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Dermatology 2 > Parasitic skin diseases in small animals > Flashcards

Parasitic skin diseases in small animals Flashcards

1
Q

What is meant by flea allergy dermatitis?

A
  • Flea bite hypersensitivity
  • Pruritic dermatitis due to hypersensitivity to salivary proteins of flea (type I or IV)
  • Does not indicate infesation
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2
Q

What organisms, other than fleas, can animals develop hypersensitivities to?

A
  • Insects e.g. mosquitoes, flies, lice

- And mites e.g. Sarcoptes, Otodectes

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3
Q

Briefly outline mosquito bite hypersensitivity (cause, species, prevalence)

A
  • Presume antigens in mosquito saliva
  • Cats mainly, but no exclusive
  • Summer-autumn
  • Usually animals with outdoor access
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4
Q

What is canine nasal (eosinophilic) folliculitis/furunculosis?

A

Inflammation of hair follicles

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5
Q

How does furunculosis develop?

A
  • Inflammation of follicle wall so bad, breaks down, keratin from hair follicle gets into dermis and causes foreign body inflammatory reaction
  • Keratin breaks down very slowly, long time for inflammation to reduce
  • Furunculosis may occur in deep pyoderma
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6
Q

Describe the development of canine nasal folliculitis/furunculosis

A
  • Comes up very quickly, within 12 hours, wildly pruritic and lots of reaction
  • Cause unknown, bites and stings from insects strongly suspected
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7
Q

Describe the common clinical signs of FAD in the dog

A
  • Pruritus: scratching, biting skin, jumping up suddenly, excessive licking, overgrooming
  • Secondary results: alopecia, skin inflammation +/- skin infection, crusting, lichenification
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8
Q

Which areas of a dog are classically most affected with FAD?

A
  • Caudal dorsum

- Tail base, thighs, inguinal area

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9
Q

Describe the common clinical signs of FAD in the cat

A
  • Variable
  • Miliary dermatitis
  • Alopecia (due to overgrooming)
  • Eosinophilic granuloma complex lesions
  • Head and neck pruritus
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10
Q

What is miliary dermatitis?

A

Gritty, crusty papular lesions of the skin

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11
Q

Describe the clinical signs of pediculosis

A
  • Operculated eggs attached to hairs may be seen
  • Often asymptomatic
  • may see poor hair coat, scaling, papules, crusts, variable pruritus
  • Heavy infestation can cause anaemia and lethargy
  • Infestation may reflect poor hygiene, nutrition or immunity
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12
Q

Describe the clinical signs associated with mosquito hypersensitivity

A
  • Papules
  • Eruptions
  • Hairless regions most affected e.g. bridge of nose, preauricular skin, occasionally footpads
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13
Q

Describe the appearance of canine nasal (eosinophilic) folliculitis/furunculosis

A
  • Acute eruption mainly affecting muzzle and ears
  • Papules
  • Nodules (+/- ulcerated)
  • variable pruritus but can be intense
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14
Q

List common differential diagnoses for flea allergic dermatitis in the dog and cat

A
  • Environmental atopy (but would commonly see signs on feet, ventrum and face)
  • IN cat, clinical signs are same as food atopy or environmental atopy
  • Other ectoparasites
  • Microbial infections
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15
Q

Briefly outline the life cycle of lice

A
  • Adults survive off host for 3 days
  • Life cycle approx 3 weeks
  • Nits can cause indirect infestation from bedding, blankets, esp. if large no. of dogs
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16
Q

Describe the diagnosis of FAD in the dog or cat

A
  • Flea comb
  • Vigorous coat brushing and examine debris on moistened paper
  • Microscopy of flea dirt collected on combing or tape stip
  • Known down fela spray for demonstration of dead fleas e.g. permethrin on dogs
  • Examine faeces for tape worm segments
  • False negatives common, esp. in cat as groom well
  • Intradermal allergy testing for FAD
  • In vitro/serological testing for FAD
  • Response to therapy
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17
Q

Why is examination of the faeces for tapeworm segments a valid method for the diagnosis of the presence of fleas on a dog or cat?

A

Dipylidium caninum is spread by fleas

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18
Q

Discuss the use of intradermal allergy testing for FAD

A
  • May test with other environmental allergens
  • Up to 30% false positive reactions with flea saliva
  • FAD can involve type I or type IV reactions, can take 48 hours to see reaction but this is rarely assessed
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19
Q

Discuss the use of in vitro/serological testing for FAD

A
  • Measure antigen specific IgE (type I)
  • Does not document type IV reaction
  • Negative does not exclude FAD
  • Rarely done
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20
Q

Discuss the use of response to therapy as a method of diagnosis

A
  • Best method
  • Range of effective products available
  • Diagnosis is confirmed by response to thorough flea control trial
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21
Q

Outline the management of FAD

A
  • Pupae not responsive to treatment so need to cover emerging adults
  • Can take 140 days for pupae to emerge so need to cover this period i.e. treatment may take more than 3 months treatment
  • Permethrin household adulticide, lasts 6-7 weeks, repeat
  • Whole life cycle usually complete in 3-4 weeks, can be as short as 2 or as slow as 6mo depending on environmental conditions
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22
Q

What control measures are available for fleas?

A
  • Mechanical removal (flea comb, vacuum house)
  • Repellents (limited in cats to only flumethrin)
  • Adulticides, larvicides, ovicedes
  • Products that inhibit development e.g. IGRs, chitin synthesis inhibitors (lufenuron)
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23
Q

Which drugs have an effect on environmental and adult life stages of fleas? Discuss

A
  • Imidacloprid
  • Selamectin
  • Indoxacarb
  • BUT incomplete, imidacloprid only in hair and dandruff that falls off animal
  • Need to use household spray as well for complete coverage
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24
Q

List the drugs that are effective against adult fleas

A
  • Dinetofuran
  • Permethrin, flumethrin, tetramethrin
  • Fipronil
  • Pyriprole
  • Nitenpyram
  • Afoxolaner, flurolaner, sarolaner, spinosad
  • Imidacloprid
  • Selamectin
  • Indoxacarb
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25
Q

List the drugs that are effective against the environmental life stages of fleas

A
  • Pyriproxyfen
  • S-methoprene
  • Lufenuron
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26
Q

Give an example of a spot on product consisting of a pro-drug that is only activated by the parasite

A

Indoxacard

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27
Q

Give an example of a spot on produce that kills fleas and sarcoptic mage, but has no action against demodicosis

A

Selamectin

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28
Q

Give examples of flea adulticides that will not lose efficacy with repeated bathing

A

Spinosad, isoxazolines

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29
Q

Give an example of a very short acting (24h) knock down flea adulticide

A

Nitenpyram (rarely used)

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30
Q

Give an example of an oral product effective against fleas and ticks (and likely demodicosis but off label), and lasts for 3 months

A

Flurolaner

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31
Q

How is pediculosis diagnosed?

A

Demonstration of live/eggs with magnifying glass or under microscope from coming, unstaned acetate tape strip or hair pluck

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32
Q

Outline the treatment for pediculosis

A
  • Relatively easy as entire life cycle is on host
  • Many flea adulticides are effective incl. imidacloprid, fipronil, selamectin, permethrin
  • Treat all in contacts
  • recommended environmental cleaning incl. removal and washing of bedding
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33
Q

Outline the management of mosquito hypersensitivity

A
  • avoid outdoors, esp. dawn and dusk
  • Use insect repellents (permethrins are toxic to cats, flumethrin can be used)
  • Symptomatic treatment with glucocorticoids
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34
Q

Outline the management of canine nasal eosinophilic folliculitis/furunculosis

A
  • Glucocorticoids, antihistamines

- Insect repellents

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35
Q

Outline the life cycle of Cheyletiella

A

Life cycle 3-4 weeks, may survive off host for 5-6 weeks

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36
Q

List the surface and deep mites that affect dogs and cats

A
  • Surface: Cheyletiella, Otodectes, Neotrombicula

- Deep: Sarcoptes,, Demodex

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37
Q

Describe the clinical signs of Cheyletiella

A
  • Pruritus, scaling
  • Esp dorsal trunk
  • Walking dandruff
  • Often very dramatic in rabbits, less so in dogs and cats (often just pruritus)
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38
Q

What are the key differential diagnoses for a condition that presents similarly to Cheyletiella?

A
  • Flea infestation
  • Scabies
  • Atopy
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39
Q

What species are at risk of cheyletiellosis and define the risk?

A
  • Dogs, cats, rabbits, guinea pigs, humans

- HIGHLY contagious

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40
Q

How is cheyletiellosis diagnosed?

A
  • Microscopic examination of superficial skin scrapings, unstained tape strips, coat brushings/combins
  • Brushings/combings most sensitive, few in coat if mild and otherwise easy to miss. Collect debris, place in LP on slide
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41
Q

Outline the management of cheyletiellosis

A
  • Environmental treatment important, household flea spray
  • Contaminated materials must be burnt, steam cleaned or chemically treated
  • no licensed products but effective treatments available
  • Topical: fipronil q3-4 weeks, selenium sulphide shampoo weekly, amitraz (not for cats) q2weeks 3x
  • Systemic: selamectin spot on q2-4 weeks, isoxazolines (anecdotal)
42
Q

Describe the clinical signs of Otodectes cynotis

A
  • Ear irritation
  • Head shaking
  • Excessive ear wax
  • Occasional irritation of face or body
43
Q

What are important differential diagnoses for a presentation similar to that for Otodectes cynotis?

A
  • Malassezia

- Flea infestation

44
Q

How is Otodectes diagnosed?

A
  • Visualise ear mites by otoscopy

- Detect ear mites/eggs in cerumen

45
Q

How long is the life cycle of Otodectes?

A

3 weeks

46
Q

Describe the treatment of Otodectes cynotis

A
  • Topical in ears: acaricidal in ears 2xdaily for 3 weeks. Surolan, canaural licensed but contain no anthelmintic, but effective
  • Systemic: selmectin, moxidectin spot-ons, sarolaner licensed
  • Regular ear cleaning
  • Must treat in contact animals
47
Q

Why must topical ear drops be used for 3 weeks in the treatment of Otodectes cynotis?

A

Eggs are resistant to treatment so have to treat over 3 weeks to cover life cycle and kill adults

48
Q

Describe the occurrence of trombiculosis

A
  • Seasonal (summer and autumn)

- regional geographic distribution

49
Q

Which species are affected by Neotrobicula autumnalis?

A
  • Dog, cats, occasionally humans

- NB humans infested from environment rather than dog or cat

50
Q

What is the clinical significance of trombiculosis in dogs?

A
  • Can cause discomfort

- But also associated with seasonal canine Illness

51
Q

Briefly outline Seasonal Canine Illness

A
  • Disease that kills dogs in Thetford forest, Clumber park, Sherwood forest
  • Acute gastroenteric disease, collapse, often fatal
  • Have large number of harvest mites in them
  • Very regional, unknown cause
52
Q

Describe the clinical signs of trombiculosis

A
  • Papules
  • Crusts
  • Pruritus
  • esp. interdigital spaces, pinnae (Henri’s pocket) ventral abdomen, anal region
  • Visible orange larvae
53
Q

How is trombiculosis diagnosed?

A
  • Demonstration of larvae on skin

- Skin scrapings in liquid paraffin

54
Q

Describe the treatment for trombiculosis

A
  • No licensed product but various products used
  • Fipronil q2weeks
  • Selamectin limited efficacy
  • Isoxazolines to be determined
55
Q

How long is the life cycle of Sarcoptes scabiei?

A

3 weeks

56
Q

Which species of Sarcoptes affects dos and foxed?

A

Sarcoptes scabiei var. canis

57
Q

Is there a risk to humans from Sarcoptes scabiei?

A

Yes - zoonotic

58
Q

Describe the clinical signs of Sarcoptic mange

A
  • Intensely pruritic
  • Positive pinnal-pedal scratch reflex
  • Papules, crusts, especially on pinnal margins, elbows, hocks, sternum
  • Other areas may be affected
59
Q

What methods are used in the diagnosis of sarcoptic mange

A
  • Clinical signs (if dog cannot stop itching, high suspicion), acute onset, unresponsive to prednisolone
  • Skin scrapings
  • Treatment trial
  • IgE serology
  • ELISA serology
  • Histopathology
60
Q

Describe the method for skin scrapings in the diagnosis of sarcoptic mange

A
  • Multiple, minimum 6 deeps scrapings
  • Difficult to detect (50% sensitivity)
  • Choose primary lesions in areas avoiding secondary cahnges
  • Look for mites, eggs, mite faeces using LP and coverslip
61
Q

Discuss the use of IgE serology in the diagnosis of sarcoptic mange

A

Cross-reactivity with house mites, may give false negative/false positive for house mites

62
Q

Discuss ELISA serology in the diagnosis of sarcoptic mange

A
  • Detects anti-sarcoptes IgG, highly sensitive and specific
  • Can have false positive due to cross-reaction with Abs to house dust mites
  • False negatives may occur as seroconversion takes 3-4 weeks
63
Q

Discuss the use of therapeutic trials in the diagnosis of sarcoptic mange

A
  • Good if no mites detected but are suspicious

- Helps distinguish from atopic dermatitis

64
Q

Evaluate the use of histopathology in the diagnosis of sarcoptic mange

A
  • Litlle use in diagnosis as are unlikely to see mites

- Non-specific inflammatory picture with eosinophils and mast cells more likely

65
Q

What is Norwegian scabies?

A

Simply means a large number of mites found, need to look for underlying immunosuppression

66
Q

Give the treatment options for sarcoptic mange

A
  • Steroids ineffective
  • Systemic acaricidals effective e.g. selamectin, moxidectin
  • Licensed use: 2 spot on applications 4 weeks apart
  • Off label: 3 spot on applications 2 weeks apart
  • Sarolaner: oral tablet monthly, licensed
  • Topical: amitraz solution or lime sulphur, both weekly for 4 weeks
67
Q

Compare the use of spot on treatments for sarcoptic mange in the licensed method, or as the off label method

A
  • Licensed: safe, well tolerated
  • Off label: never for collies/herding breeds, elderly, young, debilitated animals, animals at lower margin of bodyweight band
68
Q

Compare the use of amitraz and lime sulphur in the treatment of sarcoptic mange

A
  • Amitraz: long coats need clipping, +/- prewash with keratolytic shampoo. toxicity concerns for pet and in cotact peple, use gloves, aprons, face-shileds. No longer used due to isoxazolines being better and safer
  • Lime sulphur: effective, well tolerated, stains, pungent, dyes white hair yellow, but works where other treatments have failed
69
Q

Describe the management of sarcoptic mange

A
  • Zoonotic, as well as contagious
  • Avoid contact, decontaminate or destroy items e.g. bedding, brushes
  • Treat all in contacts with acaricide
  • Use insecticidal spray for environment
  • Glucocorticoids may help control intense pruritus
70
Q

How long is the Demodex life cycle?

A

10-12 days

71
Q

When does demodicosis usually occur?

A

In animals with immunoincompetence e.g. young animal, underlying dsiease

72
Q

Explain how infection with demodex occurs

A
  • Is a normal inhabitant of canine skin

- Not contagious, passed form dam to offspring in first few days of life

73
Q

Outline the potential consequences of demodicosis

A
  • Excessive multiplication in hair follicles and sebaceous glands leading to follicular disease on skin, folliculiis, alopecia, furunculosis, often with erythema
  • Can cause deep pyoderma
74
Q

Described the distribution of demodicosis on an animal

A

Can be localised or generalised

75
Q

Describe localised demodicosis

A
  • <6 multifocal lesions
  • Well circumscribed, scaling, alopecia, +/- erythema
  • Often young dogs
  • Not usually pruritic
  • Occasionally secondary to bacterial/Malassezia infection
  • 90% self cure, 10% progress to generalised condition
76
Q

What is the criteria for generalised demodicosis?

A
  • Any of:
  • > 6-10 lesions
  • Entire body region
  • 1 or more feet affected
77
Q

Describe generalised demodicosis

A
  • Feet affected worst prognostically
  • Secondary bacterial infection common, potentially severe leading to pyrexia, lymphadenopathy, depression, occasional death
  • More frequently pruritic than localised form
  • Generalised alopecia and erythema
  • Comedones and pustules (+ follicular casts) common
78
Q

Why does pododemodicosis carry a poor prognosis?

A

More refractory to treatment than other areas

79
Q

Compare the appearance of Demodex injai to canis

A

Extra long bodies, 50-100% longer than canis

80
Q

Describe the key features of Demodex injai

A
  • Sit in pilosebaceous units
  • Especially on dorsal trunk of adult dogs
  • Especially terriers and WHWT
  • Often present with excessive greasiness
  • Key differential is atopic dermatitis
81
Q

Compare Demodex to Demodex canis

A
  • Short bodies, 50% length of D. canis
  • Mainly located on skin surface an follicular openings, interdigital surfaces
  • Now thought to be variant of D. canis
82
Q

When is demodicosis classes as juvenile onset?

A

1-12mo, especially common 3-6mo

83
Q

What is the prognosis for juvenile onset demodicosis?

A

Good, usually resolves with sexual maturity if localised, as immune response improves

84
Q

What is the main consequence of juvenile onset demodicosis?

A

Should not be bred from

85
Q

When is demodicosis classed as adult onset?

A

4yo or more, uncommon

86
Q

How does adult onset demodicosis occur?

A
  • Usually secondary to immunosuppression

- Endocrinopathic, neoplastic, infectious etc.

87
Q

What is the prognosis for adult onset demodicosis?

A

Guarded if underlying cause cannot be corrected, may end up with recurrent demodicosis

88
Q

Describe the diagnosis of demodicosis

A
  • Deep skin scrapes, squeeze skin before scraping
  • +/- plucks (esp. face and feet), not useful alone but good ajuncive
  • +/- if skin scarred or very thick e.g. Shar Pei (may see mites, folliculitis, furunculosis)
  • Preparation thin otherwise will not see anything
89
Q

Identify the treatment options for demodicosis

A
  • Localised usually self resolves
  • Generalised may self resolve but better to use acaricide e.g. sarolaner, moxidectin, amitraz
  • Advocate
  • Sarolaner
  • NOT steroids
  • Avermectins off license
  • Treatment of secondary infection, underlying cause, relapses
90
Q

Discuss the use of amitraz in the treatment of canine demodicosis

A
  • Precautions and indications must be followed
  • Can be toxic
  • Weekly application
  • Clip and degreasing bath first
  • Care re. MAOI cross reactions
  • Contraindicated in Chihuahuas and care with other small breeds
91
Q

Discuss the use of Advocate in the treatment of canine demodicosis

A
  • Imidacloprid and moxidectin spot on
  • Licensed for monthly use, but info for weekly use in serious cases
  • Do not go off license in collies/herding breeds
92
Q

Discuss the use of isoxazolines in the treatment of canine demodicosis

A
  • Sarolaner licensed, other unlicensed
  • Use at same frequency as for fleas/ticks
  • Can take up to 60 days to see significant effect
93
Q

Discuss the use of steroids in the treatment of canine demodicosis

A
  • Cannot be used

- Immunosuppression is the underlying problem and steroids will add to this

94
Q

Discuss the use of avermectins in the treatment of canine demodicosis

A
  • Superseded by isoxazolines
  • Milbemycin daily PO, some risk of side effects and costly
  • incremental dose increase over 10-24 days in all cases and close monitoring for adverse effects
95
Q

Outline the treatment monitoring for canine demodicosis treatment

A
  • Regular scrapings i.e. monthly
  • Same sites scraped
  • Record numbers of each stage of life cycle (egg, larvae, nymph, adult)
  • Record dead vs alive
  • Treat until have 2 negative scrapings with minimum 1 month interval
  • Treatment may be required for months
96
Q

Describe Demodex cati

A
  • Follicular
  • Long slender mite
  • Uncommon
97
Q

Where is Demodex cati found?

A
  • In follicles and sebaceous glands
  • can be locaslised to head and neck
  • Or generalised
98
Q

What is generalised feline demodicosis usually associated with?

A

Underlying immunosuppression e.g. FIV, FeLV, diabetes mellitus

99
Q

Describe the clinical signs of Demodex cati

A
  • +/- waxy otitis externa
  • Patchy alopecia, erythema, scale
  • May have comedones, secondary pyoderma
  • Pruritus variable
100
Q

What are the 2 demodex species that infect cats?

A

Demodex cati and gatoi

Dermatology 2 (23 decks)

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