ENDO > Week 4 > Flashcards

Week 4 Flashcards

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1
Q

What are the advantages of Cytology-FNA/FNCS?

A
  • Quick
  • Simple
  • Cheap
  • Possible to do in-house
  • Helpful in establishing a diagnosis
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2
Q

What are the disadvantages of Cytology-FNA/FNCS?

A
  • May not give definitive diagnosis
  • Samples may be non-diagnostic
    • poor technique
    • some lesions do not exfoliate readily
  • Cannot grade tumours
  • Cannot assess local infiltration
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3
Q

What are “Skipocytes” / ”basket Cells” / ”Smudge cells”?

A
  • Damaged cells with disrupted cytoplasm/ bare nuclei
  • Nuclei enlarge
  • Chromatin coarse
  • Nucleoli may become visible
  • Look nasty!
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4
Q

What would be your d/d if you saw Inflammation with tissue cells on cytology?

A
  • Primary neoplasia with secondary inflammation
    Or
  • Primary inflammation with secondary hyperplasia,
    fibroplasia or granulation tissue
  • If in doubt – take a biopsy
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5
Q

What are some findings seen on Cytology of inflammatory lesions?

A
  • Septic inflammation
  • Pyogranulomatous inflammation – neutrophils plus
    macrophages
  • Steatitis / panniculitis – subcutaneous fat inflammed
  • Granulomatous inflammation – mainly macrophages
    and some neutrophils
  • Eosinophilic inflammation
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6
Q

What are the Causes of acute inflammation?

A
  • Bacterial infection – look on 100X for bacteria
  • Foreign body
    • More granulomatous process if been there for a
      while
  • Trauma
  • Tumour necrosis
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7
Q

What does bacteria look like on a cytology slide?

A
  • Most cocci are Gram +ve
    • Staphs in clusters
    • Streps in short or long chains
  • Most small rods are gram negative
  • Filamentous rods - Actinomyces / Norcardia
    • CAREFUL CAN BE ZOONOTIC
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8
Q

When do bacteria indicate infection on cytology?

A
  • Marked inflammatory response
  • Bacteria in neutrophils – tells us that bacteria were
    there in the body - not due to contamination
    afterwards
  • Degenerate neutrophils
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9
Q

When do bacteria indicate contamination on cytology?

A
  • No inflammation
  • Mixed population of bacteria
  • Not within neutrophils
    • Suggests contamination – not part of pathological
      process
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10
Q

What is the appearance of Degenerate neutrophils on cytology?

A
  • Karyolysis - nucleus swollen, pale staining, ragged
    outline
  • Due to bacterial infection or tissue necrosis e.g.
    necrotic tumour
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11
Q

What is Karyolysis?

A

The complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases.

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12
Q

What is the appearance of Non-degenerate neutrophils?

A
  • Similar to those in circulation
  • +/- karyorrhexis / pyknosis - condensed dark staining
    blobs of nuclear material
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13
Q

What is karyorrhexis?

A

the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm. It is usually preceded by pyknosis

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14
Q

What do Benign tumours look like on cytology?

A
  • Cells small and similar size
  • Small uniform nuclei
  • Low nuclear:cytoplasmic ratio
    • Depends of what tissue your looking at
  • Smooth granular chromatin
  • +/- 1 or 2 small nucleoli - smooth regular shape
  • Smooth / invisible nuclear membrane
  • Cytoplasm visible around nucleus
  • Ordered cell arrangement
  • Cells and nuclei parallel (streaming)
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15
Q

What are the Criteria of malignancy in tumours?

A
  • Abnormal location
  • Cell features
  • Architecture
  • Nuclear features
  • Cytoplasmic features
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16
Q

What is the Architectural Criteria of Malignancy on cytology?

A
  • Haphazard cell arrangement
  • Loss of cohesion
  • Loss of contact inhibition
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17
Q

How does Loss of cell adhesion occur in malignant tumours?

A
  • Caused by down regulation of the adhesion molecules
    ↑ Malignancy
    ↓ Cohesion
    → Usually associated with increased exfoliation
    → Hypercellular sample
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18
Q

What are the Cell features of Malignancy on cytology?

A
  • Macrocytosis – large cells

- Anisocytosis - variation in cell size

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19
Q

What is the Nuclear criteria of malignancy on cytology?

A
  • Anisokaryosis – variation in nuclear size
  • Multinucleation
  • Coarse or clumped chromatin
  • Nucleoli: prominent, large, angular, irregular, variably
    sized
  • Increased mitotic activity and atypical mitoses
  • Nuclear fragmentation and thickening of the membrane
  • High or variable N:C ratio
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20
Q

What are the Cytoplasmic Criteria of Malignancy on cytology?

A
  • Basophilia
  • Vacuolation
  • Distended with secretory product (signet-ring)
  • Cytoplasmic features can be influenced by non-
    neoplastic processes such as inflammation
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21
Q

What do Epithelial skin tumours look like on cytology?

A
  • Sheets or cohesive clusters
  • Often well defined cell borders
  • Cells can be:
    • Angular squamous cells
    • Cuboidal or columnar
    • Roundish, polygonal
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22
Q

Give some examples of Epithelial skin tumours.

A
  • Trichoblastoma (basal cell tumour)
  • Trichoepithelioma (hair follicle tumour)
  • Squamous cell carcinoma
  • Sebaceous cell tumours-adenoma, carcinoma,
    epithelioma
  • Anal sac apocrine adenocarcinoma
  • Perianal gland adenoma
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23
Q

What is the cytological appearance of Mesenchymal skin tumours?

A
  • Arise from connective tissue, muscle, bone &
    cartilage, nerve, endothelial cells
  • Cells in non cohesive aggregates or individually
  • Cell borders are variably defined and often indistinct
  • Embedded in matrix
  • Spindle shaped cells with cytoplasmic tails common
  • Cells can be oval or plump
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24
Q

Give some examples of Mesenchymal tumours.

A
  • Fibroma and fibrosarcoma
  • Lipoma and liposarcoma
  • Perivascular wall tumours
  • Haemangiopericytoma
  • Myopericytoma
  • Anaplastic sarcoma with giant cells
    (malignant fibrous histiocytoma)
  • Haemangioma / haemangiosarcoma
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25
What is a hemangiopericytoma?
A type of soft tissue sarcoma that originates in the pericytes in the walls of capillaries
26
How do Mesenchymal skin tumours progress?
↑ Malignancy → Cells get plumper Tails get shorter N:C ratio increases
27
What are the difficulties with looking at Mesenchymal tumours?
- Generally difficult to distinguish various types of mesenchymal tumours - Fibrosarcoma, Peripharal Nerve Sheath Tumour, haemangiosarcoma may all appear similar - HSC may appear very aggressive
28
What is the cytological appearance of Lipomas?
- Adipocytes with small nucleus and abundant (single vacuole/globule) cytoplasm - Free fatty droplets - NB cells may fall off slides during staining / fixation - Avoid methanol fixation (Soln. A) – try heat fixation instead and use soln’s B & C only - Subcutaneous fat appears identical!
29
What is the cytological appearance of a Liposarcoma?
- Fatty background - Pleomorphic spindle cells, some with variably sized cytoplasmic fat vacuoles - Other cells similar to lipocytes with larger vacuoles
30
What is the definition of Alopecia?
- Loss of hair | - Partial or complete
31
What is the definition of primary Alopecia?
Failure to grow normally
32
What is the definition of secondary Alopecia?
Grows normally but subsequently damaged or lost
33
What is the definition of true Alopecia?
- Direct damage to hair follicle unit → loss of whole hair | follicle unit
34
What is the definition of apparent Alopecia?
- Hair shaft damaged but not lost from hair follicle unit | - Hair cropped short
35
What do broken distal tips on a trichogram suggest?
Probable pruritus – investigate as pruritus case
36
What are the causes for Alopecia?
``` - Hair follicle inflammation (folliculitis/furunculosis/bulbitis) → Hair follicle unit damaged - Hair cycle abnormality - eg Endocrine → Hair stops growing - Hair morphological abnormalities → Hair malformed, breaks off - Congenital Aplasia → Never grows ```
37
What is the Signalment for Alopecia?
- Age of onset - <1yo: demodicosis, dermatophytosis, superficial pyoderma, congenital alopecia - Middle-aged/older: endocrinopathies, neoplasia - Breed - Small terriers/boxers: predisposed to HAC - Dachshunds: pattern baldness - Doberman: dysplastic hair follicle diseases - Sex - Entire male: Sertoli cell tumours - Entire female: post-partum telogen defluxion
38
What do you look for in the general history in a case of Alopecia?
- PUPD? - suggestive of HAC - Weight gain, lethargy ? - suggestive of hypothyroidism - Small hunting dogs (eg JRT)? - Trichophyton infection (rodent/hedgehog contact) - Lesions on owner/in-contact animals? - dermatophytosis, ectoparasites
39
What do you look for in the dermatological history in a case of Alopecia?
- Lack of hair regrowth after clipping? - hypothyroidism, HAC - post-clipping alopecia - Seasonality? - Recurrent flank alopecia - Allergic pruritus - Response to past treatment? - Pruritus? - If yes, investigate as per the pruritic animal
40
What do you look for on general physical exam in a case of Alopecia?
- Obesity, bradycardia: - Hypothyroidism - Unilateral testicular enlargement: - Sertoli cell tumour - Feminisation of male dog: - Sertoli cell tumour
41
What do you look for on a dermatological exam in a case of Alopecia?
- What is normal?? - Preauricular/pinnal alopecia of cats - Sphinx cats - Irish water spaniels - Alopecia can be ‘normal’
42
What do you need to consider on a dermatological exam in a case of Alopecia?
1. Distribution of lesions? - Localised - Multifocal/diffuse patchy - Symmetrical/diffuse 2. True or apparent alopecia? 3. Presence of other lesions?
43
When is localised alopecia commonly seen?
- Demodicosis - Dermatophytosis – zoonotic! - Superficial pyoderma
44
When is localised alopecia less commonly seen?
- Post-clipping alopecia - esp GSD, Chows, Husky-types - Cause? - Treatment – wait…regrow in 6-12mo - Steroid injection/post-vaccine vasculopathy - Tail gland hyperplasia - Cicatricial alopecia (scarring) - Traction alopecia (bows in hair!)
45
When is Multifocal/ diffuse patchy alopecia commonly seen?
- Demodicosis - Dermatophytosis – zoonotic! - Superficial pyoderma
46
When is Multifocal/ diffuse patchy alopecia less commonly seen?
- Dermatomyositis - Sebaceous adenitis - Alopecia areata
47
How do you diagnose True or apparent alopecia?
- Trichogram - Ease of epilation at periphery - Easily epilated → true - Requires some effort → apparent - Broken distal tips → apparent
48
How does the presence of Pustules give further clues to underlying cause of Alopecia?
- Pustules - Pyoderma - (autoimmune diseases)
49
How does the presence of comedones give further clues to underlying cause of Alopecia?
- Demodicosis - Dermatophytosis - Hypothyroidism - HAC - Longterm glucocorticoid use
50
How does the presence of follicular casts give further clues to underlying cause of Alopecia?
- Indicates follicular disease - Bacterial infection - Demodicosis - Dermatophytosis - Sebaceous adenitis - Primary keratinisation disorder - Endocrinopathy?
51
What would be the inital tests you would perform in a case of Alopecia?
- Skin scrapings - Dermatophyte culture - Wood’s lamp - Trichograms
52
What would you look for on skin scrapings in a case of alopecia?
- all cases! | - Demodicosis
53
What would you perform a dermatophyte culture in a case of alopecia?
- All cases of focal/?multifocal alopecia - Especially - young/elderly/immunosuppressed animals - Small hunting dogs - Dogs in household with cats - In-contact people with lesions - High risk of zoonotic infection: children, elderly, immunocompromised - If follicular casts seen
54
What would you look for on a trichogram in a case of alopecia?
- Bulb - Stage of growth? - Telogen predominates in endocrine disease - Shaft - Melanin clumping? Colour-linked follicular dysplasia - Dermatophyte spores? (lactophenol cotton blue helps demonstrate) - Follicular casts? - Distal tip - Broken? Traumatic damage/pruritus
55
What would you do if there is no definitive diagnosis after performing initial tests in a case of alopecia?
- Rule out pyoderma - Cytology of impression smears, pustule contents - Assess response to 3-week course of appropriate antibiotic or antibacterial baths - Further tests as indicated: - Endocrine function tests – if endocrinological cause suspected - Skin biopsy….
56
What should you sample when performing skin biopsies in a case of alopecia?
- A variety of sites: - Early lesions if possible - Middle and periphery of expanding lesions - Adjacent apparently normal area -Wedge biopsy across margin often useful mark direction of hair growth - Send to experienced dermatopathologist if possible
57
In which conditions causing alopecia should you perform skin biopsies?
- Folliculitis - bacterial - demodicosis - dermatophytosis - Endocrinopathies - All have similar ‘atrophic’ pattern - Atrophy of - epidermis, hair follicles and sebaceous glands - Orthokeratotic hyperkeratosis and follicular keratosis
58
What is the Classic picture of alopecia seen in Endocrinopathies?
``` - Symmetrical non-pruritic alopecia but - often more subtle changes seen before this.. - ceruminous otitis - recurrent microbial infection - generalised seborrhoea - Usually proceed to hairloss within 6 months - Hair in affected areas usually dull, dry and epilates easily – telogen predominates - Hair regrowth can be - Absent - Very slow - Abnormal e.g. woolly coat ```
59
What is the Most common endocrine disease of dogs that can cause Alopecia?
Hypothyroidism
60
How does Alopecia present in Hyperadrenocorticism (HAC)?
Symmetrical alopecia, sparing extremities
61
What is Alopecia X?
- Poorly understood - Young dogs 2-5yo - Esp Chows, Pomeranians, Samoyed, husky, miniature poodle - Alopecia starts trunk/perineum then speads; head spared - Remaining ‘puppy-like’ coat
62
How do you diagnose Alopecia X?
- eliminate other endocrinopathies | - biopsy
63
How do you treat Alopecia X?
- Castration?, - Oral melatonin? - Deslorelin implants?
64
What is Hyperoestrogenism in males caused by and what is the clinical presentation?
- Sertoli cell tumour (interstitial cell tumour, seminoma) - Skin changes - Alopecia, hyperpigmentation - Gynaecomastia - Linear preputial erythema - Attraction to other male dogs - Occasional bone marrow suppression (oestrogens from neoplasm)
65
What are the treatment options for Hyperoestrogenism in males?
neuter (check for metastasis)
66
What is the cause of Canine recurrent flank alopecia?
associated with photoperiod. Usually onset Nov-March
67
What is the signalment of Canine recurrent flank alopecia?
- Genetically influenced - Boxers, Airedale, English Bulldog, Schnauzer, Rhodesian Ridgeback predisposed - Mean age onset 4yr (range 1.5-11 years)
68
What are the clinical signs of Canine recurrent flank alopecia?
Usually thoracolumbar, abrupt onset, well-demarcated alopecia
69
How do you diagnose Canine recurrent flank alopecia?
- Rule out hypothyroidism, HAC, other follicular dysplasias. - endocrine tests - biopsy
70
What are the treatment options for Canine recurrent flank alopecia?
- Usually benign neglect… Normally regrows spontaneously in 3-8mo (range 1-14mo) - Oral melatonin (unlicensed) at onset of alopecia? - Warn owner that 80% recur, though not always every year
71
What is Anagen defluxion?
- Abrupt cessation of mitosis in anagen - Usually associated with - severe systemic disease - cytotoxic drugs - toxins (eg selenium)
72
What is Telogen defluxion?
- Hair follicles into premature telogen - Usually with stressful events (pregnancy, parturition, lactation) - Regrow in several months once stressor removed
73
What is the clinical presentation of Pattern baldness?
- Non-inflammatory - Predisposed breeds - Includes - Pinnal (Dachshunds) - Caudal thighs (Greyhounds) - Post-auricular, ventral neck, ventrum, caudomedial thighs (Dachshunds, Greyhounds, Chihuahua) - Diagnose on biopsy - Treatment - ?oral melatonin
74
What is the clinical presentation of Follicular dysplasias?
- Heritable breed-specific coat abnormalities - Usually give - focal or diffuse symmetrical alopecia - Affect dorsum/flanks - Diagnose on biopsy
75
What is Colour dilution alopecia?
- Associated with blue (dilute black) or fawn (dilute brown) coat colours - Esp Doberman,Dachshund, Yorkshire terrier, whippet, greyhound - Often secondary bacterial folliculitis
76
What is the clinical presentation of Colour dilution alopecia?
- Dystrophic change associated with dilute-colour hair only: large melanin granules and abnormal, weakened hair - May lead to shaft fracture and alopecia
77
What is Black hair follicular dysplasia?
- Bi-coloured/tricoloured puppies - Melanin clumping on trichograms, defective hair shafts - > fracture
78
What is Feline Focal/multifocal patchy alopecia?
- Very similar to dogs except - Incidence of dermatophytosis much higher - Incidence of pyoderma much lower
79
How do you diagnose Feline Focal/multifocal patchy alopecia?
- Skin scrapes for demodicosis - Investigations for dermatophytosis - Biopsy
80
What is Feline symmetrical alopecia and what is its clinical presentation?
- One of the 4 common cutaneous reaction patterns of cats… -Total/partial hair-loss, acquired - No other gross skin abnormalities - Often symmetrical - Can be caused by many diseases – need systematic investigation to find primary cause
81
What is the definition of a papule?
- Small solid elevation of skin <1cm diameter - Often erythematous - May → crusts of serum, pus or blood
82
What is the definition of a pustule?
- Small (<1cm) skin elevation, filled with pus | - Often start as papule
83
What are the different appearances of Pustules?
- Can be - Intraepidermal - Subepidermal - Follicular - Different diseases cause lesions at different sites - Colour varies - White, yellow, green, red - +/- Microrganisms - Some sterile (eg pemphigus foliaceus)
84
How often do you see pustules?
- Very fragile so rarely seen | (deeper lesions less fragile than superficial)
85
How do you usually see pustules?
- Usually see ruptured pustules as - Epidermal collarettes (circular spreading ring of crusts due to exfoliative process) - Honey-coloured crusts adherent to skin
86
Give some examples of Pustular/ papular diseases in dogs.
- Superficial bacterial pyoderma - Impetigo, folliculitis, acne - Ectoparasites - Flea bites, Sarcoptes, Demodex - Hypersensitivities - Flea, environmental atopy, food-induced atopy, contact
87
Give some examples of Pustular/ papular diseases in cats.
- Milliary dermatitis – multiple causes! A cutaneous reaction pattern - Dermatophytosis - Insect-bite hypersensitivity, flea bites, Cheyletiella
88
What are the main causes of Causes of milliary dermatitis in cats?
- Fleas - Cheyletiella, Otodectes, Trombicula - Flea allergy dermatitis, - environmental atopy, - food-induced atopy - dermatophytosis
89
What do you want to know from a history in a case of Pustular/ papular diseases?
- Breed - Age of onset - In-contact animals/humans affected - Pruritus: - presence/absence, severity - preceded or followed lesion development - Course of disease - Seasonality - Response to past treatment, including parasiticides - Results of prior tests - Concurrent systemic signs - Travel abroad
90
What do you need to look for on physical exam in a case of Pustular/ papular diseases?
- General examination – signs of systemic disease? - Dermatological examination - Distribution of lesions - Pyoderma rarely affects face, unless chronic - Variety of lesions - Large, green pustules - ?pemphigus/HAC - Scabies – often see papules only - Bacterial pyoderma – usually see all stages of development of pustule - Lesions come in waves? All lesions at same stage of development? possible pemphigus
91
Which diagnostic tests do you perform in cases of Pustular/ papular diseases?
- Ectoparasites - Dermatophytosis - Wood’s lamp, - Fungal culture – esp cats (NB 2-3 weeks to result) - Secondary microbial infections - Bacterial pyoderma/ Malassezia dermatitis - acetate tape strips/impression smears, stained with Diff-Quick - cytology of fresh pustule contents, if available
92
What should you do if you have a strong suspicion of pemphigus foliaceus?
Eliminate secondary microbial infection | then biopsy
93
What should you do if you have no strong suspicion of pemphigus foliaceus?
- Thorough parasite control program (including sarcoptic mange (dogs), fleas) - Eliminate secondary infection - Bacterial pyoderma/Malassezia dermatitis - Re-evaluate after 3-6 weeks
94
What should you do if after elimination of microbial infection and ectoparasites Lesions are resolved, but still pruritic?
Work-up as for hypersensitivities
95
What should you do if after elimination of microbial infection and ectoparasites All symptoms are resolved but rapid relapse?
- Initial therapy too short? - Poor owner compliance? - Antibiotic dose adequate? - Check re underlying health/endocrine/ metabolic disease - If all normal, ?primary bacterial pyoderma
96
What should you do if after elimination of microbial infection and ectoparasites there is No change or worse?
- Repeat skin scrapings re Demodex - Repeat impression smears for microbes/acantholytic keratinocytes - Culture intact pustule – bacterial resistance? (off antibiotics minimum 5 days) - Biopsy (esp pustule, if possible)- eg pemphigus foliaceus? - Serum biochemistry/haematology, urinalysis if systemic illness
97
What is Scale?
Rafts of immature keratinocytes which accumulate at the skin surface
98
What is scale caused by?
- Due to hyperkeratosis (increased depth of cornified layer) - Caused by increased or disrupted epidermal turnover - Loose or tightly adherent - Form scurf when desquamate
99
What are the 2 types of scale?
- Parakeratotic hyperkeratosis - cells have nuclei - Malassezia dermatitis - zinc-responsive dermatosis - superficial necrolytic dermatitis - Orthokeratotic hyperkeratosis - Increase in normal keratinocytes - Common inflammatory disorders, keratinisation disorders - nO nuclei
100
What is crust and what can it be associated with?
``` - When exudates (serum, pus or blood) dry on skin surface - Often also involves surface squames, hair, topical medications - Can therefore be associated with - scaling - pustular - ulcerative/erosive diseases ```
101
What is the Diagnostic approach for scaling, crusting?
- History, signalment, general/dermatological examination - Rule out ectoparasites - Routine tests, treatment trials - Fleas, Demodex, Sarcoptes, Cheyletiella - Rule out microbial infection - Cytology, cultures, response to treatment
102
What should you do if pruritic lesions remain?
- Exclusion diet trial + Food induced atopy - Probable environmental atopy (or biopsy if clinical signs do not fit)
103
What should you do if non pruritic lesions remain?
- Evaluate for metabolic/endocrine disease + HypoT4, HAC, sex/adrenal hormone imbalance, DM, Superficial necrolytic dermatitis - Biopsy
104
What are you looking for on biopsy of scale diseases?
- Primary keratinisation disorders - Neoplasia - Cutaneous lymphoma Paraneoplastic syndromes - Immune mediated - Pemphigus, lupus - Other underlying disorders* - Leishmaniasis - FeLV, FIV, - Superficial necrolytic dermatitis - Adverse drug reactions - Nutritional - Zinc-responsive dermatosis - EFA deficiency - Generic dog food disease
105
What are Primary keratinisation disorders?
- Defects in normal keratinisation process… - abnormal formation of keratinocytes +/or - abnormal sebaceous gland function - Rare; often breed-related; tend to occur in younger animals - Diagnosis of exclusion - Treat symptomatically
106
Give examples of Primary keratinisation disorders in dogs?
- Primary idiopathic keratinisation disorder (‘idiopathic seborrhoea’) - cocker/springer spaniels - Nasodigital hyperkeratosis - Ichthyosis - golden retriever
107
What is the clinical presentation of Primary idiopathic keratinisation disorder (‘Idiopathic seborrhoea’)?
- Spaniels - Scaling, often thick and adherent - Erythema, greasy scale of lips, periocular skin, ventral neck/body, feet, tail; otitis externa - Secondary pyoderma and Malassezia dermatitis common - Other breeds - Often dry truncal scale
108
What is the clinical presentation of Ichthyosis (‘fish scale disease)?
- Golden retriever - Often young dogs - No other clinical signs, unless secondarily-infected
109
What is the clinical presentation of Nasodigital hyperkeratosis?
- Cocker/Springer spaniels and old dogs - Also can be seen with other diseases: e.g. hypothyroidism, pemphigus foliaceus, cutaneous lupus, NME, distemper, Zn-responsive dermatosis - Frond-like hyperkeratosis that may fissure and become infected
110
How do you treat Nasodigital hyperkeratosis?
- warm-water soaks, - topical salicylic acid, - propylene glycol, - topical synthetic retinoids?
111
What is the clinical presentation of callus?
- On bony prominences in heavy dogs on hard surfaces - Normal protection mechanism but can also fissure and become infected
112
What does callus involve?
- Hyperkeratosis - Increased depth of cornified layer - Acanthosis - Increased depth of epidermis
113
How do you treat callus?
- Don’t excise! - As for naso-digital hyperkeratosis - Control infection - Encourage to lie on soft bedding - DogLeggs?
114
Name 2 Primary keratinisation disorders in cats.
- Feline acne | - Stud tail/tail gland hyperplasia
115
What is the clinical presentation of feline acne?
- Dark waxy scales on chin - May be primary disorder, but often secondary (e.g. to dermatophytosis, demodicosis) - Often develop secondary Malassezia, pyoderma and furunculosis
116
What are the treatment options for feline acne?
- depends on cause. Includes: - Chlorhexidine or chlorhexidine/miconazole washes - Antiseborrheic washes - Topical antibiotics, eg fusidic acid if secondarily infected (occasionally systemic antibiotic) - Neutering - Benzoyl peroxide product? (sparing as potentially toxic/irritant/bleaching; veterinary products no longer available) - 0.5% tretinoin (topical retinoid)? – unlicensed
117
What are Secondary keratinisation disorders?
- Almost any disease affecting the normal physiology of | the skin can cause scale
118
Give 2 examples of neoplastic Secondary keratinisation disorders.
- Exfoliative dermatitis secondary to thymoma (cats) | - Epitheliotropic lymphoma
119
Give 3 examples of immune-mediated Secondary keratinisation disorders.
- Cutaneous lupus - Pemphigus foliaceus - Sebaceous adenitis
120
What is Sebaceous adenitis and it's common clinical presentation?
- Autoimmune destruction of sebaceous glands - Esp Standard Poodle, Akita, Samoyed, English Springer Spaniel - Tightly-adherent frond-like scale, follicular casts - Hair loss - Generalised, focal or multifocal
121
What is the clinical presentation of Sebaceous adenitis in Vizslas?
annular/serpiginous areas of alopecia/fine white scale
122
How do you diagnose and treat Sebaceous adenitis?
- All may be secondarily-infected → pruritus - Need multiple biopsies often to diagnose - Treatment of choice = ciclosporin. Otherwise symptomatic control
123
Name 2 other underlying Secondary keratinisation disorders.
- Leishmaniasis | - Superficial necrolytic dermatitis
124
What is Superficial necrolytic dermatitis and what is its clinical presentation?
- Secondary to end-stage liver disease, pancreatic atrophy, glucagonomas, diabetes mellitus - Affects joints, pressure-points, lips, feet - Erythematous plaques/erosions covered with thick adherent scale
125
What are the treatment options for scaling/crusting disease?
- Best treatment is correction of underlying cause but not always possible. Therefore need symptomatic management using: - Antiseborrheic shampoos/foams - Emollients/moisturisers - EFAs - Antimicrobials - Retinoids
126
How do you use Anti seborrhoeic shampoos/foams in the treatment of scaling/crusting disease?
- Action: - Keratolytic – reduce cohesion between cells of stratum corneum - Keratoplastic – restore normal epidermal epithelialisation and keratinisation; reduce skin turnover - +/- Degreasing - Aim to use the mildest effective product – minimises risk of drying effect. - Follow with moisturising rinse if necessary
127
How do you use emollients in the treatment of scaling/crusting disease?
- Soften and soothe skin - Reduce trans-epidermal water loss - e.g. Vaseline, lanolin, paraffin, vegetable and animal oils
128
How do moisturisers work in the treatment of scaling/crusting disease?
Increase water content of stratum corneum
129
When would you use essential fatty acids in the treatment of scaling/crusting disease?
Especially if dry scale
130
How do Topical/systemic antimicrobials work in the treatment of scaling/crusting disease?
treat or prevent secondary microbial infections, if required
131
How do retinoids work in the treatment of scaling/crusting disease? Give examples.
- Anti-proliferative, anti-inflammatory, immune- modulatory - Systemic - Vitamin A - Isotretinoin, Acitretin (synthetic retinoids) - Risk of significant side-effects (highly teratogenic, KCS, joint pain, vomiting, diarrhoea, dry skin, hyperostosis) - Used under consultant dermatologist’s guidance only - Topical - Tretinoin 0.5% (unlicensed)
132
What are the Types of Ear disease?
- Pinnal disease - Diseases affecting the ear flap - Otitis externa - Inflammation of the outer ear - Otitis media - Inflammation of the middle ear - Otitis interna - Inflammation of the inner ear
133
Give some examples of a pruritic disease affecting the Pinnal margins?
- Scabies | - Neotrombicular autumnalis
134
Give some examples of a non-pruritic disease affecting the Pinnal margins?
- Vasculitis - Pinnal margin seborrhoea - Squamous cell carcinoma
135
Give some examples of a pruritic disease affecting the Pinnal surface?
- Atopic dermatitis - Food allergy - Pemphigus foliaceus - Fleas (cats) - Contact irritant dermatitis
136
Give some examples of a non-pruritic disease affecting the Pinnal surface?
- Pemphigus foliaceus - Alopecia in hyperadrenocorticism or hypothyroidism - Contact irritant dermatitis
137
Give an example of a pruritic disease affecting the Pinnal body?
Aural haematoma
138
Give an example of a non-pruritic disease affecting the Pinnal body?
Auricular chondritis
139
What is the signalment of Ear margin seborrhoea?
- Relatively uncommon - Marked breed predilection in Dachshunds - Can be a feature of hypothyroidism
140
What is the clinical presentation of Ear margin seborrhoea?
- Adherent keratin on both medial and lateral sides of the pinna - Follicular casts and plugs may trap hair - Rubbing produces erosions and ulceration - Pruritus is variable - Fissuring and secondary infection can be problematic
141
What are the Differential diagnoses for Ear margin seborrhoea?
- Early vasculitis - Early localised scabies - Many other seborrhoeic conditions if widespread
142
What is the treatment for Ear margin seborrhoea?
- Emollient rinses, vaseline, propylene glycol | - Surgery
143
What is the normal Temp, Humidity and pH of the ear?
- Temp 38.2–38.4 ˚C - Humidity 88.5% - pH 6.1/6.2
144
Which glands are present in the ear?
- Sebaceous glands | - Ceruminous glands
145
What is otitis associated with?
Otitis associated with rise in temp, humidity and pH
146
How is cerumen formed and how can this lead to otitis?
- Lipids + sloughed keratinocytes form cerumen - Cerumen traps small FB - Anti-bacterial/yeast - Epithelial migration moves wax from TM to the external space - Epithelial migration disturbed by inflammation, wetness, hyperplasia and physical blockage
147
What is the Normal flora in ear canal?
- Gram +ve cocci predominate (but no growth in some dog’s ears) - Similar species to those found on the skin - Micrococcus spp. - Coagulase negative staphylococci, Staphylococcus schleiferi and Staphylococcus pseudintermedius - Streptococcus species - Malassezia
148
What is the most important factor in Otitis externa pathophysiology?
- HUMIDITY - as this changes the epithelial defences and microbiological proliferation (yeast & bacteria)
149
What is useful to consider when treating Otitis externa?
- Primary disease - e.g. atopic dermatitis, Otodectes cyanotis - Secondary disease - e.g. Malassezia, Staphylococci & Pseudomonas spp. - Predisposing factors - e.g. Hairy &/or pendulous ears, stenosis - Perpetuating factors - e.g. Ear canal hyperplasia, stenosis and scarring
150
Give examples of Predisposing causes of otitis.
- Conformation - Excessive hair growth in canals (e.g. poodle) - Hairy concave pinna (e.g. cocker spaniel) - Pendulous pinna (e.g. basset hound) - Stenotic canals (e.g. shar pei) - Excessive moisture - Environment (heat & high humidity) - Water (swimmer’s ear, grooming, cleaners) - Obstructive ear disease - Feline apocrine cystadenomatosis - Neoplasia - Polyps - Primary otitis media - PSOM in CKCS, tumour or sepsis - Treatment effects - Altered normal microflora (e.g. inappropriate cleaner) - Trauma from cleaning or plucking
151
Give examples of Primary causes of Otitis.
- Parasites - Otodectes cynotis - Demodex spp. - Scabies - Foreign bodies - Grass awns - Hypersensitivity - Atopic dermatitis, food hypersensitivity, medications - Keratinisation disorders - Primary idiopathic seborrhoea - Hypothyroidism - Glandular disorders - Cocker spaniels, English springer spaniels & Labrador retrievers have increased ceruminous glands - Miscellaneous - e.g. feline proliferative & necrotising otitis externa
152
What is the clinical presentation of Otodectes cyanotis?
- Common cause of otitis - hypersensitivity disease - Carrier / non-clinically affected state - Hypersensitivity disease - Ectopic disease - Most ear creams are effective with localised disease - Selamectin or moxidectin spot-on - Likely that the isoxazoline group are effective (1) - May need a cleaner ± steroids
153
What is the clinical presentation of Foreign body otitis?
Grass seeds most common - Late spring to end of summer - Often stimulate violent response in the affected individual – sudden onset - Can be hidden in discharge and migrate into middle ear - Painful - chemical restraint is essential in most.
154
What is the clinical presentation and prevention measures of Hypersensitivity otitis?
- OE is a common complication of atopic dermatitis and food allergy (CAFR) - Primary otitis is often not recognised and so inadequately treated - Dogs and cats present when there is secondary infection - Prevention of recurrence - Treat 1˚ disease - Ensure perpetuating factors are treated - Ensure owner knows to intervene early!
155
Which bacteria causes acute secondary disease to otitis?
- Gram-positive bacteria - Staphylococcus species - Streptococcus species - Corynebacterium species
156
Which bacteria causes chronic secondary disease to otitis?
- Gram-positive bacteria - Enterococcus species - Gram-negative bacteria - Pseudomonas species - Proteus species - Escherichia coli
157
Which yeasts can cause diseases secondary to otitis?
- Malassezia spp.(common) - Malassezia pachydermatis - Lipid dependent Malassezia spp. - Candida sp. (uncommon)
158
Which fungi can cause diseases secondary to otitis?
Aspergillus spp. (very uncommon
159
What Changes in the external canal wall can perpetuate otitis?
- Inflammation causing failure of epithelial migration - Acute change: oedema, hyperplasia - Chronic change: proliferative change, canal stenosis, calcification of pericartilaginous fibrous tissue
160
What Changes in glandular tissue can perpetuate otitis?
Hyperplasia of ceruminous and sebaceous glands, hidradenitis
161
What Changes in the tympanum can perpetuate otitis?
- Dilation, rupture, diverticulum (false middle ear – | cholesteatoma
162
What Changes in the otitis media can perpetuate acute and chronic otitis?
- Acute - foreign material - mucopurulent exudate - Chronic - biofilm formation - granulation material - bony change in the bulla
163
What are the clinical signs of otitis externa?
- Aural pruritus or headshaking - Mild to marked exudate - Malodour - Head tilt - Deafness
164
What are the physical findings in otitis externa?
``` - Erythema, swelling, scaling, discharge (otorrhea), malodour and pain - Secondary - pinnal lesions are common - pyotraumatic dermatitis - haematoma ```
165
Describe how Secondary disease follows the primary cause in otitis externa?
- Many / most cases are not presented until secondary disease is present - In many dogs and cats - Malassezia -> Staphylococci -> Gram –ve rods - If treated inadequately potential for anti-microbial resistance - In many cases Pseudomonas aeruginosa is end point
166
What are the Progressive pathological changes that occur with time in otitis externa?
- Epidermal hyperkeratosis and hyperplasia - Dermal oedema - Fibrosis - Ceruminal gland hyperplasia and dilation - Abnormal epithelial cell migration - Tympanic membrane alterations - Otitis media
167
What are the clinical signs of Otitis Media?
- Variable clinical signs - Often non-specific – pain? - Most often signs of concurrent OE are the most obvious clinical signs - Deafness - Pain on eating - Signs of OI if progression
168
What are the consequences of otitis media?
- Conductive deafness - Loss of drum* - High pressure fluid/mucous in the middle ear - Chronic OE or OM ± cholesteatoma - Horner’s syndrome / facial paralysis - Ear and lip droop, asymmetrical lips, dribbling - Keratoconjunctivitis sicca, neurogenic dry nose - Anisocoria with ipsilateral miosis, ptosis of the upper eyelid etc. - Vestibular syndrome (otitis interna [OI])
169
What is the clinical presentation of Primary Secretory Otitis Media (PSOM) in the CKCS?
- Presented for deafness or neck pain! - Marked mucoid build-up in the middle ear - Bulging middle ear noted on otoscopy - Repeated flushing and myringotomy (3-5 times) - Sputolysin (mucolytic) has been used by some - Steroids are used to reduce mucous production
170
What are the investigative steps in otitis media?
- Appearance of the drum on video otoscopy - Sampling of the middle ear for - Bacteriology - Fungal culture - Cytology via myringotomy or ruptured TM - Palpation of granulation tissue in the middle ear - BAER (hearing testing) - Imaging
171
What is a Myringotomy?
surgical incision into the eardrum, to relieve pressure or drain fluid.
172
When is there an indication for Myringotomy?
- Bulging TM with pain or neurological signs (Horner's, vestibular signs, facial paresis) - Tympanosclerosis (an "exploratory myringotomy") - Radiographic/MRI bulla changes and intact TM - Evidence of tissue or fluid behind the TM - Medically unresponsive vestibular disease with an intact TM - Chronic otitis cases longer than 6 months that have not responded to treatment for otitis externa (requires judgement)
173
How do you perform a Myringotomy?
1. Clean and dry the external ear canal 2. Incision may be made using a 5-French polypropylene catheter (cut end to make sharper) or an open-ended tomcat catheter or a small wire (clitoral) swab 3. Passed through either hand held or video otoscope 4. Position: - caudoventral aspect of the pars tensa to avoid damaging the tympanic germinal epithelium and the structures of the middle ear. 5. Sampling: - Pass swab(s) for cytology and bacteriology instilling and then withdrawing a small amount of sterile saline solution 6. Flush with saline (± other agents depending on the cytology results)
174
What is BAER and how is it performed?
- Brainstem auditory evoked response - Click applied to tested ear (white noise to other) - Peaks of response respond to transition through differing structures (e.g. peak I = vestibulocochlear nerve) - Normal dog – threshold <10dB
175
How is radiography used to diagnose otitis media?
- Insensitive way of assessing OM - See thickening of the wall of the bulla in chronic disease - Changes absent in many cases of OM - Lateral oblique and open mouth views.
176
How is MRI used to diagnose otitis media?
- Far better appreciation of soft tissue structures - Expensive – may take significant part of the client’s budget ! - CT can be useful cheaper alternative in many cases.
177
How common is Otitis interna and how do cases develop?
- Incidence is unknown - rare - Cases may develop through - extension of OM (majority) - Haematogenous and ascending infection via the auditory tube
178
What are the clinical signs of Otitis interna?
- Head tilt to the affected side - Spontaneous or rotatory nystagmus - Asymmetric limb ataxia with preservation of strength - Falling - Vomiting and/or anorexia
179
What are the differential diagnoses of Otitis interna?
- Other peripheral vestibular diseases - Idiopathic vestibular syndrome - Neoplasia (vestibulocochlear nerve) - Hypothyroidism
180
How do you diagnose Otitis Interna?
- Establish the presence of systemic disease and/or localised disease (OE/OM) - Pruritus, headshaking and pain around the TMJ may be useful indicators of local disease - Complete neurological examination - Otic examination ± myringotomy - MRI (possibly CT)
181
How do you treat Otitis Interna?
- In the absence of another cause, long term use of systemic antibiotics has been advocated. - Ability to cross the BBB - Based on culture of the middle ear?
182
What do you need to look for in the history with cases of otitis externa?
- General health / other skin disease - e.g. inappetence /difficulty eatingsigns of atopic dermatitis - Specific ear history points - Unilateral / bilateral - Pruritus / head shaking / scratching - Smell - Head tilt - Signs of facial paralysis
183
What examination should you perform with cases of otitis externa?
- General clinical examination / other skin disease - Neurological problems - Ear carriage - Pinna and outer meatus and upper vertical canal - Smell
184
How do you perform Otoscopy?
- Is this possible? - Assistance from VN or owner for restraint - Pain - Do not look? - Admit for chemical restraint? - Treat for short period and then reassess? - Look at the good ear first - Head forward and slightly downwards - Straighten canal and use a small cone - Cones must be sterilised between use*
185
What are you looking for on otoscope examination?
- Is the surface of the epithelium smooth? - Is the surface of the canal red? - Is the lumen open and consistently so? - What is the nature of the discharge? - Epithelial migration?
186
What are the examination points to look for on ear examination?
-Smell - Useful as a measure of infection in many cases - Canal - Wall - swelling ulceration, hyperplasia, hair, masses - Lumen - wax, pus, ear mites, foreign bodies and occlusion - Drum - Present or absent, changes in colour, bulging? - Wax - What is normal ? - No wax is unusual - Heaped up or spread along the canal - a crude measure of epithelial migration - Colour - Smell - Texture
187
What is the possible pathogen associated with dry coffee grounds exudate?
Otodectes cynotis
188
What are the possible pathogens associated with moist brown exudate?
- Staphylococcus spp, | - Malassezia
189
What is the possible pathogen associated with Purulent yellow/green exudates (malodorous)?
- Gram-negative especially | - Pseudomonas sp
190
What are the possible pathogens associated with Ceruminous discharge (often little smell)?
- Allergy - Endocrine (esp hypothyroidism) - keratinisation defects - Bacteroides spp
191
What are the key techniques in a Cytology & wax exam?
- Usually possible even when otoscopy is not - Best practice – perform in ALL cases - Affected by treatments which are often oily - Consider taking bacteriology swab with cytology and then submit, store or dispose
192
What should you sample for in an ear exam?
- Parasites - Mix gently in LP and coverslip - Wax samples - Poor stickiness - Use staining rack - Apply methylene blue* only and coverslip - Purulent samples - Stain as for cytology
193
What is the purpose of bacteriology in an ear exam and what can it be affected by?
- Confirms and/or identifies bacteria present in the ear canal - Presence of bacteria ≠ disease - Commonly affected by - Previous antibiotic ear creams - Previous otic cleaners - Provides susceptibility data - MIC and disk diffusion techniques - Flawed when considering topical treatment - e.g. MIC resistance > 64µg marbofloxacin needed, in cream delivering 3000µg/ml = 45 X more - This still may be ineffective for some bacteria with very effective efflux pumps systems or that produce large amounts of biofilm
194
What is the diagnostic purpose of flushing the ear?
- See epithelium of the ear canal - Hyperplasia - Ulceration - Masses - Defects - Check integrity of the drum - Very difficult to assess correct level of drum in many dogs
195
What is the therapeutic purpose of flushing the ear?
- Dilutes and removes bacteria, yeasts and inflammatory mediators - With appropriate cleaners anti-microbial effects - Removes pus which may inactivate antibiotics - Removes old treatments
196
What are the different options for flushing solutions in the ear?
- Normal saline - Safe, widely available - Sterile - Dilute povodine iodine - This has been recommended by some authors, whilst others state ototoxicity - Chlorhexidine - Known to be problematic at higher concentrations 0.15 % safe in dogs – NOT cat - Others – for use after the drum is known to be intact - cerumolytics emulsify ear wax for easy removal e.g. squalene, alcohols - aqueous solutions aid in removing pus, mucus and serum from the ears - drying agents decrease moisture in the ears and desiccate the surface keratinocytes e.g boric acid
197
When should you use anaesthesia in an ear exam?
- In severe / chronic otitis, anaesthesia is needed to perform adequate flushing - Endotracheal tube protects aspiration of flushing solution - Hearing is often present with sedation - Especially medetomidine (e.g.Domitor®) - Adequately assess the ear - Pain - Otitis media common, but not diagnosed
198
Describe the method of ear flushing using a Manual otoscope and syringe.
- Spreul needle - Cut down gauge 6 urinary catheter - Large catheter cover - Precise, but time consuming - Can make the ear sore through rubbing of speculum - Equipment inexpensive
199
Describe the method of ear flushing using video otoscopy
- Precise - Able to record data if data capture technique - Custom made curettes, biopsy and grabbing tools - Small bore channel -> slow cleaning in some cases - May not fit the smallest ears - Turn round in a busy clinic can be a problem – need two otoscope heads
200
What are the steps in treating otitis?
- Remove/reduce microbes - Reduce swelling, discomfort or pain - Normalise canal lumen and function - Polypharmacy is the rule – medications contain - Antibiotic - Antifungal - Anti-inflammatory agent - Except for Recicort (triancimalone)
201
Give some examples of drugs that are otoxic?
- Gentamicin - Polymixin B - Ticarcillin and imipenem - Propylene glycol - Chlorhexidine at moderate concentrations - If have to use these avoid concurrent use of drugs that might increase ototoxicity
202
What would be the first line of treatment in a case of acute otitis?
- First-line ointment (antimicrobial /steroid /antifungal) - based on cytology and otoscopy - Once to twice daily therapy for 7-14 days - Sufficient amount (0.7-1.0 mls for a large dog) - Combined with a suitable cleaner e.g. - TRIZChlor – watery, disinfectant & doesn’t sting - Cleanaural – more cleaning/ceruminolytic - Malacetic otic – intermediate cleaning and drying - Always warm these before use
203
Would would you do if faced with a more severe case of otitis?
- Consider putting a charcoal swab in the fridge at time of the first appointment - Send a swab off if rods regardless of time course - If the ear is very swollen - Steroids for 1-2 days before further otoscopic examination - If a great deal of discharge / unclear time course - Admit for flush etc – treat as chronic case
204
What are the cytological reasons for bacterial culture in otitis?
- Rods are seen. The most suitable antibiotic treatments can only be chosen if the organisms are known - Marked purulent discharge without organisms being noted. Possibility of finding a pathogen that is relevant, but also may grow organisms that are irrelevant clinically - Pyogranulomatous inflammation. Organisms are often difficult to see with cytology in this uncommon ear inflammation, so culture is obligatory
205
What are the clinical reasons for bacterial culture in otitis?
- In the event of treatment failure. - If there is a suspicion of meticillin-resistant Staphylococcus species* (MRS). - If considering video otoscopy or ear flush for diagnosis or treatment in a bacterial otitis as in the event of an adverse event following these procedures, systemic antimicrobials may be required.
206
Describe re-checks in cases of otitis?
- Obligatory - Improvement ? - Owner compliance - The next stage - Use cytology in cases where improvement is suspected, culture more appropriate when treatment failing - May need to restore epithelial migration - Period of cleaning beyond microbiological and anatomical cure - Identify underlying cause
207
Describe the treatment of chronic allergic otitis.
- Long term Malassezia and S. pseudintermedius - Avoid use of antibiotics - Control microflora through - Cleaning - Use local topical steroids to - Control inflammation - This usually results in better overall control, but no licensed products - Control whole disease effectively, but need a product with an anti-inflammatory action
208
What is Pseudomonas otitis?
- A common problem - Gram negative rod - Highly drug resistant capsule and bacterial wall - Constitutive resistance to many antibiotics - Rapid development of resistance
209
What is the clinical presentation of Pseudomonas otitis?
``` - Often follow a poorly managed or untreated Malassezia or Staphylococcal otitis - Swelling, pain and malodour common - Green to browny black discharge - May be associated with - Immunosuppression - Swimming - Prior use of antibacterials ```
210
What is the treatment plan with severe disease?
- Always flush if purulent material - Presume drum ruptured – collagenase produced by bacteria makes this likely - Therefore presume OM – consider likelihood of OI - Warn owner that flushing / treatment / disease risks - Horner’s syndrome / facial paralysis - Hearing loss - Cost – expensive if severe to treat medically - Possibility of need for TECA - Non-licensed products (get signed release) - Increased risk in the cat
211
What is the process of treatment of otitis?
- Assess skin and ears - Cytology - Bacteriology - consider further bacteriology from deep in canal/middle ear later - Flush to clean & observe (? granulation tissue) - Use a disinfectant cleaner - Apply a suitable antibiotic - Provide anti-inflammatory and analgesia
212
What is stenosis?
- A consequence of - Chronic low grade trauma - Severe acute disease – untreated - Trauma - Mucinosis ± conformation in the Shar pei - Treatment can be concurrent with or if inappropriate after infection control
213
What are the approaches to treatment of otitis?
- Potent topical steroids - Commercial medications for extended course - e.g. Easotic, Posatex, Aurizon - Beware local & systemic steroid side-effects (small dogs) - Long periods of treatment needed - Oral steroids - Prednisolone 1-2 mg/kg PO - Tacrolimus 0.1% ointment - Applied to the ear twice daily (care) - Intralesional steroids
214
Describe the end stage ear in cases of otitis?
- When the any or a combination of the following becomes unacceptable - Welfare of pet or family - When ear disease is intractable or very quickly recurrent due to - stenosis - marked granulation in the middle ear - ceruminous and sebaceous gland hyperplasia - Cost of repeated medical interventions is unacceptable - Inability to treat the ear by the owner
215
What are the procedures for treatment in otitis?
- Lateral wall resection - No role in the end stage ear - Limited role in chronic otitis - Unless primary disease removed - Often worsens the situation - Total ear canal ablation - For the chronically painful ear – welfare choice! - Low risk of complications in hands of a specialist - Economically justified in many cases
216
How do you prevent further disease in cases of otitis?
- Always treat the underlying disease - Atopic dermatitis / food allergy - Steroids – pinna & meatus v. steroids in the canal - Hypothroidism - Use cleaners to - Maintain a clean and dry ear - Support the return of epithelial migration - Gently remove loose hair
217
Name the three parts of the ear?
- External ear - Middle ear - Inner ear
218
What are the Primary causes of Otitis Externa?
- Parasites - Otodectes cynotis - Demodex canis/cati - Sarcoptes scabiei - Notoedres cati - Cheyletiella spp - Hypersensitivity and allergic disease - Hypothyroidism - Keratinization disorders - Autoimmune disorders
219
What are the Predisposing causes of Otitis Externa?
- Anatomic and conformational factors - Excessive moisture - Iatrogenic factors - Obstructive ear disease
220
What are the Perpetuating causes of Otitis Externa?
- Bacteria (Staph. Intermedius, Pseudomonas aeruginosa, Proteus mirabilis, Escherichia coli, Corynebacterium spp, Enterococcus spp, Streptococcus spp) - Yeast (Malassezia pachydermis, Candida spp) - Otitis media - Progressive pathologic changes
221
What are the Major indications for ear surgery?
- Trauma (mainly pinna but sometimes external ear canal) - Aural haematoma - Neoplasia (pinna, external ear canal, middle ear, etc.) - Certain cases with chronic otitis externa - Chronic otitis media - Infection (extension of chronic otitis externa) - Middle ear polyps - Cholesteatoma
222
What are the Surgical diseases of the pinna?
Trauma | Neoplasia
223
What are the Most common neoplasms of the pinna in dogs?
- Benign - Pinnal histiocytoma - Papilloma - Malignant - Mast cell tumour - Squamous cell carcinoma
224
What are the Most common neoplasms of the pinna in cats?
- Benign - Basal cell tumour - Malignant - Squamous cell carcinoma - Mast cell tumour - Fibrosarcoma
225
What is the aetiology of an Aural haematoma?
- The aetiology of aural haematoma remains unknown - Proposed associations have included - Otodectes cynotis - Otitis externa - Trauma - Autoimmunity - Hypersensitivity
226
What are the Management options for an aural haematoma?
- Surgical incision, drainage, and suture - Drainage with an indwelling drain (Penrose, tube, teat tube, etc.) - Drainage and glucocorticoid instillation - Closed-suction drainage
227
What are the Complications of drainage of aural haematomas?
- Cosmetic alterations - Recurrence of haematoma - Pinna necrosis
228
What are the Surgical management options for Otitis Externa?
- Lateral wall resection | - Vertical canal ablation
229
When is a Lateral wall resection indicated?
- Persistent, or recurrent, otitis externa with mild, potentially reversible, hyperplasia of the epithelium and adnexae - Neoplasia of the lateral wall of the vertical canal - Very rarely in the management of otitis media to facilitate flushing and drainage of the bulla
230
What are the common neoplasms of the external ear canal in dogs?
- Benign - Papilloma - Cutaneous histiocytoma - Mast cell tumour - Basal cell tumour - Ceruminous gland adenoma - Sebaceous gland adenoma - Malignant - Ceruminous gland adenocarcinoma - Other carcinomas - Squamous cell carcinoma
231
What are the common neoplasms of the external ear canal in cats?
- Benign - Ceruminous gland adenoma - Malignant - Ceruminous gland adenocarcinoma - Squamous cell carcinoma
232
What is the prognosis for a Lateral wall resection?
- The procedure does not cure the animal of its underlying disease but improves the micro- environment of the ear - LWR will fail if there are chronic, irreversible, hyperplastic changes to the luminal epithelium or if there is ongoing otic inflammation
233
What are the complications of LWR?
- Postoperative pain/discomfort - Incisional dehiscence - Persistent otitis externa - Persistent, unrecognised otitis media - Failure to provide adequate drainage of the horizontal canal
234
When is a Vertical canal ablation indicated?
- Only rarely indicated - Vertical canal only is diseased - Hyperplastic otitis externa, trauma, neoplastic disease and polyps restricted to the vertical ear canal
235
What are the complications of a Vertical canal ablation?
- Postoperative pain/discomfort - Incisional dehiscence - Persistent otitis externa - Persistent, unrecognised otitis media - Stenosis of horizontal canal - Facial paralysis
236
What are the Surgical management options for Otitis Media?
- Total ear canal ablation and bulla osteotomy | - Ventral bulla osteotomy
237
What are the indications for TECA BO?
- Chronic, or recurrent, otitis externa associated with irreversible, hyperplastic changes in the luminal epithelium - Failure of more conservative surgery to alleviate otitis externa or media - Neoplasia of the external ear canal - Otitis media
238
What are the complications of TECA BO?
- Postoperative pain/discomfort - Deafness - Incisional dehiscence - Facial nerve paralysis - Vestibular disturbances - Haemorrhage - Horner’s syndrome - Recurrence/abscess formation
239
What are the classic features of Horner’s syndrome?
- Anisocoria with ipsilateral miosis - Ptosis of the upper eyelid - Narrowing of the palpebral fissure - Enophthalmos - Protrusion of the third eyelid
240
When is a Ventral bulla osteotomy indicated?
- cases with middle ear disease and the following circumstances, - Cases in which a TECA is not required - Certain brachycephalic breeds of dog - Often used in the cat - anatomy of the bulla - inflammatory polypoid disease in the absence of chronic otitis externa
241
What are the Complications of VBO?
- Postoperative pain/discomfort - Deafness - Incisional dehiscence - Facial nerve paralysis - Vestibular disturbances - Haemorrhage - Horner’s syndrome - Recurrence/abscess formation
242
What is a Cholesteatoma and how is it treated?
- Slowly enlarging, cystic lesions within the middle ear cavity - Lined with stratified squamous epithelium and keratin squames - Thought to arise when a pocket of the tympanic membrane comes into contact with, and adheres to, inflamed mucosa within the middle ear. - Treatment – TECA BO or VBO
243
Describe Inflammatory polyps in cats.
- Aetiology unknown - Often emanate from tympanic bulla - Nasopharyngeal - Horizontal ear canal - Otitis media
244
What do you need to remember to look an on ear examination in cats?
Do not forget to examine the ear canals in cases of nasopharyngeal polyps and the nasopharynx in cases of polyps in the external ear canal
245
What is the clinical presentation and treatment option of Primary secretory otitis media?
- Cavalier King Charles spaniels - Syringomyelia (Chiari-like malformation of the calvarium/caudal fossa) - Commonly bilateral - Affected dogs will have reduced hearing - Bulging pars flaccida - Myringotomy + flushing of affected tympanic bulla - May require multiple treatments
246
Where should an ear tag be placed?
- The tag should be placed between the two cartilage ribs which run the length of the ear, in its middle third - Metal tags should be placed on the proximal boarder of the ear in its middle third
247
How can infection occur with ear tagging and how can it be treated?
- Infection and abscesses can develop at the tagging site - Treatment - If present, lance abscess (unusual) - Clean with antibacterial washes e.g. Chlorhexidine - Apply topical antibiotics e.g. Oxytetracycline spray - In bad cases (hot, swollen, painful ear +/- pyrexia) administer broad spectrum antibiotics (e.g. long acting penicillin) - In severe cases it may be necessary to remove the tag
248
How can trauma occur with ear tagging and how can it be treated?
- Tags can become caught on objects in the environment and torn out causing haemorrhage - Treatment - Usually unnecessary - Haemorrhage - Clean with anti-bacterials - Clamp or tie off vessels or - Compression e.g. bandage - Infection - Surgical repair is possible for aesthetic purposes e.g. show cattle, but rarely performed
249
Which animals should have a nose ring?
All adult bulls should be rung to aid safe handling. Whilst it can be performed at any age, it is best done when animals are between 6 and 12 months
250
Describe copper nose rings.
- Copper bull nose rings come in a number of different sizes. - They are sold with a small screw which fixes the ring together after fitting.
251
How do you fix a bull nose ring?
- After fitting the ring, the screw is used to hold the ring together. - It can be tightened by hand or with pliers and then the screw “handle” is broken off to permanently fix the ring in place.
252
How do you restrain for nose ringing?
- In a crush or suitable stanchion - Halter +/- nose tongues - Light sedation with xylazine / detomidine may be necessary for fractious animals - Alternatively, heavy sedation with xylazine / detomidine (inducing recumbency) in a well bedded straw box
253
What anaesthesia will you provide for nose ringing?
Whilst local infiltration of the septum with procaine is theoretically possible, practically it is very difficult to administer
254
What is the technique for nose ringing?
- The ring is placed through the soft tissue of the nasal septum in front of the cartilage. It must not be placed through the cartilage itself - Four methods: - A “nose punch” is used to cut out a circular punch of tissue - The sharp end of the ring is driven through the septum by hand - The sharp end of the ring is driven through the septum using a applicator designed specifically for the job - A scalpel blade (size 11) is used to cut a slit through which the ring is passed - Which every method is used prepare carefully and ensure everyone is aware of their respective roles, prior to commencing the procedure
255
How are nose rings applied using a 'Nose Punch'?
Rings can be fitted through a hole created by a “Nose Punch” which cuts a small punch of skin out from between the nostrils in front of the cartilage which divides them.
256
How are nose rings applied using a 'Bull Ring Applicator'?
Rings can be fitted using a “Bull Ring Applicator”. One end of the ring is “sharp” and can simply be driven through the skin dividing the nostril either by hand or more simply using an applicator.
257
What do you need to be aware of after application of a nose ring?
- After application, the septum must be allowed to heal before the ring is used to restrain the animal - Occasionally animals can tear the ring from the nose. - - Whilst repair is theoretically possible, in most cases the nose should be allowed to heal by secondary intention
258
What is the background of dehorning in adult cattle?
- Dehorning is a major procedure and should not be considered “routine” - Clients must be advised to disbud when animals are young rather than dehorn them as yearlings or adults - From the Welfare Codes - “Ideally a veterinary surgeon should do it, and only if it is necessary for the herd’s welfare. It should not be a routine procedure” - Avoid summer months when flies (and the risk of fly strike) are prevalent
259
What restraint should be used for dehorning adult cattle?
- Good quality crush - Halter +/- bulldogs - Secure to side to crush to minimise movement of the head as far as possible - Light sedation with xylazine / detomidine may occasionally be necessary for fractious animals - Alternatively, heavy sedation with xylazine / detomidine inducing recumbency, in a well bedded straw box (much less common) - If a good quality crush is not available - Very fractious animals
260
What Anaesthesia & Analgesia should be applied when dehorning adult cattle?
- Cornual nerve block - Basic method as per calves - Palpate temporal ridge (runs from lateral canthus to the horn) - Mark point half way between lateral canthus and horn with thumb. Direct needle under the ridge - ~19 / 20 gauge, 1” needle; depth of needle insertion ~1-3cm - Always withdraw prior to injection, 5-10mls procaine each side, then massage. - Subcutaneous branches of second cervical nerve - Can provide substantial innervation to the caudal aspect of the horn in some adults - Subcutaneous local infiltration with procaine - Allow time for anaesthesia (at least 10 mins) - Anaesthesia can be checked by pricking around the horn base with a needle - NSAIDs - Preoperative analgesia should always be given
261
What is the method of dehorning in adult cattle?
- Remove horn close to / flush with the scull - Four methods available, choice will depend on the size of the horns, availability of equipment and operator preference - Scoop / gouge dehorners - E.g. “Barnes” dehorners. Good for smaller horns - Shears / guillotines - Quick. Require considerable strength to operate - Anecdotally, can “fracture” the frontal bone in large animals - Embryotomy wire - Slow. Require less strength but greater stamina. - Better haemostasis - Bone saw - Relatively quick. Effective in the hands of a skilled operator
262
Describe the use of Scoop / Gouge Dehorners in dehorning adult cattle.
- Barnes dehorners can be used to remove small to medium / large horns quickly, however they are a little cumbersome and require some strength to operate. - They can be purchased in a variety of different sizes.
263
Describe the use of Shears / Guillotines in dehorning adult cattle.
- Heavy duty dehorning shears can be used to remove small to very large horns quickly and cleanly, however they are cumbersome and require long arms, plenty of room and considerable strength to operate.
264
Describe hemorrhage in dehorning adult cattle.
- Significant haemorrhage occurs if horns are large (3-4 arteries). - Haemorrhage is significantly less if a wire is used (heat and dust generated limit bleeding)
265
What are some methods of haemostasis in dehorning adult cattle?
- Grasp and pull or twist the artery slowly with haemostats causing them to break below the bone line where they clot - Can be difficult or impossible to grasp in some cases. - In this case matches can be driven into the arterial canal and broken off. - Work around the wound circumferentially with a hot iron - Will not stop large arteries, blood rapidly cools iron - Apply a tourniquet around the base of the horns and the poll with baler twine or bands e.g. section of inner tube - Must be removed after a few days
266
What is the after care procedure for dehorning adult cattle?
- Many clinicians will treat the wound with oxytetracyline spray - Ideally animals should be returned to a clean environment - Advise the client that animals must be regularly checked during the first 24 hours to ensure any haemorrhage has stopped - Rule of thumb is that if individual drops of blood can be identified and counted its usually not a problem i.e. very fast drops – slow run should be dealt with - Stress should be minimised following the procedure e.g. no group changes or change of environment - In large horns the frontal sinus extends into the horn and is therefore left open following dehorning. Animals should be fed off the floor and not from a rack to prevent foreign material falling into the sinus
267
What are the Problems and Complications associated with dehorning adult cattle?
- Haemorrhage (discussed previously). Animals may bleed to death or close to death in extreme cases - Infection at the surgical site - Rarely a significant problem - Manage as any superficial infection (clean and topical ABs. Systemic ABs in severe cases) - Sinusitis - Foreign material may gain entry to the sinus especially if animals are fed from racks - Can be severe in some cases requiring systemic treatment and potentially trephination of the sinus - Fly strike - Avoid dehorning during the fly season
268
Describe “Cosmetic” Dehorning.
- Very unusual, but possible in show or pedigree animals - General anaesthesia or heavy sedation and local anaesthesia - Aseptic preparation and procedure - Clip and clean - Incise and reflect skin around horns - Dehorn and close skin with sutures to achieve primary healing
269
Describe Disbudding Goat Kids.
Disbudding goat kids is more complicated than disbudding calves and problematic
270
What is Pruritus?
Itching, rubbing, licking, scratching, chewing
271
What are the differential diagnoses for pruritis in horses?
- Parasite Infestation- - common causes: lice, mites - re-emerging causes: Habronema spp., pinworms (oxyuris equi) - other causes: Ticks, Onchocera spp., bacterial and fungal infections - Allergic dermatitis- - Insect hypersensitivity- Culicoides spp., fly bites - Atopy - Contact allergy - Food allergy (RARE!)
272
What are the 2 types of lice associated with Pediculosis?
- Biting/chewing- Werneckiella equi equi (previously Damalinia equi) - Sucking- Haematopinus asini
273
What is the Disease Profile of Pediculosis?
- Highly host specific - Entire life cycle is spent on the horse - Transmission → direct or indirect - Contagious - Can live off host → right environment → 2-4 weeks - Seasonal- more common autumn/winter
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What is Pediculosis associated with?
- Debilitated - stressed - diseased animals - poor nutrition - overcrowding
275
What are the clinical signs of Pediculosis?
- Evidence → self trauma - Variable hair loss → horses bite/ rub - flanks, jaw, outer limbs - Broken hairs, excoriation, scaling - Mature lice + eggs = visible to naked eye - mane, tail, forelock - Occasionally with haematopinus asini → anaemia, hypoproteinaemia
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How do you diagnose Pediculosis?
- Tape strips / coat brushings best way to get samples - Also warm hands! And bright light - Easy identification under light microscope
277
What are the treatment options for Pediculosis?
- Topical insecticides – permethrins - Kill adults BUT not eggs - Treat all in contacts at the same time, steam clean rugs - Treatment at 3 x at 10-14 day intervals → allow for egg hatching and incubation period - Sucking lice: ivermectin 0.2mg/kg q 14days x 3 - Licensed products - permethrin ( Switch, Coopers Fly Repellent Plus ) - Cypermethrin ( Deosect) - piperonylbutoxide+pyrethrum (dermoline shampoo)
278
What is the disease profile of Chorioptes equi?
- Surface mite → feeds on epidermal debris - Heavily feathered breeds - eg. cobs, shires, Clydesdales - BUT can be seen in short coated horses - Adults can survive off-host → 2 months - Transmission → direct or indirect contact - Mite populations often greatest in winter during periods of cold weather
279
What are the clinical signs of Chorioptes equi?
- Moderate → severe pruritus - usually on limbs ( hind limbs >forelimbs) but NOT exclusively (can be ventrum and dorsum) - Particularly → heavy horses- - crusting, scaling, exudative lesions, - blood staining, hair matting, skin thickening - Secondary infection - Stamping of hind limbs - Rubbing heels against gates and fences - Chewing limbs - Dragging belly a long floor - In short haired breeds , often no stamping but more generalised “moth-eaten” appearance
280
How do you diagnose Chorioptes equi?
- Superficial coat brushings/ multiple scrapes eg. With medical spatula - tape strips- distal limb - Visualisation of mite → light microscope / naked eye on a black background
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What are the treatment options for Chorioptes equi?
- Environment- pressure wash, jayes fluid, move horses outside - Treat ALL in contacts at same time, even if do not seem affected x3 times 1 week apart , then monthly - Can be VERY difficult to eliminate - Clip hair !! - No UK veterinary licensed products - There are publications describing the use of - Selenium sulphide shampoo- q 14 days 3 applications - Fipronil spray- skin/hair must be saturated
282
What is the disease profile of Trombicula autumnalis?
- “harvest mite”- adults are free living in vegetation - occurs in UK at harvest time Jul-Aug - in areas where chalk soil - Sometimes present in hay/straw
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What are the clinical signs of Trombicula autumnalis?
- Intense pruritus - Orange/brown sticky patches serum - Distal limbs, face, neck , thorax of horses at pasture
284
How is Trombicula autumnalis diagnosed?
- ID parasite on tape strip/skin scrapes | - Larvae → 6 legs, orange colour
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How is Trombicula autumnalis treated?
- Self limiting infection - No licensed products – tx as for Chorioptes - Occasional need for systemic glucocorticoids
286
Give some examples of Mites rarely seen or that rarely cause pruritus in horses.
- Psoroptes spp. – used to be notifiable in UK - Sarcoptes scabiei – used to be notifiable in UK - Demodecosis- check for underlying diseases causing immunosupression - Dermanyssuss gallinae (red mite)- if horses housed with poultry - Forage mites
287
How do ticks present in horses?
- seen occasionally , head, distal limb, groin and tail, most common spring and summer, - don't forget they are important for other disease transmission - Lesions: local reaction or general hypersensitivity, papular or pustular area → crusts, erosions, ulcers, hair loss at site, pathogenesis unknown. - TX: mechanical removal, kill tick topically, oral ivermectin 200µg/KG
288
What is the disease profile of Culicoides Hypersensitivity?
- “Sweet itch” - Type I ( within 6h of the bite) and Type IV Hypersensitivity reaction to salivary proteins → females Culicoides spp. - Evidence for possible genetic basis and breed predisposition(Icelandic pony, shires, welsh pony) - Starts at 2-4 y.o - Seen late spring- late autumn - Recurrent seasonal pruritus → often progressive - Significant welfare and management problem
289
What are the differential diagnoses for Culicoides Hypersensitivity?
- Mite infestation - Pediculosis - Dermatophilus congolensis - Dermatophytosis - Onchocerca cervicalis - Mane and tail dystrophy syndrome - Fly, midge, mosquito worry
290
How is Culicoides Hypersensitivity diagnosed?
- Clinical signs - Mane, tail, rump, ventral midline - Papules, crusts, ulcers, thickened skin - Seasonality and clinical signs - Intra-dermal testing can support diagnosis - Skin biopsy non-specific
291
How do you Eliminate exposure to biting midges in the management of Culicoides Hypersensitivity?
- Insect proof the stable- line with netting, fine mesh screens, fans as midges are not strong fliers - stable horse from mid afternoon to mid morning when midges most active - Total body covers eg. Boett blankets, permethrin impregnated rugs
292
Which topical insecticides are used in the management of sweet itch?
- don’t forget belly - Pyrethrums- coopers fly repellent, - Switch pour on, fly tags, citronella
293
How do you control the itching in Culicoides Hypersensitivity?
- systemic or topical corticosteroids (cortavance- hydrocortisone) - cavalesse cream and oral treatment – nicotinamide vit B3 (marmite) - Soothing shampoos- aloe/oatmeal - Benzyl benzoate – care as can be irritant - Tx of any secondary infection – abi, medicated shampoos
294
What is the disease profile of Onchocerciasis- Onchocerca cervicalis?
- Nematode lives in nuchal ligament- produces microfilariae → migrate to the skin → ingested by the intermediate host culicoides spp. - Disease seen in spring when vector present in high numbers - Usually in horses > 4 yo
295
What are the clinical signs of Onchocerca cervicalis?
- Lesions- face (annular lesions forehead suggestive), neck, ventral abdomen and chest - start as thinning hair coat, progress to generalised alopecia, scaling, crusting, plaques - May become severely excoriated, ulcerated, oozing, lichenified - Leukoderma develops and is irreversible - Ocular lesions
296
How is Onchocerca cervicalis diagnosed?
- skin biopsy- mince preparation or histopath – demonstration of microfilaria
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How is Onchocerca cervicalis treated?
- ivermectin 200µg/KG PO- single dose often causes remission of clin signs within 2-3 weeks, if not repeat dose at monthly intervals 2-3 times. Can get adverse rxn to TX ? Death of microfilaria- ventral oedema or pruritus 1-10 days post TX. - Concurrent TX with oral prednisolone 0.5mg/kg PO may help reduce this problem - Prevalence had reduced with advent of regular de- worming with ivermectin
298
What is the disease profile of Cutaneous Habronemiasis?
- Nematodes Habronema muscae, H. Majus, Draschia megastoma- deposited on wounds by flies (house and stable fly). - Adults live in the stomach → produce larvae, these are passed in faeces and ingested by maggots of the intermediate hosts. - Intermediate hosts deposits larvae near mouth of horse → swallows them
299
What are the clinical signs of Cutaneous Habronemiasis?
- Ulcerative nodules seen spring and summer - Lesions commonly on legs, urethral process of penis, prepuce, medial canthus of eye, conjunctiva, commisures of lips or any traumatised area of skin - Pruritus most likely due to allergy to parasite , mild → severe - Lesions single or multiple, characterised by rapid development of granulomatous inflammation, ulceration, haemorrhage, exuberant granulation
300
What are the differential diagnoses of Cutaneous Habronemiasis?
- Bacterial or fungal granuloma - Eosinophilic granuloma - Squamous cell carcimoma - Sarcoid - Exuberant granulation tissue
301
How do you diagnose Cutaneous Habronemiasis?
- Deep scrapings or smears from lesions- nematode larvae - Biopsy- eosinophils, mast cells, coagulation necrosis, nematode larvae
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What are the treatment options for Cutaneous Habronemiasis?
- No one optimal tx, depends on lesion size, type, position etc - Combination of topical and systemic tx - Sx/de-baulking - Cryotherapy - Ivermectin or moxidectin 2 doses at 21 day interval - Glucocorticoids: prednisolone PO 1 mg/kg, dexamethasone 0.04mg/kg PO, intralesional triamcinolone - Cream mixtures- steroid + abi+/- DMSO - Fly control - Removal of faeces from environment
303
What is the disease profile of Atopic Dermatitis?
- Allergic skin disease VERY commonly seen in equine practice - Hypersensitivity → environmental trigger - Any breed - Any age - ? Seasonality - “indoor” related factors eg. Forage/dust mites, moulds - “outdoor” related factors eg. Grass, tree, weed pollens - Note can have more than one allergy going on in one horse at same time eg. Culicoides and atopy - Lesion distribution in the horse not well defined - Some evidence of familial inheritance? Do not breed from affected animals
304
What are the clinical signs of atopic dermatitis in horses?
- Pruritus +/- urticaria - Generalised or localised lesions - Perennial or seasonal
305
How is atopic dermatitis diagnosed in horses?
- Rule out other potential causes - Elimination/provocation testing eg. for suspected food allergy - Intradermal skin testing (IDST)- gold standard for detecting cell bound allergen specific IgE in dermis - Most useful if owners want to pursue de-sensitisation programs
306
How is allergenic avoidance enforced in the treatment of atopic dermatitis in horses?
- Not going to get an immediate response - Often difficult to confirm which allergen! - dust free environment - Keep horse at pasture /totally stabled /move to new location - Rubber matting in stable only - Regular vacuuming/ pressure washing of stable - Store foodstuffs in sealable containers to avoid contamination with forage mites - Regular washing of tack equipment and rugs at high temperatures - Can use human anti- dust mite duvet covers under rugs for a barrier
307
Describe the symptomatic treatment of atopic dermatitis in horses.
- Antihistamines - alone / to reduce steroid dose needed - Side effects: drowsiness or nervous/jittery behaviour - Hydroxyzine hydrochloride (Atarax) - 200-400mg per 500kg q 12h(1st choice) - chlorpheniramine (Piriton) - diphenylhydramine - cetirizine 0.2 mg /kg q 12h ( ingredient of cetirizine ? No sense ) - ALL UNLICENSED - Steroids- anti-inflammatory doses eg. Prednisolone 0.5-1.0mg/kg PO q24h until clinical signs controlled then EOD reduced dosing ( care laminitis risk) - Doxepin- tricyclic antidepressant , well tolerated in horse 2nd choice if hydroxyzine doesn’t work and concerned re steroid use 300-600mg per 500 kg q 12h, unlicensed
308
Give some other treatment methods of atopic dermatitis in horses.
- Topical spray Hydrocortisone aceponate (Cortavance, unlicensed in horse)- advantage only penetrates superficial dermis, not absorbed systemically - Shampoos to remove allergens, soothe eg. Oatmeal or aloe vera, need 10 minute contact time , mechanism of action unknown - Allergen specific immunotherapy – based on IDST, aim is to cause Ig switching so that Ag exposure leads to normal IgG synthesis rather than IgE production and reaction with dermal mast cells causing allergy - Requires frequent subcut INJS of increasing allergen concentration – protocols can be over 1-2 year period
309
What are the Common skin lumps and masses found in horses?
- Urticaria - Sarcoid - Melanoma - Viral papilloma - Eosinophilic granuloma - Squamous cell carcinoma
310
What is the disease profile of Urticaria?
= clinical sign NOT the disease - Very Common - Often acute presentation - Cause in most cases is not determined-idiopathic - Transient or persistent
311
What are the main causes of Urticaria?
- Insect bite (flies) / sting - Atopic dermatitis - Contact allergy RARE (wood shavings, - medications/home remedies) - Food allergy( cereals)- RARE - Drug reactions
312
What are the clinical signs of Urticaria?
- Multiple, raised oedematous papules, wheals, plaques - Variable size - Variable distribution- commonly head, neck, trunk - Lesions pit on pressure - Doughnut shape = gyrate form but appearance doesn’t correlate with underling cause! - Can be diffuse and ooze serum = angioedma - Variable pruritus
313
How is Urticaria diagnosed?
- Full history - Clinical signs - Contact- drip patterns if liquid, progressive lesions where O keeps applying a topical tx and lesions get worse! - Eliminate other problems- skin scrape - Skin biopsy in persistent cases- often unrewarding but useful for ruling out other problems - Dermatographism= write on skin with blunt object ,wheal develops within a few minutes
314
What are the differential diagnoses for Urticaria?
- Dermatophytosis ( culture/biopsy to eliminate) - Insect bites - Erythema multiforme ( clip off hair, central haemorrhagic focus in wheals) - Contact hypersensitivity (rare, doesn’t cause wheals ) - Infectious/immune mediated vasculitis- Purpura haemorrhagica, cutaneous necrosis, diffuse angiodema
315
What are the treatment/management options for Urticaria?
- Acute onset /transient / may resolve spontaneously 24-48h - SO no tx may be necessary for first episode - Remove contactant- warm water wash - Avoidance of allergen ! - Fly avoidance- barriers/repellents - Most cases → steroid responsive- IV dexamethasone 0.05-0.1 mg/Kg - Anaphylactic shock- combination adrenaline, NSAID and Steroid may be needed - Low dose steroids eg. Prednisolone 0.5-1.0 mg/kg PO SID then decreasing doses 1-2 weeks
316
What is the disease profile of sarcoids?
- The MOST COMMON skin lesion in the horse (35-90% of all skin neoplasms) - Fibroblastic tumour which may be locally aggressive, and typically non-regressive - Certain equine leucocyte antigens (ELAs) associated with increased susceptibility
317
What are the typical sites that sarcoids occur in horses?
- Predilection sites include: - Ventrum, inguinal region, axilla, periocular region - May also occur at wounds - Always suspect sarcoids with chronic non-healing wounds - Transmission most likely through biting/rubbing, fomites or insect vectors
318
What is an occult sarcoid?
very superficial, often just a ring of altered pigment with focal alopecia extending to scaly/hyperkeratotic skin
319
What is a nodular sarcoid?
- well circumscribed within the dermis or subcutis - Overlying skin appears normal initially but can become ulcerated or traumatised.
320
What is a verrucose sarcoid?
- Warty - raised, hyperkeratotic and resembling papilloma (but any “wart” on a horse is a sarcoid unless proved otherwise). - Generally slow-growing.
321
What is a Fibroblastic sarcoid?
- proud flesh”-like | - raised, ulcerative, and generally aggressive and extensive.
322
What is a Malevolant sarcoid?
- Malignant - often occur at the sites of wounds or trauma - Aggressive and deeply invasive with lymphatic spread and ulcerated nodules/
323
What is a mixed sarcoid?
two or more different types
324
How do you treat sarcoids via surgical removal?
- Sharp excision - smaller sarcoids (e.g. nodular) but failure rate high - Laser excision → higher success rate → now widely available
325
How do you treat sarcoids via ligation?
- Some owners will use hair tails – NOT a good plan! - DON’T use unless you are sure there is no root - Elastrator rings useful for some nodular and pedunculated fibroblastic sarcoids
326
How do you treat sarcoids via cryosurgery?
- Only useful for small superficial tumours (need to freeze/thaw tissues - Time-consuming, and high-recurrence rate if not used effectively
327
How do you treat sarcoids via Immunotherapy?
- BCG injection can be effective for peri-ocular nodular or fibroblastic lesions - Does not work for verrucose or occult lesions - Not currently available to vets in UK
328
How do you treat sarcoids via Chemotherapy?
- Intra-lesional injection of cytotoxic drugs → cisplatin, mitomycin C, 5-fluoro-uracil - Can be effective but significant dangers to surgeon without protective equipment and appropriate disposal of cytotoxic waste. - Topical 5-FU can be effective
329
How do you treat sarcoids via Photodynamic therapy?
- Application of chemical to lesion → significant cell damage when exposed to a certain wavelength of light - Poor penetration - only applicable to very small, superficial lesions, side-effects when animal exposed to sunlight
330
How do you treat sarcoids via Topical cytotoxic therapy?
- AW5-LUDES (“Liverpool cream”) contains 5-FU and other heavy metals - Reasonably effective in certain circumstances, requires repeated topical application every 48-72 hours - Only available through Derek Knottenbelt - Health and safety concerns
331
How do you treat sarcoids via Radiotherapy?
- Iridium wires no longer available in UK - High dose rate brachytherapy - very high activity iridium 192 source, emits primarily gamma radiation – catheters implanted into lesion; source driven through catheters by remote afterloader, treatment takes only a few minutes and is delivered in two fractions a week apart – horse not radioactive between treatments, no operator exposure - Excellent cosmesis and success around 95%, but expensive (£3800 -£4800 dependant on lesion size , available at AHT only for periocular lesions - Treat early for best results!
332
What is the clinical presentation of Viral papillomas?
- Common, but only seen in young horses (<3 years old) - Warts/verrucae,/“grass warts” often on muzzle or lips - Less commonly on eyelid, external genitalia and distal limbs - Initially small 1mm diameter raised grey/white papules followed by rapid growth to multiple hyperkeratotic lesions up to 2cm in diameter - Numerous keratinous projections
333
What are the treatment options for Viral papillomas?
- Typically respond spontaneously - Other treatments included autogenous tumour vaccines - Viral aetiology (equine papillomavirus, a DNA papovavirus) - Is contagious and therefore appropriate isolation may be required
334
What is the disease profile of aural plaques in horses?
- Common disease of adult horses - Ear papillomas - ? Fly transmission - Almost always an incidental finding - However, rarely, if ever, regress - Cosmetic problem only - DO NOT attempt treatment - Many anecdotal/isolated case reports have been attempted - Extremely variable and generally result in localised pain and discomfort
335
What is the Third form of cutaneous viral papilloma?
- equine genital papilloma - Older horses, do not regress - Probably precursors to some genital squamous cell carcinomas
336
What is a Melanoma?
A grey horse disease? - Any skin mass could be a melanoma - Any unexplained disorder could be a melanoma - All grey horses will get them eventually! (Reassure owners they are not the same as human melanomas but they can/will become pathologically malignant) - Common sites include perianal region, parotid salivary gland, sheath…. and guttural pouch
337
What is the physiology of a Melanoma?
- Altered melanin metabolism results in hyperplasia then subsequent malignancy - Typically, but not exclusively grey or white horses - Middle aged to older horses
338
What are the treatment options for Melanomas?
- Benign neglect/monitor - Standard approach but all lesions will progress - Cimetidine? - Evidence is contradictory - Surgical removal - Wide surgical excision required for larger lesions - Intra-lesional treatments - Cisplatin, mitomycin C (health and safety concerns) - Vaccines/immunotherapy??
339
What is the disease profile of Eosinophilic granulomas in horses?
- Nodular lesions commonly in the saddle area - Precise cause and pathogenesis - Often occur in spring and summer so often attributed to fly hypersensitivity or atopic dermatitis - Other authors suggest trauma - Often called collagen necrosis or similar names although not entirely accurate histopathologically
340
What are the treatment options for Eosinophilic granulomas in horses?
- Intra- or peri-lesional steroids (methylprednisolone or triamcinolone) - Systemic steroids (prednisolone or dexamethasone)
341
What is the disease profile of Squamous cell carcinomas in horses?
- Malignant neoplasm of keratinocytes - Can spread either along lymphatic chains or by direct transplantation - Sites: face, eyelids/cornea/globe, genitalia - Can occur anywhere but typically at mucocutaneous junctions - Risk factors: susceptibility to UV light, smegma? - Second most common cutaneous tumour - Most common tumour genitalia - Also common periocular lesion, esp third eyelid
342
What does the treatment of Squamous cell carcinomas in horses depend on?
Treatment dependent on location
343
How do you treat Squamous cell carcinomas in horses via Surgical excision?
- Third eyelid excision - Penile reefing/distal phallectomy/en bloc penile resection
344
How do you treat Squamous cell carcinomas in horses via Brachytherapy?
- Iridium-192 very effective for periocular lesions - Plesiotherapy- Strontium-90 (ß-emmitter) useful for small lesions and corneal lesions (probe 0.8cm D) - Both only available at AHT and are expensive
345
How do you treat Squamous cell carcinomas in horses via Chemotherapy?
- Cisplatin, 5-FU can be effective - Mitomycin-C (an antibiotic with anti-neoplastic activity) has been shown to be effective topically and intra- lesionally, often in conjunction with surgical removal
346
How do you treat Squamous cell carcinomas in horses via NSAIDs?
e.g. piroxicam has been used in isolated case reports
347
What are the common causes of crusting and scaling in horses?
- Infectious - Dermatophilosis (Rain Scald) - Dermatophytosis (Ringworm) - Bacterial infection- Staphylococcus spp. --> follicullitis/furunculosis/pyoderma - Dermatosis of lower limb - Leucocytoclastic vasculitis - Pastern dermatitis - Photo dermatitis - Seborrhea - Localised keratinisation defects - Cannon keratosis - Linear keratosis - Immune-mediated - Pemphigus foliaceus – RARE - Coronary band dystrophy- RARE - Idiopathic - Multisystemic eosinophilic epitheliotrophic disease (MEED)- RARE - Generalised granulomatous disease (SARCOIDOSIS) – UNCOMMON
348
What is the disease profile of Dermatophilosis in horses?
- Dermatophilus congolensis - G +ve facultative anaerobic actinomycete - Thought to exist in quiescent state (no clinical signs) in chronically infected animals until conditions are favourable for proliferation - Skin damage- other skin disease, insect bites, environmental trauma etc - Wet skin – sweating, rain, washing - Contagious - Immunocompromised/malnourished animals - Short lived immunity so can get recurrent infections
349
What are the clinical signs of Dermatophilosis in horses?
- Follicular/non follicular tufted papules → rapidly coalesce → exudative → matted hair (= paintbrush lesions) - When plucked leave erosions/ulcerations- may bleed or be purulent - Commonly seen on - rump and top line- rainfall - Saddle area- trauma/ sweating under tack - Face and neck- trauma/sweating under tack - Pasterns, coronet, heels= mud fever/grease heel/scratches – poorly drained pasture/muddy - Lesions may be painful e.g. Distal limb swelling, oedema, lameness - Can be on white skin - Rarely pruritic - Healing stage → dry crusts, scaling and alopecia - Lesions smaller in summer
350
How is Dermatophilosis diagnosed in horses?
- History - Clinical exam - Impression smears- cytology - G +ve branching, filamentous - Chain like coccus “railway tracks” - Culture- microaerophilic / high CO2 - Skin biopsy
351
What are the differential diagnoses for Dermatophilosis in horses?
- Staphylococcal follicullitis - Dermatophytosis - Pemphigus foliaceaus - Photo dermatitis - Other causes of pastern dermatitis
352
How do you manage Dermatophilosis in horses?
- Prevent wetting e.g. stable horse - Remove rugs etc to prevent sweating - Keep tack and grooming kit clean/individual use - Most cases spontaneously regress within 1 month if kept dry - Remove crusts, dispose carefully
353
What is the topical treatment used for Dermatophilosis in horses?
- Chlorhexidine shampoos eg. 4% chlorhexidine DOUXO® Pyo shampoo DUOXO® mousse - Silver sulphadiazine (Flammazine )cream - NOT steroids !!
354
What is the systemic treatment used for Dermatophilosis in horses?
- If horse systemically ill - If severe, generalised, chronic infection - Antibiotics- penicillin/ TMPS
355
What is the disease profile of Staphylococcus Infection in horses?
- Sporadic infection - G +ve Staphylococcus aureus - Common Spring and Summer- post clipping/ during coat change - Especially fine skinned horses- TB’s - PAINFUL - Contact areas of tack, saddle patch, riders legs - Potentially contagious if shared tack, equipment
356
What are the clinical signs of staphylococcus Infection in horses?
- Lesion starts as focal papule - Hairs stick up against lie of the coat, can be glued by small crusts - Can progress to furunculosis – nodules, draining tracts, ulcers, crusts - Can get cellulitis, lymphatic engorgement (= runners)
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How is staphylococcus Infection diagnosed in horses?
- Clinical signs - Swab and culture and exudate - Remember Staphylococcus aureus is a commensal – look for pure growth
358
What are the differential diagnoses for a staphylococcus infection in horses?
- Pemphigus foliaceaus - Other bacterial infection- Strep/ dermatophilosis - Onchocerciasis – this is pruritic
359
How is staphylococcus infection managed in horses?
- NSAIDS → pain - Avoid contact with tack, rider, rugs other horses - Topical antiseptic shampoos – Chlorhexidine/ povidone iodine based - Systemic antibiotics
360
What is the clinical profile of Dermatophytosis in horses?
- HIGHLY CONTAGIOUS and COMMON - Potentially ZOONOTIC - Transmitted via contact with infected animals/environment- tack, rugs, grooming kit, bedding, fencing, transport vehicles, people 2 causes in horse - Trichophyton equinum and verrucosum - Microsporum gypseum and equinum - Incubation period 1-6 weeks - Young animals esp. susceptible - Some immunity with age/post infection – unusual for a healthy horse to get dermatophytosis a second time. - Spores very resistant , survive for long periods in environment - Disease is endemic in many livery/racing yards
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What are the clinical signs of Dermatophytosis in horses?
- Common at sites of tack contact- - face, neck, dorsolateral thorax, girth ( legs- rarely) multiple lesions - Initially change in angle of hairs → small often circular patches - Amongst hairs- amounts of finely keratinised squames → (=Cigarette ash!) - Fungus produces keratolytic enzymes → weakening hairs → easily broken / epilated - Focal areas coalesce → extensive scaling and flaking - Healing occurs from the centre - most active fungal growths at margins of the lesion- imp for sampling - Variable pain - Variable pruritus - Difficult to tell which fungal spp. is involved just by clinical presentation
362
How is Dermatophytosis diagnosed in horses?
- Hair plucks at periphery of lesions - Microscopy - Culture (can take up to 30 days) - sabouraud’s medium + red phenol - dye agar turns red if +ve - Microsporum spp. Add drop vit B to culture as tricky to grow - Woods lamp NOT useful in horse - Skin punch biopsy- fungal spores within hair follicles
363
How is dermatophytosis managed in horses?
- ID of species not critical for treatment - Most infections are self limiting (5-10 weeks) - Wear gloves to tx as potentially ZOONOTIC - Two main principles: 1. Treat active infection to decrease spore formation 2. Eliminate infective spores from environment - Topical/ systemic drugs – anti-fungal action
364
What is the clinical profile of Pastern Dermatitis in horses?
- COMMON! Often winter! Often multifactorial! Chronic wetting of the skin! White legs but not exclusively! - INFECTIOUS – bacteria, fungus, virus, parasite vs - NON-INFECTIOUS- trauma, immune mediated, neoplastic
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What are the differential diagnoses of pastern dermatitis in horses?
- Dermatophilosis- crusts on top of pus, not that painful - Staphylococcal dermatitis – extremely painful - Pastern and cannon leukocytoclastic vasculitis-not painful - Other autoimmune disease eg. SLE , immune mediated necrotising vasculitis
366
What are the clinical signs of pastern dermatitis in horses?
- Mild- alopecia, erythema, mild serum exudation - Progression to – papules, significant serum exudation → crusts → scabs - +/- pain on palpation - +/- lameness - +/- cellulitis
367
How is pastern dermatitis in horses diagnosed?
- Clinical signs - Coat brushings - Skin scrapes - Swabs from exudate – culture/sensitivity - Skin biopsy – often poor return, may help in recurrent or refractory cases - Eliminate other causes e.g. Chorioptes spp.
368
What is the general approach to the management/treatment of pastern dermatitis in horses?
1. Clean and clip area 2. Debride crusts- e.g. Dermisol cream/Sudocream +clingfilm wrap+ → stable bandage 12h overnight 3. Next day- gently wash area with dilute Chlorhexidine , dry and clip → more if needed 4. If crusts still there repeat STEP 2 5. It’s a fine balance between over wetting and needing to wash area 6. Apply topical treatment 7. Dispose of crusts carefully /don’t re-use same towel to dry
369
Which topical treatments can be used in the management/treatment of pastern dermatitis in horses?
- Chlorhexidine- 4% chlorhexidine DOUXO® Pyo shampoo and DUOXO® mousse - Antiseptic, anti-fungal eg. Malaseb shampoo - Antibiotic creams eg. Flammazine cream - Combined antibiotic+steroid cream eg. Fuciderm, - Care with repeated use of topical steroid- could delay epithelisation / cause thinning of skin , BUT may help with pain/inflammation
370
How can pastern dermatitis in horses be prevented?
- AVOID over wetting skin- use barrier creams for exercise eg. Petroleum jelly - CARE DO NOT to aggressively wash and scrub area - Clean, dry bedding, avoid prickly straw - Dry paddocks
371
What is the cause of Pastern Leukocytoclastic Vasculitis in horses?
Cause unknown ? Associated with bacterial infection
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What are the clinical signs of Pastern Leukocytoclastic Vasculitis in horses?
- in almost all cases affects white limbs, often follows BV’s Lat and med limb - Firmly attached crusts on distal limbs
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How is Pastern Leukocytoclastic Vasculitis in horses diagnosed?
See vasculitis, karryorrhexis of neutrophils
374
How is Pastern Leukocytoclastic Vasculitis in horses treated?
- Topical - Systemic steroids eg, prednisolone/dexamethasone - Avoid sun
375
What is the disease profile of Photo dermatitis?
- SUNBURN: - Primary direct damage to the epidermis by UV light - Commonly unpigmented, pink skin eg. palomino, cream horses - Areas maximally exposed to the sun, nose, muzzle – erythema, scaling, necrosis - Prevent using sun cream
376
Describe Photosensitisation in horses.
- Occurs following normal light exposure - Indirectly caused by photodynamic agents in skin due to - Ingestion of plants containing photodynamic agents → direct absorption into blood eg. UK Hypericum perforatum – St. Johns Wort - failure of the liver to de-toxify phlloerythrin (by- product of chlorophyll digestion) hepatotoxic plants eg. Senecio jacobea= Ragwort
377
What is the signalment of Photosensitisation in horses?
Check paddocks  ID plants - Ragwort → usually unpalatable when alive BUT when cut palatability ꜛ eg. In hay - Toxic effects → not seen → months after ingestion - Can affect multiple horses in a group - Not all horses have liver failure BUT its prudent to rule out
378
What are the clinical signs of Photosensitisation in horses?
erythema, oedema, pain, vesicles, serum exudation, skin necrosis, ulceration, sloughing, possible other signs of liver disease, secondary bacterial infection
379
How is Photosensitisation in horses managed?
- sun avoidance ( stable in day, turnout at night), - UV masks, high factor sun screens, avoid grazing with toxic plants. - use topical creams to remove crusts and soothe eg. Dermisol/aloe vera.
380
What is the disease profile of Auto-immune dermatoses in horses?
- Pemphigus foliaceus – RARE - Antigen in horse not known - Lesions often start on face → generalised over several months - Early lesions → papules and crusts - Annular thick crusts, annular erosions with/without epidermal collarettes, annular alopecia, oozing, matted hair coat, scaling
381
How is Pemphigus foliaceus diagnosed in horses?
- Skin biopsy – acantholysis, neutrophils, eosinophils - Direct smear of pustules/erosions- cytology - Immunohistochemistry
382
How is Pemphigus foliaceus in horses treated?
- Rarely can resolve spontaneously – foals - Aggressive treatment- immunosuppressive doses systemic steroids , prednisolone PO SID starting at 2 - 4mg/Kg or dexamethosone - Immunomodulators- Azathioprine - Gold salts- aurothioglucose - Approx 50% cases relapse after prolonged treatment
383
What are the common causes of ulcers and erosions in horses?
- Saddle sores/tack rubs- most resolve, can leave leucoderma - Chemical irritants - Vasculitis - post infection eg. Streptococcus equi equi → PURPURA HAEMORRHAGICA- urticaria, oedema of head, limbs, petichiation of mm, exudation, skin slough - Treatment : steroids, antibiotics, nursing - drug related - Photo-activated - Type III + Type I hypersensitivity
384
What are some Other causes of ulcers and erosions in horses?
- Chemical or thermal burns - Coital exanthema (EHV3) - Pemphigus vulgaris/ Bullous pemphigoid - Inherited defects- Cutaneous asthenia, epidermolysis bullosa, aplasia cutis - Ulcerative lymphangitis eg. Corynebacterium paratuberculosis - Glanders and Farcy- NOTIFIABLE (Burkholderia mallei) - Epizootic lymphangitis – NOTIFIABLE (Histoplasma farciminosum) - Vesicular stomatitis – NOTIFIABLE
385
Name some Hair coat disorders in horses?
- Normal hair shedding related to photoperiod - Hirsuitism- equine cushings disease (PPID) - Seasonal abnormal shedding - Anagen defluxation - Telogen defluxation-
386
What is seasonal abnormal shedding in horses?
- alopecia, face, shoulders, rump - skin is normal - horse otherwise healthy - pathogenesis unknown - Spontaneous recovery over several months
387
What is Anagen defluxation in horses?
disease (infectious, metabolic, fever) can disrupt the hair cycle → sudden hair loss, hair shaft breakage
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What is Telogen defluxation in horses?
stress (pregnancy, fever, severe illness, surgery, anaesthesia) causes abrupt, premature cessation of growth of anagen hairs, within 1-3 months a large number of telogen hairs are shed Both spontaneously resolve when inciting cause corrected
389
What is Leukotrichia/Leukoderma in horses?
acquired loss of coat colour without loss of skin pigment e.g. Freeze brand bandage rub patches of white hair non progressive
390
What is Vitiligo in horses?
gradual appearance of non-pigmented skin without other changes e.g. Pink peri-ocular areas of Arabs
391
What is Spotted Leukotrichia in horses?
- Shire, TB, Arab - Non-inflammatory white haired spots on normal skin - Get increased number of static spots
392
What is Reticulated Leukotrichia in horses?
- White hair patterns - Can be painful - Quarter horse , TB, SB - Cause unknown
393
How can coat changes in horses be diagnosed and treated?
- All 4 conditions can be differentiated by clinical signs or histopathology of biopsies. - No treatment
394
What are the differential diagnoses of alopecia in horses? Don't worry about trying to remember them all.
- Anomalous: - congenital hypotrichiosis- Percheron - mane and tail follicular dysplasia - asynchronous shedding - Metabolic: - telogen defluxation - PPID (hypertrichiosis) - Neoplastic: - Occult sarcoid - Lymphoma - Inflammatory/infectious: - ectoparasite - Dermatophytosis - Dermatophilosis - Inflammatory/autoimmune: - culicoides hypersensitivity - Atopic dermatitis - Alopecia Areata - Cutaneous lupus erythematosus - MEED/ sarcoidosis - Drug eruptions Toxic: - contact dermatitis - scalding (urine/faeces) - heavy metal- Selenium, arsenic, mercury Traumatic: - scarring Vascular: - ischaemic damage → minaturisation of BVs
395
What is the signalment of Linear Keratosis in horses?
- Relatively common | - All ages/breeds, TB and Quarter horses, rare in ponies
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What are the clinical signs of Linear Keratosis in horses?
- Initially small areas hyperkeratosis--> develop alopecia - Lesions develop in a linear direction - Neck, chest, quarters - No pain, pruritus
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How is Linear Keratosis in horses diagnosed?
- Clinical presentation - skin scrapes to eliminate other diseases - skin biopsy- regular/irregular hyperplasia - Hyperkeratosis - lymphocytic follicullitis

ENDO (4 decks)

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