 Reproductive Status: Equine Coital Exanthema is often associated carrier state is unclear: the scars that persist after
persist after healing may
EQUINE COITAL EXANTHEMA (ECE)
SYNONYMS
• Genital Horsepox
• Equine Venereal Balanitis in Stallions
• Eruptive venereal disease
• Equine venereal vulvitis/balanitis
• Coital vesicular exanthema
• Equine coital pyrexia (If fever occurs)
OVERVIEW
 EHV-3 causes equine coital exanthema, a highly contagious
venereal disease resulting in vesicular lesions on the penis and
prepuce of stallions and on the vulva of mares.
 The disease is generally limited to the reproductive tract, and
infection does not appear to affect fertility.
 Lesions have been reported in the nostril of a foal by the side of a
dam with coital exanthema, an example of horse-to-horse
transmission of coital exanthema virus without coitus.
 Although coital exanthema is uncommon and resolves
spontaneously, some stallions may not be willing to breed mares
when affected, leading to economic losses.
 Like other herpesviruses, a short-lived immunity develops after
SIGNALMENT
infection. The disease occurs sporadically worldwide.
 Species: Horses
 Age: Equine Coital Exanthema can affect horses of various
ages, from foals to adults. However, it is more commonly seen
in sexually mature horses that are involved in breeding
activities.
 Sex: Both male and female horses can be affected by Equine
Coital Exanthema. Mares (female horses) may develop lesions
on their vulva, while stallions (male horses) may develop
lesions on their penis.
 Breed: All horse breeds are susceptible to Equine Coital
Exanthema. The disease is not specific to any particular breed.
with breeding activities. Horses involved in breeding, both as
stallions and mares, are more likely to be affected. It's less
identify potential carriers, but such asymptomatic carriers have not
been identified. Immunity is short-lived, but evidence from
common in geldings (castrated males) or non-breeding stallions shows that recurrence is not likely within a single breeding
horses. season.
• Recrudescence may occur after stimuli such as stress,
SYSTEMS AFFECTED
systemic disease, or trauma to the genital area.
 Reproductive System: ECE mainly affects the genitalia of horses.  The virus is transmitted mainly through direct contact during sexual
In mares, it can cause lesions and sores on the vulva and vaginal intercourse; nevertheless, non-coital transmission has been
mucosa, leading to swelling and discomfort. In stallions, it can lead occasionally described, associated with the genito–nasal contact
to similar lesions on the penis. These lesions and discomfort can by behavioral nuzzling/sniffing. Contaminated fomites are
affect breeding activities. frequently implicated in the spread of this virus, during reproductive
maneuvers in breeding facilities
 Integumentary System: Since the lesions associated with ECE  During periods of reactivation from latency, production and
appear on the genitalia, they are considered a part of the excretion of infectious virus serve as the source of infection for
integumentary system. The sores can be painful and may lead to other animals. EHV-3 latency has been demonstrated
inflammation of the skin and mucous membranes in the affected experimentally by reactivation and re-excretion after the
area. administration of glucocorticoids to seropositive mares and also
naturally, by isolation of the virus from seropositive mares that
 Respiratory System: use of a contaminated endoscope was remained isolated from other equids during 11 months
involved in an outbreak of an atypical presentation of EHV-3
ETIOLOGY, EPIDEMIOLOGY, TRANSMISSION
infection resulting in unilateral rhinitis in training Thoroughbred
horses
 Equine coital exanthema is caused by equine herpesvirus
type 3 (EHV-3).
 This virus has a single antigenic type but also has small and
large plaque variants in tissue culture, indicating that variation
may occur in the severity of field outbreaks.
 Equine coital exanthema is a benign venereal disease of horses
that likely occurs worldwide. It affects both sexes. Although the
primary route of transmission is venereal, outbreaks have been
documented in which transmission occurred via contaminated
supplies and instruments or by the use of a single glove for
rectal examination of many mares. It is probably for this reason
that EHV-3 has also been isolated from horses that have not been
bred.  (1) Equid alphaherpesvirus 3 (EHV-3) infects the stratified
 Equine coital exanthema is probably transmitted only in the epithelium of epidermal tissues present at mucous–cutaneous
acute phase of the disease; after the lesions have healed, horses margins and skin of external genital organs; (2) the virus
do not appear to shed the virus. However, the existence of a
 replicates and laterally spreads; (3) lytic replication occurs
and the virus is shed; (4) destruction of epithelial cells elicits
a vigorous, localized inflammatory response; (5) the virus
does not breach the basal membrane, and thus systemic
dissemination is limited; square to dots: After active infection the
virus induces latency; the anatomic site has been not yet
demonstrated but it has been inferred to be in the sciatic and/or
sacral ganglion cells.
CLINICAL SIGNS
EHV-3 Lesions in Both Sexes:
• Lesions are restricted to the external genitalia in both
mares and stallions.
• They start as small raised papules, progress to vesicles,
then pustules, and finally become raw or encrusted
erosions or ulcers.
• Local inflammation, redness, and swelling are common.
• Uncomplicated cases resolve within 10 to 14 days, leaving
depigmentation and cutaneous scars. Some severely affected
horses may become febrile and inappetent.
• without therapeutic intervention.
Clinical Signs in Mares:
• Develop 4 to 8 days after sexual contact.
• Appear as multiple, circular, red nodules on the vulvar
and vaginal mucosa, clitoral sinus, and perineal skin.
• Nodules develop into vesicles, pustules, and ulcers that may
coalesce into larger lesions.
• Edema can develop in the perineum and may extend
between the thighs.
• Occasionally, ulcers occur on the teats, lips, and nasal
mucosa.
• Secondary bacterial infection, often by Streptococcus
spp. (S. zooepidemicus-common), is common and can cause
fever.
• Skin healing is complete within 3 weeks, but clitoral and
vaginal ulcers heal more slowly. Skin lesions persist as
unpigmented scars, but pregnancy rates are not reduced.
 The gold standard for diagnosis of EHV infection is the
 Serum neutralizing antibodies peak 2-3 weeks after infection
 Complement fixing antibodies are not present beyond 60 days
A sequential progression of the clinical stages of ECE lesions, from
vesicular to pustular to ulcerative and then to healed white scars
Clinical Signs in Stallions:
• Similar to those in mares and found on both the penis and
prepuce.
• Intromission is painful, leading to reluctance to copulate.
• Copulation during the ulcerative stage may cause ulcers
TREATMENT AND PREVENTION
to hemorrhage into the ejaculate, reducing sperm viability.
DIAGNOSIS
 Tentative diagnosis based on clinical signs.
 Confirmation involves electron microscopy to identify the virus
in cells from ulcer margins.
 Typical intranuclear herpesvirus inclusion bodies can be seen
in cytologic or histologic preparations.
 Acute and convalescent serum samples can be used for
serum neutralization or complement fixation tests for
diagnosis, but interpretation must be cautious due to potential
cross-reactivity with EHV-1 and EHV-4.
 Many diagnostic laboratories offer conventional PCR assays
for the detection of EHV-1, EHV-4, and EHV-3 DNA.
isolation of the virus from various samples, including
nasopharyngeal swabs, blood, fetal tissues, and placental tissues.
and may remain detectable for up to a year.
after infection.
DIFFERENTIAL DIAGNOSIS
• Coital exanthema lesions are characteristic; however,
inflammation of the penis or vulva may also occur due to
• trauma, bacterial infection, or contact hypersensitivities.
• Vesicular stomatitis may also uncommonly affect
genitalia.
• Contagious Equine Metritis (CEM)
• Dourine
• Neoplastic Conditions
• Genital lesions caused by EHV-3 infection usually heal
• Sexual rest is essential to allow ulcers to heal and prevent
the spread of the disease.
• Affected horses should be isolated until all lesions have
healed.
• Disposable equipment should be used for examinations to
prevent transmission.
• During the acute phase of the disease, mares should be
bred only by artificial insemination.
• All horses should be examined carefully before they are
allowed to breed, considering the incubation period of up
to 10 days.
• Daily cleaning of the lesions and the genitalia with
antiseptics
• Reducing inflammation with glucocorticoid anti-
inflammatory drugs
• The use of antibiotic ointments to prevent secondary
infections is advisable. (Administration of broad-spectrum
antimicrobials )
• Additionally, an attempted treatment could be made using a
5% acyclovir topical cream formulation
• No vaccine is available for Equine Coital Exanthema (ECE).
DOURINE
- The term "dourine" likely originates from the French word "dourin,"
which means stiff or inflexible. This name may refer to one of the clinical
signs observed in affected horses, particularly the stiffness or paralysis
that can occur due to the neurological involvement of the disease.
SYNONYMS
 Covering Disease,
 Morbo Coitale Maligno,
 Slapsiekte,
 El Dourin,
 Mal de Coit,
 Beschalseuche,
 Sluchnaya Bolyezn
 Lappessa
 Dirressa
OVERVIEW
 Disease of equidae
 Natural infections reported only in horses and donkeys
 Causative agent—classically thought to be Trypanosoma
equiperdum; however, position with the trypanozoon group is
uncertain, with overlap noted between this and T. evansi and T.
brucei brucei.
 Only a small number of laboratory strains of uncertain origin exist
from the early 20th century. No recent isolates have been obtained.
 Venereal—only transmission; transmissible by direct contact
 Tropism for genital mucosa; cannot survive outside host
 Mortality high; debilitation; predisposition to other diseases
 Signalment: Breeding Mares and Stallions
ETIOLOGY
 Dourine is a parasitic venereal disease of equines caused by the
flagellate protozoan Trypanosoma equiperdum of the order
Trypanosomatida, family Trypanosomatidae and subgenus
Trypanozoon. Other species within this subgenus are T. brucei and
T. evansi. Recent genomic studies propose that T. equiperdum,
along with Trypanosoma evansi, are subspecies of T. brucei. One
hypothesis asserts that the disease condition “dourine” is actually a
host-specific immune response to either T. equiperdum, T. brucei
or T. evansi infection
 It is very closely related to the causative agents of African
trypanosomiasis (Trypanosoma brucei) and surra (T evansi), and
whether it should be considered a distinct species is controversial.
Strains of T. equiperdum appear to differ in pathogenicity
 This agent does not survive very long outside its hosts and is not
transmitted by fomites, therefore, parameters associated with
resistance to physical and chemical actions (i.e. temperature,
chemical/disinfectants, and environmental survival) are not
meaningful.
EPIDEMIOLOGY
 Dourine is not transmitted by an invertebrate vector. It is
transmitted during breeding or infected mares may occasionally
pass infection to foals. Average mortality associated with acute
disease approaches 50% (especially in stallions)
Hosts
 Horses, mules and donkeys
 No known natural reservoir of the parasite other than infected
equids
 Rats, mice, rabbits and dogs can be infected experimentally;
rodents are used to prepare antigen for diagnostic tests
Transmission
• Natural transmission occurs directly from animal to
animal during coitus:
mainly from stallion to mare, but may also be transmitted
from mare to stallion
infection is not always transmitted by an infected animal
at every copulation
• There is currently no evidence that arthropod vectors play
any role in transmission
• Rarely, foals may be infected via the mucosa
(conjunctiva), during parturition or by drinking milk from an
infected dam. Foals may then transmit disease when they are
sexually mature
Sources of Infection
• T. equiperdum may be found in vaginal secretions of
infected mares, and seminal fluid, mucous exudate of the
penis, and sheath of stallions
• Rarely, infected mares have been reported to pass the
infection to their foals, possibly from infected mare to fetus
via placenta.
• Trypanosomes have been detected in the mammary
secretions of some infected animals.
PATHOGENESIS
1. Transmission: Dourine is typically transmitted through coitus
(venereal transmission) but can also be spread through
contaminated equipment or blood-to-blood contact.
2. Initial infection: Once the parasite enters the horse's body, it
multiplies locally at the site of entry, often the genital mucosa or
skin lesions.
3. Dissemination: Trypanosoma equiperdum can spread through
the bloodstream to various organs, causing systemic infection. It
can affect the lymphatic system, leading to lymphadenopathy
(enlarged lymph nodes).
4. Clinical signs: The clinical signs of dourine can vary but often
include fever, anemia, edema (especially in the genital area),
genital lesions or swelling, and neurological symptoms. These
symptoms can appear in acute or chronic forms, with the chronic
form often leading to severe debilitation.
5. Immune response: The horse's immune system responds to the
parasite by producing antibodies. However, in some cases, the
immune response may not effectively clear the infection, leading to
persistent parasitemia (presence of parasites in the blood) and
chronic disease.
6. Chronic stage: In chronic cases, the horse may experience
neurological issues due to the parasite affecting the central
nervous system. This can result in weakness, incoordination,
paralysis, and even death.
Occurrence
• Dourine is endemic in some African, Asian and Latin
American regions, as well as the Middle East and Eastern
Europe.
• It was once spread more widely, but has been eradicated in
many countries.
 • In Italy, an outbreak occurred in 2011.
• Eradicated in North America
• The disease was introduced into North America by a
Percheron stallion imported into Illinois from France in 1882.
Outbreaks occurred in the United States in Illinois [1886],
Nebraska [1892 and 1898], South Dakota [1901], and Iowa
[1903], before the disease appeared in Canada in 1904.
• Dourine is believed to have originated in Asia, and may have
been introduced into Europe through the importation of
Arabian stallions. Outbreaks were reported in Germany,
France, Austria, and Switzerland, as well as in Algeria.
SYTEMS AFFECTED
• GI—weight loss; emaciation
• Cardiovascular—intense anemia, dependent edema
• Intergumentary - urticarial
• Lymphatic—peripheral lymphadenopathy
• Nervous—meningoencephalitis, progressive weakness,
paresis, and paralysis
• Musculoskeletal—progressive weaknessReproductive—
abortion
• Ophthalmic—keratoconjunctivitis
CLINICAL SIGNS
Both Sexes
 The initial lesions of dourine often involve the genitalia.
• Three phases of disease recognized:
 Genital edema (leading to increased permanent
thickening of tissues) and tumefaction
 Pathognomonic widespread raised cutaneous plaques 1—10
cm in diameter
 Anemia, neurological compromise (hindquarter weakness;
ataxia, hyperesthesia an hyperalgia), emaciation, death
 Approximately 50% of affected animals die of acute
disease in 6—8 weeks.
 Vesicles or ulcers may be present and can result in
permanent white scars known as leukodermic patches.
 Depigmentation can occur in the genital region, perineum,
and udder
 Some horses in Italy experienced severe swelling of the
ventral abdomen and legs, especially the hindlegs, without
genital involvement.
 Edematous patches known as "silver dollar plaques" (up to
10 cm in diameter and 1 cm thick) can appear on the skin,
particularly over the ribs.
 These cutaneous plaques typically last for 3 to 7 days and
are considered pathognomonic for the disease, although they
have occasionally been reported with T. evansi.
 Not all T. equiperdum strains exhibit these plaques.
 Horses in Italy were reported to have smaller, variable
wheals and plaques that lasted for hours to days and
waxed and waned in different body areas.
 Pustular dermatitis was also described in this outbreak.
 Can potentially exhibit neurological signs, including
restlessness, weakness, stiffness, lameness,
incoordination, and paralysis.
 Ocular symptoms: conjunctivitis and keratitis are common
in some cases.
 Anemia, intermittent fever, and progressive weight loss
are typical in affected animals.
 The clinical course of the disease can vary from chronic to
acute, with waxing and waning symptoms and potential
relapses, often triggered by stress. The recovery and long-
term outcomes in animals with dourine are controversial, and
subclinical infections have been reported.
In Mares
• Mucopurulent vaginal discharge.
• Edematous vulva.
• Vulvitis, vaginitis with polyuria, and signs of discomfort.
• Raised and thickened semitransparent patches on the vaginal
mucosa.
• Potential for abortion.
• Edema can extend to the ventral abdomen, perineum, and
mammary gland in mares.
• A serum-like or cloudy, whitish mammary secretion may be
observed.
In Stallions
 Stallions develop edema of the prepuce and glans penis,
and can have a mucopurulent discharge from the urethra.
Paraphimosis is possible. Edema can spread to involve
the ventral abdomen and perineum, including the
scrotum in stallions
 Plaques and depigmented lesions, as in females
 Inguinal LN enlargement
Morbidity and Mortality
• Morbidity variable
• Chronic, mild disease
• Acute, severe disease
• Mortality
• Untreated cases: 50 to 70%
• Endemic areas
• Drug treatment may be possible
• Treatment may result in inapparent
DIAGNOSIS
carriers
• Dourine diagnosis typically involves:
• Serology in combination with clinical signs.
• Supporting evidence from histopathology and
epidemiological information regarding non-insect
transmission.
• The Complement Fixation (CF) test is commonly used,
especially for international trade and eradication efforts.
• No serological test is entirely specific for dourine, leading
to cross-reactions with other Old World trypanosomes,
notably T. brucei and T. evansi.
• False positives in the CF test can occur, particularly in
donkeys and mules, due to anticomplementary effects in
equid serum.
• Indirect fluorescent antibody tests and chemiluminescent
immunoblot assays may help resolve cases with inconsistent
or nonspecific reactions.
• Other serologic tests used include ELISAs,
radioimmunoassay, counter immunoelectrophoresis, agar gel
immunodiffusion (AGID), and card agglutination.
• Immunostaining is employed to detect trypanosomes in
tissues.
• Dourine diagnosis can involve the identification of the parasite,
but it's challenging.
• T. equiperdum cannot be distinguished microscopically from T.
evansi.
• Trypanosomes may be found in lymph, edematous fluids of
the external genitalia, vaginal or preputial washings or
scrapings, mammary gland exudates, or plaque content.
• Detection is more likely soon after edema or plaques first
appear and only occurs for a few days within plaques.
 • Rarely, T. equiperdum may be found in thick blood films, animals may improve clinically but remain carriers of the
but it's present very briefly in the blood and is usually parasite\
undetectable. • Stallions have sometimes been castrated in an attempt to
• Concentration techniques like capillary tube centrifugation or prevent disease transmission;
mini anion exchange centrifugation can improve success • however, geldings can still transmit the disease if they
rates. display copulatory behavior.
• PCR assays are more sensitive than culture and can • Disinfection
identify the parasite to the subgenus Trypanozoon level. 1% sodium hypochlorite
• Differentiating T. equiperdum from T. evansi remains 2% glutaraldehyde
genetically challenging. 2% formaldehyde
• In the nervous form, the organism can be recovered from the Heat at 50 to 60°C
lumbar and sacral spinal cord, sciatic and obturator nerves, • Successful treatment reported in some endemic region-
Trypanocidal drugs
DIFFERENTIAL DIAGNOSIS
and CSF.

• Coital exanthema
• Contagious equine metritis
• Surra
• Nagana
• Anthrax
• Equine viral arteritis
• Equine infectious anaemia
• Purpura haemorrhagica
• Other conditions leading to weight loss and emaciation:
malnutrition, verminosis, dental pathology, chronic

TREATMENT AND PREVENTION

infections

• Control of the disease depends on compulsory notification

and slaughter of infected animals. Herd eradication.
Infected animals euthanized
• Movement control enforced by legislation in most countries
• Good hygiene at assisted matings is also essential
• fences may help control the spread, although stallions
have been reported to serve mares over fences
• New animals – Quarantine, serological testing, cease
breeding if detected
• One recent study found that bis (aminoethylthio) 4-
melaminophenylarsine dihydrochloride (cymelarsan) was
effective in a small number of acutely or chronically infected
horses, and relapses were not observed up to a year after
treatment. Further evaluation of this drug is still required.
• Pharmaceutical therapy is not recommended because

THRUSH
DEFINITION
 Thrush is a degenerative keratolytic condition of the frog, the
central and collateral sulci of the frog, characterized by
disintegrating horn and the presence of grey to black material in
the affected areas
PATHOGENESIS/ ETIOLOGY
 Unhygienic, moist stabling conditions with poor foot care.
 Infection by keratolytic organisms: multifactorial, but often
Fusobacterium necrophorum is involved.
 Thrush usually starts superficially on the surface of the frog,
particularly in the central and paracuneal sulci, before extending
deeper into the stratum corneum of the frog and occasionally
reaching the germinal layers of the epidermis and the dermis
 Horses with deep and/or narrow sulci are more prone to
developing thrush than those with wide and shallow sulci.
SYSTEMS AFFECTED
 Thrush typically affects the center and grooves (central and lateral
sulci) of the frog
 Black discharge in the sulci of the frog with very offensive odour.
 Lameness only when sensitive tissues involved.
SIGNS
 Mainly hind limbs affected.
 Horses with thrush usually present because the affected foot has
a characteristic foul odour and discharge, and the surface of the
frog is ragged.
 Affected animals are often not lame, but deeper damage,
especially between the bulbs of the heel, can be painful
DIFFERENTIAL DIAGNOSIS
 Canker
DIAGNOSIS
 The characteristic odour and appearance of the frog are usually
sufficient to make a diagnosis of thrush, but it may need to be
distinguished from early canker
The symptoms and progression
of thrush differ from those of canker in several ways:
(1) thrush is a degenerative condition of the superficial layers of the frog,
whereas canker is a proliferative condition affecting the basal layers
(2) thrush is confined to the frog and paracuneal sulci, whereas canker
may extend to any part of the hoof
(3) horses with thrush are less likely to be lame; and
(4) remedies that usually cure cases of thrush frequently fail to improve
TREATMENT
canker.
 Thrush is effectively treated with debridement of ragged and
undermined frog, transferring the horse to hygienic and dry
conditions
 An astringent solution (eg, copper sulfate solution) may be applied
with daily hoof cleaning.
 Applying topical antiseptics and astringents (e.g. povidone–iodine,
2% tincture of iodine or proprietary preparations of formalin [but
formalin in its aldehyde state is best avoided])
 Prognosis
 The prognosis is almost always good. Horses with narrow frogs
and deep sulci are likely to experience recurrence if they have to
stand on moist unhygienic surfaces.
PREVENTION
 Keeping hooves clean of dirt, debris and excess moisture is the
best way to prevent thrush

CANKER
DEFINITION
 Equine proliferative pododermatitis, or canker is a debilitating
disease of the hoof characterized by chronic proliferation of horn-
producing tissues, mainly in the frog region but sometimes also
undermining the sole, heel bulbs, and, less commonly, the hoof
wall
PATHOGENESIS/ ETIOLOGY
 The disease classically starts in the central or paracuneal
(collateral) sulci and then rapidly spreads to the crura of the frog
 It may extend to the sole or bulbs of the heel, and occasionally
even to the walls of the hoof
 Canker classically occurs in the hooves of horses that are
standing for prolonged periods on a wet ground surface that is
contaminated with feces
 The etiology and pathogenesis of canker are unknown, but
anaerobic bacterial infection affecting the germinal layer of the
epithelium has been hypothesized in the literature
 infectious agents such as anaerobic bacteria, viruses, fungi, and
spirochetes have been isolated from diseased tissue, but the
causal relationship between specific organisms and canker
remains unclear.
 It has not yet been established whether canker in fact represents
one or more disease processes or etiologic agents
SYSTEMS AFFECTED
 Musculoskeletal
SIGNS
 The duration of the disease is usually chronic, over several weeks
to months
 It may affect one or more feet. Canker has a characteristic
proliferative appearance from which extend finger-like projections, dressings saturated with 10% benzoyl peroxide in acetone have
and it is usually associated with a yellow, creamy exudates also been used successfully
 The lesion is typically located on the frog, but may have extended
to involve any other part of the hoof PROGNOSIS
 Palpation of the affected area is likely to elicit a painful response
 Early in the course of the disease the horse may be sound or  The response to treatment in this disease is highly variable and,
slightly lame, but as the disease becomes more advanced the therefore, the prognosis must always initially be guarded. A
lameness becomes progressively worse cautious long-term outlook is advised because it is not currently
known whether individual animals may have a predisposition
DIFFERENTIAL DIAGNOSIS towards developing this disease
 Thrush
DIAGNOSIS
 Diagnosis is usually based on the physical appearance of the foot
but a biopsy and histopathology are required for confirmation.
 the pathognomonic appearance of hoof tissue, most frequently
foul-smelling, cheesy masses with filamentous or cauliflower-like
epithelial proliferations, often extending from the caudal part of the
frog to the heel bulbs and bleeding on manipulation; affected
horses often also have upright hairs at the heel bulbs
 Culture is generally unrewarding because the tissue typically
yields a variety of organisms.
 Because no definitive single causative agent has been identified,
a variety of treatments have been proposed
 Extensive surgical debridement of all affected tissues.
Debridement can cause extensive haemorrhage and is best
performed with the horse under general anaesthesia and following
placement of a tourniquet
TREATMENT
 Careful prolonged post-operative management with daily
bandaging, application of topical therapeutic dressings (e.g.
benzoyl peroxide in acetone and metronidazole) until the defect is
dry and covered with a layer of new horn. Additional debridement
of necrotic dermis may be required during bandage changes
 In refractory cases, 0.05% enrofloxacin or clindamycin in Tricide®
(Molecular Therapeutics LLC), applied either as a wet-to-dry
dressing or as a dry-to-dry dressing after the dressing has been
soaked and dried, has been successful. Alternatively, topical

LAMINITIS
DEFINITION
 Laminitis is a disease in which a series of pathophysiological
events cause injury to the dermal and epidermal lamellae
 This in turn weakens the attachment between the lamellae and, at
its most extreme, causes separation of the hoof capsule from the
underlying tissues
 Laminitis has been defined as acute if it is within 72 hours of onset
of clinical signs and has not been accompanied by displacement
of the distal phalanx
 It has been defined as chronic once the distal phalanx has
displaced in relation to the hoof capsule (regardless of duration)
 Laminitis that is present for more than 72 hours’ duration and is
not accompanied by displacement has been defined as subacute
PATHOGENESIS/ ETIOLOGY
 There are 3 distinct major forms of laminitis based on the
underlying cause and mechanisms—laminitis associated with
severe systemic disease (sepsis associated);
 laminitis associated with insulin dysregulation (endocrinopathic
laminitis);
 and laminitis associated with excessive weight-bearing on a foot
(supporting limb laminitis)
 The lamellae suspend P3 within the hoof capsule—epidermal
lamellae extend like sheets from the stratum medium of the inner
hoof wall, interdigitating with dermal lamellae that are ultimately
connected to P3.
 Endocrinopathic laminitis is intrinsically linked to insulin
dysregulation in horses/ponies and encompasses laminitis
associated with EMS, PPID, and exogenous corticosteroid
administration
 Current evidence suggests that excess insulin overstimulates
growth factor receptor IGF-1R, which triggers a response in
lamellar epidermal cells that involves disruption of normal cell
adhesions
 Sepsis-associated laminitis occurs with severe systemic
inflammation, usually as a result of infection (e.g. pneumonia) or
the absorption of bacterial products (particularly endotoxin) from
the gastrointestinal tract (e.g. colitis, natural/experimental
alimentary carbohydrate overload)
 Marked local inflammation including infiltration of the lamellae with
neutrophils is characteristic
 Supporting limb laminitis appears to be the result of ischemia due
to reduced lamellar perfusion due to both increased load and
reduced unweighting/load cycling on a limb.
 Pasture-associated laminitis may involve pathophysiologic
elements of both endocrinopathic and sepsis-associated forms
 Once the lamellar attachments are weakened, the nature and
severity of the resultant pathology are determined by the extent of
lamellar damage.
 Severe, wholesale acute lamellar detachment can result in
downward P3 “sinking” within the hoof capsule.
 In many endocrinopathic cases chronic laminitis pathology is very
slowly progressive and substantial pathology is often already
present by the time clinical signs are first recognized
 Systemic septic diseases including colitis (bacterial, Potomac
horse fever, grain overload), anterior enteritis, colonic volvulus,
septic peritonitis, pneumonia, metritis/retained fetal membranes
 Insulin dysregulation due to EMS or PPID
 Pastures rich in nonstructural carbohydrate, particularly in
combination with EMS or PPID
 Excessive weight-bearing on a limb due to pain or dysfunction of
the opposite limb
 Exertional Rhabdomyolysis
 Exposure to black walnut (Juglans nigra) heartwood shavings
 excessive work on hard surfaces Corticosteroid administration
 Excessive intake of cold water (empirical reports only)
 Ingestion of the toxic plant hoary alyssum (Berteroa incana) in hay
or pasture
SYSTEMS AFFECTED
 Musculoskeletal—foot
SIGNS
 Rare (absent) in foals or weanlings
 Pony breeds more susceptible to theendocrinopathic form
 Chronic laminitis is common in broodmares
 Laminitis is divided into 3 phases—developmental, acute, and
chronic
 Historical Findings
 Acute or recurrent lameness of variable severity in 1 or more
limbs
 Reluctance to move± more frequent recumbency


Lameness worse when circling or on hard ground
Recent systemic disease or access to excess grain or lush
pasture ±Severe, prolonged contralateral limb lameness.
Developmental phase
◦ No clinical signs; however, primary disease and pathologic processes
that lead to lamellar damage are under way
Acute laminitis
◦ Increased digital pulse amplitude and hoof wall/coronary band
temperature
◦ ± Distal limb edema
◦ Incessant shifting weight in fore- and hindlimbs ◦ In mild cases, subtle
lameness
With increasing severity, obvious lameness at the walk; worse circling
on a hard surface
◦ Characteristic stance—forelimbs extended forward and hindlimbs
underneath the body
◦ In severe cases, unwillingness to move and recumbency
± Difficulty lifting limbs due to reluctance to bear weight on opposite
limb
◦ Tachycardia, tachypnea, and sweating may be profound
◦ Highly variable response to hoof testing. ± Generalized hoof pain or
focal pain in toe region. ±Reaction to tapping the hoof wall
Chronic laminitis
◦ Defined by ≥48 h of clinical laminitis and/or radiographic displacement
of P3 within the hoof capsule
◦ Increased digital pulse amplitude
◦ Variable lameness
◦ ±Prolonged periods in recumbency
◦ Palpable coronary band cleft
◦ Prolapse of the sole in the toe; ±P3 penetration through the sole
± Uneven hoof growth rings, wider in quarters/heels, narrower in dorsal
hoof wall
◦ Characteristic “dished” appearance to dorsal hoof wall
◦ ± White line separation, seedy toe, and abscess
◦ ±Persistent tachycardia and hypertension
◦ Weight loss in moderate to severe cases

DIFFERENTIAL DIAGNOSIS
 Other painful conditions such as rhabdomyolysis, tetanus, or
pleurodynia secondary to pleuropneumonia
 Rule out by absence of increased digital pulse amplitude and
digital hyperthermia
 Unilateral limb laminitis or laminitis that is more severe in 1 digit
must be differentiated from hoof abscess or P3 fracture. Rule out
by hoof testing and radiographs
Pathologic Findings
 Abnormalities due to inciting cause(s)
 ±Stress leukogram
DIAGNOSIS
 Testing of the pituitary adrenal axis in cases of suspected PPID
(Cushing disease). Baseline adrenocorticotropic hormone
concentration or thyrotropin-releasing hormone response test
preferred to dexamethasone suppression test
 Baseline insulin concentration or preferably dynamic testing (oral
sugar test) for the diagnosis of insulin dysregulation of PPID or
EMS
 Plasma creatinine and albumin concentrations with NSAID use to
monitor for toxicity
 Standard lateromedial radiographs to assess P3 position relative
to the hoof capsule. Radiopaque marker placed on dorsal hoof
wall at the coronary band aids in measurements. A steel rod of
known length can be used to correct for magnification
 Radiographs obtained at onset of clinical signs to document
progression
 P3 rotation, dorsal hoof wall to P3 distance, and coronary band to
the extensor process of P3 distance can guide progression and
prognosis
 Digital venograms may be useful in chronic cases to determine
vascular compression or thrombosis. ± Guide hoof wall resection
or coronary grooving. Adhere to published descriptions of this
technique to avoid common artifacts
 Avoid perineural anesthesia unless there is difficulty isolating
lameness to the foot
 Chronic—sagittal sectioning of the feet reveals characteristic
formation of lamellar wedge and palmar rotation of P3
 Acute—lamellar histopathology recommended, gross changes
TREATMENT
may not be obvious
AIMS
Treat underlying cause(s)
Acute—limit mechanical damage, control inflammation
Chronic—provide mechanical support, encourage normal hoof growth
Provide adequate analgesia and supportive
care
Developmental Phase
 Laminitis is irreversible; focus is prevention during the
developmental phase and minimizing progression in the early
acute phase
 With septic disease/endotoxemia, aggressive systemic treatment
with anti-inflammatory and antiendotoxic therapy as well as
continuous cooling of the feet. Ideally, an ice and water mixture is
applied from the proximal metacarpal/metatarsal region to (and
including) the hooves and is regularly replenished. Maintain ice
boots for up to 7 days
 Preemptive shoe removal and application of frog/sole support
Acute Phase
 Once clinical signs are apparent, limit mechanical damage
 Strict stall confinement
 Continuous cooling of the feet after the onset of lameness in
sepsis-associated cases
 Light sedation may encourage recumbency
 In less painful horses, shoe removal, excessive toe conservatively
trimmed
 Bed on sand or apply silicone impression material or Styrofoam
padding to the sole
 Styrofoam pads custom sized to the foot and taped on overnight.
Once crushed down, remove pad and cut off the toe portion
 Reapply pad with an additional second pad underneath to
preferentially load the caudal foot
 Heel elevation (10–20◦) to reduce deep flexor tendon tension and
redistribute distracting forces from the dorsal wall to
quarters/heels
 Judicial NSAID use; excessive analgesia may encourage
locomotion and increase mechanical damage
 Sling support during standing periods especially with rapid P3
sinking
Chronic Phase
 Medical management of underlying endocrinopathy (EMS or
PPID), diet management, restrict nonstructural carbohydrate
consumption (soaked hay, commercially formulated feeds)
 Ongoing farriery and a closeclient–veterinarian–farrier relationship
are required for successful management
 Avoid radical trimming or shoeing. Gradualchanges over >1
shoeing interval to avoiddestabilizing the foot and worsening of
clinical signs
 Shoe/pad/trim or other farrier techniques that redistribute weight
from hoof wall to frog and caudal sole, minimize breakover forces,
and reduce deep flexor tendon tension
 Radiographs should be used as a guide for trimming and shoeing
 In acute phase, absolute strict stall confinement
 Stall rest for at least 1 month, and up to ≥6
 months, after an acute laminitis; depends on severity

Activity
Very, very gradual reintroduction to exercise

DIET
Avoid excessive carbohydrate in grain, hay, and pasture

Obese and/or EMS horses benefit from controlled, gradual weight

loss
 With significant P3 rotation (>15◦) or where the dorsal tip of P3 is
penetrating the sole or causing solar prolapse, deep flexor
tenotomy may be beneficial
In chronic cases, coronary grooving or dorsal hoof wall resection

can relieve tension on the coronary band, reduce sublamellar
venous compression, and facilitate better quality hoof wall
regrowth.
DRUG(S) OF CHOICE
  NSAIDs—phenylbutazone (2.2–4.4 mg/kgevery 12 h) tends to
provide superior analgesia to flunixin meglumine (1 mg/kg every
12 h)
 Acepromazine (0.02–0.04 mg/kg IV or IM every 6 h) during the
acute phase

 Avoid corticosteroid administration

 Monitor for signs of toxicity with long-term NSAID use.

 Aggressive and early treatment of primarydisease in systemically

ill horses
 Identify horses with EMS/PPID or insulindysregulation and strict

PREVENTION

dietary control toavoid hay/grain and pasture high in soluble

carbohydrate; maintain an ideal body weight
 For high-risk horses, avoid pasture turnout when nonstructural
carbohydrate levels are likely to be highest—midmorning to late
afternoon, spring and fall, during flowering and early seeding or
after frosts

Exertional Rhabdomyolysis/
Azoturia
DEFINITION
 Exertional rhabdomyolysis (otherwise known as
azoturia or ‘Monday morning disease’) is a syndrome
of muscle pain that occurs during or following exercise
 Necrosis of skeletal muscle fibers. Rhabdomyolysis in
horses occurs associated with exercise and in
nonexercising horses on pasture.
 It can be caused by several different conditions that
each affect skeletal muscle function in different ways
and result in a common clinical presentation.
PATHOGENESIS/ ETIOLOGY
 Sporadic cases may be caused by dietary imbalances
or overexertion (rapid increase in work intensity or
duration).
 Chronic/recurrent cases may be related to defects in
intracellular calcium regulation or glycogen metabolism.
 Highly strung mares and fillies are affected more than
colts.
 Tends to be an increased incidence in certain breed
lines and families of horses
 Exercise-induced skeletal muscle necrosis results in
release of CK and myoglobin into circulation, often with
stiffness, cramping, and pain; severe myoglobinuria
can result in renal tubular damage and renal
insufficiency
 ER can occur as an acquired disorderassociated with
overexertion, heat exhaustion,viral infections, and prevalence in halter Quarter Horses (∼ 28%)
other factors; however, it is most commonly associated In Belgian drafts, prevalence approaches 40%
with heritable muscular disorders including RER and
PSSM. Geographic Distribution
Acquired Causes
 Exercise exceeding level of training
Worldwide
 Exhaustive exercise SIGNS
 Dietary electrolyte and mineral imbalance
 Electrolyte depletion during exercise.
 Vitamin E and/or selenium deficiency General Comments
 Influenza  Frequency and severity of rhabdomyolysis episodes
can be very variable between and within individuals
Inherited Causes  Clinical signs can occur any time from immediately
 In Thoroughbred RER, defective calcium regulation before exercise until sometimes hours after exercise
resulting in a low threshold for muscle contraction;  Subclinical disease (elevated CK/AST only) can occur
±analogous disorder in Standardbreds with few clinically visible abnormalities, and may be a
 In PSSM, heritable defect of glycogen metabolism particular risk in endurance horses
recognized in QuarterHorses, Paints, some drafts, and
related breeds Historical Findings
 Possible triggering factors—training regime changes,
Risk Factors ration changes, prior rest period
High starch (grain) diet  Variable signs from mild stilted gait to severe sweating,
>24 hr of stall rest in horses with underlying muscle disease stiffness, and recumbency.
Sudden interruption of exercise routine.  Repeated episodes may be observed
Infectious respiratory disease
Nervous temperament (Thoroughbreds, polo horses). Physical Examination Findings
 Exercise intolerance
Lameness (Thoroughbreds)
Genetic predisposition  Stiffness,
High level of fitness (Thoroughbreds, Arabians)  stilted gait
 Sweating
 Reluctance to move
SYSTEMS AFFECTED
 Swollen
 and/or fasciculating muscles
 Tachycardia,
 Musculoskeletal
 tachypnea
 Renal
 Distress
Incidence/Prevalence  Recumbency
RER affects ∼ 5–7% of racing Thoroughbreds  Pawing, stretching, discomfort
 Discolored
PSSM affects ∼ 6–10% of Quarter Horses, higher
 (red/brown) urine
 Muscle atrophy
 Usually normal between episode
 Thoroughbreds, Quarter Horses, Appaloosa, Paint,
Belgian draft, Percheron, Arabian, Standardbred,
Warmblood, many other light breeds
SIGNALMENT
 Mean Age and Range
 For PSSM, mean age of onset of signs in Quarter
Horses is ∼ 5 years (range 1 day tolate maturity)
In Thoroughbred racehorses, 2-year-olds most
 
frequently affected
Arabian endurance horses, clinical disease >5 years of
 
age and often in older horses.
Predominant Sex
 
 In Thoroughbreds and Standardbred racehorses, 2–3-
year-old females more likely to be affected. Sex bias
resolves withincreasing age
Sex predilection not reported for the other disorders.
 fold CK increase is considered suspicious. This test
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
 Association between exercise and onset of signs in
addition to physical examination and laboratory
findings facilitates differentiation from other conditions
 Conditions causing reluctance to move, acute
recumbency, and/or discolored urine, including:
◦ Lameness/laminitis
◦ Diseases causing intravascular hemolysis or bilirubinuria
◦ Lactation tetany
◦ Aortoiliac thrombosis ◦ Tetanus
◦ Neurologic disease ◦ HYPP
◦ Colic
◦ Pleuropneumonia  APPROPRIATE HEALTH CARE
 Aims of treatment—reduce discomfort and anxiety,
prevent further damage, normalize hydration, acid–
 Elevated serum CK, AST, and lactate dehydrogenase base and electrolyte status, and restore or protect
Myoglobinuria renal function
±Hypochloremia, hypocalcemia, hyponatremia,  Severe rhabdomyolysis is an emergency. Inpatient
hyperkalemia (severe disease) management recommended to facilitate fluid therapy.
±Metabolic alkalosis or acidosis Further muscle damage can occur with transport; less
±Elevated serum creatinine and urea nitrogen severe cases can be managed as outpatients
OTHER LABORATORY TESTS  Nursing Care
 IV or oral fluid therapy with balanced electrolyte
solutions until myoglobinuria resolves
Urinary fractional excretion of electrolytes
 Alkalinizing fluids in myoglobinuric horses with
 Blood selenium and serum/plasma vitamin E
metabolic acidosis to protect against renal injury
OTHER DIAGNOSTIC PROCEDURES
 Deep bedding, particularly for recumbent patients
 PCR testing of blood or hair for GYS1 mutation in
 Slinging to prevent prolonged recumbency and further
PSSM breeds.
muscle trauma
_ Semimembranosus muscle biopsy in non-PSSM
breeds (Warmbloods, Arabians).
 After mild episode, commence gentle exercise (at
 _ Submaximal exercise test—serum CK activity before
reduced intensity and duration than prior to episode) in
15 min of walk and trot exercise, then 4–6 h later >2–3-
24–48 h if clinical signs of stiffness have resolved
 With severe episode, remain stall confined until
has
recovered
 greatest utility in PSSM
PATHOLOGIC FINDINGS ACTIVITY
 Low-intensity exercise (hand-walking) initiated when
 In RER, nonspecific muscle changes (increased clinical signs and serial CK improves
centrally located nuclei, myocyte degeneration and
regeneration) Diet
 In PSSM, abnormal polysaccharide inclusions if >2
years of age, subsarcolemmal vacuolations.  Low-starch diet (grass hay) according to caloric
 Arabian horses with ER—abnormal cytoplasmic requirements
desmin accumulation in myocytes  In RER-susceptible horses, avoid >2.2 kg (5 lb) of
grain per day
 In PSSM-susceptible horses, no grain
TREATMENT
 Fat supplements (rice bran, vegetable oil) and soluble
 fibers (beat pulp) if higher caloric requirements exist
 Eliminate high-starch supplements (molasses)
 Susceptible horses should not be stall rested
 for >24 h at a time . Frequent exercise is preventative
 Daily turnout or forced daily exercise (riding or lunge
work) is ideal. Interruption of routine exercise is a
CLIENT EDUCATION
prominent risk factor
 Discuss breeding management when underlying
hereditary muscle disorder is suspected
DRUG(S) OF CHOICE
 For significant distress and pain, xylazine (0.2–0.4
mg/kg) or detomidine (0.01–0.02 mg/kg IM or IV);
 butorphanol (0.01–0.04 mg/kg IM or IV or as a CRI at
23.7 μg/kg/h after a loading dose of 17.8 μg/kg IV); or
lidocaine (CRI at 30–50 μg/kg/min after a loading dose
of 1.3 mg/kg IV slowly)
 Flunixin meglumine (1.1 mg/kg IV or PO) or
phenylbutazone (2.2–4.4 mg/kg IV or PO)
 Phenylbutazone (2.2–4.4 mg/kg IV or PO)
 Muscle relaxants—methocarbamol (5–22 mg/kg IV
slowly every 6–12 h) or dantrolene sodium 4–6 mg/kg
PO every 12–24 h)
 Give dantrolene within 4 h of feeding for adequate
absorption
 Young anxious Thoroughbreds may benefit from
stress-reducing management changes, such as
feeding and exercising them before others and low-
dose sedatives before training.
PROGNOSIS
 Horses with sporadic acquired ER have good
prognosis with appropriate management
 Horses with mild to moderate signs of PSSM or RER
usually respond to a disciplined routine of daily
exercise and appropriate dietary changes
 PSSM horses with late onset of signs have good
prognosis if the triggering management changes are
identified and addressed
 Horses with repeated and severe episodes of muscle
necrosis have poor
 prognosis for athletic function if they display limited
response to appropriate dietary and training changes

PREVENTION
 Daily exercise and avoiding stall rest are critically
important for prevention in susceptible horses
 Eliminate/reduce high-starch feeds. Grass hay (1.5–
2.0% body weight) with supplemental fat sources (rice
bran, oil, commercial high-fat feeds) to meet higher
caloric needs. Susceptible horses fed minimal grain
 heal on their own, although the warts can remain for 5 to 6 months.
 In inside horses one or both ears there are white flakey patches
that appear called Aural plaques.
PAPILLOMATOSIS
 Aural plaques is delineated lesion that affect the concave
aspect of the pinna with a flat surface of whitish keratinous crust
covering a shiny and erythematous skin surface. Lesion are
single/ multiple, coalescing, not pruritic and can resist bridling or
SYNONYMS: handling of ears. In some cases, it can cover almost the entire
 Papillomavirus infection surface of one or both pinnae.
 While, Squamous cell carcinoma of the penis and prepuce is
 Papillomatosis
 Warts an ulceration or mass lesion and can be complicated by
 Condyloma acuminata secondary bacterial infection.
Approximately affected horses have:
OVERVIEW  o40% of purulent or blood-stained preputial discharge
 o10% of preputial edema / inability to prolapse the penis
 Papillomas commence as benign proliferative epithelial  o80% on the glans of the penis and prepuce can have papillomas
neoplasms associated with the presence of EcPV (Equus caballus neighboring the neoplastic tumor.
papillomavirus).
 Occasionally progress to malignancy.
CAUSES AND RISK FACTORS:
 Cutaneous warts in horse are benign and self-limiting
 The virus also associated with neoplastic disease squamous  There have been 7 confirmed EcPVs isolated from different
cell carcinoma of the penis and prepuce in horses. lesions. Lesion may contain one or more forms of EcPVs. Recenty,
a possible novel virus has been discovered.
3 Forms of Papillomas:  EcPV is DNA papillomavirus, penetrates stratified squamous or
1.Skin (warts) mucosal epithelium via trauma, which may or may not culminate
2.Genital in infection.
3.Aural Plaque  Can transmitted to direct or indirect contact through biting
insects and contaminated tack or buckets.
SIGNALMENT:
 Skin barrier breakage is needed for infection to be established
and inoculation of the skin may occur in the foal from infected
 Common in 1 and 3 years of age sites on the dam during parturition.
 Congenital papillomas: Newborn foals
 No breed or sex predisposition  Connective tissues and can be a PAPILLOMA or
FIBROPAPILLOMA
SIGNS
PATHOGENESIS:
 Prone to squamous cell carcinoma of the penis or prepuce:
Older horse (20 years)
 There are 7 Equine caballus papillomavirus (EcPV) EcPV-1
through EcpPV-7
 The warts can be seen in muzzle, lips, eyelids, external genitalia,
 First the virus infects the basal keratinocytes then replicates its
distal legs and Axilla. The lesion may be solitary or multiple up to
genome in the differentiating spinous and granular layers causing
100 and can causes problems due to physical location and
excessive growth or also called wart formation.
esthetics. Warts are solid outgrowths of epidermis that are sessile
 The expression of the late structural proteins of the virus is
or pedunculated.
limited to the differentiated cells of the squamous layer where the
 Papillomas may look like gray, pink, or white; surface is
new virus particles are encapsulated and shed into the
hyperkeratotic with numerous frond-like projections.
environment as the cells die.
 Solitary lesions can be larger. While head papillomas typically
 The tumor contains epithelial cells
PAPILLOMA: contain little connective tissue and result of basal-cell
hyperplasia without viral antigen production.
FIBROPAPILLOMAS: mostly fibrous tissue, with very little epithelial
tissues, uncommon in horses but common in cattle, sheep and wild
ruminants.
DIAGNOSIS:
DIFFERENTIAL DIAGNOSIS:
 Verrucose Sarcoid- extensive areas are usually affected with
markedly thickened skin around and evidence of hypotrichosis at
the periphery of the lesion.
 Squamous cell carcinoma – in facial, genital and vulval
proliferative forms.
 Melanoma
DIAGNOSTIC PROCEDURE
 Biopsy & Histopathologic examination – establish definitive
diagnosis of papillomatosis
 Immunohistochemistry – to detect viral antigen within the lesion
 Electron microscopy – hexagonal viral particles can be found in
all form of equine papillomatosis (except congenital)
GROSS AND HISTOPATHOLOGIC FINDING
True papillomas consist of a hyperplastic epidermis with scant

dermal tissue, whereas in fibropapillomas the dermal component
tends to predominate.
 RT-PCR or PCR and Serologic test: detection of viral DNA
MEDICATION
 Imiquimod 5% cream -generalized papillomatosis and applied
in a thin film to cover the surface of the lesion every 48h until
resolution
Anecdotal treatment with immunostimulatory agents:
 Used for persistent papillomatosis and include:
 INTRALESIONAL INJECTIONS OF INTERFERON ALPHA
 INTERLEUKIN 2
 CISPLATIN
 BACILLUS CALMETTE-GUERIN
 TREATMENT

1.Surgical excision – treatment of choice

2.Cryosurgery – also effective
3.Topical antibacterial – secondary infection may require treatment
oCreams
oGels
oWashes

PREVENTION
Papillomaviruses are resistant to freezing or desiccation. Formalin,
detergents or high temperatures decrease infectivity. Avoid
transmission of the virus among horses that are stabled or pastured
together by isolation of affected horses and prevention of
immunologically susceptible horses from entering the contaminated
premise.

Preventing insect bites

oRepellent sprays. May decrease irritation in the affected horses and

limit spread of the virus among horses.

Regular genital sanitation

oTo prevent the onset of disease due to poor hygiene as a promoter of
genital carcinoma or induction of genital papillomatosis.

EXPECTED COURSE AND PROGNOSIS

1-9 MONTHS: Spontaneous regression of warts
Genital papillomas may transform into squamous cell carcinoma
Surgical excision: excellent prognosis
SARCOID
2. Lip related to the high level of viral gene expression, matrix
3. Margins metalloproteinase upregulation, and production of viral oncoproteins.
4. Periocular
oNeck 4.E5 and E6 protein products enhance cell proliferation and invasion in
oLower limbs EqS02a cells, while E7 improves cell anchorage independence, all
OVERVIEW oVentral body: characteristics of neoplastic cells.
Is a dermal fibroblast neoplasm with a minor epidermal component, 5. Inguinal
with a variety of clinical forms. Locally aggressive with a high propensity 6. Preputial 5.BPV-1-infected fibroblasts show increased phosphorylated p38
for recurrence after surgical excision, but does not metastasize. 7. Perineal expression due to BPV-1 E5 and E6 expression, indicating cellular
mechanisms for neoplastic transformation in infected cells.
SIGNALMENT 6 CLINICAL TYPES OF EQUINE SARCOID
Breed Predilection 1.OCCULT – focal, roughly circular, non-raised areas of alopecia with 6.The study reveals increased expression levels of regulatory T cell
 QUARTER HORSE – Higher risk foci of scaling, lichenification or papules. May start with subtle hair color/ markers and BPV-1 E5 copy numbers in lesional skin samples from
 Appaloosas quality change and common in relatively hairless body areas. It remains horses with sarcoids, indicating local immune suppression.
 Arabians static for years and slowly enlarge or progress to verrucous forms.
 Thoroughbred 8. Sarcoids do not regress unlike most papillomavirus infections,
 STANDARDBREDS – Lower risk 2.VERRUCOUS (WARTY) – irregular papillomatous and scaly plaques likely because BPV expression in equine cells triggers immune
to peduncles, often surrounded by a zone of mild lichenification with evasion mechanisms.
Predilection sites: altered coat quality. Less common on the limbs except for coronary
oParagenital band areas. It is a slow growing.
oAbdominal CAUSES AND RISK FACTORS
oInguinal 3.NODULAR – is a firm, well-defined dermal or subcutaneous nodules  Caused by complex association between BPV (BPV-1, BPV-2
oVentral thorax of variable size ≥0.5–20 cm. Solitary, small to occasionally myriad and BPV-13)
oHead clusters. The predilection site were inguinal, preputial, periocular areas.  Inheritable traits of the horse, with environmental influences.
Suspected genetic and familial predisposition.
Mean Age: 3-9 YEARS  Potential BPV transmission via:
Range: 6 MONTHS TO 15+ YEARS 4.NODULAR AND ULCERATED “FIBROBLASTIC” – a irregularly  Flies, fomites, direct wound contamination
Predominant Sex: NO GENDER PREDISPOSITION nodular locally invasive lesions with prominent ulceration and exudation.
System affected: SKIN Often resembling exuberant granulation tissue called “proud flesh”. A fly PATHOPHYSIOLOGY
Genetics: INCREASED RISK LINKED TO MHC I GENES worry, myiasis and bacterial infections commonly complicate.  Complex and multifactorial.
 ELA-A3  BPV infection potentially causal to BPV DNA detected within
 MHC II GENES: 5.MIXED SARCOID - variable mixtures of two or more types. fibroblast nuclei in most sarcoids, low levels in epidermis (BPV-1,
 ELA-W13 BPV-2 and BPV-13). BPV-1 variants are horse specific. The viral
 MHC II and NON-MHC GENES ON: 6.MALEVOLENT – it is a rare, invasive and irregularly nodular lesions proteins are oncoproteins E5 and E7.
 ECA-20 that can infiltrate lymphatics and potentially local lymph nodes.  Environmental factors, epizootic disease outbreaks with
 ECA-22 (involved in host immune response) apparent transmission between horses. Insect transmission likely
PATHOGENESIS: identical BPV-1 DNA in sarcoids and flies in same regions.
SIGNS: 1.The virus infects fibroblasts, and the infection is nonproductive. Viral Worldwide occurrence without seasonal or geographic
HISTORICAL FINDINGS: DNA can be detected in lesional tissue, although viral load varies only predilection suggest other transmission routes. It may be direct
oSingle or multiple lesions in a variety of body regions. slightly with clinical type of sarcoid. wound, contact and indirect fomites.
oOccur at sites of previous injury. May progress into more aggressive
forms spontaneously. 2.Intralesional viral load directly correlates with disease severity. BVP DIAGNOSIS
virus capsids are not found in equine sarcoids due to host-specificity DIFFERENTIAL DIAGNOSIS:
PHYSICAL EXAMINATION FINDINGS: and the cellular environment of keratinocytes required for the host oCutaneous habronemiasis
These are frequent happen in the: species. oPhycomycosis
oHead: oFibromas
1. Pinnae 3.Fibroblasts isolated from sarcoids are highly invasive, an attribute oGranulation tissue
oSquamous-cell carcinoma, especially of the penis and eyelid Alignment of neoplastic fibroblasts perpendicular to the epidermis in Good patient hygiene
oOther skin tumors, including melanoma by examination of a biopsy of a “picket fence” pattern may occur. Good management hygiene practices
the lesion There is also a neoplastic fibroblast that is spindle-shaped or fusiform
oPapillomatosis with pointed nuclei and large, irregular, pleomorphic nuclei. POSSIBLE COMPLICATION:
oOccult: The mitotic rate is usually low and the epidermis is hyperkeratosis Wound break and wound infections
Infectious folliculitis (Dermatophytosis, Bacterial) and acanthosis, with elongated truncated reteridge projections into Restricted movement
Dermatophilosis dermis and absence of classical PV changes.
Pemphigus foliaceus
oVerrucous: MEDICATION
Papillomas CHEMOTHERAPY
Developmental hemartomas o5-FU – intralesional injection
Squamous cell carcinoma
o Nodular: TOPICAL CYTOTOXIC AGENTS:
Bacterial, fungal, habronemiasis, pythiosis, hypodermiasis. oAW-3-LUDES ( 5-FU/ thiouracil/ heavy metal salts
Sterile inflammation: oXTERRA (Eastern bloodroot and zinc chloride
Exuberant granulation tissue oANIMEX (Blood root extract)
Foreign body reactions CISPLASTIN -cure rates 80% and intralesional injection effective
Eosinophilic granuloma
CYSTS: IMMUNOSTIMULATION:
Dermoid oIMIQUIMOD 5% GEL – for small sarcoid
Follicular oMYCOBACTERIAL PRODUCTS – for periocular sarcoids
Other neoplasms: oAUTOLOGOUS VACCINE
Fibroma/ fibrosarcoma ANTIVIRAL
Melanoma oACYCLOVIR 5% CREAM
Neurofibroma/ sarcoma oCIDOFOVIR 1% GEL
Cutaneous lymphoma
Squamous cell carcinoma TREATMENT
Mast cell tumor Good wound hygiene and fly control before and after surgery
Need restricted activity post-surgery depending on body site.
DIAGNOSTIC PROCEDURE: Surgical consideration:
Alopecia lesions to screen for other differentials oCONVETIONAL SURGERY
oSURFACE SKIN CYTOLOGY Most effective and cure rate 82% and recurrence rates 50-70%.
oFUNGAL CULTURE Surgery combined with another treatment modality have highest
FINE NEEDLE ASPIRATION OF NODULAR LESION success.
SKIN BIOPSY
oa definitive diagnosis, recommended if tx. will be undertaken once oCRYOSURGERY
diagnosis is confirmed, and to ensure margins clear for excisional Useful for lesions but difficult to excise. Accurately determining
biopsy. adequate depth.

GROSS CHANGES oLASER THERAPY

reflect clinical types, from alopecic to nodular and ulcerated. Smaller Radiation
satellite lesions surrounding main tumor.
oINTRALESIONAL RADIATION
HISTOLOGIC CHANGES Effective and the cure rates 60-94%
Dermal proliferation of transformed fibroblasts. The dermis is
dominated by proliferation of immature fibroblasts and collagen fibers PREVENTION:
forming whorls, interlacing bundles, and disorganized arrays. Fly control
PHOTOSENSITIZATION
Stored feed contains enough chlorophyll to produce critical tissue Erythema
levels of phylloerythrin in affected animals, including substances or Edema
OVERVIEW plants common causes of hepatogenous photosensitization. Serous exudation
UV-induced dermatitis caused by a photodynamic agent in the skin Crust formation
which increases the sensitivity of the skin to sunlight. Decreased skin TYPE IV (IDIOPATHIC PHOTOSENSITIZATION)
pigmentation and hair cover facilitate cutaneous penetration of UV. The primary cause of photosensitization remains unclear, as it has oLesions may be sensitive to touch and pruritic it may be:
not been determined whether it is due to hepatic insufficiency or other Chronic
Photosensitization is a condition in which skin becomes overly factors. Crust formation
sensitive to ultraviolet light (sunlight). This condition is not sunburn, Sloughing of the skin
although the difference can be difficult to distinguish. Photosensitization SIGNALMENT:
occurs when certain compounds, which are activated by light, are All ages and breeds oConjunctivitis, keratitis and corneal edema
present in skin that is exposed to ultraviolet (UV) light. The Paint horses, Light colored fur – primarily affects oLiver failure signs are:
photodynamic compounds are energized by the UV light and cause Light-skinned horse / Light pigmented/ Little hair: most severe lesion Icterus
chemical reactions that damage cells in the skin and lead to ulceration GEOGRAPHIC DISTRIBUTION: common in sunny areas. Pruritus
and fluid accumulation. Many chemicals, including some that are fungal Weight loss
and bacterial in origin, may act as photosensitizing agents. Affected SYSTEM AFFECTED: Diarrhea
areas are usually those that are lightly pigmented or that have little hair, Skin/ Exocrine – is restricted to light-skinned, sparsely haired areas Abdominal pain
such as the lips, eyelids, and tips of the ears. such as coronary band, muzzle, ears, eyelids, tail, vulva. Altered mentation
Hepatobiliary – is a secondary photosensitization and can be
4 CLASSIFICATIONS OF PHOTOSENSITIZATION: associated with any cause of hepatic insufficiency. More commonly with PATHOGENESIS:
1.TYPE I (Primary Photosensitization) hepatic insufficiency caused by the ingestion of hepatotoxic plants. Penetration of light rays to sensitized tissues causes local cell death
2.TYPE II (Aberrant Pigment Metabolism) Nervous system and tissue edema. Irritation is intense because of the edema of the
3.TYPE III (Hepatogenous Photosensitization) lower skin level, and loss of skin by necrosis
4.TYPE IV (Idiopathic photosensitization) SIGNS: or gangrene and sloughing is common in the terminal stages.
TYPE I / PRIMARY PHOTOSENSITIZATION HISTORICAL FINDINGS:
Exogenous photodynamic agents (PSs) can enter organisms through oRestlessness Nervous signs may occur and are caused either by the photodynamic
oral ingestion, parenteral administration, or direct absorption through oScratching agent, as in buckwheat poisoning, or by liver dysfunction.
skin. In livestock, oral ingestion is the most common route. oRubbing of the ears, eyelids and muzzle
Photosensitization occurs when plants are in lush green stages and oShade-seeking behavior Hepatogenous photosensitization involves production of a toxin, by a
growing rapidly. Livestock are affected within 4 to 5 days of transitioning oDemarcated skin lesions: higher plant, fungus, or cyanobacterium (algae), that causes liver
to pasture, with susceptibility varying between species. Redness, blister formation, weeping and crusting damage or dysfunction, resulting in the retention of the photosensitizing
oLiver failure agent phylloerythrin.
Is a secondary photosensitization.
TYPE II / ABERRANT PIGMENT METABOLISM Altered mentation CAUSES:
are porphyrins that may accumulate in an organism with disturbed Weight loss PRIMARY PHOTOSENSITIZATION is associated with ingestion,
heme synthesis. The only known examples in domestic animals are the Abdominal pain injection and contact with a photodynamic agent.
two rare inherited conditions of congenital porphyria erythropoietica(pink Diarrhea Photodynamic plants are:
tooth) and congenital protoporphyria erythropoietica described in oSt. john’s wort (Hypericum perforatum)
Limousin cattle. PHYSICAL EXAMINATION FINDINGS: oBuckwheat (Fagopyrum esculentum)
oCutaneous lesions (Primary and Secondary Photosensitization) oBurr trefoil (Medicago denticulate)
TYPE III/ HEPATOGENOUS PHOTOSENSITIZATION ois restricted to sparsely haired, light-skinned areas on the dorsal oSpring parsley (Cymopterus watsoni)
Hepatogenous photosensitization is a common disorder in livestock, aspects of the body. In face, muzzle, eyelids, ears, coronary bands, oBishop’s weed (Ammi majus)
affecting phylloerythrin, a chlorophyll-excreted end product. Obstructed vulva and tail. In severe cases, dark-skinned areas. oOat grass (Avena fatua)
biliary secretion can accumulate in the body, making the skin sensitive oDemarcation between lesions and normal skin is quite clear in oRape (Brassica spp. )
to light, and can occur in animals fed hay or hepatotoxic chemicals. multicolored animals. oDutchman’s breeches (Thamnosma texana)
Hepatotoxic chemicals: CARBON TETRACHLORIDE. oAlsike clover (Trifolium hybridum)
oACUTE SIGNS: oAlfa alfa (Medicago spp.)
oVetches (Vicia spp.) excited or high-energy state. These excited molecules may cause skin of secondary photosensitization. Complications are hemorrhage,
oHogweed (Heracleum sphondylium) damage directly damage but damage occurs mostly through the pneumothorax spread of infectious hepatitis, peritonitis where bile or
oGluten production of reactive oxygen metabolites and free radicals. ingesta contamination.

Drugs or Chemicals related photodynamic agents: oThere 2 categories of Photosensitization PATHOLOGIC FINDINGS
1.Primary photosensitization oPRIMARY PHOTOSENSITIZATION – the lesions are limited to the
oPHENOTHIAZINES When a preformed or metabolically derived photodynamic agent. skin; edema, serous exudate, scab formation, skin necrosis.
oTHIAZIDES Plant or fungal products or chemicals. oSECONDARY PHOTOSENSITIZATION -is dependent on primary
oACRIFLAVINES Reaches the skin by ingestion, injection or contact. disease process.
oMETHYLENE BLUE 2.Secondary (hepatogenous) photosensitization
oSULFONAMIDES Occurs in cases of liver disease when phylloerythrin acts as a MEDICATIONS
oTETRACYCLINES photodynamic agent. oFor CUTANEOUS LESIONS – to decrease severity of inflammation in
oCOAL TAR DERIVATIVES early stage
oFUROSEMIDE PHYLLOERYTHRIN Prednisone and flunixin meglumine
oPROMAZINE oA porphyrin compound formed by microbial degeneration of chlorophyll Corticosteroid creams
oCHLORPROMAZINE in the intestine, normally conjugated in the liver and excreted in the bile. Systemic antibiotics -to manage secondary bacterial infections.
oQUINIDINE oLIVER DYSFUNCTION / BILIARY STASIS accumulation of o TREATMENT FOR HEPATIC AND EXTRACUTANEOUS
oROSE BENGAL phylloerythrin in the blood and body tissues, DISORDERS
Mycotoxins: including the skin. Treat underlying liver disease
oPhycocyanin Some toxins derived from grasses directly phototoxic and
Produced by blue-green algae hepatotoxic, which makes the above classification of photosensitization CONTRAINDICATIONS
oPhytoalexins less clear. oPRIMARY PHOTOSENSITIZATION
By celery and parsnip Avoid use of drugs that may promote photosensitization
DIAGNOSIS Tetracyclines, sulfonamides, phenothiazines
SECONDARY PHOTOSENSITIZATION oDIFFERNTIAL DIAGNOSIS: oSECONDARY PHOTOSENSITIZATION
oAssociated with CHRONIC LIVER FAILURE or BILIARY PRIMARY PHOTOSENSITIZATION Anesthetics, barbiturates or chloramphenicol
OBSTRUCTION -History of exposure to plants = St.John’s wort, buckwheat Sedatives:
 Chronic active hepatitis - Chemicals = Phenothiazines, tetracyclines Xylazine or diazepam
 Hepatic abscessation
 Neoplasia (cholangiocellular carcinoma, lymphosarcoma) SECONDARY PHOTOSENSITIZATION PATIENT MONITORING
 Chronic megalocytic hepatopathy (Senecio spp., Crotalaria spp. -Photodermatitis accompanied by liver failure signs. Icterus, weight loss, oPRIMARY PHOTOSENSITIZATION
Heliotropium spp. ) diarrhea, abdominal pain, neurologic lesion. Evaluate skin lesions every few days and debride necrotic lesions as
 Burning bush required.
 Fireweed (Kochia scoparia) CBC/ BIOCHEMISTRY/ URINALYSIS oSECONDARY PHOTOSENSITIZATION
 Mycotoxicoses (blue green algae (Microcystis spp.) oPRIMARY PHOTOSENSITIZATION – liver enzyme activities. SDH, Manage skin lesions as for primary photosensitization
 Lupines (Phomopsis leptostromiformis ) GGT, AST, ALP, bilirubin and bile acid concentration are normal. Monitor liver enzyme activities, serum bile acids and bilirubin
 Cholelithiasis / cholangitis oSECONDARY PHOTOSENSITIZATION -increased liver enzyme concentration weekly until improvement
activities SDH, GGT, AST, ALP. Hyperbilirubinemia and bilirubinuria will Repeat liver biopsy in 4-6 weeks
RISK FACTORS: support the diagnosis.
oExposure to plants and chemicals that cause primary
photosensitization. Chronic liver failure or biliary obstruction. Lack of IMAGING
skin pigment or sparse hair cover. oMay detect changes in liver size and abnormalities in the hepatic
oExposure to sunlight. parenchyma abscesses, neoplastic masses, dilated bile ducts,
choleliths, cases of secondary photosensitization.

PATHOPHYSIOLOGY: LIVER BIOPSY

oExposure to UV, molecules of the photodynamic agent enter an oMay yield diagnostic, prognostic and therapeutic information in cases