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Veterinary Dermatology > Equine Congenital Miscellanous Ch 14 and 15 > Flashcards

Equine Congenital Miscellanous Ch 14 and 15 Flashcards

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1
Q

Stains for elastin?

A

Acid-orcein giemsa, Verhoff and van Gieson

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2
Q

Treatment for chronic progressive lymphedema

A

No curative tx exists, tx is palliative (aggressive tx/control of bacterial infection/mite infestation), exercise, massage, compressive bandaging, clip feathering and keep clean

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3
Q

CS neonatal ulcerative dermatitis, thrombocytopenia, neutropenia

A

Ulcerative and crusting skin disease in neonatal foals - along muzzle, periocular, perineal, axillary, inguinal regions; neck/trunk can be affected commonly
Oral lingual ulcers, petechiae, ecchymoses typically seen
Bleeding tendency (eg hematoma)
Otherwise healthy or mild to moderately lethargic

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4
Q

Which types of hypotrichosis are fatal?

A

Lethal hypotrichosis - autosomal recessive
Hypotrichosis and partial anodontia - sex linked recessive in males
Inherited epidermal dysplasia (baldy calf syndrome) - autosomal recessive
Congenital goiter and hypothyroidism

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5
Q

hypotrichosis that leads to dysplastic teeth?

A

ectodermal dysplasia

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6
Q

define follicular dysplasia

A

clinically variable degrees of hair loss and histopath shows dysplasia of hair follicles/shafts

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7
Q

What are the 4 types of follicular dysplasia in cows?

A

Semi-hairless: Herefords, Polled Herefords, Ayrshires; autosomal recessive, thin coat of short, fine, curly hairs at birth. Later a sparse coat of coarse, wiry hairs which is thickest on the legs
Viable hypotrichosis: Guernseys, Jerseys, Holsteins, Ayrshires; autosomal recessive, hair only on legs, tail, eyelids, and pinnae at birth
Color related follicular dysplasia: black and white or tan and white Holsteins; normal or mildly affected at birth, then hair loss and scaling only in black or tan coated areas
Follicular dysplasia of black cattle: black Angus, black Brangus-cross; generalized hair loss begins at 3-5 years old

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8
Q

what hairless disorder seen with wild temperament (bovine)

A

semihairlessness - Herefords, Polled Herefords

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9
Q

semihairlessness mode of inheritance

A

simple autosomal recessive

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10
Q

what are synonyms with cutaneous asthenia

A

dermatosparaxis, cutis hyperelastica, ehlers-danlos

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11
Q

Aside from fragile skin what is seen in these cases?

A

Joint laxity
Skin hyperextensibility
Delayed wound healing
Cutaneous edema esp of eyelids, dewlap, distal limbs

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12
Q

What is the most common type of EB and what is the inheritance?

A

Junctional EB
Autosomal recessive inheritance

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13
Q

What are the clinical features of hereditary zinc deficiency?

A

Normal at birth but develop diarrhea by 3-8 weeks of age
Lethargy, depression, poor appetite, increased lacrimation and nasal discharge
Erythema, scaling, crusting, and alopecia begins on face
Spreads to neck, flanks, perineum, ventrum, distal limbs, and mucocutaneous
Dark-coated areas often fade, especially periocular and results in “spectacles” appearance

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14
Q

What are the two forms of ichthyosis?
Forms:

A

1) severe form “ichthyosis fetalis”
Simple autosomal recessive trait
Norwegian red polls, Friesians, and Brown Swiss
2) milder form “ichthyosis congenita”

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15
Q

What are the clinical signs of severe form?

A

Dead at birth or die within a few hours or days
Entire skin is alopecic and covered with thick scales and hyperkeratosis, divided into plates by fissures
Skin around lips, eyelids, and other body orifices tend to be everted

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16
Q

ocular changes with milder form - ichthyosis congenita

A

cataracts

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17
Q

What is porphyria IMPORTANT

A

KNOW EVERYTHING EVER
Abnormal accumulation of various photodynamic porphyrins in the blood and body tissues as a result of aberrant porphyrin synthesis

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18
Q

What is the classical clinical sign of porphyria?

A

Photodermatitis

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19
Q

know porphyria pathway

A

understand where in the pathway is the defect and why that matters - decreased levels uropor

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20
Q

Name two types of porphyria

A

erythropoietic porphyria and protporphyria

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21
Q

what is the defect in erythropoietic porphyria?

A

Decreased levels of uroporphyrinogen III cosynthetase result in increased levels of uroporphyrin I and coproporphyrin I in blood and tissues
Autosomal recessive trait
Clinically, retarded growth, anemia, discolored teeth and urine, and photodermatitis are seen

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22
Q

which tool can be used to distinguish the two types of porphyria?

A

On Wood’s light examination, teeth and urine fluoresce a bright orange or red with erythropoietic porphyria

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23
Q

coat marker for cardiomyopathy in cows

A

Curly (“wooly”) coat is a phenotypic marker for cardiomyopathy in Herefords and Polled Herefords

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24
Q

What breed is affected by sticky coat syndrome?

A

Golden Guernseys
Kids born with sticky and matted hair coats that do not dry normally
Remains in older goats

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25
Q

What breed has a viable hypotrichosis?

A

Polled Drosets
Are hypotrichotic at birth, especially on the face and legs

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26
Q

What defects are seen in New Zealand Romney lambs

A

Cutaneous asthenia (dematosparaxis, cutis hyperelastica, and Ehlers-Danlos syndrome), congenital collagen dysplasia characterized by loose, hyperextensible, abnormally fragile skin
Autosomal dominant

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27
Q

What is the most common form of EB in sheep?

A

Most reported cases of ovine epidermolysis bullosa resemble dystrophic epidermolysis bullosa
Thought to be autosomal recessive

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28
Q

What is the collagen abnormality in EB for sheep?

A

Deficient collagen VII (anchoring fibrils)

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29
Q

What are the clinical signs of aplasia cutis?

A

Piglets are born with one round/elliptical ulcer, 3-8cm in diameter, esp over the back, loin, or limb.
Occasionally reported: hydroureter, hydronephrosis, skull/ear defects
Occurs in individual piglets or with familial incidence in litters

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30
Q

What breed/inheritance pattern of dermatosis vegetans?

A

Hereditary; often congenital
Simple autosomal recessive mode of inheritance in Landrace pigs with no sex predilection

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31
Q

dermatosis vegetans clinical lesion

A

skin/hoof lesions are present at birth; but occasionally develop at 2-3 wks of age
Symmetric, erythematous, maculopapular dermatitis on ventral abdomen, medial thighs → spread to entire trunk
Lesions expand peripherally, coalesce, and develop into dry, brown/black papillomatous, crusted plaques
Nonpruritic, nonpainful
Coronary bands become erythematous, edematous, then covered with yellow/brown substance
Hooves become irregularly ridged and dysplastic
In piglets: gradually deteriorate, have stunted growth; die at 5-6 wks old
Respiratory signs happen → death (pneumonia, bronchopneumonia)
Piglets can survive but remain stunted

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32
Q

what are tassals?

A

Wattles is another name for this condition
Presumed autosomal dominant; no breed/sex predilection
Congenital cylindrical, teat-like structures, 5-7 cm long, hanging from ventral mandibular region

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33
Q

What is aural hematoma and chondritis?

A

Hereditary condition causing multiple small, fluid-filled, flat plaques on the lateral aspects of the pinnae that heal with scarring & deformation

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34
Q

What are the classic histopathology findings of eosinophilic granulomas in horses? Be able to ID on histopath (Fig 15.10-15.15)

A

nodular -to-diffuse areas of eosinophilic, granulomatous inflammation of the dermis, and often the panniculus
Multifocal areas of collagen flame figures are a characteristic finding, and small foci of eosinophilic folliculitis or furunculosis may be seen
Lymphoid nodules may be prominent
Older lesions can have marked dystrophic mineralization

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35
Q

list five dfdx for nodules in horses

A

bacterial (staph coag pos, corynebact pseudotuberculosis, actino, nocardiosis, abscess (esp c pseudotuberculosis), tuberculosis, glanders; fungal (eumycotic mycetoma, phaeohyphomycosis, sporotrichosis, zygomycosis, rhinsporidiosis), parasitic (hypodermiasis, habronemiasis (fly), parafilariasis), immunologic (urticaria, EM, amyloidosis), misc_ eosinophilic granuloma, axillary nodular necrosis, unilateral papular dermatosis -TABLE 15-1 Scott equine dermatitis

36
Q

typical lesions axillary nodular necrosis?

A

3 or less (occasionally up to 10) nodules, 1-10cm in diameter, typically present in the girth area (behind the elbow)
Lesions may be seen caudal to the shoulder and on the proximal, medial aspect of the forearm
Lesions are unilateral, rounded, well-circumscribed, and firm, and the overlying skin and hair coat appear normal
Some lesions may develop crateriform ulcers
Multiple lesions may be arranged in chains and may be connected by a thin cord of palpable tissue (diseased artery?)

37
Q

Sterile Eosinophilic Folliculitis and Furunculosis has been seen as a reaction pattern associated with what disease in the horse?

A

This reaction pattern has been seen in horses with atopic dermatitis, insect-bite hypersensitivity, food allergy, and onchocerciasis

38
Q

Histopath findings of SEFF?

A

Infiltrative-to-necrotizing eosinophilic mural folliculitis and furunculosis and occasionally focal collagen flame figures
Focal areas of eosinophilic mural folliculitis, luminal folliculitis, and furunculosis may be seen in biopsy specimen from horses with insect-bite hypersensitivity, atopic dermatitis, and food allergy in the corresponding clinical lesions

39
Q

What are the clinical characterizations of multisystemic eosinophilic epitheliotropic disease?

A

Characterized by exfoliative dermatitis, ulcerative stomatitis, wasting, and infiltration of epithelial tissues by eosinophils, lymphocytes, and macrophages

40
Q

hat are the dermatologic signs associated with MEE

A

Dermatitis usually begins insidiously with scaling, crusting, oozing, alopecia, and fissures on the coronets and/or the face
Oral ulceration is often an early finding
Some initially develop well-demarcated ulcers on the coronary bands, muzzle, and mucocutaneous junctions
Vesicles and bullae are rarely seen in these areas, and urticarial eruptions may be seen in the early phase of disease
Dermatosis then develops into a generalized exfoliative dermatitis with scaling, crusting, easy epilation, alopecia, and focal areas of ulceration
Pruritus is variable, and peripheral lymph nodes may be enlarged

41
Q

What are the treatment options of multisystemic eosinophilic epitheliotrophic disease

A

Characterized by exfoliative dermatitis, ulcerative stomatitis, wasting, and infiltration of epithelial tissues by eosinophils, lymphocytes, and macrophages

42
Q

What are the dermatologic signs associated with MEE

A

Dermatitis usually begins insidiously with scaling, crusting, oozing, alopecia, and fissures on the coronets and/or the face
Oral ulceration is often an early finding
Some initially develop well-demarcated ulcers on the coronary bands, muzzle, and mucocutaneous junctions
Vesicles and bullae are rarely seen in these areas, and urticarial eruptions may be seen in the early phase of disease
Dermatosis then develops into a generalized exfoliative dermatitis with scaling, crusting, easy epilation, alopecia, and focal areas of ulceration
Pruritus is variable, and peripheral lymph nodes may be enlarged

43
Q

What are the treatment options of MEE

A

Large doses of glucocorticoids can be helpful early in the disease
Often progressive and results in euthanasia

44
Q

What are the clinical features of linear alopecia

A

Circular areas of alopecia in a linear vertically oriented configuration
On the neck, shoulder, and/or lateral thorax
There can be mild surface scaling and crusting but are otherwise nonpainful and nonpruritic

45
Q

What are the histopathology findings of linear alopecia?

A

Early infiltrative lymphocytic mural folliculitis with variable outer root sheath edema
Later on in dz there is a lymphohistiocytic mural folliculitis with epithelioid cells and multinucleated giant cells
Apoptotic keratinocytes and eosinophils can be found in the wall of follicles

46
Q

What are the breakdown products of a lipocyte

A

Glycerol and fatty acids
Fatty acids are potent inflammatory agents

47
Q

What breed appears to have a high incidence of panniculitis?

A

Shetland ponies

48
Q

What stain is commonly used to detect lipid droplets?

A

Sudan stain (reveals intra and extracellular lipid droplets)

49
Q

What is Ceroid

A

A wax-like light brown to yellow homogenous material found in lipocytes macrophages, giant cells, and connective tissue
Similar to lipofuscin

50
Q

What are the clinical signs associated with sarcoidosis?

A

Insidious onset
Starts with scaling, crusting, and alopecia on the face, trunk, and/or legs and progresses to multifocal or generalized exfoliative dermatitis
Variable pruritus and sometimes painful
Occasional horses will develop isolated hyperkeratotic, crusted, alopecic plaques on the legs
Peripheral LNs may be enlarged
Most horses go on to develop a wasting syndrome characterized by exercise intolerance, poor appetite, weight loss, edema, and persistent fever
Sometimes lung involvement and GI involvement

51
Q

What infectious disease can mimic sarcoidosis?

A

Infection w/ Mycobacterium spp. (report was regarding M. intracellulare serotype 8)

52
Q

What are the histopathologic findings ofsarcoidosis

A

Nodular to diffuse sarcoidal granulomatous dermatitis that may affect all portions of the dermis
Multinucleated histiocytic giant cells
Small #s of lymphocytes, plasma cells, & neuts
Not mentioned in the textbook but from our histo learning - you will also see those spikey rete pegs

53
Q

Mgmt options of sarcoidosis?

A

May spontaneously resolve
If only skin disease, may achieve remission with glucocorticoids alone & be able to eventually stop therapies
If relapses, may require long-term glucocorticoids - effective if caught early before onset of wasting syndrome
Prednisolone or Prednisone 2-4mg/kg PO SID
Dexamethasone 0.2-0.4mg/kg PO SID
Omega 3/6 FA as adjunctive
Pentoxifylline as adjunctive

54
Q

What are the major and minor criteria for Sweets syndrome in humans? basics of how graded

A

Major (must have both)
Abrupt onset of painful erythematous plaques
Histopath evidence of dense neutrophilic infiltration w/o leukocytoclastic vasculitis
Minor (must have at least 2):
Pyrexia
Associated w/ underlying hematologic or visceral malignancy, inflammatory dz, or pregnancy, or preceded by respiratory or GI infection, vaccination, or drug administration
Excellent response to systemic glucocorticoids or potassium iodide
Abnormal lab values (3 of 4): increased sedimentation rate, positive C-reactive protein, leukocytosis, neutrophilia

55
Q

What environments precipitate anhidrosis?

A

Humid environment
Increased prevalence in southern & central FL
Increased prevalence in show & riding instruction operations vs ranches

56
Q

How much sweat can a horse lose per day?

A

45L

57
Q

What is the proposed etiology of anhidrosis

A

Due to a gradual failure of the glandular secretory cell processes, initiated by desensitization and subsequent downregulation of the cell receptors d/t continued epinephrine-driven hyperactivity stimulated by climatic stress

58
Q

What is aquaporin-5?

A

A member of a family of integral membrane water channel proteins, located in the apical luminal membrane of the equine sweat gland. These channels have been implicated as routes of the rapid osmotically driven water passage across the plasma membrane of many cell types. The level of apical AQP-5 expression is diminished with anhidrosis.

59
Q

What are the acute signs of anhidrosis?

A

Labored breathing, flared nostrils, fever, partial/complete lack of sweating
Prominent sign of impending anhidrosis is tachypnea
Not usually tachycardic.
Often drink less water
Collapse, death

60
Q

What are the chronic disease signs OF ANHIDROSIS

A

Dry hair coat, excessive scale, and partial alopecia face/neck may be seen
Residual areas of sweating under jaw, mane, saddle, base of ears, axillae, groin, perineum
Skin is hot and dry
Pruritus, pu/pd, poor appetite, loss of body condition may occur
Chronically: inelastic, scaly skin, hair coat: dry, rough, hair loss

61
Q

How do you test for anhidrosis?

A

History, PE, and response to intradermal injection of epinephrine:
evaluate sweat response to intradermal serial inj of dilutions of epi or salbutamol/albuterol (beta adrenergic agonist) and terbutaline – measure how much they sweat at each dilution. Note: KNOW HOW THEY TEST/MEASURE THE SERIAL DILUTIONS.
Epi is measured at 1:1000, 1:10,000, and 1:1,000,000 with 0.5 ml epi intradermally
Anhidrotic horses may only respond to epi 1:1000 dilution after 5+ hrs
quantitative: same test but uses absorbent pads to capture sweat over each intradermal injection
lab findings: hyponatremia, hypochloremia +/- hyperkalemia; hypochloremia alone; high urinary fractional excretion of chloride may be supportive
histo may be supportive

62
Q

Histopath findings of anhidrosis and EM findings of anhidrosis

A

Histo: thinning of sweat gland secretory epithelial cells, superficial blockages of some glandular ducts. Dilated intercellular spaces, cells lose secretory vesicles. Flattened secretory epithelium, fewer cytoplasmic vesicles.
Ultrastructural: flattening, degranulation, and degeneration of secretory cells.

63
Q

Treatment options for anhidrosis:

A

-environmental mgmt. is very important: remove severe climatic stress. Sweating ability can be restored if p moved to cooler drier climate away from hot humidity
-reduce work
-place in air conditioning, low humidity stalls
-supplements:
- Vit E? helps restore sweating and coat appearance -better in recovery
- iodinated casein
- feed supplements with amino acids
- Injections of adrenocorticotropic hormone
-diuretics to assist with water retention
-electrolyte supplementation to counteract electrolyte loss – saline via orogastric tube

64
Q

List at least three causes of generalized hyperhidrosis?

A

High ambient temp
Vigorous exercise
Severe pain
Drugs (epi, acetylcholine, promazine, colloidal silver, prostaglandin F2alpha)
PPID
pheochromocytoma

65
Q

List at least three causes of localized hyperhidrosis?

A

Local injections of epi
Dourine
Horner’s syndrome (secondary to hypothalamic, brain stem, or spinal cord lesions; guttural pouch infections; careless intravenous injections)

66
Q

What is coronitis?

A

Inflammation of the coronary bands
See flakes, crusts, exudate, or ulceration of the area
Rarely: vesicles, pustules, necrosis
“Winging out” (uplifting of hair at coronary band) is an early sign
Chronic disease may lead to hoof wall defects

67
Q

What is coronary band dysplasia?

A

Coronary bands are symmetrically diseased
Scaly, hyperkeratotic, crusty, variably erythematous lesions
Causes not discomfort, but chronic coronary band disease can lead to hoof wall deformities
Ergots and chestnuts may also be affected

68
Q

Be able to list at least 5 differentials for coronary band disease:

A

Pemphigus foliaceus
Vasculitis
Photodermatitis
Sarcoidosis
Epidermolysis bullosa
Erythema multiforme

69
Q

Define stereotypic behaviors:

A

Stylized repetitive apparently functionless motor responses or sequences
Endogenous opioids may be involved in the propagation of stereotypes

70
Q

What is head shaking syndrome?

A

Abnormal condition where the horse flicks, nods, or shakes its head in the absence of obvious extraneous stimuli, and with such frequency and violence that the horse becomes difficult or dangerous to use or appears distressed
Head shaking is not a diagnosis, but a clinical syndrome with numerous causes

71
Q

What are some of the causes of head shaking?

A

Diseases of nasal cavity - allergic or vasomotor rhinitis, sinusitis, foreign body
Diseases of the ear - trombiculiasis, ear mites, foreign body
Diseases of the eye - melanotic iris cyst, uveal or retinal lesion
Diseases of the nervous system - encephalopathy, cervical spinal injury, trigeminal neuralgia
Diseases of the skeletal system - maxillary osteoma, temporohyoid osteoarthropathy, premaxillary bone cyst
Diseases of the soft tissues of the head - parotid gland melanoma, guttural pouch mycosis, buccal lesions
Miscellaneous - stereotypic behavior, photic optic-trigeminal nerve summation, idiopathic

72
Q

What other behaviors are associated with head shaking?

A

Variable frequencies and intensities of sneezing, snorting, nasal discharge, and rubbing the muzzle
Clamping the nostrils, wiggling or flipping the upper lip, and engaging in protective behaviors to avoid contact between human handlers and the head

73
Q

What is anagen defluxion?

A

AKA anagen effluvium
Temporary growth defects in the hair shaft caused by various severe stressors (infectious disease, metabolic diseases, high fevers), most commonly affects calves
Hair loss occurs suddenly (within 7-10 days of the stressor)
Hair loss may be regional, multifocal, or fairly generalized and is bilaterally symmetrical
Skin in affected areas appears normal unless secondarily inflamed by trauma, contact dermatitis, or photodermatitis. Pruritus and pain are absent

74
Q

What are clinical lesions of psoriasiform dermatitis?

A

More or less symmetrical lesions begin on the face and pinnae; commonly involve the neck, distal legs, and ventrum
Early erythema and scaling progress to crusting, thickened skin, and variable degrees of hair loss
Neither pruritic or painful; animals otherwise healthy
Waxing/waning can be seen, but does not fully resolve

75
Q

What are some of the other names for anagen defluxion in sheep?

A

Anagen effluvium
Wool break
Wool slip

76
Q

What breeds are commonly affected by juvenile pustular psoriasiform dermatitis?

A

Landrace and other white breeds

77
Q

Clinical lesions of JPPD juvenile psoriaform lichenoid dermatitis:

A

Symmetric distribution of erythematous macules and papules starting on the ventral abdomen and medial thighs
Often extends to involve most of ventrum and sometimes lateral trunk
Lesions enlarge and develop central craters and become covered in bran-like scale
Can sometimes develop into annular, arciform, serpiginous, and polycyclic shapes

78
Q

What disease causes annular areas of erythema in sows?

A

Recurrent dermatosis of sows
Occurs in farrowing house, disappears after leaving farrowing house

79
Q

What is idiopathic neutrophilic necrolytic hyperkeratotic dermatosis?

A

Rare disease found worldwide that causes waxing & waning erythema, crusts & vesiculopustules on the axillae, groin, ventral abdomen, face, distal extremities, & perineum

80
Q

What is the normal shedding pattern of llamas?

A

Shed every 1-2 years beginning in the spring

81
Q

What is aplasia cutis congenita?

A

Rare and perhaps congenital
Developmental failure to form certain layers of skin and fusion of skin
Dermis, epidermis, and fat may all be missing, or single layers may be absent

82
Q

What are the three types of Epidermolysis bullosa?

A

1) Epidermolysis bullosa simplex
Blister cleavage occurs within stratum basale of epidermis
2) Junctional epidermolysis bullosa
Blister cleavage occurs within the lamina lucida of BMZ
3) dystrophic epidermolysis bullosa
Blister cleavage occurs within sublamina densa area of BMZ

83
Q

is the most common form in horses?

A

Junctional form

84
Q

What breed is overrepresented in JEB in horses?

A

Draft horses (belgians, trait breton, trait comtois, american saddlebreds)

85
Q

When are lesions most commonly noticed in JEB in horses

A

Foals may be born with lesions or develop lesions within the
first 2 days of life

86
Q

clinical lesions of JEB in horses

A

Primary lesions: vesicles & bullae - these are transient & rupture easily therefore are usually absent when foals are initially examined
Will see well-demarcated ulcers w/ peripheral epidermal & mucosal collarettes, & pronounced crusting
Hoof wall separation progresses to complete sloughing
Enamel hypoplasia
Depression, cachexia, often die of septicemia
Location: coronets, mucocutaneous junctions of lips/anus/vulva/eyelids/nostrils, bony prominences, oral cavity, +/- cornea, esophagus

Veterinary Dermatology (4 decks)

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