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Leah GIL > Week 6 > Flashcards

Week 6 Flashcards

1
Q

Define immunological memory

A
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2
Q

What is the role of lymph nodes

A

filter & trap pathogens

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3
Q

What is the role of the spleen

A

filter blood
remove damaged RBCs
store platelets

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4
Q

What is the role of tonsils

A

first-line defence against ingested or inhaled pathogens

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5
Q

What is the role of thymus

A

maturation & education of T cells

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6
Q

What is the role of bone marrow

A

site of blood cell production (including lymphocytes)

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7
Q

What is the role of Peyers patches

A

important for gut associated lymphoid tissue (GALT) & immune response in digestive system

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8
Q

Describe major histocompatibility complex

A

MHC1 presents intracellular antigens to cytotoxic T cells

MHC2 presents extracellular antigens to helper T cells

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9
Q

Explain the roles of cytokines

A
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10
Q

Explain MHC class 1

A
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11
Q

Explain MHC class 2

A
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12
Q

What are the roles of T lymphocytes

A
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13
Q

What are the roles of B lymphocytes

A
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14
Q

What is GALT

A

Lymphoid tissue associated with lining of intestinal tract

Located immediately below epithelium of mucosal tissue

Primary lymphoid organ in ruminants (B cell proliferation)

Secondary lymphoid organ in other species

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15
Q

What does GALT contain

A

organized structures such as:
- Peyer’s Patches (PP)
- isolated lymphoid follicles
- Cryptopatches (aggregates of lymphoids)

scattered lymphocytes (intra-epithelial & in lamina propria) in intestinal villi

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16
Q

Where can Peyer’s patches be found

A

Located in jejunum and ileum

They can be visible inside lumen of intestines during inflammation

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17
Q

Describe peyers patches in group 1 species (ruminants, pigs, horses, dogs, humans)

A

Ileum
- 80-90% of Peyer’s Patches
- Form single continuous structure that extends forward from ileocecal junction
- Densely packed lymphoid follicles, contain only B-cells
- Reach maximal size & maturity before birth (prior to encounter of gut microbiota)

Jejunum
- Multiple discrete accumulations of follicles
- Persist throughout life
- Mainly B-cells, up to 30% T-cells

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18
Q

Describe peyers patches in group 2 species (rabbits, rodents)

A

Peyer’s Patches located at random intervals in ileum & jejunum

Development starts 2-4 weeks after birth & persist into old age

Development dependent on gut microbiota

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19
Q

Label the Peyers patches histology

A
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20
Q

Name the immunocytological content of GALT

A

Intestinal villi
- intraepithelial lymphocytes & lymphocytes in lamina propria

Peyers patches

Follicle associated epithelium
- M cells in between villous epithelium

sub-epithelial dome
- dendritic cells, macrophages, neutrophils, B & T cells

interfollicle areas
- T cells

follicle areas with germinal centres
- B cells

Lamina propria
- T cells

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21
Q

Describe M cells (part of GALT)

A

Regular distribution of M cells across follicle associated epithelium

Have apical microfolds with adhesion molecules (so antigens can be transported)

M-cells sample antigens & transport them to basolateral pocket to facilitate contact with immune cells on other side of barrier

They are transporter cells which transport antigens to dendritic cells which can present the antigen to lymphocytes

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22
Q

Compare Peyer’s patches to lymph nodes

A
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23
Q

Describe antigen sampling in GALT

A

Follicle associated epithelium sample soluble antigens

M cells & dendritic cells sample particulate antigens (eg bacteria)

Antigen is captured by dendritic cells & presented to T cells (in local LN if naïve animal)

Antigen specific T cells will be activated by second co-stimulatory signals

Activated Th cells secrete cytokines
- Promote differentiation & proliferation of:
*B cells –> plasma cells
*T cells –> CTL

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24
Q

How do lymphocytes of GALT stay at site of infection if infection is intestinal?
(Activated T & B cells normally recirculate from PP to LN into circulation)

A

During infection, mucosal adhesion molecules are upregulated on local endothelial cells

Activated T cells express mucosal adhesion receptor (done by dendritic cells)

As antigen specific lymphocytes re-circulate through local LN & site of infection, they adhere & remain at local site (& all other mucosal tissue) ie homing

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25
Q

Describe mucosal B-lymphocytes in GALT

A
  1. B cells are activated by cytokines from Th lymphocytes
  2. Differentiate into plasma cells
  3. IgM secreted first (but very large & vulnerable to intestinal enzymes)
  4. Cytokines stimulate plasma cells to class switch their antibody isotype from IgM to secretory IgA (protected from enzymatic digestion)
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26
Q

What are the 2 isotypes of IgA

A

IgA1 - predominant IgA subclass found in serum

IgA2 - predominant IgA subclass found in secretory lymphoid tissues e.g., GALT
- Secretory component is added to IgA antibody in lamina propria as it passes through mucosal epithelial cells
- –> protected from enzymatic digestion

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27
Q

Describe how the secretory component is added to IgA in GALT

A

Secretory IgA captures antigens in lumen:

  1. IgA binds to receptor on basolateral aspect of epithelial cell
  2. IgA-receptor complex is internalised into epithelial cell
  3. IgA-receptor complex is translocated to apical aspect where secretory component is wrapped around IgA molecule
  4. On mucosal surface of cells secretory IgA is either released into lumen or captures antigen directly
  5. Secretory IgA interferes with binding of pathogen to receptors on the epithelial cells to prevent pathogen invasion
    - –> Immune exclusion rather than immune elimination
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28
Q

Describe IgG in GALT

A

Mucosal immunity also stimulates IgG production in circulation which can go into lumen but…
Mostly in serum & lamina propria

Neutralises bacterial toxins
- limit toxic effects

Opsonises invading pathogens, enhancing their phagocytosis or complement mediated lysis
- reduce numbers or eliminate pathogen
- –> Immune elimination

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29
Q

Name some parasites that exploit M cells & use them as portals of entry into body

A

Salmonella

Listeria

Yersinia

Some E. coli

Rotavirus

Cryptosporidium

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30
Q

Define hypersensitivity

A

when an animals immune response reacts to normally innocuous environmental antigens

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31
Q

Define type 1, 2, 3 & 4 hypersensitivity

A
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32
Q

Describe the phases of type 1 hypersensitivity

A

phase 1:
- sensitisation phase (no clinical signs yet)
1. allergen exposure via respiratory or skin
2. antigen presenting cells capture antigens
3. causes naive T cells to differentiate
4. release cytokines causing B cell proliferation
5. class switch for B cells from IgM to IgE
6. IgE binds to mast cells

phase 2:
1. same allergen encountered
2. primed IgE coated mast cells bind to antigen of allergen
3. release of cytoplasmic granules
4. immediate hypersensitivity - pruritis, broncho-constriction, oedema

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33
Q

Describe anaphylaxis (example of type 1 hypersensitivity)

A
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34
Q

What kind of hypersensitivity is atopic dermatitis in cats

A

type 1 hypersensitivity

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35
Q

Describe type 2 hypersensitivity

A
  1. mediated by IgG antibodies that recognise antigens on cell surface
    - intrinsic or extrinsic antigens
  2. activates classical complement pathway
  3. destruction of cells (phagocytosis)
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36
Q

How is type 2 hypersensitivity different to type 1

A
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37
Q

Describe Myasthenia Gravis (example of type 2 hypersensitivity)

A
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38
Q

Describe type 3 hypersensitivity

A
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39
Q

Describe equine recurrent airway obstruction (RAO) (example of type 3 hypersensitivity)

A
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40
Q

Describe canine blue eye (example of type 3 hypersensitivity)

A
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41
Q

Describe type 4 hypersensitivity

A
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42
Q

How is TB (type 4 hypersensitivity) diagnosed?

A
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43
Q

What are the 5 main clinical signs of inflammation

A
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44
Q

Describe chronic inflammations

A

Can occur if there is no return to steady state conditions following acute inflammation

Often infectious cause, may be immune mediated
- e.g. chronic colitis/inflammatory bowel disease in dogs
- –> Constant immune output occurs

Granuloma may form –> e.g. enteric granuloma seen commonly in ruminant Johne’s disease (paratuberculosis)

Granuloma may take long time to develop & is e.g. of delayed type hypersensitivity (Type IV) response

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45
Q

give examples of causes of chronic inflammation

A

Autoimmune disorders
- e.g. diabetes, rheumatoid arthritis, IBD

Exposure to toxins
- e.g. pollution, exposure to chemicals

Chronic exposure to irritant or foreign material
- e.g. foreign body granuloma

Auto-Inflammatory (Hyper-Inflammatory) Syndromes
- Hyper-inflammatory Syndrome in Weimaraner

Infection
- e.g. bacteria:
* e.g. gingivitis, Johne’s disease

Trauma
- e.g. injury

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46
Q

Give some examples of both

A
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47
Q

Describe granuloma formation

A
  1. Macrophages (Histiocytes – macrophages in tissues) fail to clear foreign agent & become chronically infected
  2. Activated macrophages constantly secrete TNF-α & other proinflammatory cytokines which promote influx of T-cells
    - Removing TNF-α causes breakdown of granuloma
  3. T cells around periphery secrete IFN-γ
  4. Stimulated macrophages can further mature into epithelioid cells
  5. Epithelioid cells sustain granuloma
  6. Prolonged stimulation leads epithelioid cells to fuse together & form multinucleated ‘Giant Cells’ or Langhans cells
  7. Giant cells are capable of phagocytosis & cytokine secretion
  8. T-cell & macrophages stimulate fibroblasts promoting fibrosis which can lead to organ damage
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48
Q

What are the pros and cons of granuloma formation

A

pros:
1. Granuloma form focal killing point in which micro-organisms may eventually be killed
2. Granuloma prevent dissemination since it ‘walls off’ micro-organisms

cons:
1. Break-down of granuloma can have serious effects since bacteria can disseminate
2. Granuloma may cause severe tissue necrosis & hence affect organ function
3. Granuloma can cause fibrosis & tissue thickening impairing organ function

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49
Q

What is Chronic enterocolitis in dogs & cats

A

Chronic Diarrhoea (>14 days)

Causes:
- Idiopathic
- Chronic infection
- Allergic response (e.g. food)
* –> thus, immunosuppressive therapy may be effective
- May be a genetic component

Although granuloma may not be present, cytokines & immune cell infiltrate & maintain chronic inflammatory state

Chronic enteropathy is most common gastrointestinal disorder in older cats, with rising prevalence over past decade

Classified into 4 forms

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50
Q

What are the 4 Forms of chronic enterocolitis in dogs & cats

A
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51
Q

Describe lymphocytic plasmocytic enteritis (form of chronic enterocolitis in dogs & cats)

A

Most common form of chronic enterocolitis in dogs & cats (commonly middle aged)

Characterised by increased lymphocyte & plasma cell infiltrate into lamina propria (Ileum & colon common)

In cats it may be difficult to differentiate from small cell lymphoma

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52
Q

Describe eosinophilic (gastro)enteritis (form of chronic enterocolitis in dogs & cats)

A

Less common that lymphocytic plasmocytic enteritis

No. of different breeds- usually younger animals

Infiltrate is predominantly eosinophils

Chronic parasitic infections/allergy e.g. food.

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53
Q

Describe neutrophilic colitis (form of chronic enterocolitis in dogs & cats) & causes

A

Neutrophil infiltrate

Possible causes:
- Idiopathic
- Response to normal bacterial microbiota
- Invasion of Campylobacter spp
- Trichomonas foetus infection

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54
Q

What is Hypereosinophilic syndrome in cats?

A

A variant of eosinophilic enteritis

Overproduction of eosinophils in bone marrow

Widely disseminated eosinophilic infiltration of multiple organs

Organs commonly affected include:
- Bone marrow
- Small intestine
- Liver
- Spleen
- mesenteric & peripheral lymph nodes
- Skin lesions

Poor prognosis

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55
Q

Describe granulomatous colitis (form of chronic enterocolitis in dogs & cats)

A

Rare - Seen in young Boxer dogs, French bulldogs

Thickened, partially obstructed segment of bowel (ileum & colon most commonly)

Large foamy, Periodic acid-Schiff (PAS) +ve macrophages present in colonic mucosa (pro-inflammatory macrophage type)

True granulomas are not present.

Caused by E. coli

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56
Q

What are the methods of antigen sampling in gut

A
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57
Q

How are lymphocytes recruited to peripheral lymphatic organs such as GALT?

A

Lymphocytes leave LN, enter blood, then emigrate back from capillaries to intestine

Addressins (adhesion molecules) on high endothelial venules interact with homing receptors on lymphocytes to ensure they reach mucosal surface

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58
Q

How is bacterial DNA recognised in mammals

A

Bacterial DNA CpG dinucleotides are un-methylated

Most mammalian CpG di-nucleotides are methylated

TLR-9 in mammals recognises un-methylated CpG in bacterial DNA & initiates inflammation

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59
Q

Describe bacterial chromosomes & plasmids

A
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60
Q

Describe plasmids

A

Typically circular

DsDNA

Separate from the chromosomal DNA

Some have a suicide gene to ensure maintenance

Some are transmissible by conjugation

Variable in sizes

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61
Q

Describe bacterial replication

A

Binary fission

They have a generation time
- Length of time required for single bacterial cell to divide to 2 daughter cells

Binary fission leads to clones of bacteria

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62
Q

If bacterial replication leads to clones how do bacteria evolve?

A

Mutation of genes

Transfer of genes

Rearrange their DNA

Delete genes

New genes inserted

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63
Q

What are the methods of transferring genes between & within bacteria

A

Introduction of new DNA into and between bacteria:
- Transformation
- Conjugation
- Transduction
- Recombination

Movement of DNA already in bacteria:
- Transposition
- Recombination

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64
Q

Describe transformation in bacteria

A

Transformation is the uptake of naked DNA

DNA contacts the bacteria and is taken up

Some bacteria are…
- Naturally competent. They can take up DNA without treatment. Have competence mechanisms
- Require treatment to become competent (laboratory competent)

Once naked DNA is taken up into cells there are two options:
- It is degraded by nucleases
- It recombines into the genome

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65
Q

Describe conjugation in bacteria

A

Bacterial conjugation is transfer of genetic material between bacteria through direct cell-to-cell contact (horizontal gene transfer)

It’s transfer of genetic information from a donor cell to a recipient

donor must host conjugative or mobilisable genetic element (plasmid or transposon)

Most conjugative plasmids have systems ensuring that recipient cell doesn’t already contain similar element

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66
Q

Describe transduction by bacteriophages

A

Viruses that infect bacteria are known as bacteriophage

Each virus is specific for a specific species of bacteria

They need to bind (specific receptor)

Then inject their genome and this infects the bacteria

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67
Q

What are the types of bacteriophage & transduction

A

Lytic and generalised transduction

Temperate phage and specialised transduction

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68
Q

Describe generalised transduction by lytic bacteriophage

A

Process by which any bacterial DNA may be transferred to another bacterium via a bacteriophage

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69
Q

Describe specialised transduction by lysogenic bacteriophage

A

Lysogenic (viruses that insert their DNA into bacterial chromosome)

Bacterial genes that get transferred depend on where phage genome is inserted on chromosome

When prophage excises it may do this imprecisely or package adjacent bacterial DNA

These packaged particles can then infect another bacteria with bacterial DNA

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70
Q

What happens to DNA that enters bacteria

A

Degraded – non specific (no recombination general nucleases degrade DNA)

Degraded – by specific restriction endonucleases (DNA restriction)

It manages to integrates with genome (DNA recombination)

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71
Q

Describe Homologous, directed & non-homologous recombination/insertion

A

Homologous recombination - Where 2 DNA sequences are same they can intercalate their strands. During replication these can get spliced

Non homologous – less efficient, DNA doesn’t match but can be in random positions

Directed - Insertion elements have repeats which lead to homologous/directed insertions in specific sites or enzymes that direct integration at set sites
- These have hot spots for insertions & are more effective

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72
Q

What is DNA restriction in bacteria

A

It’s not good for bacteria to constantly take up DNA so they have restriction system

They have Restriction endonuclease(s)

Which degrade DNA not made in their own cell

These restriction nucleases don’t degrade self-DNA as they act on specific sites

Bacteria methylates its own DNA where its own restriction nuclease cut so blocking enzyme (They don’t chew up their own genome)

Works on any DNA including non-self plasmids

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73
Q

What are frameshift mutations

A

Either addition or loss of single base moving reading frame in an out of position

Frame shift adds or removes base to change codon position relative to reading frame

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74
Q

What is transposition

A

Transposons are sequences of DNA that can move around to different positions within genome

Transposons encode their own transposases

Transposase cut out & re-insert the DNA flanked by inverted repeats (IR)

The process directed by these enzymes is transposition

They pop into (integrate) and out of DNA

If they insert into a gene they will disrupt it

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75
Q

What are insertion sequences

A

IS elements are a type of transposon. They are….
- short DNA sequence that acts as simple transposable element
- are small relative to other transposable elements
- only code for proteins implicated in the transposition activity
- are different from transposons, which carry accessory genes

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76
Q

What is the clinical relevance of mutations

A

If a mutations is beneficial to bacteria this will become more fit

Alteration of antibiotic binding sites
- E.g. mutations ribosomal binding sites can reduce binding of ribosome targeting drugs

Avoidance of vaccines
- If mutations alters amino acid sequence of epitope that antibodies bind to then this can reduce or abrogate binding

Alteration of metabolism
- Can be no. of reasons mutations in promotors can upregulate or down regulate critical functions. Making bacteria less or more competitive

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77
Q

Define genetic drift

A

Changes of over time by mutations of genomes

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78
Q

What are antimicrobial growth promoters and what is the problem with them

A

substances added to the feed or water of animals to promote growth and improve feed efficiency

Prolonged and large scale use will select for antibiotic resistance

Leading to a reservoir of transferable antibiotic resistance

Banned in UK and EU

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79
Q

Describe bacterial metabolism of xenobiotics (drugs)

A

Gut flora bacteria can transform (alter) compounds. This can have different effects
- Drugs activated
- Drugs inactivated
- Toxic metabolites (and carcinogens)

Different compounds in food can also alter composition of gut flora
- Can lead to increased bacteria associated either with ‘improved’ or ‘reduced’ gut health

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80
Q

What are methods used to enumerate bacteria

A

Qualitative
- General assessment of level low, med, high

Quantitative
- Enumeration normally vs. volume or weight

Visual examination
- microscopy total count or general assessment

Culture:
- Viable counts where you dilute count colonies & calculate original no. of bacteria

Molecular detection
- Detecting species by quantitation of their nucleic acid

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81
Q

What are methods for assessing presence of bacteria

A

Slides/smears
- May work for some very characteristic spirochetes but rods & cocci can’t be distinguished in faeces
- Useful in discrete normally body sites/tissues where you would expect sterility or only single common morphologies (you can spot abnormal types or mixed infections)

Culture:
- For faeces, the most common method is culture.

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82
Q

What can impact gut flora

A

Age

Stress

Use of drugs

Genetics

Diet

Illness

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83
Q

What genes are essential for bacterial colonisation

A

Surface structures, for adhesion and stop wash out

LPS and membrane integrity for tolerance of harmful factors

Motility to get to target niches

General gene regulation for stress responses to turn on genes required to adapt to GI-environment

Specific transporters to take up GI-specific nutrients

84
Q

What is natural competitive exclusion and competitive exclusion products

A

“Natural” competitive exclusion: Existing bacterial flora present competitive barrier to incoming bacteria so can exclude & prevent colonisation &/or infection

Competitive exclusion products: Deliberate use of desired microbial cultures to colonise animals that out-compete pathogens from colonising specific niches (so can exclude & prevent colonisation &/or infection)
- Applied commercially

85
Q

Describe competitive exclusion

A

Presence of one bacteria inhibits other due to it competing & winning in acquisition of growth factors

‘Nutrition’ is NOT free

There is Competition (for….)
- Space
- co factors elements etc..
- Electron acceptors (Humans Oxygen)
- Carbon sources

Only compete if they require same type of nutrition

86
Q

Describe how antibiotics can disrupt flora

A

Antimicrobials can remove sensitive organisms from a particular niche

Space left is then repopulated by intrinsically resistant bacteria

Thus antibiotics can disrupt existing flora or allow over growth of undesirable organisms

87
Q

Name viruses that cause major clinical signs associated with GI tract

A
88
Q

What are key features of parvoviruses

A
89
Q

What are parvoviruses of veterinary importance

A
90
Q

Describe feline parvovirus infection

A

also known feline infectious enteritis (FIE) or feline panleukopenia

faecal-oral transmission

infects lymph nodes of naso- & oro-pharynx & then spreads to other tissues
- needs rapidly dividing cells to propagate

then infects intestinal cells & bone marrow

kittens most susceptible

91
Q

Describe parvoviruses pathogenesis

panleukopenia, enteritis & cerebellar hypoplasia

A
92
Q

What are the clinical signs & treatment of feline parvovirus

A
93
Q

How is feline parvovirus controlled

A
94
Q

How is feline parvovirus diagnosed

A
95
Q

Describe canine parvovirus 2 infection

A
96
Q

Describe corona viruses

A

enteric & respiratory pathogens

commonly mutate

97
Q

Describe transmissible gastroenteritis virus (TGEV) (porcine corona virus)

A
98
Q

Describe porcine epidemic diarrhoea virus (PED) (porcine corona virus)

A
99
Q

Describe Porcine delta coronavirus (PDCoV) (porcine corona virus)

A
100
Q

Describe swine acute diarrhoea syndrome coronavirus (SADS-CoV) (porcine corona virus)

A
101
Q

Describe betacoronaviruses (bovine corona virus)

A
102
Q

Describe canine coronavirus

A
103
Q

Describe feline coronavirus

A
104
Q

What are the 2 main forms of feline infectious peritonitis

A

wet FIP
- effusions

dry FIP
- pyogranulomatous lesions

105
Q

What might lead you to suspect a case of wet FIP (feline infectious peritonitis)

A
106
Q

What are the features of pestiviruses

A
107
Q

Describe bovine viral diarrhoea virus (pestivirus)

A

Causes:
- diarrhoea
- decreased fertility/milk yield
- abortion/congenital defects
- immunosuppression
- mucosal disease

2 genotypes:
- BVDV 1 - classical form of disease
- BVDV 2 - haemorrhagic syndrome (severe acute BVD)

108
Q

Describe epidemiology of mucosal disease (BVDV)

A

BVDV can cross placenta

infection during pregnancy may have various effects on foetus
- if infected before development of foetal immunocompetance calf aborted or PI calf
- if infected after calf aborted or born with congenital defects

mucosal disease only develops in PI (infected in utero) animals around 2 years of age
- invariably fatal

109
Q

How is BVD (bovine viral diarrhoea) controlled

A
110
Q

Describe the structre of paramyxoviridae

A
111
Q

describe rinderpest virus (Morbillivirus) & its clinical signs

A

cattle plague
highly infectious
respiratory & alimentary tract disease
high mortality

clinical signs:
- nasal discharge
- pyrexia
- oral & nasal erosions & ulcerations
- diarrhoea with mucus, blood & debris
- dehydration

112
Q

describe canine distemper (morbilillivirus)

A

young dogs
transmitted by direct contact
replicates in urinary tract
spreads to tonsils & lymph nodes & then CNS

clinical signs:
- pyrexia
- depression
- ocular & nnasal discharge
- vomiting
- diarrhoea
- hyperkeratosis of nose/pads
- neurological signs if poor immune response

113
Q

Describe Newcastle disease

A
114
Q

What are some strains of Newcastle disease

A
115
Q

What are viral membrane glycoproteins

A
116
Q

Compare lentogenic & mesogenic strains of Newcastle virus

A
117
Q

How is Newcastle disease diagnosed

A
  1. egg inoculation
  2. harvesting allantoic fluid after 7 days
  3. Haemagglutination test to detect viruses in allantoic fluid
118
Q

How is Newcastle disease controlled

A
119
Q
A

acid-fast staining

120
Q

Describe method of staining Mycobacteria (acid-fast staining)

A
121
Q

How long do Mycobacteria take to grow & what problem does this pose for diagnosis?

A

slow (2-16 weeks)

takes very long to culture so disease can spread while waiting

122
Q

what is Johne’s disease

A
123
Q

What are the clinical signs of Johnes disease?

A
124
Q

What are the clinical characteristics/pathogenesis of Johne’s disease?

A
  1. MAP colonises in intestinal epithelial cells by attaching to surface receptors
  2. body forms granulomas to attempt to contain infection
  3. causes disruption of normal digestive functions & leads to malabsorption
  4. intestinal mucosa becomes damaged which leads to diarrhoea
  5. contributes to weight loss
125
Q
A
126
Q

Describe oesophageal infections

A

Relatively uncommon due to rapid passage of material through oesophagus & tough stratified epithelium

Some viral infections can cause ulcers

Most notable infections:
- BVDV (Bovine viral Diarrhoea virus) & mucosal disease (Ovine Herpes virus 2)
- Newcastle disease in poultry

127
Q

How can infections spread from GIT to other body systems

A

Liver & spleen, GI Tract is a route for infection
1. Portal vein
2. Hepatic artery (billiary system)
3. Contagious spread from adjacent system

128
Q

Describe Campylobacter jejuni

A

Zoonotic

Associated with diarrhoea in dogs

Gram negative

Flagellated and Motile

Microaerophilic

Optimum growth temperature for C. jejuni is 42ºC.

Grown on nutrient media or isolation using Campylobacter selective medium

Can be seen as commensals in intestinal tract of warm-blooded animals

The genera contains a number of species
- C. jejuni, C. coli, C. lari

Important because it is a common contaminant of meat

129
Q

How can GI tract diseases enter food chain

A
130
Q

How can campylobacter be identified (sample collection)

A

Samples depending on stage of production

On farm:
- Environmental samples
- Faecal swabs
- Boot swabs

At abattoir:
- Gut contents
- Neck Swabs from birds
- Skin samples

At retail:
- Swabs
- Juice from meat packages
- Whole meat samples

131
Q

What is Multi Locus Sequence Typing (MLST)

A

MLST looks at single base pair changes

Done by sequencing 7 housekeeping (essential) genes & clustering strains based on differences

These clusters are called clades

Researchers have collected lots of strains from different sources & compared their MLS

So if clinical isolate clusters in MLST clade it indicates potential source of infection

MSLT systems exists for range of bacteria

They get developed where there is clinical need to understand sources of infection

132
Q

Describe campylobacter in birds

A

Mainly infects lower intestinal tract

There is an inflammatory response during initial colonisation

A correlation with Campylobacter colonisation and
- reduced weight gain
- Hock burn (which is associated with wet bedding i..e more watery faeces)

133
Q

Are campylobacter sp. Clear pathogen in dogs?

A

Diarrhoeas in dogs & other domesticated animals has been associated with Campylobacter

However, Campylobacter is often found in healthy animals so what does this mean?

Presence of large number of Campylobacter may indicate infection

In older dogs evidence is unclear for campylobacter causing diarrhoea but there is some evidence in puppies

It may be that disease is associated more with young or debilitated animals which are often increased at risk

134
Q

How can brachyspira (spirochete that causes disease in pigs & poultry) be diagnosed

A

Selective media - Blood agar plus selective antibiotics

Stained faecal smear for spirochaetes

Silver stain faecal smear

PCR tests

135
Q

What is Lawsonia and how can it be diagnosed

A

Curved Gram-negative rod
Obligate intracellular pathogen
Microaerophilic
In piglets & foals

Diagnosis:
- Clinical signs
- Demonstration in mucosa or faeces by immunofluorescence or PCR
- Staining of tissue sections
- Serological tests

136
Q

Describe Lawsonia intracellularis

A

Invades enterocytes

Causes lack of differentiation

Undeveloped cells do not shed

Leads to pseudo-stratified epithelium
- Thickening of gut & thus poor absorption

137
Q

What are enterobacteriaceae

A

Gram negative rods which are oxidase negative, facultative anaerobes & grow on MacConkey

Major enteric pathogens
- Escherichia coli (also commensal)
- Salmonella enterica
- Yersinia species

Opportunistic pathogens

138
Q

How can you differentiate between different enterobacteriaceae

A

Differentiation by growth characteristics and biochemistry
- Motility Test
- Citrate utilization Test
- Indole Test
- Methyl Red (MR) Test
- Voges–Proskauer (VP) Test
- Triple Sugar Iron (TSI) Agar Test
- Urease Test

More common now for molecular tests to confirm species by:
- PCR of unique genes
- Whole genome sequence (WGS)
- Ribosomal genome sequence
- Mass Spectrophotomerty

139
Q

Describe E. coli

A

Most members of this genus are low virulence

They may cause opportunistic infections

Pathogenic strains possess virulence factors which allow them to cause disease

Basic genomes of E. coli are same but they will have gained some very specific properties.

3 main criteria
- Adhesion factors
*Presence or absence of LEE island
- Type of enterotoxin present
- Species associated with

140
Q

What factors can lead to pathogenic E. coli in young farm animals

A

Poor colostrum immunity

ETEC receptors present

Build-up of pathogenic E. coli

Stress and environment

141
Q

What are the 2 species of Salmonella

A

S. bongori

S. enterica

142
Q

What are the sources of Salmonella infection

A

Organisms found in:
- Contaminated water sources
- Carrier animals
- Faecal contaminated environment

Foodborne
- Eggs (from infected birds)

GI content contaminated food:
- Raw Meat
- Offal
- Animal Feed
- Plant material (Faecal contamination and uptake)

143
Q

What are clinical signs of Enteric Salmonella

A

Profuse foul-smelling diarrhoea

Fever

Depression

Anorexia

Severely affected animals may become recumbent

144
Q

Describe Salmonella invasion

A
  1. TTSS-1 injects effector proteins into host enterocyte
  2. Triggers actin changes that leads to engulfment of bacteria into vacuole
  3. There are multiple TTSS-1 effectors but overall effect of different effector proteins is to
    - Trigger invasion by actin and tubulin remodelling
    - Trigger cytokine response
    - trigger Enteropathogenic response (fluid secretion)
  4. Once bacteria is internalised in vacuole, host will try & attack bacteria moving antimicrobial vacuoles to form phagolysozome out of Salmonella containing vacuole.
  5. These fusion is inhibited by TTSS-2
145
Q

Describe Salmonella intracellular survival (in vacuole)

A
  1. TTSS-2 injects SPI-2 effectors
  2. These jam up in cytoskeletal movements in cell so cell can’t mature vacuoles
  3. This means Salmonella is in protected space
  4. Salmonella replicates in controlled vacuole
  5. In this space it’s safe from adaptive responses as antibodies only survey outside cells
146
Q

Describe Septicaemic salmonellosis

A

Common to specific host serotype combinations

Host may vary in susceptibility with age

Sudden high fever, depression, recumbence, rapid death

Mucosa is route to deeper tissues Salmonella can spread in blood & lymph inside macrophages

Organisms can spread to other organs liver & spleen (oviduct in birds)

147
Q

Describe Salmonella in eggs

A

Carrier state observed after recovery from enteric infection of
- S. Enteritidis
- S. Gallinarum

Bacteria found in macrophages

These reach oviducts and contaminate eggs

Biosecurity & vaccination have reduced infection & egg contamination

FSA guidance is that Lion Brand Eggs (or equivalent) in UK are now considered Salmonella ‘free’

148
Q

Describe phylum firmicutes

A

The ‘majority’ Gram positive

Found in various environments

The group includes commensals and pathogens

BUT exceptions
- Mycoplasmas lack cell walls (e.g. of genetic reduction)

Some Gram positive genera:
- Produce endospores
- Have porous pseudo-outer-membrane that causes them to stain Gram-negative

149
Q

Give examples of Firmicutes

A
150
Q

Describe phylum bacteroidetes + e.g.

A

Gram negative

Wide distribution in the environment, (soil, water GI tracts)

Rarely pathogenic

examples:
- Bacteroides (abundant in the faeces)
- Porphyromonas, (oral cavity)

151
Q

Describe phylum proteobacteria

A

All Gram Negative

A major Phylum (with subgroups)
- Alphaproteobacteria
- Betaproteobacteria
- Gammaproteobacteria
- Deltaproteobacteria
- Epsilonproteobacteria

Includes commensals and pathogens

Members can be facultative/obligate anaerobes or even microaerophilic

Notable Genera clinically relevant to GI tract:
- Escherichia, Salmonella, Vibrio (in humans), Helicobacter, Campylobacter

152
Q

Name an important family of gammaproteobacteria

A

Pseudomonas found in lots of environments & can cause ear infections, burn infections, wool/skin in sheep infections

It’s good at forming biofilms in infections as it often produces exopolysaccharides (slime made form sugars)

These films can make it more intransigent to treatment

153
Q

Name important epsilonproteobacteria

A

Both are microaerophilic

Helicobacter is important in stomach infections

Campylobacter causes GI infection in humans & is foodborne zoonotic as its carried by number of large animals

154
Q

Give examples from phyla actinomycetota

A
155
Q

Describe Bifidobacterium

A

Gram Positive, Anaerobes

Can be branched

Common commensal bacterium

Niche gastrointestinal tract of mammals

A major constituents of probiotic food supplements

156
Q

Describe Genus bacteroides

A

A major component of mammalian gastrointestinal flora

Gram negative, bacilli (morphology as in rod), anaerobes

Non-endospore-forming

Variable motility between species

Will use simple sugars when available, but main source of energy is polysaccharides from plant sources

157
Q

Describe Genus Lactobacillus

A

Gram Positive

Facultative anaerobic / microaerophilic bacteria

Major part of group can convert lactose & other sugars to lactic acid

Common and benign

Present on mucosa of reproductive and GI tract

Production of lactic acid makes its environment acidic which inhibits growth of some harmful bacteria

This ‘MAY’ help protect the gut against less pH tolerant bacteria

158
Q

Describe Genus streptococci

A

Gram Positive, Coccoid, facultative-anaerobes

Members of phylum Firmicutes

Cellular division on a single axis so they grow in chains or pairs

Found in many body sites as commensals

Can cause opportunistic disease

159
Q

Describe Enterococcus sp. (faecalis & faecium)

A

Gram Positive, Facultative anaerobe

Commensal bacterium

Niche gastrointestinal tracts mammals

A major constituents of some probiotic food supplements

Can cause opportunistic infections

One of the ESKAPE pathogens

160
Q

What are ESKAPE pathogens

A

6 nosocomial pathogens that exhibit multidrug resistance & virulence

Enterococcus faecium, Staphylococcus aureus, Enterobacter Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa & spp.

161
Q

Describe genus Clostridia

A

Gram Positive, Endospore forming, Rod shape, obligate anaerobes

162
Q

What is genome

A

Genetic material of animals, plants & bacteria consists of DNA

Genome includes both genes (coding regions) & noncoding DNA

In viruses genome can be double stranded or single stranded RNA or DNA

163
Q

Describe mitochondrial DNA (eukaryotes)

A

In animals mitochondrial genome is typically single circular chromosome that is approx. 16-kb long & has 37 genes

Not all proteins necessary for mitochondrial function are encoded by mitochondrial genome

Mitochondria divide by binary fission similar to bacterial cell division

Mitochondria & thus mitochondrial DNA, usually comes from egg only

Sperm’s mitochondria enter egg but don’t contribute genetic information to embryo – Maternal inheritance

164
Q

define microbiome

A

Combined genetic material of microorganisms in particular environment – population level

165
Q

What is metagenomics

A

study of structure & function of entire nucleotide sequences in bulk sample

166
Q

Describe the intestinal microbiome

A

Gut composed of widely divergent microbial lineages whose genomes contain functionally similar sets of genes that would give rise to coordinated single metabolic outcome

Diversity & abundance level of microbes, genes, proteins & metabolites will influence energy balance, gut motility, inflammatory tone, mucosal integrity, appetite & signalling

Gut key player (i.e., pathogens) may also negatively influence gut barrier
- –> promoting inflammation

Good flora can produce good products & also exclude detrimental bacteria

Detrimental bacteria may produce toxins or interact with cells stimulating unwanted responses in gut mucosa

167
Q

Describe Influence of Microbiota gut brain axis (MGBA) on behaviour

A

via cell structural components (ie LPS) & with release of microbial metabolites which act on intestinal epithelium, then released into bloodstream & cross blood-brain barrier

production of pro-inflammatory cytokines by immune cells

stimulate enteric nervous system & its sensory neurons or induce secretion of neuropeptides by entero-endocrine cells

Affects:
- anxiety-like behaviour
- memory capacities
- social behaviour
- feeding behaviour

168
Q

What are coding regions of a gene

A

portion of gene’s DNA or RNA that is composed of exons

169
Q

What are Long interspersed nuclear elements & short interspersed nuclear elements

A

Long interspersed nuclear elements (LINEs):
- expressed as RNA & encode reverse transcriptase that creates DsDNA copy that can then insert

Short interspersed nuclear element (SINE) sequences:
- Widely distributed in eukaryotic genomes & have crucial roles in genome organization, genome evolution & modulating gene expression

170
Q

What are the Applications of PCR & qPCR in veterinary medicine

A

pathogen detection

quanitification of gene expression

detection of gene mutations

171
Q

Why might diarrhoea occur more commonly in younger animals

A

not very developed immune system

GI tract not fully developed

Incomplete gut flora

lack of exposure

exploring environment with mouth

172
Q

How might an animal ingest viruses shed within faeces

A

Viruses shed in diarrhoea can create aerosols

foodstuffs, drinking water & fomites can be contaminated & spread disease

poor disinfection of environment

173
Q

Define fomite

A

objects or materials which are likely to carry infection

174
Q

Describe common features of enteric virus infections

A
175
Q

How can enteric virus infections cause malabsorption

A
176
Q

What are the 4 main mechanisms of viral diarrhoea

A
177
Q

What are the main viruses that affect GIT

A
178
Q

Describe rotaviruses

A
179
Q

What is important about viruses with a segmented genome?

A

have their genetic material divided into separate segments (each encoding for different genes)

allows for genetic diversity (each segment can undergo reassortment to create new viral variants)

increases adaptability to survive in different conditions

some have antigenic variation (encode for proteins that undergo frequent changes to avoid immune system)

180
Q
A
181
Q
A
182
Q

Where do rotaviruses infect & effect

A
183
Q
A
184
Q

What is the importance of rotavirus

A
185
Q

How is rotavirus diagnosed

A
186
Q

How is rotavirus controlled

A
187
Q

What are the steps of PCR

A
  1. reaction mix is heated to 95 degrees
  2. hydrogen bonds of DNA nucleotides are broken down
  3. double stranded DNA will be denatured
  4. reaction mix is cooled down to annealing temperature
  5. primers align with complementary sequence of target DNA
  6. primers form hydrogen bonds with target DNA
  7. reaction mix is heated to reach optimum temperature for DNA polymerase
  8. heat stable DNA polymerase extends primers in 5’->3’ direction
  9. temperature raised to 95 degrees again to start next cycle
188
Q

Compare microbial culture to PCR

A
189
Q

Compare PCR to immunodiagnostics (ELISAs & snap tests).
1. What do they detect?
2. How quick are they?
3. How accurate are they?

A
  1. PCR detects pathogen DNA & immunodiagnostics detect Ab that animal produced when in contact with pathogen
  2. snap tests immediate. PCR & ELISA 24-72h
  3. PCR more accurate
190
Q

Define silent or synonymous mutation

A
191
Q

define missense mutation

A

nucleotide substitution that leads to change of an amino acid
Impact can vary:
- new amino acid might have similar properties to the old one or the substitution is in a part of the protein that does not affect its structure or function and has no impact
- It can cause a major change in the protein

192
Q

Define nonsense mutation

A

A point mutation that changes a codon for an amino acid into a stop codon and causes the premature termination of translation. If that happens close the 3’ end of the strand than that might not have much impact on the proteins.

Most non-sense mutations lead to non-functional proteins.

193
Q
A
194
Q
A
195
Q
A
196
Q

Which organism causes Johne’s disease

A
197
Q
A
198
Q

How is canine coronavirus transmitted

A
199
Q

Define diarrhoea

A

Increase in frequency, fluidity, volume & water content of faeces

200
Q

What factors can cause disease

A

Secretion of exotoxin

Invasion of target cells leading to cell death

Invasion of host cells & lymphatic’s leading to systemic disease

201
Q

What is hypersecretion (pathogenic mechanism)

A

A functional disturbance of the intestinal epithelial cells

Increased out flow or decrease re-absorption of water
crypt cells can pump chloride ions (Cl-) into the crypt space

Cl- ions attract sodium ions (Na+) into crypt space, increasing local osmotic pressure

As osmotic pressure increases, water is pulled into intestine

Some enterotoxins can trigger & lock ON chloride secretion leading to hypersecretory diarrhoea

Done by activating adenylate cyclase

Example cause:
- ETEC (enterotoxigenic E. coli)

202
Q

What are examples of pathogenic mechanisms

A

Hypersecretion

Villous atrophy

Infiltrative and proliferative distortion of mucosa

Mucosal necrosis

203
Q

What is villus atrophy (pathogenic mechanism) + example pathogens

A

Destruction of the epithelial cells on villi or in the crypts

Villi become often stunted or fused

Example pathogens:
- Attaching and effacing E. coli (EHEC, VTEC)
- Rotavirus (mild villous atrophy)
- Canine parvovirus (severe villous atrophy)

204
Q

What is infiltrative & proliferative distortion of mucosa (pathogenic mechanism)

A

Recruitment of large numbers of Macrophage & T-lymphocytes in lamina propria & sub-mucosa

Leading to crypt compression and villous distortion

Therefore reduce absorptive capacity

Example Paratuberculosis (Johne’s disease)

205
Q

What is mucosal necrosis (pathogenic mechanism)

A

Infection leads to cell death

Severity and extent depend on virulence of pathogen

Majority of Diarrhoea from reduced absorption

Example pathogens:
- Brachyspira hyodysenteriae

206
Q

What are the advantages & disadvantages of preventative vaccination

A

Leah GIL (12 decks)

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