242
3 March 2002
CE Article #5 (1.5 contact hours)
Refereed Peer Review
KEY FACTS
■ Small equine sarcoids should be
monitored carefully; larger
tumors and those undergoing
morphologic changes should be
treated aggressively.
■ Squamous cell carcinomas can
be locally invasive and
metastatic.
■ Melanomas should be carefully
monitored even though they are
slow-growing and nonmetastatic.
Vol. 24, No.
Comments? Questions?
Email: compendium@medimedia.com
Web: VetLearn.com • Fax: 800-556-3288
Common Equine
Skin Tumors
Mississippi State University
Jenny M. Foy, DVM
Ann M. Rashmir-Raven, DVM, MS, DACVS
Michael K. Brashier, DVM, MS, DACVIM
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
frequently affect the legs, ventral trunk, and head. They are believed to be the result of infec-
tion with bovine papillomavirus or a similar agent. SCCs are the second most common equine
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
body and predominantly occurring in paints, Appaloosas, and albinos. Equine melanomas are
the most common skin tumor in horses with a white or gray coat. They are believed to be the
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.
D
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.
SARCOID
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
Figure 1—Verrucous (warty) sarcoid on the left pinna.
missures of the lips, are most commonly affected. In
northern climates, lesions occur predominantly on the
head and abdomen. In warmer climates, the limbs are
more often involved. 1–3 Lesions frequently occur in
traumatized areas.1,2 Sarcoids may be related to scar tis-
sue and the rapidly dividing cells that heal the wound.4
Although the etiology of equine sarcoid tumors has
not yet been definitively established, there is ample evi-
dence to support a viral agent, including transmissibil-
ity, occurrence in an epizootic form, and the tendency
for lesions to occur at previous wound sites. 1–4 A
genome closely resembling bovine papillomavirus has
been consistently isolated from equine sarcoid tissue.
Although patent viral particles have not been conclu-
sively demonstrated with electron microscopy or anti-
body testing, in a recent study, tissue sections from sar-
coids revealed viral DNA by polymerase chain reaction
in the dermal layer within the fibroblasts of the tumor.
Bovine papillomavirus DNA was also detected in 65%
of the samples of normal skin obtained from sarcoid-
affected horses.5 This finding may indicate that bovine
papillomavirus infects the skin of horses and remains in
a latent phase within the fibroblasts of the dermis until
some other factor triggers transcriptional activation.
This would explain the high incidence of tumor recur-
rence after surgically complete excision because surgical
trauma may induce proliferation and expression of
latent virus, resulting in regrowth of the tumor.5 Flies,
shared grooming equipment, and common rubbing
posts may be transmission routes.3,6
Clinical studies suggest a genetic predisposition for
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
appear to have a lower risk than all other breeds.4,7,8
Clinical Presentation
Sarcoid tumors generally appear with linear or focal
dermal thickening that has a pale color and a firm tex-
ture due to fibroblastic proliferation and the small num-
ber of capillaries within the tumor. The epidermis varies
from thick, rough, and hyperkeratotic to ulcerated.3,9
Sarcoid tumors can also occur in the subcutaneous tis-
sue as firm, movable masses with an intact covering of
skin.10 Four distinct forms of sarcoids are recognized.
Less severe types can quickly progress to more aggressive
forms, especially if the area is traumatized.3
Occult sarcoids seem to favor the skin around the
mouth, eyes, neck, and other relatively hairless areas of
the body, including the medial aspects of the forearm
and thigh. These lesions manifest as a slightly thickened
area of skin with a mildly roughened surface that is
devoid of hair. These sarcoids are generally slow-grow-
ing. Occult sarcoids can progress to verrucous (warty)
growth or, if traumatized, may develop into fibroblastic
lesions.1,3 As long as occult sarcoids remain in a static
state, the tumor should be left untreated to avoid pro-
gression to a more aggressive lesion.1
Verrucous sarcoids show a predilection for the face,
body, groin, and sheath areas. Lesions are generally
small, rarely exceeding 6 cm in diameter, with a dry,
horny surface and a cauliflowerlike appearance (Figure
1). These tumors are generally slow growing and
become aggressive only when injured. Any type of
insult can cause a rapid change to a fibroblastic sarcoid
over variable areas of the lesion.1
Predilection sites for nodular sarcoids include the
groin, sheath, or eyelid. These lesions are generally sub-
244 Equine
Figure 3—Fibroblastic sarcoid on the right distal hindlimb.
cutaneous, easily movable nodules (Figure 2). Occa-
sionally, dermal attachments prevent movement of the
tumor relative to deeper tissue. The skin over larger
nodules may become thin and ulcerate followed by the
progression of the tumor to a fibroblastic character.
Any trauma to the area may produce similar results.1
Fibroblastic sarcoids are usually found on the groin,
eyelid, lower limbs, previous wound sites, and sites of
other sarcoid types subjected to insult. Fibroblastic sar-
coids are variable in appearance. Some are well-circum-
scribed, fibrous nodules in the dermis covered by intact
epidermis, and others are large masses with ulcerated
surfaces that hemorrhage easily and are often covered
by purulonecrotic debris (Figure 3).1 These lesions usu-
ally have an aggressive nature and will spread locally in
the dermis. The fibroblastic sarcoid will often resemble
exuberant granulation tissue.3
Diagnostic differentials that must be considered when a
sarcoid is suspected vary widely and include dermatophy-
tosis, linear hyperkeratosis, blisters, burns, rub marks,
papillomatosis, hyperkeratosis, SCCs, fibromas, neurofi-
bromas, equine eosinophilic granulomas, melanomas,
pythiosis, fibrosarcomas, and lymphosarcomas.3
Diagnosis
Although biopsy of occult, nodular, and small verru-
cous tumors is often not recommended to avoid chang-
ing the morphology and behavior of a lesion, definitive
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
Treatment
There is a wide range of treatments available for equine
sarcoids; no one therapy has been shown to be universally
effective in eliminating sarcoid tumors. The treatment
modality selected is determined by location, size, and
aggressiveness of the tumor; clinical experience; and the
availability of services, equipment, and facilities.12 Tumor
regrowth is a common occurrence regardless of the
treatment modality used.
Equine sarcoids removed by conventional surgical
excision have been shown to have a 50% to 64% recur-
rence rate, with most regrowth occurring within 6
months. 1 Surgical excision is better used to reduce
tumor volume and improve the killing efficiency of
combination therapies. When using surgical excision, a
0.5- to 1-cm-diameter margin of normal tissue is rec-
ommended.1,12 This often results in a large skin defect
in areas with little skin mobility and slow epithelializa-
tion. Application of a split-thickness skin graft may
facilitate epithelial covering of the wound and result in
faster healing, reduced production of excess granulation
tissue, and improved appearance.1,3,12
Cryotherapy with liquid nitrogen is a cost-effective
treatment in many cases. The sarcoid is destroyed by ice
crystals that form inside the cells, rupturing the walls
and killing the tissue.4 It is strongly recommended that
tissue freezing be monitored using implanted tissue
temperature probes.1 The use of at least two or three
freeze–thaw cycles is necessary. Healing is by second
intention or delayed closure, which may result in scar-
ring and hair depigmentation.1,3
246 Equine
Figure 4A
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
tumors allows accurate dissection with minimal damage
to surrounding tissue, uncomplicated healing, and
excellent cosmetic results1,12; however, laser excision
should still be combined with other treatment modali-
ties to avoid tumor regrowth.4
EqStim (nonviable Propionibacterium acnes ; Neogen
Corporation, Lansing, MI) has shown good results. Pro-
tocols differ widely, including intralesional and/or intra-
venous injections given once weekly for 6 to 8 weeks.
Susceptible lesions generally show improvement after two
to three treatments and eventually necrose and slough.13
There are many topical products available for treating
sarcoids. Daily topical application of the antimetabolite
5-fluorouracil and podophyllin, an irritant cathartic, has
been used to treat patients with sarcoids. This treatment
must be continued for 30 to 90 days.1,10 5-Fluorouracil
is a fluorinated pyrimidine antimetabolite that interferes
with nuclear DNA biosynthesis, leading to cell death or
increased susceptibility to the immune system.1,10
A bloodroot extract that contains Sanguinaria
canadensis, puccoon, gromwell, distilled water, and
trace minerals (AnimexTM, NIES Inc., Las Vegas, NV)
has been used to treat various types of skin lesions,
including sarcoids. It is an escharotic salve that pene-
trates the lesion, killing the affected cells while leaving
Compendium March 2002
Figure 4B
the surrounding healthy tissue intact. A rapid response
to the salve is usually noticed, and the lesion sloughs in
7 to 10 days (Figure 4). We consider this product to be
the treatment of choice for small sarcoids that can be
easily bandaged. Similar products are also available. A
topical treatment that contains a caustic chemical plus
an extract of the bloodroot plant (XXTERRATM, Lar-
son Laboratories, Inc., Fort Collins, CO) has also been
used and is believed to change the antigenicity of the
sarcoid cells so the immune system recognizes them as
being foreign, resulting in tissue rejection.4
A topical ointment (AW-3-LUDES, D.C. Knotten-
belt, Division of Equine Studies, Leahurst, Neston,
South Wirral, UK) has shown some success in treating
sarcoids. It contains a variety of heavy metals and the
antimitotic compounds 5-fluorouracil and thiouracil.14
The ointment is administered on successive or alternate
days for three to five treatments. A response should be
evident in the following 5 to 10 weeks and will be
noticed as preferential necrosis and sloughing of the
sarcoid tissues.14
Various radioisotopes have been used for interstitial
brachytherapy of equine sarcoids. Permanently
implanted seeds of radon-222 or gold-198 and remov-
able needles of radium-226, cobalt-60, or iridium-192
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
Figure 6—SCC on the vulva of a mare.
normal skin. The developing tumor eventually destroys
the overlying epidermis, leading to ulceration, necrosis,
and a generalized foul odor.3,21 These lesions gradually
enlarge and may develop a craterlike appearance. The
productive lesions develop as papillary masses with a
cauliflowerlike appearance.21 Diagnostic differentials
include sarcoids, melanoma, exuberant granulation tis-
sue, and pythiosis.3,23
In SCC of the male genitalia, tumors usually arise
from the glans penis or the inner lining of the penile
sheath and spread to the corpus cavernosum (Figure
5).21 Early clinical signs include preputial edema, dis-
charge, intermittent hemorrhage, dysuria, pollakiuria,
weight loss, and urinary incontinence.21 The regional
lymph nodes should also be assessed for metastasis by
inguinal and rectal palpation.21 Regular examination
and washing of the prepuce and penis will aid in early
detection of SCC and may even assist in preventing its
development.21 SCC affecting female genitalia typically
originates at the clitoris and progresses toward the vagi-
nal vestibule and mammary glands (Figure 6).21 Hyper-
trophy of the clitoris and surrounding tissue as well as
roughening of the ventral commissure may be noticed
early in the disease. Advanced lesions are generally
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
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,
or the lungs may also occur.21 The prognosis is poor for
oral SCC that has metastasized.3,21 Similarly, SCC of
the nasal cavity and paranasal sinuses previously had a
poor prognosis; however, a recent study using course-
fractionated cobalt-60 radiotherapy provided good to
excellent long-term results.28
Diagnosis
Diagnosis of SCC can be accomplished by cytologic
or histologic examination.21 Depending on the site and
size of the lesion, excisional, wedge, punch, or elliptical
biopsy can be performed. Histologically, the tumor
consists of nests and cords of epithelial cells that infil-
trate the dermis.21 Other diagnostic methods include
fine-needle aspiration of nodular lesions, cytologic
examination of superficial scrapings from ulcerated
lesions using a dull blade, and impression smears.21
Treatment
With SCC, treatment is most successful when the
lesion is recognized and therapy is initiated early in the
course of the disease.29 Debulking the tumor along with
cryosurgery, intratumoral hyperthermia, and cisplatin
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.

MELANOMA
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-
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
or more melanomas at some location by 15 years of
age.3,34,37 There appears to be no gender predilection for
these tumors. The most common areas of the skin
affected are underneath the tail (Figure 8) and external
genitalia. 38 Other regions less commonly affected
include the ear, eyelid, neck, parotid salivary gland,
guttural pouches, lips, and limbs. 3,33,34,37 When
melanomas do occur in horses of other colors, they may
be at greater risk for becoming malignant (Figure 9).6
The etiology of melanomas in horses has not been
clearly defined. It is thought that melanomas in old gray
horses are due to disturbed melanin metabolism, leading
to the formation of new melanoblasts, or to increased
activity in resident melanoblasts, resulting in a focal area
of pigment overproduction in the dermis.6 Controversy
exists as to whether exposure to increased levels of ultra-
violet radiation may play a role in the pathogenesis of
melanomas in horses. 6,33 Because of their frequent
occurrence in shaded body regions, sun exposure may
not be a risk factor for melanoma formation. However,
reducing solar exposure in predisposed horses may be
warranted.
Figure 8—Melanoma lesions on the underside of a horse's tail.
Clinical Presentation
Ninety-five percent of melanomas are slow-growing
and show no signs of regional or distant metastasis.
These tumors are of little clinical significance except
when they inhibit the use of riding tack or interfere
with urination, defecation, and coitus.37 Melanomas
commonly appear as black or gray, solitary, discrete,
firm, spherical or flat nodules in the skin or subcutis
and may have a pedicle. Tumors frequently coalesce,
and hundreds or more variable-sized nodules may be
present without affecting the well-being of the horse.
Many small tumors may be present, producing a cob-
blestone appearance.3,34 Overlying skin may be intact or
may be slightly alopecic. Lesions may ulcerate and pro-
duce a black, tarry discharge.3
Occasionally, melanomas will exhibit slow growth for
several years followed by a sudden rapid growth phase
associated with malignant transformation of the tumor.
These tumors become locally invasive and may metasta-
size.37 Sites of metastasis include regional lymph nodes,
lungs, liver, serosal surfaces, spleen, kidney, brain, bone,
and heart. If the tumor metastasizes to internal organs,
clinical signs will be determined by the affected organ.
252 Equine
Figure 9— Amelanotic melanoma on the underside of a
horse's tail. This lesion was ulcerated, aggressive, and rapid
growing, unlike melanomas that commonly occur in this
location in gray horses (see Figure 8).
Cachexia may be seen when almost any internal organ is
affected. 36,37 In rare cases, melanomas exhibit rapid
growth and malignant properties from the onset.39
Diagnosis
Diagnosis of equine melanomas is generally based on
gross appearance, which can be confirmed using histol-
ogy. Lesions are composed mostly of melanocytes and
melanophages.40
Treatment
Treatment is often not necessary for small
melanocytic tumors located in uncompromising loca-
tions. Rarely, tumors may spontaneously regress over
time.34 Large masses, or masses located in areas where
they can be a nuisance, are treated with surgical exci-
sion. When possible, a wide margin should be attained
with surgical excision.3,34,37 Cryosurgery can be used in
conjunction with surgical excision. However, tumor
regrowth is a problem with this technique also.3,34,37
Intralesional injection of BCG has been associated
with disappointing results in the treatment of
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
rejection have been developed.33 Although studies per-
formed with these vaccines have shown promising
results,33 we have not experienced success with their use.
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ARTICLE #5 CE TEST
CE
The article you have read qualifies for 1.5 con-
tact hours of Continuing Education Credit from
the Auburn University College of Veterinary Med-
icine. Choose the best answer to each of the follow-
ing questions; then mark your answers on the
postage-paid envelope inserted in Compendium.
1. Equine sarcoids are believed to be associated with
_______________ or a similar virus.
a. equine herpesvirus c. morbillivirus
b. bovine papillomavirus d. lentivirus
2. Which of the following breeds has a decreased chance
of developing sarcoid tumors relative to all other
breeds?
a. Appaloosa c. standardbred
b. Arabian d. quarter horse
3. Which of the following is not a type of equine sarcoid?
a. occult c. papillary
b. verrucous d. nodular
4. Biopsy of latent sarcoids should be avoided because
a. they may hemorrhage profusely and result in acute
blood loss.
b. it may cause an undesirable change in the behavior
of the lesion.
c. metastasis may occur in the lymph nodes and spleen.
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
metastasis?
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