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derm Flashcards

1
Q

Ehlers danos syndrome

A

group of genetically heterogenous connective tissue disorders linked with genetic defects affecting collagen or other extracellular matrix proteins

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2
Q

Hereditary equine regional dermal asthenia (HERDA) is seen in what breed

A

American quarter horses

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3
Q

Hereditary equine regional dermal asthenia (HERDA) gene mutation

A

PPIB: peptidyl prolyl isomerase B gene

** acts as a chaperone involved in proper folding of collagens

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4
Q

Hereditary equine regional dermal asthenia (HERDA) C/S

A

usually seen at 2 years old when broken into saddle– skin tears, or wounds with prolonged healing times
**develop disfiguring scars
-skin is loose and hyperelastic

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5
Q

What is the prevalence of Hereditary equine regional dermal asthenia (HERDA) in
Quarter horses?

A

3.5%

**inc prevalence in cutting horses (up to 28%)
**w/in pleasure/working-cow horses (up to 12.8%)

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6
Q

Warmblood fragile foal syndrome gene mutation

A

PLOD1 (procollagen lysin, 2-oxglutarate 5- dioxygenase 1) gene
**codes enzyme for collagen biosynthesis

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7
Q

Warmblood fragile foal syndrome C/S

A

is af atal defect of connective tissue involving severe skin malformations in enonatal foals

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8
Q

Chronic progressive lymphadema is seen in what breeds?

A

draft breeds: clydesdales, belgian drafts and shires

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9
Q

chronic progressive lymphadema lesions

A

start at early age
-progressive swelling of legs & development of severe chronic skin changes such as hyperkeratosis & dermal fibrosis with thick skin folds & nodules
-secondary skin infections– contrib to chronic changes
-severe discomfort

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10
Q

Junctional epidermalysis bullosa gene mutations

A
  1. LAMA 3: american saddlebreds
  2. lamC3– belgian and other drafts
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11
Q

Junctional epidermalysis bullosa clinical signs

A

mechanobullous dz: development of ulcers adn bilsters in the skin at pressure points (hocks/stifle) or mucocutaneous junctions (mouth & anus)
oral lesions: premature eruption of teeth & loss of enamel= bleeding mouth

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12
Q

Hypotrichosis is a disease of what breeds?

A

curly coated breeds: american bashkir, culry horses and missouri fox trotters

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13
Q

hypotrichosis clinical signs

A

alopecia @ birth or develops early during neonatal period
defects in ectodermal structures: teeth, hooves, eyes or seat glands

– normal shedding periods, some permanent loss of main & tail

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14
Q

Pemphigous foliaceus describes a group of what disorders?

A

autoimmune vesiculobullous disorders characterized histologically by:
-intraepidermal acantholysis
-intercellular deposition of immunoglobulin

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15
Q

What are the clinical lesions primarily recognized in Pemphigous foliaceus?

A

-scaling
-crusting

–>generalized exfoliative dermatitis, ventral or peripheral edema, fever depression

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16
Q

What are characteristic histologic findings of Pemphigus foliaceus?

A

-intragranular to subcorneal cleft and vesicle formation assoc with acantholysis

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17
Q

Why is recommended to review on slide exam of biopsies in cases of pemphigus foliaceus?

A

certain strains of Trichophyton spp of dermatophytes may also cause acantholysis
**any histology suggestive of pemphigus foliaceus must be stained for fungi

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18
Q

What are recommended treatments for pemphigus foliaceus?

A

-immunosuppressive doses of corticosteroids
-prednisolone: 1 mg/kg
-dexamethasone: 0.08-0.1 mg/kg PO q24h, then tapering

-gold salts (historic tx)
-azathioprine: 1-3 mg/kgPO q24-48h

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19
Q

Why is oral prednisole preferred to prednisone?

A

–some horses are unable to metabolize prednisone into active metabolite of prednisolone

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20
Q

What is the prognosis for horses diagnosed with pemphigus foliaceus?

A

–lifelong administration of steroids required

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21
Q

Pemphigus vulgaris is a rare autoimmune skin disease ancedotally reported in horses characterized by:

A

-circulating IgG directed against the epidermal transmembrane protein desmolgein-3

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22
Q

What are clinical signs of pemphigus vulgaris?

A

vesicles
ulcerations– @ mucocutaneous & cutaneous areas

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23
Q

What is bullous pemphigoid?

A

an autoimmune vesiculobullous and ulcerative disorder that affects the cutaneous basement membrane zone (BMZ)

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24
Q

What is the pathophysiology of bullous pemphigoid?

A

complement activaitng anti-BMZ antibodies bind to glycoprotein ag in lamina lucida of BMZ
–collagen activation results in degranulation of mast cells & chemotaxis of neuts &eos
-eosinphils release tissue destructive enzymes with resultant injury to the BMZ, loss of demoepidermal adherence & blister formation

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25
Q

Equine bullous pemphigoid is characterized clinically by:

A

-painful, crusted or ulcerated lesions of skin (face & axilla), mucous membrane and mucocutaneous junctions

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26
Q

Besides the skin, bullous pemphigoid lesions can occur where?

A

GI tract

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27
Q

in horses alopecia areata occurs in what areas?

A

–areas of nonpruritic alopecia
–most common affected i nhorses: mane, tail & face

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28
Q

What is seen in biopsy in cases of alopecia areata?

A

lymphocytic infiltrated surrounding the base of the hair follicle

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29
Q

In cases of alopecia areata does hair regrow?

A

most horses regrow hair, but this. may take up to 2 to 3 years

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30
Q

alopecia areata is often mistaken for what other differential?

A

ringworm

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31
Q

What is the definition of atopic dermatitis?

A

abnormal immunological response to environmental allergen like pollens, barn dust, and molds

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32
Q

What is the etiology of atopic dermatitis?

A

type I (immediate) hypersensitivity response mediated by IgE– allergen specific IgE

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33
Q

What are clinical signs of atopic dermatitis?

A

-pruritus
-alopecia
-erythema
-urticaria
-papules

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34
Q

Confirmation to formulate allergen-specific immunotherapy is based on what diagnostic tests?

A

-intradermal testing (IDT)
-serum allergy testing

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35
Q

with intradermal skin testing, what does a positive reaction mean?

A

the horse has antibodies ot the allergen that , on intradermal exposure, cause wheals to form
–>does not necessarily mean the horses clin signs are caused by reacting allergen

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36
Q

What is the benefit of performing intradermal skin testing?

A

-hyposensitization
– should be performed for 12 months to assess success

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37
Q

What are treatments recommended in atopic dermatitis?

A

-corticosteroid (dex, pred)
-antihistamine hydroxyzine pamoate: cetirizine, doxepin, diethylcarbamazine
-essential fatty acids

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38
Q

Urticaria is characterized by

A

transient focal swellings in the skin or mucous membranes (wheals– areas of dermal edema)

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39
Q

Wheals result from:

A

vasodilation and transudation of fluid from capillaries and small blood vessels

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40
Q

What is the immunologic mechanism that causes urticaria?

A

type I hypersensitivity (IgE)

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41
Q

Non-immune mediated urticaria may be induced by:

A

Type II: cytotoxic, involving antibody and complement

Type III: immune complex

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42
Q

Urticaria can be seen in what other diseases?

A

–pemphigus foliaceus
-dermatophytosis
-vasculitis

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43
Q

Milk allergy is urticaria usually seen in cows when?

A

cows during the drying off period

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44
Q

What is the pathogenesis of milk allergy?

A

-INC intramammary pressure presumably causes milk proteins to gain access to circulation
-induce type 1 hypersenstiivity

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45
Q

Milk allergy is seen in what cattle breeds?

A

Channel Island breeds

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46
Q

Diagnosis of Milk allergy is made how?

A

by observing an edematous swelling at site of intradermal injection of cows milk or milk protein casein diluted 1:1000

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47
Q

What are recommended treatments for cattle with milk allergy?

A

antihistamines

**culling d/t cows are likely to suffer recurrence of milk allergy

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48
Q

Erythema multiform is an immunologic skin reaction, what is seen on skin bopsy?

A

programmed keratinocyte cell death (apoptosis) in prominent change seen on biopsy

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49
Q

What are clinical lesions of erythema multiform?

A

macules, papules, urticarial lesions, vesicular bullous lesions
–target-like lesions
-scaling, crusting, erosions or ulcers
–variable pruritus and pain

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50
Q

What are DDx for erythema multiforme?

A

-urticaria
-amyloidosis
-other nodular papuler diseases
–> drug eruption should be considered

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51
Q

What are characteristic histologic lesions of erythema multiforme?

A

lichenoid pattern with keraitnocyte apoptosis

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52
Q

describe the histopathologic changes seen iwth vasculitis

A

inflammatory changes in the walls of blood vessels

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53
Q

in what cases are cutaneous vasculitis seen?

A

-photoaggravated dermatitis
-drug reactions
-purpura hemmorrhagica

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54
Q

What are cutaneous lesions of vasculitis?

A

crusts
scales
edema
purpura
necrosis
ulceration

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55
Q

what are the treatment recommendations for vasculitis?

A

-corticosteroids: dexamethasone
-reducing UV light exposure
-topical corticosteroids
-pentoxyifylline
–antibiotics– prone tos econdary bacterial infections

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56
Q

Drug eruptions can occur when:

A

–initial administration as a immunologically mediated hypersensitivity reactions
OR
–repeated exposure to a drug

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57
Q

What medications are seen to cause drug eruptions

A

-antibacterial agents (semisynthetic penicillins & sulfas)
-local anesthetics
-anticonvulsants
-antipyretics (esp phenylbutazone)

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58
Q

Drug eruptions can present as a wide variety of cutaneous manifestations including

A

-urticaria
-angioedema
-diffuse erythema
-papular rashes
-intense pruritus
-sharply demarcated ulcers secondary to vasculitidies
-vesicular & bullous eruptions
-photosensitization

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59
Q

When are drug eruptions typically seen?

A

–cutaneous lesions are typically seen 24 to 48 hours after drug administration

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60
Q

define irritant contact dermatitis

A

cutaneous reaction to an irritating concentration of an offending agent
**chemically damages skin

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61
Q

Define allergic contact dermatitis

A

represents cutaneous reaction in a sensitized animal to nonirritating concen of the offending agent
**delayed type hypersensitivity (type IV)

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62
Q

Treatment of contact dermatitis

A

-symptomatic treatment
-washing the affected region with water
-pentoxifylline

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63
Q

What is the causative agent of rain scald, lumpy wool, strawberry foot rot?

A

-gram-positive , non-acid-fast, branching filamentous, aerobic bacteria
**parallel rows of coccoid zoospores

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64
Q

What are the 3 conditions that must be present for Dermatophilus to manifest?

A

-carrier animal
-moisture
-skin abrasions

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65
Q

Mechanical transmission of dermatophilosis can be caused by:

A

-biting & non-biting flies, ticks and fomites

66
Q

Distribution of dermatophilosis is worldwide, however what areas are predisposed?

A

areas with increased rainfall

67
Q

Where are lesions caused by dermatophilus congolensis typically seen?

A

-dorsal surface of animal– rain scald
-lower extremities– dew poisoning
**body areas predisposed to infection are areas most susceptible to maceration & trauma

68
Q

Diagnosis of dermatophilosis is made by?

A

“railroad-track” cocci on impression smears
–bacterial culture or histpathology
–removal of thick crusts, remove hair–> paintbrush lesions

69
Q

What is the recommended treatment of rain scald?

A

-remove from wet environment
-removal painful crusts, wash with iodophors or lime sulfur
-antibiotics-TMS, oxytet

make sure to have proper removal of crust lesions, they are important in contagion

70
Q

define bacterial folliculitis (superficial pyoderma)

A

inflammation of hair follicles secondary to bacterial infection

71
Q

define furunculosis

A

follicular infection that breaks through the follicular wall (“boil”)

72
Q

define impetigo

A

bacterial infection that causes subcorneal pustules but does not involve hair follicles

73
Q

Bacterial folliculitis is typically caused by what bacteria?

A

-coagulase-positive staphylococcus species
–Staph aureus, Staph pseudointermedius

74
Q

What are C/S of folliculitis/furunculosis/impetigo

A

crusts
epidermal collarettes
encrusted papules

75
Q

what is an uncommon manifestation of staph spp infection of the skin resulting in nodular lesions?

A

-botryomycosis
***may req sx excision as well as long-term antibiotics

76
Q

What antibiotics are typically used for bacterial skin infections?

A

systemic:
-TMS
-enrofloxacin
-doxycycline
-ceftiofur sodium
-vancomycin
-aminoglycoside

local: mupirocin ointment 2%, SSD, tris EDTA/4% chlorhexidin

77
Q

Define cellulitis

A

severe deep, suppurative process in which a poorly defined area of infection tends to dissect through tissue planes

78
Q

What are the major pathogens for cause of cellulitis?

A

Staph aureus & Staph (pseud)intermedius

79
Q

What are C/S of cellulitis?

A

-acute swelling
-lameness
**involving one or more limbs
-inc rectal temperature
-INC HR
-laminitis
-poss. sequelae– osteomyelitis, bacteremia

80
Q

cellulitis treatment

A

broad-spectrum antibiotics (ie TMS)
NSAIDS
hydrotherapy
support wraps

81
Q

Causative agent of pigeon fever?

A

Corynebacterium pseudotuberculosis

82
Q

What is a diagnostic that can be performed to help diagnose equine corynebacterium pseudotuberculosis internal abscesses?

A

synergistic hemolysis inhibition test

83
Q

Does treatment of pigeon fever typically require antibiotics?

A

Not if abscesses are solitary, not causing pain or fever

84
Q

Digital dermatitis of cattle is a major cause of lameness in cattle, stages of lesions

A

1st stage: small (~1-2 cm) focal lesions reddened, circumscribed area (strawberry heel warts) that are extremely painful, exudative

2nd stage: larger (2-6cm) ulcerations lesions

3rd stage: healing lesions, rough, encrusted surface, gray in color

4th stage: chronic proliferative lesions, hyperkeratosis, black papilliform projections

5th stage: healing of lesion

85
Q

Washed surfaces of lesions with Digital Dermatitis appearance

A

-extremely painful
-red & granular
-white-yellow, gray, brown, black papillary areas with red, granular areas
-lesions bleed easily

86
Q

What are differentials for individuals with Digital dermatitis?

A

interdigital necrobacillosis (foot rot; foul in the foot; interdigital phlegmon)
interdigital hyperplasia (corns, interdigital fibroma)
interdigital dermatitis
traumatic injury with granulation tissue

87
Q

What are differentials for herd problems of lameness localized to the digit?

A

-digital dermatitis
-interdigital dermatitis
-laminitis
-excessive sole wear from caustic or abrasive flooring
-improper or no hoof trimming

88
Q

Which herds of cattle are predisposed to developing digital dermatitis?

A

freestall herds– more commonly affected than stanchion (tie stall) housed cattle or pastured cattle
**dairy cattle

89
Q

Which bacteria is most commonly implicated in digital dermatitis?

A

Treponema spp spirochetes

90
Q

What are histopathologic criteria to establish a diagnosis of digital dermatitis

A

-circumscribed plaque of eroded acantholytic epidermis attended by parakeratotic papilllomatous proliferation profusely colonized by spirochete-dominant bacterial flora
-loss of stratum granulosum
-invasion of stratum spinosum by spirochetes
-infiltration of neutrophils, plasma cells, lymphocytes, eosinophils into the dermis

91
Q

treatment of digital dermatitis

A

-application of topical antibiotics: oxytetracycline, lincomycin
-systemic antibiotics– PPG, ceftiofur, req milk withholding
-foot baths: 5% formalin, oxytetracycline, lincomycin, copper sulfate, zinc sulfate, sodium hydroxide

91
Q

What are preventative measures for digital dermatitis?

A

-improve environmental hygiene
-providing dry, comfortable bedding
-improving ventilation
-sanitize –foot trimming equipment, mobile tilt tables, & livestock trailers

92
Q

Interdigital dermatitis is a condition defined as

A

condition of acute or chronic inflammation confined to the epidermis of the interdigital skin

93
Q

interdigital dermatitis lesions

A

small circular ulcers in the interdigital epithelium
severe cases: characterized by ulceration, necrosis & underrunning of the hoof horn
-varying degrees of lameness
-moist, white to gray serous exudate
-skin irritation results in hyeprtrophy
-inc growth rate of the axial hoof wall along excessive horn production along axial wall & sole

94
Q

Which digits are most commonly affected with interdigital dermatitis: cattle in tied systems

A

hind digits are most commonly affected

95
Q

How does interdigital dermatitis differ from interdigital necrobacillosis (foot rot)

A

infection extends into the dermis, leading to fissure formation, infection of deeper structure if left untreated, & cellulitis if the pastern & fetlock regions

96
Q

Which bacteria commonly causes the virulent foot rot (VRF) in sheep?

A

D. nodosus– gram-neg rod-shaped anaeorbic bacterium

97
Q

in sheep interdigital necrobacillosis is characterized by:

A

inflammation of interdigital skin, resulting in lameness and loss of body condition
–skin appears pink, most, sensitive to touch
–characterized by underrunning of hoof horn leading to separation of hoof from underlying soft tissue

98
Q

The occurrence of interdigital dermatitis is influenced by what?

A

local climatic conditions– wet pasture required for transmission

99
Q

What is the recommended time to rest pastures after interdigital dermatitis the outbreak?

A

-VFR (virulent foot rot) in sheep– 14 days
-D nodosus cannot survive off host for more than 7 days

100
Q

Papillomas are associated with what virus?

A

bovine papillomavirus (BPV)

101
Q

Warts in horses are commonly seen on what locations?

A

-on the face– more common

102
Q

Congenital warts in horses are termed?

A

hamartomatous lesions (epidermal nevus)
**not associated with a virus

103
Q

Pseudocowpox is caused by

A

bovine herpesvirus-2 (BHV-2)

104
Q

Pseudocowpox lesions can predispose to

A

**mastitis

105
Q

Diagnosis of pseudocowpox

A

-isolation of the virus– BHV-2 serum neutralization tester or histologic demonstration of herpesvirus particles

106
Q

Dermatophytosis (ring worm) is caused by

A

microsporum and trichophyton spp
–refers to infections of the keratinized tissues of the skin

107
Q

Describe ringworm lesions

A

lesions are circular, superficial or deep, thick crusts, diffuse moth-eaten appearance with desquamation & alopecia, small crust over follicle, hair is lost
– usually of face, axillary/girth area may spread over the trunk, rump, neck, head & limbs

108
Q

What is the most common and reliable method of diagnosing dermatophytosis?

A

fungal culture
**direct microscopic exam

109
Q

Dermatophytosis treatment

A

-50% captan for tack
-lime sulfur
-bleach (1:10)
-shampoos– containing miconazole, ketoconazole, and/or 3-4 % chlorhexidine
-20% sodium iodide (NaI)

110
Q

Effective control of ringworm in cattle has been achieved in regions implementing what strategies?

A

-systemic vaccination

111
Q

Sporotrichosis causative agent

A

– yeast Sporothrix schenckii– pathogenic b/c can switch from yeast to mycelial phase (branching, septate hyphae)
**zoonotic potential

112
Q

what is the cause of equine epizootic lymphangitis in East Africa

A

Histoplasma capsulatum vaar farcimonsum (farcy)

113
Q

Clinical manifestations of lice are most apparent during what season?

A

winter

114
Q

What are recommended treatment for lice?

A

ivermectin– sucking lice
-topical insecticide– pyremthroids, permethrins, selenium sulfide, imidacloprid, phoxim, ifpronil

115
Q

Tombiculidiasis is caused by larval stages of mites (harvest mites, chiggers), what are the most common species

A

Eutrombicula alfreddugesi (N. america)

116
Q

What are the C/S of trombiculidiasis?

A

crusts & papules– on face, neck and extremities
-variable pruritus

117
Q

Describe the appearance of mites that cause trombiculidiasis

A

-red-orange larvae in the center of a papule
– 6 legged larvae with round body

118
Q

Where do psoroptes mites live?

A

-on surface of epidermis

119
Q

horses with psoroptic mange have what lesions?

A

-pruritus
-papules, crusts, alopecia seen on the base of the mane, tail, ears & intermandibular rea

120
Q

Describe appearance of psoroptic mites

A

-round bodies, long segemented pedicles

121
Q

What is the treatment of psoroptic mange?

A

topical insecticides– deltamethrin, coumaphos, diazinon, malathion, toxaphene & lime sulfur
**treat contaminated environment

122
Q

Which breed of horses are predisposed to the development of chorioptic mange?

A

draft horses

123
Q

in horses chorioptic mange can be treated with what?

A

-lime sulfur
-fipronil– applied once weekly for at least 1 month

124
Q

Which forms of mange are reportable in the US?

A

psroptic mange
chorioptic range

125
Q

Demodectic mites usually live where?

A

in hair follicles and sebaceous and sweat glands
**host specific

126
Q

Demodex caballi is a normal inhabitant of:

A

-pilosebaceous apparatus of the eyelids and muzzle and may found in skin scrapings of these areas on horses in the absence of skin lesions

127
Q

What are the 3 most common species responsible for culicoides hypersensitivity?

A
  1. Culicoides varipennis
  2. Culicoides obsoletus
  3. Culicoides nubeculosus
128
Q

which breed of horse is predisposed to the culicoides sensitivity?

A

Icelandic horses

129
Q

Culicoides hypersensitivity therapy is aimed at insect control, especially what:

A
  1. stabling horses at sunrise and sunset, peak culicoides feeding hours
  2. ultrafine setting or screens placed in windows (0 squares to the square inch)
  3. fly control, especially keeping horses away from standing water and using permethrin repellants, usually 2% permethrin sprays. Freq spray, must be applied mroe often than label recommendations. have had success with nonpesticide herbal spray, or roll-on
  4. Overhead or stall fans (drafts interfere with insects flight)
  5. “dresses” that physically obstruct the insects from reaching the skin
  6. hyposensitization is controversial; success may vary with hte presence of an adjuvant or the actual antigen used
  7. oral prenisolone to manage pruritus
130
Q

Ventral midline dermatitis in horses is caused by what ectoparasites

A

-onchocerca cervicalis infestation
-black flies (Simuliidae)

131
Q

Screwworm infestation has been eliminated from the United States, through which methods?

A

release of sterile males– d/t mating tendency of female fly
**reportable disease

132
Q

What are management strategies to prevent blow fly strike?

A

**practices that decrease the incidence of wound or skin irritations
- sheep are clipped below the tail and between the hind limbs (“crutched”)
-castration, shearing, docking & lambing avoided during the summer season

133
Q

what is a common cause of filarial dermatitis?

A

cutaenous conchocerciasis

134
Q

the incidence of cutaneous onchocerciasis has been decreased due to

A

ivermectin for routine deworming

135
Q

Where are O. cervicalis is typically found where?

A

coiled in the funicular part of the ligamentum nchae, where they produce calcified nodules

136
Q

What are preferential areas of microfilarial localization?

A

-ventral midline
-lower eyelid
-lateral limbus of the eye

137
Q

cutaneous onchocerciasis is transmitted by what organism?

A

Culicoides (acts as an intermediate host)

138
Q

What are the differentials for cutaneous onchocerciasis?

A
  • H. irritans
    -hypersensitivity reaction to culicoides
    -dermatophytosis
    -infestation with mange mites
139
Q

What is the treatment for cutaneous onchocerciasis?

A

ivermectin or moxidectin

140
Q

Cutaneous stephanofilariasis is seen what region of US?

A

-western & southwestern regions of US

141
Q

Where do stephanofilaria inhabit what area of the skin?

A

epidermis

142
Q

Stephanofilaria is transmitted by what organism

A

female horn fly (H. irritans)

143
Q

What are two species of Hypoderma that parasitize cattle and cause warbles?

A

Hypoderma bovis
Hypoderma lineatum

144
Q

Hypoderma cysts develop around the what larvae?

A

L1 larvae–> L3 larvae (grubs) that emerge through breathing pore, fall to the ground & pupate

145
Q

How long does it take for hypoderma life cycle to complete?

A

1 year

146
Q

Economical loss of hypoderma (warbles) infestation in cattle is due to?

A

-fly worry
-gadding– stampede behavior
**stampede injury and decreased feeding & milk production

147
Q

What are differentials for hypoderma warbles in horses?

A

-eosinophilic granuloma (nodualr collagenolytic granuloma, nodular necrobiosis)
-mastocytoma
-sterile nodular paniculitis
-amyloidosis

148
Q

Why does care need to be taken to remove hypoderma larvae in their entirety?

A

– because breaking the larvae & rupturing the cyst during removal can result in severe systemic reaction

149
Q

What are medications to administer to prevent migrating hypoderma larvae?

A

**systemic insecticides only means of eliminating the migrating larvae
-organophosphates
-marcocyclic lactones

150
Q

With systemic medications in the treatment of hypoderma (warbles), what is the recommended timing?

A

–not to administer systemic insectivides than 8 to 12 weeks before anticipated first appearance of grubs along the back
–northern US– not recommended from Oct 1st to March 1st; this is when H. bovis larvae are in the esophagus

151
Q

Sheep keds is caused by what organism?

A

Melophagus ovinus
–wingless fly approximately 6 to 7 mm in diameter with a ticklike appearance

152
Q

The sheep ked Melophagus ovinus has been shown to be a vector for what organisms?

A

Rickettsia raoultii
Rickettsia slovaca

153
Q

Melophagus ovinus life cycle occurs where in relation to the host?

A

– entire life cycle is spent on the host

154
Q

Infestation of sheep keds is more common in what months?

A

winter months

155
Q

Sheep keds (melophagus ovinus) infestation results in economic loss form what:

A

-dec dressed carcass weight of lambs
-reduced clean dry weight of fleece, wool staining
-reduced value of sheep skins b/c of nodular defects

156
Q

Treatment of sheep keds (melophagus ovinus)

A

– shearing all sheep in affected flock
–two topical applicaitons of malathion, diazinon, or coumpahos 14 to 21 days intervals to kill emerging adults

157
Q

Cutaneous habronemiasis (equine summer sore) is caused by larvae of what flies?

A

-harbonema microstoma
-Habronema muscae
-Draschia megastoma

158
Q

What are common areas of cutaneous habronemiasis

A

–natural areas of body moisture: medial canthus of eye, male genitalia, nictitating membrane (“third eyelid”) & distal extremities

159
Q

Describe the life cycle of cutaneous habronemiasis?

A

-H. muscae and De. megastoma develop in the house fly, M domestica and H. microstoma
- L3 larvae are deposited around the horses mouth and swallowed to pass to the stomach where they mature as adults

160
Q

Diagnosis of cutaneous habronemiasis is confirmed by:

A

– confirmed by biopsy– presence of calcified concretions (sulfur granules)

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