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242 Vol. 24, No.

3 March 2002

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Common Equine
Skin Tumors
Mississippi State University
■ Small equine sarcoids should be Jenny M. Foy, DVM
monitored carefully; larger Ann M. Rashmir-Raven, DVM, MS, DACVS
tumors and those undergoing Michael K. Brashier, DVM, MS, DACVIM
morphologic changes should be
treated aggressively.
ABSTRACT: Sarcoids, squamous cell carcinomas (SCCs), and melanomas are three of the
most common dermal neoplasms that occur in horses. Sarcoids are the most common and
■ Squamous cell carcinomas can frequently affect the legs, ventral trunk, and head. They are believed to be the result of infec-
be locally invasive and tion with bovine papillomavirus or a similar agent. SCCs are the second most common equine
metastatic. skin tumor and commonly affect the eye, adnexa, and external genitalia. Ultraviolet radiation
contributes to the occurrence of this tumor, affecting nonpigmented, hairless areas of the
■ Melanomas should be carefully body and predominantly occurring in paints, Appaloosas, and albinos. Equine melanomas are
monitored even though they are the most common skin tumor in horses with a white or gray coat. They are believed to be the
slow-growing and nonmetastatic. result of abnormalities in melanin metabolism. Many equine skin tumors respond to appropri-
ate therapy, which may include surgical debridement or excision coupled with the use of select
chemotherapeutic agents, immunostimulants, radiation, brachytherapy, and cryotherapy. Early
recognition and treatment will produce the most satisfactory outcome.

ermal neoplasms are the most common equine tumors, of which sar-
coids, melanomas, and squamous cell carcinomas (SCCs) are the most
common. The causes of cellular transformation are multifactorial (e.g.,
viral infections, trauma, inflammation, ultraviolet radiation). Sarcoids are the
most common of the three tumors. They are nonmetastatic but frequently recur
locally. They occasionally undergo locally aggressive growth that can make it
hard to differentiate them from SCC, proliferative granulation tissue, cutaneous
habronemiasis, and other conditions. SCC is the second most common tumor,
generally occurring on nonpigmented areas of the skin and mucous membranes.
Metastasis can occur, making early diagnosis important. Melanomas occur most
commonly in gray-coated horses. Although they are usually benign, malignant
transformation can occur. With early diagnosis and treatment, equine skin
tumors can often be treated or managed successfully.

Sarcoids are the most common skin tumors in horses. They are locally inva-
sive, nonmetastatic, fibroblastic tumors composed mainly of connective tissue.
Sarcoids rarely regress spontaneously.1–3 These tumors usually affect horses 1 to 6
years of age, although they have been reported in horses older than 15 years of
age. Sarcoids can occur on any part of the body, either singly or in clusters. The
ventral abdomen, limbs, and head, especially around the eyes, pinnae, and com-
Compendium March 2002 Equine Skin Tumors 243

Figure 2—Nodular sarcoid in the left inguinal region.

sarcoids, and a familial tendency has been identified.

Quarter horses have been shown to be at twice the risk of
developing sarcoids as thoroughbreds. Appaloosas and
Arabians are also at increased risk, while standardbreds
Figure 1—Verrucous (warty) sarcoid on the left pinna. appear to have a lower risk than all other breeds.4,7,8

Clinical Presentation
missures of the lips, are most commonly affected. In Sarcoid tumors generally appear with linear or focal
northern climates, lesions occur predominantly on the dermal thickening that has a pale color and a firm tex-
head and abdomen. In warmer climates, the limbs are ture due to fibroblastic proliferation and the small num-
more often involved. 1–3 Lesions frequently occur in ber of capillaries within the tumor. The epidermis varies
traumatized areas.1,2 Sarcoids may be related to scar tis- from thick, rough, and hyperkeratotic to ulcerated.3,9
sue and the rapidly dividing cells that heal the wound.4 Sarcoid tumors can also occur in the subcutaneous tis-
Although the etiology of equine sarcoid tumors has sue as firm, movable masses with an intact covering of
not yet been definitively established, there is ample evi- skin.10 Four distinct forms of sarcoids are recognized.
dence to support a viral agent, including transmissibil- Less severe types can quickly progress to more aggressive
ity, occurrence in an epizootic form, and the tendency forms, especially if the area is traumatized.3
for lesions to occur at previous wound sites. 1–4 A Occult sarcoids seem to favor the skin around the
genome closely resembling bovine papillomavirus has mouth, eyes, neck, and other relatively hairless areas of
been consistently isolated from equine sarcoid tissue. the body, including the medial aspects of the forearm
Although patent viral particles have not been conclu- and thigh. These lesions manifest as a slightly thickened
sively demonstrated with electron microscopy or anti- area of skin with a mildly roughened surface that is
body testing, in a recent study, tissue sections from sar- devoid of hair. These sarcoids are generally slow-grow-
coids revealed viral DNA by polymerase chain reaction ing. Occult sarcoids can progress to verrucous (warty)
in the dermal layer within the fibroblasts of the tumor. growth or, if traumatized, may develop into fibroblastic
Bovine papillomavirus DNA was also detected in 65% lesions.1,3 As long as occult sarcoids remain in a static
of the samples of normal skin obtained from sarcoid- state, the tumor should be left untreated to avoid pro-
affected horses.5 This finding may indicate that bovine gression to a more aggressive lesion.1
papillomavirus infects the skin of horses and remains in Verrucous sarcoids show a predilection for the face,
a latent phase within the fibroblasts of the dermis until body, groin, and sheath areas. Lesions are generally
some other factor triggers transcriptional activation. small, rarely exceeding 6 cm in diameter, with a dry,
This would explain the high incidence of tumor recur- horny surface and a cauliflowerlike appearance (Figure
rence after surgically complete excision because surgical 1). These tumors are generally slow growing and
trauma may induce proliferation and expression of become aggressive only when injured. Any type of
latent virus, resulting in regrowth of the tumor.5 Flies, insult can cause a rapid change to a fibroblastic sarcoid
shared grooming equipment, and common rubbing over variable areas of the lesion.1
posts may be transmission routes.3,6 Predilection sites for nodular sarcoids include the
Clinical studies suggest a genetic predisposition for groin, sheath, or eyelid. These lesions are generally sub-
244 Equine Compendium March 2002

diagnosis is based on histologic examination of the

affected tissue in other sarcoid forms. 11 The entire
tumor should be sectioned centrally in a plane perpen-
dicular to its epidermal surface. Punch biopsies are not
recommended. Equine sarcoids are typically biphasic,
with an epidermal and a dermal component. Histology
will show epidermal hyperplasia and dermal fibroplasia.
Pegs of hyperkeratotic epithelium extend into the
depths of the dermal lesions. The epidermal compo-
nent is sometimes absent, and the dermal component
can be limited. Hyperkeratosis and acanthosis are typi-
cally seen if the sarcoid has an intact epidermis. Epider-
mal inclusion cysts containing keratin (representing
dilated, degenerated hair follicles) may be present.
Immature fibroblasts make up the dermal component.
Collagen fibers are often present, and cytoplasmic
boundaries are not well defined. A distinctive feature of
equine sarcoids is the picket-fence pattern created when
the fibroblasts at the dermal–epidermal junction line
up perpendicularly to the basement membrane. The
mitotic rate is invariably low.1,11,12

Figure 3—Fibroblastic sarcoid on the right distal hindlimb. There is a wide range of treatments available for equine
sarcoids; no one therapy has been shown to be universally
cutaneous, easily movable nodules (Figure 2). Occa- effective in eliminating sarcoid tumors. The treatment
sionally, dermal attachments prevent movement of the modality selected is determined by location, size, and
tumor relative to deeper tissue. The skin over larger aggressiveness of the tumor; clinical experience; and the
nodules may become thin and ulcerate followed by the availability of services, equipment, and facilities.12 Tumor
progression of the tumor to a fibroblastic character. regrowth is a common occurrence regardless of the
Any trauma to the area may produce similar results.1 treatment modality used.
Fibroblastic sarcoids are usually found on the groin, Equine sarcoids removed by conventional surgical
eyelid, lower limbs, previous wound sites, and sites of excision have been shown to have a 50% to 64% recur-
other sarcoid types subjected to insult. Fibroblastic sar- rence rate, with most regrowth occurring within 6
coids are variable in appearance. Some are well-circum- months. 1 Surgical excision is better used to reduce
scribed, fibrous nodules in the dermis covered by intact tumor volume and improve the killing efficiency of
epidermis, and others are large masses with ulcerated combination therapies. When using surgical excision, a
surfaces that hemorrhage easily and are often covered 0.5- to 1-cm-diameter margin of normal tissue is rec-
by purulonecrotic debris (Figure 3).1 These lesions usu- ommended.1,12 This often results in a large skin defect
ally have an aggressive nature and will spread locally in in areas with little skin mobility and slow epithelializa-
the dermis. The fibroblastic sarcoid will often resemble tion. Application of a split-thickness skin graft may
exuberant granulation tissue.3 facilitate epithelial covering of the wound and result in
Diagnostic differentials that must be considered when a faster healing, reduced production of excess granulation
sarcoid is suspected vary widely and include dermatophy- tissue, and improved appearance.1,3,12
tosis, linear hyperkeratosis, blisters, burns, rub marks, Cryotherapy with liquid nitrogen is a cost-effective
papillomatosis, hyperkeratosis, SCCs, fibromas, neurofi- treatment in many cases. The sarcoid is destroyed by ice
bromas, equine eosinophilic granulomas, melanomas, crystals that form inside the cells, rupturing the walls
pythiosis, fibrosarcomas, and lymphosarcomas.3 and killing the tissue.4 It is strongly recommended that
tissue freezing be monitored using implanted tissue
Diagnosis temperature probes.1 The use of at least two or three
Although biopsy of occult, nodular, and small verru- freeze–thaw cycles is necessary. Healing is by second
cous tumors is often not recommended to avoid chang- intention or delayed closure, which may result in scar-
ing the morphology and behavior of a lesion, definitive ring and hair depigmentation.1,3
246 Equine Compendium March 2002

Figure 4A Figure 4B
Figure 4—Fibroblastic sarcoid before (A) and after (B) application of AnimexTM. This lesion healed without further complications.

Carbon dioxide laser excision and ablation of sarcoid the surrounding healthy tissue intact. A rapid response
tumors allows accurate dissection with minimal damage to the salve is usually noticed, and the lesion sloughs in
to surrounding tissue, uncomplicated healing, and 7 to 10 days (Figure 4). We consider this product to be
excellent cosmetic results1,12; however, laser excision the treatment of choice for small sarcoids that can be
should still be combined with other treatment modali- easily bandaged. Similar products are also available. A
ties to avoid tumor regrowth.4 topical treatment that contains a caustic chemical plus
EqStim (nonviable Propionibacterium acnes ; Neogen an extract of the bloodroot plant (XXTERRATM, Lar-
Corporation, Lansing, MI) has shown good results. Pro- son Laboratories, Inc., Fort Collins, CO) has also been
tocols differ widely, including intralesional and/or intra- used and is believed to change the antigenicity of the
venous injections given once weekly for 6 to 8 weeks. sarcoid cells so the immune system recognizes them as
Susceptible lesions generally show improvement after two being foreign, resulting in tissue rejection.4
to three treatments and eventually necrose and slough.13 A topical ointment (AW-3-LUDES, D.C. Knotten-
There are many topical products available for treating belt, Division of Equine Studies, Leahurst, Neston,
sarcoids. Daily topical application of the antimetabolite South Wirral, UK) has shown some success in treating
5-fluorouracil and podophyllin, an irritant cathartic, has sarcoids. It contains a variety of heavy metals and the
been used to treat patients with sarcoids. This treatment antimitotic compounds 5-fluorouracil and thiouracil.14
must be continued for 30 to 90 days.1,10 5-Fluorouracil The ointment is administered on successive or alternate
is a fluorinated pyrimidine antimetabolite that interferes days for three to five treatments. A response should be
with nuclear DNA biosynthesis, leading to cell death or evident in the following 5 to 10 weeks and will be
increased susceptibility to the immune system.1,10 noticed as preferential necrosis and sloughing of the
A bloodroot extract that contains Sanguinaria sarcoid tissues.14
canadensis, puccoon, gromwell, distilled water, and Various radioisotopes have been used for interstitial
trace minerals (AnimexTM, NIES Inc., Las Vegas, NV) brachytherapy of equine sarcoids. Permanently
has been used to treat various types of skin lesions, implanted seeds of radon-222 or gold-198 and remov-
including sarcoids. It is an escharotic salve that pene- able needles of radium-226, cobalt-60, or iridium-192
trates the lesion, killing the affected cells while leaving have been used.15 The principal advantage of radiother-
248 Equine Compendium March 2002

apy is the continuous delivery of radiation locally to the

tumor while sparing the adjacent healthy tissue. For
recurrent, aggressive, and surgically inaccessible sar-
coids, this modality should be considered.1,3,4,15
Immunotherapy is a common treatment for equine
sarcoids. The most commonly used immunomodulator
is bacille Calmette–Guérin (BCG), an attenuated strain
of Mycobacterium bovis.10,12 The exact mechanism of
action of BCG is unclear, but it is believed that it may
induce a tumor-specific immunity.6,10 Muramyl dipep-
tide, a structural component of the mycobacterial cell
wall, is the immunostimulating component of BCG.10,12
The antineoplastic response of BCG involves a delayed-
type hypersensitivity response against the neoplasm
into which it is injected. The tumor is destroyed by
macrophages, which generate a proteolytic activity and
synthesize cytotoxic oxygen-derived free radicals, and
by cytotoxic lymphokines produced by sensitized T
lymphocytes and natural killer cells. 10,12 Because
patients may go into anaphylactic shock after two or
more injections, premedication with flunixin meglu-
mine and corticosteroids is recommended.10,12,16
Autogenous vaccines are another category of Figure 5—SCC on the penis of a horse.
immunotherapy that has been used experimentally to
treat sarcoids.12,17 The transfer of sarcoid tumors, tumor
homogenates, or cell-free tumor extracts can stimulate ments are necessary for this method to be effective. The
the production of new tumors or the regression of antineoplastic effects of radiotherapy, immunotherapy,
existing tumors. Transfer of whole tumors and tumor and chemotherapy are enhanced by hyperthermia.1,3
extracts to the limbs (as opposed to the neck) is likely
to result in tumor production rather than tumor regres- SQUAMOUS CELL CARCINOMA
sion. 12,17 Sarcoid regression has occurred in several SCC is the second most common tumor diagnosed in
horses with refractory sarcoids following transplanta- horses, accounting for 20% of equine neoplasms.19 It is
tion from one horse into another horse. Because other the most commonly diagnosed neoplasm of the eye,
less invasive treatments frequently work well and tumor conjunctiva, ocular adnexal structures, and external gen-
transplantation bears risks, such as tumor production italia but can also affect the stomach, esophagus, nasal
and transmission of other diseases, this procedure passages, paranasal sinuses, hard palate, pharynx, larynx,
should be attempted only in the most refractory of perianal tissue, ear canal, tongue, hoof, and guttural
cases and with horses known to be negative for equine pouches.20–23 Tumors reportedly metastasize in 18.6% of
infectious anemia. cases.24 Local lymph nodes are most commonly affected
Intralesional implants that allow a high local drug by metastasis, but SCC may also spread to the lungs.25
concentration for extended periods have been devel- Older horses are at higher risk for SCC, and there
oped. The implants consist of a high–molecular-weight appears to be a higher incidence of the disease in draft
collagen matrix that contains a chemotherapeutic agent breeds, Appaloosas, American paints, and pintos.6,21–23,26
(cisplatin and to a lesser extent 5-fluorouracil) and a The presence of smegma, persistent phimosis, or
vasoactive modifier (epinephrine)1 or sterilized sesame repeated trauma may predispose stallions and geldings
oil to effect a slow release and an elevated tumor:plasma to developing lesions of the external genitalia. 21 Solar
drug concentration ratio.18 Results with cisplatin in oil radiation appears to contribute to ocular lesions.
have been extremely good.18
Intratumoral hyperthermia induced by radiofrequency Clinical Presentation
(orthovoltage) has been successful in treating equine sar- Early clinical signs of SCC include thickening, mild
coids. A thermoprobe is used to heat the tissue to 59°C exfoliation, and ulceration of the skin.21 Mature lesions
for 30 seconds.1 Malignant cells are more susceptible to can be erosive or productive in nature.3 Erosive lesions
high temperatures than are normal cells. Multiple treat- usually appear as small superficial nodules covered with
250 Equine Compendium March 2002

Figure 7—SCC of the left eye. Note the characteristic muco-

purulent discharge.

given a guarded prognosis.21

Lesions affecting the eyelid frequently begin as white,
raised plaques at the edge of the eyelid and proceed to
extensive ulceration and destruction of the eyelid, rapidly
invading the periorbital tissues (Figure 7).3 The earliest
stages may appear with blood-stained tears and progress
rapidly to a granulomatous and ulcerated lesion.3
Oral SCC is often missed in the early stages, and
fetid breath, blood-stained saliva, and nasal mucus may
be the first reported signs.3,21 Lesions of the pharynx
Figure 6—SCC on the vulva of a mare. appear with stertor and dysphagia.3,21,27 Metastasis to
the retropharyngeal lymph nodes is common. Metasta-
sis to the parotid salivary glands, cervical lymph nodes,
normal skin. The developing tumor eventually destroys or the lungs may also occur.21 The prognosis is poor for
the overlying epidermis, leading to ulceration, necrosis, oral SCC that has metastasized.3,21 Similarly, SCC of
and a generalized foul odor.3,21 These lesions gradually the nasal cavity and paranasal sinuses previously had a
enlarge and may develop a craterlike appearance. The poor prognosis; however, a recent study using course-
productive lesions develop as papillary masses with a fractionated cobalt-60 radiotherapy provided good to
cauliflowerlike appearance.21 Diagnostic differentials excellent long-term results.28
include sarcoids, melanoma, exuberant granulation tis-
sue, and pythiosis.3,23 Diagnosis
In SCC of the male genitalia, tumors usually arise Diagnosis of SCC can be accomplished by cytologic
from the glans penis or the inner lining of the penile or histologic examination.21 Depending on the site and
sheath and spread to the corpus cavernosum (Figure size of the lesion, excisional, wedge, punch, or elliptical
5).21 Early clinical signs include preputial edema, dis- biopsy can be performed. Histologically, the tumor
charge, intermittent hemorrhage, dysuria, pollakiuria, consists of nests and cords of epithelial cells that infil-
weight loss, and urinary incontinence.21 The regional trate the dermis.21 Other diagnostic methods include
lymph nodes should also be assessed for metastasis by fine-needle aspiration of nodular lesions, cytologic
inguinal and rectal palpation.21 Regular examination examination of superficial scrapings from ulcerated
and washing of the prepuce and penis will aid in early lesions using a dull blade, and impression smears.21
detection of SCC and may even assist in preventing its
development.21 SCC affecting female genitalia typically Treatment
originates at the clitoris and progresses toward the vagi- With SCC, treatment is most successful when the
nal vestibule and mammary glands (Figure 6).21 Hyper- lesion is recognized and therapy is initiated early in the
trophy of the clitoris and surrounding tissue as well as course of the disease.29 Debulking the tumor along with
roughening of the ventral commissure may be noticed cryosurgery, intratumoral hyperthermia, and cisplatin
early in the disease. Advanced lesions are generally have been used as previously described to treat sarcoids.
Compendium March 2002 Equine Skin Tumors 251

In addition, in both genital and ocular cases, topical

treatment of superficial, ulcerative SCC with 5-fluo-
rouracil ophthalmic drops and creams has been success-
ful in our experience.23,30,31 Radiation therapy can be
used in the same manner as described for sarcoid treat-
ment. Beta irradiation (strontium-90) has been used
successfully to treat SCC and is particularly good for
ocular lesions because the orbit and adnexa can be pre-
served.32 Course-fractionated cobalt-60 radiotherapy
has provided good to excellent long-term results in sev-
eral cases with severe involvement of the paranasal
sinuses.28 Bloodroot extracts may have some value.19 In
our experience and that of others, despite aggressive
therapy with many of these treatment modalities, recur-
rence of the disease is common.26 In some cases, recur-
rence may be minimized by protection from solar radi-
ation; fly masks, evening turnout strategies, and
sunscreen may be beneficial.

Melanomas are common tumors that can occur in
horses and mules of any coat color, but incidence is
much higher in gray and white horses.3,33,34 Arabians,
Thoroughbreds, and Percherons may be at increased
risk for developing this disease.33,35 In one study of 264
gray-skinned horses in France, the prevalence of
melanomas in the overall population was 31.4%. The
incidence, size, and number of melanomas was signifi- Figure 8—Melanoma lesions on the underside of a horse's tail.
cantly correlated with age, with a prevalence of 67% for
ages older than 15 years.36 Other sources suggest that
approximately 80% of all gray horses will develop one Clinical Presentation
or more melanomas at some location by 15 years of Ninety-five percent of melanomas are slow-growing
age.3,34,37 There appears to be no gender predilection for and show no signs of regional or distant metastasis.
these tumors. The most common areas of the skin These tumors are of little clinical significance except
affected are underneath the tail (Figure 8) and external when they inhibit the use of riding tack or interfere
genitalia. 38 Other regions less commonly affected with urination, defecation, and coitus.37 Melanomas
include the ear, eyelid, neck, parotid salivary gland, commonly appear as black or gray, solitary, discrete,
guttural pouches, lips, and limbs. 3,33,34,37 When firm, spherical or flat nodules in the skin or subcutis
melanomas do occur in horses of other colors, they may and may have a pedicle. Tumors frequently coalesce,
be at greater risk for becoming malignant (Figure 9).6 and hundreds or more variable-sized nodules may be
The etiology of melanomas in horses has not been present without affecting the well-being of the horse.
clearly defined. It is thought that melanomas in old gray Many small tumors may be present, producing a cob-
horses are due to disturbed melanin metabolism, leading blestone appearance.3,34 Overlying skin may be intact or
to the formation of new melanoblasts, or to increased may be slightly alopecic. Lesions may ulcerate and pro-
activity in resident melanoblasts, resulting in a focal area duce a black, tarry discharge.3
of pigment overproduction in the dermis.6 Controversy Occasionally, melanomas will exhibit slow growth for
exists as to whether exposure to increased levels of ultra- several years followed by a sudden rapid growth phase
violet radiation may play a role in the pathogenesis of associated with malignant transformation of the tumor.
melanomas in horses. 6,33 Because of their frequent These tumors become locally invasive and may metasta-
occurrence in shaded body regions, sun exposure may size.37 Sites of metastasis include regional lymph nodes,
not be a risk factor for melanoma formation. However, lungs, liver, serosal surfaces, spleen, kidney, brain, bone,
reducing solar exposure in predisposed horses may be and heart. If the tumor metastasizes to internal organs,
warranted. clinical signs will be determined by the affected organ.
252 Equine Compendium March 2002

melanomas.33,34 The use of intralesional injection of cis-

platin has been very effective in the treatment of
tumors less than 3 cm in diameter. They often resolve
following a single treatment.3 The use of cisplatin in
the treatment of larger masses is made more effective if
the mass is debulked before treatment is administered.
Regrowth of the tumor may occur 7 to 8 months fol-
lowing treatment. Treatments can be repeated using the
same procedure.3
Cimetidine, a histamine receptor agonist, has been
used to treat equine melanomas. Histamine stimulates
T suppressor cell inhibition of both cell-mediated and
humoral immunity. Cimetidine appears to block H2-
receptors on these cells, thereby enhancing immune
function and targeting of these tumors.3,33,37 Studies
evaluating the use of cimetidine for melanomas have
shown varying results, but regression of tumors should
be evident within 3 months of initiating treatment. If
no improvement is seen, cimetidine will probably not
be effective and should be discontinued.33,37 Cimetidine
is administered at 2.5 mg/kg tid or (less satisfactorily)
7.5 mg/kg once or twice daily and continued for 2 to 3
weeks following resolution of tumor growth. Some
horses may require treatment their entire life.
Techniques to prepare vaccines and monoclonal anti-
bodies to promote immunologic recognition and tumor
Figure 9— Amelanotic melanoma on the underside of a
rejection have been developed.33 Although studies per-
horse's tail. This lesion was ulcerated, aggressive, and rapid
growing, unlike melanomas that commonly occur in this
formed with these vaccines have shown promising
location in gray horses (see Figure 8). results,33 we have not experienced success with their use.
1. McConaghy FF, Davis RE, Hodgson DR: Equine sarcoid: A
Cachexia may be seen when almost any internal organ is persistent therapeutic challenge. Compend Contin Educ Pract Vet
affected. 36,37 In rare cases, melanomas exhibit rapid 7(1):1022–1030, 1994.
growth and malignant properties from the onset.39 2. Nasir L, Reid SW: Bovine papillomaviral gene expression in
equine sarcoid tumours. Virus Res 61(2):171–175, 1999.
Diagnosis 3. Pascoe RR, Knottenbelt DC: Manual of Equine Dermatology.
Diagnosis of equine melanomas is generally based on London, WB Saunders Co, 1999.
gross appearance, which can be confirmed using histol- 4. Meszoly J: Sarcoids benign and baffling. Equus 283:91–102,
ogy. Lesions are composed mostly of melanocytes and 2001.
melanophages.40 5. Carr EA, Theon AP, Madewell BR, et al: Bovine papillomavirus
DNA in neoplastic and nonneoplastic tissues obtained from
horses with and without sarcoids in the western United States.
Treatment Am J Vet Res 62(5):741–744, 2001.
Treatment is often not necessary for small 6. Scott D, Peterson D (eds): Large Animal Dermatology. Philadel-
melanocytic tumors located in uncompromising loca- phia, WB Saunders Co, 1988.
tions. Rarely, tumors may spontaneously regress over 7. Angelos J, Oppenheim Y, Rebhun W, et al: Evaluation of breed
time.34 Large masses, or masses located in areas where as a risk factor for sarcoid and uveitis in horses. Anim Genet
19(4):417–425, 1988.
they can be a nuisance, are treated with surgical exci-
8. Bolin D: Equine sarcoid. Equine Dis Q 7(3):5–6, 1999.
sion. When possible, a wide margin should be attained
9. Knottenbelt DC, Kelly DF: The diagnosis and treatment of
with surgical excision.3,34,37 Cryosurgery can be used in periorbital sarcoid in the horse: 445 cases from 1974 to 1999.
conjunction with surgical excision. However, tumor Vet Ophthalmol 3(2–3):169–191, 2000.
regrowth is a problem with this technique also.3,34,37 10. Piscopo SE: The complexities of sarcoid tumors. Equine Pract
Intralesional injection of BCG has been associated 21(8):14–18, 1999.
with disappointing results in the treatment of 11. Martens A, De Moor A, Demeulemeester J, Ducatelle R:
Compendium March 2002 Equine Skin Tumors 253

Histopathological characteristics of five clinical types of equine 33. Jeglum K: Melanomas, in Robinson N (ed): Current Therapy in
sarcoid. Res Vet Sci 69(3):295–300, 2000. Equine Medicine. Philadelphia, WB Saunders Co, 1997, pp
12. Bertone AL, McClure JJ: Therapy for sarcoids. Compend Contin 399–400.
Educ Pract Vet 12(2):262–265, 1990. 34. Fintl C, Dixon PM: A review of five cases of parotid melanoma
13. Robinson J: Equimmune, Eqstim for horses. VIN Equine in the horse. Equine Vet Educ 13(1):17–24, 2001.
Boards, 1997. 35. Mullowney P: Dermatologic diseases of horses: Part IV. Envi-
14. Newton SA: Periocular sarcoids in the horse: Three cases of suc- ronmental, congenital, and neoplastic diseases. Compend Contin
cessful treatment. Equine Vet Educ 12(3):137–143, 2000. Educ Pract Vet 7(1):S22–S32, 1985.
15. Turrel JM, Stover SM, Gyorgyfalvy J: Iridium-192 interstitial 36. Fleury C, Berard F, Balme B, Thomas L: The study of cutaneous
brachytherapy of equine sarcoid. Vet Radiol 26(1):20–24, 1985. melanomas in Camargue-type gray-skinned horses (1): Clinical-
pathological characterization. Pigment Cell Res 13(1):39–46,
16. Vanselow BA, Abetz I, Jackson AR: BCG emulsion
immunotherapy of equine sarcoid. Equine Vet J 20(6):444–447,
1988. 37. Hare JE, Staempfli HR: Cimetidine for the treatment of
melanomas in horses: Efficacy determined by client question-
17. Kinnunen RE, Tallberg T, Stenback H, Sarna S: Equine sarcoid
naire. Equine Pract 16(5):18–21, 1994.
tumour treated by autogenous tumour vaccine. Anticancer Res
19(4C):3367–3374, 1999. 38. Fleury C, Berard F, Leblond A, et al: The study of cutaneous
melanomas in Camargue-type gray-skinned horses (2): Epidemi-
18. Theon AP, Pascoe JR, Carlson GP, Krag DN: Intratumoral
ological survey. Pigment Cell Res 13(1):47–51, 2000.
chemotherapy with cisplatin in oily emulsion in horses. JAVMA
202(2):261–267, 1993. 39. Moore CP, Collins BK, Linton LL, Collier LL: Conjunctival
19. Bastianello S: A survey of neoplasia in domestic species over a malignant melanoma in a horse. Vet Ophthalmol
40-year period from 1935–1974 in the Republic of South 3(2–3):201–206, 2000.
Africa. Ondersteport J Vet Res 50:91, 1983. 40. Valentine BA: Equine melanocytic tumors: A retrospective study
20. Burney DP, Theisen SK, Schmitz DG: Identifying and treating of 53 horses (1988–1991). J Vet Intern Med 9(5):291–297,
squamous cell carcinoma of horses. Vet Med 87(6):588–594, 1995.
21. MacFadden KE, Pace LW: Clinical manifestations of squamous
cell carcinoma in horses. Compend Contin Educ Pract Vet
13(4):669–675, 1991.

22. Perez J, Mozos E, Martin MP, Day MJ: Immunohistochemical
study of the inflammatory infiltrate associated with equine squa-
The article you have read qualifies for 1.5 con-
mous cell carcinoma. J Comp Pathol 121(4):385–397, 1999. tact hours of Continuing Education Credit from
23. Paterson S: Treatment of superficial ulcerative squamous cell car- the Auburn University College of Veterinary Med-
cinoma in three horses with topical 5-fluorouracil. Vet Rec icine. Choose the best answer to each of the follow-
141(24):626–628, 1997. ing questions; then mark your answers on the
24. Gelatt KN, Myers Jr VS, Perman V, Jessen C: Conjunctival postage-paid envelope inserted in Compendium.
squamous cell carcinoma in the horse. JAVMA 165(7):617–620,
25. Murray D: Granulomatous and neoplastic diseases of the skin of
horses. Aust Vet J 54:338, 1978.
1. Equine sarcoids are believed to be associated with
_______________ or a similar virus.
26. Mair TS, Walmsley JP, Phillips TJ: Surgical treatment of 45
horses affected by squamous cell carcinoma of the penis and pre-
a. equine herpesvirus c. morbillivirus
puce. Equine Vet J 32(5):406–410, 2000. b. bovine papillomavirus d. lentivirus
27. Jones DL: Squamous cell carcinoma of the larynx and pharynx
in horses. Cornell Vet 84(1):15–24, 1994. 2. Which of the following breeds has a decreased chance
28. Walker MA, Schumacher J, Schmitz DG, et al: Cobalt-60 radio- of developing sarcoid tumors relative to all other
therapy for treatment of squamous cell carcinoma of the nasal breeds?
cavity and paranasal sinuses in three horses. JAVMA a. Appaloosa c. standardbred
212(6):848–851, 1998. b. Arabian d. quarter horse
29. King TC, Priehs DR, Gum GG, Miller TR: Therapeutic man-
agement of ocular squamous cell carcinoma in the horse: 43 3. Which of the following is not a type of equine sarcoid?
cases (1979–1989). Equine Vet J 23(6):449–452, 1991. a. occult c. papillary
30. Fortier LA, MacHarg MA: Topical use of 5-fluorouracil for b. verrucous d. nodular
treatment of squamous cell carcinoma of the external genitalia
of horses: 11 cases (1988–1992). JAVMA 205(8):1183–1185,
4. Biopsy of latent sarcoids should be avoided because
a. they may hemorrhage profusely and result in acute
31. Yeatts R, Engelbrecht NE, Curry CD, et al: 5-Fluorouracil for
the treatment of intraepithelial neoplasia of the conjunctiva and
blood loss.
cornea. Ophthalmology 107(12):2190–2195, 2000. b. it may cause an undesirable change in the behavior
32. Theon AP, Pascoe JR: Iridium-192 interstitial brachytherapy for
of the lesion.
equine periocular tumours: Treatment results and prognostic c. metastasis may occur in the lymph nodes and spleen.
factors in 115 horses. Equine Vet J 27(2):117–121, 1995. d. it will cause extreme pain to the horse.
254 Equine Compendium March 2002

5. SCCs account for ____% of tumors in horses. b. disturbed melanin metabolism.

a. 60 c. 10 c. bacterial infection.
b. 20 d. 80 d. trauma.

6. Which of the following contributes to SCC develop- 9. The most common growth pattern exhibited by
ment? melanomas is
a. solar radiation a. rapid growth with aggressive metastasis.
b. pigmented skin b. slow growth for many years with no signs of metas-
c. bovine papillomavirus tasis.
d. gray haircoat c. slow growth for many years with a sudden growth
spurt and metastasis.
7. What tissue is most commonly affected by SCC d. none of the above
a. lymph node c. heart 10. Which of the following is recommended for treating
b. lung d. brain equine sarcoids?
a. surgical excision alone
8. The development of melanomas in older gray horses is b. cimetidine
associated with c. topical antimicrobial agents
a. increased exposure to ultraviolet light. d. intralesional cisplatin