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BVETMED2 > Principles of science > Flashcards

Principles of science Flashcards

1
Q

Why is a particular dose of drug given

A

Because it is shown that the drug can reach the target tissue/organ at the desired concentration to give a therapeutic effect

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2
Q

what is the effective dose (ED50) of a drug defined as

A

The dose of drug that produces 50% of the maximal response in 50% of the population

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3
Q

What is the therapeutic index of a drug

A

The amount of the drug that causes therapeutic effect in comparison to toxic effects

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4
Q

What are the factors affecting absorption of a drug

A
  • Molecular weight
  • Lipid solubility - higher=more readily absorbed
  • Chemical nature - Weakly acidic/basic. Dependant on area of the body can become ionized and absorbed less readily
  • Area of absorbing surface
  • Local blood flow
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5
Q

What is bioavailability

A

Fraction of administered drug that reaches systemic circulation in an active form

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6
Q

Why are drugs given via a particular route

A

Because you may be aiming to achieve a different thing e.g

  • rapid onset
  • high plasma concentration
  • long term administration
  • restriction to local site
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7
Q

What s volume of distribution

A

Measure of the volume of fluid required to contain the amount of drug at its plasma conc.

enables us to know if the drug will reach systemic circulation, ECF or ICF

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8
Q

Why are drugs given at variable intervals

A
  • Drugs are elimated via bile, kidneys and liver (metabolism)
  • Drugs metabolised to make them more water soluble, Cytochrome p-450
  • Enterohepatic (re)cycling - Drugs transfered from drug conjugates to bile. Released in the intestines & hydrolysed back into free drugs reabsorption
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9
Q

Whats first order kinetic & zero order kinetics

A
  • First order - Rate at which plasma drug concentration & elimination. Decreases is proportional to concentration. Half life is dependant on dose
  • Zero order - Linear decrease in concentration time. Fixed amount of drug removed per unit time
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10
Q

What type of drugs can be used to slow heart rate

A
  • Muscarinic agonist
  • Beta adrenoreceptor antagonist - e.g propranolol, atenolol
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11
Q

What drugs would be used to increase heart rate

A
  • Muscarinic antagonist - commonly used as premedication to anaestesia when vagal stimulation dominates - atropine
  • Beta adrenoreceptor agonist - isoprenaline (non selective)
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12
Q

What are the 4 classes of antidysrhythmics

A
  1. Class I - Block voltage gated dependant Na+ channels e.g lidocaine
  2. Class II - antagonise Beta adrenoreceptors e.g propranolol
  3. Class III - Blocks K+ channels involved in repolarisatione e.g Amiodarone
  4. Class IV - Inhibit Ca+2 channels e.g Diltiazem

Arrythmias caused by excessive sympathetic tone

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13
Q

What drugs are used to increase cardiac contractility

A
  • Sympathomimetics - Selective B1 adrenoreceptor agonist e.g dopamin/dobutamine
  • Phosphodiesterase inhibitors - elevated cAMP levels increases force of contraction and acts as a vasodilater e.g milrione
  • Cardiac glycosides - Positive inotrope with a very narrow therapeutic window. Blocks k+ site on na/k ATPase, increasing intracellular Na, decreasing amount of Na in Na/Ca exchange, increasing intracellular Ca. e.g digoxin. Also has a negative chronotropic effect by increasing vagal tone
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14
Q

What drugs are used to decrease contractility of the heart

A
  • Beta adrenoreceptor antagonist
  • Na channel blockers
  • Ca channel blockers
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15
Q

Describe the drug actions that are used to interfere with vasoconstriction

A
  • Alpha 1 Selective adrenoreceptor antagonist - Both arteries/veins dilated e.g Prazosin
  • Inhibit RAAS system by
  1. Beta antagonist to block renin secretion
  2. ACE inhibitors - captopril
  3. Angiotensin I receptor blocker - Saralasin
  • Endothelin 1 - constriction peptide formed by ECE in endothelial cells e.g propranolol
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16
Q

what drugs mimic vasodilation system

A
  1. Stimulate cGMP production vai gylceryl trinitrate. increase intracellular NO, increase cGMP and protein kinase G leading to relaxation
  2. Stimulate cAMP. agonist at Beta adrenoreceptor , isoprenaline
  3. Inhibit phosphodiesterase to elevate cAMP
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17
Q

What drug actions can bring about vasodilation

A
  • Block voltage gated calcium channels e.g amlodipine
  • Increased sensitivity of K+ channels, increasing hyperpolarisation. inhibits calcium channel and causes relaxation. e.g pinacidil
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18
Q

what is the definition of a side effect

A

An unwanted action that a drug produces at therapeutic dose

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19
Q

Whats and adverse drug reaction and the different types

A

Used to describe unwanted that occurs at therapeutic dose

  • Type A - Expected but exagerrated
  • Type B - Abnormal response not related to does (allergy)
  • Type C - After prolonged use
  • Type D - Occur at remote time to treatment
  • Type E - occurs when treatment halted abruptly
  • Type F - Occurs when expected response not seen
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20
Q

What is hydropic degeneration of a cell

A

Cellular swelling caused by hypoxia. Low 02 leads to reduction in ATP, Na moves into cell causing ER to rupture and vacuolise. Commonly occurs in metabolicly active cells e.g hepatocytes or renal. Seen in some viral infections e.g foot and mouth and causes blisters.

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21
Q

What is fatty change and what is it caused by

A

Accumulation of fatty substances in cytoplasm of cells that arent supposed to be fat stores. Causes include

  • Starvation or overeating
  • Lack of lipotropes ( aid in the removal of fat)
  • Anaemia
  • hypoxia and ishaemia
  • Ketosis & diabetes melitus
  • Bacterial/fungal
  • Chemical toxin
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22
Q

What is mucoid degeneration

A

Degeneration of connective tissue. E.g valvular endocardiosis

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23
Q

Explain what is ment by Pyknosis, Karyorrhexis and Karyolysis

A
  • Pyknosis - Appearance of Very dense, heavily stained chromatin
  • Karyorrhexis - Nucleus has broken up into several dense pieces
  • karyolysis - Dissolution of the nucleus
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24
Q

What is necrosis and what are its 3 causes

A

Necrosis - Substantial death of a number of cells within the living body

  1. Loss of blood supply - can be due to hypoxia, ischaemia or infarction. Compression of blood vessel leads to organ swelling and cessation of venous outflow and arterial blood flow. ishaemic necrosis occurs.
  2. Non living agents - can be physcal. e.g a burdizzo castration gone wrong. Suppose to crush spermatic cord and testicular blood vessels leaving scrotal vessels intact. If all crushed undergo necrosis. can also be chemical e.g oak poisining
  3. Living agent - e.g Black disease caused by clostridium novyi type B
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25
Q

How does necrosis present histologically

A
  • Where agent has maximal effect theres a sphere of necrosis.
  • Next to this is a area where the tissue is damaged but not yet dead, zone of degeneration
  • Next to this is a dark zone where the body is reacting to the dead tissue, inflammatory zone
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26
Q

What are the 3 types of necrosis

A
  1. Coagulstive - Firm and drier appearance. Cell architecture preserved but cells appear larger. caused by bacteria (clostridium) virus (herpesvirus).
  2. Liquefactive - tissue transformed into liquid mass. 2 types. Malacia - Affects the CNS. e.g Thiamine deficiency causing cerebrocortical necrosis. Abscess - Pus producing organisms. Cause necrosis and attract neutrophils which they also kill. These release proteolytic enzymes, which digest necrotic tissue, & kill tissue cells
  3. Caseous necrosis - Cheese like necrosis. mixture of coagulative and liquefactive necrosis. Large proportion of necrotic tissue is macrophages. caused by specific organisms e.h mycobacterium which invade macrohphages.
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27
Q

What is the consequence to necrosis

A
  • If basement membrane intact then erosion
  • If basement membrance breached, and host immune system reacts causing ulceration
  • Internal necros causes the formation of fibrous tissue
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28
Q

What is fat necrosis and gangrene

A

Fat necrosis

  • Adipocytes broken down to fatty acids to form soaps.
  • Caused by release of pancreatic enzymes, damaging mesenteric fats by trauma or Vit E deficiency

Gangrene

  • Wet - Degredation of dead tissue. Life threatening. New or excisting bacteria putrefy dead tissue
  • Dry- Air moving over the extremeties removes all the fluid content, mumyfying it
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29
Q

Describe how an definitive haemostasis plug is formed & what are the control mechanisms

A
  • Vessel is severed exposing collagen in the subendothelin
  • Adhesion of platelets requires van wilebrand factor. platelets activate and undergo conformational changes
  • Platelets release granules containing ADP & thrombaxane A2
  • Thrombaxane A2 causes expression of GPIIb, allows adhesion of platelets.
  • Thrombin activated and causes the conversion of fibrinogen into fibrin, acts as a mesh and forms definitive haemostatic plug

  • Antithrombin III is a endogenous inactivator of coagulation factors*
  • Endothilin secretes NO (increase cGMP) and prostacyclin (increase cAMP) to stop the formation of thrombi*
  • Also platelet activation & adhesion blocked by raising cAMP or cGMP levels*
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30
Q

What are the injectible anti coagulant drugs

A
  • Heparin - Bins to Antithrombin III & thrombin. Has a short half life
  • Heparin like low molecular molecules - Enhance inhibitory action of antithrombin III but does not bind to thrombin, meaning theres less Anti platelet activity. Longer half life than heparin
  • Hirudin - Binds directly to thrombin and inhibits
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31
Q

What is the oral anticoagulant commonly used

A

Warfarin - Structurally similiar to Vitamin K. Prevents reduction of Vitamin K needed as a co factor for the clotting cascade.

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32
Q

what protein aids in the breakdown of clots

A
  • Tissue plasminogen activator (tPA) - Acts specifically on plasminogen inside the thrombus. Plasminogen => Plasmin. Plasmin dissolves fibrin into fibrinogen.
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33
Q

what is melanin and what can go wrong pathologically

A

Melanocytes in epidermis produce melanin, a endogenous brown pigment that protects against UV damage

  • Hyperpigmentation - Due to increased number of melanocytes or increased production (can be caused by hyperadrenocorticism).
  • Hypopigmentation - Can be congenital or aquired (Cu deficiency). Damage to basement membrane can cause melanin to leak into dermis.
  • Melanoma - Tumour of melanocytes, common in grey horses
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34
Q

What is bilirubin and what are the causes of jaundice

A

Bilirubin is a yellow pigment found in macrophages at the site of macrophage breakdown

  1. Pre-hepatic jaundice - Excessive production of bilirubin due to haemolysis. Increase in unconjugated bilirubin in blood caused by large haemorrhage or infection e.g babesiosis
  2. Hepatic jaundice - Hepatocyte damage meaning a decrease in conjugation => increased unconjugated bilirubin in blood. Caused by liver damage due to toxins/chemicals or a hepatocellular tumour
  3. post hepatic jaundice - Obstruction of bile excretion. Causes an increased amount of conjugated bilirubin in the blood & is caused by tumours, inflammation or gall stones
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35
Q

What are the two types of calcification

A
  • Dystrophic calcification - Local depostition in necrotic tissue. No regulation of cellular Ca+2 metabolism leads to increase in blood Ca. irreversible change
  • Metastic calcification - Depostion of Calcium in normal tissue. Disturbed Ca+2 metabolism leads to increase in blood. Can be caused by increased PTH, Chronic renal failure.
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36
Q

What are the 3 mechanisms of oedema

A
  1. increased Intravascular hydrostatic pressure - increased blood volume in microvasculature. RHS heart failure can lead to Ascitis ( oedema of peritoneum) & LHS heart failure causes pulmonary oedema
  2. Decreased osmotic pressure - decrease in plasma proteins (albumin) causes a decrease in absorption at venous end of capillary beds and builds up in the intersitium. Caused by severe liver disease (cirrhosis) causing a decrease in production or malnutrition/malabsorption. Also protein losin enteropathy (haemorrhage associated with parasites)
  3. Increase in capillary permeability - Infamation causes vasodilation. increase permeability => increasin in protein escaping into intersitium raising osmotic pressure and causing oedema.
  4. Decrease in lymphatic drainage - caused by
  • lymph vessel constriction
  • internal blockage
  • lymphitis
  • surgical removal of LN
  • Congenital malformation (aplasia/hypoplasia)
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37
Q

What are the 2 type of haemorrhage and what are the consequences

A
  1. Rhexis - Usually a big hole in the blood vessel. Can be inherited or aquired by vascular erosion by microorganisms, Inflammatory reaction of abscess
  2. Diapedesis - Various small holes. can be caused by:
  • Endothelial injury due to endotoxins
  • Decrease in platelet numbers or function
  • decrease in coagulation factors
  • Vit k deficiency

Consequences - >20% loss = hypovaleamia. Decrease in tissue perfusion & haemorrhagic shock.

Intracranial haemorrhage will cause increased intracranial pressure, comprimising blood supply & possibly causing hernation of brain stem through foramen magnum.

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38
Q

What is hyperaemia and congestion

A
  • Hyperaemia - Active process that increases arterial dilation and blood flow ( inflammatory )
  • Congestion - Passive process that decreases outflow of blood. can be local (obstruction of flow e.g torsion) or general ( decrease passage of blood through heart/lungs. RHS heart failure causes hepatic congestion (nutmeg liver) and LHS pulmonary congestion
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39
Q

What is infarction and what causes it

A

Area of peracute ischemia that undergoes coagulative necrosis of tissu, often leading to a wedge shaped areas of necrosis.

Causes

  • Thromboembolic arterial occlusion
  • Vasospasm
  • Exetrinsic compression of vessel
  • Torsion or traumatic rupture
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40
Q

What is disseminated intravascular coagulation

A

DIC - Widespread activation of clotting factors can cause many thrombi in microvasculature

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41
Q

What is hypercoagulability and give an example of how its caused

A

over production of thrombi, blocking vessels. caused by an increase in coagulation factors or decrease in coagulation inhibitors. Glomeruli amyloidosis causes a loss of protein in urine, one being antithrombin III

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42
Q

What are the differences between arteial, cardiac and venous thrombi

A
  • Arterial - Occur at site of endothelial damage with increased turbulance. Dull, pale red apearance due to reduced time for RBC to encorporate into thrombate. grow downstream
  • Cardiac - Caused by arrythmias and dilated cardiomyopathy. Damaged heart valves can be targeted by bacteria
  • vonous - Sites of stasis. Slow blod flow allows RBC’s to incorporate.
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43
Q

what is shock and what are its 3 stages

A

Characterised by systemic hypertension. Impaired tissue perfusion and cellular hypoxia

  1. Non-progressive - Decrease in BP detected by baroreceptors causes Adr release. increase in CO & arterial vasoconstriction, also increase in RAAS. causes tachycardua, peripheral vasoconstriction and renal retention of water
  2. Progressive - Widespread hypoxia causing anaerobic respiration and lactic acid formation. Leads to metabolic acidosis and arterioles dilate and blood pools in microcirculation. decreases CO and risk of DIC.
  3. Irreversible - Energy stores depleted and impairs membrane transport. Lysosomal release and cell integrity lost leading to necrosis. Organs begin to fail and ishemic bowls can cause intestinal flora to leak into circulation.
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44
Q

What are the 3 types of shock

A
  1. Cardiogenic - Failure of the heart to pump blood adequately. Caused by intrinsice mycardial damage, ventricular arrythmias, extrinsic compression and outflow tract obstruction
  2. Hypovalaemic - Decrease blood volume. Haemorrhage or fluid loss e.g vomitting. blood loss of >35% means CO & BP decrease, also adequate tissue perfusion cant be maintained
  3. Blood maldistribution - Peripheral vascular resistance decrease. Due to neural/cytokine induced vasodilation. Normal blood volume but decreased effective circulating BV.
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45
Q

What are the types of Blood maldistribution shock

A
  1. Septic - Overwhelming bacterial infection which comprimises the mucosal integrity, allowing bacteria toxins into blood. Bacterial endotoxins induce systemic release of excessive amount of vascular and inflammatory mediators. Results in DIC, peripheral blood poolin & leukocyte induced damage.
  2. Anaphylactic - Exposure to insect or plant antigen. Interaction with igE and mast cell causing widespread degranulation. systemic vasodilation = hypofusion/tension
  3. Neurological
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46
Q

Why can treating rabbits with penicillin potentially be fatal

A

Penicillin can potentially kill commensual organisms, leading to super infection of clostridial bacterial leading to fatal enterotoxaemia

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47
Q

What are gamma delta t cells

A

T cells that are important in ruminants and pigs. They recognise stress proteins not MHC. These cells induce apoptosis

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48
Q

How does MALT work in the GIT

A
  • Peyers patches recognise antigen
  • They are lined with Mcells which sample luminal contents, presenting them to the DC’s and lymphocytes on their basolateral side
  • Plasma cells are stimulated by Th2 to produce IgA or IgE
  • IgA secreted in submucosa & transported across mucosal epithelium and into lumen. Uses polymeric immunoglobin receptors to do this (plgR)
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49
Q

Explain the term mucosal tolerance

A
  • Exposure to ANY antigen stimulates an immune response
  • If antigen doesnt stimulate inflammatory response, Tregs secret IL-10, which down regulate immune system… mucosal tolerance
  • Harmful antigen will cause inflammatory response via recognition of PAMP via TLR. inflammatory cytokines inhibit Tregs.
  • Occasionally IgE responds to food antigen. known as dietary hypersensitivity. mass dedgranulation of mast cells
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50
Q

Describe Maternal transfer of Ig’s

A
  • Migration of Bcells to mammary glands
  • Small amount of Ig transfer via placenta in dogs/cats but no ruminants.
  • IgG from colostrum absorbed by FcRn receptors in intestinal epithelia. but these receptors last 24 hours
  • Provides systemic IgG for 8-12 weeks.

Failure of passive transfer can be due to poor colostrum quality (early birth or nutritional defiecieny) or indequate intake or absoprtion

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51
Q

What is neonatal isoerythrolysis

A
  • Mare can make antibodies that are reactive to RBC’s of the foal.
  • doesnt usually occur on first foal because mare hasnt been expose to ‘foreign’ antibodies as of yet so hasnt developed the antibodies (unless mare has had a blood transfusion)
  • Exposure to foals RBC’s can occur at birth.
  • Causes anaemia and jaundice
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52
Q

Describe the differences in the avian respiratory system

A
  • Have small lungs and 9 air sacs
  • Trachea is 2.7x longer and 1.29x wider = 4.5x increase in tracheal deadspace. this is compensated by larger tidal volumes & lower respiratory rate (ore time for gaseous exchange)
  • Trachea => Mesobronchi => Ventrobronchi => Parabronchi => dorsobronchi => mesobronchi
  • Parabronchi has hundres of tiny anastomising air capillaries surrounded by blood capillaries
  • During expiration air moves out of air sacs (specically abdominal) and pass through parabronchi, undergoing gaseous exchange… meaning gaseous exchange occurs during inspiration and expiration
  • Air and blood travel at 90 degress of eachother creating efficient C02/02 gradients along parabronchi
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53
Q

What drugs are used for respiratory depression

A
  • Etamiphylinne camsylate - acts on central chemoreceptors, chaging sensitivity to C02
  • Doxapram - acts on central/peripheral cheorecptors (carotid body), increase tidal volume and respiratory rate

Used for apnoeic newborns or to reverse respiratory depression from overdose

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54
Q

What drugs are used to treat cough

A

Antitussives are used for the comfort of the animal. Cough recpetors in medulla express opoid receptors that have a negative effect. therefore opoid receptor agonists used. Codein and butorphanol

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55
Q

How do you treat an accumulation of mucus

A
  • Mucolytics - Bromohexine - alters viscosity
  • Nasal decongestants - Pseudoephedrine - can release endogenous noradrenaline from presynaptic terminals. Act on adrenoreceptors to increase calcium and cause constriction. decreasing blood flow to secretory glands
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56
Q

What are the various drugs that can cause bronchodilation

A
  • Muscarinic receptor agonist - atropine. Inhibits vagal input, inhibiting vasoconstriction. also inhibits mucociliary clearance/GIT function.
    Ipratropium - Adverse effects reduced becuase it is inhaled
  • B2 agonist (selective) - Clenbuterol. decrease in Calcium causes relaxation. improves ciliary clearance. but can cause tachycardia, hypotension and hypokalemia. Can be inhaled
  • Methylxanithines - Theophyllin - inhib phosphodiesterase => increase camp and decrease calcium. antiinflammatory properties. can cause vomitting (gastric intolerance) tachycardia and restlessness.
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57
Q

What factors must be considered when making a vaccine

A

Variability of pathogen

  • Strains/serotype that need to be in vaccine
  • What antigens stimulate response
  • Does pathogen demonstrate immune evasion strategies

Variability of host

  • Antibody enough or do u need cell mediated immunity?
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58
Q

What are ideal traits for a vaccine

A
  • Cheap production
  • Consistent production
  • Long shelf life
  • Easy to administer
  • No adverse effects
  • Long lasting immunity with single dose
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59
Q

What are the two types of passive immunisation

A
  • Maternally derived antibodies - Rotavec vaccines which cover rotavirus, coronavirus and E.coli K99. Administered to pregnant cow 3-12 weeks pre-partum. stimulate antibodys in colostrum
  • Anti-serum - Tetanus antitoxin purified from the blood of horses which are hyperimmunised with tetanos toxoid. provides immediated protection.
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60
Q

What are the 5 types of active vaccinations

A
  1. Toxoid - Some bacteria (clostridial spp) produce endotoxins. Toxin is inactivated but antigenic structure remains to stimulate immune response
  2. Inactivated - Pathogen chemically treated to kill it, contains adjuvant & requires 2 doses 2-4 weeks apart
  3. Attenuated - Grow virus under abnormal conditions ( e.g 37 degress instead of 35). Drives natural selection towards lower virulence. (e.g grown in snow leoprad kidney until strain evolves). Non adjuvinated & only 1 dose required
  4. Recombinant - Genes encoding antigen cloned into viral vector (canarypox)
  5. DNA vaccine - Antigen genes closed & inserted into vector & recombinant plasmid DNA. recombinant protein stimulates immune response
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61
Q

What is an adjuvant

A

Chemicals added to vaccines to boost immunogenecity. Increase Ig levels and influence specific Ig isotope formation & th1 or th2 balance

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62
Q

What is DIVA

A

(Differentiating Infected from Vaccinated Animals)

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63
Q

Why are first vaccines administered at 8-12 weeks

A

Immune system isnt fully developed until 6 weeks of age. MDA’s can interfere with any vaccines up until 12 weeks of age.

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64
Q

what affects do vaccines for viruses, bacteria and parasites have

A
  • Virus - Designed to stimulate neutralising antibodys. therefore surface antigens very important
  • Bacteria - Stimulate antibody for opsinisation, compliment & neutralisation. sometimes cell mediated immunity required, can be achieved by addition of adjuvant (leishmania)
  • Parasite - Irradicate the L3 stage
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65
Q

What vaccine is given to rabbits

A

Myxomatosis - 0.1ml intra dermally injected, rest of the does given sub cutaneous. This produces better cell mediated immunity

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66
Q

What are the possible reasons for vaccines failing

A
  • Vaccine doesnt contain appropriate antigens for serotype/strain
  • Vaccine expire or not stored properly
  • Not administered correctly
  • Animal too young or old
  • MDA’s
  • Immunosupressed
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67
Q

What is pka

A

Dissociation constant for an acid. high value = strong acid.

PH = Pka + log([A-][HA])

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68
Q

What is a buffer, and descirbe the extracellular and intracellular buffer

A

A buffer is a solution of weak acid and its conjugate salt. Accept H+ to minimise changes in PH

Intracellular : H2O + CO2 <=> H2CO3 <=> H+ +HCO3-

open system because H2CO3 can never run out

Extracellular: Haemoglobin

  • CO2 from metabolism diffuses into RBC
  • Carbonic anhydrase in RBC allows formation of H2CO3, which dissociates in HCO3- and H+
  • HCO3- secreted into plasma and CL- replaces it (chloride shift). this acts as a buffer for CO2
  • H+ reacts with HbO2 froming HbH & releasing 02
  • RBC’s reach lungs where 02 tension is high, so favours backwards reaction re forming HbO2 and releasing H+. thus CO2 and H+ removed in lungs.
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69
Q

Describe respiratory regulation of PH

A
  • PH decrease
  • Respiration stimulated
  • PCO2 decreases
  • H2CO3 decrease
  • Increase PH
  • Respiration depressed
  • PCO2 increase
  • H2CO3 increase
  • PH decrease

continous cycle trying to keep ph within limits.

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70
Q

What are the 3 mechanism for controlling ph by the kidneys

A
  1. Re-absorption of HCO3- - CO2 from blood moves into tubular cell froming H2CO3 => HCO3-. H+ passes into the lumen in exchange for Na+. the HCO3- moves into the blood.
  2. Excreting acid urine - H+ moves into the lumen in exchange for Na+. H+ combines with HPO4-2 => H2PO4- which is excreted.
  3. Excretion of NH3 - NH3 produced from metabolism in tubular cell & diffuses into lumen to form NH<strong>4</strong>+. can not pass back into cell as its charged and is excreted. important in prolonged periods of acidosis.
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71
Q

Describe respiratory acidosis

A
  • Decreased PH and increased CO2
  • Caused by hypoventilation, no elimination of CO2
  • HCO<strong>3</strong>- normal in acute conditions and positive in chronic
  • Caused by Airway obstruction, depression of respiratory centre, neuroloical disease and any disease prevent lung expansion
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72
Q

Describe respiratory alkalosis

A
  • Increase in PH & decrease in CO2
  • Due to hyperventilation
  • HCO3 negative in chronic conditions
  • Caused by Fear/anxiety, PAin, Hyperthermia, Corticosteroids, Decrease in arterial 02 ( causing anemia/hypofusion/hypoxaemia)
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73
Q

Describe metabolic acidosis

A
  • Decrease in PH and decrease in HCO3-
  • PCO2 decreased in chronic conditions
  • Causes include increased acid ( lactate, diabetic ketacidosis, uraemic acids) or lose of base (diarrhoea)
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74
Q

Describe metabolic alkalosis

A
  • Increased PH and increased HCO3-
  • Increased PCO2 in chronic conditions
  • Causes include decrease in acid (vomitting or increased renal loss) And addition of base (sodium carbonate)
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75
Q

What are the 3 stages of inflammation

A
  • Initial - First arteriole constriction which last seconds. Followed by hyperaemia for minute/days. Capillaries Dilate due to chemical mediators. Opening of pre-capillary sphincters, large engorgement of blood.
  • Exudative - Increase vascular permeability due to endothelial contraction. Contraction caused by histamine released from mast cells. Opening of tight junctions due to contraction. Allows escape of exudate
  • Migration of leukocytes - margination of neutrophils allowed by slowing blood flow. roll along the endothelium towards site of damage. this is allowed by the expression of selectins which bind to glycoproteins on the surface of the leukocytes. Undergo changes in morphology as they under go emigration through the leaky blood vessels. Move along chemotactic gradient (chemotaxis) produced by chemokines (IL-8) & C5a.
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76
Q

What are the cells of acute inflammation

A
  • Neutrophils - 6 hour half life & replaced twice daily, most are lost through mucous membranes. Release granules into exudate that enhance inflammatory response.
  • Eosinophil - Large numbers in parasitic infection. cause greenish gross appearance
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77
Q

during inflammation what causes pyrexia

A
  • Pyrogens act on control centres in the hypothalamus of the brain to increase body temperature
  • Released from neutrophils ( phagocytosis), Gram - bacteria (when broken down), Damaged tissue cells & tumour cells, especially when they mastasised
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78
Q

What is the role of inflammatory effusion

A
  • Dilutes toxic agent
  • Contain IgG which acts as a opsin
  • Can contain fibrin which immobilises irritant
  • Wash away irrittant and bring them to LN
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79
Q

What are the fluid types that allow us to identify the different types of inflammation

A
  • Serous - mild vascular injury. Vesicles on skin. resolves when irritant is overcome
  • Catarrhal - occurs on goblet cells and mucous glands. Can be watery or gelatinous
  • Fibrinous - Severe endothelial injury, escape of fibrinigoen. Common on serous surfaces. Will peel away from underlying tissue
  • Diphtheritic - Severe fibrinous exudate. Considerable necrosis of underlying tissue. Attempts to remove will tear tissue. Internal surface of fungal infection. common in nose and gutural pouch
  • Haemorrhagic - Severe acute/peracute inflammation whe haemorrhage is main compoent. If widespread, associate with death but if localised = bruise
  • Purulent - Pus due to dead neutrophils releasing proteolytic enzymes. Can be detrimental if ruptures in body cavity. End result is fibrous scar
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80
Q

What are the cells of chronic inflammation

A
  • Lymphocytes
  • Plasma cells - Deposited at damaged tissue
  • Macrophages - derived from circulatory monocytes. phagocytose, present antigen and stimulate fibroplasia & fibrosis
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81
Q

What is granulamatous inflammation

A

Caused by organisms of low virulence and great persistance.

histology - Central core of irritant surrounded by chronic inflammatory cells encapsulated in a fibrous capsule

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82
Q

What is granulation tissue and what occurs when theres an excess

A

Granulation tissue froms at the site of skin injury. Formation of connective tissue and new microscopic blood vessels. When skin doesnt grow over and granulation tissue continue to grow forms proud flesh.

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83
Q

What affects the ability of an animal to heal ?

A
  • Ability of species to cope - E.g Ox’s can wall off peritonitis whereas in horse can be fatal
  • Age - Old animal has less scope of healing ability, also very young animals have immature immune system
  • Nature of damage - highly specialised tissue (e.g neurones) wont heal
  • Amount of tissue damaged - If its still functional
  • Subsequent fibrosis - Progressive destruction of tissue causes furthur injury to adjacent normal tissue (e.g liver cirrhosis)
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84
Q

What is the difference between repair and regenration

A
  • Repair - Replacement of damaged tissue by fibrous scar tissue, does not retain function
  • Regeneration - Replacing damaged tissue with normal tissue of the same type. Functional status is repaired
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85
Q

What are the 3 categories of regeneration

A
  1. Liable - Constantly replineshses tissue in life E.g skin & bone marrow
  2. Stable - Limited ability to replace E.g Renal tubules and liver
  3. Perminant - Poor or no regenration. Highly specialised cells e.g Cardiac or neurones
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86
Q

What are the 4 stages of skin healing

A
  1. Haemostasis - Blood escapes damaged vessels. Fibrin clot formed
  2. Inflammation - develops within 24 hours. Adds exudate. Macrophages release enzymes digesting scab and promoting repair
  3. Epithelial regeneration - Within 48 hours. small amount of granulation tissue. blood vessels grow
  4. Consolidation - Final scar is small. Sutures can be removed 7-10d
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87
Q

What causes joint inflammation

A

In livestock mostly caused by infectous agents that entered circulation via naval. in small animals usually immune mediated. Infection can also come from adjacent tissue, deep lacerations or poor aseptic techniques

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88
Q

What are the 3 routes of entry for lung inflammation

A

Pneumonia

  • Airborne agent - Bronchopheumonia (mannheimia haemolytica), infectous droplets cranio ventral portion of lungs. Forms large lymphoid follicles that obstruc airways
  • Haematogenous - Interstital pneumonia. Distribution throughout lung, viral (viral infection e.g canine distemper) thickens alveolar wall
  • Traumatic implantation - Rare, tends to cause pleural inflammation
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89
Q

What causes inflammation of alimentary tract & what are the consequences

A

Usually inflammation of mucous membranes (Catarrhal), can cause damage to villi. Resulting in Malabsorption & progressive loss of fluid with protein. (granulomatous enteritis - Johnes disease)

90
Q

What is the cause of pancreatic inflammation and the outcome

A

Acute pancreatic necrosis is the main cause in dogs. Release of pancreatic enzymes into surrounding fatty tissues. Can cause death soon after painful episode or continue normally asymptomatically until little pancreatic tissue remains. Can lead to diabetes mellitus

91
Q

When does metritis commonly occur

A
  • At service (livestock), often mild
  • At parturition & is usually life threatenting
92
Q

What is ‘left shift’

A

In episodes of severe acute inflammation, Neutrophil need be so excessive that immature forms are released from bone marrow

93
Q

What are the 3 types of systemic allergy

A
  • Urticaria (hives) - characterised by red itchy skin rash
  • Angioedema - Severe swelling of tissues, especially eyelids & lips
  • Anaphylaxis - Widespread mast cell degranulation, life threatening because Histamine causes vasodilation, Cause hypotension & reduced blood flow to the brain
94
Q

What are examples of allergic respiratory diseases and what are the clinical signs and treatment

A

e.g’s Feline asthma & canine allergic bronchitis.

Clinical signs - Coughing, weezing & excercise intolerance

Mast cells cause bronchospasms & systemic eosinophilia may been seen

Corticosteroid & allergen avoidance are treament options

95
Q

Whats an example of a immune mediated gastrointestinal disease

A

Irritabal bowl disease (IBD) - classified by type of cellular infulatrate. Loss of mucosal tolerance and inappropriate immune reactivity to dietary or enteric microbes. Cause :

  • Increased intestinal permeability to antigen
  • IgA deficieny
  • Innapropriate IgE response
  • Defective Tregs

Treatment includes antibiotics to reduce the bacterial load, hypoallergenic diet & corticosteroid or ciclosporin

96
Q

What is autoimmunity and what are the possible causes

A

Innapropriate immune response to self antigen

Factors:

  • Genetic - predominately MHC genes
  • Hormonal
  • Environmental - diet, stress, infection
97
Q

What is type I hypersensitivity

A

The production of IgE instead of IgM or IgE in response to an allergen. IgE becomes sensitised and subsequent reexposure leads to degranulation of mast cells, causing vasodilation, oedema, smooth muscle contraction and increased mucous secretions.

98
Q

What is type II hypersensitivty

A

IgG or IgM response to fixed self antigen. one form is immune mediated haemolytic anaemia. Rbc’s are brocken down causing jaundice, pale mucous membranes, tachycardia. Can be diagnosed by positive saline augoagglutination

99
Q

What is type III hypersensitivity

A

Caused by accumulation of Antibody-antigen complexes. gives rise to inflammatory response that causes destruction of blood vessels - Vasculitis. E.gs include Feline infectous peritonites or Glomerulonephritis.

100
Q

What is type IV hypersensitivity (delayed onset)

keauno has shit banter lol

A

Mediated by CD4 th1 cells and CD8 cells. Reactive CD4 th1 cells release interferon gamma which activates macrophages to secrete pro-inflammatory mediators. CD8 cells kill healthy cells. Can be due to Hypothyroidism, Hypoadrenocorticism, exocrine pancreatic insufficiency

101
Q

What is secondary immune deficiency

A

An aquired form of immune deficiency

  • Retrovirus induced immunosuppression - FeLV
  • Toxin induced immunosuppresion - poisons
  • Malnutrition, stress, chronic disease - drugs
102
Q

What is tolerance and what are the two mechanism of T-cell tolerance

A

Tolerance - Deliberate state of unresponsivness to antigen by the immune system

  • Central - Clonal deletion of self reactive T-cells in Thymus (negative selection)
  • Peripheral -
  1. Active suppression - T regulatory (Tregs) cells function to strategically supress the immune system
  2. Clonal anergy - T cells unresponsive in absense of danger signals (inflammatory response)
103
Q

What is the main prostaglandins involved in inflammation and what are their roles

A

PGE2

  • Gastric cytoprotection
  • vasodilation of renal blood flow

PGI2

  • Gastric cytoprotection
  • vasodilation of renal blood flow
  • Prevents platlet aggregation and is a vasodilator
104
Q

Explain the mechanism of action of Non steroidal anti inflammatory drugs (NSAID’s) & what are the clinical uses of them and what are the side effects

A

the majority of NSAID’s act as Non selective COX inhibitors. COX-1 is involved in normal physiological processes producing prostaglandins. whereas COX-2 is induced by bacterial toxins and cytokines. Thus inhibits the inflammatory mediators (PGE2).

Clinical uses:

  • Control pain in acute and chronic inflammatory conditions
  • Decrease swelling
  • Reduce fever

Side effects:

  • Damage to GIT (increase acid & decrease bicarbonate)
  • Nephrotoxicity when dehydrated (suppression of protective afferent artery vasodilation)
  • Hepatotoxicity
105
Q

What are glucocorticosteroids and what is their mechinsm of action

A

Glucocorticosteroids are anti inflammatory drugs that inhibit the formation & action of pro-inflammatory mediators but also induce the formation of anti-inflammatory mediators (mimicing cortisol)

Mechanism:

  • Decrease in inflammatory mediators, inhibiting the induction of COX-2
  • Induce lipocortin, reducing lipid mediators
  • Decrease in stored mediator release
  • Decrease in inflammatory cell production in BM
  • Decrease in circulating compliment components
106
Q

What are the clinical uses of glucocorticosteroids, what are the side effects & contra indications and the duration of effects

A

Clinical uses:

  • Allergic disease ( anaphlaxis )
  • Inflammatory conditions of skin/eye
  • Immunosuppression with prolonged use (making it useful for autoimmune/chronic inflammatory conditions)
  • Induce parturition of cattle/sheep

Contra indications:

  • Renal disease
  • Diabetes mellitus

Side effects:

  • Suppression of wound healing
  • inhibition of osteoblasts & increased osteoclast activity
  • Induction of iatrogenic cushing syndrome
  • Can cause adrenal atrophy due to endogenous cortisol
  • Rapid withdrawel can cause addisonian crisis ( acute sudden death due to decrease in cortisol)
107
Q

Why does chronic inflammation occur?

A
  • Inflammatory stimuli not effectiively removed
  • Stiumulus overwhelms system
  • Stimulus by passes immune response (parasite)
  • Lack of effective resolution & repair
  • Immunosuppressed
108
Q

Explain the difference between first and second generation H1 receptor antagonists

A

first generation H1 antagonist had side effects such as antipruritic, antiemetic, anti nausua and sedative. Second generation drugs do not cross the blood brain barrier to access the H1 receptors in the CNS. Meaning these side effects are negated.

109
Q

Define the term malformations, Congenital defects and heridatory defects

A

Malformations - Disorders of growth which occurs during gestitation

Congenital defect - Disorder of growth detected at birth

Hereditary defects - Genetically transmitted disease

110
Q

What are the main cause of defects and What are some various types of defects

A
  1. Chromosome - results in early abortion/resorption
  2. Viral disease - Can cross placenta E.g bovine virus diarrhoea can cause cerebellor hyperplasia
  3. Toxins - ‘Corn lilly’ can produce cyclopia when ingested in 12-14 days into pregnancy
  4. Drugs - Griseofulvin (ring worm treatment) given to pregnant queen results in kittens with cleft palate (aspiration pneumonia)
  5. Ionising radiation
  6. Nutritional deficiency - Copper deficiency in pregnant ewe = Degredation of white matter. Can be ‘sway back’ which is seen at birth or Enzootic atoxia which is a delayed onset of upto 6 months
  7. Physical factors - umbilical cord can wrap around limbs causing amputations
  8. Anoxia - can be caused by aneamic mother

Various types of defects include :

  • Cyclops
  • Bulldog calg in dextor calfs
  • Cleft palate (failure of palatine bones to close)
  • Cystic kidneys
  • Cardiac defects
111
Q

What is atrophy and what are its causes

A

Decrease in size of cells & organ After organ has reached it normal size. Occurs in normal physiology with the thymus and uterus post partum

Cause:

  • Decrease in blood supply
  • Compression
  • Work load
  • Denervation ( temporal muscle in cats when trigeminal damaged
112
Q

What is hypertrophy and what are the 4 different types

A

Hypertrophy is an increase in size of individual cells

  1. Funtional hypertrophy - In response to increase in physiological need e.g heart diseases
  2. Compensatory hypertrophy - when one of a paired organ is impaired e.g kidney
  3. Obstructional hypertrophy - Hollow organs thicken around an obstruction e.g bladder/intestines
  4. Hormone mediated hypertrophy - Induced by anabolic steroid. Thyroid hormone has general hypertrophic effect on cells. E.g hyperthyroidism cause cardiac hypertrophy
113
Q

What is hypoplasia

A

Reduction in size of cells due to failure to grow to normal size

E.g pituitary dwarfism

114
Q

What is aplasia

A

Failure of an organ or tissue to develop

115
Q

What is hyperplasia and what is it caused by

A

Hyperplasia is an increase in size of an organ to due increased number of cells

Cause:

  • Hormonal E.g parathyroid hyperplasia in chronic renal failure.
  • In response to cell loss/damage. Regeneration
116
Q

What is metaplasia

A

Transformation of one type of tissue into another. occurs in connective tissue and epithelium.

E.g in prostate of dogs, Transitional epithelium to stratified squamous epithelium.

117
Q

What is dysplasia

A

Abnormal growth within tissue. Loss of normal arrangement

118
Q

What is epitheliogenesis imperfecta

A

A congenital discontinuinity of squamous epithelium. Autosomal recessive disorder in cattle.leaves animal prone to bacterial infection

119
Q

Describe papillomavirus properties and pathogenesis

A

Papillomavirus is a double stranded DNA virus which is NON enveloped.

Pathogenesis:

  • Entry via lesion in the epithelium
  • Infection of dividing basal cells of the skin
  • Expression of early proteins in basal epithelium causes proliferation
  • Virus particles only produced in upper layer of epithelium, where cells are differentiated
  • Transmission via exfoliated cells
120
Q

What are the different types of Papillomavirus

A

Bovine

  • 10 different strains
  • Clinically presents as skin tumour on head, neck & shoulders
  • Most frequent in calves and yearlings. spontaneously regress after 6 months
  • Viral protein E5 binds to receptor for platelet derived growth factor (PDGF), causing cell proliferation. Also stops communication with neighbouring cells. E5 downregulates MHC I, meaning it avoids immunosurveilance
  • Malignant tumours from BPV-4 requires co factor… Bracken fern contains mutagens

Canine

  • Presents as oral papillomatosis, benign tumours on lips, tongue, palate which spontaneously regress

Equine

  • Causes benign skin tumours
  • BPV-1/2 Can cause equine sarcoids. Frequently reoccur after surgical removal.
  • Commonly mistaken for ringworm or granulation tissue
121
Q

Describe the properties of Retrovirus and how it cause neoplasia

A

Retroviruses are enveloped RNA viruses. They posses Reverse transcriptase which transcribes RNA into DNA. This viral DNA is then incorporated into the host genome by Integrase.

Transforms the Cell in 3 different ways:

  1. Carry Oncogenes within viral genome. This can often lead to defects in the viral genome.
  2. Activate cellular pro-oncogenes Via insertional mutagenesis
  3. Inactivate Anti-oncogenes
122
Q

Describe the pathogenesis of Feline leukaemia virus (FeLV) and the possible outcomes

A

FeLV causes lymphomas and transmitted oronasally

Pathogenesis:

  • Initial viral replication in lymphocytes of tonsils = Primary viraemia which presents as pyrexia
  • Causes uncontrolled expression of MYC, causing uncontrolled cell proliferation
  • immunosuppression = secondary infection

Outcome

  • 20-30% - seroconvert without detectable viraemia
  • 30-40% - transient virameia, remain latently infected in BM, may reactivate if animal immunosuppressed
  • 30%- persistenly viraemic. Infects dividing stem cell of BM. Larger amounts released, infects epithelia in salivary glands and intestines. Animal becomes immunosuppressed, anaemic and has lymphoma.

FeLV detected by immunochromatography

123
Q

Define neoplasia

A

Uncontrolled purposeless cell proliferation.

Continous without cause & forms from single mutation

Rate of growth exceeds normal for the tissue

124
Q

Define the terms carcinoma, sarcoma, sarcoid and granuloma

A

Carcinoma - Malignancy of epithelial origin E.g squamous cell carcinoma

Sarcoma - Malignancy of mesenchymal origin. E.g Osteosarcoma

Sarcoid - Low grade fibrosarcoma, skin of horses & cats. viral involvement

Granuloma - NOT neoplastic. Chronic inflammatory reaction

125
Q

What are the two theories for tumour heterogeneity

A
  1. Clonal expansion - Genetic & epigenetic changes overtime. Traits with selective advantage outcompete others
  2. Cancer stem cell theory - States that cancer is driven by small number of cancer stem cells that can reporduce & sustain cancer.

Importance in treatment. Because treatments that shrink cancer cells will have no effect if the stem cell theory is correct because stemm cells stil proliferating

126
Q

what is a proto-oncogene & give examples of oncogenes

A

A normal gene that becomes an oncogene following mutation or over expression

  • RAS - involved in kidney signalling pathway, controlling transcription of genes
  • MYC - Transcription factor
127
Q

Describe the process of carcinogenesis

A
  1. Initiation - Introduction of irreversible genetic change by mutagenic initiator (e.g chemical carcinogens that damage DNA). Cells can remain morphologically quiescent for years. Have mutations which give growth advantage. e.g resistant to apoptosis.
  2. Promotion - initiated cells exposed to certain stimuli, driving proliferation. Begins to grow more rapidly and less controlled than normal cell. May lead to benign tumour, this is reversible step.
  3. Progression - Conversion of benign tumour into malignant & metastatic. This conversion is Irreversable. Increase in cell heterogeneity.
128
Q

Why does tumour incidence increase with age?

A
  • Accumulation of genetic changes over time
  • Immune function decreases
  • Lag between transformation & clinically detectable tumour
129
Q

How does hormones influence tumours

A
  • Spayed bitches reduce incidence of malignant tumours on mammary glands.
  • Castration of dogs causes regression of perianal tumours
130
Q

When does a tumour become vascularised and what makes it distinctive

A

Tumours larger than 2mm must become vascularised. Production of tumour angiogenesis factor causes host vessels to branch into tumour. Tumour vessels are tortous, irregular, leaky and less efficient. Density of vessels can be used for prognosis. Malignant tumours can also outgrow blood supply and cause necrosis.

131
Q

Name the differences between benign and malignant tumours

A
132
Q

Explain the metastatic cascade

A
  1. Cells must detatch and migrate from primary malignant tumour
  2. Adhere to vesel wall
  3. Invasion of vessel
  4. Transport of micrometastasis
  5. Evasion of host defences
  6. Exit vessel & migrate to form second tumour

Some tumors preferentially migrate. E.g Mammary gland tumours commonly metastasises to the lung

133
Q

What are the routes of metastisis

A
  • Local invasion
  • Intraorgan spread
  • Intra-vascular/lymphatic - A few tumour cells within blood vessel suggests intra-vascular metastatic potential
  • Serosal spread (pancreatic carcinoma)

Spread via lymphatics Easier as they have thinner walls & lower pressures

134
Q

What are the effects of the tumour on the host

A
  • Replaces functional tissue = malfunction
  • Can cause compression on tissues
  • Can grow into blood vessels causing haemorrhage or infarction
  • Cachexia - Weakness/wasting of the muscle due to systemic cytokines
  • Paraneoplastic effects - Innapropriate production of hormones. E.g parathyroid hormone related peptide released promotes osteoclasts, therefore resorption occurs causing release of Ca+2 = Hypercalcaemia. excess Calcium can be deposited e.g in alveoli, can also cause
  • . Another E.g is hypertrophic osteopathy. symmetrical lameness & extensive periosteal new bone in distal limb
135
Q

How do tumours evade immune response

A
  1. Failing to show antigenic molecules or mask them
  2. May express antigens of normal tissue
  3. Express immunosuppresives

Tumours have immune cells surrounding them sugesting that immunosurveilance detects them

136
Q

what is the initial test to distinguish between gram possitive cocci (Staphyloccus & Streptococcus)

A

Catalase test. Bacteria inoculated with hydrogen peroxide. Presence of catalase enzyme will produce bubbles.

Positive result = Staphylococcus

Negative result = Streptococcus

137
Q

What test distinguishes between pathogenic and non pathogenic Staphylococcus

A

Coagulase test. Bacteria suspended with saline & plasma. If coagulase present it causes conversion of pro-thrombin => thrombin which converts fibrinogen => fibrin. Can visibly see bacteria clumping from insoluble fibrin.

Pathogenic Staphylococcus include S.aureus, S.intermedius & S.hyicus

Negative result could be S.epidermis or S.xylosus. These are of low virulence and are oppertunistic. adhere to plastics.

138
Q

What are the 2 main pathogenecity factors of staphylococcus

A
  • Haemolysins - 2 types. 1) alpha - Produced by S.aureus & S.intermedia. Produces zone of B-Haemolysis on blood agar. causes necrosis. B)Beta toxin - A sphingomyeinase converting sphingomyelin into ceramide. Causes sensitisation of RBC’s to weaker haemolysins, Also damages cell membrane causing cell leakage.
  • TSST - 1: Toxin shock syndrome toxin is a superantigen. Cross links invariable region of MHC class II & T-cell receptors. Without antigen processing. Then reacts with variable region causing T-cell proliferation & over production of TNFalpha (cause cardiovascular shock)
    *
139
Q

What are the cell surface pathogenecity factors

A
  • Fibronectin binding protein - On surface of S.auereus, Allowing them to adhere & colonise on damaged tissues.
  • Protein A - Anti-opsin. binds to Fc receptor on IgG, leaving Fab region free to bind to antigen BUT can no longer bind to WBC via Fc. S.auereus
  • Capsule - Produced in vivo & inhibits phagocytosis, C3 cant stabilise on surface
140
Q

What are the properties of streptococcus, what are the 4 main groups and what are its pathogenecity factors.

A
  • Catalase negative
  • Aerotolerant
  • survival outside body is poor

4broad groups:

  1. Pyrogenic
  2. Viridians
  3. Lactic
  4. Faecal

Pathogenecity: Hyaluronic acid capsule - Anti phagocytic

M protein - Anti phagocytic

141
Q

Describe group A-G of streptococcus

A
  • Group A - S.pyogens. Infections of the tonsils, human throat infection & scarlet fever
  • Group B - S.agalactiae. is B-haemolytic & causes chronice bovine mastitis
  • Group C - 4 species
  1. S.equisimillis- arthritic joints in pigs aged 1-2 weeks
  2. S.zooepidemicus - Wound infections, abortion in cattle
  3. S.dysgalaticae - Acute bovine mastitis & joint ill
  4. S.Equi - Strangle in horse,stongly B-haemolytic
  • Group D - Faecal streptococci, opppertunistic, wounds, UTI, antimicrobial resistance
  • Group G -S.canis - Severe acute kennel cough
142
Q

What are Erysipelothric

A

Slender gram positive rods that are catalase negative.Non motile. Normaly inhabit lymphoid tissue of pig. has 23 serotypes. Causes diamond shaped skin lesions & poly arthritis

143
Q

What is listeria

A

Catalase postive, motile gram positive rod. Present in faeces, soil and silage. Growth at 4 to 45 degrees. Can cause septicaemia, abortion and CNS disease. Can survive in cells by producing listeriolysin which lyses phagosome. Cellmediated response required to eradicate.

144
Q

What are Aracanobacterium

A

Catalase negative,non motile gram positive rods that are surrounder by B-haemolysin. A.pyogens commonly inhabit upper respiratory tract & causes liver abscesses and summer mastitis. produces several extracellular toxins such as haemolysin, proteases and neuraminidase

145
Q

What is actinomyces

A

Filamentous & branching gram positive rods that are catalase positive. Part of normal mouth baterium but are inoculated upon trauma

146
Q

What is A.Viscosus

A

Cause thorasic lesions in canine & A.bovis causes lumpy jaw

147
Q

What is Nocardia

A

Gram positive, aerobic ,partially acid fast. Branching rods containing mycolic acid. Making them resistant to a number of antimicrobials, making them harder to treat. Cause granulamatous lesions & survive in macrophages

148
Q

Describe mycobacterium and its pathogenesis in tuberculosis

A

Strict aerobes that are slow growing. Repell aquoes stains becuase of mycolic acid therefore must use zeihl neelsen stain. this is where smear heated & decolourise with 3% HCL in ethanol, giving a red stain.

Pathogenecity - Inhalation/ingestion. Uptake into macrophages. Migration to LN where they form granulomas. Type IV hypersensitivity. shed via respiratory tract and udders.

149
Q

How do you test for TB

A

Comparative intradermal tuberculosis test

Pure protein derivitive of avian tuberculosis injected intradermally. And so is Bovine tuberculosis. Cell mediated responce measured by the size of the swelling 72 hours after injection. Allows for differentiation between exposure to tuberculin and exposure to bovine tuberculin.

150
Q

Define the terms pathogenicity, virulence and pathogenesis

A
  • Pathogenicity - Ability of infectous agents to cause disease
  • Virulence - Measure of ability to cause disease
  • Pathogenesis - Process of disease progression
151
Q

How do bacteria adhere and aquire nutrients

A
  • Adhesion - Must adhere to surfaces to avoid being flushed out. Have fimbrae. The K88 fimbrae bind to receptor mannose
  • Aquiring nutrients - Initial survival dependant on ability to aquire iron. Bacteria produces siderophores, take iron of chelators, e.g haemoglobin. Siderophores bind to bacteria on outer membrane
152
Q

How do bacteria evade host defences

A
  • LPS plays a role in preventing phagocytosis. The M protein destroys C3 convertase, preventing C3a formation = decreased opsinisation. release antichemotoxins which are ant-opsinins.
  • Can hide intracellularly to avoid humoral/cellular defences. 3 mechanisms to survive in cell:
  1. Inhibit phagosome-lysosome fusion (salmonella)
  2. Lyse phagosomal membrane & escape into cytoplasm
  3. Resist inactivation by lysosomal factors
153
Q

How do bacteria cause damage to the host

A
  • Exotoxins - produced by G+ve bacteria. Heat liable proteins e.g anthrax
  • Endotoxins - Lipid A portion of LPS. Outer membrane of G-ve. interacts with macrophages membrane receptors. Cause release of tumour necrosis factor (TNF) then IL-1, acts on hypothalamus to cause fever.
154
Q

Describe properties of clostridium and its 5 different types

A

Anaerobic gram positive spore forming bacterium. inhabit soil and faeces. Motile and produce many toxins.

Types:

  • A - Alpha toxin. causes enteritis in pigs & chickens.
  • B - Has alpha, beta & epsilon toxins. Causes lamb dysentry
  • C - Has alpha and beta toxins. Causes enterotoxaemia in sheep. death without premonitory signs. also nectrotic enteritis is lambs & pigs
  • D - Has alpha and epsilon toxins. causing enterotoxaemia in sheep and causes in lambs.
  • E - Less important. necrotic enteritis in australia
155
Q

Decribe the clinical signs of C.botulinum and C.tetani

A

C.botulinum

  • Ingestion of toxins, usually from inadequetely heat treated canned food or hay silage with contaminated rotting carcase
  • Enters circulation & peripheral NS. blocks Ach release at NMJ, causing a flaccid paralysis and death

C.tetani

  • Found in soil and faeces
  • Grows superficially on deep anaerobic wounds
  • Releases tetanospasmin, blocking release of neurotransmitter for inhibitory synapses (glycine)
  • Causes uncontrolled excitory synaptic activity, paralysis by constant contraction.
156
Q

Describe basic features of bacillus and the characteristics of Anthrax

A

Gram positive spore forming rod bacteria. Aerobic and found in soil and faeces. most are not pathogens.

B.anthrax

  • Capsule enables it to resist phagocytosis and survive in vivo
  • spores ingested and germinate in lymphatics
  • Appear on smear as dark blue chain of square ending rods in capsule
  • Produce B toxin in vivo, 3 protein exotoxin.
  • Leads to death of phagocytic cells, increased capillary permeability and thrombosis. death by systemic shock due to haemorrhage, hypotension and oedema.
157
Q

How do penicillins act against bacteria and what are the 4 classes of penicillins

A

They disrupt the cell wall synthesis by non competitvely inhibiting Transpeptidases, No peptidoglyan cross links. As bacteria grow, They burst under osmotic stress! therefore.. If used with a bacteriostatic drug NOT effective. Cidal drugs

  1. Natural - Narrow spec agains +Gve. beta lactomase sensitive (produced bby staphylococcal infections)
  2. Anti-Staphylococcal penicillins - Narrow spec & resistant to B-lactamase
  3. Aminopenicillins (amoxycillin) - Broad spec. Sensitive to B-lactamase
  4. Extended spec penicillines - Broad spec

Penicillins are organice acids therefore are ionised at Physiological PH=> poor oral availability. Except aminopenicillins

158
Q

What are cephalosporins

A

Cephalosporins are antimicrobial drugs that non competiitively inhibt Transpeptidases.. no peptidoglycan Cross links. developed from penicillins to improve the spectrum. Also B-lactamase sensitive.

  • 1st gen - Broad spec and resistant to Beta lactamase
  • 2nd gen - Improved effectivenss against +Gve
  • 3rd gen - Improved effictiveness against -Gve
159
Q

What are quinolones and fluorquinolones

A

Quinolones are narrow spec -Gve antibiotics that inhibit the super coiling of bacterial DNA.

Fluoroquinolones Have there structere altered and now Wide spectrum. Highly lipophilic, meaning they can cross INTO cells making them effective against intracellular pathogens. Oral availability good and volume of distribution good.

Poor against obligate anaerobes

160
Q

What are Nitroimidazoles

A

Antibacterial drug that is only effective against obligate anaerobes. Highly lipophilic and has good oral availability and volume of distribution. Requires hepatic metablism before it can be excreted

161
Q

Describe the properties of sulphonamides

A
  • Competitve inhibitor of glutamic acid, Blocking production of nucleotides
  • Broad spectrum
  • Weak acid with good oral availability
  • Good volume of distribution
  • Extent of plasma binding varies in species
  • Not good vs obligate anaerobes
  • Rate of metabolism & excretion varies within species & with urine PH ( more acidic less excretion)
162
Q

Describe dihydrofolate reductase inhibitors (DHR)

A

DHR’s are wide spectrum antibacterial drugs. Orally active and cleared via hepatic metabolism. Not good vs obligate anaerobes.

163
Q

Describe properties of chloramphenicol

A
  • Inhibit peptidyl transferase, inhibiting peptide formation. Bacteriostatic
  • Broad spec including obligate anaerobes
  • Orally active
  • Requires hepatic metabolism
164
Q

Describe properties of tetracylins

A
  • Inhibit tRNA joining A site. bacteriostatic
  • Broad spectrum
  • Hydrophilic and lipophilic
  • Renally excreted
165
Q

Describe the aminoglycosides

A
  • Binds to ribosome causing wrong amino acids to bind. Wastes all metabolic energy making pointless proteins
  • Narrow spec -Gve with some anti staphylococcal activity
  • Poorly distributed - confined to extracellular
  • Renally excreted
166
Q

Describe the properties of macrolides and Lincosamides

A
  • Cause peptide chain to dissociate duuring translocation
  • Narrow spec +Gve
  • Good vs olbligate anerobes
  • Good vs special organsims (mycoplasma and mycobacteria)
  • orally active distribute widely
  • Hepatic metabilism prior to metabolism
167
Q

What are the 3 ways in which antibacterials target bacteria

A

1. Target DNA & cell division

  • Inhibit nuclei acid syntheis (sulphonamides)
  • Interfere with DNA synthesis (rifampin)
  • Prevent cell division (cisplatin)

2. Protein synthesis - ribosomes of prokaryotes are 70s and eukaryotes 80s. Bacteriostatic effect

  • Bind to 30s subunit - tetracyclines
  • Bind to 50s subunit - chloraphenicol

3. Plasma membrane - Alter permeability

E.g Ionophore cause formation of pores

168
Q

What is the mechanism of antibacterial resistance

A

Antibacterials put selective pressure of bacteria meaning a change in phenotype can cause survival. Can be transfered by conjugation (horizonatal), transduction (virus induced) & Transformation (uptake from cytoplasm)

  • Increased production of metabolite that competes with drug.
  • Loss of cell permeability, increases trasportation of drug out of cell.
  • Over production of drug target
169
Q

What is Pseudomonas

A

P.aeruginosa

  • Aerobic gram negative Rod
  • Secretes a green pigment called pyocyanin
  • oppertunistic infectous agent, damaged tissue
  • Has an effective efflux system pumping out disenfectant quicker than it diffuses in
  • Resistant to some antibiotics, therefore when antibiotics given kills competing bacteria
170
Q

What is bordetella

A
  • Strict aerobic gram negative Rod
  • Grows on MacConkey medium
  • secondary infection of ciliated epithelium of trachea following damage to tissues by virus or mycoplasm
  • Filamentous haemogglutinin alows adherence
  • Leukotoxins destroys neutrophils
171
Q

What is pasteurella multocida

A

Gram negative rod bacteria that inhabits the upper respiratory mucosa and GI tract.

  • Primary pathogen - Fowl cholera & atrophic rhinoitis
  • Secondary pathogen - Bovine pneumonia, wound infections and enzootic pneuomonia
172
Q

What is mannheimia haemolytica

A

Non fermenting gram negative Rod. Usually secondary to mild viral infection. Bovine respiratory disease. Secrete leukotoxins & fills alveoli with serous fluid
.

173
Q

Outline the bacteria classification

A
174
Q

What are enterobacteria and what are the two types

A

Gram negative bacteria, oxidase negative that are facultative anaerobes.

  1. Lactose fermenters - Harmless commensual of the gut E.g E.coli and Enterobacter
  2. Non lactose fermenters -pathogens of the gut E.g salmonella

Neutral red added to detect any acid produced from lactose fermentation

175
Q

Describe Escherichia coli and what makes it pathogenic

A

E.coli normally inhabits LI, & is a indicator of water contamination

  • Rare strains with special properties e.g fimbrae, reversable Na+ pumps=>diarrhoea & metabolite loss =>acidosis are enteropathogens of gut. an example is enterotoxigenic Escherichia coli (ETEC)
  • Many strains are pathogenic outside of the gut and are known as extraintestinal pathogens.
  • Pathogenecity factors include K antigens, Fe aquisition , haemolysins & compliment resistance
176
Q

Describe salmonella enterica, How its isolated and its effects on the host

A

Is a Non lactose fermenting gram negative rod. Produces H2S.

Must use enrichment because present in very small numbers and then place on a strong selective medium and use phenal red. Will remain red as no acid is produced but colonies appear black due to H2S.

Can identify using API test

Agglutinisation with specific antisera determines grouping based on O side chain of LPS and flagellae, Kaufmann-white scheme. However an inverted segment of DNA allows ‘switch phasing’ of flagellae.

Causes cytotoxicity of enterocytes, septicaemia and enteritis. Can survive in macrophages, so after recovery can be intermittently released in faeces, active carriage.

177
Q

What is camplobacter and why is it a public health risk

A

Camplybacter is a curve gram negative rod. Motile and is microaerophilic (5-10%)

C.jejuni is the largest cuse of food poisining in man. When chicken slaughtered intestinal contents splattered onto abdominal wall. Inadequate thawing causes bacteria to be viable. Causes necrosis of the spithelial cells of GIT, erosion of mucosa and cyptic abcsesses.

178
Q

What is immune evasion and give an example of how its achieved

A

Balance between host immune protection & pathogen immune evasion.

E.g vaccinia virus - multiple modulatory proteins. inhibits inflammatory & immune response

179
Q

Give an example of a mechanism of rapid virus spread

A

Expresses actin tail. repells viral proteins away from already infected cells. repelled to adjacent non infected cells to ensure rapid spread

180
Q

What are the pathological effects of a virus on cells

A

Direct effects

Cytopathic effects (CPE) - changes visible under light microscopy

  • host cell shuts off
  • lysosomal damage
  • inclusion bodies
  • syncitia formation (measles)

Indirects effects - immune mediated pathology

181
Q

what is viral tropism and what are the factors effectingf it

A

Is the specificity of a virus to a cell type, tissue or species.

Determined by:

  1. Appropriate cell surface receptor
  2. requirements of a virus for expression of intracellular gene products to complete infection
  3. accessibility
  4. overcoming host immune defences
182
Q

how do viruses affecting the GI gain entry and what is their pathogenesis

A

Entry

  1. Via ingestion - Must be bile and stomach acid resistant. Can also gain access via a buffer
    E.g milk. Also can be activated by proteases (rotavirus has its outer capsid cleaved)
  2. Via oropharynx - primary infection of lymphocytes. spread to GI via blood

Pathogenesis

  • Destruction of spithelial cells, replaced by transitional cells which lack enzyme production & absorbitive function
183
Q

What is rotavirus, what affects does it have on the host and how is it diagnosed

A
  • Non enveloped, RNA segmented virus
  • Group A causes diarrhoea in calves. short inoculation (1-4 days)
  • Infects vili tips
  • Less differentiated cells secrete less disaccharides, causing a decrease in glucose coupled transporters.
  • Build up of undigested lactose promotes bacterial growth, exerting furthur osmotic effects = diarrhoea. milk scours

Diagnosis - by antigen detection in faeces by ELISA. antibody detection not useful due to passive immunity

184
Q

What is the pathogenesis of respiratory tract viruses and give an example

A
  • Lysis of cells - erosion of mucosa
  • Loss of ciliated cells=>decreased ciliary clearance => increase in spread of virus
  • Mucus, accumulation of fluid and inflammatory cells inhibits airflow, increasing sucseptibility to secondary infection

Equine influenza virus

  • Segmented ss RNA enveloped virus
  • transmission via aerosol & direct contact
  • Diagnosis - Antigen detection by ELISA or nasal swabs
185
Q

Describe pathogenis pf viruses affectin Haematopoeitic & lymporeticular system and give an example

A
  • Primary replication at lymphoid tissue at site of entry
  • Viraemia to sites
  • Destruction of lymphoid cells causing immunosuppression

Feline pandeukopenia virus

  • Non enveloped ss DNA virus
  • Targets rapidly diving cells
  • Entry via oropharynx, infects tonsils and infects blood
  • Destroys white blood cells without preference
  • Also targets crypts, causing diarrhoea
  • Diagnosis - Antigen detection via ELISA from faeces
186
Q

Give 3 examples of viruses effecting the skin

A

Pox virus

  • Encodes all enzymes required for replication, therefore independant of nucleus and can replicate in cytoplasm

Pathogenisis

  • Targets skin abrasions, spreading locally
  • Replicates in epithelial cells & causes cytoplasmic swelling/rupture. Inflammatory cells attracted
  • Dilation of blood vessels, increases permeability and causes dermal oedema forming papule
  • Degeneration and formation of intradermal vesicle. Ruptures releasing viral proteins

ORF

  • Lesions of lips and gums
  • Spreads direct or via formites
  • Vaccination can cause clinical signs therefore shouldnt be given to herds free of ORF

Myoxoma

  • Generalised infection of rabbits
  • Causes conjunctivitis, swelling of muzzle and subcutaneous nodules.
  • Transmitted by arthropods
187
Q

Give an example of CNS virus

A

Rabies

Bite containing virus inoculated into muscle. Uses motor nerves to travel to the VNS and furthur replicate

Clinical signs include a foamy mouth (paralysis of pharyngeal muscles inhibits swallowing, animals can becomes aggressive or paralyses

Diagnosed by immunofluorescence of brain smear

188
Q

How does Equine herpes virus affect the host

A
  • Gains entry via respiratory tract, infecting lymphocytes and causing viraemia
  • Causes vasculitis and haemorrhaging causing abortion in pregnant mares
  • Blood vessels of spine can be affected and cause ataxia or paralysis
  • Diagnosed by PCR from nasal swab
189
Q

What are the effects of canine distemper virus on the host

A
  • Enveloped ss RNA virus
  • Gains entry via upper respiratory tract causing a viraemia
  • Spread to lymphoid organs & epithelial cells (widespread)
  • Clinicals signs include cough, conjunctivitis, v&d, seizures and hyperkeratosis (hard pad)
  • Clinical signs are dependant on age, strain of virus and environmental stresses upon hosy
  • Diagnosed by serology (IgM), PCR or CSF
190
Q

What are the three ways in which you can directly detect a viral pathogen

A

Virus isolation

  • Virus need cells to replicate. CPE’s can be see on cells
  • Virus is amplified and easier to detect
  • BUT can take several days, requires live virus and can be cultured

Directly visualise

  • Electro microscopy. Use negative staining. Heavy metals bind to backround and not substrate.
  • Can be used for virus that cant be cultured & can identify new agents
  • BUT requires specialised machinery and personal. sample often needs to be purified

PCR

  • Taq polymerase used to amplify DNA. Short oligoucletide primers specific to virus structure used. If its RNA then must be first coverted into cDNA by reverse transcriptase
  • Very sensitive and doest require live virus
  • High sensitivity means dager of contamination
191
Q

Wat are the two Diagnostic tests that detect virus antigen

A

Antigen ELISA

  • Plates coated with antibody specific to virus, virus then binds. Second virus specific antibody is added which carries enzyme label. enzyme acts on substrate generating colour
  • Fast, Virus can be dead and test is specific
  • No amplification means low sensitivity

Immunoassays

  • Virus antigen in cells detected by specific antibody. Antibody carries either fluorescent marker or enzyme which reacts with substrate.
  • Fast, non living viruses can be used and is specific
  • No amplification, relatively low sensitivity
192
Q

What are the three virus diagnostics used by identifying host immune response

A

Neutralisation assay

  • Serum mixed with virus. antibodies in serum bind. mixture added to cells. if antibodys are present they do not infect cels

Haemagglutination inhibition assay

  • Some viruses have the ability to agglutinate red blood cells. E.g influeza. Serum mixed with virus. Red blood cells added to mixture. If theres NO antibodies, RBC’s agglutinate

Antibody ELISA

  • Plate coated in antigen. Antibody in serum binds to antigen. Second antibody whic recognises
    *
193
Q

Describe the normal innate response to viruses and a way viruses evade this

A

Type 1 interferons are secreted by viraly infected cells. IFN’s act in a paracrine manner making cells resistant to viral replication by:

  1. Increasing degradation of viral mRNA
  2. Reduced synthesis of virus protein & increased antigen presentation (MHC class I)
  3. NK cells destroy cells with reduced MHC class I

Pestiviruses** (BVDV) produce **NON structural proteins** that interfere with signlling to **prevent IFN production. Pox virus** interferes via **blocking IFN receptors

194
Q

What are the 5 ways in which viruses evade immune response

A
  1. Taking up residence in privilidged sites in the body E.g CNS, eyes and testis. No immune response in these areas to protect against damage from inflammation. E.g’s Rabies in CNS and BVDV in testis
  2. Avoiding the extracellular matrix where Ig’s are lurking by syncitia formation E.g parainfluenza-3 virus.
  3. Integrating viral DNA into genome inducing malignant transformation. cell proliferation propogates virus ( Retroviruses, FeLV). Some also integrate into germline, main concern when considering xenotransplants
  4. Secrete an antigen decoy in large quantities, saturating the binding sites of Ig’s. Infectous virus particles are therefore not neutralised (E.g Ebola). Decoy antigen can also be expressed on surface, distracting immune system away from antigen of attachment. Impacts on developing vaccines (E.g Retroviruses)
  5. Antigenic variation:
  • Antigenic drift - Genes subject to mutation. slight change making antigen not recognisable
  • Antigent shift** - Fast process, whole **genes swapped between viruses radically changing proteins expressed. E.g mutation in feline panleuokpenia virus allowed spike antigen to bind to transferrin on canine entoerocytes. Also feline calicivirus. Also equine infectous anaemia is a persistent infection occuring in cycles, with each cylce due to new antigenic variant thats mutated.
195
Q

How do viruses evade cell mediated immunity

A
  1. Superantigens - Cross link MHC to TCR non specifically outside peptide binding groove. Causes clonal expansion of T-cells, diluting antigen specific T-cells (E.g retroviruses)
  2. Resistance to apoptosis - Produce sepsins which inhibit caspase cascade. Also produce analogues of anti-apoptosis proteins (Bcl2)
  3. Preventing presentation to CD8 T cells:
  • Block TAP transporter, preventing MHC presentation
  • Prevent MHC transport, retined in ER
  • Misdirects newly synthesised MHC into cytosol to be dissolved by proteosome.

This however increases susceptibility to NK cells due to lack of MHC. therefore can produce fake MHC

196
Q

What immune evasion strategies to Retroviruses and lentiviruses use

A
  • Direct immuno suppression - Direct destruction of T helper cells and cells of monocyte lineage (macrogohages and DC’s). Increases susceptibility to cancers (reduced tumour surveleince) and oppertunistic infections. (e.g FIV)
  • Indirect immunosuppression - Produce cyotokine analogue that acts to mimic regulatory Tcells, downregulating the immune system ( E.g herpesvirus, ORF and epstein bar virus)
197
Q

Describe pathogenesis of Feline immunodeficiency virus

A
  • Acute primary phase - Transient viraemia, fever, lymphodenopathy as virus replicates in lymphoid tissue
  • Asymptomatic phase - immune response fails to eradicate virus & persistant infection develops. animal remains healthy
  • Feline AIDS - lyphopenia develops. CD4 T cells number reach critical low levels, causing immunosuppression
198
Q

How do pesttiviruses evade immune response

A

Example BVDV. Has 2 stains, cytopathic and non cytopathic. Infection with ncp early in gestation causes abortion/resorption. If infection occurs 80-125 days into gestation, foetus may survive with persistant infection. T & B cells reactive to virus are eliminated as its treated as self. developing calf is tolerant but sheds large amount of virus. Can mutate and become cytopathic causing ulcerations to mucosal epithelium.

199
Q

How do herpesvirus evade immune response

A

Latency - Initial infection causes clinical signs. Virus then enters quiescence. viral genome maintained in host cell with no replication. Recrudescence occurs when host immunity lowered:

  • Stress
  • Medication (corticosteroids)
  • Pregnancy

Examples:

  1. Feline herpesvirus -1 : Transmission to kittens, develop latent infection. Vaccination useless post infection
  2. Equine herpesvirus-1/-4: Causes abortion in pregnanct mares. Causes depression, fever and nasal discharge. -1 strain can also cause neurolgical clinical signs in which euthanasia is required. Large proportion of healthy horses are latently infected with EHV. Vaccination is licensed but every horse on yard needs to be vaccinated and many boosters required.
200
Q

What is canine parvo virus and how is it an example of an emerging & evolving disease

A

Disease:

  • Acute enteric disease in young dogs ( diarrhoea, vomitting, dehydration and shock)
  • Loss of intestinal barrier allowing bacterial infection
  • Immunosuppression
  • Myocarditis in pups

Pathogenesis:

  • Replicates in pharyngeal lymphoid tissue
  • Viraemia proceeded by targeting of rapidly dividing stem cells
  • In pups <2weeks causes myocarditis
  • In older pups invade crypts

Aminoacid change mutation in FPLV capsid protein (VP2) allowed host change from feline panleukopenia virus to efficiently attach to canine vili.

201
Q

What is influenza and how is it an example of an emerging and evolving viral disease

A

Causes enteric disease in birds and respiratory disease in horses, swine & humans

Pathogenisis:

  • Replicates in Upper respiratory tract in humans
  • Replicates in ciliated epithelium and nasal mucosa in horse & bronchioles

Influenza is subject to antigenic shift. 2 viruses infect same cell, causing reassortment of viral segments. Recombination causes new strain. Pigs act as mixing vessels causing pandemics.

202
Q

What is the life cycle of influenza, what determines pathogenicity and what is the importance of the siliac acid galactose bond?

A

Life cycle

  • Attachment - Attaches to virus receptor via HA, binds to sialic acid
  • Penetration - Endocytosis. Acidic PH in endosome causes conformational change in HA causing exposure of cleavage site. HA cleaved to HA1 & HA2.
  • Uncoating - Viral genome released
  • Replication
  • Viral synthesis
  • Release - Virus progeny released. Neuraminidase cleaves sialic acid to prevent virus binding to infected cell.

Cleavibility of HA determines pathogenicity. Normally linked by argenine residues and only cleaved by limited proteases in few cells. Whereas highly pathogenic strains easily cleaved by proteases found in the majority of cells, allowing viral replication throughout body.

In humans the bond between galactose and siliac acid gives it a kinked shape, whereas in avain is linear. This determines what strain binds to which species. HOWEVER in lower respiratory tract, siliac acid is linear in humans, therefore close contact with avain can cause infection.

203
Q

What is the meanind of urban cycle, dead end host and sylvatic cycle

A

Urban clycle - Transmission of virus between human and arthropod

Dead end host - Infected but not sufficient replication in blood to infect arthropod when feeding

Sylvatic cycle - Transmission between arthropod and other vertebrates

204
Q

What are factors affecting the emergence, spread and persistence of viruses

A

Emergence

  • Movement of vector
  • Climate change
  • Movement of animals
  • New vector

Spread

  • R0 - Ability to infect
  • Population of vector and host
  • Movement of animals
  • Host range

Persistance

  • Ability to evade immune system
  • Segmented genome alows genomic shift
205
Q

Give examples of arthropod diseases

A

West nile virus

  • Disease in birds in the USA
  • Human and horses are dead end hosts
  • Rapid spread due to migration of birds
  • Mosquito vector

Louping ill

  • Tick borne virus
  • Disease in sheep causing encephalomyelitis, ataxia, leaping gait and parlysis
  • Cattle, horses and humans are dead end hosts

Bluetongue virus

  • Affects domestic ruminants
  • Spread via midges
  • Causes ulceration of upperlip and erosion of tongue
  • Clinical signs include oedema, fever, congestion, necrosis of skeletal & cardiac muscle
  • Haemorrhage of pulmonary artery

African horse sickness virus (AHSV)

  • Affects ruminants
  • Midge vector
  • Pathogenisis - Cell associated viraemia, causing vasculitis => increased permeability of vessels
  • Mild form presents as supraorbital oedema
  • Cardiac form presents as oedema in the head, neck and chest
  • Pulmonary form presents as pulmonary oedema and has a mortality rate up to 95%
206
Q

What is a notifiable disease and what are the criteria

A

A disease that must be reported to the AHVLA if suspected (Legal requirement)

  • Endemic diseases (Bovine TB)
  • Exoctic disease not usually seen in the UK
  • Zoonotic disease (Rabies)
207
Q

What is PETS

A

Pet Travel Scheme

Requirements:

  • Microchip
  • Rabies vaccination
  • Pet passport
  • Tapeworm treatment
  • Travelling via approved route
208
Q

What is Foot and mouth disease, how is it controlled and is it transmitted

A

Highly transmissable virus that has 7 serotypes. Can be transmissed via fomites, vesicular fluid, milk, faeces, salivia & aerosol. Can be diagnosed from serum or vesicular fluid.

Control based on disease status of control. Basis of control:

  • Import control
  • Early detection
  • Tracing to identify source
  • Movement control
  • Intensive surveillance

Prophylactic vaccination: Seeks to maintain immunity against 1 or more serotypes. 2billion administered a year.

209
Q

What Is a prion disease

A

PrPsc is a disease associated isoform of the PrPc protein. PrPc is alpha helix recylcing protein which is continously produced on neurones. PrPsc Has a beta pleated sheet structure, allows it to aggregate and form plaques. Can convert PrPc into PrPsc. Replicate inside Follicular DC’s.

Causes Neuroinflammation. Astrocyte proliferate and hypertrophy. Theres an influx of microglia but not WBC’s due to BBB. No B or T cells because proteins are recognised as self antigens & therefore any reactive lymphocytes would have been destroyed. Histologically causes vacuolisation (reversible) inside neurones, extracellular plaques of aggregated proteins.

Exceptionally resistant to conventional sterilisation techniques. Requires 121 degrees for 1 hour. New methods in 1980’s reduced temp of sterilisation and no solvent used.

210
Q

How is prion disease diagnosed and give two examples

A

Diagnosis - Western blot

  • PrPsc is a surrogate marker
  • Proteins seperated into molecular weight & bloted onto paper.
  • Antibody specific to prion protein detect protein and bind resulting on 3 lines on paper
  • 3 lines represent same protein but differently glycosolated
  • To distinguish between PrPc and PrPsc proteases are used as PrPsc is protease resistant

Antibodies are produced by:

  1. Immunising PrP knockout mice with PrP
  2. Immunice with PrP from different species
  3. Add T-cell epitope to PrP

Bovine spongiform encephelopathy (BSE) - neurological symptoms affects cows of 4-5 years. was transmitted by meat and bone meal

Scrapie - Occurs in sheep of 2-5 years, death within 6-7 months. Persistant in environment for over 16 years.

211
Q

What produces the Extracellular matrix, what are its two main components and what is its function

A

ECM is a network of locally secreted macromolecules. Produced by fibroblasts. Cells determine ECM turnover and production

Function:

  • Cell shape
  • Cell migration
  • Cell proliferation
  • Cell function

the 2 main components are Glycoaminoglycans (GAG) and fibrous protein (collagen)

212
Q

Describe properties of GAG’s and fibrous proteins in ECM and give examples

A

GAG

  • Polysaccharides which are covalently linked to protein core
  • Negatively charged, attract sodium and thus water
  • Strong at with standing compressive forces
  • Example - Hyaluronan. Unsulphated and is not covaletly linked to protein. synthesised at PM and not golgi. Functions as a space filler, lubricant and facilitates shape change. Can link to Protein of Proteoglycans.

fibrous protein

  • Collagen. 3x alpha helix, forms a triple helix which is covalently cross linked
  • High tensile strength
  • Fibril associated collagens (type IX) influence fibrular collagen structure (type II). Allowing for alternate structure and resistance of tensile strength in more than one plane
213
Q

Explain how proteoglycans can increase ECM synthesis, control tissue breakdown and act as a co receptor

A

ECM synthesis

  • Transforming growth factor beta (TGF-b) increases ECM production
  • Decorin (PG) inhibits TGF-b.
  • TGF-b upregulates decorin synthesis. this is a built in negative feedback system.

Co-receptor

  • Syndecan is a transmembrane protein. Brings FGF towards its receptors. Intracelullarly domain binds to actin.

Modulate tissue breakdown - By binding to enzymes or their inhibitors

  • Bind to enzyme/inhibitor to restricts its range of action
  • Bind & store enzyme/inhibitor to directly control
  • Bind to enzyme/inhibitor to modulate activity
  • Bind to enzyme/inhibitor to control effective concentration
214
Q

What are the 3 cell junctions

A
  • Tight - Prevent leakage. Transmembrane proteins that dimerise.
  • Anchoring - Can be cell to cell or cell to matrix. Also can be actin dependant or intermediate filament dependant
  • Gap - Allow chemical and electrical signals to pass. 2-4nm gap. Flow of ion
215
Q

What is gular flutting

A

Contraction of the throat muscles of birds, pushing air through moist air sacs, releasing heat upon expiration. a form of thermoregulation

216
Q

What is the thermoneurtral zone

A

Range of temperature in which a homeotherm can regulate its body temperature by adjusting heat loss at negligible energy cost

217
Q

What physiological responses occur to control thermoregulation

A
  • Vasodilation of superficial veins for heat loss or vasoconstriction of deep veins for heat conservation
  • Sweat glands - Controlled by sympathetic innevation & circulating catecholamines
  • Adrenals - Release adrenaline, speeding up metabolism and producing heat
  • Piloerection - Maximises boundary layer, increasing insulation
218
Q

What thermoregulatory problems due neonates face and what adaptation do they have to combat this

A
  • Wet surface area from foetal fluids
  • Limited subcutaneous fat
  • Large surface area:volume ratio
  • Poorly developed coat
  • Poorly developed central control of hypothalamic set points

Born with large amount of brown fats that are activated at birth by cold shock and placental seperation. Increase in adrenaline, cortisol and T3. increased activity of mitochondrial uncoupling protein, increasing the amount of non shivering thermogenesis

219
Q

What are the physiological consequences of hypothermia & hyperthermia and what causes fever

A

Hypothermia - Depletion of glycogen stores causes

  • Decrease of CO & BP
  • Increased Blood viscosity
  • Decrease oxygen cosumption and GFR

Hyperthermia - Loss of water and salts leading to organ dysfunction

Fever - Release of TNF, IL-6 and IL-1. causes the release of PGE2 causing and increase in the hypothalamic set points.

220
Q
A

BVETMED2 (10 decks)

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