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Animal Science Lecture Notes.docx

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Department
Animal Science
Course
AN SC100
Professor
Craig Wilkinson
Semester
Fall

Description
Animal Health 100 1. Health: State of physical, mental, and social well-being. a. Growth → Broiler chickens grow rapidly b. Reproduction → Hogs reproduce efficiently c. Behaviour → Horses work harder 2. Disease: An agent or anatomical alteration. Ex. Feline leukemia a. Infectious b. Non-infectious c. Sentinel (indicator) Context 1. Old diseases come back as new 2. Medical advances 3. People in poorer countries have little access to health care for themselves and animals a. Increase in population of undeveloped countries and decrease in developed b. Developed cutting back on meat consumption, undeveloped increasing 4. Changing of relationships with animals Animal Health/ Food Safety and Trade 1. Each country governs their own, but WTO and NAFTA set rules a. Disease outbreaks could be catastrophic 2. Travellers could take home infections, and Trade can move infections with dry goods Participants 1. Frontlines of animal production, animal habitat or companion owners a. Ranges from Intensive, large scale, highly technical food animal production facilities with monitoring by well-trained livestock managers and vets i. Commercial producers are encouraged to adopt herd health programs and focus on prevention→ Hobbyist farmers may have less training and less economic incentive to engage in prevention b. To clusters of companion animals observed with varying degrees of intensity by owners c. To wildlife populations with no regular health monitoring 2. Vets and other professionals a. 80% of vets in US are private practices b. Decrease in government vets c. Animal health technologists work in vet practices d. Vets involved in food animal practice are key to detecting and responding to emerging diseases. Ex. West Nile GUEST LECTURER DR. LANDALS 1. Human-animal bond changing over time, expanded need for awareness of welfare 2. Vet oath: promote animal health and welfare, relieve animal suffering and protect the health of the public 3. Legislated Responsibilities a. Set and enforce standard of vet med at a level minimally acceptable to society: kick out unskilled practices b. Enhance society by setting self-imposed standards at a level higher than minimal, keep updated 3. Government a. Federal i. Canadian Food Inspection Agency (CFIA): Food safety, protection of Animal Health ii. Agriculture and Agri-food Canada: Livestock support and regulation. Ex. Organic Production iii. Public health agency of Canada: monitors emerging diseases iv. Health Canada: Approves drugs in Canada b. Provincial i. Alberta Agriculture and Rural Development (AARD): Animal welfare laws, animal health act  Provinces have Chief Provincial Vet c. Municipal/ Local i. Restaurant inspection and outbreak investigations 4. International Organization a. WTO i. Global rules of trade and reference OIE codes b. OIE (World Organization for Animal Health) i. Objectives:  Transparency  Scientific Information  International Solidarity: countries set a standard  Sanitary safety  Promotion of Vet services  Food Safety and Animal Welfare ii. Collects and disseminates info on diseases including changes in disease status iii. Terrestrial and Aquatic Animal Health Code Manual c. WHO i. Diseases affecting humans, including zoonotic d. FAO (food and agriculture organization) i. Food and animal health in developing countries, international effort to defeat hunger ii. Improve agriculture, forestry and fisheries GUEST LECTURER ELLEN GODDARD Production cost increases= less product available Reduced demand= lower price= lower supply Rinderpest outbreak highlights need to create international body to regulate trade in animals and meat products: recall affects reputation 5. Supporting institutions a. Education and research 6. Others a. Media and Pet supply Identified Gaps in the Framework 1. Need for development of technological tools for preventing and detecting or diagnosing animal diseases 2. Lacking funds 3. Need coordination among nations 4. Education and training lacking 5. Improving awareness of economic, social and human health effects of animal diseases Genetic technologies: SHADI AND YOUNES PRESENTATION 1. Polymerase Chain Reaction a. amplifies DNA, confirms presence of micro-organism not anti-bodies 2. Bioinformatics a. To characterize components of living things through sequencing 3. Genotyping a. SNP array geno-typing 4. Cloning a. increase number of desired genotype Comparative medicine 1. Accuracy: how to treat and reduce adverse effects 2. Rules around research a. Human environment health and safety followed b. Living conditions of animals c. Use animals only if necessary and keep animals to minimum d. Will not cause impact to species or environment or the individuals behaviour e. Endpoint: how much disease is the animal allowed to be exposed to f. Post approval monitoring: doing what the rules said g. Process: has scientific merit and makes sure it has a good protocol h. Protocol review: they must have thought of all the things that could go wrong Ethical Use of Animals in Teaching and Research Albert Schweitzer: Nobel peace prize winner, medical doctor who opened hospitals who brought along animal ethics Bernard Rollin: livestock and animal research, ethics column in Vet Journal Laws Around Research Canadian Regulatory Framework 1. Federal legislation and controls: Criminal code highlights how you transport animals and has consequences for intentional cruelty to animals. No federal Animal Welfare Act, instead: 2. Canadian Council on Animal Care (CCAC): all animal codes under this, all research at universities are funded by CIHR and NSERC. 3. Vet professions act: have to do it like a vet would, if non-compliance with these then funding is stopped 4. ACUC: membership required, have to have a person from each category to do research (scientist, community) and have an authority who may have to stop experiment if necessary. 5. Three R’s: a. Reduction: in animal use→ strategy used b. Replacement: of animals by alternatives→ science simulators c. Refinement: of techniques→ better equipment and training d. Respect: for the animals and people you’re working with Immunity: defense against invasions 1. Micro-organisms a. Bacteria, Viruses, protozoa all see animal body as a source of nutrients and shelter b. Constantly seek to invade, avoid immune system and reproduce to pass to new host Development of New Vaccines and Immunology 1. Beginning of Immunology a. Small pox: virus related to cow pox i. Debilitating disease with 40% mortality, leading cause of blindness ii. Who estimated 15M contracted and 2M died; Eradicated in 1979, used quarantine iii. As early as 10 century, variolation (scratching of skin with the infection) used to cause small pox and hopefully induce immunity iv. Noticed cowpox caused immunity to small pox, Edward Jenner tested this v. 1 vaccine in 1800, Clinch obtained and vaccinated 700 people in Newfoundland 2. Immunology Pioneer a. Louis Pasteur i. P. multocida: Fresh caused death but when aged it didn’t because it wasn’t able to retain the disease and therefore made the chicken immune ii. Anthrax and Rabies: Grew Bacillus anthracis at a high temperature to become avirulent and used attenuated as a vaccine in sheep.  Rabies hides in the nerve and takes weeks to travel to the brain  Rabies vaccine using dried spinal cord from rabies infected rabbits using similar methods  Anthrax is transferable from animals to humans  By 1900, virus toxin still unknown, but still a filterable particle o Before antibiotics, vaccines were thought to be the only answer Definitions: 1. Avirulent: No disease but still reproduces 2. Attenuated: Shortened life by high temperature 3. Pathogen: An agent possessing the ability to cause a disease in an animal in an environment a. Primary: Causes a disease nearly every time it invades, even in low numbers b. Opportunistic: Low virulence and causes disease only if administered in high doses 4. Pathology: Study of events and reactions, particularly changes in the body tissue and organs, occurring in the development of a disease (pathogenesis). 5. Etiology: Determination and study of factors that contribute to the disease 6. Diagnosis: Determination of the nature of the case (not determination of etiology) 7. Prognosis: Forecast of probable outcome and course of a disease 8. Pathogenic: How dangerous it is 9. Virulence: Degree of pathogenicity, determined by fatality rates and or the ability to invade 10. Antigen: Foreign substance that can bind to specific lymphocyte receptors and induce an immune response 11. Anti-body: Immunoglobulin molecule synthesized on exposure to an antigen 12. Desiccation: Skin dry 13. Desquamation: shedding the surface 14. Turbulence: Spiral bones that hit sides of nasal passage with air and collect debris Several Levels of Defense 1. Primary: a. Physical barrier: Impair entry of micro-organisms through the epithelium into the body i. Skin: physical injury often opens up entry for microorganisms, skin carries dense resistant bacteria ii. Respiratory tract: traps microbes with ciliated epithelium and mucus secreting cells (goblet)  Provides mucus layer atop the cilia which has anti-septic properties due to lgA and lysosome action  Mucocillary escalator: cilia beating transport these particles out of the respiratory tract to the pharynx and then is swallowed  Coughing= expulsion of large particles iii. Gastro-intestinal: Gastric juices act as a bactericide due to acidity  Gastrointestinal mucins: glycoproteins secreted into the intestine to form a mucous gel which serves as a barrier  Inner layer of mucus is rich in defensins (non-specific) and lysozymes that help destroy bacteria  Mucus is transported out of the body in feces. More mucus= more digestive problems  Horses use hindgut digestion to digest grasses, uses symbiotic bacteria iv. Others: Desiccation, Desquamation, and Turbulence b. Innate immunity: Doesn’t require vaccines, but doesn’t work well with viruses. “Always on” i. Inflammation: exposure to microbial invasion, trauma, heat or chemicals that result in tissue damage  Releases alarmins (tissue damage) to trigger innate or  Toll like receptors that recognize pathogen associated molecular patterns (PAMPs) (microbial invasion) which are highly conserved molecules (lipopolysaccharide) found on the surface of micro-organisms. 1. TLRs or Alarmins trigger innate immune defenses of Sentinel Cells - result is inflammation 2. Vasoactive Molecules or Cytokines are released, activating vascular changes, phagocytic cell activity, and systemic responses 3. These activate neutrophils and macrophages, resulting in the killing of bacteria, and tissue repair processes 5 Classical signs of inflammation: 1. Redness (rubor) 2. Heat (calor) 3. Pain (dolar) 4. Swelling (tumor) 5. Loss of function (fuctio laesa) Inflamation ‡ infection Use “itis” to indicate inflammation except for pneumonia (lung inflammation) Ex. Nephritis =kidney inflamation 2 Types of inflammation 1. Acute 2. Chronic  Sudden onset  Onset slow  Short duration  Long lasting  Not imply severity  Often results in impaired functions  May be mild or severe  May begin with acute that does not resolve 2. Secondary: i. Acquired Immunity: Purpose is to deal with micro-organisms that gained entry into body and escaped primary defenses. “Turned on”  Cell mediated immunity: WBC (leukocytes) form essential part of secondary defenses a. Granulocytes: neutrophils, eosinophils, and basophils adhere to, engulf, and digest foreign particles b. Mononuclear cells: i. Monocytes: phagocytic; engulf foreign material and promote immune response ii. Lymphocytes (T-cells): non-phagocytic; signalling, cytotoxic (killer) cells iii. Lymphocytes (B-cells): Antibody production (humoral immunity); memory cells  Humoral immunity: Antibody production a. Antibodies: soluble antigen receptors b. Antibody proteins are known as “immunoglobulins” c. Immunoglobulins, 5 types in mammals: IgG, IgM, IgA, IgE, IgD i. Immunoglobulin G – highest concentration in blood, major role in antibody-mediated defense mechanisms – the immunoglobulin found in colostrum ii. IgM - complement activation, facilitating phagocytosis, neutralizing viruses, and agglutination. iii.IgA - in external secretions of nonruminants, important in protecting the intestinal, respiratory, and urogenital tracts, mammary glands and eyes iv. IgE - low concentrations in many species. Immune response to many helminth (parasitic worm) infestations and in mediating allergic reactions. d. Produced by “B cells” – a type of lymphocyte e. Ab’s are very specific to particular invading material - the “antigen” f. an “antigen” must be recognized as foreign g. Antigen receptors must reliably bind foreign antigens on their first encounter h. Achieved by scrambling and rearranging the peptide sequences that comprise the antigen- binding site (millions of conformations), allows them to bind to almost any invading microorganism The anti-body response 1. Initial invasion (infection) stimulates production of proteins called "antibodies" by plasma cells (a type of lymphocyte) 2. Antibodies bind specifically to antigen and hasten its destruction or elimination by various types of lymphocytes and other cells and their products. 3. Stimulates production of “memory” cells to initiate a quicker and larger response the next time 2 types of humoral immunity 1. Active 2. Passive  Immunity produced by the body  Protection of individual by administering antibodies produced in another individual  In response to an administration of an  No immune response triggered to the antigen antigen in the recipient  Triggers the body's immune response  No memory and memory Active: exposure to, or vaccination with live, attenuated or dead infectious agent to produce an immune response.  Exposure to antigen causes animal to mount a protective immune response that may be antibody- or cell-mediated or both.  Reimmunization or exposure to infection results in a secondary immune response. Disadvantage: Protection is not conferred immediately, often requires “boosters.” Advantage: once established immunity is long-lasting and capable of re-stimulation Passive: production of temporary immunity by administration of preformed antibodies from a resistant to a susceptible animal.  Recombinant: insert gene that makes expression of protein that looks like the diseased one  Bacterins kill organism completely Advantage: Gives immediate protection Disadvantage: Antibodies are gradually broken down and immunity wanes and can block development of active immunity until passive drops off Animals receive anti-bodies in the colostrum, humans receive antigens passed through placenta → 1 24 hours baby is able to absorb antibodies because gut is “leaky”, after 24 hours the gut seals off →After the 24 hours, give them plasma or serum for immunity -Effective level of antibodies graph -Test tube of blood picture Ex. Tetanus: if you step on a nail and you don’t know whether you’ve been vaccinated, nurses will re- vaccinate with tetanus anti-toxin derived this way 5 major components to acquired immunity 1. Cells that trap and process antigen and then present it for recognition to the cells of the immune system 2. Cells that have receptors for the processed antigen bind and respond to the antigen (antigen sensitive cells) 3. Cells that once activated by antigens will produce specific anti-bodies, or will participate in the cell-mediated immune responses against the antigen (effector cells) 4. Cells that will retain the memory of the event and react rapidly to that specific antigen if its encountered at a later time 5. Cells that regulate the response and ensure that it functions at an appropriate level (inhibit immune responses) Innate compared to Acquired The C onc ept of Sel f vs. Non S elf Immunological Goals • R e c o g n itio n a n d e lim in a tio n o f foreign proteins (antigens) witho ut •T o r e d u c e s tr e s s damaging normal cells and tissues. Self v•T o re d u c e d is e a s e e x p o s u re 1. Recognition and elimination of foreign proteins (antigens) without damaging normal cells and Failur e s r esult in •tissues.in ta in /in c re a s e n a tu ra l – T o le r a n c e ability to respond to infection – A u to im m u n e d is e a se 2. •T o ra is e th e le v e l o f d is e a s e aresistance by vaccinationd fails to fight infection – A lle r g ic r e a ct io n b. Autoimmune disease: reaction against infection and self c. Allergic reaction: exaggerated reaction to non-pathogens, hypersensitivity reaction (bee sting) When is the immune system compromised? Stress (cumulative), body condition, parasitism, nutrition Ex. Cows become sick because of consuming tall grass with high levels of toxic alkaloids Trace minerals affecting immunity? Copper, selenium, zinc, manganese. How can an Animal’s immune Stresses system be compromised? → If you have none, your immunity lowers, if you have too much could be poisonous Weaning Shi ppi ng • S tre s s Disease Mixing • C o n d itio n Resistant Diet Disease • P a ra s itis m Susceptible Weather • N u tritio n Vaccination and Immunization (don’t always get immunization by vaccination) Types: 1. Intramuscular 2. Subcutaneous 3. Oral 4. Intranasal 5. Eye drops Reasons for Vaccine Failures 1. Incubating disease at the time of vaccination 2. Something happened to the vaccine to make it ineffective (not kept cool) 3. Physiologic status of the vaccinated animal may make it less responsive or unresponsive to the vaccine 4. The host may be exposed to an overwhelming amount of the infectious agent (dose above immunity of disease=sickness) Vaccine factors 1. Antigenic components: signal different parts of protein/virus (not all vaccines are created equal) 2. Homologous antigens: viruses are using same antigen (exact same virus) 3. Heterologous antigens: virus using 2 antigens (strains) therefore cross protection 4. Cross protection: protected against 2 strains 5. Adjuvants: boosts immune response (Keep those who have bad reactions away from these) Administration factors 1. Environmental/Storage Stress 2. Improper Injection Equipment 3. Sterilization Practices 4. Mixing Products in Syringes 5. Route of Injection: if you inject an intra-nasal when it needs to be intramuscular, it won’t work 6. Aseptic Technique: give an injection may cause infection (vaccinating many animals with 1 needle) Animal Factors 1. Maternal Blockade 2. Immune suppression 3. Concurrent Diseases: other disease being incubated that’s why you do a physical before vaccinating 4. Drugs - eg: Corticosteroids : suppresses immune system 5. Nutritional status 6. Age 7. Hormones 8. Incubation of disease 9. Stress Side note to reactions to vaccines (definitions): Malaise= feeling crappy  Not a reaction, just normal response from immune system Anaphylaxis: bad hyper sensitive reaction Granuloma: WBC set up local reaction (in cats there will be a bump around needle entry) Fibro sarcoma: Cancers that happen from vaccines Neurological reactions: rare Infectious Diseases Definition: disease that is caused by a living agent  May or may not be contagious, most are transmissible Ex. Tetanus: non contagious because it releases toxins in anaerobic environment Infection: disturbances caused by entrance, growth and activity of the agent in the body (abnormal symptoms) Means of disease transmission (often requires direct contact) 1. Pathogenic organisms: most harmless, some opportunists a. Bacteria: Prokaryotic i. Reproduce by fission (cell wall elongates, dividing wall separates two parts) ii. Microscopic characteristics 1. Size: 1-100microns 2. Shape: coccus, baccillus, spirillium/ vibrio, filiment 3. Arrangement: single, pairs, chains, clusters, irregular clumps 4. Gram stain: + = purple, - = pink 5. Other stains: acid fast (mycobacterium) 6. Spores: in rod shapes with clubbing of ends. Resistant to heat, dessication and chemicals. (Bacillus, clostridium) 7. Flagella: motility, delicate thread like. Many bacilli, spirilli and vibrios have (few cocci) iii. Macroscopic characteristics 1. Culture a. Plates: size, morphology, activity of colonies (hemolysis: breaking down of nutrients), media b. Tubes: biochemical reactions, anti-microbial susceptibility, serological response (antibodies in blood bind to antigens of the bug. Ex. E.coli 0157 H7, 0 lipopolysaccharide, H flagellin) iv.Molecular and genetic characteristics 1. Allow identification of many subtypes of bacteria a) Gene Sequencing b) Polymerase Chain Reaction Detection c) Identification of unculturable bacteria (technology allows to identify a dead bacteria) d) Analysis of whole communities of bacteria Case study: Clostridium strains 1. Symptoms: depressed, fever, off feed, no stomach movement, stiff gait  Vaccinating helps boost memory cells→ treated then later died 2. Post mortem results  Petechial hemorrhage (purple bruises) in axilla (armpit) and myocardium(heart)/ pericardium  Histology (muscle stained) found basophilic rods  Vasculitis = multi focal (inflammation of blood vessels)  Blood test = inflammatory response 3. Diagnosis: clostridium type D (spore type)  Everything on farms vaccinated for this because they are in soil, feed and manure.  Use a polyvalent vaccine that has 7 or 8 key antigens  Rule out anthrax and lightning strikes because of swelling and lameness Types of clostridium 1. Clostridium tetani (tetanus): rigid paralysis a.Causes generalized hypertonia (paralysis of muscles, mostly jaw) b.Commonly present in feces c. Begins producing toxins in 4-8 hours, incubation 1-3 weeks d.Treatment: debride (cut) wound e.Effects more greatly in horses than dogs 2. Clostridium botulinum (botulism): flaccid paralysis f. Often from carcasses or decaying plant material g. Epizootics occur in water fowl (ducks feed of decaying food) 3. Clostridium chauvoei (Black leg) h.Non-contagious and soil borne i. Happens in hot months, anaerobic, motile and spore forming b. Viruses: Acellular i. Characteristics:  Contain DNA or RNA core and protein “capsid” coat  Often have an envelope (phospolipid) derived from host cell membranes  Genetic elements (DNA/RNA) that can replicate independently of a cell’s chromosomes  Obligate intracellular reproduction (“parasitic” on host cell mechanisms)  Must replicate in their specific host cell  Very small compared to bacteria and fungi (20 – 300 nm) ii. Morphologies 1. Helical symmetry Ex. Tobacco mosaic virus (plants) looks like paramyxoviruses with distemper similar to measles 2. Isohedral symmetry (20 sided polygon) 3. Enveloped: outside coating Ex. Rabies 4. Complex Ex. T4 bacteriophage (invades bacteria) Animal Viruses 1. RNA viruses a. Coronavirus: in most animals (SARS and MERS-CoV) b. Rhabdovins: Rabies c. Retroviruses: HIV, FeLV (feline leukemia) Ex. Bovine Viral Diarrhea  Acute, highly contagious and rapid contraction  Virus in feces and spread by fomites  All ages susceptible but most susceptible at 6-24 months (drop in antibodies from colostrum)  Cows symptoms include weight loss, decrease in milk production and mummification of calf  Calves symptoms are a fever, diarrhea and dry cough  Transplacental infection: calf infected before its born, may be aborted or have a physical malfunction  After birth, the cerebellum is half the size so it will never walk properly  Prevent by decreased exposure, isolation and vaccination  Strains: o Cytopathic: high virulence o Non-cytopathic: low virulence 2. DNA viruses a. Herpe virus: herpes in every animal b. Pox virus: largest virus (cow and small pox) c. Parasites: i. Protozoa: Eukaryotic 1. Ciliated Ex. Balantidium Coli: Parasitizes many species of hosts 2. Amoeboid Ex. Entamoeba histolytica: Cause of amoebic dysentery (intestines: presence of blood) 3. Flagellate Ex. Giardia lamblia; Trichomonas vaginalis 4. Spore forming Ex. Isospora and Eimeria spp. (coccidia) ii. Helminthes 1. Platyhelminthes (flatworms) a) Cestodes (tapeworms): Endoparasitic, segmented (head attached to a neck), no gut (absorbs nutrients), hermaphroditic Ex. Taenia saginata of beef b) Trematodes (flukes): non-segmented, simple ventral sucker, 2-4 hosts Ex. Fasciola hepatica – sheep liver fluke 2. Nematodes (round worms) Ex. Guinea worm (dracunculus): endo-parasite that infects almost any organ, Vermiform (cylindrical and non-segmented), no intermediate host Ex. Bovine ostertagiasis 1. Symptoms: Weight loss and diarrhea, herd outbreaks (mostly young cattle) 2. Life cycle: No intermediate host, eggs passed in feces then 3 stage larvae emerge and sit on grass where they are eaten and they moult in the rumen, develop in the lumen of the abomasal gland 3. Pathogenesis: Causes severe damage, bumps and folds in the stomach 4. Two forms 1. Calves start to graze then results in spike of larvae 2. Symptoms occur in yearlings resulting from maturation of larvae ingested from earlier autumn which went into dormant phase and then activated next spring when yearlings graze a. Type 2 can be diagnosed by leaking protein from intestines and blood plasma becomes less concentrated which leaks (ventral edema: swelling of tissue) b. Treated by ivermectin (dewormer) and controlled by deworm routines or rotational grazing iii. Arthropods 1. Endo and ecto-parasites Ex. Sarcoptes scabei (mange): mites 2. Arachnids: mites, ticks, spiders 3. Insects: lice, fleas Ex. Dermacentor albipictus (moose tick) d. Fungi: Eukaryotic, lacking chlorophyll, facultative anaerobes/ strict aerobes, chemotrophic, dimorphic. i. Mykos: fungus ii. Mycosis: disease caused by fungus 1. Superficial: hair skin, cornea Ex. Ring worm: skin fungal disease o Hedgehogs common carrier but don’t show lesions o Animals show it as ring of hair loss o Humans show it as a red circle. Redness is the hyphae growing o Transmissible from animals to humans o Diagnose by skin scrapings Ex. Yeast (Candida albicans) o Reproduce by budding (bud=blastospore) o Pseudohyphae o Pasty colonies o Causes yeast infections in dog ears Ex. Mould o Multicellular, long branching filamentous o Has hyphae (2-10 micron) and spores 2. Subcutaneous 3. True systemic (in organs and spread) 4. Opportunistic: nasal, oral, urogenital iii. Mycology: study of fungi Developments: 1. Increase in number of immuno-compromised patients (immune suppressed for surgeries so mycotic infection can take advantage) 2. Grow fungus on plates and test right on plate= new antifungal drugs 3. Some that we used to kill are now becoming resistant e. Prions: Acellular i. Infectious particle which resist inactivation ii. Causes spongiform encephalopathies: appearance of the brain with large vacuoles in the cortex and cerebellum Ex. Scrapie (sheep), BSE, CWD, TME,CJD, GSS, FFI, Kuru, Alpers syndrome  Loss of motor control, dementia, paralysis iii. Both infectious and hereditary 2. Intervening agents a. Inanimate vectors or fomites: in feed and water, transport vehicles, bedding, needles i. Vector: animals carry disease one place to another ii. Fomite: physical object that carries disease from one animal to another b. Animate vectors i. Arthropods ii. Mammals 3. Portal of entry a. Routes or pathways into the body often depends on the infectious agent and vector involved i. Most common are cuts, punctures or abrasions ii. Through mucous linings, mouth, eyes, GI, respiratory tract and uro-genital tract Disease resistance 1. An animal will inevitably be exposed to pathogenic organism 2. An animal capable of warding off a particular pathogen are considered “Resistant” because they have immunity 3. Animals in good health normally have Primary and Secondary defenses that maintain their disease resistance So how do diseases occur? Epidemiology: collection of statistical tools used to elucidate the associations of exposures to health outcomes (where did it come from and what happened to it).  Discover and establish causal relationships, Triad (triangle or teeter totter) Exposure vs. Infection Depends on: 1. Dose: number of bacteria that challenge the animal (more there is less likely to fight) 2. Pathogenicity: organism’s ability to reach the animal, invade and infect, then multiply enough to cause disease a. Invasiveness: the organism’s ability to spread from the initial invasion site or to gain entry to the circulatory system. b. Production of harmful substances: Pathogenicity of an organism is often due to toxins or enzymes it produces that interfere with the function or metabolism of the animal 3. Immune status: animals ability to fight off the disease (includes both primary and secondary defenses) a. Why does one have immunity and the other doesn’t? Non-Infectious disease 1. Developmental: may have as a young animal 2. Anomoly (cleft pallet); Allerigic/Autoimmune(itchiness due to reaction against own cells) 3. Metabolic: liver diseases, diabetes 4. Nutritional(deficiency in diet); Neoplastic(cancerous);Neurologic(tumor in brain causes seizure)* 5. Inflammatory; Immune;Iatrogenic(the doctor did it or misdiagnosed);Idiopathic(unknown) ;Infectious 6. Traumatic(bruise instead of black leg); Toxic(lead poisoning, automobile battery) 7. Vascular: cardio/heart diseases (coagulation, blood type problems) Types of non-infectious diseases 1. Physical and chemical diseases a. Toxicological problems that may relate to nutrition 1. Fungal (mycotoxicosis) 2. Plant 3. Nutrient toxicoses 2. Circulatory diseases: various etiologies 3. Digestive diseases: nutritional, traumatic, metabolic 4. Reproductive diseases a. Abortion: plant toxins or developmental problems b. Dystocia: calf gets overweight not enough calcium c. Failure to lactate d. Repeat breeders Case study “Hardware Disease” in Cattle (reticuloperitonitis)  Not infectious but involves an infection due to a traumatic injury to reticulum Symptoms 1. Digestive upset and develop fever 2. May not produce enough milk 3. Develops heart problems later 4. Congestive heart failure: brisket(chest) swollen Pathway: Rumen →Reticulum →Omasum→Abomasum (Most like our stomach) 1. Heavy stuff ends up in reticulum: nail sticks out in front of diaphragm and heart 2. May puncture heart /pericardial sac: causes infection around the heart (heart disease) Prevent: 1. Put magnet in cow to capture sharp metal bits, does not help with sharp plastic. Ex. Tires have steel wires that may get mixed in with feed Ex. Feed machine may loose bolts Outcomes: 1. Diffuse peritonitis: infection spreads 2. Acute local peritonitis 3. Vagus nerve affected→ rumen stops working 4. Cardiac tamponade: heart can’t beat properly→ death Many diseases are primarily associated with life stages or particular groups: Developmental= young growing animal (broiler chicken) Neoplasia= more commonly older Production Diseases  induced by management practices  Recently, "Production related diseases" expanded to include other traits, such as infertility, and diseases such as mastitis and lameness that might involve infectious agents but are exacerbated by nutritional or management factors  Relates to expected productivity of animal  Maintenance of “health” in a high-production animal includes: o Fertility  return to oestrus(heat) after calving or farrowing(pigs)  Dystocia rate  Bull fertility o Dietary Management  nutritional and metabolic disorders o Multifactorial Diseases – relationship and participation in infectious diseases Non-infectious diseases in cattle  Energy Metabolism Associated Disease o Fat cow syndrome. o Ketosis o Retained Placenta o Infertility  Diseases Associated With Low Fiber/Acidosis o Bloat, laminitis, indigestion/off feed, liver abscesses, displaced abomasum  Calcium/Phosphorus Metabolism Diseases/Complications o Hypocalcemia (Milk Fever)  Hardware Disease (Traumatic Reticuloperitonitis and Pericarditis) Case study “Downer cow” Symptoms:  cow is recumbent, won’t/can’t get up, not alert  up after calving and shifting on feet, has not discharged fetal membranes  hasn’t eaten, low temperature, increase heart rate to 120bpm (tachycardia), extremities feel cool(hypothermic), pupils dilated  rumen not growling every 45 seconds(GI depression), mild muscle tremors, no feces Diagnosis:  Milk fever (Parturient paresis) caused by calcium dropping low and results in muscle contraction o Caused by exposure to lots of calcium before birth, during birth all calcium is used for milk so she isn’t efficient absorbing calcium after o Prevent by lowering calcium before birth so she gets used to absorbing calcium (acidify diet) o Treat with calcium slowly, too much too fast=death o Hypocalcemia causes muscle tremors, pupil dilation and retained placenta  Ketosis caused by metabolism of fats which results in ketones in urine o Treat with glucose through IV or glucocorticoids to improve glucose distribution o Prevent with maximum energy intake of high quality food Developmental Orthopedic Diseases in Horses -These diseases are found in young growing horses -Horses bones grow from the metaphysis and up 1. Osteochondrosis dissecans o Bone cartilage problem o Flap develops from articular cartilage due to failure of cartilage to be properly converted into bone, this can go down to the bone 2. Epiphysitis and physitis o Inflammation at growth plate when bone is weak o Causes deformation of leg 3. Subchondral bone cysts o Failed endochondral ossification 4. Osteochondisis of vertebral column o Cervical vertebrae does not form correctly, pinching the spinal column Dogs Hip dysplasia  Socket is flat and angle between socket and ball is straight  Not a stable joint, can cause more bone to form to try and correct the stability  Large dogs: Risk in 5 month and older dogs  Feed for large dogs have to be low in energy so they grow slowly and evenly  Treatments can be surgical or medical (rest, anti-inflammatory) o Femoral head ostecotomy in smaller dogs: removal of ball so all is scar tissue Bovine Ocular Squamous Cell Carcinoma (cancer eye)  High heritability, white faced breed  Prolonged exposure to UV light Zoonoses 1. Zoonoses are dynamic a. Flow and ebb: more some years, less other years b. Vector population: ex. mosquito populations from year to year change c. Climate changes and habitat alteration change d. Mutations and alterations Emerging disease Definition: When incidence has increased or expected to increase, and circulation of potentially different infectious disease  Emerging for a particular sub population  An agent endemically present in one species may emerge in another Types: 1. Qualitative a. Host: who and what is the target population b. Agent: what is the agent and how do we recognize it c. Interaction: what are the mechanisms of infection, transmission and what is the mode of propagation (reproduction) 2. Quantitative a. Incidence: magnitude of increase b. Time: temporal pattern of increase, duration of the outbreak c. Space: location and area affected Factors: 1. Ecological changes such as those due to agricultural or economic development, or anomalies in climate (slash and burn) 2. Human demographic changes and behaviour 3. Travel and commerce 4. Technology and industry 5. Microbial adaption and change 6. Breakdown of public health measures: Alberta shut down routine post mortems because budget too tight Pre-emergence “spill over”→ Local Emergence→ Global emergence Emergence: land use, international travel and climate that drives zoonotic diseases to wildlife Un-emergence: ex. Malaria and measles → goes down in number of cases over time People involved with zoonoses 1. Virchow: founder of medical disciplines like comparative pathology (disease common to animals and humans) 2. Osler: coined “one-medicine” and studied pathology a. Studied hog cholera b. Determined parasite causing bronchitis in dogs Zoonoses and early vet med  Founded on study and eradication of zoonoses as much as one animal diseases  Testing program for Bovine tuberculosis (into bones when affecting humans) and Brucellosis (develop undulant fever which comes and goes, and makes you sterile) o Eventual elimination of TB o Caught by unpasteurized milk o TB is why vet schools were made Famous zoonoses 1. Bubonic plague (black death) 2. Influenza 3. Bovine TB 4. Brucellosis 5. Anthrax and Rabies 6. Malaria and yellow fever “New” zoonoses 1. West Nile: in birds and horses 2. Canine parvo: came from cats and mutated to affect domestic dogs and wolves 3. Canine distemper: related to human measles, crossed into felines and wiped out 1/3 lion population in Serengeti 4. Post weaning multisystemic 5. Chytrid disease and iridovirus of amphibians: tracking mud of transporting as pets 6. Exotic: Newcastle disease in poultry from cormorants carrying it and adapted to it Ex. Avian Influenza  Gets around with movement of birds  Establishing good biosecurity methods on poultry farms is an important defense  Chicken in contact with pigs which caused H1N1  Risk: duck with low pathogenic flu and human with low pathogenic flu get mixed and causes increased pathogenicity Factors unique to Asian countries Importance of Asia as a reservoir of disease emergence  High human population density- most rapidly growing population  Cultural predilection to “novel” food species- mixing ducks and chickens in the same environment  Want more high protein diets  Close association between humans, soils, vegetable food sources. They live right where their food comes from Ex. Backyard chickens, can have egg laying chickens but cannot slaughter them for food after they stop laying eggs Case study Nipah virus(named due to town it came from)  40% mortality, no treatment or vaccine Symptoms:  Pork slaughter house workers caused swelling of the brain  Saw disease on pig farms, sudden death of pigs  Unusual pattern noticed by epidemiologists Outcome:  Military killed 1.3 mil
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