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Finals > Pathological And Epidemiological Mechanisms Of Disease > Flashcards

Pathological And Epidemiological Mechanisms Of Disease Flashcards

1
Q

How does salmonella attach and invade epithelial cells

A

Depends on fimbrae and flagella

Injects effector proteins resulting in uptake

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2
Q

How does salmonella elicit an immune response

A

Invasion stimulates cell to provide IL-8
Inflammation and inflammatory diarrhoea
Salmonella remains in vacuole and survives

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3
Q

How does salmonella persist within cells

A 
Growth rate slows
Replication
Escaping bacteria are ubiquitinated
Virulence downregulated
Glucose and fatty acids catabolised
Transcytosis 
Move to liver and spread to other organs
Find the organ it is shedding from and remove it
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4
Q

Features of campylobacter jejuni

A

Severe disease in humans
Chickens are carriers
Host needs to be immunologically compromised for infection to occur

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5
Q

How does the body respond to campylobacter

A

Neutrophils to site of infection
Epithelial cell junctions open to let them out
Campylobacter enters
More inflammation and cycle repeats until epithelium is shed or an adaptive immune response is generated
Doesn’t spread around the body

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6
Q

Why are infections worse in neonate

A

Few antibodies - only from mother
Poor adaptive immune response
Pathogens subvert the immune response to get in - adaptive immune response in adults slows them down

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7
Q

What causes the greatest mortality in household pets

A

Cancer 41%

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8
Q

What does neoplasia mean

A

The pathological process that results is the formation of a neoplasm

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9
Q

What does neoplasia mean

A

A new growth that occurs over time and is uncoordinated with normal tissue
Consist of neoplastic cells and supporting cells that allow blood vessels in and produce growth factor to allow tumour to grow

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10
Q

What type of disease is cancer

A

Genetic disease
Changes are genetic mutations that have to be inherited by the next generation of cells
Epigenetic changes

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11
Q

What are epigenetics

A

The inheritance of patterns of gene activity that do not depend on the nucleotide sequence

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12
Q

What causes cell mutations

A

Intrinsic factors - DNA replication or repair errors
Extrinsic factors - chemicals, radiation, infectious agents

Need a driver mutation for cancer to occur

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13
Q

What are the hallmarks of cancer

A 
Self sufficient growth
Insensitive to anti growth signals
Evasion of cell death
Unlimited replication
Angiogenesis
Tissue invasion and metastasis
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14
Q

What are oncogenes

A

Stimulatory genes that promote self sufficient growth.

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15
Q

How are growth factor receptors involved in tumour growth

A

They are produced excessively as a result of duplication of growth factor genes in the nucleus
Binding of ligands to the receptors causes massive stimulation for cellular proliferation

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16
Q

What genes are suppressed in cancer cells

A

Tumour suppressor genes

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17
Q

What is the clonal evolution model

A

Tumour population is heterogenous
Multiple subclonal populations at different stages of neoplastic transformation
One or more subclones will dominate
Most cells have potential to form new tumours

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18
Q

What is the stem cell model

A

Stem cells
Unlimited proliferation
Self renewal
Daughter cells formed which follow differential pathways
Only the cancer stem cells can form new tumours

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19
Q

Starting from a single cell explain the basic steps that occur during development of cancer

A

Cell undergos 6 driver mutations that affect specific genes
Protein expression and function is altered
Cell function and behaviour is altered
Cell proliferates forming more mutant cells

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20
Q

What is the difference between stem cell model and clonal evolution model of cancer

A

Stem cell model - only stem cells and self renew and proliferate unlimitedly. Daughter cells formed which differentiate

Clonal evolution model- subclonal populations at different stages of transformation. Most of the cells can form new tumours.

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21
Q

Features of cartilage

A

Light
Flexible
Less vascular and cellular than bone
Bad at repair

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22
Q

What is cortical bone

A

Rigid outer shell

90% bone is cortical

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23
Q

What is trabecular bone

A

Occurs at the ends of long bones and in the inner parts of flat bones
Provides strength as provides a complex system of internal supports
Bone marrow occupies space in between trabeculae

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24
Q

What is lamella bone

A

Parallel or concentric layers of lamellae
Consist of highly organised arrangement of mineralised collagen fibres
Intervertebral discs

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25
Q

What is woven bone

A

Disorganised collagen fibres
Mechanically weak
1st bone to be made in repair

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26
Q

What is bone covered by

A

Periosteum - scenes fibrous outer membrane

Endosteum - thin connective tissue lining the marrow

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27
Q

Features of the avian skeleton

A

Lightweight
Many hollow bones - pneumatic with air sacs for gas exchange instead of marrow
Flexible necks - many cervical vertebrae
Fused collarbone and breastbone (keel)

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28
Q

What is the composition of calcified bone

A

Organic matrix 20-30%
Inorganic matrix 60-70%
Cells 2-5%
Water 5-10%

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29
Q

What is the organic matrix of bone

A

Type 1 collagen
Triple helix of polypeptide chains
Cross linked for strength

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30
Q

What is osteogenesis imperfecta

A

Mutation of collagen causing loss of the triple helix
Poor mineralisation and bone fragility
Collagen poor quality and less than normal

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31
Q

Clinical signs of osteogenesis in dogs

A 
Osteopenia
Multiple fractures
Bone deformities
Pain
Pink teeth as thin enamel
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32
Q

Clinical signs of osteogenesis in cats

A 
Bone pain
Poor bone mineralisation
Stunted
Reluctant to move
Depression and decreased appetite
Poor prognosis
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33
Q

What are the non collagenous properties of bone

A

Proteoglycans - space filling
Adhesive glycoproteins - RGD containing proteins
Gla protein and osteocalcin - regulate mineralisation

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34
Q

What is bone mineralisation

A

Calcium phosphate deposited as hydroxyapatite in the gap regions of collagen fibrils
Mediated by osteoblasts and chondrocytes

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35
Q

What are osteoclasts

A

Cells that reabsorb bone

Macrophage lineage

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36
Q

What are osteoblasts

A

Synthesise bone

Derived from mesenchymal stem cells

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37
Q

What are osteocytes

A

Long lived resident bone cell

Mechanoreceptors which can slowly remodel bone

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38
Q

What is the difference between bone modelling and remodelling

A

Bone remodelling requires the prior resorption of bone by osteoclasts.
Normal bone maintenance instead of change in response to load

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39
Q

What are the steps of bone remodelling

A

Osteoclasts activation by osteoblasts and osteocyte signalling, cytokines and hormones
Resorption of mineral in acidic lacunae and collagen degraded by proteases
Reversal - osteoclast apoptosis and osteoblasts replace them
Formation of new bone by osteoblasts which produce type 1 collagen matrix onto the resorbed surface
Mineralisation as osteoblasts deposit hydroxyapatite onto the collagen matrix
Osteoblasts become osteocytes and communicate via canaliculi

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40
Q

What are the regulators of bone remodelling

A 
Mechanical load
Microdamage
Hormones
Mineral homeostasis
Local regulators
Cytokines
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41
Q

Explain calcium homeostasis

A

Thyroid detects calcium levels too high so releases calcitonin.
Decreased bone resorption and calcium absorption. Calcium excretion through kidneys increases
Parathyroid detects levels too low so secretes PTH to increase bone resorption and calcium absorption. Calcium excretion is decreased. Vit D activated.

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42
Q

How does vitamin d contribute to calcium absorption and release

A

Causes liver to release calcidiol
This reduces excretion of calcium by kidneys and increase calcium absorption
Kidneys release calcitrol which causes increased calcium release

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43
Q

What systemic hormones regulate bone

A

Growth hormone - increases bone remodelling
Glucocorticoids- inhibit bone formation
Thyroid hormones - increase bone formation and resorption
Oestrogens - increase bone remodelling
Androgens - increase bone formation
Leptin - reduces bone mass

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44
Q

What are the local regulators of bone remodelling

A

TGF-B stimulates and inhibits bone resorption and promotes formation
IGFs stimulate osteoblast proliferation
BMPs promote osteoblast differentiation
Receptor Activator NfkB and RANKL allow for direct osteoblast and osteoclast precursor contact

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45
Q

What is intramembranous ossification

A

Flat bones
No cartilage template
Bone develops directly from fibrous connective tissue membrane
Osteoblasts form a centre of ossification where osteoid is deposited and mineralised

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46
Q

What is endochondral ossification

A

Long bone formation
Bone collar forms
Cavitation of cartilage where cells start to differentiate
Periosteal invasion of a blood vessel and formation of trabecular bone
Formation of secondary ossification site with an epiphyseal blood vessel
Cartilage remains at articular surface and growth plate

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47
Q

What genes are important for skeletal development

A

FGF genes - stimulates proliferation and limb outgrowth
Sonic hedgehog - limb development
Indian hedgehog - cartilage development and endochondral ossification
TGFB - signalling
RUNX2 - encodes core binding factor alpha 1 which is essential for differentiation of osteoblasts and conversion of cartilage into bone

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48
Q

What are the phases of bone repair

A

Reactive phase
Reparative phase
Remodelling phase

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49
Q

What is the reactive phase of bone repair

A

Vascular and inflammatory phase
Blood clot forms
Fibroblasts and macrophages infiltrate and proliferate to form granulation tissue

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50
Q

How does salmonella persist intracellularly

A 
Evades immune system
Provides nutrients
Protected replication
Persistence
Targets epithelial cells and macrophages
Entry by invasion or phagocytosis
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51
Q

What is the reparative phase of bone repair

A

Chondroblasts formed to produce cartilage by fibroblasts in the granulation tissue and periosteal cells in the fracture gap
Osteoblasts formed by periosteal cells distal to fracture which produce woven bone
Fracture gap bridged by soft callus
Endochondral ossification
Woven bone replaced by lamellar bone
Soft callus replaced by trabecular bone

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52
Q

What is the remodelling phase of bone repair

A

Trabecular bone replaced by cortical bone

Bone remodelled to recover original strength and shape over 3-5years

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53
Q

What are skeletal dysplasia

A

Abnormalities of cartilage and bone
Can be inherited or spontaneous
Abnormal shape or size of skeleton, disproportion of the long bones, spine and head

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54
Q

What are chondrodysplasias

A

Disorders of cartilage that cause the skeleton to develop abnormally
Linked to abnormalities in bone length
Achondroplasia and hypochondroplasia are causes of dwarfism
Common in cattle
Normal for dachshunds and bassets - mutation of FGF4

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55
Q

What is spider lamb syndrome

A

Chondrodysplasia in lambs causing skeletal deformities
FGF3
Long bent limbs and twisted spines

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56
Q

What is osteoporosis

A

Metabolic bone disease
Gradual lose of bone causing fragility
Low trauma fractures
Pain, deformity and functional impairment
Reported in dogs, horses, cats and chickens
Free range chickens get keel fractures

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57
Q

How might omega 3 prevent osteoporosis

A

Shifts the balance in favour of bone formation so can prevent bone fragility

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58
Q

What is rickets and osteomalacia

A

Swellignof joints and bending of the long bones in young
Cartilage not properly calcified as bone
Insufficient vit D, sunlight, phosphorous cause it

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59
Q

What are the causes of metabolic disease in reptiles

A

Lack of calcium in diet
Not enough UV access so reduced vit D formation
Secondary to diseases of liver, kidney, thyroid, parathyroid and intestine
Incorrect housing temperature

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60
Q

What are the clinical signs of metabolic bone disease in reptiles

A 
Soft shell
Bowed legs
Arched spine
Lumps on leg longbones and spine
Rubber jaw
Fractures
Jerky movement
Anorexia
Weakness
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61
Q

What is osteoarthritis

A

Degenerative joint disease
Cartilage destruction
Subchondral bone thickening and growth of osteophytes
No cure
Loss of articular cartilage causes new bone formation at the edges

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62
Q

What is inflammation mediated by

A

Cells of the innate immune system

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63
Q

What are the phases of normal wound healing

A

Vascular response
Lag phase
Proliferative phase
Remodelling phase

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64
Q

How is inflammation initiated

A

Platelet aggregation
Platelets activated by coming into contact with collagen or fibrin from damaged tissue or bacteria
Increase the expression of cell adhesion molecules which bind fibrin and other platelets

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65
Q

What factors are released by platelets

A

Clotting factors
Cytokines and growth factors
Chemokines
Proteases and inhibitors

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66
Q

Aside from forming a clot what do platelets do

A

Recruit neutrophils, macrophages and lymphocytes to the site of injury

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67
Q

What is the complement system

A

Chemical part of innate immune system
Classical pathway - antibody-antigen complexes
Alternative pathway - bacterial proteins

Initiates phagocytosis and cell lysis - the complement is chemotactic for leukocytes

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68
Q

What is the clotting system

A

Coagulation cascade of proteins and proteases convert fibrinogen to a fibrin clot
Activates platelets to initiate inflammation
Initiated by both intrinsic and extrinsic activation mechanisms

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69
Q

What are neutrophils

A

Decontaminating phagocytes
Secrete inflammatory cytokines
Release proteases like neutrophil elastase and neutrophil collagenase
Generate reactive oxygen free radicals to kill bacteria

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70
Q

What are macrophages

A

Highly phagocytic
Release inflammatory cytokines
Then release anti inflammatory cytokines
Release chemokines
Produce aggressive proteases to promote cell infiltration and tissue debridement

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71
Q

What is the action of phagocytic cells

A

Engulf bacteria to form phagosome
Lysosomes fuse with phagosome to form phagolysosome
Microbe killed by chemicals such as hydrogen peroxide and lactoferin before being released as fragments

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72
Q

What are mast cells

A

Resident within tissues
Activated by injury, IgE binding or by complement
Degranulate to release histamine and proteases
Synthesise leukotrines and prostaglandins from fatty acids

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73
Q

What does histamine do

A 
Chemotactic
Vasodilatory
Activated capillary endothelium
Causes increase blood vessel permeability
Oedema and swelling
Pain and itching
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74
Q

What do eosinophils do

A

Phagocytic granulocytes

Release cytotoxic granular contents to attack large targets

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75
Q

How do monocytes and neutrophils get into tissue

A

Rolling against blood vessel wall
Shedding of L-selectin - this is margination and pavementing
Adhesion to endothelium
Enters between endothelial cells by diapedesis
Migration into the tissue to phagocytose and destruct C3b coated bacteria

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76
Q

What is the NF-kB pathway

A

Resides in the cytoplasm in an inactive complex with IkB
NF-kB released from IkB
Goes to nuclease and causes gene transcription
100 NF-kB genes that relate to inflammation, lymphocytes activation and inhibition of apoptosis

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77
Q

What is the activation mechanism of the innate immune response to pathogens

A

Pathogen associated molecular patterns (PAMPS) bind to toll like receptor
Activation of NF-kB which causes gene transcription in the nucleus
Pro cytokines formed
Danger associated activation patterns (DAMPS) bind to PRR which activates caspase 1
Caspase 1 binds to pro cytokines to form activated cytokines

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78
Q

What is the arachidonic acid pathway

A

Arachidonic acid metabolism produces pro inflammatory prostaglandins, leukotrines and thromboxanes
In response to pro inflammatory cytokines, TGFb is generated and arachidonic metabolism switches to production of anti inflammatory lipoxins

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79
Q

What is TNFb

A

Transforming Growth Factor beta
Induces production of IkB
Suppressor of cytokines signalling

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80
Q

What do lipoxins do

A

Decrease - chemotaxis, transmigration, superoxide generation, inflammatory cytokines, NF-kB, proteases, endothelial cell adhesion

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81
Q

What do resolvins do

A

Decrease - leukocytes, inflammatory cytokines, NF-kB, hyperalgesia, pain, proteases, leukocyte adhesion

Increase - apoptosis, inhibitory cytokines, chemokine scavengers

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82
Q

How is resolution of inflammation completed

A

TGFb, lipoxins and resolvins - promote chemokine scavenging

  • aid phagocytosis of neutrophils
  • limit leukocyte infiltration
  • inhibit inflammatory cytokine release
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83
Q

What is the extracellular matrix

A

Surrounds, supports and regulates cells
With it life would have limited size and function with no mechanical strength or definite shape
Key regulator in inflammation
Contains collagen, elastic proteins, proteoglycans and adhesive glycoproteins

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84
Q

What are adhesive glycoproteins

A

Cell matrix interactions
Regulate cell attachment, migration and phenotype
Fibroconectin is in all tissue expect basement membrane

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85
Q

Where are elastic fibres found

A

Ligament
Skin
Blood vessels
Any tissue requiring elasticity

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86
Q

How do cells interact with each other

A

Cell to cell CAMs (cell adhesion molecules) - cadherins

Cell to matrix CAMs - integrins

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87
Q

What is the structure of cadherins

A

Extracellular adhesion
Transmembrane domain
Intracellular signalling

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88
Q

What is the structure of integrins

A

Extracellular binds matrix proteins
Hydrophobic cell membrane anchor
Cytoplasmic cell signalling

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89
Q

What diseases are associated with acute inflammation

A 
Meningitis
Tendinitis
Tonsillitis 
Appendicitis 
Laminitis
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90
Q

What diseases are associated with chronic systemic inflammation

A 
Alzheimer's 
IBS
Nephritis
Parkinson's
Arthritis 
Asthma
Atherosclerosis
Colitis
Dermatitis
Cancer
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91
Q

What are the markers of inflammation

A

Glutathione - peptide antioxidant. Marker of oxidative stress
Malondialdehyde- marker of oxidative stress
C-reactive protein- general inflammatory marker released by macrophages and adipocytes. Binds to dead cells to promote innate immunity and formation of complement
Pro inflammatory cytokines

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92
Q

What are the drivers of systemic inflammation

A 
High levels of pro inflammatory cytokines
Low levels omega 3
Hyperglycaemia
High oestrogen levels
Stress
Low serotonin
Low exercise levels and obesity
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93
Q

What is leukocyte adhesion deficiency

A

Dysfunctional inflammation
Decrease or absence of B2 integrin found on neutrophils and macrophages
Life threatening bacterial infections, chronic skin infections and delayed healing
Death as a result of sepsis

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94
Q

What is glazmanns thrombasthenia

A

Absent or defective platelet integrin
Defective platelet aggregation
Prolonged bleeding time and susceptibility to bruising

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95
Q

What effect does stress have on healing

A

Healing is slower due to increased production of cortisol

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96
Q

What does cortisol do

A 
Modifies T cell responses
Impairs fibroblast function
Increases vasoconstriction
Reduces histamine release
Reduces serotonin
Down regulates proteases
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97
Q

What is the function of skin

A

Barrier against injury, chemicals, radiation

Acts as a sensory organ, thermal regulator and determinant of external identity

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98
Q

Features of the epidermis

A 
Stratified epithelium
Cornified keratinocytes - dead cells
Basal keratinocytes- proliferative cells
Melanocytes
Langerhans cells
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99
Q

What are keratinocytes

A

Principle cell of the epidermis
Produces keratin
Maturation is in 4 layers - basal, prickle cell, granular and horny

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100
Q

What are melanocytes and langerhan cells

A

Melanocytes - in basal layer and produce melanin

Langerhans cells - antigen presenting cells which act as the first stage of the adaptive immune response to pathogens

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101
Q

Structure of the dermis

A

Separated from epithelium by basement membrane
Collagen type 1, elastic fibres and adhesion glycoproteins
Provides strength, elasticity, thermoregulation and vascular network for the epidermis
Divided into papillary and reticular layers
Mostly fibroblast cells and sensory nerve endings

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102
Q

What is the papillary dermis

A

Thin collagen fibre bundles

Rich in blood capillaries and nerve endings

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103
Q

What is the reticular dermis

A

Thick collagen fibres and elastic fibres
Gives skin it’s stretch and elasticity
Contains hair follicles and sweat glands

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104
Q

What is the structure of the hypodermics

A

Merges with dermis
Loose fatty connective tissue
Collagen fibres anchor it to underlying fascia
Adipocytes act as a store of energy, mechanical cushion and insulation

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105
Q

What are the types of wound healing

A

Regeneration - complete recovery. Superficial wounds, foetal repair and liver regeneration

Fibroblasia - recovery of function but remains distinct from undamaged tissues

Impaired healing - original function not recovered. Incomplete healing

Fibrosis- too much connective tissue. Function may be impaired

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106
Q

What are the types of repair

A

Primary - wound edges entirely apposed. Small vessels cut. Little re-epithelialisation needed

Secondary - large wound with separate wound edges. Fills with clot then granulation tissue then scar tissue. Needs extensive re-epithelialisation

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107
Q

What are the phases of wound healing

A

Vascular response
Lag phase
Proliferative phase
Remodelling phase

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108
Q

What is the vascular response to a wound

A

Constriction causing ischaemia
Increased stickiness of vessel wall
Increased vascular permeability to allow plasma proteins to leave vessel
Fluid drawn into tissue by presence of proteins in extracellular space
Platelet aggregation, complement activation and clotting
Vasodilation

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109
Q

What is the proliferative stage of wound healing

A

Fibroblasts and capillaries enter wound and proliferate to high density
Fibrin clot degraded
Provisional extracellular matrix produced in excess in prostaglandins and collagen - granulation tissue
Fibroblasts differentiate into contractile apoptotic myofibroblasts which reduce wound size
Keratinocytes contact type 1 collagen and proliferate until wound is closed, laying down basement membrane - re-epithelialisation
Keratinocytes differentiate to regenerate epidermis

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110
Q

What is the remodelling phase of wound healing

A

Granulation tissue fills wound and epithelialisation is complete
Capillary growth stopped
Fibroblasts, endothelial cells and macrophages apoptose
Recover normal skin content
Fine fibres replaced with thick fibres
In scar tissue cells are sparse and o melanocytes regenerate

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111
Q

What are the 3 stages of burns

A

First - damage to epidermis, inflammation and oedema
Second - dermis damage and separation from epidermis
Third - extensive da,age and necrosis of dermis. Graft required

Does not heal normally

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112
Q

What are the 3 stages of frost injuries

A

First - damage to epidermis
Second - damage to dermis and separation from epidermis. Capillary damage
Third - full depth damage and necrosis of dermis. Blood vessels damaged irreversibly and amputation or debridement may be needed

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113
Q

What do chemical injuries damage

A

Denaturation of proteins

Necrosis

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114
Q

What wounds have problems healing

A

Infected by viruses or fungi
Putrid infections
Pyogenic infections - MRSA
Anaerobic infections - clostridia

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115
Q

What is gangrene

A

Wet - infected wound preventing adequate venous drainage

Dry - no infection but poor blood supply and tissue hypoxic. Occurs in feet from cold, vascular dx or diabetes

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116
Q

What are the 3 types of fibrosis

A

Hypertrophic scars - tensile force applied during repair increasing matrix deposition

Lymphoedema - excess protein causing fibrotic changes

Keloid scars - proliferation of matrix deposition able to beyond site of injury. Humans only

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117
Q

What is proud flesh

A 
Horses
Overgranulation
Mechanical loading of skin not supported by underlying tissues
Distal limbs
Sx
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118
Q

What is a common element in chronic wounds

A

Tissue ischaemia

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119
Q

What are venous ulcers

A

Faulty valves in venous return

Ischaemia and repercussion injuries damage skin

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120
Q

What are pressure sores

A

Poor blood supply and reperfusion
Form on pressure points
Deep necrosis with infection

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121
Q

What are diabetic ulcers

A

Due to systemic vascular disease, neuropathy, susceptibility to infection and poor remodelling

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122
Q

What are arterial ulcers

A

Narrowing of arteries, thrombosis and diabetes causes ischaemia

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123
Q

What is the function of stem cells

A

Repair tissue damage and replace lost cells

Can differentiate into different specialised cell types

124
Q

What are the potencies of stem cells

A

Totipotent - form all types of cells and tissues
Pluripotent - can form most cells including those from all germ layers
Multipotent - many different cell types but usually only those derived from a single germ layer
Oligopotent - few cell types
Unipotent - one cell type

125
Q

What do stem cells do to prevent cell ageing

A

Add TTAGGG onto the ends of telomeres

126
Q

What are the types of stem cells

A

Tissue stem cells - limited to differentiation within that tissue
Embryonic - puri or totipotent
Induced pluripotent stem cells - genetically modified from adult cells

127
Q

What do haemapoietic stem cells differentiate into and what are their markers

A

Lymphoid progenitors- B, T and NK cells
Myeloid progenitors - macrophages, neutrophils, eosinophils, basophils, platelets, rbcs

Have CD34 and Sca-1 markers

128
Q

What do neural stem cells differentiate into and what are their markers

A

Neurones, oligodendrocytes, astracytes

PSA-NCAM markers

129
Q

What do mesenchymal stem cells differentiate into and what are their markers

A

Osteoblasts, chondrocytes, adipocytes

Hypoimmunogenic cells that have no expression of MHC I and II

STRO-1 marker

130
Q

What do intestinal stem cells differentiate into and what are their markers

A

Paneth cells, goblet cells, endocrine cells, columnar cells

ASCL2, Smoc2, Lrig1

131
Q

How are embryonic stem cells derived for medical use

A

Stem cells taken from blastocyst
Cultured in lab
Differentiation

132
Q

What are the problems of using embryonic stem cells in medicine

A

Able to form all types of cells so teratoma formation is possible leading to cancer
Ethical debate

133
Q

How can you create stem cells for medicine without using an embryo

A

Take a cell from the body and genetically reprogram it to form iPS cell
Culture in lab
Differentiation

134
Q

What are the problems with iPS cells

A

Differentiated iPS may stop being differentiated in situ so risk of teratoma formation
Not known if iPS cells are truly pluripotent
Don’t have the same immune privilege as bone marrow stem cells
Use of viral vectors to transfect genes may introduce oncogenes into iPS

135
Q

What have stem cells been used for in veterinary

A

Racehorses treated by stem cells being injected directly into diseased tendons

136
Q

What is a tendon

A

Connective tissue connecting muscles to bone

Longitudinal collagen fibres

137
Q

What is a ligament

A

Bands or sheets of connective tissue connecting bone

138
Q

Anatomy of tendons

A

White
Fibroelastic
Can withstand enormous load
Has a myotendinous junction and a osteotendinous junction

139
Q

Features of a myotendinous junction

A

Collagen fibrils of tendon interdigitate with projections of muscle cells and attach to basement membrane
Weak
Muscle cells attach to basement membrane by hemidesmosomes

140
Q

Features of the osteotendinous junction

A

Gradual merging
Tendon fibres merge with fibrocartilage then mineralised cartilage then bone
Connective tissue surrounding temdon is continuous with periosteum

141
Q

Features of the osteoligamentous junction

A

Ligament fibres merge with fibrocartilage then mineralised cartilage then bone

142
Q

What is the organisation and structure of tendons

A 
Collagen microfibrils
Fibrils 
Fibres
Primary fibre bundles
Secondary fibre bundles
Tertiary fibre bundles
Endotendon surround tertiary fibre bundles
Final tendon structure surround by epitenon
143
Q

What is the blood supply to tendons

A

Well organised but minimal vascular network

Supplied by bone and vessels in the sheath and epitenon

144
Q

What are the differences between tendons and ligaments

A

Tendons are cylindrical and have a separate sheath
Ligaments are sheets and can also be cylindrical.
Tendon fibres run in one directions, ligament fibres dont
Collagenous content of ligaments is lower than tendons
Elastic content is higher in ligaments
Less extensive blood supply in ligaments

Both 60% water

145
Q

What are the non collagenous components of tendons and ligaments

A

Elastic fibres made of elastin and fibrilin
Glycosaminoglycans
Proteoglycans

146
Q

What are the two types of tendon cells and what is their role

A 
Tenoblasts and tenocytes 
Arranged in rows parallel to collagen fibres
Regulate tendon structure and function
Remodel extracellular matrix
Tissue growth, maintenance and repair
Respond to tensile and compressive loads
147
Q

What are ligament cells called and what is their function

A

Ligamentocytes

Differ in matrix deposition in response to external stimuli

148
Q

Why do tendons fail

A

Usually fail at junctions of muscle and bone
Failure in the middle usually due to chronic tendonosis or acute tendonitis
Fatigue damage - 5% strain
Rupture - 8% strain
Overuse and injury when repeated strain causes accumulated microdamage

149
Q

Which tendon is usually damaged by horses

A

Superficial digitor flexor tendon
Core lesion of a blood filled hole in the centre of the tendon caused by tendonosis and made worse by hypoxia and poor repair

150
Q

Why do ligaments fail

A

Rupture in the middle when the strain is at a fast rate
Rupture at the bone junction when the strain is a slow rate
Already poor vasculature is disrupted so slow healing
Sprains are traumatic acute injuries

151
Q

What is extrinsic healing of tendons

A

Repair cells migrate from outside the repair tissue

152
Q

What is intrinsic healing in tendons and ligaments

A

Local migration of fibroblastic cells from surround tissue, epitenon and endotenon

153
Q

How can tendons and ligaments be replaced

A

Autografts
Allografts - rejection problem
Permanent prostheses - Fb responses, scar formation and tissue necrosis. No problem with donor site
Tissue engineering - no rejection, quality control before implantation. Difficult to replicate mechanics and micro architectures. Long rehab

154
Q

What is a Protozoa

A

Single cell eukaryotic
Nucleus
Sexual reproductive stages
Babesia bigemina or Cryptosporidium

155
Q

What are metazoans

A

Parasites
Multicellular eukaryotic organism
Complex lifecycle and sexual reproduction
Worms - haemochus contortus

156
Q

What is infectious disease

A

Caused by and agent that can spread between individuals in a population

157
Q

What is contagious disease

A

Infectious disease that is contracted by an individual who comes into direct contact with an infected individual

158
Q

How can contagious disease be transmitted

A 
Sex
Mother and offspring
Fighting or grooming
Nosocomial - contamination of environment
Oro-faecal
Aerosol
159
Q

What is vertical disease transmission

A

An infection passed from one generation to the next in utero

Pseudovertical transmission from mother to offspring in the peri natal period

160
Q

Features of parvoviruse

A

Can be contagious
Can be transmitted indirectly via fomites or environmental contamination
Resists desiccation and some disinfectants

161
Q

How do some parasites have an indirectly infectious lifecycle

A

They are eaten by another parasite which then finds a host and transfers it over

162
Q

What is an aerosol

A

Solid or liquid particles suspended in air
Very tiny particles that can spread far
Most infections target the upper respiratory tract

163
Q

What affects aerosol spread

A

Amount of the agent shed
Survival of the agent in the environment - oxygen toxic to some, UV radiation, heat
Weather conditions
Host susceptibility

164
Q

Features of SARS

A 
2-10 days incubation
7-14 days infectivity
Super shedder
No sub clinical infection
Good aerosol spread
Effective spread from physical contact
165
Q

Features of H1N1

A 
2-3 days incubation
2-5 days infectivity
Subclinical infection
Very efficient aerosol spread
Good physical contact spread
166
Q

What is foot and mouth disease

A

Non enveloped RNA virus
Need a large number for infection
Thrives in cool temperatures
Can travel 100km in air

167
Q

Features of Aujeskies disease virus

A

Pigs
Herpes virus enveloped DS DNA
Spread between farms up to 14km
Cool damp weather

168
Q

How do some pathogens spread over long distances

A

Airborne vector or host

E.g. Migrating waterfowl carry influenza

169
Q

Name some pathogens that survive in soil or slurry

A 
Enteric pathogens
E.coli - survive for months
Rotavirus - 6 months
Cryptosporidium- 3 months
Salmonella - recycling through GI tract of animals so survives in the soil
170
Q

What are mechanical vectors

A

Blood feeding insects
Transmit viruses and bacteria via saliva into blood
Does not require any of the parasitic lifestyle to take prt in the vector so some pathogens can have multiple vectors

171
Q

Signs of inflammation

A

Heat - increased local blood flow
Swelling- oedema
Redness - vasodilation
Pain - hyperasthesia of nerves

172
Q

What do neutrophils release

A

Proteases
Oxidative burst
Cytokines IL8

173
Q

What are acute phase proteins

A

Present in plasma, increased synthesis by liver in response to IL1, IL6
Serum Amyloid A - recruits neutrophils, cholesterol transport, induces enzymes for extracellular matrix proteolysis
Fibrinogen - blood clotting
Alpha acid glycoprotein - binds drugs and protein inhibitors
C-reactive protein - binds phosphocholine and assists complement binding and opsonises bacteria
Mannose binding lectin - activates complement

174
Q

What are the 4 proteolytic cascades

A

Complement system
Kinin system
Coagulation system
Fribrinolysis system

175
Q

What are the features of the complement cascade

A

Mannose binding lectin
Antigen/antibody complexes
Pathogen surfaces
Bind to C1,4,2 or 3b to form C3 convertase
C3 becomes C3a for opsonisation
C5 convertase converts C5 into C5a and C5b
C5a anaphylotoxin
C5b bind C6,7,8,9 to form Membrane attack complex which punches holes in cell membrane

176
Q

What are the features of the kinin pathway

A

Recruits and activates neutrophils
Activates monocytes and cytokines release
Release of prostaglandins - pain

177
Q

What are the features of the blood clotting cascade

A

Extrinsic pathway -damage to tissue outside the vessel. Tissue thromboplastin.
Intrinsic pathway - damage to vessel. Cascade of clotting factors.
Together these activate X
Prothrombin to thrombin
Thrombin turn fibrinogen to fibrin
Fibrin and Factor VIII form blood clot

178
Q

What are the features of the fibrinolysis system

A

Plasminogen reacts with tissue plasminogen activator to form plasmin
Plasmin converted to fibrin
Thrombin activateable fibrinolysis inhibitor creates fibrin degradation products with fibrin

179
Q

What happens when the endothelium is damaged

A

Exposed sub endothelial collagen and Von Willebrand factor
Platelets adhere to collagen
Recruits circulating vWf, collagen and factor VIII

180
Q

What do activated platelets release

A

Serotonin
VWf
ADP
Thromboxane A2 - vasoconstrictor

181
Q

How does the adaptive immune response discriminate between self antigens, non threatening food antigens and pathogens

A

Two component signal
Antigen 3D-B-cell epitope and linear Tcell epitope
PAMP - receptors of the innate immune system

182
Q

What do PAMPs do?

A

Toll like receptors on surface of monocytes

Induce signals inside the cell and discriminate between bacteria and viruses

183
Q

What does C type lectin dectin 1 do

A

Responds to fungal sugars
Stimulates dendritic cells to mature and produce IL6 and IL23
Causes monocytes to activate respiratory burst, release IL10 and CXCL2

184
Q

What are damage associated molecular pattern

A

Released by stressed cells undergoing necrosis that act as endogenous danger signals to promote the inflammatory response

185
Q

How is a fever caused

A

Production of interferon and TNFa
They bind to opioid receptors on nerve cells in hypothalamus
COX-2 activated in hypothalamus causing increased PGE2
Altered firing rate of temperature sensitive neutrons in the anterior hypothalamus
Faster they fire the higher the temp

186
Q

General points about the inflammatory response

A

Conserved response of living tissue to external threats or damage
Many different stimuli trigger an inflammatory response
Products release from dead or damaged cells also causes inflammation
If some parts of the inflammatory response are unregulated they can cause more tissue damage
First step in healing

187
Q

What is the main feature of a gram +be cell wall

A

Peptidoclycan

188
Q

What enzyme is effective against peptidoglycans

A

Lysosyme present in tears and milk

189
Q

What is a feature of gram -vet bacteria

A

Lipopolysaccharide

190
Q

How do bacteria activate monocytes

A

Monocytes bind to the toll like receptors which activate pro inflammatory cytokines

191
Q

What are the properties of activated macrophages

A

Enhanced phagocytosis
Enhanced production of reactive oxygen species
Enhanced NO production
Enhanced phagosome lysosome fusion
Increased expression of MHC
Increased production of interferons, cytokines and chenokines

192
Q

What is the oxidative burst

A

Neutrophil killing
Hydrogen peroxide produced - Not selective in what it kills
NADP oxidase and myeloperoxidase produced

193
Q

Features of macrophages

A

Long lived
Migrate to tissues in blood and lymph
Phagocytic
Adaptive response - antigen presentation

194
Q

Features of neutrophils

A 
Short lived
Stored in circulation and bone marrow 
Chemotaxis to inflamed sites
Phagocytic 
Oxidative killing
195
Q

What do tcells do

A

Recognise short peptides on antigen presenting cells
CD4 make cytokines that activate and control immune response - MHCII
CD8 kill infected cells and make cytokines - MHC1

196
Q

What does MHCII antigenic presentation do

A 
Activate CD4 helper Tcells which secrete cytokines
Direct the immune response
Activate NK cells
Help expansion of cytotoxic Tcells
Help B cell antibody production
Essential for immune system
197
Q

How does IgM antibody kill

A

By fixing complement

198
Q

Which antibodies are secreted by B lymphocytes

A

IgM and IgA

199
Q

How many IgG isotopes does the horse have

A

7
Some fix complement
Some enhance phagocytosis by binding FC receptors

200
Q

What antibacterial actions do antibodies have

A

Recognise unique surface proteins and polysaccharides
Prevent adhesion and invasion
Opsonise bacteria
Activate complement
Specific antibodies neutralise secreted endotoxins

201
Q

What bacterial virulence factors inhibit immunity

A

Capsular polysaccharides block opsonisation
Antiphagocytic M proteins
Protein A binds IgG FC and inhibits opsonisation
Bacterial toxins kill leukocytes
Coagulase converts fibrinogen to fibrin and protects from phagocytosis and complement

202
Q

How do bacteria escape macrophage killing

A 
Interfere with phagolysosome fusion - Tb
Disrupt phagosome membrane and entry into cytoplasm
Resists killing 
Prevent antibody binding
Highly variable surface proteins
203
Q

What is the immune response to viral infection

A 
Interferon
NK cells
IgM
T cells
IgG
204
Q

What is the virus induced inflammatory response in response to tissue damage and viral PAMPs

A

Epithelium releases interferon b
Fibroblasts release interferon b
Macrophages release interferon a, IL1, IL6
Tcells and NK cells release interferon y

205
Q

What do interferons do

A

Alert neighbouring cells via receptors that turn on genes to increase viral resistance
Produce enzymes that degrade RNA or inhibit protein synthesis
Increase expression of MHC
Activate immune cells
Activate NK cells
Mediate fever response and sickness behaviour

206
Q

What do NK cells do

A

Monitor cell health and MHC expression
Kill unhealthy cells
Make interferon y and are activated by interferon y
MHC receptors inhibit killing
Some receptors increase killing
Active early in viral infections
Antibody receptors act to enhance killing of infected cells later in the infection cycle

207
Q

How can viruses avoid destruction by NK cells and IgG antibody attack

A

They bud into lumen side of mucous membranes

208
Q

When viruses bud into lumen of cells how are they stopped

A

IgA antibody secreted by B cells
Transcytosed across epithelium to the lumen
Bind and neutralise virus

209
Q

Features of MHCI

A 
Expressed on all cells
Highest conc on leukocytes
Interferon increases expression
Inhibits NK cell
Presents antigen to CD8 T cells
Can only fold with a peptide in the groove
Healthy cell has a self peptide
210
Q

How does MHCI work

A 
Virus infects cell
Virus makes protein
Protein degraded by proteosome 
Small peptide translocated into E.R
MHCI fold in presence of peptide
Folded MHCI transported to cell surface
Foreign MHCI/ peptide complex displayed on cell surface
211
Q

How does MHCII work

A 
Antigen presenting cell
Ingestion of virus or cell debris
Destruction in lysosome
Assembly of MHCII with foreign peptide
Presentation of complex on cell surface
212
Q

Which antibody is associated with parasites

A

IgE

213
Q

What are host factors affecting parasite immunity

A

Age - older more resistance
Immune status
Genetics

214
Q

What are parasite factors affecting immunity to parasites

A

Life cycle
Species
Specificity
Immune modulation - evading of immune response

215
Q

What is the role of IgD in horses

A

Very early role in making B cells

216
Q

What is class switching

A

All B cells start making IgM
Switching occurs when B cells divide
Section of DNA is removed so variable region gene is linked to VDJ heavy chain
Can continue to remove DNA and switch when B cells replicate but can not change back

217
Q

How to T cells help antibodies change class

A

Th17 secretes IL17 and IL21 so IgM becomes IgG
Th1 secretes INFy so IgM becomes IgG
Treg secretes TGFb so IgM becomes IgA in gut
Th2 secretes IL4 so IgM becomes IgE

218
Q

What do macrophages release and what cells do these activate

A

INFy, IL12 - Th1 and INFy
TGFb, IL6 - Th17
IL10, TGFb - Treg
IL4 - Th2

219
Q

What are the features of IgE

A

Half life 72 hours
Binds to Fc on cell surfaces
Basophils have a variety of IgE receptors
Low levels in blood as Usually very localised - specificity needed at site so B cells switch class on arrival

220
Q

What cells is IgE found on

A

Mast cells

Also monocytes and dendritic cells

221
Q

When a parasite binds to IgE on mast cells what is released

A 
Histamine
Leukotrines
Pro inflammatory cytokines 
Proteases
Eosinophil chemotactic factor
222
Q

What do mast cells do

A

Attract and activate eosinophils

223
Q

What do eosinophils do

A 
Once activated they express IgE and IgG receptors
Release IL3' IL5, IL8, leukotrines, PAF
Peroxidase
Collagenase
Major basic protein 
Eosinophil cationic protein
224
Q

What does the vaccine for Dictyocaulus Viviparous do

A

Irradiated L3 larvae
Non patent infection
IgG, IgE, yd T-cells and eosinophils are increased in immunised animals
Immunity is not sterilising
Takes a couple of weeks for an immune response and to build up immune memory

225
Q

What is the pathology of A. perfoliata

A

Gross thickening and fibrosis
Erosion of epithelium
Acute inflammatory response IL1, IL6
Infiltration of leukocytes, mast cells, eosinophils
Sub mucosal oedema fibrosis
IgE mast cells migrate to top of epithelium

226
Q

What are vaccine adjuvants

A

Substances that enhance the immune response to an antigen
Alum enhances antigen presentation and Th2 response
Freund’s adjuvant - gram -ve Th1 response
Ribi adjuvant - gram +ve
ISCOM - stimulates Th1 and 2, cytotoxic Tcells

227
Q

What are the most relevant components of the vaccination immune response

A

Antibodies with memory Tcell and Bcell responses

228
Q

What do typical antibacterial vaccines contain

A

Bacterin

Inactivated form of bacterial toxin

229
Q

Why do many bacterial vaccines require regular boosters

A

To maintain antibody levels

230
Q

What are inactivated virus vaccines

A

Virus grown in culture or embryonated eggs
Virus harvested and inactivated
Protective responses includ serum antibody, B cells and Tcells
Inactivated virus may reduce immunogenicity of vaccine
Seen as safer for pregnant women

231
Q

What are the examples of inactivated virus vaccines

A

Rabies
Feline leukaemia
Foot and mouth disease

232
Q

How is influenza vaccine made

A

Grow virus in eggs
Extract polymers
Combine with adjuvant
Induces neutralising antibody, Bcell and T cell memory

233
Q

What are subunit vaccines

A

Contain certain virus proteins but no nuclei acid
Can extract from cultured virus, synthetic protein, recombinant protein made in lab
Relays on antibody response

234
Q

What is a live attenuated vaccine

A

Passage virus in cell culture or eggs and repeat many times
Change its characteristics so it prefers different growing conditions and becomes less virulent in target host
Can still replicate in host but not to a level that causes disease but stimulates a full immune response

235
Q

How is the bovine respiratory syncytial virus vaccine made

A

Non structural proteins 1 and 2 block interferon response
Non essential for replication in vivo
Essential for pathogenesis
Deletion mutant can infect calves but non pathogenic- still induces immune response

236
Q

Features of intranasal vaccination for bovine respiratory syncytial virus

A

Temperature attenuated so adapted to grow at low temp
Low risk
Instant effect
Stimulates full range of antibody reactions
Good local response including IgA

237
Q

What does morbidity mean

A

Proportion of animals that gets sick

238
Q

What does mortality mean

A

Proportion of animals that die

239
Q

What are the phases of disease

A

Infection
Incubation period
Clinical period
Death/recovery/chronic/carrier

Along side this is the latent and infectious period

240
Q

What are the phases in a disease outbreak

A 
Infection
Spread
Exponential sprea
Levelling off
Dying down
241
Q

Why does a disease die down

A

Lack of susceptible animals

Suitable control measures - culling, vaccination, treatment, increased biosecurity

242
Q

What does disease spread require

A

Susceptible animals
Infectious agents
Transmission from diseases animals to susceptible animals

243
Q

What model represents disease spread

A

SIR
Susceptible
Infected
Removed

Dynamic model - numbers in each class change over time

244
Q

How can SIR be used to calculate change in numbers in classes

A

Transition rate = speed that the numbers change
S–b – I – v – R
S(t)+I(t)+R(t)=N is number of animals in pop.
b = contact rate
v= recovery / death rate

Between S and I transition rate is bI
Between I and R transition rate is v
If D is duration of infection v= 1/D
N(b/v)=R0 basic reproduction number or measure of transmission

245
Q

What does R0<1 mean

A

Outbreak dies down

246
Q

What does R0>1 mean

A

Outbreak becomes epidemic

247
Q

What does R0=1 mean

A

Disease becomes endemic

248
Q

How can transmission (R0) be influenced

A

Vaccination reduces number of susceptibles - b smaller so R0 smaller
Culling reduces number of infected
- I smaller so R0 smaller

249
Q

What other models for disease are there

A

SEIR - Susceptible exposed infectious recovered
MSIR - maternal immunity, susceptible infectious recovered
Carrier state - susceptible infectious recovered carrier
SIS - susceptible infectious susceptible- diseases with non-susceptible recovery

250
Q

When is SIR not very useful

A

When there is variability such as seasons

251
Q

What is epidemiology

A

Began with the 1854 cholera outbreak in London
Study of the behaviour of disease in populations
The study of distribution and determinants of health related states in populations and use of this study to address health related issues

252
Q

What are the 5 objectives of epidemiology

A

Determination of origin of the disease
Investigate and control disease with unknown course
Gain knowledge on disease ecology and natural history
Planning, monitoring and assessment of disease control programmes
Assessment of economic effects - benefit of control programmes

253
Q

When is it possible to control disease

A 
Amount of disease presence known
Risk factors
Mode of transmission
Workable control measures
Monitoring and surveillance to keep an eye of progress
254
Q

Why do you need to assess the economic effects of disease

A

Cost of control vs cost of disease

If control costs outweigh the costs of economic loss then the need to control disease is doubtful

255
Q

What does descriptive epidemiology mean

A

Observing and recording disease and causal factors

256
Q

What does analytical epidemiology mean

A

Analysis using suitable tools and techniques such as statistics and diagnostics

257
Q

What does experimental epidemiology mean

A

Observations and analysis in controlled groups of animals

258
Q

What does theoretical epidemiology mean

A

Mathematical modelling - representation of disease simulating natural patterns of disease

259
Q

What is qualitative epidemiology

A

Natural history of disease
Causal hypothesis testing leading to investigation of causal factors and sources of infection
1st stage of epidemiological investigation

260
Q

What is quantitative epidemiology

A

Measurement

261
Q

Features of an epidemiological survey

A

Quantitative
Examination of an aggregate of units
Usually a sample of a population
Cross sectional - events at a particular point in time
Longitudinal- events over a period of time
Screening - looking for healthy animals that appear to carry disease

262
Q

What are the features of epidemiological monitoring and surveillance

A

Monitoring - routine observations on health, production and environment
Surveillance - collation and interpretation of monitoring data to identify changes in population health status

263
Q

Features of epidemiological studies

A

Comparing groups of animals where they have things in common but also are different
Experimental - purposely put together - clinical trials
Observational - naturally occurring disease in the field. Crossectional - animals categorised according to presence of disease and factors. Case-control - compare healthy with diseased group. Cohort - compare groups with and without causal factor and measure prevalence of disease

264
Q

What are the features of epidemiological modelling

A

Mathematical modelling using equations

Using biological simulation such as experimental animals simulating pathogenesis of disease

265
Q

What does Koch say about causality

A

Present in all cases of disease
Not present in another disease as a non pathogenic organism
Can be isolated and transferred to cause disease in another animal

266
Q

What are Evan’s rules

A

Proportion with disease significantly higher in exposed than in not exposed
Exposure to cause more common in those without disease but with constant risk factors
Number of new cases sig. higher in exposed than not exposed
Bell shaped curve of disease following incubation
Spectrum of host responses following exposure
Measurable host response following exposure
Experimental reproduction with greater frequency in exposed
Elimination or modification decreases frequency
Prevention or modification of hosts response decreases disease

267
Q

How is causality determined

A

Epidemiology studies association between caus, risk factors and disease
Association needs statistical significance
Studies on groups of animals
Group size determined by level of expected difference between exposed and non exposed

268
Q

What are the two types of association

A

Non-statistical - agent can be found in animals both with and without disease

Statistical - noncausal and causal. Causal can be directly or indirectly associated
Eg. A causes b and c but b+c not necessarily associated with each other so connection is non causal
A can cause dehydration via diarrhoea so that association is indirectly causal

269
Q

What does endemic mean

A

Disease constantly present in population

Kennel cough

270
Q

What does epidemic mean

A

Disease present in much higher than expected numbers

FMD 2001

271
Q

What does pandemic mean

A

Widespread epidemic affecting a large proportion of population
HIV

272
Q

What does sporadic occurrence mean

A

Happens only irregularly

Rabies

273
Q

What does prevalence of disease mean

A

Number of instances of disease in known population

P= no. People with disease / number of individuals in population at risk at that time

274
Q

What does incidence of disease mean

A

Number of NEW cases occurring in a known population over a specified period

I = no. New cases in a certain period / sum of length of time all individuals were at risk

Cumulative incidence - number of non diseases cases becoming sick during period

CI = no. Animals becoming sick during period / number of healthy animals present at start of incidence

275
Q

What is One Health

A

Worldwide strategy for expanding interdisciplinary collaborations and communications in all aspects of health care for humans, animals and the environment

276
Q

How is the one health vision achieved

A

Education
Communication
Clinical care of cross species disease
Cross species disease surveillance and control
Better understanding of cross species transmission
Development and evaluation of new diagnostic methods, medicines and vaccines
Inform and educate political leaders

277
Q

Why is One Health important

A

World population increasing so contact with wild animal habitats increases so risk of exposure to new disease
Increasing awareness, knowledge, and understanding of interdependency of health of humans, animals and the environment.
Growing bond with animals
Need protection of food from disease, contamination and acts of terrorism
Contamination of waters by personal care products and pharmaceuticals
Antimicrobial resistance does not distinguish between man and animal

278
Q

What are the benefits of One Health approach

A

Improve animal and human health globally with collaboration of all health sciences
Developing centres of education through enhanced collaboration between schools
Increases professional opportunities
Adding to scientific knowledge for innovative programs to improve health

279
Q

What risk factors create the perfect microbial storm

A 
Adaptation of microbes
Global travel and transportation
Host susceptibility 
Intent to do harm
Climate change
Economic development and land use
Human demographics and behaviour
A breakdown of both public and animal health infrastructures
Poverty
Social inequality
280
Q

Give examples of non communicable conditions and risks crossing species

A

Among pets, pet owners and their children
Obesity
Exposure to second hand tobacco smoke

281
Q

Where does One Health enter the practice

A

Awareness of infectious and non infectious diseases
Info,ration for customers, pet owners and farmers on disease and zoonotic disease risks
Occupational health hazards
Cooperation where applicable
Responsible use of veterinary antimicrobials
Encompasses mental health through human animal bond

282
Q

Give some examples of vet-human cooperation

A

Rabies introduction from abroad - vet practice is port of call. Subsequently human world involved
West Nile virus US - jackdaw walked into A&E and dropped dead

283
Q

How does avian influenza spread

A

Aquatic birds to poultry, horses and pigs
Poultry also spread to pigs
Pigs spread to humans

284
Q

What is Ecchinococcus granulosus

A

Dog tapeworm
Hydatid cyst of ruminants, horses and humans
Sheds segment full of eggs then grows a new one

285
Q

What is BSE

A

Nervous disease in cows

Causes vCJD in humans if eat nervous system of cows

286
Q

What organisations are involved in One Health

A

WHO
World Organisation for Animal Health
Food and Agriculture Organisation of the United Nations
National governments
National and international medical and veterinary organisations

287
Q

What do you need to know about infectious diseases

A

Source
Risk factors for getting disease
How to prevent

288
Q

What does virulence mean

A

Degree of pathogenicity within a group or species of parasites as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host

289
Q

What is disease risk

A

The likelihood of occurrence and likely magnitude of biological and economic consequences of a disease to animal or human health

290
Q

What is a risk factor

A

Characteristic of a host, pathogen, time or environment that influences risk of disease

291
Q

What is serological epidemiology

A

Investigation of disease and infection through measurement of variables in serum
Minerals, trace elements, hormones,enzymes, antibodies

292
Q

Why test for antibodies

A

Provides evidence of current exposure and previous exposure
Efficient and cheap
Serology can be used to quantify level of antibodies - keep diluting, the longer you can the higher the conc of antibodies in the blood originally

293
Q

What is the antibody prevalence in an individual

A

Detectable antibody - animal exposed to antigen
Levels decline without rechallenge - the half life depends on the antibody
Need a cutoff point to determine if an animal is +vet or -ve for an antibody
Two samples taken with a time interval may show rise in serum levels

294
Q

Features of serological tests and antigen

A

Tests for determination of types of antigen in serum
-produced by pathogenic microorganisms
- triggers antibody response by host
- specific for species and type of microorganism
Bigger the ability of test to distinguish between variety of species / type the bigger the analytical specificity

295
Q

How accurate are serological tests

A

Can cause false positives and negatives
False + - group cross reaction, non specific inhibitors, non specific agglutins

False - - natural or induced tolerance, improper timing, improper test selection, non specific inhibitors, antibiotic induced immunosuppression, incomplete antibody, insensitive tests

296
Q

What does test sensitivity mean

A

Number of true positives

297
Q

What does test specificity mean

A

Number of true negatives

298
Q

Why is specificity and sensitivity of serological tests important

A

Low sensitivity means too many false positives which can cause many animals to be unjustly treated or killed
If specificity too low then too many false negatives and diseased animals stay in the population and don’t receive proper treatment. Increased risk of spread

299
Q

Why is there a difference between specificity and sensitivity in tests for disease control and clinical disease

A

Disease control needs to distinguish between positive and negative animals
Clinical disease needs to distinguish between diseased animal and animals with similar conditions

300
Q

How are sensitivity and specificity calculated

A

Need information of true status
Have a known test with known result e.g. Post mortem
Derive negative samples from known negative populations e.g. Brucellosis free herds

Express results in a 2x2 table
Ideal test would have 0 false positives or negatives
True positive status / (positive test and false negative test) = sensitivity
True negative status / (false positive test and negative test) = specificity

301
Q

What is the predictive value

A

Depends on sensitivity and specificity and prevalence
Gives a proportion or %
Tells us have big the probability is that a test positive animal is truly positive

Probability of a positive test = positive test / (positive + false positive)
Negative = negative test / negative + false negative

302
Q

Why is specificity and sensitivity important depending on prevalence

A

High prevalence - low sensitivity not a problem
Low prevalence - tests with higher sensitivity needs to be used
Consequences for costs of control as low predictive value may mean many false positives

303
Q

What is a likelihood ratio

A 
LR+ is ratio of population of affected individuals that test positive and the proportion f healthy animals that test positive
(a/(a+c))/(b/(b+d))
a = positive animals test positive
b= negative animals test positive
c= positive animals test negative
d= negative animals test negative
304
Q

2x2 table to show not all animals show sign of disease

A

Infection. Present. Absent
Present. Clinical dx subclinical dx
Absent Sequellae. Healthy

305
Q

What happens when clinical signs last longer than infectivity

A

No pathogen present

Determines what diagnostic test to use

306
Q

What does infectivity mean

A

Evidence of an infectious agent

307
Q

What is the attack rate

A

The proportion of a defined population affected during an epizootic

Finals (3 decks)

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