized vaccine, Lapinized vaccine, Avianized vaccine, and recently tissue culture adapted vaccine is produced in calf kidney cells after upto 100 passages of the virus, these give a high level of attenuation for cattle and advantage its failure to spread by contact, the vaccine does not activate latent infections, it is safe for use in pregnant animals. The vaccine is produced in lyophilized form after reconstitution in normal saline s/c injection of 100 TCID5Q of virus induces high level of protection and life long immunity up to 8-11 years. This type of vaccine produced in Egypt from "Kabete 0 strain" in lyophilized form in vials of 200 and 100 doses which reconstituted in 200 and 100 ml cooled saline respectively and 1 ml injected s/c, branding ear tagging or ear punching help to identify vaccinated animals. Animals recovered
  • 37. RINDERPEST (22) from natural infection as well as vaccinated animals have life long immunity, this acquired immunity is transmitted to their offspring via colostrum which persist for 5-6 months and prevent the development of active immunity by vaccination during this period, therefore the minimum age for vaccination in calves 5-6 months, but if no colostral antibodies, is indicated to vaccinate the calves in the first week and revaccination again after 6-8 months. Plate 1 A 1. RP causes a high mortality. 2. Excessive salivation follows appearance of oral lesions. 3. Erosions produced by RP on the dental pad and the hard palate resemble FMD lesions. 4. Erosions on the gums caused by RP. 5. Lesions on the buccal mucosa and gums RP. 6. Erosions at the base ofthe tongue. 7. Before dying from RP. cattle frequently assume the classical “Milk fever” position. 8. Fundic portion ofthe abomasum with congestion and hemorrhage RP. Plate 1 B 1. “Zebra striping” in the distal colon and rectum RP References 1. Callis, J. J.; Dardiri, A. H.; Ferris, D. H.; Gay, J. G.; Mason, J. and Wilder, F. W. (1982) "Illustrated manual for the recognition and diagnosis of certain animal diseases" Mexico- United, Commission for the prevention ofFoot and mouth disease. 2. FAO/OIE/WHO (1995) "Animal Health Year Book" 36 Rome, Roma 3. Hungerford. T. G. (1990) "Rinderpest In: Hungerford's diseases of livestock" 9 Edit., McGraw - Hill Book Company Sydney, NewYork, London, Tokyo, toronte, PP 386 - 387 4. Kahrs, R. F.(l 981) "Rinderpest In: Viral diseases of cattle" The Lowa State University Press /Ames, Iowa (32): 275 - 281 5. Radostits, 0. M.; Blood, D. C.; and Gay, C. C. (1994) "Veterinary Medicine A textbook of the diseases of cattle, sheep, pigs, goats, and horses ".8& Edit. Baillier Tindall, England 6. Reid, H.W. (1981) Rinderpest, In: " Diseases of cattle in the tropics" (Ristic, M. and MCIntyreJ., eds) Martinus NijhoffPublishers, The Hague, Boston / London (11): 133 -152 7. Rossiter, P. B. (1992) Rinderpest, In: "Veterinary Diagnostic Virology" (Castro,A.E.,and Heuschele, W. P., eds) Mosby Year Book St. Louis, Baltimore, Boston, London, Toronto (40): 123 - 126 8. Rossiter, P. B. and Wamwayi, H. M. (1989) "Surveillance and monitoring programs in the Rinderpest" A review Tropical Anim. Hith. Prod. 21, 89 - 99 9. Scott, G. R. (1990) Cattle plague, in "Handbook on Animal Diseases in the tropics" (Sewell, M. H., and Brocklesby, D. W., eds) 4 & Edit. Bailliere Tindall, London, Philadelphia, Tokyo PP 287 - 292. 10. Scott, G. R.; Taylor, W. P. and Rossiter, P. B. (1986) "Manual on the diagnosis of Rinderpest" FAO Animal Production and Health Series No. 23 Rome. 11. Uirich Werneiy, and Oskar - Rueger Kaaden (1995) "Infectious diseases ofcamelides" 1 Si Edit. Blackwell Wissenschafts-Verlage, Berlin, Oxford, Edinbuurg, Boston, London.
  • 38. VIRAL DISEASES (23) FOOT AND MOUTH DISEASE I, Introduction I. 1. Synonyms:- Foot and mouth disease (FMD), Aphthous fever, Aftosa, according to OIE list (A) or ja I. 2. Definition:- FMD is a highly contagious, viral disease of cloven hoofed animals, characterized clinically by fever, vesicular eruptions on the buccal mucosa, the skin ofthe interdigital space and the coronary band. I. 3. History:- FMD was the first animal infection proved to be caused by a virus and the first published data was in Italyl514. In Egypt the first outbreak was detected in 1953, and later outbreaks occurred. II. Etiology FMD viruses belong to the genus Aphthovirus, of the family Picomaviridae, single stranded RNA molecule, ether and chloroform resistant, there are 7 immunologically and serologically, distinct serotypes with different degrees of virulence, within these serotypes there are more than 65 subtypes which are antigenically different based on genomic analysis {A (32), O (11), C (5), SAT} (7), SAT2 (3), SAT3 (4), and Asiai(3)}. There are biotypical strains which become adapted to a particular animal species and virulent to others. In Egypt type A was identified during outbreaks in 1953, 1956, 1958, and type SATj was isolated and identified in 1960, but type Oj substrain wras identified and the most prevalent since 1972 and during the different outbreaks later until now. II. 1. Growth in tissue culture:- FMD Vs grow well in calf kidney or bovine thyroid cell cultures, piglet kidney cell cultures and produce cytopathic changes and the virus is most stable between pH 7.4-7.6 II. 2. Resistance:- FMD Vs are acid and alkali labile, sunlight quickly inactivates the viruses, the vinises can survive after drying in and upon inanimate material from one week to months, they also can remain viable at - 20 °C for 2 years, and in frozen meat for up to 80 days especially in the lymph nodes. The virus may persist for a year or more in infected premises, for 10-12 weeks on clothing and feed. FMD Vs are inactivated by 2 % sodium hydroxide and it is considered the best disinfectant especially after cleaning with 5 % sodium carbonate, also 2 % formalin kills the viruses within a few hours. The virus is destroyed by boiling or autoclaving.
  • 39. FOOTAND MOUTH DISEASE (24) III. Epidemiology III. 1. Distribution:- FMD is world wide distributed, it occurs enzootically in Africa, the Middle East, Asia and most countries of South America. In contrast only a few countries all over the world are free from infection such as the USA, Canada, Australia, New Zealand, Japan and Great Britain, with a few sporadic outbreaks, the disease is eradicated in most European countries. III. 2. Transtnission:- A. Sources of infections are clinically active animals, carriers and those in the incubation period. Such animals shed the virus in all body secretions and excretions such as saliva due to discharging the vesicular fluids which contain high concentrations ofthe virus, milk, feces, urine and semen. All meat tissues and meat products especially bone, bone marrow, viscera, blood vessels and lymph nodes, remain infective and act as a source of infection for long periods, especially if quick frozen used and to a lesser extent meat chilled or frozen by a slow process due to the development of acidic pH. B. Infection with FMD virus occurs by both inhalation (air borne disease) and ingestion, aerosols of infective droplets generated by infected cattle and pigs under suitable environmental conditions may spread the virus indirectly downwind (wind borne) over a distance of 100 km. C. FMD virus is transmitted and spread either directly by the movement of diseased animals, humans or apparently healthy carrier ones, or transmitted indirectly by transportation of the virus on inanimate objects, vehicles for animal transport, packing material, stable utensils, clothing, feed stuffs, uncooked and unprocessed meat and meat products, milk and its products, and semen. FMD virus can be spread via unsusceptible domestic animals as dogs, cats, migrant birds, poultry, rats and maybe insects such as ticks. III. 3. Host susceptibility:- A. All cloven hoofed animals are susceptible to FMD virus, among the domestic animals cattle and buffaloes, have the highest morbidity rates, followed by pigs, sheep and goats. In Egypt buffaloes are equally susceptible as cows to FMD. B. Many rodents, birds and wild ruminants such as elephants, ungulates and capybara are susceptible and may provide reservoirs of infection for domestic animals.
  • 40. ___________________________________________________ VIRAL DISEASES (25) C. Clinical disease in humans occurs especially in children but is usually rare, infection occurs by drinking infected milk, accidental infection of laboratory workers with the virus, people handling infected animals may become carriers and have the virus in their nasopharynx for more than 24 hours. D. Some sheep, goats and cattle may remain carriers ofthe disease to susceptible animals for up to 6 months after recovery due to continuous low multiplication of the virus in the pharyngeal tissues and mammary glands. 4. Factors influencing susceptibility:- A. In susceptible populations, all ages, sexes, and breeds are infected and develop clinical signs. B. Fatality rates in neonates (calves, lambs and kids) are higher than adults. III. 5. The economic importance ofthe disease:- A. Production of meat and milk is seriously impaired due to the severity of the acute stage ofthe disease and prolonged convalescence period. B. Impairment of the international trade and transit due to restriction ofthe movement of livestock and animal products between countries. C. Occasionally high mortality up to 50 % in calves. D. Mild form of the disease in humans may occur. IV. Pathogenesis The FMD virus gains access to the blood stream after infection either by inhalation or by ingestion, multiplication and transitory viremia occurs for 4-6 days, followed by localization and multiplication ofthe virus in the predilection tissues such as the epithelium of the buccal cavity, pharynx, esophagus, stomachs, feet, teats and occasionally muscles especially cardiac muscles and skeletal muscles, multiplication of the virus results in continuous irritation and / or degenerative changes with formation of the vesicles at these sites which rupture, producing . . secondary bacterial infections and ulcers. V. _Clinical signs K 1. Cattle and buffaloes:- A. The IP in natural infection is 3-8 days, high morbidity rate up to 100 %, but usually low in enzootic areas with mild clinical signs, mortality rate in adults 0.2-5 %, except the malignant form of the disease, in calves it is high upto 50 - 70 % (Plate 1 C photo 4).
  • 41. FOOTAND MOUTHDISEASE (26)__________________________________________ The course of the disease is usually 2-3 weeks without complications and 6 weeks ifcomplications occur. B. High fever (40-41 °C), for the first 1-4 days, associated with depression, anorexia, cessation ofrumination, increased thirst, and a marked drop in milk production. C. Acute painful stomatitis due to vesicle formation, the body temperature returns to normal after rupture ofthe vesicles, serous nasal discharge, severe ropy salivation and smacking ofthe lips (Plate IB photos 2-3). D. The characteristic vesicles (1-2 cm in diameter) appear on the mucous membranes ofthe mouth, tongue, dental pad, muzzle, udder, teats, on the feet especially in the interdigital space and the coronary band, these vesicles are thin walled contain straw colored fluid and rupture within 24 hours, leaving a painful raw eroded surface, which heals within a week, unless complicated by secondary bacterial infection (Plate 1 B photos 4-8 and Plate 1 C photos 1-3). E. Severe lameness may be complicated by the loss ofthe horny covering ofthe foot and sometimes complete recumbence (Plate 1 C photos 1-2). F. Lactating cows develop vesicles and ulcers on the udder and teats which predispose to mastitis (Plate 1 C photo 3). G. Loss ofcondition, abortion and infertility troubles may occur. Common sequel io FMD in cattle:- A. A chronic syndrome of dyspnea, anemia, diabetes mellitus, over growth of hair, loss ofthermal regulation "Panting" probably due to pituitary lesion. B. Mastitis and abortion may occur during the acute stage or during convalescence with subsequent infertility trouble. C. Myocardial degeneration and deaths in calves (Plate 1 C photos 4-5). D. Sloughing ofthe claws (Plate 1 C photo 2). V. 2. Camels:- There is agreement that camels play an important role as viral reservoirs in the epidemiology of FMD. However FMD in camels creates an especially difficult situation since camels excrete the virus over a certain period oftime, yet produce no antibodies. V. 3. Adult sheep and goats:- Mainly lameness at first, followed by vesicle formation in the buccal cavity and salivation.
  • 42. VIRAL DISEASES (27) V. 4. Young animals:- Calves, lambs, kids and piglets, sometimes deaths without previous clinical signs due to myocardial necrosis and degeneration, some surrviving animals after FMD attacks exhibit severe dyspnea when exercised and are known as " Panters". V. 5. Pigs:- salivation, vesicles on the snout, rupture leaving shallow ulcers, foot lesions are more easily detected on the coronary band, lameness and the pigs walk on the tips of their toes, sometimes sloughing ofthe hooves. V. 6. Human:- FMD in human inapparent infection, rarely development of vesicles on the hands, feet, oral mucosa, headache and nausea. VI. Postmortem lesions A. Vesicles, erosions and ulcers are found in the buccal cavity, esophagus, stomachs, feet, udder, sometimes trachea and bronchi. B. The pericardium may contain serous fluid. C. In the malignant form of the disease or the newly bom animals, acute degeneration of the cell fibres and necrosis, manifested by the appearance of a small grayish foci in the myocardium (myocarditis) produce a striped appearance known as "Tiger heart" (Plate 1C photo 5) similar lesion may be found in the skeletal muscle. VII. Diagnosis VII. 1. Field diagnosis:- FMD should be suspected from the epidemiological pattern of the disease, rapid spread, high morbidity, low mortality, except the malignant form, high mortality in neonates, clinical signs as salivation, lameness, vesicles, and erosions. VII. 2. Laboratory diagnosis:- Specimens for laboratory use A. For virus isolation or viral antigen detection fresh vesicular fluid and epithelium from ruptured vesicles suspended in equal amounts of glycerol and 0.04 M phosphate buffer pH 7.2-7.6, whole blood sample (huffy coat) in early stage of the disease on heparin from feverish or suspected diseased animals is indicated, esophageal pharyngeal fluid from acute, convalescent and recovered animals, and lymph nodes, kidney, adrenal glands, heart tissues, thyroid or other tissues collected at necropsy are also indicated, and should be frozen. B. For serological examination paired sera should be collected from suspected diseased animals immediately and 3 weeks later to detect antibody titer.
  • 43. FOOTAND MOUTH DISEASE (28) Isolation and identification ofFMD virus by:- A. Inoculation of vesicular fluid or epithelium in primary or secondary calf kidney or bovine thyroid cell cultures, piglet kidney cell cultures or in susceptible permanent cell lines such as BHKo], baby mice (2-7 days old) and the diagnosis ofvirus by using known antiserum is highly efficient. B. The direct complement fixation test (CFT) on the original epithelial suspension is a rapid method to detect the positive infection within few hours, type specific and strain specific complement fixing antisera used for typing. C. Recently polyacrylamide gel electrophoresis, and polymerase chain reaction (PCR) are used in diagnosis of FMD in Egypt. Serological examination:- Neutralization test, ELISA and fluorescent antibody technique is also indicated for detection of virus or viral antigen as well as its antibodies. ELISA tests for antibody to virus - infection - associated (VIA) antigen may be employed to differentiate between humoral responses to vaccination and natural infection. Experimental transmission in:- A. Unweaned white mice used to detect the virus in suspected material by intraperitoneal (i/p) inoculation, paralysis in the hind legs and death within 7 days, the infection is confirmed by CFT. B. Guinea pig inoculation used to detect FMD virus in suspected material by the intradermoplantar injection offresh vesicular fluid into one foot pad, vesicles appear on all the pads in 1 -7 days and in the mouth 1-2 days later. C. Large animal inoculation test may be used. VII. 3. Differential diagnosis:- A. FMD should be differentiated from diseases with vesicular syndrome, based on the different species susceptibilities to their viruses as in Table 1. Also cross immunity test in guinea pigs may be used to differentiate FMD from VS. B. FMD should be differentiated from mucosal disease complex as Mucosal disease, RP, Malignant catarrhal fever and Bovine infectious rhinotracheitis. C. FMD should be differentiated from pox herpes complex as Papular stomatitis, Cow pox, Bovine mammalitis. D. FMD should also be differentiated from diseases causing lameness as Contagious footrol and Bovine ephemeral fever.
  • 44. VIRAL DISEASES (29) Items Cattle Swine Sheep & goat Horse guinea pigs and unweaned mice FMD 4“4- + 4- - 4- Vesicular stomatitis (VS) 4-4- 4- 4-4- 4“ Vesicular exanthema y ? - - - VITL Prognosis A. Favorable in adult animals without complications. B. Unfavorable or bad in neonates due to the high fatality of the disease. TX, Treatment FMD is a notifiable disease, isolation and slaughter to control outbreaks in epizootics, but usually in endemic areas as in Egypt, symptomatic treatment as broad spectrum antibiotics, mild disinfectant and protective dressings io inflamed area in mouth and feet to prevent secondary infection, systemic antivirals may be indicated, supportive treatment as glucose solution intravenously in acute cases. X. Prevention and control measures X. 1. FMD Free countries:- A. Prevent the importation of live animals from FMD infected areas and all imported animals should be quarantined for 21 days and tested for the presence of FMD virus in the pharyngeal tissues and for the presence of the antibodies, if possible importation should be directed towards the young stock, which have not been previously vaccinated, so if positive for the antibodies, there is evidence of exposure to infection. B. Importation of frozen meat or meat products and all biological products as semen from FMD infected areas should be prohibited. X. 2. FMD occasionally epizootics occurs infree areas:- A. As soon as the diagnosis of the disease is established all cloven hoofed animals in the exposed groups should be immediately slaughtered and burned or buried. B. Proper disinfection of all materials in infected premises as motor vehicles, farm feeding utensils, machine, bedding, animal products and water proof clothing using 1-2 % sodium hydroxide, fonnalin or 4 % sodium carbonate.
  • 45. FOOTAND MOUTH DISEASE (30) C. When all possible sources of infection are destroyed the farm should be left unstocked for 6 months and restocking permitted only when "sentinel test" animals are introduced and remain uninfected. D. Human movement to and from infected premises must be reduced to a minimum; persons working and their clothing must be disinfected by spraying or boiling E. Strict quarantine measures on the infected focus within a 16-24 km diameter, no animal movement can be permitted, human and motor traffic must be reduced to a minimum, ring vaccination using killed vaccine around the infected focus may be indicated < X. 3. FMD endemic areas:- During outbreaks, strict quarantine measures, 1 restriction of animal and human movements, closing of markets, destruction of all { sources of infection and vaccination. Vaccination is the basis of most control ( measures and the vaccines must be type specific, but production of the vaccines i from locally isolated virus is becoming a more common practice. Two types of ] vaccine are used: (1) Inactivated vaccines may be monovalent, bivalent and trivalent vaccines, inactivating agent as formalin or recently betapropiolactone or acetylethylenimine (Aziridine), modern vaccines contain aluminum hydroxide or saponin, the antibodies appear and reach a peak 3 weeks post vaccination, the duration of immunity in cattle is 6-8 months and vaccination every 6 months is required. The duration of immunity after natural infection in cattle ranges from 1/2-4 years, and calves receive antibodies via the colostrum of immune cows which are protective for 1-2 months. ) FMD vaccines in Egypt A. Aziridine inactivated tissue culture Oj vaccine is used now and it gives immunity for 8 months, booster dose after 6 months and requires 2 vaccination per year, the dose in cattle and buffaloes is 2 ml and in calves, and sheep 1 ml s/c in dewlap and if the calves were born to vaccinated dams it should be vaccinated at 6 months of age with booster dose at 10 months and if the calves were born to non vaccinated dams it should be vaccinated at 4 months of age with a booster dose at 8 months. B.Formalin inactivated tissue culture 0] vaccine. C. Oil adjuvent 0] vaccine (2) Living attenuated vaccines may be used but it is not safe because the virus is attenuated for one animal species it can remain virulent for others.
  • 46. VIRAL DISEASES (31) Plate 1 B 2. Excessive salivation cow with FMD. 3. Buffalo with ropy salivation due to FMD. 4. Intact vesicle on the tongue of a bovine. 5. Extensive area denuded of epithelium on the tongue of a cow. 6. A recent ruptured vesicles on the mucosa above dental pad in a cow. 7. Irregular ulcers on the mucosa above dental pad in a buffalo. 8. Ruptured vesicle on the upper lip and buccal surface of a cow. Plate 1 C 1. Ulcer in the interdigital space of a buffalo 2. Sloughing ofthe claw of a buffalo as a common complication 3. Vesicle at the end of the teats in a cow 4. Calf mortality in FMD. 5. Necrotic streaks in the myocardium (Tiger heart) occasionally seen in FMD. References 1. Abd El-Samea, M. M.; El-Sawalhy, A. A.; Hamouda, F. K.; Selim, A. M. and Metwally, N. (1994) "The duration of maternal derived antibodies in buffalo calves borne from FMD vaccinated dams" 2 Vet. Med. Congress Zagazig: 569-575 2. Blaha, T. (1989) "Foot and mouth disease. In: Applied Veterinary Epidemiology" 121 Edition Elsevier Science Publishers, Amsterdam, oxford, New York, Tokyo, PP 17-26 3. Brooksby, J. B. (1981) "Foot and mouth disease. In: Diseases of cattle in the tropics" (Ristic, M. and MCIntyreJ., eds) Martinus NijhoffPublishers, The Hague, Boston /London (10): 123 -132 4. Brown, F. (1986) "Foot and mouth disease one of remaining great plagues " A review Proc. Roy. Sco. Lond. B, 229,215-226 5. Callis, J. J. and Gregg, D. A. (1992) "Foot and mouth disease. In : Veterinary Diagnostic Virology " (Castro, A. E., and Heuschele, W. P., eds ) Mosby Year Book St. Louis, Baltimore, Boston, London, Sydney, Toronto (32): 100 - 103 6. Callis, J. J.; Dardiri, A. H.; Ferris, D. H.; Gay, J. G.; Mason, J. and Wilder, F. W. (1982) "Illustrated manual for the recognition and diagnosis of certain animal diseases" Mexico- United, Commission for the prevention of Foot and mouth disease. 7. Donaldson, A. I. and Doel, T. R. (1992) "Foot and mouth disease: The risk for great Britain after 1992 " A review Vet. Rec., 131,114-120 8. FAO/OIE/WHO (1995) "Animal Health Year Book" 36 Rome, Roma. 9. Genral Veterinary Services (1994) "Foot and mouth disease (in Arabic). TTc, NARP, Ministry of Agriculture, Egypt 10. Hamoda, F. K. 1.(1988) "Interference with locomotion in relation to infectious diseases of cattle" M.V.Sc. Thesis, Dept, of Animal Medicine, Fac. of Vet. Med. Zagazig University 1 l.Kahrs, R. F.(1981) " Viral diseases ofcattle" The Lowa State University Press/Ames, Iowa (29) :255 - 262. 12. Radostits, 0. M.; Blood, D. C.; and Gay, C. C. (1994) "Veterinary'Medicine A textbook of the diseases of cattle, sheep, pigs, goats and horses".8^ Edit. Baiilier Tindall, England 13.Scott, G. R. . (1990) Foot and mouth disease, In: "Handbook on Animal Diseases in the tropics" (Sewell, M. M. H.. and Brocklesby, D. W„ eds) 4 & Edit. Bailliere Tindall, London, Philadelphia, Tokyo PP 309 - 312, 14.Uirich Werncry, and Oskar - Rueger Kaaden (1995) "Infectious diseases of camelides" 1 21 Edit. Blackwell Wissenschafts-Verlage, Berlin, Oxford, Edinbuurg, Boston, London.
  • 47. BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (32) BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX L Introduction I. 1. Synonyms:- Bovine viral diarrhea-Mucosal disease (BVD-MD), Bovine viral diarrhea (BVD), Mucosal disease (MD), according to OIE list (B) or I. 2. Definition:- BVD-MD is an acute or chronic infectious viral disease of cattle, characterized clinically by fever, diarrhea, ulceration and erosion of the alimentary mucosa, salivation, respiratory signs, leukopenia, abortion and congenital anomalies. I. 3. History:- BVD-MD was diagnosed for the first time in the world in USA 1946 from a herd outbreak of an acute fatal rinderpest like syndrome with ulceration of the alimentarv mucosa and diarrhea. Later the disease was detected «/ in different countries of tlie world and confirmed in Egypt for the first time in 1975. H, Etiology BVD-MD virus is classified as a small RNA virus of genus Pestivirus, it is antigenically closely related to the viruses causing Border disease in sheep and Hog cholera in pigs. There is a wide range of strains that produce cytopathic and non cytopathic effects in tissue culture, and many ofthem infect cattle and sheep. II. 1. Growth in tissue culture:- BVD-MD virus grows well in a primary bovine kidney cell culture (BK) producing cytopathic effects after 96 hours from inoculation. II. 3. Resistance:- BVD-MD virus is stable at temperatures below 10 °C and at a pH range of 3-9. The virus is unstable in the environment, the virus is killed by lysol, iodophors and aldehydes. HI. I. Distribution:- BVD-MD is widely distributed in Africa, Europe, North America and the Middle East including Egypt. III. 2. Transmission:- A. Source of infection, the virus isolated from nasal discharge, saliva, semen, feces, urine, tears, milk, placental fluid, fetal tissues and animals with persistent BVD virus infection are the major source of infection to susceptible I non immune cattle.
  • 48. _______________ VIRAL DISEASES (33) The virus is a common contaminant of biological materials such as fetal calf serum and cell culture lines which plays an important role in transmission of the virus. B. The disease is transmitted by direct contact between susceptible animals via ingestion or inhalation of materials contaminated by infected oculonasal discharges, saliva, urine, also transplacental transmission occurs, as well as venereal infection of susceptible female cattle through service or by insemination with semen from a persistently infected bull usually resulting in early embryo loss and repeat breeding. III. 3. Host siisceptibility:- A. BVD-MD virus and related pestiviruses infect cattle, buffalo, sheep, goats, pigs and deer naturally. B. Cattle and buffaloes are the only species which develop clinical forms ofthe disease C. The importance ofsheep, goats and pigs sources ofinfection for cattle is still unknown. III. 4. Factors influencing susceptibility:- A. Cattle of all ages, sexes, and breeds are equally susceptible, but the majority of acute and chronic cases occur at 6-24 months ofage. B. Calves usually show congenital anomalies. III. 5. The economic importance ofthe disease:- A. Abortion, stillbirths, reproductive failure and congenital defects. B. Increased neonatal mortality. C. Prenatal and postnatal growth retardation. D. BVD-MD virus infection in calves may enhance diseases due to other pathogens especially respiratory diseases in calves such as IBR, Parainfluenza 3, pasteurellosis as a result of immune dysfunction (biological immunosuppression). 1Y> Pathogenesis A. In general it is not completely understood, but after natural infection ofnon immune susceptible cattle, the BVD-MD virus spreads via the blood stream and produces erosions and ulcers on the epithelium of the muzzle, nostrils, and alimentary tract.
  • 49. BO’INE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (34)------------------------------- B The virus has an affinity for lymphocytes causing leukopenia and lymphoid depiction in lymph nodes and peyers patches, the virus has immunosuppressive or immunodepleting effect, so BVD-MD vims infection in calves may enhance diseases due to other pathogens especially IBR, parainfluenza 3, pasteurellosis as a result of immune dysfunction. C. The virus can cross the placental barrier and invade the fetus and the results depend only on the stage of pregnancy, in early stage up to 100 days, abortion or mummification of the fetus occurs resulting in infertility and repeat breeding; in the middle and late stages, congenital defects and or persistent lifelong infection without clinical signs is a common sequel, as a result of these congenital anomalies, abortion and stillbirths may occur and calves may be born weak with a low body weight, incoordination, varying degrees of blindness due to cerebellar hypoplasia (Plate 1C photo 8) or degeneration, microphthalmia, cataracts, optic nerve injury', and other CNS lesions such as musculoskeletal malformations, and a variety' of skin lesions such as alopecia. Fetuses infected in early stage up to 125 days will be positive for the virus and persistent lifelong infection later and negative for antibodies, (immune tolerance), in contrast the fetuses infected in the late stage 180 days or later the calves will be positive for neutralization antibody' (active immunity) even before colostrum intake and such calves will be negative for virus. V. Clinical signs There is a variety of clinical forms ofthe disease, which may all occur in the same herd or appear separately, those clinical forms vary in severity from inapparent, subclinical infection or mild febrile disease to an acute fatal syndrome, a chronic debilitating infection can also occur. V. 1. Acute fatal syndrome (acute MD):- IP varies from 2-3 weeks, morbidity rate is low 5-10 %, mortality rate is high up to 90 %, the course of the disease is 1-3 weeks, this form usually occurs at age 6-24 months, it is sporadic in nature, it is characterized by fever 40-41 °C and depression, anorexia, weakness, cessation of rumination, increased heart rate and respiration, severe leukopenia, salivation profuse watery diarrhea occur 2-4 days from the onset ofthe clinical signs the feces are foul smelling and may contain mucus or blood, erosions and ulcers on the oral, alimentary tract mucosa, muzzle, nostrils and pharynx.
  • 50. VIRAL DISEASES (35) mucopurulent nasal discharge, lameness due to laminitis, coronitis and erosive lesions of the skin in the interdigital cleft, corneal opacity begins in the center and extends outwards (in contrast to Malignant catarrhal fever), pregnant females may abort, dehydration and death occurs after 5-8 days from the onset of signs. V. 2. Chronic form:- Develops as a sequel to either subclinical infection or non fatal clinical cases, and is characterized by progressive emaciation and weakness, inappetence, continuous or intermittent diarrhea, ocular and nasal discharge, chronic bloat, chronic erosions in the oral mucosa (Plate 1C photo 7) and skin over the perineum, around vulva, scrotum, prepuce, in the interdigital cleft and around coronary band, if in a pregnant female a variety of fetal abnormalities, abortion and fetal mummification, the chronic form is difficult to distinguish from the "unthrifty poor doers" with a persistent viremia in calves as a result of in utero infection, which is characterized by retardation of growth until development of a fatal form or other infections as pneumonia. V. 3. Inapparent, subclinical or mild infection:- This form is more common, and characterized by high morbidity 80-100 % and low' fatality 0-20 %, mild fever, leukopenia, inappetence and mild diarrhea V. 4. Congenital defects in calves:- These include cerebellar - ocular agenesis, ocular defects, musculoskeletal deformities (Plate 1C photo 6), alopecia, and intrauterine growth retardation. VI. Postmortem lesions The carcass is dehydrated, the gross abnormalities are confined to the alimentary tract, and characterized by shallow erosions with very little inflammation around them on the mouth, pharynx, esophagus, forestomachs, also in the muzzle, larynx and congenital defects in calves may be observed. VII. Diagnosis VII. I. Field diagnosis:- Clinical diagnosis is based on the history, the epidemiological patterns, clinical signs especially fever, diarrhea, oral lesions, abortion and congenital anomalies in newdybom calves. VII. 2. Laboratory diagnosis:- Specimens for laborator}7 use as shown in Table 1. There are two main keys to establish BVD-MD virus infection, one is to isolate the virus and the second is to detect the specific antibodies.
  • 51. BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (36) Isolation and identification ofBVD-MD virus by:~ | Purpose BVD-MD 1 diagnosis in I live animals Samples_______ __ Paired sera (with 3 weeks in between Single sera, with heparinized blood, (buffy coat) and nasal, oropharyngeal secretion, tears, urine and feces_______ Tissues samples from spleen, lung, kidney, lymph nodes as mesenteric Laboratory test Serology as SN Serology as SN and virus isolation Comments SingR sera are of no value Both tests are essential Diagnosis in dead animals Antigen detection tests and virus isolation Select alimentary tract tissues with macro scopic lesions I Detection of persistent Single serum sample SNT and virus isolation Both tests are essential I J111ccnon_______ Abortion inquiries, Fetus Tissue samples, thyroid, spleen, salivary' gland, fetal fluid______________ ______ Antigen det­ ection tests, virus isolation, SNT Preferred samples Dam Paired sera with 3 weeks in between SNT Serological response often completed at abortion time Investigation of congenital | abnormality Single serum sample SNT and virus isolation Precolostral serum is essential A. Isolation of the virus by inoculation of the specimens into a variety of cell cultures as primary bovine kidney cell culture (BK) and incubation, if vacuolation and or degeneration with detachment of cells will be noticed after 2-7 days indicates presence of cytopathic strains, but if no changes in cultures, non cytopathic strains are suspected and the virus is confirmed by indirect methods as IFT, SNT, using specific known antisera; indirect ELISA may be used to detect extra cellular virus in samples such as serum or cell cultures, also a sensitive and specific PCR may be used for detection of the virus, as well as the immunoperoxidase procedure.
  • 52. VIRAL DISEASES (37) B.The diagnosis of primary postnatal BVD-MD vinis infection, detection of its specific antibodies are required using virus neutralization (VNT), IIF, ELISA, immunodiffusion and CFT, precolostral serum samples from neonatal calves may be also tested for the virus antibodies to confirm the cause of teratogenesis, abortions, mummification, stillbirths or weak calves. VII. 3. Differential diagnosis:- BVD-MD should be differentiated clinically from A. Diseases with oral lesions and diarrhea as Malignant catarrhal fever, RP, alimentary form of Infectious bovine rhinotracheitis (IBR). B. Diseases with oral lesions and without diarrhea, as Foot and mouth disease, Vesicular stomatitis, Bluetongue, Necrotic stomatitis, Bovine papular stomatitis. C. Disease with diarrhea and without oral lesion as parasitic scours, Salmonellosis, Johne's disease, Tuberculosis, Enterotoxaemia and non infectious as copper, cobalt, selenium, vitamin A deficiency. VIII. Prognosis The prognosis for acute form with profuse watery diarrhea and oral lesions is unfavorable, most acute clinical cases will die in spite oftrials for treatment, but animals with subclinical, mild or chronic infections are favorable, such animals should be destroyed to prevent dissemination of the virus in the herd. IX. Treatment There is no specific treatment but in general symptomatic treatment is recommended as a course of antibiotics to control secondary infections, electrolyte fluid therapy to prevent dehydration, antidiarrhea drugs and supportive treatment. X. Prevention and control measures Control measures should be directed to limiting the spread of the disease via application of all hygienic precautions and clinical cases should be isolated and slaughtered; limiting the risk of transplacental infection via detection and identification ofpersistently infected animals and vaccination of susceptible cattle and buffaloes by:- A. Killed or inactivated virus vaccine usually safe, used in pregnant females, no post vaccinal complications but generally considered less immunogenic, its
  • 53. 1 BOVINE VIRAL DIARRHEA-MUCOSAL DISEASE COMPLEX (38) A recommended as early as 2-4 weeks ofage in calves and should be followed by booster dose annually at 6-8 months and its used in pregnant animals in late stage of pregnancy in two doses with 2-3 weeks intervals, this type of vaccine may be used singly or in combination with others viruses as IBR, PI - 3, this type ofvaccine is produced in Egypt. B. Modified live virus vaccine (MLV) may be used but it may be immunosuppressive, sometimes post vaccination BVD-MD appears within 3 weeks of vaccination, should not be given to pregnant cattle, should be given to the calves after 6 months, sometimes MLV contaminated with a virulent BVD virus strain, this type ofvaccine not recommended in Egypt. Plate 1C 6. Cerebellar ataxia in a calf infected in utero; teratogenic effect (BVD). 7. Erosions on the dorsal surface ofthe tongue (BVD). 8. Cerebellar hypoplasia shown in BVD compared with a normal cerebellum on the left. References 1. Callis, J. J.; Dardiri, A. H.; Ferris, D. H.; Gay, J. G.; Mason, J. and Wilder, F. W. (1982) "Illustrated manual for the recognition and diagnosis of certain animal diseases" Mexico- United, Commission for the prevention of Foot and mouth disease. 2. Duffell, S. J. and Harknen, J. W. (1985) "Bovine virus diarrhea-Mucosal disease infection in cattle " A review Veterinary Record 117,240 - 245. 3. El Sawalhy, A. A.; El Bagoury; Salem, S. A. and Youssef, M. A. (1995) "Bovine viral diarrhea complicated with Rota virus infection among foreign breed herd in Sharkia Governorate" 3 Sci. Cong. Egyptian Society for cattle diseases 66-77 4. FAO/O1E/WHO (1995) "Animal Health Year Book" 36 Rome, Roma 5. Hungerford, T. G. (1990) "Hungerford's diseases of livestock" 9 — Edit., McGraw - Hill Book Company Sydney, NewYork, London, Tokyo, toronte, PP 378 - 384 6. Kahrs, R. F.(l 981)" Viral diseases of cattle" The Lowa State University Press / Ames, Iowa 89-106 7. Kahrs, R. F (1981) "Bovine viral diarrhea, In: Diseases of cattle in the tropics" (Ristic, M. and MClntyreJ., eds) Martinus NijhoffPublishers, The Hague, Boston/London (15): 189- 195 8. Potgieter, L. N. D. (1992) "Bovine viral diarrhea In: Veterinary Diagnostic Virology " (Castro, A. E., and Heuschele, W. P., eds) Mosby Year Book St. Louis, Baltimore, Boston, London, Sydney, Toronto 88-92 9. Radostits, 0. M.; Blood, D. C.; and Gay, C. C. (1994) "Veterinary Medicine A textbook of the diseases of cattle, sheep, pigs, goats and horses".8& Edit. Baillier Tindall, England, London lO.Scott, G. R. (1990) "Bovine viral diarrhea-Mucosal disease, In: Handbook on Animal Diseases in the tropics" (Sewell, M. H., and Brocklesby, D. W., eds) 4 & Edit. Bailliere Tindall, London, Philadelphia, Tokyo PP 278 - 281
  • 54.
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  • 56. __________________________________________________________VIRAL DISEASES (41) BOVINE HERPES VIRUSES 1. Bovine herpes virus 1 (BHV-1) infection causes a variety of syndromes in the bovine with the same virus as Infectious bovine rhinotracheitis (IBR) or Infectious pustular vulvovaginitis (IPV) in females, Infectious pustular balanoposthitis (IPB) in bulls, alimentary tract (enteritis), ocular (conjunctivitis and keratoconjunctivitis), abortion and encephalitis forms of herpes virus infection, encephalitis and enteritis is restricted to newborn animals and is often lethal; ocular and respiratory infections commonly occur simultaneously; but it is uncommon to see the respiratory and genital involvement in the same animal. 2. Bovine herpes virus 2 (BHV-2) infection is characterized by skin lesions including Bovine herpes mammilitis (BHM) and Allerton virus infection. 3. Also herpes virus infection causes Malignant catarrhal fever (MCF) and Pseudorabies which are immunologically distinct from (BHV-1) and (BHV-2) INFECTIOUS BOVINE RHINOTRACHEITIS I. Introduction I. 1. Synonyms:- Infectious bovine rhinotracheitis (IBR), Infectious pustular vulvovaginitis (IPV), IBR/IPV, Red nose, bovine herpes virus 1 infection, according to OIE list (B) or J5jjuAi uiy>i j UuS'i I. 2. Definition:- IBR is a highly infectious disease of cattle and buffaloes caused by bovine herpes virus 1 and characterized clinically by rhinotracheitis, conjunctivitis, fever, short course and high recovery’ rate. I. 3. History:- IBR/IPV virus was firstly isolated in Germany, Western United States, and Egypt in 1928,1955 and 1976 respectively. IL Etiology. IBR/IPV virus is an alphaherpesvirus (BHV-1), all these strains have different tissues affinities but arc immunologicaly the same and cause IBR, IPV, IPB, one of the characteristics of (BHV-1) is its ability to become latent following primary infection with a mild strain of the virus or following vaccination with an attenuated strain.