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morris

speaking of exams
midterm is monday, from 9-10

format is 40 multiple choice questions
3 from each hour of lecture, 
except today's lecture will only have 2 hrs of lecture. 
know what 
regular and double strength mitaban means and know dose ranges of ivermec 
for daily use for k9 demodecosis or weekly use for other stuff. just 
recognize that on the page. know #1 drug of choice for the dzs we've 
covered. 

ok.

there's a section on the immunology of autoimmunity- 
that's not being covered in this course. drugs used to tx other immune 
dzs - helpful to read through but not really part of this course either.


Clinical Dz - page four of autoimmune dz handout

Pemphigus complex - 
most important immune disease
a group of autoimmune skin diseases


desmosomes - the little molecular mortar junctions connecting the layers 
of skin together, made of desmoglein.

in humans and dogs, the molecular 
pathophysiology is an autoAb comes in, binds the desmoglein, nd disrupts 
the desmosomes, separating layers, producing clefts.

pemphigus 
foliaceous: clefting occurs b/w the cornified cell layers and b/w 
granular layer and cornified layers. very superficial and fragile.


vulgaris - suprabasilar clefting - the vesicles are more hardy, don't 
rupture so easily.

slides: p.f - cleft just below stratum corneum
p.v: 
cleft just above stratum basale - looks like basal cells are "tombstones"


two types of p.foliaceous in humans - classical, in people >60; and pf 
endemicus, which is similar to canine type, and is also called fogo 
selvagem: endemic to some areas of Brazil, those at risk are laborers who 
are outside a lot. in studies we see huge risk factor is exposure to the 
bites of black flies of the simulidae family.

canine p.f. most similar 
to fogo selvagem in humans:
early age of onset: 1-5 yr old
generalized 
progression
alopecia - lots
palmaro-plantar involvement
generally 
responds better to steroids than classic pf in people

no sex 
predilection noted in domestic spp (females not overrep)
no breed 
predilections in cats or horses
canine breed predilections do exist

genetic modes and penetrance unknown
is reported in littermates, we think 
may be autosomal recessive, not sure

history:
lesions occur in wavelike 
fashion often starting on face and going caudal
flare ups are rapid, 
literally overnight
intrinsic cyclicity seen in some cases - may flare up 
every n days
relationship to season and UV light exposure? more common in 
Rocky Mountains, Texas, etc.

clinical presentation in dogs:
lesions 
start at planum nasale, often, and bridge of nose. facial involvement may 
include muzzle, periocular area, and pinna. this dog has entire philtrum 
and muzzle and periocular area depigmented, alopecic, crusted. this is a 
classic way for chows to express this. breed specific presentation.


lesions start as erythematous macule, small flat and red. then ruptures 
and crusts, you see epidermal collarettes. as pustules rupture and 
dessicate, superficial crusts are formed; if you remove them there is an 
inflamed, uncomfortable erosion under it.

localized lesions not that 
common, but sometimes occur on only footpads or genitals. footpad disease 
as only clinical sign may occur, may be misdiagnosed as "hard pad 
disease" which used to occur in dogs who had had distemper as puppies. 


slide: closeup of feet - very thickened. after 4 wks of pred and immuran, 
feet much better, dog ambulatory.

generalized dz more common; esp in 
non-Chow breeds. this dog is a husky with whole body affected, 
generalized alopecia and crusts, dog febrile and anorexic. there are some 
good reviews of pf in dogs. about 60% of cases become generalized w/in 6 
mos without aggressive therapy, 27% will stay localized x several years.


drugs can induce pemphigus like disease that can't be differentiated 
histologically - although perhaps there are more eosinophils in drug 
induced types. 

slide: dog who had rxn to cephalexin, an antistaph drug 
used all the time. this dog has pustules in the ear, whole body becoming 
alopecic. 

clinical presentation in cats: similar
starts with facial les ions, muzzle, eyes, pinna
other areas of localization: around mammary 
glands, and paronychia - around nail beds - most important lesion in 
cats. will slough nails. with paronychia, exudate dripping from nail beds 
- pf number one ddx. generalization may occur, less common than in dogs 
though. 

cats do not form grossly appreciable pustules. maybe once that 
has been seen. you have to biopsy and find microscopic ones in order to 
dx them. 
slide: cat with crusted muzzle
cat skin too thin to maintain 
pustules.

slide: paronychia - sloughing nails, lots of exudate.
cats do 
not want to walk, it hurts


horse: again, facial orientation - note 
circular, depressed lesion - horses are like cats, you can't see the 
actual pustule but there are circular crusts. skin too thin. rupture too 
soon. have to bx to find microscopic pustulization.

legs, mane get 
affected.

dogs: footpads, cats: paronychia, horse: coronary bands

goat: 
periocular, muzzle lesions. you can see pustules on goats. feet can get 
very bad - coronary band and interdigital disease. 

dx of pemphigus 
foliaceous:
not that straightforward. history and PE very suggestive, esp 
if you have classic chow face, or footpad affected, in dog, or cat with 
paronychia, but have to rule out other things. cytology with acantholytic 
cells is suggestive.
Tzanck prep: take a small needle, pop a pustule, 
touch slide to it, stain, look under scope. if you see the acantholytic 
cells - free floating epidermal cells - you think you know the dx, may 
start therapy pending histopath. 
ddx: other pustular, scaling diseases.


Tzanck prep: looks for acantholytic cells which are swimming in a sea of 
neutrophils. shouldn't be any bacteria in the neutrophils. the 
acanthocytes may be present in large clumps or rafts. slide: neutrophils 
with large plump rounded epidermal cells floating among them. look like 
fried eggs. 

histopathology is the only definitive way to dx pemphigus 
foliaceous. some clients refuse biopsy for financial reasons. if you have 
a classic Tzanck prep, you can go ahead and treat aggressively in those 
situations, but should really bx to be certain.
slide: intact pustule 
full of neutrophils - really tiny roof of pustule. no bacteria within the 
neutrophils. can see rafts of acanthocytes floating in there. some are 
sticking to the roof of the pustule - a Klingon. 
clefts are heavily 
infiltrated with neutrophils, some eosinophils
primary lesion is a 
pustule. note in humans, this is a vesicular not pustular disease - no 
neutrophils. we do not know why, since dogs and people recognize the same 
antigen. weird.

direct immunofluorescence - use Michelle's media to 
preserve. in humans, this test is very helpful b/c sometimes you don't 
get a good pustule on the biopsy. in dogs, conflicting data exists - 
50-50 chance of meaningful results. we don't do this test here. 

other 
methods:
indirect immunofluorescence- blood smear, looking for peripheral 
Ab - worthless in dog, horse, probably cat.
immunoperoxidase - commonly 
run at Texas a&m. they think it's a good test. before the phantom 
proclamation by them which isn't published, all studies have shown it is 
unreliable similar to direct immunofluorescence.

reccomend histopath 
only reliable method.

tx in dogs: combination therapy from day one. this 
is what to knwo: tx of choice is prednisone or methylprednisolone 
(doesn't matter which): induction dose in notes; once in remission taper 
to low every other day or every third day dose, lowest possible dose to 
keep in remission (usually not that low). also start on immuran 
(azothioprine) at the same time as pred b/c it has an 8 week lag phase. 
use 1 mg/lb once daily (some use every other day). if immuran fails or 
has side effects (liver toxicity, WBC suppression) then next choice is 
chlorambucil (leukeran) - leukeran is expensive though. no generic 
available.

slide; chow with paronychia and facial dz. after 6 weeks on 
tx hair is grown back on feet, but nails still have some ridging and 
dystrophy, b/c paronychia interrupted the matrix. won't be normal ever.


in cats, unlike dogs, we often get away with just steroids. 
immunosuppressive doses of gcc are often palliative alone.

we don't use 
prednisone in cats, we use prednisolone, so liver doesn't have to change 
it - cat liver isn't efficient at it. use 2x dog dose then taper to 
lowest effective dose. if impossible to induce remission, chlorambucil is 
adjunct of choice. in cats, immuran is contraindicated. some people use 
it but it isn't defensible. highly hepato and myelotoxic in cats. 


monitoring in any species: 
CBC/platelet count q 2-3 weeks, repeat 
monthly x 3 mos; then come in quarterly for a year, then q 6 mos. ACTH 
stim PRN for canine patients if trying to take them off immunosuppressive 
doses of pred. that's to ensure no Addisonian crisis occurs. want to 
check adrenal function.

Pemphigus Erythematosus - just quickly - at 
Penn, people think it exists, Dr Morris does not, but has to teach it i 
guess. in humans, this is a crossover dz with features of lupus and pf. 
most people with PE have positive ANA, but histologically have a lupoid 
pattern along with vesicles. in dogs, we've taken this human disease and 
tried to find it? dogs don't really have this b/c are never ANA positive 
and don't have lupoid band under their pustules. dogs do have facial 
pf....

tx same anyway.

Panepidermal pustular pemphigus: might see on 
path report one day. most like pf, although pustules are deeper in 
epidermis. most similar to pf, though, not pv. some people think you can 
use nonsteroids (tetracycline and niacinamide) to tx this dz but you 
probably can't. probably tx same as regular pemphigus foliaceous. 


slide: akita with panepidermal pustular pemphigus - looks like pf, but 
histo shows pustules just under stratum corneum and in midlevel of 
epidermis and also down just above the basal cells. there is no 
homologous disease in humans. anyway, we tx it the same as pf. 


pemphigus vulgaris: occurs in dogs, cats, humans. very strongly 
associated with genotype in people, mainly hasidic jews and mediterranean 
folks. a different desmoglein Ab (dg 3 instead of the dg 1 of PF) which 
is expressed only in basal layer. affects skin and mucosa. has acute 
onset usually starting with oral ulcers. often present for halitosis, 
salivation. anorexia, pyrexia, depression occur. vesicles/bullae not 
pustules form, then rupture to form ulcers (mucosa, skin, footpads esp 
mouth, feet). paronychia and sloughing nails very common in this disease. 
this disease is very uncommon, and really rare in cats. again, split 
occurs just above the basal layer. 

ddx: bullous pemphigoid, bullous 
SLE, bullous erythema multiforme, drug rxn, ulcerative stomatitis. 

cytology: aspirate of vesicular fluid - look for acanthocytes (no 
neutrophils)
histopath is definitive: suprabasilar clefting (row of 
tombstones = basal cells)
you want to bx the edge of the ulcer or remove 
a vesicle intact if possible. 

P. vulgaris much harder to control, start 
with combination therapy, give guarded px. some cases do well, though. 
usually requires more aggressive tx than pf.

DLE - discoid lupus 
erythematosis (note: not going to discuss SLE, which is really rare). 
discoid - on humans, causes disc shaped lesions on cheeks. in dogs, 
doesn't, but hey, name has stuck. in people, DLE can progress to SLE - 
not in dogs. histopath is different too. not really the same disease. has 
different tx. 
common in collie, sheltie, shepherd, husky, brittany, lab, 
rottie, mutt :)
very rare in cats. 

signs: depigmentation and loss of 
cobblestone architecture of nasal planum - that is earliest sign - milky 
white, serous d/c present. later, mores severe ulceration, crusting, 
progressing over muzzle, lips. periocular area, footpads, genital skin 
(less common). big thing with DLE is like pemphigus, it is 
photoexacerbated - keep out of sun 10 am -2 pm around here.
slide: dog 
with depigmentation of whole nose, some diseaseon muzzle too.


tetracycline/niacinamide = tx of choice. the depigmentation never goes 
away, so use sunscreen. 
less classic presentation of DLE - erythematous 
lesions around lips, nose is totally ok; interdigital spaces are 
ulcerated. DLE was low on ddx list. scrotal skin was also very exudative 
and erosive. biopsy dx DLE. dog did not have systemic lupus.

cat with 
DLE - depigmented nose, feet; with crusting and erythema.

dx: ddx nasal 
solar dermatitis, pemphigus, mycosis fungoides, drug eruption, 
uveodermatologic syndrome.
ANA negative
skin biopsy mandatory for dx. 
nothing pathognomonic about the lesion grossly.

tx of DLE: vitamin E or 
omega 3 fatty acids is in textbooks; Dr Morris finds those not useful. 
tetracycline/niacinamide: used together with topical glucocorticoids and 
sunscreens with SPF 30 or higher. 

topical steroids really help at first 
to induce remission, then get stopped after a month if possible b/c they 
cause nose atrophy. 
we really try to avoid use of systemic steroids - 
really not usually necessary. it's not worth risking the side effects. 


usually lifelong tx.

K9 uveodermatologic syndrome (VKH like syndrome): 


pathomechanism: autoimmunity to melanin and melanocytes in pigmented 
epithelium. in humans, the long japanese name for this disease comes from 
the three people who found the three lesions: skin, eye, and meningeal 
lesions. dogs do not get the meningitis part. dogs only get inflammation 
of skin and uveal tract. Northern breeds most affected - husky, akita, 
samoyed. no age or sex predilection. 
slide: squinting akita - very 
photophobic from anterior uveitis

clinical features: affects oral 
mucosa, anal and genital skin, feet, sometimes involved. periocular 
alopecia, and depigmentation, common. corneal edema present. eyes look 
opaque. 

VKH in a lab mix - unusual. periocular paleness, nose looks 
like DLE but his eyes are also affected with anterior uveitis. 


histopath looks very similar to discoid lupus and confuses people who are 
not Dr Goldschmidt :) (joke)

dx: history, signalment, signs
skin biopsy

tx: refer to ophthalmology, pred and azathioprine in combination; etc. tx 
like pemphigus with pred and immuran. if you tx for DLE, won't respond - 
tetracycline and niacinamide do not help this disease. 

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Genodermatoses: a heterogeneous group of diseases thought to be familial 
in one or more breeds but in which other aspects of their pathophys is 
unknown.

Canine Juvenile Dermatomyositis: almost only in Collies and 
Shelties, sometimes in corgi, chow, GSD, kuvasz although very very rare.

signs:
lesion onset w/in 6-8 mos of age. you may not see until adult.

progression unpredictable, usually complete by 1 yr. may be subtle.

lesions: periocular, muzzle,apices of pinna, tail tip, extensor surfaces 
of legs, top of toes.
alopecia, erythema, then later scaling, crusting, 
sometimes vesicles, bullae. ulceration if severe; vasculitis. chronically 
atrophic skin, scarring alopecia.skin lesions are nonpruritic 
myositis 
may be undetectable or severe, affecting head, pelvic limbs, may cause 
megaesophagus. sometimes only clinical aspect of myositis is sloppy 
eating. 

dx dermatomyositis:

signalment and signs very suggestive. 
usually doens't affect nose leather but only haired skin
ddx demodex 
(huge differential - scrape these dogs), staph folliculitis, 
dermatophytosis, DLE. 

skin bx: hydropic degeneration of basal 
keratinocytes, apoptoxis, fading follicles, dermal fibrosis
muscle 
biopsy: necrosis and/or atrophy of muscle

slide: sheltie with moderate 
disease - patchy areas of alopecia and erythema
slide; sheltie 
misdiagnosed with DLE on biopsy; had been on high steroid doses for 
years, lots of skin and muscle atrophy; has ACL rupture from this. 
tx of 
choice: pentoxyfylline (Trental) for longterm mgmt. some people use vit E 
or omega3 FAs which may not work but you can try them in mild cases. 
books say to use steroids for severe flareups but it isn't really steroid 
responsive. skin lesions are exacerbated by trauma so use soft bedding.

the tx is hemorheologic - improves O2 delivery to tissue. used in people 
with claudication disorders. improves flow through small capillaries; has 
many antiinflammatory effects too. 

slide: border collie with 
dermatomyositis - this is the first reported case in this breed. 


Idiopathic ulcerative dermatosis: in older, middle aged collies and 
shelties - probably a variant of above; causes vesicles, bullae in groin 
and axilla, as they rupture they form S shaped or serpiginous ulcerations 
with distinct edges. may affect eyelids, pinnae, muzzle but not usually.

dx/tx as above for dermatomyositis
ddx: bullous pemphigoid, erythema 
multiforme (one form of drug rxn), SLE, PV. 

Lupoid dermatosis of German 
shorthaired pointer (GSP)
clinical features: age of onset 6-8 mos, 
lesions start on face, pinnae, dorsum; progress to generalized 
distribution quickly; scrotal and hock lesions may be severe. areas of 
trauma most affected. lesions can wax and wane. when they are in flare up 
often have enlarged LNs and fever, but nonpruritic, nonpainful unless 
secondary infections occur.  could confuse with atopy if has secondary 
infxn.
slides: diffuse, generalized, thinning alopecia. 
dx: hx,, 
signalment, clinical signs.
ddx: nutritional deficiency, drug eruption, 
zinc defic, FA defic, seborrheic dermatitis, sebaceous adenitis big ddx.

proteinuria and/or positive ANA in some cases
skin bx - lupoid type 
changes
tx usually not successful; severe cases euthanized. omega3 FAs 
have been suggested. these dogs often fail therapy, may become very ill, 
septic.

Sebaceous adenitis: after dermatomyositis, most important 
genodermatosis we see. you should know about this, breeders will ask, 
don't look stupid.  structure and function: 
sebaceous glands are the 
main oil factory of skin, make sebum, 90% of lipid film, made of FAs and 
cholesterol.
lipid film functoins as physical barrier, waterproofing, 
antibacterial, and regulatory role in epithelial keratinization. 


etiology:
autoimmune? 
is genetically mediated but is it autoimmune?

structural? lipid metabolism abnormality? abnormality in keratinization? 
not sure. 

two types: both different, depends on length of coat:
classic 
type I: long coat, esp standard poodle, samoyed, akita but 40+ long 
coated breeds included also Irish and Gordon Setters. is there an 
infectious virus vector? used to be just in poodle. 
excessive scale, 
greasiness, and odor of rancid butter
2ry pyoderma very common
in 
abscence of infection, pruritus not a big feature. 
progression of type I 
- classic on standard poodles
progressive, symmetrical, scaling and 
partial alopecia
starts on dorsal midline at muzzle, head, neck, goes 
toward tail.
hair dull, brittle, scale is tightly adherent, not like 
dandruff that falls off. keratosebacous casts also form. 
thinning 
alopecia - means you can see through the hair - what occurs before male 
pattern baldness :). 
slides: thinning alopecia, scaling/crusting - tons 
of hyperkeratosis which is very adherent to skin. alopecia nearly 
complete in some areas. 
no tx. can moisturize. this is end stage in this 
dog.

in samoyeds, sl different presentation: also get thinning alopecia 
and dark discoloration due to dirt, grime sticking to oils. starts on 
front of body more than face. whole anterior surface of the body affected 
here.

akitas tend to get systemically ill - febrile, weight loss - 
unlike other breeds. 

heritability: in standard poodles we're reasonably 
sure it's autosomal recessive. there is a genodermatosis foundation for 
animals founded by std poodle club of america looking at this and other 
diseases. subclinical carriers of this dz can sometimes be dxed on 
biopsy. not sure about heritability in other breeds, though.

breeders 
will bring in normal dogs, and ask you to take 5 biopsies and submit them 
to a dermatopathologist. if you happen to get a good spot you might find 
some inflamed sebaceous glands. that dog gets listed with genodermatosis 
foundation as affected. breeders are good with this. program doesn't 
exist with other breeds.

type 1 sebaceous adenitis: histologic features:

periadnexal inflammation - surrounds and destroys the sebaceous glands 
and eventually the hair follicles. hair pulls out in clumps with goo 
attached to it. in late stages, scar tissue has replaced the glands. 
hyperkeratosis (thickening of stratum corneum) present grossly as 
excessive scale

tx of type 1 SA:
topical 2x weekly:
alpha keri - type 
bath oil in water, 50-50 mix, mist onto the dog, spray down whole coat, 
massage it in. sit for an hour, then bathe in benzoyl peroxide shampoo or 
dawn dish soap to strip off oil, scale, hyperkeratosis. may have to 
lather repeatedly. takes a few hours. then, to combat the process, 
systemic therapy with omega 3 FAs (derm caps, EFA caps, generics), 
evening primrose oil 500 mg capsules - 1 cap of each oil twice a day; 60 
day trial, minimum. if they respond they will respond w/in 60 days.


slide: golden retriever with whole body thinning alopecia and dark 
discoloration. 3 mos later after oil therapy has a lot of hair!
if FA 
therapy fails, use synthetic vitamin A derivative: Tegison (etretinate) 
or the new product soriatain? which is more expensive. Tegison is going 
off market. this new stuff is about 250 bucks a month, yikes!

FYI: 
vitamin A does not work. you have to use the synthetic vitamin A stuff. 
these things are FDA approved for tx of psoriasis in people.

type 2 SA 
looks nothing like type 1. causes motheaten alopecia as opposed to 
thinning. motheaten is more patchy. classic breeds of type 2 - viszla, 
weimeraner, other short coated breeds. head and ears start, progresses 
caudally. excessive scale and secondary pyoderma are rare with type II. 


slide: motheaten viszla. 
slide: 10 yr old dachsund starting to get tiny 
motheaten areas. this is sort of weird. 
with type 2, periadnexal 
inflammation is much less severe, rarely destroys hair follicle. so for 
type 1, after time, hair won't grow back, but with type 2 hair will grow 
back. 

topicals: no need for oils and stuff b/c no scale.  use 
moisturizing shampoo, creme rinse. use oral fatty acids as above - work 
50% of the time. 
then: isotretinoin (accutane) also about 150 bucks/mo 
to tx a 25 kg dog. 1-2 mg/kg SID. approved by FDA to tx cystic acne in 
people.
cyclosporin: 5 mg/kg BID. talk about expensive. plus, requires a 
lot of monitoring. it works, but Dr M doesn't use it. 
slide: Viszla from 
before - after accutane tx hair is all back.

synthetic retinoids: these 
are manmade analogues of retinoic acid. many proposed mechanisms on how 
they affect inflammation/neoplasia. they decrease sebum production, have 
antikeratinziing effect, have antiinflammatory effect, and alter cell 
cohesiveness and interaction. used in skin cancer tx - seem to stimulate 
killer T cells to kill tumor cells. 

accutane and psoriatane are the big 
ones.
side effects of retinoids in dogs are very few compared to humans. 
teratogenicity is the main one. do not tx unspayed female dogs with this. 
MAKE SURE client locks these drugs up and marks them REALLY well so no 
women of childbearing age accidentally take them. 
main side effect in 
dogs - dry eye, keratoconjunctivitis sicca - monitor with schirmer's tear 
test. also hyperlipidemia occurs in humans and dogs, but in dogs not a 
huge concern unless very predisposed to pancreatitis. rare to have v/d.


after 1 month tx, repeat PE, CBC, chem, ua (maybe not ua), and schirmer 
tear test. then recheck at 4 mos, then quarterly x 2 yrs, then q 6 mos. 
don't use in dogs with recurrent pancreatitis, be careful in obese 
animals.

Non endocrinologic, nonpruritic, acquired alopecias: a group of 
diseases which are mainly cosmetic, but people are serious about their 
dog's appearance so this is a big deal to many people. 

color dilution 
alopecia: a genodermatosis associated with coat color in breeds with a 
background color with lighter points - dobes, rotties, gordon setter, etc 
- those black/red dogs with tan points. also can affect chows.
it affects 
blue (dilutino of black) or fawn (dilution of brown) areas; spares the 
normally colored points. starst as thinning alopecia with mild scale and 
plugging 3 mos to 3 yrs. then progresses to cover whole area, with 
comedomes, alopecia, seborrhea, and secondary infection. 

slide: 
chihuahua with fawn dilution of dark haircoat - alopecic areas are all in 
darker fawn areas, the light points are normal. 
slide: dobe with total 
body alopecia except on his points. 
etiology: genetically mediated 
abnormality in melanin transfer to hair shaft
melanin clumping and 
cuticular abnormalities create weakness of the hair shafts, which then 
fracture, and fall out. highest frequency of this is in blue and fawn 
dobermans. blue min pin, blue dachshund, blue chow, blue poodle, dane, 
whippet, yorkie, chihuahua, fawn irish setter; also other pointed breeds.


dx: microscopic exam of plucked hairs often reveals large clumps of 
melanin resulting in fraying and fracturing of hair shafts. definitive dx 
if needed is by skin biopsy - sometimes helpful very early in a case. no 
effective therapy up til 2 yrs ago. we still say affected dogs should be 
culled from breeding programs. staph managed and treated; use benzoyl 
peroxide to flush blackeads from follicles and has some antistaph 
activity. however, synthetic retinoids - psoriatane - work well with this 
disase but financially unfeasible.

black hair follicle dysplasia: also 
familial, tends to occur in bi-tri colored dogs in area where black hair 
should be. also in solid breeds. mild scale and folliculitis may occur. 
bearded collies, basset, schipperke, other. 
slide: lhasa x papillon 
cross - black areas are totally bald. white areas are totally fine. 

slide: black lab trying to be a chocolate lab and hair is gone. severe 
total body thinning alopecia. he's fine - gets frequent secondary staph 
infections - gets a lot of benzoyl peroxide baths. 
etiology and 
pathogenesis same as color mutant alopecia. histology the same. 


follicular dysplasias: far murkier - non color linked abnormalities in 
hair development. follicles making abnormal hair. age of onset varies 
from 3 mos to several years, many seem to be acquired, not congenital. 
several syndromes described in various breeds. 

husky/malamute: loss of 
truncal guard hairs at 3-4 mos, spares head and limbs, reddish 
discoloration, abnormal texture

curly coated breeds: portugese water 
dog, water spaniel: progressive truncal alopecia starting 2 yrs, abnormal 
texture

others: airedale, boxer, etc.

dx/tx follicular dysplasia:

signalment, PE, signs
ddx: post-clipping alopecia (northern breeds - 
shaved for the summer - hair never grows back); pattern baldness (curly 
breeds). bx: distored follicles
cosmetic problem but synthetic retinoids 
have worked in some cases.

seasonal flank alopecia - we see this here.

clinical presentation: originally reported in boxer, schnauzer, eng 
bulldog. a cyclic, seasonal alopecia mainly over flanks/saddle region; 
usually either very darkly pigmented or hair grows back too fast to see 
it. unilateral or bilateral. most lose hair in fall, regrow in 
spring/summer. occurs in many breeds. some dogs lose hair in 
spring/summer, regrow in fall. may skip a year, progress to permanent 
alopecia, or never recur after first one or more episodes. 

etiology 
unknown - similar signs with many endocrinopathies, though, so look for 
hypothyroidism, hyperadrenocorticism, ovarian imbalance type I and II. 

hormone assays are normal in dogs with this disease. 

slide: young dog 
with what looks like seasonal flank alopecia; turned out to be sertoli 
cell tumor related, went away after castration.
some class this as a 
follicular dysplasia - usually will respond to retinoids - but maybe 
would have gone away anyway? however, there is a cheaper tx option. most 
plausible pathogenesis - something to do with pineal gland and melanin 
synthesis making hairs fracture. but why is flank? no clue, really. 
dx: 
history of cyclic recurrence. if first time, r/o hormone disorder. skin 
bx: characteristic atrophy of hair follicles with comedome production - 
witch's foot. 
tx:Psoriatane will work, but $$$$; melatonin working in 
many dogs.

pattern baldnesses - pinnal, ventral
this is really vexing. 
there is no tx. hey, Dr Morris doesn't have a tx for his, why should the 
dog. Propecia costs a lot and may not work that well b/c pattern baldness 
is more common in female dogs than males, so 5DHT may not be the cause. 
Rogaine causes necrosis of the right atrium in dogs if systemically 
absorbed. some people report response to melatonin. 
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