Download Equine Crusting Dermatosis

AAEP RESORT SYMPOSIUM / 2015
Equine Crusting Dermatosis
Anthony A. Yu DVM, MS, DACVD

Take Home Messages:
1) Equine crusting dermatoses can be either infectious or noninfectious. It behooves the referring veterinarian to rule-out
infectious causes before starting immunomodulatory therapy,
such as in the case of Trichophyton equinum that can cause
pemphigus-like lesions as a result of its exfoliative toxin.
2) Appropriate selection and length of therapy is key to
resolution of the crusting dermatoses. Hence identifying the
underlying etiology by combining clinical distribution pattern
and correct diagnostic procedures will result in a successful
therapeutic outcome.
3) It is not uncommon to identify concurrent etiologies when
addressing crusting dermatoses in horses.
Author’s address—1460 Gordon Street South, Guelph, ON
Canada N1G 4W4; e-mail: [email protected].
I. EQUINE CRUSTING DERMATOSIS INFECTIOUS
Pyoderma (Bacterial Skin Infections)
Bacterial folliculitis (superficial pyoderma) is usually caused
by a coagulase positive Staphylococcus species. Both S.
aureus and S. intermedius have been isolated.1,2 In one study, S
aureus accounted for twice as many isolates as S intermedius;
the same study isolated some strains of S hyicus as well.3
Interestingly, in another study, lysozymes from equine
neutrophils were only slightly bactericidal for S. aureus.4
Many isolates are resistant to penicillin G.3 Occurrence of
pyoderma has been linked to poor nutrition and husbandry in
some cases.5
Clinical signs of staphylococcal pyoderma are most often
crusts, usually in a circular pattern suggestive of
dermatophytosis (this may be the reason that equine pyoderma
is under-diagnosed), epidermal collarettes (circular skin lesions
with an exfoliative border as seen in dogs with superficial
pyoderma) or encrusted papules similar to the miliary
dermatitis reaction pattern in cats.6, 6a These infections tend to
be variable in their intensity of pruritus. Histology usually
shows folliculitis and/or furunculosis, but bacterial colonies are
not always seen. A truncal form of bacterial folliculitis
(contagious acne, contagious pustular dermatitis, Canadian
horsepox) is often associated with poor grooming,trauma from
tack and saddle, warm wet weather and heavy work. It is
painful and interferes with working and riding. It is usually
caused by a coagulase positive Staphylococcus species (but
may also be caused by Corynebacterium pseudotuberculosis.7
This organism is more commonly a cause of deep pyoderma
(as discussed below). In horses, folliculitis often develops in
the saddle and lumbar region, particularly in the summer. The
affected area initially may be swollen and very sensitive; this
is followed by formation of follicular papules and pustules.
These may become confluent or rupture, forming plaques and
crusts. Deep pyoderma followed by ulceration may develop
over large areas of the body, especially on the neck, sides of
the thorax, inner surface of the thighs or on the prepuce.
A pastern bacterial infection (pastern folliculitis) is often seen.
Again, the causative agent is usually a coagulase positive
Staphylococcus species. As with most “primary pyodermas”,
the mechanism(s) whereby the organism gains its foothold is
unknown (not contagion, not poor sanitary conditions). The
lesions are usually limited to the posterior aspect of the pastern
and fetlock regions; one or more limbs may be involved. The
initial lesions consist of papules and pustules. If left untreated,
the lesions coalesce and may produce large areas of ulceration
and suppuration, which may be quite painful. The disease is
usually not associated with systemic signs and the general
health of the horse is not affected.
A relatively uncommon nodular disease termed
‘botryomycosis’ mimics actinomycosis or a deep fungal
infection but is most often caused by Staphylococcus species in
the horse. These may require surgical excision as well as longterm antibiotics.
Public Health Considerations – Staphylococcus spp
In a 2000 study, methicillin-resistant, coagulase-negative
staphyloccal species were cultured from healthy horses in
Japan; the authors concluded, “These organisms must be
considered a potential threat to horses and veterinarians who
care for them.”8 In a 2006 study from the Netherlands,
methicillin-resistant coagulase negative staphylococci were
AAEP RESORT SYMPOSIUM / 2015
found frequently.9 The organism was usually Staphylococcus
sciuri, as opposed to S. epidermidis, which was found in the
humans in close contact with these horses. No methicillinresistant Staphylococcus aureus (MRSA) was found in healthy
horses.
In contrast, a single strain of MRSA was isolated from both
humans (13%) and horses (4.7%) on horse farms in Canada and
New York state.10 In looking at horses admitted to a university
teaching hospital (Ontario Veterinary College), MRSA was
isolated from 120 (5.3%) of 2,283 horses. Of these 120 horses,
50.8% were positive at the time of admission, and clinical
infections attributable to MRSA were present or developed in
14 horses. Horses colonized at admission were more likely to
develop clinical MRSA infection. Administration of ceftiofur
or aminoglycosides during hospitalization was the only risk
factor associated with nosocomial MRSA colonization.
Another strain of MRSA was isolated from a small number of
horses at the Veterinary University, Vienna, Austria.11
Of most concern is the finding of humans reporting skin lesions
following contact with a community MRSA-positive affected
foal, despite short-term contact with standard protective
barriers. The isolates from the foal were indistinguishable from
the ones from the humans.12
The antibiotic usually used for many bacterial skin infections
in the horse is trimethoprim sulfa per os (15-30 mg/kg q12h for
2-6 weeks, longer for deep infections).6 Interestingly, dosing
intervals for intravenous administration of trimethoprimsulfamethoxazole in horses may not be appropriate for use in
donkeys or mules. Donkeys eliminate the drugs rapidly,
compared with horses.13 In cases of Staphylococcus sp
resistance to TMS, enrofloxacin may be used. The dose is 7.5
mg/kg PO once daily or 5 mg/kg IV once daily. Use of
enrofloxacin in young horses (less than 2 years old) should be
avoided, due to concerns of damage to the articular cartilage.14
A recent report of the usage of an oral gel formulation of
enrofloxacin 100mg/ml of gel) showed good clinical efficacy
for infections in several organs; however, almost one-third of
the horses had some diarrhea, and 10% had oral lesions.15 The
authors felt that this latter side effect could be overcome by
following administration with a tap water rinse of the oral
cavity. Interestingly, enrofloxacin binds to melanin in equine
hair, although the clinical implication is unknown.16 In one
report of 15 horses, vancomycin was used, alone or in
combination with an aminoglycoside, to treat MRSA and
enterococcal infections. The average vancomycin dosage was
7.5 mg/kg q8h given IV over 30 minutes. The antibiotic, alone
or in combination with an aminoglycoside, was safe and
effective. Because of the problems with emerging resistance,
the authors recommended vancomycin use in horses be limited
to cases in which culture and susceptibility indicate
effectiveness and no reasonable alternative treatment.17
For localized lesions, mupirocin ointment or silver sulfadiazine
cream may be effective. Shampoo ingredients including
benzoyl peroxide, accelerated hydrogen peroxide, ethyl lactate,
miconazole or chlorhexidine are helpful.
Dermatophilosis is caused by an actinomycete bacteria,
Dermatophilus congolensis. Three conditions must be present
for Dermatophilus to manifest itself: a carrier animal, moisture
and skin abrasions. Chronically affected animals are the
primary source of infection; however, they only become a
serious source of infection when the lesions are moistened, this
results in the release of zoospores, the infective stage of the
organism. Mechanical transmission of the disease occurs by
both biting and nonbiting flies, and possibly fomites. Because
normal healthy skin is quite impervious to infection with D.
congolensis, some predisposing factor that results in decreased
resistance of the skin is necessary for infection to occur,
prolonged wetting of the skin being one of the most important.
The disease is usually seen during the fall and winter months,
with the dorsal surface of the animal most commonly affected.
Occasionally the lesions involve the lower extremities when
animals are kept in wet pastures ("dew poisoning"), or if horses
are left in the stall while the stall is cleaned with high-pressure
water hoses. In the early stages of the disease, the lesions can
be felt more easily than they can be seen. Thick crusts can be
palpated under the hair coat. Removing the crusts and attached
hair exposes a pink, moist skin surface, with both the removed
hair and the exposed skin assuming the shape of a “paintbrush”.
The under surface of the crusts are usually concave with the
roots of the hairs protruding.
Diagnosis is by demonstrating the “railroad track” cocci on
impression smears: a portion of one of the crusts should be
minced and mixed with a few drops of sterile water on a glass
slide, gram stained and examined microscopically.
Alternatively, bacterial culture or histopathology may be
utilized for diagnosis. A thick crust composed of alternating
layers of parakeratotic stratum corneum, dried serum, and
degenerating neutrophils is the most characteristic change. A
superficial folliculitis may be a prominent feature of the
disease.1 In sections stained with gram stain, the branching,
filamentous organisms can be observed in the crusts and in the
follicles.
Treatment is removal from the wet environment, removal of
crusts (with care, as these may be painful), washing with
iodophors or lime sulfur, and antibiotics (penicillin: 22,000
mg/kg procaine pen G intramuscularly twice daily or
trimethoprim sulfa orally: as above for staphylococcal
pyoderma) for 7 days.18 As the crusts are important in
contagion, these should be disposed of rather than brushed on
to the ground.
Dermatophytes and Malassezia
Dermatophyte infections, like pyoderma, can be variably
pruritic. The most common equine dermatophyte species
isolated from horses are Trichophyton equinum, M. equinum,
T. mentagrophytes and T. verrucosum.1,3,19 Tack (bridles,
halters, saddle blankets) often act as fomites. The lesions
usually appear first on the axillary/girth area and may spread
over the trunk, rump, neck, head and limbs. Initial lesions may
be urticarial in nature progressing to multiple focal sharplydemarcated scaling, crusting areas. Lesions may be superficial
AAEP RESORT SYMPOSIUM / 2015
or deep. Superficial infections are more common and are
manifested by the development of thick crusts, or more
generally a diffuse moth-eaten appearance with desquamation
and alopecia. Less commonly, deeper structures are infected
through the hair follicles causing small foci of inflammation
and suppuration. A small crust forms over the follicle and the
hair is lost but extensive alopecia and crust formation do not
occur.
Diagnosis is by fungal culture; biopsy is less reliable
(Trichophyton species may cause acantholysis, mimicking
pemphigus on histopathology).20 Hair is the specimen most
commonly collected for the isolation of dermatophytes. Using
forceps, hairs should be selected that appear stubbled and
broken, especially at the advancing periphery of an active, nonmedicated lesion. In addition, surface keratin may be gathered
by forceps or skin scrapings from similar areas and inoculated
onto the culture medium. The hair and surface keratin of large
animals have large numbers of saprophytic fungi and bacteria.
Hence, it is recommended to cleanse the skin prior to taking
samples for culture. This may be done by gently cleansing the
area to be sampled with soap and water, allowing it to air dry
before acquiring samples..
Sabouraud’s dextrose agar has been used traditionally in
veterinary mycology for isolation of fungi; however, other
media are available with bacterial and fungal inhibitors, such
as Dermatophyte Test Medium (DTM). DTM is essentially
Sabouraud’s dextrose agar containing cycloheximide,
gentamicin, and chlortetracycline as antifungal and
antibacterial agents and to which the pH indicator phenol red
has been added. Dermatophytes utilize protein in the medium
first, with alkaline metabolites turning the medium red. Most
other fungi utilize carbohydrate first, giving off acid
metabolites, which do not produce a red color change. These
saprophytic fungi will later use the protein in the medium,
resulting in a red color change. However, this usually occurs
only after a prolonged incubation (10 to 14 days or more).
Consequently, DTM cultures should be examined daily for the
first ten days. Some Aspergillus species and others cause a red
color change in DTM, so microscopic examination is essential
to avoid an erroneous presumptive diagnosis. It has been
recommended that one to two drops of a sterile injectable B
complex vitamin preparation be added to culture plates when
culturing horses, as one strain of T. equinum (T. equinum var.
equinum) has a unique niacin requirement. However, the
author does not routinely do this. Skin scrapings and hair
should be inoculated onto Sabouraud’s dextrose agar and/or
DTM and incubated at 30C with 30% humidity. A pan of
water in the incubator will usually provide enough humidity.
Cultures should be checked every day for growth. DTM may
be incubated for 21 days, but cultures on Sabouraud’s agar
should be allowed 30 days to develop. The author has usually
used split culture plates with DTM on one side and rapid
sporulating media on the other, with a well of water in the
center. It is routinely incubated at room temperature. T.
verrucosum has been reported not to grow on DTM.21
Topical treatment alone is often curative. While 50% captan (2
tablespoons of the powder in 1 gallon of water) has been touted
in the past, and while certainly safe for tack, its effectiveness
has been questioned. Lime sulfur diluted 1 cup to 1 gallon of
water, or bleach 1:10 with water, are both effective, but messy
and odiferous. Miconazole or ketoconazole veterinary
shampoos are becoming more widely used, and may be as
effective. In Europe and Canada, an enilconazole rinse is highly
effective.
Systemic treatment is occasionally needed. Griseofulvin’s
efficacy in horses (as well as an effective dose) has not been
thoroughly researched. However, a dosage of 100 mg/kg daily
for 7-10 days has been advocated. Griseofulvin is a teratogen,
and should not be used in pregnant mares. Alternatively, 20%
sodium iodide (NaI) may be given IV (250 ml/500 kg horse
every 7 days, 1 to 2 times). This also is contraindicated in
pregnant mares as it may cause abortion or congenital
hypothyroidism. While medications such as itaconazole and
fluconazole have been used to treat horses with systemic
mycotic infections, there have not been any studies on their
effectiveness in dermatophytosis. However, their safety record
in horses in the face of the doses used (5 mg/kg q 24h) are
encouraging.22-24 Vaccination against T. equinum may reduce
the incidence of new infections and protect a high percentage
(> 80%) of vaccinates from infection. This data is based on
results with an inactivated vaccine containing both conidia and
mycelial elements.25
The exact species of Malassezia growing on horses’ skin is just
beginning to be investigated.26 In one study, the Malassezia sp.
isolated were identified as M. furfur, M. slooffiae, M. obtusa,
M. globosa and M. restricta.27The author has examined several
mares with a Malassezia infection between their mammary
glands, which was intensely pruritic. The mares rubbed their
tail and ventral abdomen. Physical examination showed a dry,
greasy-to-the-touch exudate. Cytology of the exudate showed
numerous yeast organisms, which were identified on culture as
Malassezia species.
Treatment with a topical 2%
miconazole/chlorhexidine shampoo was curative. The author is
aware of other, similar cases. However, healthy non-pruritic
mares may also have large numbers of yeasts in the intramammary area.28
REFERENCES
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4.
Scott DW, Manning TO: Equine folliculitis and
furunculosis. Equine Practice 1980; 2(6):11-32.
Shimizu A, Kawano J, Ozaki J, et al. Characteristics of
Staphylococcus aureus isolated from lesions of horses. J
Vet Med Sci 1991; 53:601-606.
Chiers K, Decostere A, Devriese et al. Bacteriological
and mycological findings, and in vitro antibiotic
sensitivity of pathogenic staphylococci in equine skin
infections. Vet Rec 2003; 152:138-141.
Pellegrini A Waiblinger S, Von Fellenberg R.
Purification of equine neutrophil lysozyme and its
antibacterial activity against gram-positive and gramnegative bacteria. Vet Res Commun 1991; 15:427-435.
AAEP RESORT SYMPOSIUM / 2015
5.
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Inokuma H, Kanaya N, Fujii K, et. al. Equine pyoderma
associated with malnutrition and unhygienic conditions
due to neglect in a herd. J Vet Med Sci 2003;65:527-529.
White SD. Equine bacterial and fungal skin diseases: a
diagnostic and therapeutic update. Clin Tech Equine
Pract, 2005; 4:302-310.
Weese, JS, Yu AA. Infectious Folliculitis and
Dermatophytosis. Vet Clin Equine. 2013:29(3):559-576
Heffner KA, White SD, Frevert CW, et al.
Corynebacterium folliculitis in a horse. J Am Vet Med
Assoc 1988;193: 89-90.
Yasuda R, Kawano J, Onda H, et al. Methicillin-resistant
coagulase-negative staphylococci isolated from healthy
horses in Japan. Am J Vet Res 2000; 61:1451-1455.
Busscher JF, van Duijkeren E, Sloet van OldruitenborghOosterbaan MM. The prevalence of methicillin-resistant
staphylococci in healthy horses in the Netherlands. Vet
Microbiol 2006;113:131-136.
Weese JS, Rousseau J, Traub-Dargatz JL, et al.
Community-associated methicillin-resistant
Staphylococcus aureus in horses and humans who work
with horses. J Am Vet Med Assoc 2005;226:580-583.
Cuny C, Kuemmerle J, Stanek C, et al. Emergence of
MRSA infections in horses in a veterinary hospital: strain
characterisation and comparison with MRSA from
humans. Euro Surveill 2006;11(1): 44-47
Weese JS, Caldwell F, Willey BM, et al An outbreak of
methicillin-resistant Staphylococcus aureus skin
infections resulting from horse to human transmission in
a veterinary hospital. Vet Microbiol 2006;114(1):160–164
Peck KE, Matthews NS, Taylor TS, et al.
Pharmacokinetics of sulfamethoxazole and trimethoprim
in donkeys, mules, and horses. Am J Vet Res 2002;
63:349-353.
Egerbacher M, Edinger J, Tschulenk W. Effects of
enrofloxacin and ciprofloxacin hydrochloride on canine
and equine chondrocytes in culture. Am J Vet Res 2001;
62:704-708.
Epstein K, Cohen N, Boothe D, et al. Pharmacokinetics,
stability, and retrospective analysis of use of an oral gel
formulation of the bovine injectable enrofloxacin in
horses. Vet Therapeutics 2004; 5:155-167.
Dunnett M, Richardson DW, Lees P. Detection of
enrofloxacin and its metabolite ciprofloxacin in equine
hair. Res Vet Sci 2004; 77:143-151.
James A. Orsini, Corinna Snooks-Parsons, Lynne Stine,
et al. Vancomycin for the treatment of methicillinresistant staphylococcal and enterococcal infections in 15
horses. Can J Vet Res 2005; 69: 278–286.
Outerbridge CA, Ihrke PJ: Folliculitis: Staphylococcal
pyoderma, dermatophilosis, dermatophytosis. In
Robinson NE (ed): Current Therapy in Equine Medicine
5. St. Louis: Saunders, 2003;197-200.
Kane J, Padhye AA, Ajello L. Microsporum equinum in
North America. J Clin Microbiol. 1982;16:943-947.
Scott DW. Marked acantholysis associated with
dermatophytosis due to Trichophyton equinum in two
horses. Vet Dermatol 1994; 5:105-110.
Scott DW, Miller WH. Equine dermatology. St. Louis:
Saunders, 2003; 96.
22. Foley JP, Legendre AM. Treatment of coccidioidomycosis osteomyelitis with itraconazole in a horse. A
brief report. J Vet Intern Med 1992;6:333-334.
23. Korenek NL, Legendre AM, Andrews FM, et al.
Treatment of mycotic rhinitis with itraconazole in three
horses. J Vet Intern Med 1994;8:224-227.
24. Taintor J, Crowe C, Hancock S, et al. Treatment of
conidiobolomycosis with fluconazole in two pregnant
mares. J Vet Intern Med 2004;18:363-364.
25. Pier AC, Zancanella PJ: Immunization of horses against
dermatophytosis caused by Trichophyton equinum.
Equine Pract 1993;15(8):23-27.
26. Nell A, James SA, Bond CJ, et al. Identification and
distribution of a novel Malassezia species yeast on
normal equine skin. Vet Rec. 2002; 150:395-398.
27. Crespo MJ, Abarca ML, Cabanes FJ. Occurrence of
Malassezia spp. in horses and domestic ruminants.
Mycoses 2002; 45:333-337.
28. White SD, Vandenabeele SIJ, Drazenovich N, Foley J.
Malassezia species isolated from the intermammary and
preputial fossa areas of horses. J Vet Int Med,
2006;20(2):395–398
II. EQUINE CRUSTING DERMATOSES
NON-INFECTIOUS
Photosensitization Syndromes
Melanin, found in pigmented skin, absorbs and scatters light
(<300-1200 nm). Photosensitization develops when
photodynamic agents are activated by ultraviolet light (200400 nm; typically UVA = 320-400 nm) as they circulate
through superficial vessels of non-pigmented skin and results
in local tissue injury from production of oxygen free radicals.
Subsequently, damage to cell membranes and DNA ensues
leading to the release and production of additional
inflammatory pathways, resulting in erythema and pruritus,
progressing to edema, serum exudation, crusting, scaling, and
fissure formation.1
Pathomechanisms
Photosensitization syndromes have been classified as either
primary, where the patient ingests the photodynamic agent or
secondary, where the photoactivated by-products of normal
metabolism are not removed from the bloodstream due to an
underlying hepatopathy.2,3
a)
Primary photosensitization disorders are either welldefined such as with Hypericum perforatum (St. John’s
wort) that contains hypericin, or speculative, as in the case
of alfalfa hay where neither the photodynamic agent nor
the characteristics of the alfalfa (e.g., cutting, stage of
maturation) are well understood. Fortunately, as most of
the causative plants are unpalatable, outbreaks of primary
photosensitization are rare (see below). Idiosyncratic
reactions to medications (e.g., phenothiazines, thiazides,
potentiated sulfonamides, tetracyclines) have also been
implicated as a cause of primary photosensitization.
AAEP RESORT SYMPOSIUM / 2015
such as chronic weight loss, icterus, and neurologic signs.
b) Secondary photosensitization results from accumulation
of phylloerythrin, a photodynamic metabolite of
chlorophyll.2,3 Normally, phylloerythrins are absorbed
into the portal circulation and excreted in the bile. In the
face of hepatic disease, the excretion is compromised,
and elevated concentrations of the photodynamic agent
remain in circulation, make their way to the skin and
result in photosensitization reactions. Ingestion of plants
containing pyrrolizidine alkaloids or exposure to
chemical agents (e.g., carbon tetrachloride) may induce
hepatic injury and produce secondary photosensitization.
Grazing pastures containing alsike and red clover is
probably the most common cause of secondary
photosensitization of horses, followed by ingestion of
tansy ragwort.4,5 Alsike (Trifolium hybridum) and red
clover (Trifolium pratense) are often found in grass seed
marketed as a pasture mix. Most cases of
photosensitization from ingesting clover are reported
from late spring through late fall in years when there has
been a particularly wet spring or heavy late summer rains
allowing abundant clover growth.4 As little as 20% of
alsike clover in pasture or when fed as hay has been
associated with signs of poisoning as early as 2-4 weeks
after initial exposure. It is unclear as to whether the
entire alsike or red clover plant, some component of the
plants, a toxic metabolite produced by the plants, or a
fungal toxin present on the plants is responsible for the
disease.6 The presence and consumption of the flower
appears to be most often associated with the development
of signs. Cymodothea trifolii, a fastidious fungus that
causes “black blotch” or “sooty blotch” disease of clover
and alfalfa, has also been linked to development of liver
disease in horses.4
Tansy or common ragwort, Senecio jacobaea, is a weed
of the sunflower family that contains pyrrolizidine
alkaloids. In North America, ragwort has become a
problem weed in pastures, rangelands, and clear-cuts on
both the east and west coasts, particularly in Oregon.5
Ragwort can be lethal when animals (especially cattle and
horses) ingest 3-7% of their body weight in ragwort over
one to two days. However, acute poisonings seldom
occur because the low palatability of the plant usually
results in only small quantities being consumed per day.
Chronic ingestion leads to progressive loss of hepatic
function manifested outward by chronic weight loss and
secondary photosensitization.
Clinical Signs
There is no breed, sex, or age predilection for the problem.
Lesions tend to be limited to the hairless, white or lightly
pigmented areas of skin. Erythema, swelling and pain often
represent acute stages of the condition. Lesions may then
evolve to serum exudation, thickening, and fissuring over
several weeks. In severe cases, necrosis and sloughing are
noted. Systemically, patients affected due to secondary
photosensitization may present with other signs of hepatopathy
Diagnosis
A history of plant, drug or toxin exposure is clearly important
in the evaluation of horses presented with photosensitization.
As owners are often unaware of exposure, direct inspection of
the farm, hay, and pasture by the referring veterinarian and/or
extension agent may be warranted.
When examining a horse with suspected photosensitization, it
is important to remember that non-pigmented equine skin can
also suffer sunburn. Detection of icterus on physical
examination and increased serum hepatic enzyme activities
(e.g. -glutamyltransferase, alkaline phosphatase, sorbitol
dehydrogenase) especially in several horses within a group is a
key characteristic of secondary photosensitization.
Histopathologic examination of hepatic biopsy from clover
toxicity samples reveals bile duct proliferation and perilobular,
centrilobular, and periportal fibrosis. If fibrosis is limited to
centrilobular regions with the absence of “bridging” fibrosis
(extending from the centrolobular to periportal regions) the
prognosis is usually favorable and horses can fully recover
from clover toxicity.6 In contrast, with ragwort or other
pyrrolizidine alkaloid toxicity, fibrosis is typically much more
extensive and megalocytosis is a characteristic histopathologic
finding. Thus, it should not be surprising that the prognosis for
chronic ragwort toxicity is generally guarded to poor with
humane euthanasia required for most affected horses.
Treatment
Identifying and avoiding the offending photosensitizing agent
is key to a favorable prognosis. Moving pastures for at least 2
weeks will help rule-in a photosensitization disorder if a
significant improvement is noted followed by a relapse when
challenged. Regardless of the cause, treatment of
photosensitization is supportive, primarily consisting of topical
wound care.
Occasionally, systemic anti-inflammatory
medications (Prednisolone at 1 mg/kg/d per os for 7 days, then
0.5 mg/kg/d for 7 days) and antimicrobial agents may be
required. Prevention of further skin injury is accomplished by
limiting exposure to ultraviolet light for a minimum of 14 days
by stabling horses during the day (affected horses can be turned
out at night), covering affected areas using UV protectant
material (blankets/face mask/leg bandages), or applying sun
block to non-pigmented skin.2,3
Pastern Leukocytoclastic Vasculitis (PLV)
PLV is also a photo-aggravated condition, but is limited to the
pastern region. This disease is poorly understood and affects
mature horses. It is unique to the horse and often, but not
exclusively, targets unpigmented distal extremities.7,8 PLV is
believed to be due to immune complex deposition on the
vasculature of the distal limbs, triggering a vasculitis and
resulting in well-demarcated circular, erythematous, exudative
lesions with tightly adherent crusts.7
The prevalence of
clinical signs in the summer suggests that it is a
photoaggravated condition. The medial and lateral aspects of
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the pasterns are the areas most commonly affected. Lesions
appear painful rather than pruritic. Limb edema and lameness
are common sequelae. Chronic cases may develop a rough or
warty surface.7 Dermatopathologic findings of leukocytoclastic vasculitis include vessel wall necrosis and
thrombosis involving superficial small dermal vessels.
Treatment of this condition is multimodal and incorporates
high dose glucocorticoids (prednisolone at l mg/kg BID or
dexamethasone at 0.1 mg/kg q 24 h for 2 weeks, tapering over
4-12 weeks), pentoxifylline (8-10 mg/kg BID), reduced UV
light exposure and topical corticosteroids. Antibiotics are often
not required unless notable purulent discharge is detected.
Prognosis is good to fair for complete recovery with
elimination of medications. Some patients require lifelong
pentoxifylline treatment once daily to every other day.
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
Scott DW, Miller WH. Photosensitization, in Equine
Dermatology, Philadelphia, PA, WB Saunders,
2003;620-621.
Woods PR. Internal diseases that have skin lesions.
Vet Clin North Amer: Equine Practice 1995;11:111126.
Boord M. Photosensitivity, in Robinson NE (ed):
Current Therapy in Equine Medicine, 5th edition.
Philadelphia, PA, WB Saunders, 2002;174-176.
Nation NP. Hepatic disease in Alberta horses: A
retrospective study of alsike clover poisoning (19731988). Can Vet J 1991;32:602-607.
Mendel VE, Witt MR, Gitchell BS, et al. Pyrrolizidine
alkaloid-induced liver disease in horses: An early
diagnosis. Am J Vet Res 1988;49:572-578.
Petersen AD, Schott HC. Cutaneous markers of
disorders affecting adult horses. Clin Tech Equine
Pract 2005;4:324-338.
Standard,
AA.
Miscellaneous.
Veterinary
Dermatology 2000;11(3):217-223.
Pascoe RRR, Knottenbelt DC. Immune mediated
diseases, in Pascoe (ed) Manual of Equine
Dermatology. London, WB Saunders, 1999;165-166.
III. PEMPHIGUS
Pemphigus foliaceus is the most common autoimmune skin
disease in the horse and was first described in this species in
1981.1,1a,2 Several forms of pemphigus exist including
pemphigus foliaceus, pemphigus vulgaris (very rare), druginduced pemphigus, and paraneoplastic pemphigus. The most
commonly reported form is that of pemphigus foliaceus.
Pemphigus foliaceus in humans is a result of the production of
autoantibodies directed against cell adhesion proteins, in
particular the desmosomal antigens (desmoglein 1 (DSG1) in
pemphigus foliaceus; desmoglein 3 in pemphigus vulgaris), of
the stratified squamous epithelium. The antibody-antigen
complex, through multiple pathways, then incites
acantholysis.3 A similar pathway is hypothesized for the dog
and horse based on the detection of DSG1 via immunoblotting/
immunoprecipitation studies.4,5 Several trigger factors have
been proposed including drugs, systemic disease, neoplasia,
stressful situations, and lastly allergies (foods, inhalants,
insects) based on the presence of case clusters and
seasonality.1,1a,6
Signalment
Pemphigus presents in both adult horses (5 years of age or
older) and in foals (less than one year of age).7,8 This age
dichotomy may not be obvious in all populations.6 Younger
horses often carry a better prognosis and potential for
spontaneous remission without relapses. Of the specific horse
breeds, Appaloosas, Quarter Horses and Thoroughbreds appear
to be at greater risk although this may have some geographic
variability.1,6,7 At this time, there does not appear to be any
evidence of sex predilection. Pemphigus has been known to
have a waxing and waning course, and recently there may also
be a seasonal incidence of the condition potentially due to
allergen load (pollens, insects) and/or the increased use of
preventative medications (dewormers, vaccines, supplements,
etc.)6,9
Clinical Signs
Classic clinical findings of vesicles and pustules are rarely
noted in the horse, as lesions of pemphigus progress rapidly to
crusts, exfoliation, erosions, alopecia, and scaling. In fact,
transient, persistent or recurrent urticaria may precede actual
crusts.1,1a Pruritus, pain, and edema resulting in a stiff-gaited
lameness are variable. Lesions tend to begin on the face or
limbs and spread to the rest of the body within days to weeks.
A localized form restricted to the coronary bands can also be
seen. Mucosal lesions are extremely rare. Although internal
organs are not involved, systemic signs including depression,
poor appetite, weight loss, fever, and lethargy are often noted.
CBC and serum chemistry profile changes may include
anemia, leukocytosis, neutrophilia, hyperglobulinemia, and
hypoalbuminemia.
Differential Diagnosis
Differential
diagnoses
include
dermatophilosis,
dermatophytosis, Staphylococcal folliculitis, systemic
granulomatous disease/equine sarcoidosis, multisystemic
exfoliative eosinophilic dermatitis and stomatitis, drug
eruption, external parasite hypersensitivity, and keratinization
disorders.
Diagnosis
Diagnosis is based on history, clinical findings, skin cytology,
and dermatohistopathologic findings. Cytologic sampling is
ideally performed from intact pustules; however, impression
smears from both the skin and under surface of a teased crust
will often be rewarding. Single or rafts of acantholytic cells,
that are 10-20 times the size of surrounding neutrophils, can be
found on cytologic evaluation using a Diff-Quik stain.
Characteristically, there is little to no evidence of bacteria, and,
neutrophils/eosinophils have a healthy appearance (no
AAEP RESORT SYMPOSIUM / 2015
evidence of toxic changes). Based on these findings, multiple
skin biopsies should be taken to confirm the diagnosis. Primary
vesicles or pustules if present are ideal, with crusted sites being
the next best choice for multiple biopsies. Surgical preparation
of biopsy sites is NOT recommended, as the crusts may contain
the
acantholytic
cells
necessary
for
diagnosis.
Dermatopathologic findings include subcorneal and/or
intraepidermal pustules, spanning multiple hair follicles,
associated with marked acantholysis, neutrophils and
occasionally eosinophils. As Trichophyton equinum may
mimic the clinical and histological appearance of pemphigus
(crusts and acantholytic cells), fungal stains should be
performed on all biopsies suggestive of pemphigus.10
Immunohistochemical staining has taken precedence over
immunofluorescence due to the ability of the former method to
detect autoantibodies within formalin-fixed tissues (e.g.
immunoperoxidase) rather than the need for special handling
of skin samples for direct immunofluorescence.1,1a The use of
immunoprecipitation has been reported in one horse with
paraneoplastic pemphigus.5 This technology is currently
available for use in human dermatology to confirm the
diagnosis and act as a prognostic tool when evaluating response
to therapy. Species-specific tests are being investigated for the
dog and hopefully for the horse in the near future.4
Monitor CBC for bone marrow suppression
(thrombocytopenia),
drug
reaction
(eosinophilia)
and
glomerulonephritis
(proteinuria)
Eliminate inciting factor (i.e. tumor extirpation in
paraneoplastic pemphigus)
o
o
Prognosis
Management in horses may take weeks to months to control
and is not without complications including hepatopathies and
reported laminitis when using glucocorticoids or bone marrow
suppression and adverse drug reactions with adjunctive
immunosuppressive therapy.12,13 Typically, an initial response
is noted within 7-14 days, then medication can be tapered 20%
every 1-2 weeks based on individual responses. Young horses
have an excellent prognosis for remission and little chance of
relapse, while mature horses tend to have a less favorable
prognosis (46%) and typically lifelong therapy is necessary for
control of the condition.1,1a,6,7 If a trigger factor can be
identified and eliminated, therapy should be tapered and
potentially discontinued.
REFERENCES
Treatment
Before starting therapy, baseline and follow-up bloodwork
(complete blood count, biochemical profile) are recommended
to monitor the effect of the immunosuppressive regimen.
Multimodal therapy is often necessary for the treatment of
pemphigus in horses and includes the following:
o
o
o
o
o
o
o
Essential fatty acids
Vitamin E – 13 IU/kg/day
Decreased exposure to sun/photoaggravation
High doses of corticosteroids
o Dexamethasone at an induction dose of 0.02
- 0.1 mg/kg/day PO or IV/IM for 7-10 days,
then tapering to 0.01 - 0.02 mg/kg q 48-72
hours
o Prednisolone at 1.5 - 2.5 mg/kg/day for a 710 day period, then taper over several weeks
to a maintenance dose of 0.5-1 mg/kg q 48
hours. Preferentially used if low albumin6
Pentoxifylline 8-10 mg/kg 2-3X/day. Taper once
steroids have been minimized.
Azathioprine at 2-3 mg/kg PO daily for 3-4 weeks,
then taper to every other day.
Low (1-7%)
bioavailability therefore can be costly to maintain11,12
Injectable gold salts –
o Aurothioglucose - no longer available.
o Aurothiomalate
o Test dosages of 20 mg and 50 mg at weekly
intervals
o If no abnormal reactions, 1 mg/kg IM weekly
for 6-12 weeks, then taper to every 2-3 week
injections, and finally weaned off entirely
o Often used in conjunction with steroids
during the initial induction phase
1.
1a.
2.
3.
4.
5.
6.
7.
8.
9.
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Johnson ME, Scott DW, Manning TO. A case of
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Yager J, eds. Veterinary Dermatol 2000;11:172175.
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drug-related pemphigus foliaceus in four dogs.
Vet Dermatol 2002;13:195-202.
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10.
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Scott DW. Marked acantholysis associated with
dermatophytosis due to Trichophyton equinum in
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