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101 Cards in this Set

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what clinical signs would typify a dermatophyte lesion in a horse? what areas of the body are most likely to be affected initially?
commonly start in areas of abrasion. More common in winter months. more common in dirty damp, poorly ventilated enviroment
focal areas of alopeica with variable scaling and crusting.
variable pruritus
what is the best way to definitively diagnose a dermatophyte infection in the horse?
fungal culture, addition of nicacin to DTM
widespread dermatophyte infections are often treated initially with a shampoo to remove debris etc.. followed by a residual solution that is generally sprayed and/or brushed and/or dabbed on and left to dry. Give an example of a shompoo/residual germicide combination that you would use in your practice to routinely treat dermatophytosis.
shampoo:
miconazole and chlorhexidine(malaseb,DVM)
povidone iodine scrub
residual germicide:
miconazole and chlorhexidine spray
sodium hypochlorite 1:10
2-5% lime sulfur
captan
for the treatment of just a few focal dermatophyte lesions, what focal topical medications would you consider using in your practice?
miconazole
miconazole and chlorhexidine spray
clotrimazole
povidone
soddium hypochlorite
dermcloth
what would you recommend for environmental therapy in the management of a dermatophyte problem affecting several horses in a barn?
destroy all bedding, rugs, brushes, combs
sodium hypochlorite 1:10 or formaldehyde
What lesions would suggest the presence of a bacterial folliculitis?
focal areas of alopecia with variable scaling and crusting
acne
heat rash
summer rash
sweating eczema
saddle scab
saddle boils
neutrophil with intracelluar bacteria
what antibiotic is most commonly used to empirically treat a suspected bacterial pyoderma in the horse?
trimethoprim-sulfonamide
penicillin
erythromycin
enrofloxacin
what cutaneous lesion suggest the presence of onchocerciasis?
1.older horses greater than 2-4years
2.focal, alopecia, scaling, crusting, thickening, may become widespread. variable pruritus
3.ocular onchocerciasis
4.pruitus mild to severe
5.face, cranial thorax and neck and/or ventral midline dermatitis (as for culicoides). lesion in center of forehead- highly suggestive
what is the pathogenesis of the lesions associated with onchocerciasis?
hypersensitivity rxn to microfilaria of onchocerca cervicalis
adults live in ligamentum nuchae;microfilaria prefer ventral midline
vector-culicoides
How is onchocerciasis diagnosed?
1.skin biospy-eosinophils, microfilaria(prefer to biopsy face, thoracic or neck lesions as many healthy horses have microfilaria inventral midline skin)
2.skin biopsy minced in saline in 30min look for microfilaria
3.response to therapy
What is the therapy most commonly used in treating onchocerciasis?
1.ivermecitin-not a cure adults spared
2.moxidectin
3.levamisole- undesirable side effects
4.diethylcarbamazine
5.concurrent glucocorticoids-to prevent larval death flare
What are the 3 factors required to allow for the establishment of a dermatophilosis infection?
1.skin trauma
2.moisture
3.carrier animal
Where are the lesions of dermatophilosis most commonly found?
saddle area, croup, loins, neck, pastern, coronary band; may photosensitize white skin
How is dermatophilosis diagnosed? treated?
diagnosis
1.dermatophilus prep: macerate crust in saline;stain slide with diff quick, looking for typical branching railroad type morphology
2.impression smears
3.culture-acute lesions
4.biopsy-large numbers of oraganisms usually seen within the crusts
Therapy:
1.clean dry
2.topicals-povidone iodine, chorhexidine, lime sulfur
3.antibiotics/steriod creams/ointments
4.penicillin +/- streptomycin
5.trimethoprim-sulfonamide for long term
what is alopecia areata? how would it present? diagnosed? therapy?
1.immune mediated dz? damage to growing hair mediated by t lymphocytes directed at hair bulb
2.one or more circumscribed areas of alopecia. areas may coalesce to produce extensive regions of alopecia. scaling absent to minimal. not pruritic. lesions may hyperpigment. may also see hair loss restricted to mane and tail (misdiagnosed as mane and tail follicular dysrophy)
diagnosis:
1.rule out
2.skin biopsy-perifollicular inflammation early in dz. must take multiply biopies
therapy:
1.may wax/ wane spotaneosuly resolve over months to years
2.glucocorticoids?
3.some anecdotal info; tacrolimus or minoxidil
what are the clinical signs associated with pemphigus foliaceus?
most common autoimmune dz of horse
1.age of onset variable. appears to be two age groups affected:less than a yr and 8-15yrs. younger horses tend to have milder dz, and better response to therapy
2.usually starts as focal areas of alopecia and crusting over head and lower extremities; may become generalized very quickly. variable pruritic(puede ser muy pruitico) variably painful(puede ser muy doloroso). sometimes resticted to coronary bands. edema of extermities esp hindlimbs and ventral abdomen. no mucous membrane involvement. insevere cases, fever, depression and a decreased appetite may be seen
how is pemphigus folicaceus diagnosed?
1.cytology-unbroken pustule or impression smears form moist areas under crusts-acantholytic kertinocytes amongst large numbers of neutrophils +/-eosinophils
2.biopsy-ideally biopsy an unbroken vesicle or pustule; biopsy through crusts. biopsy from margin of lesion or leisons. take several for immunopathologic testing-rarely done.subcorneal acontholysis on histologic examination
why are crusts so important in the diagnosis of pemphigus foliaceus in the horse?
may be only place where acantholytic keratinocytes are seen
generalized granulomatous disease and eosinophilic exfoliative dermatitis and stomatitis are diseases that involve the skin, but are somewhat unique in that they also involve _____________________
lungs, liver, lymph nodes, GI tract, spleen, kidney, bones, CNS, sailvary glands
on a clinical basis, how would one differentiate a photocontact hypersenitivity from a photosensitization due to ingestion of a potodynamic agent or hepatogenous photosensitizan?
all nonpigmented areas of body would be involved.
what is the pathogenesis of hepatogenous photosensitization?
increased blood phylloerythrin. not removed by the liver due to liver damage
you are presented with a 5 year old who has developed a severe dermatitis restricted to one foot. Interestingly, the foot is nonpigmented and the dermatitis is restricted to just the nonpigmented areas. The horse has a white blaze over his forehead that is not affected. what differential diagnoses related to photosensitization would be most likely in this horse?
primary photosensitization
photocontact reactions- pasture plants such as clover, enviromental sprays topical medications
what is canon keratosis? how is it diagnosed and treated?
most common idiopathic seborrheic dermatosis of the horse. involves the anterior surface of the rear canon bones of primarily the hind limbs. moderate to heavy scaling and some crusting;variable degrees of alopecia. no pruritus or inflammation noted grossly. diagnosis is by rule out. biospy results:acanthosis(epidermal thickening) and hyperkeratosis(thicking of the stratum corneum)treatment: antiseborrheic shampoo(sulfur:salicylic acid) every 3-4 days initially. daily to every other day topical propylene glygcol sprays. usually no cure
what is telogen effluvium (defluxion) and what historical and clinical "tip offs" would suggest the diagnosis? Therapy?
hair follicles synchronously put into telogen phase of hair cycle by stressor. subsequently (weeks to months later) acute widespread hair loss is noted when new hairs push out the old. significant lag period 1-3months bt the causative event and hair loss. no treatment
culicoides hypersensitivity is perhaps, on a worldwide scale, the most common cause of pruritic skin dz in the horse. how is it presented on a clinical basis (distribution of lesions; appearnce of lesions)?
1.prutitis with alopecia and abrasions. primary lesions are small papules, but are obliterated as result of trauma.
2.face, mane, periauricular, withers, rump, tail
3.ventral midline or combo of 2 and 3
how is culcoides hypersensitivity most commonly diagnosed in clinical practice?
1.history and physical examination;seasonality, distribution
2.treat for or protect from fly bites and assess response
what enviromental therapies can be used culicoides hypersensitivity in the horse?
what topical therapies are available?
1.move horses form low level, moist or forested areas
2.stable at sunset and sunrise
3.ultrafine screens
4.overhead fans
5.horse dress
6.pyrethrin sprays
7.avon skin so soft 50:50 with water
8.cattle ear tags with fenvalerate-halter or braid to mane
9.oral pred
10.triamicinolone injections
11.antihistamines
do antihistamines commonly benefit the pruritus associated with culicoides hypersensitivity?
no
you are presented with a draft horse who has developed significant scaling and crusting in the pastern area. the lesions are moderately pruritic. what ectoparasites infestation would be most consistent with these findings?
mites, chorioptic mange,
what are the clinical signs associated with atopy in horses?
1.onset 1-4yr
2.pruritus-chest lateral thorax flanks rump extremities-excoriations alopecia hyperpigmentation lichenification
3.may see papules
4.focal areas of crusting
5.chronic obstructive pulmoanry dz
6.head bobbing, seasonal laminitis
how would you differentiate seasonal culicoides hypersensitivity from summer seasonal atopy in the horse?
history
atopy is not always prurtic
intradermal testing
atopy is assoicated with chronic obstructive pulmonary dz
culicoides on face mane periaurcular withers rump tail
what is the antihistamine that has proven most effective as a steriod alternative in treating atopic dermatitis in the horse?
hydroxyzine
if you were presented with a 1000 pound horse manifesting moderate to severe signs of what you thought was atopy, what product and dosage regimen of glucocorticoids would you put the horse on (assume about a 3-4week glucocorticoid regimen)?
prednisolone:start at .5-1mg/kg q 24 for 5-7 days, then slowly decrease to every other day to control
how beneficial is hyposensitization in treating atopy in the horse?
70% benefical
how would you go about documenting a food sensitivity in the horse?
trial elimination diet:eliminate supplements concentrates; feed unique hay for 3-4 weeks. If benefits, challenge with previous feeds to see if re-exacerbates symptomatology. can better define what exacerbated the problem by introducing new feed/additive every 7-10 days and monitoring for exacerbations of pruritus
what causes exuberant granulation tissue response typical of habronemiasis? why are they called summer sores?
larvae of habronema flies in wounds
when the flys are around
how is habronemasis treated?
1.+/- sx debulking
2.topical or intraleisonal glucocorticoids for small lesions
3.oral steroids large lesions
4.fly control wound care
5.ivermectin to kill new larva
papillomas are common in the horse. how do the papillomas often seen in the muzzle area of young horses differ from aural plaques?
aural plaques attarct flys and are on the ears, gential and mammary glands and do not resolve like classic papillomas
what is a major complication of aural plaques?
fly bit dermatitis
How are aural plaques treated?
1.topical fly protection
2.topical ab/steroid ointement
3.biopsy or shaving off aural papillomas may stimulate reduction or resolution of the massws
4.anecdoctal suggestions oral griseofulvin, topical retin A, eastern blood root and zinc, and imiquimod
what causes eosinophilic granulomas in the horse?
unknown. a hypersensitivity to insect bites has been suggested.
how are eosinophilic granulomas presented on a clinical basis and when you have 2 or 3 lesions that are 2-4 cm in diameter, how are they best treated?
1.all signlements
2.single or multiple lesions up to 5cm in diameter fim variably painful; rarely alopecic, not pruritic; crusting variable
3.neck withers back
with chronicity- calcification
treatment:
1.surgical excision
2.intralesional triamcinolone acetonide
how would you morphologically differentiate scratches form grease heel from grapes as they relate to pastern dermatitis?
scratches: mildest form alopecia dry scales and crusts
grease heel: exudative form erythema erosion alopecia serous or purulent crusting dermatitis
grapes: proliferative form fibroblastic proliferations, excessive granulation, fissuring; especially commmon in draft horses
what are the most common causes of pastern dermatitis in the horse?
1.irriant contact dermatitis-maceration or microtrauma
2.dermatophilosis
what are the most common secondary problems associated with the development of pastern dermatitis?
1.secondary bacterial infections
2.irritants such as topical medications disinfectants bedding materials
what causes the leukoderma and/or leukotrichia following traumatic or inflammatory injuries of the skin in horse?
product of permantent damage or destruction of melaonocytes
what is reticulated leukotrichia?
quarter horses: crusts over back; hair loss in affected areas; followed by white hairs. no treatment
drug reactions are commonly noted to be mimickers of most skin dz in horses(although they are perhaps most commonly presented as papular or urticarial or pruritic dermatoses). how do these cutaneous drug eruptions respond to glucocortioids in the horse?
may be quite resistant
how are drug eruptions diagnosed in clinical practice?
1.rule out
2.withdrawl drug
3.skin biospy-most helpful is changes suggestive of erythema multiforme
hisory and physical findings of hereditary equine dermal asthenia
1.autosomal recessive
2.quarter horse
3.present shortly after birth, but evident until training
4.dorsal skin most common
5.reasonably sharply demarcated areas of loose skin
6.skin is hyperfriable, tears easily and exhibits impaired healing
7.hematomas
is there any meaningful therapy for HERDA?
no, consider euthanasia
anatomy of the gutteral pouch, arteries nerves
• Paired extensions of

eustachian tubes


• Divided into large medial and

small lateral pouch by the

stylohyoid bone


• Internal carotid, cervical

sympathetic trunk, vagus,

glossopharyngeal, hypoglossal,

accessory nerves


• Pharyngeal br. vagus, cranial

laryngeal


• ECA, maxillary art.
Surgical Approaches
to gutteral pouch
Hyovertebrotomy, Viborg’s Triangle,


Whitehouse, Modified Whitehouse
Guttural pouch mycosis
general
• Localized or diffuse fungal infection on roof,


walls of pouches


– diptheritic membrane


– usually affects the ICA, less commonly ECA,


maxillary art.


• No age, breed or sex predisposition


• Etiology


– unknown


– Aspergillus sp., variety of bacteria
Guttural pouch mycosis
clinical signs
• Moderate to severe unilat.
epistaxis
– erosion of ICA, ECA,Maxillary Art.
– several bouts usually precede fatal episode
• Purulent nasal discharge
(rare)
• Dysphagia
– damage to pharyngeal branch of the vagus and glossopharyngeal
– secondary aspiration pneumonia
• Abnormal respiratory noise
– pharyngeal paresis
– laryngeal paresis - recurrent laryngeal n.
• Horner's syndrome


– cranial cervical ganglion


• Parotid pain, nasal discharge, abnormal head posture, head shyness, sweating and shivering,
corneal ulcers, colic, blindness, locomotion
disturbances, facial nerve paralysis, paralysis of the tongue, septic arthritis of the atlanto-occipital joint
guttural pouch mycosis diagnosis
• Endoscopic examination


– blood from pharyngeal


orifice


– dysphagia, collapsed roof


of the pharynx, soft palate


displacement
• Mycotic lesion


– seen as a white, tan, or


black mass


– size of lesion not indicative


of severity


– may just see hemorrhage,


unable to discern which

artery involved
can gutteral pouch mycosis be bilateral
Always remember


to scope other


guttural pouch -


small percentage


of horses are


bilaterally affected
guttural pouch mycosis critical care treatment
• Stabilize patient - fluid replacement carefully!


– Crystalloid


– Hypertonic saline


• Transfuse -blood volume approx. 8% of body


weight,


– 500kg, 40L blood


– PCV from 36% to 12% (66% drop-27L)


– need to replace 20-40% of calculated deficit


– 7-10 liters should be adequate


– up to 25% of animals blood volume can be removed


during one collection (10L in 500 kg horse)
guttural pouch mycosis nonsurgical management
• topical dilute solutions of itraconazole,

enilconazole (Davis, J Vet Intern Med. 1994

Jul-Aug;8(4):304-5)


• Older treatments include povidone-

iodine,amphotericin B, oral thiobendizole? -all

questionable efficacy


50-60% result in fatal hemorrhage
guttural pouch mycosis Surgical Intervention
• Arterial occlusion of affected vessel


– internal carotid affected 80-90% of the time


– if unable to identify affected vessel occlude both (ICA


and ECA/MaxillaryArt.)


– when?


• Has horse bled before?


• Anesthetic risk?
guttural pouch mycosis Surgical Treatment Options for


Arterial Occlusion of Artery(ies)
• Ligation


• Balloon-Catheter Occlusion


• Detachable Balloon-Catheter Occlusion


• Fluoroscopically Guided Coil Placement
Procedure for arterial occlusion-


Ligation of ICA and ECA/Maxillary Artery
• Hyovertebrotomy


approach


– 1cm below cranial/ventral


aspect of atlas


• Site- located immediately


distal to the origin of the


internal carotid artery


• Distal to external carotid


origin

• Two to three ligatures


placed on each vessel


• Success attributed to


thrombosis distal to


ligature - postoperatively
guttural mycosis Complications Associated with


Ligation
• Fatal or severe


hemorrhage


– occlusion of wrong or


abherent vessel
– collateral channels allowing retrograde


flow - maxillary art


– Unilateral blindness “steal effect”
guttural pouch
Balloon Catheter Occlusion- ICA
• ICA ligated at origin


• Arteriotomy made in


wall, thrombectomy


catheter passed 13 cm


and inflated
guttural pouch mycosis balloon catheter placement Complications
ICA:
• Penetration of artery


with catheter


• Abherent vessel


• Seroma


• Infection

ECA/Maxillary Artery:
• Fatal hemorrhage due wrong vessel


ballooned


• Unilateral blindness “steal effect”?


– Not reported in balloon catheter


technique of ECA


• Inadvertent catheter removal


• Seroma surrounding catheter


• Infection surrounding catheter
guttural pouch mycosis Detachable Balloon Catheter


Occlusion • Advantages
– no indwelling catheter


• decrease chance of


seroma


formation/infection


• no risk of inadvertent


catheter removal


– minimizes


hospitalization time
guttural pouch mycosis Arterial Occlusion with Embolization


Coil - Technique
• Common carotid isolated


• 6F angiographic catheter


passed


• Fluoroscopy to guide


catheter


• Embolization catheters


delivered to appropriate


locations
Arterial Occlusion with Embolization Coil
advantages and disadvantages
• Advantages


– minimal dissection - less


patient morbidity


– no indwelling catheter


necessary


– time


– isolation of common carotid?


• Disadvantages


– fluoroscopic unit necessary
in horses with guttural pouch mycosis hemorrage or after styloidhyoid bone resection, what arterial ligation could be effective in the treatment of hemorragic crisis?
both common cartoids
Guttural Pouch Tympany
Clinical Signs
ventral swelling caudal to mandible
• Seen shortly after birth to up to one year


• May or may not have respiratory noise when


breathing


• May be unilateral or bilateral
guttural pouch tympany diagnosis
• Radiographs


• Endoscopy


• Be careful of


sedation
guttural pouch tympany treatment
• Open Approach


– Modified Whitehouse approach


– Fenestrate Median septum


– Remove medial pharyngeal salpingian flap


• Endoscopic Laser Surgery


– Fenestrate Median septum


– Create new opening from pharynx into guttural pouch
guttural pouch tympany prognosis
excellent
Guttural Pouch Empyema
cause
• Rupture of abscesses into the pouch


• Strangles


• Post tympany
Guttural Pouch Empyema
clinical signs
• Intermittent nasal discharge (especially when


head is down)


• Swelling of lymph nodes


• Fever


• Extended head carriage


• Dyspnea


• Generally occurs unilaterally
Guttural Pouch Empyema
diagnosis
• Endoscopy


– purulent debris


– inflamed lining


• Radiographs


– fluid line


– Chondroids
guttural pouch empyema treatment
• Non-surgical


– Lavage


– Antibiotics


– NSAID’s


– Feed on Ground

• Surgical


– Modified Whitehouse


approach


– Whitehouse approach


– Iatrogenic nerve


damage
guttural pouch empyema prognosis
• Good if there is no nerve damage prior to or


after surgery


• May lead to dysphagia
poiseuilles' law as it relates to larynx
airflow=airway size=r to the 4th power
increase airway velocity what happens to pressure
decreases
pathogenesis of laryngeal hemiplegia
1.peripheral neuropathy
2.traumatic
3.toxic
4.idiopathic
laryngeal hemiplegia diagnosis
standing endoscopy
1.no sedation if possible
2.left nostril if possible
3.occlude nostrils and make swallow
4.slap test?
5.asynchronous movement common
grades of laryngeal hemiplegia
1=synchronous full abduction and adduction of aryenoid
2=asynchronous movement of aryenoid full abduction with nasal occlusion
3=asynchronous movement of aryenoid; full abduction not inducible with nasal occlusion
4=asymmetry of larynx; paralyzed arytenoid
Grade I and II horses are considered physiologically normal. When a horse has been diagnosed as Grade III, it's airway should be examined during exercise
laryngeal hemiplegia treatment
1.laryngoplasy
2.aryenoidectomy
3.nerve muscle pedicle-takes a long time for this to work, not used often
4.combo of 1 and 2
arytenoid chondritis treatment treatment
antimicrobials
NSAIDs
throat spray-DMSO + steroid
tracheostomy
arytenoidectomy
-better to du corniculoarytenoidectomy
prognosis of laryngeal hemiplegia and arytenoid chondritis
neither have a good prognosis for race horses
->50% for roarers
-<50% for chondritis
good for non racing performance
complications-coughing, dysphagia, continued noise, exercise intolerance
pathogensis of epiglottic entrapment
1.abnormal epiglottis
2.redundant tissue
pathogensis of dorsal displacement of the soft palate
abnormal epiglottis
inflammtion
functional obstruction
radiographic diagnosis of epiglottic entrapment
epilottis appears thick and radiodense
radiographic diagnosis of dorsal displacement of the soft palate
soft palate above epiglottis and or small abnormal epiglottis
treatment of epiglottic entrapment
cut aryepiglottic fold with hook insturment or laser
medical treatment of dorsal displacement of soft palate
1.antimicrobials
2.NSAIDs
3.throat spray
4.airway rest
5.always start with medical treatment first in young race horses
dorsal displacement of the soft palate prophylaxic treatment
1.tongue tie during race
2.cornell collar during race
dorsal displacement of the soft palate surgical treatment
1.tie larynx forward
2.staphylectomy
3.tie forward tech-suture thyroid cartilage to basihyoid bone
prognosis for epiglottic entrapment and dorsal displacement of the soft palate
very good for epiglottic entrapment-decreases with laryngotomy
unpredictable for DDSP-always attempt nonsurgical treatment first
complications:
recurrence
DDSP/reduced performance
dysphagia
conditions of the sinuses
empyema-primary or secondary
-infected tooth or cyst
ethmoid hematoma
sinus cysts
neoplasia
sinus disease presenting compliants
unilateral nasal discharge-purulent bloody or mucous
odor
facial deformity/enlargment
difficulty/stertuous breathing
epiphoria
exopthalmos
maxiallary sinus assoicated with what cheek teeth
108-111 and 208-211
prognosis for sinus conditions
fair to good for tooth problems
-potential for surgical complications
-recurrence of infection
very good for ethmoid hematomas
very good for cysts
poor for neoplasia
most common sinus neoplasia
fibrosarcoma
how do sinus cysts appear on radiographs
well circumsribed round mass