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CVSOH 4 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Define bulla.

A

Localised collection of fluid greater than 1cm in diameter and larger than a vesicle

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2
Q

Define erythema.

A

A diffuse or localised redness of the skin which disappears with diascopy

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3
Q

Define macule.

A

A flat circumscribed skin discolouration less than 1cm in diameter without surface elevation or depression

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4
Q

Define nodule.

A

Circumscribed solid elevation greater than 1cm usually extending into the dermis, large nodules may be referred to as masses

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5
Q

Define papule.

A

A small solid elevation of the skin up to 1cm in diameter, feels solid and is due to the infiltration of inflammatory cells, fluid or foreign material (calcium), with oedema and epidermal hyperplasia

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6
Q

Define patch.

A

A localised flat change in skin pigmentation larger than 1cm in diameter (big macule)

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7
Q

Define plaque.

A

A flat topped elevation of the skin greater than 0.5cm formed by a coalition of papules, flatter than a nodule

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8
Q

Define pustule.

A

A small circumscribed elevation of the epidermis filled with purulent material

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9
Q

Define vesicle.

A

Small circumscribed elevation of the epidermis filled with a clear fluid less than 1cm in diameter

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10
Q

Define wheal.

A

A sharply circumscribed raised lesion consisting of oedema, usually appears and disappears within minutes to hours

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11
Q

Why may skin be red?

A

Can be caused by erythema/blood in blood vessels or haemorrhage/blood outside of blood vessels

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12
Q

How can the cause of skin redness be differentiated?

A
  • Place a glass slide over the area of redness
  • Erythema will blanch because the blood vessels compress
  • Haemorrhage will not
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13
Q

What is a secondary lesion?

A

Secondary lesions may be created by scratching, chewing or other trauma to the skin, as a result of infections or may evolve from regressing primary lesions.

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14
Q

Define comedone.

A

Dilated hair follicle filled with cornified cells and sebaceous material

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15
Q

Define crust.

A

Dried exudate, cells, pus and scale adherent to the surface

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16
Q

Define epidermal collarette.

A

A circular lesion with a marginal rim of scale

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17
Q

Define excoriation/erosion.

A

Superficial damage to the epidermis

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18
Q

Define fissure.

A

Linear cleavage into the epidermis

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19
Q

Define hyperkeratosis.

A

Increase in thickness of the cornified layer of the skin

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20
Q

Define lichenification.

A

Thickening of the skin (as a whole, not just cornified layer) resulting in a cobblestone appearance

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21
Q

Define scale.

A

Accumulation of loose fragments of the cornified layer of the skin

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22
Q

Define scar.

A

Fibrous replacement tissue formed when there has been trauma

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23
Q

Define ulcer/ulceration.

A

Full thickness loss of the epidermis, exposing the dermis.

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24
Q

Is hypo/hyperpigmentation primary or secondary lesions?

A

Secondary

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25
Q

Name 5 dermatological diagnostic tests.

A

Acetate tape
Skin scrapings
Cytology
Flea comb
Trichogram

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26
Q

What can acetate tape diagnose?

A

Malassezia, bacteria, inflammatory cells

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27
Q

What can deep and superficial skin scrapings diagnose?

A

Deep – demodex mites

Superficial – cheyletiella, sarcoptes, chorioptes, psoroptes

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28
Q

What can a trichogram diagnose?

A
  • Demodex mites
  • Anagen, telogen
  • Mite and lice eggs
  • Evidence of pruritus
  • Dermatophytosis
  • Hair shaft abnormalities
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29
Q

What is ASIT?

A

Allergen specific immunotherapy

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30
Q

What are some considerations for ASIT?

A
  • Only use allergen test with highly compliant owners who understand limitations of the test and ASIT
  • Need to correlate with history – patient old enough to have IgE response/12 months, owner cost
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31
Q

What is allergen testing?

A

Inject histamine for positive control and saline for negative control and then inject a number of allergens. Not diagnostic but something we can use to formulate immunotherapy

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32
Q

How is allergen specific IgE serology (ASIS) testing for dogs done?

A
  1. Capture of IgE antibody by the Fc
  2. Receptor normally binds IgE to a mast cell in vivo
  3. Binding is highly specific for the IgE antibody
  4. ELISA that measures serum IgE using a panel of monoclonal antibodies specific for dog IgE
  5. Antigens coated on the ELISA plate
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33
Q

Describe the results of allergen testing for dogs.

A
  • Only a guide to the amount of IgE – calculated from positive and negative controls – arbitrary antibody units
  • Poorly validated
  • Merely measure the serum antibody
  • Positive results do not unequivocally indicate clinically significant allergic reaction to that allergen
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34
Q

Describe the results of serology allergen testing.

A
  • They are not diagnostic tests
  • They are widely misused and misunderstood
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35
Q

What diagnoses are serological tests available for?

A
  • Malassezia
  • Staphylococcus
  • Food serology not recommended for ‘food allergy’
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36
Q

What are the diagnostic dermatological methods using tissues?

A
  • Culture – bacterial, fungal, mycobacteria, susceptibility testing
  • PCR
  • Dermatopathology
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37
Q

What is the itch-scratch cycle?

A

The mechanical effect of scratching temporarily abolishes the sensation of pruritis. Pruritis recurs intensified by the damaging effects of self-trauma.

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38
Q

Name 3 possible allergic skin diseases.

A
  • Atopic dermatitis
  • Food allergy
  • Flea/insect bite hypersensitivity
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39
Q

What is canine atopic dermatitis?

A

A genetically inherited clinical syndrome that encompasses a diversity of mechanisms and can have a variety of triggers. Multifactorial and complex inflammatory syndrome, typically associated with antigen-specific IgE antibodies to environmental allergens.

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40
Q

What are the primary lesions of canine atopic dermatitis?

A

Erythema
Papules

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41
Q

What are the clinical signs of canine atopic dermatitis?

A

Pruritus

Associated with self-trauma and secondary bacterial and Malassezia infections:

  • Alopecia
  • Erythema
  • Excoriation
  • Lichenification
  • Hyperpigmentation
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42
Q

What are the published diagnostic criteria for canine atopic dermatitis?

A
  • Onset of signs under 3yo
  • Dogs that live mostly indoors
  • Pruritus is glucocorticoid responsive
  • Pruritus is the major/only sign (skin lesions can develop later)
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43
Q

What are the affected regions of canine atopic dermatitis?

A
  • The front feet and concave aspects of the pinnae are affected
  • The ear margins are not affected (think scabies)
  • The dorso-lumbar area is not affected (more consistent with flea allergy)
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44
Q

What are the licensed medications for canine atopic dermatitis?

A

Glucocorticoids
Ciclosporin
Oclacitinib (Apoquel)
Lokivetmab (Cytopoint)

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45
Q

What is an unlicensed medication for canine atopic dermatitis?

A

Antihistamines

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46
Q

How is canine atopic dermatitis treated?

A
  • Topical therapy – antimicrobial, soothing, glucocorticoids, steroid
  • Shampoos – malaseb is antimicrobial, allermyl is soothing
  • Essential fatty acids – supplements, diets and topicals
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47
Q

What are the possible adverse reactions to ASIT?

A

Pruritis
Vomiting
Urticaria
Angioedema
Anaphylaxis

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48
Q

What is CAFR?

A

Cutaneous adverse food reaction - relevance of food-specific IgE and IgG

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49
Q

How is CAFR diagnosed?

A
  • Do not use serology tests to make a diagnosis or suggest the constituents of a diet trial
  • Diagnosis by elimination of signs following a restricted protein and carbohydrate diet
  • Duration at least 6-12 weeks
  • Rechallenge/provocation with the original diet
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50
Q

What are the common triggers of CAFR in cats and in dogs?

A

Dogs = beef, dairy, chicken, wheat

Cats = beef, fish, chicken

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51
Q

When is insect bite hypersensitivity in horses common?

A
  • Common, April to October
  • Usually over 2 years old at onset
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52
Q

Where is insect bite hypersensitivity common?

A

Mane
Tail
Lateral neck
Tail to croup – ventral midline

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53
Q

What are the clinical signs of insect bite hypersensitivity?

A

Pruritis causing rubbing
Biting
Stamping
Agitation
Alopecia
Crusting and erosions – lichenification and hyperpigmentation

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54
Q

How is insect bite hypersensitivity treated?

A
  • Avoidance – manage pasture grazing and housing, stable at high risk periods, such as at dusk and dawn
  • Protective fly wear
  • Application of licensed permethrin or cypermethrin based emulsion
  • Antihistamines
  • Glucocorticoids
  • Allergen specific immunotherapy does not appear effective
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55
Q

What are the other causes of pruritus in horses?

A
  • Atopic disease
  • Insect bit hypersensitivity due to other insects
  • Mites – chorioptes typically on distal limbs
  • Pediculosis
  • Oxyurasis – perineum
  • Onchocerciasis
  • Post clipping
  • Contact reactions
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56
Q

When is ovine culicoides hypersensitivity common/

A
  • Seasonal recurrence
  • Particularly severe September to October
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57
Q

What are the clinical signs of ovine culicoides hypersensitivity?

A
  • Foot stamping, dropping to the ground and sternal recumbency
  • Non-wool areas of the body are usually affected
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58
Q

What is surface pyoderma?

A
  • Infection is confined to the interfollicular epidermal layers of the skin
  • Pyotraumatic dermatitis ‘hot spots’
  • Intertrigo ‘skin fold dermatitis’
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59
Q

What are the clinical signs of surface pyoderma?

A
  • Erythema, erosion, serosanguineous to purulent exudate
  • Often very uncomfortable – pruritic and painful
  • Matted fur
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60
Q

How is pyogranulomatous dermatitis diagnosed?

A

Cytology of exudate

Find underlying cause – may vary with location: otitis externa for facial lesions, fleas for caudal dorsum lesions

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61
Q

How is pyogranulomatous dermatitis treated?

A

Topical antimicrobial therapy and oral/topical steroids

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62
Q

What are the clinical signs of superficial pyoderma?

A
  • Intraepidermal pustules (primary) easily disrupted by grooming, scratching or bathing
  • Lesions and sometimes the pruritus are antibiotics responsive
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63
Q

What are the common underlying disorders of superficial pyoderma?

A

Ectoparasitism
Allergy
Endocrinopathies

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64
Q

Describe the lesions of superficial pyoderma.

A
  • Primary lesions may be transient and secondary lesions may predominate – crusting, erosion
  • Peripheral spread produces an annular lesion with a peeling epidermal collarette
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65
Q

What are the clinical signs of deep pyoderma?

A

Swelling/nodules
Draining tracts
Crusting
Ulceration
Often painful

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66
Q

How is deep pyoderma diagnosed?

A

Cytology and culture of draining fluid may not be representative – biopsy for deep material

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67
Q

Why is topical therapy the treatment of choice for pyoderma?

A
  • Removes scale, crust and exudate
  • Reduced the number of bacteria
  • Promotes drainage of deeper lesions
  • Can reduce pain and pruritis
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68
Q

When are antibacterial agents used in pyoderma?

A

Only if really needed. Severity, temperament, deep pyoderma. Only for superficial pyoderma if there is no way we can manage things without other therapy.

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69
Q

Name the narrow spectrum bacteriostatic antibiotic used for pyoderma.

A

Clindamycin

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70
Q

Name the 3 broad spectrum bacteriocidal drugs used in pyoderma.

A

Trimethoprim/sulphonamides
Clavulanic acid and amoxicillin
Cefalexin

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71
Q

What is dermatophilus?

A

Dermatophilus congolensis - zoonotic

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72
Q

What are the clinical signs of dermatophilus?

A

Distribution of matted hair
Crusts and erosions
Fissuring
Pain
Lameness

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73
Q

What are the differentials of dermatophilus?

A
  • Dermatophytosis, bacterial folliculitis (staph)
  • Photosensitisation
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74
Q

How is dermatophilus diagnosed?

A
  • Smears from under side of crusts
  • Dermatophilosis preparation from crusts – saline maceration
  • Demonstration of branching fam positive filamentous bacteria with internal compartments, ‘tram track’ appearance
  • Culture
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75
Q

What are the predisposing factors of dermatophilus?

A

Excessive moisture
Biting insects
Abrasive pasture
Excessive brushing

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76
Q

How is dermatophilus treated?

A
  • Clean affected area with topical antibacterial agents, such as chlorhexidine
  • Some may benefit from a 3-5 day course of penicillin/streptomycin
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77
Q

What are malassezia?

A
  • Opportunistic yeast pathogen
  • Normally resident in the external ear canal, the chin, perioral and interdigital areas
  • Lipid dependent yeasts
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78
Q

What are the predisposing factors of malassezia?

A
  • Alterations in skin microclimate – sebum production, moisture
  • Allergic and bacterial skin disease
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79
Q

What are the clinical signs of malassezia?

A

Pruritus
Erythema
Scale
Hyperpigmentation
Greasiness
Malodour

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80
Q

How is malassezia diagnosed?

A
  • Impression smears with a dry swab or direct slide contact
  • Acetate tape strip preparations
  • Culture
  • Serology – not recommended
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81
Q

How is malassezia treated?

A

Topical therapy with twice weekly bathing with shampoo products

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82
Q

Why may otitis externa be a sign of malassezia infection?

A

The ceruminous glands provide a lipid-rich medium for the organisms to survive, they are commensals in this environment

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83
Q

How can otitis externa due to malassezia infection be treated?

A

In some cases topical or oral steroids will help to control the glandular hyperplasia and cerumen production within the ear canal and starve the yeast

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84
Q

What are the primary lesions of atopic dermatitis?

A

Erythema, papules and pruritus

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85
Q

Which of these cutaneous microbial infections are zoonotic?

A

Dermatophytosis
Dermatophilosis

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86
Q

What are the 4 main manifestations/clinical syndromes of pruritic/allergic dermatitis in cats?

A
  • Self-induced alopecia/hypotrichiosis (SIAH)
  • Miliary dermatitis/popular dermatitis
  • Head and neck pruritus
  • Eosinophilic granuloma complex
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87
Q

Describe head and neck pruritus.

A
  • Self-trauma leads to excoriation, erosion and ulceration
  • Blepharitis
  • Can be ulcerative with wounds caused by scratching
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88
Q

What is miliary dermatitis?

A

Crusted papules commonly seen with flea bite hypersensitivity, food allergy and feline atopic skin syndrome

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89
Q

What are the differential diagnoses of miliary dermatitis?

A
  • Allergic skin disease
  • Ectoparasites
  • Dermatophytosis and rarely bacterial folliculitis
  • Pemphigus foliaceus
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90
Q

What does eosinophilic granuloma complex include?

A
  • Eosinophilic ulcer
  • Eosinophilic plaque
  • Eosinophilic/linear granuloma
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91
Q

Describe the lesions of eosinophilic plaques.

A

Pruritic, raised, often ulcerated

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92
Q

Where are eosinophilic plaques located?

A

Found anywhere on the body, often ventral abdomen and medial thighs

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93
Q

What can eosinophilic plaques be seen concurrently with?

A

Miliary dermatitis
Eosinophilic granuloma of the chin

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94
Q

How is the underlying cause of eosinophilic plaques investigated?

A
  • Look for evidence of fleas
  • Flea treatment trial
  • Elimination diet trial
  • Feline atopic skin syndrome
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95
Q

Describe the lesions of eosinophilic (/rodent/idolent) ulcers.

A
  • Distinct well-demarcated
  • At philtrum of upper lip or adjacent to upper canine tooth
  • Large lesions – may cause facial distortion
  • Pain and/or pruritus are rare
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96
Q

How are eosinophilic ulcers diagnosed?

A

Consider biopsy to rule out neoplasia and bacterial/fungal infections for chronic lesions

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97
Q

How are eosinophilic ulcers treated?

A
  • Small single lesions, leave the cat intreated if they are not bothered by them
  • Manifestation of allergic skin disease, treat underlying cause
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98
Q

Describe eosinophilic/linear granuloma lesions.

A
  • May or may not be pruritic
  • Linear form often seen on caudal thigh
  • Proliferative lesions in mouth
  • Poorly defined chin swelling/fat chin
  • Erosion/ulceration common
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99
Q

What may be associated with eosinophilic/linear granulomas?

A
  • Can see concurrently with cutaneous eosinophilic granulomas and plaques
  • Oral cavity disease may be associated with halitosis, anorexia and hypersalivation
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100
Q

How are eosinophilic/linear granulomas treated?

A

Oral cavity lesion – surgical debulking

Glucocorticoids, ciclosporin, topical therapy – does topical stimulate more overgrooming by trying to get medication off

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101
Q

What may CAFR be concurrent with?

A

Flea bite hypersensitivity or feline atopic skin syndrome

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102
Q

What are the possible non-cutaneous signs of CAFR?

A

Vomiting
Diarrhoea
Respiratory signs
Conjunctivitis
Hyperactive behaviour

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103
Q

How is CAFR diagnosed?

A

Elimination of signs following an elimination diet trail. Re-challenge – re-introduce the original diet in its entirely, clinical signs recur within 7 days

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104
Q

What are the problems of diet trials?

A
  • Potential problems with palatability
  • Cats can access other sources of food, such as hunting
  • Difficult to evaluate a food trials in a cat allowed outdoors
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105
Q

What are the treatment options of pruritus in cats?

A
  • Essential fatty acids – to protect the skin barrier
  • Antihistamines
  • Oclacitinib
  • Allergen specific immunotherapy
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106
Q

What is the dosage of glucocorticoids in cats?

A

Intial dose 1-2mg/kg/day of prednisolone – higher than in dogs

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107
Q

What are the adverse effects of long term glucocorticoid therapy in cats?

A
  • PUPD
  • Polyphagia
  • Weight gain
  • Diabetes mellitus
  • Iatrogenic hyperadrenocorticism (skin fragility)
  • Infections (dermatophytosis, bacterial cystitis)
  • Demodicosis
  • Gastrointestinal signs
108
Q

Describe cyclosporin usage in cats?

A
  • Calcineurin inhibitor – affects T cells
  • Check for exposure to FIV/FeLV and toxoplasma before treatment
  • Toxoplasma naïve cats on cyclosporin may be more likely to develop clinical signs of toxoplasmosis if exposed during treatment
  • 4 weeks
  • Concurrent glucocorticoids initially
109
Q

What are the adverse effects of cyclosporin in cats?

A

Vomiting
Diarrhoea
Lethargy
Anorexia
Hypersalivation

110
Q

What is flea bite hypersensitivity?

A
  • Clinical condition seen in animals which have become sensitised to antigenic components of flea saliva
  • The immunopathogenesis of the condition in the dog is thought to involve type I and type IV (delayed) hypersensitivity reactions
111
Q

How is flea bite hypersensitivity diagnosed?

A
  • History and compatibly clinical signs
  • Evidence of fleas or flea excreta in the hair coat
  • Dipylidium caninum infestation – positive response to flea control programme, elimination of differential diagnoses. Positive test response to intradermal/serology testing with flea saliva allergen is not diagnostic
112
Q

How are fleas controlled?

A
  • Shampoos, collars, sprays, powders, spot-ons
  • Consider hair coat length and bathing/swimming
  • Use of insecticidal products
  • Insect growth development inhibitors
  • Thorough vacuuming
  • Carpet shampooing and steam cleaning are not recommended – the residual humidity is ideal for hatching and larval development
113
Q

How is sarcoptic mange/scabies and chorioptic mange diagnosed?

A

Superficial skin scrapes

114
Q

How is sarcoptic mange/scabies treated?

A

Macrocyclic lactones and isoxazolines

115
Q

What are the species differences in location of chorioptic mange in large animals?

A

Horses – distal limbs, often in heavily feathered horses

Cattle – tail base, distal limbs, udder

Alpacas – tail base, distal limbs, extension to ventral abdomen, medial limbs and the ears in alpacas

116
Q

How is chorioptic mange in large animals treated?

A
  • Treat all affected and in contact animals as well as the environment – carrier status
  • Macrocyclic lectone, topicals
  • Duration of treatment is 2 life cycles = 6 weeks
117
Q

Distinguish chorioptes bovis and equi.

A

Chorioptes bovis need host to survive long term

Chorioptes equi can survive off host for several weeks

118
Q

How is chorioptes treated in camelids?

A
  • Macrocyclic lactones are less effective in camelids – may need higher doses and longer treatmnet course
  • Double dose ivermectin in camelids
  • Topicals not licensed
  • Treatment reduces mites not eliminates
119
Q

Distinguish the lesion locations of chorioptic mange and lice in cattle.

A

Chorioptes - neck, legs, tail base, rump

Lice - ear base, neck, legs, dorsum midline

120
Q

When are lice in cattle more apparent?

A

Winter months

121
Q

What are the clinical signs of louse pediculosis?

A

Pruritis
Alopecia
Excoriation
Self-wounding
Anaemia

122
Q

How is pediculosis treated?

A

Spot-on/pour-on of synthetic pyrethroids and macrocyclic lactones

123
Q

How does treatment of pediculosis depend on the louse species?

A

Biting should respond to macrocyclic lactones

Sucking may require topical therapy as well, such as cypermethrin

124
Q

What are the clinical signs of psoroptic mange?

A

Severe pruritus
Some asymptomatic

125
Q

How is psoroptes mange diagnosed?

A

Superficial skin scrapings
Serology

126
Q

How is psoroptic mange treated?

A

Treat whole flock

127
Q

Which of these systemic treatments for allergic skin disease are licensed for use in cats?

A

Cyclosprin and prednisolone

128
Q

What are the causes of erosion/ulceration?

A
  • Trauma - mechanical (pyotraumatic dermatitis, surface pyoderma), thermal and chemical injuries
  • Radiation
  • Neoplasia
  • Infection
129
Q

What is the pathogenesis of immune mediated skin disease?

A

Drugs, neoplasia, systematic disease, variety of immune mechanisms. Different diseases will target different layers of the skin causing different types of lesions to form.

130
Q

How is immune mediated skin disease treated?

A

Therapy

131
Q

What can be associated with pemphigus?

A

Neoplasia
Infectious agents
Drugs
Autoimmune disorders
Certain haplotypes
Pregnancy
Chronic skin disease

132
Q

Describe the lesions of pemphigus.

A

Fragile pustules produces layers of crust

133
Q

What are the clinical signs of canine pemphigus foliaceus?

A
  • Skin lesions on face, pinnae, footpads, trunk
  • Pruritus
  • Primary lesions – vesicles and pustules are often transient, may look like superficial pyoderma
  • Secondary lesions – trauma readily leads to crusting and erosions, scaling, alopecia
134
Q

How can canine pemphigus foliaceus be diagnosed?

A

Cytology of pustule
Bacterial culture and sensitivity
Skin biopsy for histopathology and bacterial and fungal culture

135
Q

Describe the cytology of canine pemphigus foliaceus pustules.

A
  • Numerous acantholytic keratinocytes – which are round in shape but free floating
  • Neutrophils (eosinophils in some cases)
  • No cocci
136
Q

Describe the bacterial culture and sensitivity of canine pemphigus foliaceus pustules.

A
  • Should be sterile but can see substantial secondary bacterial infection
  • Cocci may be present on cytology
  • Treat first for microbial infection then collect samples
137
Q

What is feline pemphigus foliaceus?

A
  • Most common form of autoimmune skin condition of the cat
  • Drug eruption has been documented as an underlying cause
  • There are no breed, sex or age predilections
138
Q

Where are lesions located in feline pemphigus foliaceus?

A

Pinnae, nasal planum, face, bridge of the nose, muzzle, eyes, tail and ventral abdomen and around the nipples

139
Q

What are the clinical signs of feline pemphigus foliaceus?

A
  • Claw beds can have a thick caseous green purulent discharge
  • Transient pustules and vesicles – readily replaced by erosions and overlying crusts
140
Q

How is feline pemphigus foliaceus diagnosed?

A
  • May be confused with dermatophytosis – a fungal culture will usually be negative
  • Cytology of undisturbed pustule = numerous neutrophils/eosinophils with acantholytic keratinocytes
  • Skin biopsy and histopathology
141
Q

How is pemphigus treated?

A
  • Glucocorticoids - slowly reduce over weeks
  • Azathioprine – not recommended for cats
  • Chlorambucil
  • Ciclosporin
142
Q

Describe the lesions of canine discoid lupus erythematous.

A

Photosensitive dermatosis that involves the nasal planum
Hypopigmentation
Erythema
Scaling
Erosions and ulcerations
Loss of normal architecture (leathery nose appearance becomes smooth and shiny)

143
Q

How is canine discoid lupus erythematous treated?

A
  • Topical glucocorticoids
  • Topical tacrolimus
  • UV protection
  • Vitamin E
  • Essential fatty acids
  • Nicotinamide and tetracycline
  • Oral glucocorticoids
  • Ciclosporin
  • Azathioprine
  • Chlorambucil
  • Nasal flap plastic surgery
  • Nose protectors
144
Q

What are the clinical features of equine pastern dermatitis?

A
  • Hind pasterns
  • Cellulitis, ulceration and crusting, oedema
  • Fissuring occurs because of mobility of the skin
  • Granulation tissue may be excessive if healing is delayed
  • Lameness
145
Q

What are the differential diagnoses and causes of equine pastern dermatitis?

A
  • Immune mediated – pemphigus foliaceus, vasculitis
  • Bacterial infection – staphylococci, dermatophilus
  • Parasites – chorioptic mange/thrombiculidiasis
  • Dermatophytosis
  • Contact dermatitis – likely to affect all legs
  • Photosensitisation – white socks
  • Chronic progressive lymphoedema
  • Keratinisation defects
146
Q

What are scales?

A

Scales are loose fragments of keratin debris. Most scales are dry, powdery or flaky. Can see waxy, greasy scales in some disorders and can be associated with rancid odour.

147
Q

What causes scales?

A

Scale formation is a major finding in disorders of the process of cornification

148
Q

List 4 mechanisms of scale formation.

A
  • Abnormalities in epidermal cell turnover
  • Abnormalities in keratin synthesis and/or intra-epidermal lipid synthesis
  • Abnormalities in surface keratinocyte cohesion
  • Abnormalities in sweat or sebaceous gland function
149
Q

Name 8 primary keratinisation disorders causing scale formation.

A
  • Sebaceous adenitis
  • Idiopathic nasodigital hyperkeratosis
  • Ichthyosis
  • Zinc associated dermatosis
  • Lethal acrodermatitis in English bull terriers
  • Vitamin A responsive dermatosis
  • Ear margin dermatosis
  • Feline acne
150
Q

Which breeds are more susceptible to idiopathic nasodigital hyperkeratosis and why?

A

Brachycephalics as nose is further back and muzzle further forward so keratin gets less wear

151
Q

What is ichthyosis?

A
  • Congenital/hereditary
  • Primary defects in formation of stratum corneum – increased stratum corneum production, decreased corneocyte desquamation/retention hyperkeratosis
152
Q

What are some possible underlying causes of secondary scale formation?

A
  • Inflammation – allergy, parasites, microbial infection
  • Endocrine imbalances
  • Nutritional factors
  • Environmental
153
Q

What are some nutritional causes of secondary scale formation?

A
  • Zinc responsive dermatoses
  • Hepatocutaneous syndrome
  • Fatty acid deficiency/responsive dermatosis
  • Vitamin A responsive dermatosis
154
Q

What are the clinical signs of zinc responsive dermatosis?

A
  • Erythema and alopecia
  • Scaling and crusting
  • Can be pruritic
155
Q

What is type I zinc responsive dermatosis?

A

Unable to absorb zinc

Periorbital, dorsal nose, lateral aspect of the muzzle, ventral mandible, pinnae, foot pads

156
Q

How is type I zinc responsive dermatosis diagnosed?

A

Clinical signs
Compatible histological findings
Measuring zinc levels in blood or hair not diagnostic

157
Q

What is type II zinc responsive dermatosis due to?

A

Diet low in zinc, high in phytate or calcium

158
Q

What is scaling a common clinical signs of in goats and alpaca?

A

Pyoderma
Ectoparasites
Rare primary disorders in pygmy goats

159
Q

How are scaling disorders managed?

A

Address the underlying cause – treat all secondary microbial infections

Topical therapy for scaling

160
Q

Distinguish keratolytic and keratoplastic activity.

A

Keratolytic – this causes damage to keratinocytes with subsequent shedding

Keratoplastic – affects the kinetics of basal cell turnover

161
Q

What are the 3 stages of the hair cycle?

A

Anagen = active growth

Catagen = involution of the hair shaft

Telogen = no growth, hair is retained until anagen is initiated

162
Q

Ditsinguish anagen and telogen hairs.

A

Anagen hairs have bulb like end to them and telogen have tapered paintbrush appearance

163
Q

What are the 3 pathogenic mechanisms that result in alopecia?

A
  • Destruction or distortion of normally growing hair follicles and hair shafts
  • Abnormalities of the hair cycle (causing atrophy of hair follicles and regression of hair growth)
  • Abnormalities of hair follicle and hair shaft development (causing structural defects, hair fragility and failure of normal growth of hair)
164
Q

What are some conditions that could cause alopecia by destructing/distortion of hairs?

A
  • Traumatic alopecia
  • Folliculitis - bacterial folliculitis, dermatophytosis, demodicosis
  • Inflammatory alopecia – vascular diseases, sebaceous adenitis, neoplasia
165
Q

Describe the lesions and alopecia caused by bacterial folliculitis.

A
  • Secondary to an underlying disease process, such as, atopic dermatitis
  • Pustules centred on hair follicles
  • Small areas of alopecia ‘moth-eaten coat’
166
Q

What causes dermatophytosis?

A
  • Contagious and zoonotic
  • Microsporum and trichophyton species
  • Infection by contact with infected animals, contaminated hair or scale in the environment
167
Q

What is the pathogenesis of dermatophytosis?

A
  1. Initially fungal arthrospores need to adhere to the skin – microtrauma from clipping, self-trauma
  2. Invasion of the superficial layers of the skin through production of enzymes such as proteases
  3. Contribute to breakdown of the keratinocytes
168
Q

What is the incubation period of dermatophytosis?

A

1-3 weeks

169
Q

What are the clinical signs of dermatophytosis?

A

Alopecia and scale with central healing
Pruritus is variable

More unusual presentations:
- Onychomycosis
- Granulomas
- Pustular form that resembles bacterial pyoderma or pemphigus foliaceus

170
Q

Describe dermatophytosis in Persian cats.

A

Can see severe, chronic and generalised infections. Do not mount a sufficient immune response

171
Q

How is dermatophytosis diagnosed?

A
  • Microscopy for the identification of ectothrix arthroconidia spores – but this is difficult
  • Culture of hair and scale
  • Fungal culture
  • Skin biopsies – fungal culture and histopathology
  • PCR
  • Wood’s lamp
172
Q

How does wood’s lamp diagnose dermatophytosis?

A
  • Use the lamp for several minutes to allow lesions to fluoresce
  • Only useful for M. canis isolates
173
Q

If dermatophytosis is self-limiting in healthy animals, why do we treat it?

A
  • Contagious and zoonotic
  • Shorten disease course
  • Topical therapy reduces environmental contamination > reduces risk of exposure and false positive cultures
174
Q

How can topical therapy treat dermatophytosis?

A

Help reduce environmental contamination – infection may spread up to 6 cm from the obvious lesions. Shampoos, dips/rinses, wash 2x weekly

175
Q

Can clipping treat dermatophytosis?

A

Controversial – may reduce the environmental and host load but may spread the disease on the affected animal

176
Q

How can systemic therapy be used to treat dermatophytosis?

A

Systemic therapy – eliminates infection from within the hair follicle

Itraconazole - cats
Ketoconazole - dogs

Treat for 7 days on, 7 days off

177
Q

Describe equine dermatophytosis.

A
  • Trichophyton spp. usually
  • Direct contact
  • Spontaneous resolution
  • Alopecia, crusting and scale
  • Spontaneous remission can occur – but zoonotic risk
178
Q

How is equine dermatophytosis treated?

A
  • Topical therapy with miconazole shampoo or enilconazole
  • Disinfection of the premises and grooming equipment, tack
179
Q

How is canine demodicosis diagnosed?

A
  • Deep skin scrapings – live in hair follicles
  • Hair plucks
  • Skin biopsies for chronic lesions, thickened skin. Not routine for finding demodex or other mites
180
Q

Describe generalised demodicosis.

A

More than 5 lesions, 1 major body region affected, 2 or more feet

181
Q

How is generalised demodicosis treated?

A
  • Must be treated, although some juvenile cases may spontaneously recover, perhaps due to the immune system maturing
  • Must not be used for breeding as can pass it on
182
Q

What is juvenile onset/localised demodicosis?

A
  • Mild disease that rarely becomes generalised
  • Lesions are focal areas of alopecia and erythema
183
Q

How is juvenile onset/localised demodicosis treated?

A

Do not need to treat localised disease, as there is spontaneous resolution in large proportion of cases, resistance

184
Q

What are the underlying disease processes of adult-onset demodex?

A

Immune suppression
Corticosteroid therapy
Hyperadrenocorticism
Chemotherapy
Neoplasia
Hypothyroidism?
Idiopathic

185
Q

What are the diagnostic tests for adult onset demodex?

A

History – drug therapies?
Haematology
Serum biochemistry
Endocrine function tests
Urinalysis
Lymph node biopsy
Diagnostic imaging

186
Q

How can adult onset demodex be treated?

A

Acaricidal treatment – moxidectin, isoxazolines

Bathe with chlorhexidine based shampoo 3 times a week, only if necessary, oral cefalex

187
Q

What may abnormalities with hair cycle be associated with?

A

With other cutaneous signs – thinning of the skin, comedones, recurrent pyoderma, scaling, hyperpigmentation

188
Q

What is cyclical flank alopecia?

A

Changes in daylight hours

189
Q

What is follicle dysplasia/dystrophy?

A
  • An abnormality of the morphogens that influence the development of the hair follicle that does not allow hair growth
  • Not associated with hair cycle problems
  • Congenital – Chinese crested dogs with an ectodermal defect and profound alopecia
190
Q

What is colour dilution alopecia?

A

Instead of having an even distribution of melanin and pigment across the hair shaft, it clumps together. These large clumps can distort the hair shaft and cause a weakness. The hairs then break under normal environmental conditions and will usually break around the skin surface and give the appearance of alopecia

191
Q

How is hair follicle dysplasia diagnosed and treated/

A

Diagnosis – histopathology, rule out endocrine disease?

Treatment – none

192
Q

What is perivascular dermatitis without epidermal involvement?

A

Inflammatory infiltrate around potentially dilated superficial blood vessels, can also be associated with superficial oedema, which looks like dermal pallor on histopathology.

193
Q

What species does perivascular dermatitis without epidermal involvement affect?

A

Horse and dog

194
Q

What are the consequences of perivascular dermatitis without epidermal involvement?

A
  • Acute lesion
  • Urticaria
  • Type I (type III) hypersensitivity to a wide range of allergens
195
Q

What is perivascular dermatitis with epidermal hyperplasia?

A

As well as inflammatory infiltrate around superficial blood vessels, there is thickening of the epidermis and may see rete peg formation, where the epidermis dips up and down into the dermis. May later see excess accumulation of keratin on the epidermal surface/hyperkeratosis.

196
Q

What are the consequences of perivascular dermatitis with epidermal hyperplasia?

A
  • Keratinisation defects
  • Callus
  • Allergic dermatitis type I hypersensitivity
  • Contact (irritant) dermatitis – rare
  • Sarcoptic mange
  • Atopic dermatitis
197
Q

What are the histological features of type I hypersensitivity?

A
  • Epidermal hyperplasia
  • Spongiosis
  • Hyperkeratosis and follicular keratosis
  • Dermal oedema
  • Superficial perivascular dermatitis involving mast cells and eosinophils
  • Late stage mononuclear cell infiltrate
198
Q

What is epidermal hyperplasia?

A

Marked epidermal hyperplasia for the extension of the epidermis into the dermis. Loss of pigment from dermis/pigmentary incontinence, and pigment is free in dermis or in macrophages following phagocytosis.

199
Q

How does perivascular dermatitis with epidermal spongiosis develop?

A
  1. Intercellular oedema due to vascular exudate
  2. Acute
  3. If progresses, oedema may rupture intercellular bridges and form a spongiotic vesicle

Can see this with UV damage

200
Q

Distinguish direct and indirect perivascular dermatitis with epidermal spongiosis.

A

Direct – sunburn/solar dermatitis/primary phototoxicity

Indirect – photosensitisation via photodynamic agent – plant or drug

201
Q

What is vasculitis?

A

Inflammatory cells attach the blood vessel walls, leading to a loss of blood supply to that area of skin/ischaemia. Inflammatory cells pass from vessels to dermis so hard to differentiate from normal cell movement. Other signs include a fibrin deposition within the blood vessel, and therefore thrombus formation, perivascular haemorrhage and oedema. Gives glassy pink appearance on histology.

202
Q

What is interface dermatitis?

A

Inflammatory cells, typically lymphocytes obscure the dermal-epidermal junction. Associated with thickening or clefting of the basement membrane, apoptotic/dying keratinocytes and hydropic degeneration of the basal keratinocytes. Vaculated appearance (‘bubblies’).

203
Q

What is nodular to diffuse granulomatous dermatitis?

A

Nodular accumulation. Associated with granulomatous inflammation, where granulocytes dominate.

204
Q

What is intraepidermal vesicular-pustular dermatitis?

A

Can be superficial and sub-corneal. When inflammatory cells are sparse = vesicle, when the content is highly cellular = pustule. Associated with some degree of dermal inflammatory infiltrate.

205
Q

How do pustules form?

A

Formation of pustule involves breakdown of intercellular bridges/acantholysis. Autoimmune or bacterial disease. Once broken down, fluid and sometimes free floating keratinocytes/acantholytic keratinocytes can be found within the pustule with/without inflammatory cells.

206
Q

What is the most common cause of pustules?

A

Superficial pyoderma

207
Q

What are some causes of pustules?

A
  • Bacteria in pustule
  • Degenerate neutrophils
  • Porcine exudative dermatitis – greasy pig disease/S. hyicus
  • Sterile pustular dermatitis conditions - pemphigus
  • Insect mediated dermatitis
208
Q

What causes subepidermal vesicular pustular dermatitis?

A

Autoimmune and immune-mediated skin diseases:

  • Bullous pemphigoid - autoantibody to BMZ component
  • Mechanobullous disease - inherited defect
209
Q

What are the 3 stages of skin disease centred on hair follicles?

A
  1. Perifolliculitis – inflammatory infiltrate surround the hair follicle
  2. Folliculitis – where cell invade follicular wall or lumen
  3. Furunculosis – follicular wall rupture
210
Q

Name the 3 most common causes of skin disease centred on hair follicles.

A

Deep pyoderma, dermatophytosis and demodicosis

211
Q

What is fibrosing dermatitis post inflammatory granulation?

A

Associated with replacement of normal dermal and adnexal structures, such as hair follicles and sebaceous glands, with granulation tissue. Non-specific pattern associated with the end stage of an intense destructive inflammatory reaction or signify an ongoing insidious reaction.

212
Q

What is panniculitis?

A

Inflammation of the fat, that often involves secondary inflammation of the dermis or because of dermal inflammation. Can take 3 forms: lobular – multi-nodule appearance to the inflammatory infiltrate, septal – inflammatory cells are seen in connective tissue between lobules of fat, diffuse. All 3 can be seen in 1 patient and cannot be used to identify the underlying disease process.

213
Q

What is atrophic dermatopathy?

A

Complex collection of endocrine and metabolic diseases

214
Q

What are the clinical features of atrophic dermatopathy?

A
  • Alopecia
  • Increase or decrease pigmentation
  • Coarse, dry, dull, brittle coat
  • Secondary keratinization/infection
215
Q

What is the consequence of atrophic dermatopathy?

A

Thin and hyperkeratotic epidermis

216
Q

What are the indications for skin biopsy?

A
  • Neoplasia
  • Unusual or serious generalised dermatosis
  • Condition poorly responsive to therapy
  • Other diagnostic tests not helpful
  • Vesicles, bullae, erosions, ulcerations
217
Q

What are papillomas?

A

Papillomavirus is a DNA virus that is host specific and possibly site specific

218
Q

Describe the dermatohistopathology of papillomas.

A
  • Solitary to multiple
  • May regress spontaneously due to cytotoxic immune response
  • Exophytic
  • Cauliflower like
  • Hyperplastic/keratotic squamous epithelium
  • Fibrovascular stalk
219
Q

Describe the dermatohistopathology of squamous cell carcinomas.

A
  • UV associated
  • Thin haired, unpigmented skin
  • Eyelids, ear tips
  • Invasive cords of squamous epithelium
  • Intercellular bridges
  • Keratin pearls
  • Pleomorphic, mitotic
  • Scirrhous reaction – fibrous tissue forms around the mass
  • Peripheral inflammation
220
Q

Name 3 examples of tumours of hair follicles.

A

Infundibular cyst
Infundibular keratinising acanthoma
Trichoblastoma

221
Q

What are infundibular cysts?

A

Marked thickening of the epithelial lining of the hair follicle, which pushes other structures upwards. Keratinaceous material forms within the cyst, and can rupture occasionally releasing this material on the surface of the skin.

222
Q

What are infundibular keratinising acanthomas?

A

Material protrudes out of the infundibulum, which can clinically have a tooth paste like appearance. Benign process

223
Q

Name 4 types of sebaceous gland masses.

A
  • Sebaceous hyperplasia – benign proliferation of normal sebaceous glands
  • Sebaceous adenoma – benign, may recur
  • Sebaceous adenocarcinoma – rare, infiltrative, may metastasise
  • Sebaceous cysts - older dogs
224
Q

Describe the dermatohistopathology of circumanal/hepatoid gland hyperplasia/adenomas.

A
  • Lobulated, one or more
  • Arbitrary distinction hyperplasia/adenoma
  • Benign but can be big
  • Excision may be difficult as close to anal ring
  • Partially castration responsive
225
Q

What are the characteristics of anal sac apocrine tumours?

A
  • Infiltrative
  • Metastatic
  • Pseudo-hyperparathyroidism
  • Paraneoplastic hypercalcaemia
226
Q

How do lipomas appear on histopathology

A

As normal fat cells

227
Q

Distinguish fibromas and fibrosarcomas.

A

Fibroma – mostly cat, well circumscribed, bundles and whorls of collagen, uniform fibroblasts, benign

Fibrosarcoma – more cellular, pleomorphic (can form giant cells), more mitotic figures, rapid growth, infiltrative, non-metastatic

228
Q

Describe the dermatohistopathology of sarcoids.

A
  • Bovine papilloma virus DNA in lesions
  • Hyperplastic epidermis
  • Whorls and bundles of collagen/fibroblasts
  • Lack of normal adnexa structures
  • Usually low mitoses
229
Q

What are the tumour characteristics of sarcoids?

A
  • Locally infiltrative
  • Not metastatic
  • May recur after removal and become more aggressive
230
Q

Describe the dermatohistopathology of histicytomas.

A
  • Red appearance
  • Solitary
  • Raised
  • Benign
  • Spontaneously regress due to cytotoxic lymphocytes
  • Do not recur after excision
  • Dendritic Langerhans cells
  • Highly mitotic
  • Lymphoid infiltrate
231
Q

What are the tumour characteristics of mast cell tumours in dogs?

A
  • Infiltrative
  • Local recurrence
  • Metastasise to local LNs
  • More malignant if scrotal, inguinal or preputial
  • Paraneoplastic with histamine
232
Q

What are the tumour characteristics of mast cell tumours in cats?

A

Relatively benign, rarely recur or metastasise

233
Q

Describe the dermatohistopathology of mast cell tumours.

A
  • Sheet mast cells
  • Varying differentiation and depth of infiltration
  • Eosinophils
  • Lymphoid aggregates
234
Q

Describe melanocytomas.

A
  • Usually pigmented
  • Dermal infiltrate and epidermal nests – junctional activity
  • Benign, potential to become malignant
235
Q

Describe the dermatohistopathology of malignant melanomas.

A
  • Pleomorphism
  • Mitosis
  • Invasiveness
  • Diffuse epidermal infiltration higher than junctional
  • Not more pigmented may be amelanotic
236
Q

Describe the dermatohistopathology of equine melanomas.

A
  • Grey horses - perineum, ventral tail, genital, periocular, pinnal
  • Pigmented
  • Slow growing
  • Clusters melanocytes and melanophages
  • Dermal
  • Little junctional activity
237
Q

Define discharging sinus.

A

The intense inflammatory response to infectious agents/foreign material may lead to the formation of a tract between the epidermis surface an deeper tissues – can also be seen with cat bite abscess.

238
Q

When are nodules seen?

A
  • Skin tumours
  • Deep infections – bacterial, fungal, abscesses, leishmania
  • Foreign material – plant material, tick bites, furunculosis
  • Sterile inflammation
239
Q

How can infectious nodules associated with discharging sinus tracts be investigated?

A
  • Exudate – granules may be more likely associated with infection
  • Diff-Quik, Gram stain
  • Ziehl Neelsen when mycobacteria suspected
240
Q

What are some infectious cases of nodules?

A

Bacteria – staphylococcus, mycobacteria

Fungi – mycetoma causes subcutaneous fungal infections and deep or systemic fungal infection

241
Q

Describe the nodules involved with feline tuberculosis.

A
  • Nodular ulcerated lesions
  • Subcutaneous tissue/joints/bone
  • Regional lymphadenopathy
  • Systemic pulmonary involvement
  • Zoonotic potential
242
Q

How is feline tuberculosis diagnosed?

A
  • Cytology/biopsy for Ziehl Neelsen
  • Culture
  • Assess organ involvement – imaging
  • Serological tests available (APHA and Biobest)
243
Q

What is the epidemiology of feline leprosy?

A
  • Associated with 3 mycobacterial species
  • Infection spread by bites from wildlife reservoir
  • Likely contracted by contamination of wound with soil
244
Q

How do sterile granulomas and pyogranuloma syndrome differ between tissues?

A
  • Ocular tissues including the eyelids and nictitating membrane
  • Nasal tissues leading to snoring
  • Head – dorsal muzzle and occasionally pinnae
245
Q

What are some examples of sterile inflammation that cause nodules?

A

Sterile granuloma and pyogranuloma syndrome/SGPS/sterile pyogranulomatous dermatitis

Panniculitis

246
Q

What are the differential diagnoses of SGSP?

A

Lymphoma
Mast cell tumour
Malignant and cutaneous histiocytosis
Granulomatous reactions to foreign bodies, bacteria and fungi
Panniculitis

247
Q

What are the trigger factors of SGSP?

A

Aerobic, anaerobic and fungal cultures
Leishmaniosis
Mycobacterial infections

248
Q

How is SGSP treated?

A
  • High dose oral steroids such as daily 2mg/kg of prednisolone
  • Tetracycline and nicotinamide
  • Azathioprine 2mg/kg
249
Q

What aspects of an animal’s history may be important for diagnosis of nodules?

A
  • Papillomas and histiocytomas may be seen in young dogs – can spontaneously resolve
  • UV light is a factor for cats in the UK
  • Relationship with vaccination and feline skin lesions, especially sarcoma
250
Q

What is cutaneous T-cell lymphoma?

A
  • Rare group of T-cell malignancies
  • Can be epitheliotropic or non-epitheliotropic
251
Q

What is the presentation of cutaneous T-cell lymphoma in dogs?

A
  • Generalized erythematous exfoliative dermatitis (erythroderma) with/without pruritus
  • Plaques and nodules
  • Loss of pigment
252
Q

How is cutaneous T-cell lymphoma treated?

A
  • High dose prednisolone
  • Retinoids (teratogenic)
253
Q

What are the clinical signs of pastern dermatitis?

A

Pain
Stamping
Rubbing
Biting
Lameness
Swollen limb
Local oedema
Scabs
Crusting
Hyperkeratosis

254
Q

What can make pastern dermatitis worse?

A

Wetting the region

255
Q

What are the non-contagious causes of pastern dermatitis?

A

Vasculitis
Photosensitisation (primary = ingestion, secondary = liver failure)

256
Q

What are the contagious causes of pastern dermatitis?

A
  • Dermatophilus congolensis – mud fever
  • Staphylococcus – folliculitis
  • Choroptic mange – feather mites
  • Trobicula autumnalis – harvest mites
257
Q

How is pastern dermatitis treated?

A
  • Medicated shampoo
  • Silver sulphadiazine (Flamazine)
  • Lime and sulphur
  • Sunblock
  • Analgesia
  • Dectomax (if mites)
  • Systemic antimicrobials?
258
Q

What are some causes of equine pruritus?

A
  • Infectious – Staph aureus, Dermatophilus
  • Parasites – flies, lice, mites
  • Allergy – hypersensitivity, atopy
  • Photosensitization
  • Contact reaction– “scalding”
  • PPID may lead to chronic skin infections
259
Q

What are the primary causes of equine alopecia?

A

Ringworm
Pemphigus
Rug rub
Alopecia areata – rare

260
Q

What are the secondary causes of equine alopecia?

A

Pruritus
Folliculitis

261
Q

What is the clinical presentation of equine louse infestation?

A
  • Alopecia – moth eaten pattern
  • Pruritic
  • Scale
  • Ill thrift
262
Q

How are lice diagnosed in equine?

A
  • Visible to naked eye – adults and eggs stuck on hair shafts
  • Migrate away from cold (rug, remove and look)
  • Microscopy?
263
Q

How is equine louse infestation managed?

A
  • Clipping and hogging
  • Bathing – 10ml of deosect in 500ml water per horse/125ml for ponies, important to repeat at 14 day intervals to kill hatchlings
  • Clean equipment – wash rugs, headcollars and grooming kit, 50˚C to kill
264
Q

How can sheep scab be treated?

A

3 MLs – ivermectin, moxidectin, doramectin. Ivermectin 2 injections 7 days apart, resistance, SCOPS principles

Plunge dips – organophosphates. Highly toxic, certificate of competence needed (mobile dippers)

265
Q

What is the clinical presentation of fly strike in sheep?

A

High respiration rate and heart rate
Normal rumen turnover, normal temperature
Large area of wet fleece

266
Q

How is fly strike treated?

A

Clip fleece away
Completely shear animal
Clean with hibiscrub
Pour on ivermectin
NSAIDs

267
Q

Does ringworm in cattle need treating?

A
  • Lesions will self-resolve quicker with UV
  • Can’t go market with lesions
  • Zoonosis
  • Vaccines available but uptake is slow/not commonly used

CVSOH 4 (13 decks)

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