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BVMS 2 > Module 7 Wk 4 > Flashcards

Module 7 Wk 4 Flashcards

1
Q

T/F fungi have undefined nuclei?

A

Flase - They have a defined nuclei

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2
Q

What types of repro does fungi do?

A

sexual and asexual

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3
Q

Where do you not see sexual reproduction of fungi?

A

Infection in animals and humans

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4
Q

What is the infectious form of fungi?

A

Asexual spores

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5
Q

What do we target within fungi cell wall?

A

Glucan synthesis

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6
Q

Where will you see most fungi infections?

A

Cutaneous and superficial mucous membranes

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7
Q

What are benificial fungla products?

A

Antibiotics

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8
Q

What are harmful fugal products?

A

mycotoxins

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9
Q

Why would you not feed fungal products to pregnant cows especially?

A

Can cause fungal abortions

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10
Q

When in the lab making a diagnosis what can you do?

A
  • direct microscopy
  • Culture
  • histology of tissue effected by invasive disease
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11
Q

How do yeast reproduce?

A

By budding

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12
Q

Where do yeasts grow?

A

Skin, mucous surfaces and in the body

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13
Q

What kind of infection do yeasts cause?

A

Superficial

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14
Q

What are moulds?

A

Multicellular organisms that produce hyphae and mycelium and spores

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15
Q

What are dimorphic fungi?

A

Organisms that can produce both hyphae and yeast

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16
Q

What can result from yeast daughter cells not detaching themselves?

A

Pseudohyphae

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17
Q

In catt;e what can the yeast Candida Albicans cause clinically?

A
  • Mycotic abortions
  • Ruminal infections
  • Mastitis
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18
Q

What would you see Candida albicans cause in pigs?

A

Dermatitis

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19
Q

What would you see Candida albicans cause in dogs?

A
  • Chronic enteritis and dermatitis
  • Vaginitis
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20
Q

What would you see Candida albicans cause in Birds?

A
  • Crop infections
  • enteritis
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21
Q

What shap do Malassezias apear like?

A

bottle shaped

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22
Q

What enchances Malassezia growth?

A

Lipase

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23
Q

How would you become infected with Cryptococcus?

A

Inhalation of yeast cells

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24
Q

what are moulds?

A

Molds are multinucleated, filamentous fungi composed of hyphae

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25
Q

What is the difference between septate and non-septate hyphae?

A

Septate have walls between cells and non septate dont

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26
Q

What kind of branching do dermatophytes have?

A

Sepate branching hyphae

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27
Q

What kind of spreading do dermatophytes have?

A
  • Anthropophilic (human to human)
  • Geophilic (enviro to animal)
  • zoophilic (animal to human)
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28
Q

What do dermatophytes infect?

A

Skin, hair and nails

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29
Q

What is used in the lab to detect Dermatophytes?

A
  • micoconidia and macroconidia
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30
Q

what are the two genus of dermatophytes?

A

microsporum and trichophyton

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31
Q

How can you detect ringworm?

A
  • fluresce under uv light
  • culture
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32
Q

T/f ringworm in cats and dogs is zoonotic?

A

True

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33
Q

What genus of dermatophyte causes ring worm?

A

microsporum

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34
Q

What is the difference between ectothrix and endothrix

A

Dermatophyte infections in which arthrospores are formed on the outside of the hair shaft are known as ectothrix infections and those in which the spores develop within the hair itself are known as endothrix infections.

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35
Q

Is M.canis ecto or endo?

A

ectothrix as grows on the hair

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36
Q

What is the name of the micro sporum species that geophillically effects dogs?

A

M. gypseum

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37
Q

T/F trichophytons are zoophilic?

A

Trueeee bitch

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38
Q

What shape are the macrocondia in trichophyton?

A

Club

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39
Q

What is the species of trichophyton that is cattle ringworm which is transmissible to man?

A

T. verrucosum

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40
Q

Is T. verr ecto or endothrix?

A

Ectothrix

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41
Q

What is the species of trichophyton that effects horse and dog and which one just effects horse?

A
  • T. mentagrophytes effects both
  • T. equinum just horse
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42
Q

Are Aspergillus sepate or non speate hyphae?

A

sepate branching hyphae

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43
Q

what do aspergillus fumigatus spores infect?

A

Young non-immune or immunosupressed animals

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44
Q

What does aspergillus disease mainly cause?

A

resp infection as you inhale spores

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45
Q

Describe the host defences against Aspergillus?

A
  • neutrophils swell and germinate in to hyphae
  • Invade into lung
  • Into blood vessels (angioinvasive) neutophils will kill them
  • They don’t infect no immune as macrophages in lung get rid
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46
Q

what are the two distinct forms of dimorphic fungi?

A

mould in enviro and yeast in animal tissue

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47
Q

in dimorphic fungi which form is pathogenic?

A

yeast

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48
Q

How do the spores from the dimorphic fungi enter host?

A

inhalation

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49
Q

T/F the Histoplasma capsulatum farcinimosum dimorphic fungi is notifible?

A

Trueeee

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50
Q

what is selective toxicity of antifungal agents and how does it work?

A

where we destroy the fungus but cause no or minimal damage to the animal

to do this we need to target features of the fungus not found in host

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51
Q

What do allyamines inhibit within fungal

A

Inhibits Squalene turning into lanosterol

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52
Q

What inhibits lanosterol from being engosterol?

A

azoles

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52
Q

What kind of damage and wher do amphotercins have effect?

A

pores in cell membrane and oxidative damage?

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53
Q

What are the 5 classifications of antifungal drugs?

A

Superficial/Systemic infection

Topical/Systemic administration of drug

Antifungals/ Synthetic agents

Fungicidal/Fungistatic

Chemical Subclass

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54
Q

Whats the difference between fungicidal and fungistatic?

A

Fungicidal = fungi is killed by drug
Fungistatic - fungis is inhibited by drug

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55
Q

What 3 drug classes target ergosterol in the fungal cell membrane?

A
  • allyamines
    -azoles
    -amphtericin B
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56
Q

Describe the biosynthessi of ergosterol?

A

Acetyl CoA - squalene - lanosterol - ergosterol

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57
Q

What is allyamines mechanism of action?

A

inhibits ergosterol biosynthesis via inhibition of squalene epoxidase (fungicidal)

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58
Q

T/F allyamines can only darget dermatophyte infection only?

A

True

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59
Q

Is there side effects of using allyamines?

A

could have very genral and mild GIT and skin ones

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60
Q

What routes is there for allyamines?

A

Oral and topically

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61
Q

in terms of pharmacokenetics what is importnat about allyamines?

A

highly lipophilic so persists in skin

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62
Q

What are the two types of azoles?

A

imidazoles - topical
triazoles - systemic

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63
Q

What are examples of imidazoles?

A

Clotrimazole; Enilconazole, Miconazole

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64
Q

What is the main use of imidazoles?

A

For superficail mucous membrane and skin infection

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65
Q

What are Imidazoles meachnism of action?

A

inbibition of cytP450-dependent 14-sterol de-methylase

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66
Q

Do imidazoles have a broad spectrum?

A

Yes

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67
Q

what are side effects of imidazoles?

A

GIT; anorexia; hepatotoxicity; suppression of steroid production (ketoconazole); teratogenic

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68
Q

What are triazoles for?

A

Used for serious systemic mycoses

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69
Q

what are examples of triazoles?

A

fluconazole, itraconazole, voriconazole, and posaconazole

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70
Q

What route do triazoles use?

A

oral

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71
Q

What is intraconazole drug of choice for?

A

Histoplasmosis (lung infection)

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72
Q

what are the mechanisms of resistance to azole antifungal drugs?

A

Membrane changes lead to reduced drug up-take
Mutation of the target enzyme
Over production of the target enzyme
Modification of the ergosterol biosynthesis pathway
Drug efflux due to up-regulation ABC transporters, MFS transporters
Biofilm formation

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73
Q

What are two examples of Polyenes?

A

Amphotericin B, Nystatin

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74
Q

what is the mechanism of action of polyenes?

A

They bind to ergosterol, distrupting osmotic integrity of the membrane by forming pores where ions leak from cell causing cidal and oxidative damage

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75
Q

describe the pharmacokenetics of polyenes?

A

poorly water soluble (amphotericin B
is forms a colloid in solution for injection), poor absorption from GIT

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76
Q

What are the meachnisms of resistance to polyenes relate too?

A

It is linked to reduced ergosterol in fungal cell membrane

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77
Q

What does inhibition of the enzyme that is involved in glycan synthesis cause?

A

Fungal cell wall falls apart

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78
Q

What are glucan synthesis inhibitors called?

A

echinocandins

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79
Q

what are examples of echinocandins?

A

Caspofungin; Anidulafungin, Micafungin

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80
Q

what is the mechanism of action of echinocandins?

A

block synthesis of Beta (1,3) glucan

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81
Q

what route would you use with echinocadins?

A

IV

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82
Q

what are the mechanisms of resistance against echinocandins?

A

Inhibit glucan synthase which synthesizes beta glucan, a structural component of fungal cell walls
Structural integrity lost – cidal in yeast, static in moulds
Many moulds resistant (not Aspergillus) most Candida species susceptible
Candida parapsilosis innately less susceptible – higher breakpoints
Various FKS1 (glucan synthase subunit) mutations identified also FKS2 and 3 genes all of which encode the target enzyme and up-regulation of chitin synthesis - rescue mechanism

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83
Q

what is Flucytosine an example of?

A

Antimetabolite

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84
Q

what is the mechnanism of action of an antimetabolite?

A

Incorporation of 5-FU into RNA disrupts protein synthesis (fungicidal) and further conversion of 5-FU to fluorodeoxyuridine monophosphate inhibits thymidylate synthase which interferes with DNA synthesis

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85
Q

what route would you use to give an antimetabolite?

A

oral

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86
Q

what is the pharmocokenetics of antimetabolite?

A

excreted unchnaged by the kidney

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87
Q

Describe the Mechanism of resistance to flucytosine

A

Sensitive – cascade of active enzymes, cytosine permease to take up the drug, cytosine deaminase and phosphorylase to metabolize it to its toxic form – disrupts RNA and DNA synthesis
5-FC converted to 5-FU – Fluorouracil – miscoded RNA or DNA
Loss or reduction in activity in any of the enzymes (but most commonly the phosphorylase) leads to primary emergent resistance
Common during treatment – rarely used as monotherapy, always combined with AmB

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88
Q

what does active host defence consist of?

A
  • skin immune system
  • innate immunity
  • adaptive immunity
89
Q

what does passive host defence consits of?

A
  • hair, hooves and claws
  • melanocytes
  • epidermal barrier
90
Q

Describe the main difference between Innate and adaptive immunity?

A
  • Innate immunity is imediate but non specific whereas adaptive is a delayed response yet specific
91
Q

what is the main role of melanocytes in host defence?

A

photoprotection

92
Q

what is the stratum corneam?

A

Its is a lipid bilayer of cell membrane forming a corniflied envelope

93
Q

what is the the main intercellular adhesive structures in the stratum corneum

A

corneodesmosomes

94
Q

Why is the control of desquamation importnat at the stratum corneaum?

A

For the balance of stratum corneum proteases and protease inhibitors

95
Q

what are 4 portals of entry into the skin?

A
  • epidermis
    -adnexa
  • dermis and panniculus
  • from underlying tissues
96
Q

Describe the different entr ways to the epidermis?

A
  • absorption
  • direct contact
  • colonistation
  • penetration
  • impaired barriers
97
Q

Describe entry to skin via adnexa

A
  • entry via follicule ostium where there is rupture of follicule or adnexal glands making acess to dermis to cause furonculosis (deep infection of hair follicule)
98
Q

Describe entry to skin via dermis or panniculus

A
  • blood vessels and nerves
99
Q

Describe entry to skin from underlying tissues

A

Penetation by damaged bones or extension from adjacent tissues like tumout, lymph node, gland, muscle or bone

100
Q

when looking at patterns of disease what epidmiology can effect it?

A

Breed , sex, loaction and season

101
Q

when looking at patterns of disease what clinical signs can you use?

A

Distribution:
- where are the lesions on the body?
Description:
- size, shape, colour, consistency
Lesion type:
- inflammatory (red)
- hyperplastic (thickened)
- alopecic / hypotrichotic (bald)
- tumoral / neoplastic (nodular)

102
Q

how do primary skin lesions develop?

A

Spontanously as a result of underlying disease

103
Q

what do secondary skin lesions develop from?

A

They evolve from primary skin lesions or induced via self-trauma or external factors

104
Q

what primary skin lesion can be described as a circumscribed, non-palpable spot characterised by a change in colour and is less than 1cm?

A

A macule

105
Q

what primary skin lesion can be described as a small solids elavation of skin and is less than 1cm?

A

a papule

106
Q

what primary skin lesion can be described as a sharply circumscribed epidermal elavation filled with clear fluid and is less than 1cm?

A

a vesicle and bulla if greater than 1cm

107
Q

what primary skin lesion can be described as a intra or sub epidermal or follicular elavation filled with cell debris?

A

a pustule

108
Q

what primary skin lesion can be described as a circumscribed raised lesion due to odema witha pale pin central and red rim?

A

A hive

109
Q

what primary skin lesion can be described as a well circumscribed, epithelial lined cavity containing fluid or solid material within the dermis or subcutis?

A

A cyst

110
Q

what primary skin lesion can be described as a circumscribed solid elavation that is greater than 1cm?

A

A nodule

111
Q

Give 3 examples of nodules?

A
  • abcess
  • plaque
  • neoplasm
112
Q

what secondary skin lesion can be described as a thin circular layer of scale eveolving from pustule, vesicle or bulla?

A

A collarate

113
Q

what secondary skin lesion can be described as a shallow linear break in skin surface due to scratching rubbing or biting?

A

A excuraite

114
Q

what secondary skin lesion can be described as a partail loss of epidermis which is depressed, moist , glistening?

A

An erosion

115
Q

what secondary skin lesion can be described as a linear crack from epidermis to dermis?

A

A fissure

116
Q

what secondary skin lesion can be described as a thickening anf folding of the epidermis with or withouta pigment?

A

A lichenification

117
Q

what secondary skin lesion can be described as a dead keratinocyte plus fibirin, serum and neutrophils?

A

crust

118
Q

Give examples of the sentinal detecting cells in innate immunity?

A

macrophages, mast cells and dendritic cells

119
Q

what is the effector meachnism of innate immunity?

A
  • inflammation
  • complement activation
120
Q

what are examples of the antigen presenting cells that digest and present to the effector cells in adaptive immunity?

A
  • dendritic cells
  • macrophages
121
Q

what is the effector mechanism of the adaptive immunity?

A
  • humoral
  • cell mediated
  • immunological memory
122
Q

whats the difference between innate and adaptive immunity when it comes to self/nonself discrimination?

A

Present in both to allow reaction against foreign body

123
Q

whats the difference between innate and adaptive immunity when it comes to the lag phase?

A

Lag pahses is abesnt In innate making response immediate and in adaptive it is present which means response

124
Q

whats the difference between innate and adaptive immunity when it comes to specificity?

A

Specificity is limited in innate immunity meaning the same response is mounted to a wide range of agents whereas it is high in adaptive immunity allowing response to target the agents which incited it

125
Q

whats the difference between innate and adaptive immunity when it comes to diversity?

A

Diversity is limited in innate immunity hense the limited specificity wheras it is extensive in adaptive immuity as wide range if antigen receptors

126
Q

whats the difference between innate and adaptive immunity when it comes to memory?

A

Memory is absent in innate immunity meaning get same response every time whereas in adaptive it is present meaning responses are amplified in subsequent exposures

127
Q

In the skin immune system what are the physiochemical barriers?

A
  • stratum corneum
  • surface lipids
  • antimicrobial peptides
128
Q

Describe how the stum corneum acts as a physiochemical barrier

A
  • the lipids bilayer between the corneocytes is created by planar lamellar sheets of ceramides, cholesterol and FFA
  • Profillaggrin is cleaved by proteases at the junction of granular layer and stratum corneam which forms fillagrin
  • fillagrm bundles ketatin and flattens corneocytes
  • fillagrin turns to ammino acids which allows for retention of moisture
129
Q

what are sphingolipids and free fatty acids importnat for?

A
  • physical barrier agianst water
  • permibilty barrier
  • immunological barrier
130
Q

What should the production of antimicrobial peptides be like on normal skin?

A

A low constant level of production

131
Q

What should the production of antimicrobial peptides be like on infected skin?

A
  • injured keratinocytes increases the number of antimicrobial peptides
  • This results in recruitment of mast cells and neutrophils creating inflammation
  • inflammatory sells also produce AMPs so adds to the number there
  • this stimulates angiogenisis and keratinocyte proliferation resulting in tikeningof the epidermis
132
Q

What is the function of the AMPs in host defence?

A

To activate and recruit inflammatory cells and alarm + arm keratinocytes

133
Q

What are defensins and cathelicidins examples of?

A

AMPs

134
Q

What does skin need for proper immune function?

A

microbail signals

135
Q

Describe how the commensal microbes work to create prpor immune function

A

They stimulate skin and immine cells to produce IL-1. IL-1 activates T cells which become more responsive to invading organisms.

136
Q

What are factors that effect skin microbiome?

A
  • host physiology
  • enviroment
  • immune system
  • host genotype
  • lifestyle
  • pathobiology
137
Q

What cells make up the skin immune system?

A
  • endothelial cells
  • keratinocytes
  • dendritic/ langerhans cells
  • mast cells
  • lymphocytes
138
Q

keratinocytes act as sentinel cells what do they do?

A
  • The exxpress pattern recognition receptors which respond to PAMPs and DAMPS
139
Q

Do keratinocytes have a pro inflma response?

A

yes - they react to harfmful insults producing a complex mixture of pro inflammatory AMPs, cytokines and chemokines

140
Q

T/F keratinocytes express MHC class 2 and interact with antigen- experienced T cells

A

True

141
Q

What are langerhan cells?

A

epidermal dendritic cells

142
Q

what do dendritic cells link?

A

the onnate and adaptive immunity

143
Q

what do langerhan cells interact with?

A

skin resident memory T cells

144
Q

What is the skins response to injury at the epidermal level?

A

Release of pro-inflammatory cytokines and growth factors by keratinocytes

145
Q

What is the skins response to injury at the dermal level?

A
  • stimulation of dermal inflammation
  • erythma, odema and exudation
  • release of secondary cytokines/ growth factors
  • antigen presenting cells interact with t cells
146
Q

What is orthkeratotic hyperkeratosis?

A

An increase in thickness of anuclear surface keratin

147
Q

what is parakeratosis?

A

Where a thickened keratin layer has retained nuclei which reflects and increase turnover of keratinocytes

148
Q

What is hypergranulosis

A
  • prominent granular layer associated with hyperkeratonis also see in assocaition with hyperplasia
149
Q

what is acanthosis?

A

Hyperplasia of the spinous layer due to hyperplasia and or hypertrophy

150
Q

what is hyperplasia?

A

Thickening of epidermis which has projections into the dermis

151
Q

Define Hypersensivity reactions?

A

An exageratted or inappropriate immune response to a mild pathogen or innocusus substance (allergen)

152
Q

Define autoimmine disease

A

A specific humoral or cell mediated immune response against the bodys own tissue components (auto-antigen)

153
Q

Describe what happens in type 1 hypersensitivity

A
  • There is production of antigen specific IgE
  • IgE is bound to mast cell memebranes
  • Mast cell degranulation then happens where there is a release of vasoactive mediators into fluid including histamine and prostaglandins
154
Q

What does type 1 hypersensititivty cause?

A

Severe systemic reactions lie anaphalaxis and some milder ones

155
Q

What is anaphalaxis?

A

An immediate system reaction caused by rapid IgE mediated immune release of potent mediators from tissue mast cells and peripheral basophils

156
Q

What does anaphalaxis effect?

A
  • skin and or mucosal tissues ie in the resp, git and cardi system
157
Q

What happens during anaphalaxis?

A
  • release of vasoactive mediators
  • systemic vasodilation and increase of vascular permability
  • hypertension and tissue hypoperfusion
158
Q

what are the tiggers of type 1 hypersensitivity?

A
  • food
  • medication
  • venoms
159
Q

What are examples of type 1 hypersensitivity?

A
  • atopic dermatitis
  • insect bite hypersensitivity
160
Q

What is the reaction to with atopic dermatistis?

A

Enviroment allergens

161
Q

Where on body would you expect to see atopic dermatitis effecting?

A

face, ventrum and feet

162
Q

How is the allergen introduced with atopic dermatitis?

A

Through absorbtion or inhalation

163
Q

With aptopic dermtitis there is an abnormal skin barrier what can be seen?

A
  • varaitions of fillagrin expression
  • disorganised lipid lamellae
  • altered balance of AMPs
164
Q

What are the triggers of inset bite hypersensitivitys?

A
  • fleas
  • biting midges
  • black flies
  • mosquitos
165
Q

T/F flea bit hypersensitivity can be seasonal?

A

True

166
Q

Histologically what would you see with flea bit hypersensitivity?

A

May include eosinophils in dermal infiltrate and or intraepidermal eosinophillic abcesses

167
Q

What is type 2 hypersensitivity?

A

Direct damage mediated by antibodies to exposed cell surface antigens

168
Q

what does type 2 hypersensitivity underlie?

A

Underlies varoius autoimmune disorders afftecting varoius tissues

169
Q

What are the 3 phases of type 3 hypersensitivity?

A
  • phase 1 is thwre immune complex is formed
  • phase 2 is where immune complex is deposited
  • phase 3 is where there is immune complex mediated inflammation
170
Q

In type 4 hypersensitivity what does the blanace swing from prtotection?

A

Swings to tissue damage

171
Q

What happens during type 4 hypersensitivity?

A
  • sensitised T cell population develops after initial contact with antigen
  • tissue damage due to activated macrophages and cytotoxic Tcell
172
Q

Name the 3 types of delayed hypersensitivity?

A
  • tuberculin - local/induration
  • contact - eczema
  • gramuloma - hardeing
173
Q

what is allergic contact dermititis hard to differ from?

A

irritant contact

174
Q

Name the non biting fly species of veterinary significance?

A
  • musca domestica (houes fly)
  • musca autamainis (face fly)
  • hydroyea irritans ( head fly)
175
Q

Decrbe how non-biting flies act as disease vectors?

A
  • Mouth parts adapted for ‘spounging’
  • rasping device which cant puncture skin but can agrevate wounds
  • claws on feet and polovili whihc is ideal for picking up pathogens
176
Q

What does the round nematode worm habronema cause?

A

summer sores

177
Q

what are the habronema spp transmited via?

A

musca flies

178
Q

Describe lifecycles of Habronema spp

A
  1. horse expells eggs in feaces (L1)
  2. fly lays eggs in the feaces
  3. when the fly eggs hatch they ingest eggs/L1
  4. fly larvae and parasites develop together ( trnsstadoil transmission)
  5. Adult flies emerge from pupae
  6. L3 nematodes migrate to fly mouthparts
  7. Flies deposit L3 whilst feeding near nose/ mouth
179
Q

What are the two ways habronema spp can be transmitted?

A
  • ingested = assympotomatic
  • on wound/ mucous membrane = local hypersensitivity = summer sores
180
Q

Where would Thelazia spp of round nematode found?

A

The eye

181
Q

What is the pathological signifigance of biting flies the cuicoides species?

A
  • Causes sweet itch, summer itch, queensland itch and seasonal dermatitis
182
Q

Describe the parasite transmission that causes onchocerciasis?

A
  • microfilarail stage on skin of horse
  • microfilaria are picked up by the midges when they tak a blood meal
  • develop to L3 within the fly
  • transferred to naive animals when they feed
  • larvae migrate to the nochal ligament
  • develop into adults and produce microfilaria to sustain the infection
183
Q

What nematode causes Onchoceriasis?

A

The filarail nematode called onchoceraca cervicalis

184
Q

T/F the chonallenberg virus can pass to foetus during pregnancy?

A

True

185
Q

How can we control culicoids?

A
  • Hard to control due to the extensive breeding so use repelents, insecticides and barries (fly masks)
186
Q

T/F sheeps ked have wings?

A

False

187
Q

What is the lifecycle of sheeps ked

A
  • live larvae - every 10-12days
  • adheres to wool and pupates
  • adult eerges 19-30days
188
Q

What is the pathology and significane of sheeps ked?

A
  • peirce skin and suck blood
    -bites ause intense priritis leading to wool damage
  • decrease in body condition score and case anemia
189
Q

How would you go about controlling sheep ked?

A
  • sheering removes papae and adults
  • follow up with insecticides
  • It is notifiable too
190
Q

What is myiasis?

A

The invasion a living animal with fly larvae

191
Q

What is obligate myisasis?

A

Parasitic development of the larvae on a host is a nessory stage in the lifecycle

192
Q

Hypoderma spp (warble flies) is an example of obligate myiasis, describe the life cycle

A
  1. adults emerge and deposit eggs
  2. eggs hatch and larvae (L1) penetrates skin at 3-7days
    3a. L1 migrate and often along the CT or nerve pathways at 2-4months
    3b. L1 reach spinal cord or oesophagus wall also at 2-4months
  3. larvae migrate to subdermal tissue on back of host to complete development
  4. larvae molt (L1-L3) and peirce skin to allow respiration
  5. mature L3 erupt via breathing hole
  6. pupate in soil (1-2 months)
193
Q

What is the significane of warble flies?

A
  • animals panic at the sound of flies - decreasing grazing, decrease in weight gain and injury due to panicing
  • hide damge due to perforation leading to a loss of value
  • butchers jelly reduces carcus value
194
Q

What is faculative myiasis?

A

Oppertunistic - have the ability to exploit living tissue but not a required stage in the lifecycle

195
Q

what are the three types of blow flies?

A
  • lucilia (greenbottle)
  • calliphora (bluebottle)
  • Phormia (blackbottle)
196
Q

what is the lifecycle of blowflies?

A
  1. Adult emerges from pupae, feed and mate
  2. eggs laid on feaces and hatch 10-12hrs
  3. produce enzymes to digest tissue
  4. drop to ground and bury in soil and pupate at 14days
197
Q

What are primary flIES?

A

Ones that can initiate a strike on living anaimsl without the need for existiting tissue damage - L and P

198
Q

What is a secondary fly?

A

Flies that cannot innitiate a strike, thwy attack areas of existing stick or damage - C

199
Q

What types of strike are thre?

A
  • body
    -tail
  • poll
  • penile sheath
200
Q

What is the epidemiology of blowflies?

A
  • influencing factors such as temp, ranifall and host speceptibility?
201
Q

what are the welfare problems ectoparasites cause?

A
  1. They cause forms of dermititis associated with pruritis that is oftem intense
  2. painful bites that cause irritation and restlessness
  3. Ther larvae can invade the body of an animal (myiasis) and cause tissue distruction
  4. Some are oblugate bloof feeder and can cause naemia
  5. They are effective at transmitting agents of infectious disease so act as vectors
  6. They can be difficult to control
202
Q

What is mechanical transmission?

A

When a vector simply carres pathogenic microorganisms on or in their body and transfers them to the host

203
Q

What is biological transmission?

A

Involoves the multiplication and growth of a disease-causing agent inside the vectors body

204
Q

What are the 3 primary types of dermititis?

A
  • FAD - flea allergic dermatitis
  • Pediculosis - louse infestation
  • Mange
205
Q

What are the 3 types of mange (mites)?

A
  • Psoroptes ovis
  • Sarcoptes scabia
  • Demodex canis
206
Q

What does the psoroptes ovis mite cause?

A

Ovine psoroptic mange ie sheep scab

207
Q

T/F sheep scab is a notifiable disease?

A

True

208
Q

Describe the pathogenesus of sheep scab?

A
  • Caused by allergic reaction to mite antgens in feaces
  • Genertaes inflammation and serous exudate
  • Exudate dries to form scab surrounded by moist border and inflamed skin
  • Mites active in scab border and population expands and scab extends
209
Q

What do mites feed on?

A

They feed on lipids/nutrients in the exudate

210
Q

What are the clinical signs of sheep scab?

A
  • Wet discoloured over the shoulders
  • Restlessness ie licking, biting, scratching and rubbing so wool becomes ragedy
  • wool loss
  • bleeding wounds
  • Decrease in BCS
  • sometimes death
211
Q

How would you diagnose sheep scab?

A

A skin scrape at the dges of lesion to define cause

212
Q

Is psoeoptes ovis a non-burrowing mites?

A

Yes

213
Q

Is demodex a burrowing mites?

A

yes

214
Q

How many legs do demodex have?

A

4 stuby back legs

215
Q

Descirbe juvinile onset of generalised demodecosis?

A

Is a genetically inhereted immunodeficeny and the mite population cant be controlled

216
Q

Descrive the adult onset of generalised demodecosis?

A

It is assocaited with immunisupresive condition

217
Q

What is the moste commen tick in the UK?

A

Ixodes ricinus - sheep tick

218
Q

Describe the lifes cycle of the tick

A
  1. Adult feeds in late spring/summer
  2. eggshatch at autumn time
  3. Look for host and feed for 6 days
  4. moult into nymps
  5. nymphs quest, attach and feed for 6-8 days
  6. They drop to ground and moult to adults
  7. adults quest and attach
  8. males and femals mate on host and feed for 14days
  9. females drop off and lay 100’s of eggs
219
Q

what is teh pathological significance of ticks?

A
  • mouthparts generate lesion and lock aided by substance in the salica which also contains anticoagulant to aid with feeding
  • heavy infectation can cause anemia
  • lesions can be subject to secondary infection lie attracting blow flies and bacteria
220
Q
A

BVMS 2 (18 decks)

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