1. Disease Brief Description Epidemiology Pathogenesis Clinical Signs Lesions Differential
Diagnosis
Diagnosis Treatment Control &
Prevention
Epitheliogenesisimperfecta
(aplasia cutis)
(aplasia cutis)
*A congenital skin deformity.
Foals are born with small to
extensive areas where skin is
missing. Secondary infection is
common
*The condition is fatal when
extensive
*One or more
hooves may be
deformed or absent
*Obvious at birth as
glistening red,well-
demarcated
discontinuities in
the skin or mucous
membranes
*Small defects can
be surgically
corrected
Nevus *This term is used for any area
where skin is malformed,
including abnormally pigmented
spots. Some forms of nevi
displace the normal structures
of the skin, including hair
follicles; thus, these patches are
hairless
*Defect occur in all
species
*Alopecic, with
pigmented ,pitted
surfaces
*When not
extensive, it can be
surgically removed;
otherwise there is
no effective
treatment
Dermoid sinuses or cysts *These cysts are lined with skin.
Exfoliated skin, hair, and
glandular debris accumulate in
the cysts, which can lead to
infection. The cysts are found on
the midline of the back and in
rare cases are associated with
spinal cord deficits
*Occur in
Thoroughbred
horses
*They are caused by
failure of complete
separation of the
neural tube from the
epidermis during
embryogenesis
*The lesions may be
lateral or bilateral
*Can be removed by
surgical excision
Follicular cysts
Periauricular
(dentigerous) cysts
*Develop by abnormal hair
follicle growth and by retention
of follicular or glandular
products
*They may be congenital when
the hair follicle does not develop
normally
*Although they are present at
birth, they may not be
recognized until adulthood
Albinism *Always associated with pink or
pale irises and with visual
defects and increased risk of skin
damage from solar radiation.
Albinism is different from
extreme white spotting.
*Some animals with extreme
piebaldism (spotted or blotched
with black and white) or
dominant white have associated
neurologic anomalies or
deafness in one or both ears.
*Lethal white foal
syndrome is one
that results from
breeding 2 Overo
Paints.
Vitiligo *Hereditary but not noticeable
at birth. Complete remission
may occur but is rare. It causes
no other health problems.
*Mostly seen in
Arabian horses
(Arabian fading
syndrome, pinky
syndrome).
*There is no
accompanying
systemic or
cutaneus pathology
*Affected animals
develop bleached
splotches of skin
that occasionally
also affect the hair
coat and hooves.
*Most lesions are on
face ,especially the
muzzle or
planumnasale or
around the eyes
*No treatment is
available
*Treatments used in
people with vitiligo
are unlikely to help

2. *The onset is usually
in young adulthood
Most splotches are
on the face,
especially the bridge
of the muzzle or
around the eyes.
Color loss may wax
and wane
animals
Hereditary equine regional
dermal asthenia (HERD)
*A condition in which the skin
produces abnormal collagen
and/or elastin.
*Common in
Quarter horses and
Arabian cross
horses.
*The condition is
often first noticed
during training, at
the time saddles and
tack are first placed
on a young horse.
*Handling of the
skin elicited a
painful response
and superficial
trauma led to skin
wounds.The skin
was thinner than
normal in affected
areas,with thickened
borders and harder
fibrotic masses.
The collagen fibrils
were thinner and
smaller,which
created a loose
arrangement of
collagen within the
deep dermis which
contains a
distinctive horizontal
linear zone
*Patches or large
areas of loose,
stretchy, fragile skin
*Joint problems
*Clinically there
were bilateral
asymmetrical lesions
of the trunk and
lumbar
regions,where the
skin was
hyperextensible
*Based on visible
signs and testing of
the collagen
structure.
*Wounds heal
slowly or not
completely
Epidermolysisbullosa
syndromes
*These are a group of hereditary
congenital defects that affect
the attachments between the
outer and inner layers of the
skin.
*Skin trauma results in dermal-
epidermal separation and
blisters that soon rupture,
leaving glistening, flat ulcers.
Blisters may be present at birth
or develop within the first weeks
of life. The most severe blisters
are on the lower legs (with
sloughing of hooves), mouth,
face, and genitals.
* Except for the
simplex form, most
occurrences of the
disease are fatal. All
3 forms of
epidermolysisbullos
a have been
reported in Belgian
foals.
*Most common on
the
gingivae,palate,lips,t
ongue,and feet
*Most severe
lesions are on feet
with sloughing of
hooves, claws of
footpads and oral
mucous membrane
and facial and
perigenital
skin(erosions)
Airborne Allergies (Atopy) *While the horse's immune
system normally provides
protection for the animal, the
immune system of some horses
overreacts to the presence of
one or more airborne allergens.
*Airborne allergens can
adversely affect the skin.
*Allergy testing is
also available in
some areas. Allergy
testing identify the
specific allergens
*Avoiding the
allergen, if possible
*Corticosteroids to
control the
inflammatory
reaction. If a horse is
allergic to dust in
the environment
*Feeding the horse
hay lage or some

3. other feed with little
dust may also help.
*Conversely, if the
horse has seasonal
pollen allergies, it
can be kept inside
during the months
when pollen is
normally present.
Food Allergies *Although documented cases
are rare. For example, there are
reports that certain types of
grains or hay have caused hives
in horses. In some cases, the
food allergies were associated
with high-protein food
concentrates.
- - *Trial or elimination
diet
*Strict avoidance of
the food.
ECTOPARASITES
Parasite Brief Description Epidemiology Pathogenesis Clinical Signs Lesions
Differential
Diagnosis Diagnosis Treatment
Control &
Prevention
The biting midges, “no-see-
ums,” or punkies belong to the
family Ceratopogondiae.
*Culicoid hypersensitivity in
Canada
*Queensland itch in Australia
*Kasen in Japan
*Sweat itch
*Sweet itch
*Summer dermatitis
*Culicoides spp are vicious biters
and can cause intense irritation
and annoyance. In large
numbers, they can cause
livestock to be nervous and
interrupt their feeding patterns.
These gnats tend to feed on the
dorsal or ventral areas of the
host; feeding site preference
depends on the species of biting
gnat.
*They fly only in the
warm months of the
year and are most
active before and
during dusk. They
feed often on the
mane, tail, and belly
of horses.
*These flies also
serve as the IH
for Onchocercacervi
calis; the
microfilariae of this
nematode are found
in the skin of horses.
*These flies also
transmit the
bluetongue virus in
sheep and cattle.
*Horses often
become allergic to
the bites, scratching
and rubbing these
areas, causing
alopecia,
excoriations, and
thickening of the
skin
*Onchocerciasis
*Nonseasonalderma
tosis that is similar
to sweet itch but
usually is less
pruritic and affects
the head, neck, and
belly.
*Most often
collected in the field
and not found on
the animals
*Identification is
probably best left to
an entomologist.
*Larvae may be
attacked in their
breeding grounds.
Extension
entomology
personnel should be
contacted for the
latest approved
recommendations.
*Permethrin for the
spraying of stables
and horseboxes.
*Topical insecticides
such as pyrethrins
(eg, cypermethrin or
cyfluthrin),
especially in pour-on
formulations, may
also be used to
control these adult
pests in large
animals.
*Black flies *Black flies feed on all classes of
livestock, wildlife, birds, and
people.
*Distributed
throughout the
world in areas
where conditions
permit development
of the immature
forms.
*Larvae nearly
-Because of their
tiny,serrated
mouthparts, female
black flies inflict
painful bites.The
ears,neck,head, and
abdomen of cattle
are favorite feeding

4. always are found in
swiftly flowing, well-
aerated water;
shallow
mountain torrents
are favored breeding
places.
*They are
particularly
abundant in the
north temperate
and subarctic zones,
but many species
are found in the
subtropics and
tropics where
factors other than
seasonal
temperatures affect
their developmental
and abundance
patterns.
sites
Buffalo
flies, Haematobiairritansexigua
*The buffalo fly is a primary pest
of cattle and water buffalo but
occasionally feeds on horses,
sheep, or wildlife.
*It is distributed
throughout
northern Australia
and New Guinea
and is found in parts
of southern,
southeastern, and
eastern Asia as well
as Oceania; it is not
found in New
Zealand.
* Its life cycle is
similar to that of the
horn fly; the adult
leaves the host long
enough to oviposit
on fresh manure,
where development
occurs. The life cycle
may take as few as
7–10 days,
depending on
weather conditions.
*Buffalo flies irritate
and annoy animals,
usually biting about
the shoulders and
withers. Bite
wounds may provide
a site for
screwworm
(Chrysomyiabezzian
a) infection. During
hot weather, the
flies move to shaded
parts of the body.
Affected animals
suffer blood loss and
are irritated by the
flies; feed efficiency
and production may
be affected
adversely.
*It can be identified
by their dark color,
size (approximately
half that of a stable
fly), and bayonet-
like proboscis that
protrudes forward
from the head.
*Insecticides should
be avoided in the
treatment of buffalo
fly populations.
Many of the
chemicals used to
treat these flies
result in meat
residues. Buffalo
flies have developed
resistance to the
synthetic
pyrethroids and to
some of the
organophosphates.

5. The eye gnats or the eye flies
(Hippelates spp)
*They are very small (1.5–2.5
mm long) flies that frequently
congregate around the eyes as
well as mucous and sebaceous
secretions, pus, and blood.
They gather in deep shade, such
as among densely planted
shrubs or in the shade of a
dwelling
*In the desert and
foothill regions of
southern California,
adult Hippelates
flies are present
throughout the
year; they are
annoying from April
through November.
During the peak
months, they are
noticeable in the
early morning and
late afternoon.
*Hippelates flies
also serve as vectors
forArcanobacterium
pyogenes (summer
mastitis)
and Moraxella bovis
*The eggs are ~0.5
mm long, fluted,
and distinctly
curved. They are
deposited on or
below the surface of
the soil. The larvae
hatch and feed on
decaying organic
matter, including
excrement. The
larval stage lasts 7–
11 days. During the
winter months, the
larval and pupal
stages may persist
for many weeks.
Pupation occurs
close to the surface
of the soil and lasts
~6 days. The entire
life cycle lasts ~21
days. The adults are
generally strong
flyers, flying both
with and against the
wind.
*These gnats
quietly approach
their mammalian
hosts. They usually
alight some distance
from their feeding
site and then crawl
over the skin, or fly
intermittently and
alight, thus avoiding
annoyance to the
host. They are
persistent and, if
brushed away,
quickly return to
continue engorging
themselves.
They are nonbiting
flies; however, the
labellae have spines
that scarify host
tissue and allow
entrance of
pathogenic
organisms. Hippelat
es flies often hover
around the body
orifices of calves,
yearlings, pregnant
heifers, and lactating
cows. They feed on
lacrimal fluid, fatty
body secretions,
milk droplets, and
on secretions at the
tips of the teats of
animals.
*These small flies
have sponging type
mouthparts.
Although eye gnats
have much smaller
mouthparts, they
closely resemble
house flies in form
and structure and
have short aristate
antennae.
*Repellents, such as
those recommended
for mosquitoes,
provide temporary
relief from eye
gnats.
*Applications of
insecticides on a
community-wide
basis (as would take
place with mosquito
abatement) may
provide temporary
control of adults,
but more adults
invade the treated
area after the
insecticide has
dissipated.
Face flies, Muscaautumnalis *They gather around the eyes
and muzzles of livestock,
particularly cattle. They may also
be found on the withers, neck,
brisket, and sides. Their
mouthparts are adapted for
*Face flies are found
on animals that are
outdoors and
usually do not follow
animals into barns.
*They follow blood-
feeding flies, disturb
them during the
feeding process, and
then lap up the
blood and body
*Sanitation

6. sponging up saliva, tears, and
mucus. Face flies are usually not
considered blood feeders
because their mouthparts are a
sponging type and not piercing
or bayonet-like, as are those
of Stomoxyscalcitrans.
fluids that
accumulate on the
host's skin.
Filth-Breeding flies *Filth-breeding flies:
Muscadomestica (the house
fly);
Calliphora, Phaenicia, Lucilia,
and Phormia spp (the blow flies
or bottle flies);
Sarcophaga spp (the flesh flies);
Fannia spp (the little house
flies);
Muscina spp (the false stable
flies);
Hermetiaillucens (the black
soldier flies).
*The house fly is commonly
found around livestock
operations, where it readily
breeds in accumulating manure
sources.
*It is a medium-sized (as large as
9 mm), grayish fly with four dark
thoracic stripes and sponging,
nonbiting mouthparts designed
for sucking semiliquid food
(there are no mandibles or
maxillae). The labium is
expanded into two labellae that
can transfer fluids and
semifluids.
*The life cycle of M
domestica will be used as a
representative example of the
life cycles of the assorted filth-
breeding flies.
*Large populations
of these adult flies
are often found
around facilities
associated with
animal feces
*Have been
implicated in the
transmission of
numerous
pathogens
(helminth,
protozoan, bacterial,
and viral) of people
and other animals.
*Larval stages may
be associated with
skin wounds
contaminated with
bacteria or with a
matted hair coat
contaminated with
feces
* The identification
of adult flies is
probably best left to
a specialist.
*House flies are
medium-sized,
grayish flies with
four dark thoracic
stripes. A
preliminary
identification of
blow flies or bottle
flies may be made
on the basis of the
metallic coloring of
the adults. Flesh
flies are medium-
sized, grayish flies
with a checkerboard
abdominal pattern.
*Thorough
sanitation program
to control fly
populations in and
around livestock and
facilities.
*All manure
accumulations
should be removed
at least twice a week
or handled properly,
if stored on the
premises, to
minimize fly
breeding.
*Residual sprays
providing 2–4 wks
control with one
treatment may be
applied to fly-resting
surfaces. Space
sprays, mists, or fogs
with quick
knockdown but no
residual action can
be used for
immediate
reduction of high
numbers of adult
flies.
*Use of insecticide
resin strips or
various fly baits.
Horse Flies *Tabanus spp (horse flies) are
large (up to 3.5 cm long), heavy
bodied, robust dipterans with
powerful wings and very large
eyes. They are swift fliers. These
flies are the largest in the
dipteran group in which only the
females feed on vertebrate
blood. Horse flies are larger than
deer flies; many horse flies are
highly colored.
* Adults are seen in
summer, particularly
in sunlight. Adult
females feed in the
vicinity of open
water and have
reciprocating,
scissor-like
mouthparts, which
they use to lacerate
tissues and lap up
*Restless when the
flies are present.
Site preferences
include the
underside of the
abdomen around
the navel, the legs,
or the neck and
withers.
*These flies can be
identified by their
large size, powerful
wings, compound
eyes, and lacerating
scissor-like
mouthparts. Species
identification of
intact adult and
larval horse and
deer flies is probably
*Horse fly traps
have been effective
when used around
cattle confined to
manageable areas.
*Manipulation of
these flies' aquatic
habitat has been
attempted by
removing

7. the oozing blood.
*Horse flies feed a
number of times in
multiple feeding
sites before they
become replete.
When disturbed by
the animal's
swatting tail or by
the panniculus
reflex, the flies leave
the host, yet blood
continues to ooze
from the open
wound.
*These flies may act
as mechanical
transmitters of
anthrax,
anaplasmosis,
tularemia, and the
virus of equine
infectious anemia.
best left to an
entomologist.
unnecessary woody
plants from
residential areas or
draining wet areas.
* Application of
insecticides in the
water may have
detrimental
environmental
effects.
Mosquitoes *Mosquitoes are members of
the family Culicidae.
Important genera
include Aedes, Anopheles, Culex,
Culiseta, and Psorophora.
*Although they are tiny, fragile
dipterans, mosquitoes are
perhaps some of the most
voracious of the blood-feeding
arthropods.
*Mosquitoes lay their eggs
either on the surface of standing
water
(eg, Aedes and Psorophora spp)
or on a substrate (such as damp
soil) where the eggs hatch after
inundation from rainfall,
irrigation, snow melt, etc. Larval
mosquitoes are known as
wrigglers, whereas pupal
mosquitoes are known as
tumblers. These stages are
always aquatic and are found in
a wide variety of habitats. Large
numbers of mosquitoes can be
produced from eggs laid in
relatively small bodies of water.
*About 300 species
have been described
worldwide, with
~150 species found
in the temperate
regions of North
America.
Mosquitoes are
found in such
diverse areas as salt
marshes of the
coastal plains to
snow pools above
14,000 ft (4,300 m)
to the gold mines of
India 3,600 ft (1,100
m) below sea level
*Only female
mosquitoes actively
take a blood meal so
that they can lay
eggs. Males feed on
nectar, plant juices,
and other liquids.
Mosquitoes annoy
livestock, cause
blood loss, and
transmit disease.
Also, the toxins
injected at the time
of biting may cause
systemic effects. The
feeding of large
numbers of
swarming
mosquitoes can
cause significant
anemia in domestic
animals. Although
they are known for
spreading malaria,
yellow fever,
dengue, and
elephantiasis in
people, mosquitoes
are probably best
*Adult mosquitoes
are most often
collected in the field
and are not found
on animals. Adults
are 3–6 mm long
and slender, with
small, spherical
heads and long legs.
The wing veins,
body, head, and legs
are covered with
tiny, leaf-shaped
scales. The long,
filamentous
antennae have 14–
15 segments and are
plumose in the
males of most
species. They also
have proboscides
designed for
lacerating tiny blood
vessels and sucking
up pooled blood.
Identification of the
plethora of
mosquito species
(adult, larval, and
*Drainage o
collections of still
surface water or
destruction of the
larvae by the
addition of any one
of a number of
insecticides

8. Some species have several
generations per year. The flight
habits of adult mosquitoes vary
with the species; some Aedessp
migrate many miles for their
aquatic, larval habitat. In strong
winds, mosquitoes may be
carried great distances. Some
species overwinter as eggs,
while others overwinter as
adults.
known in veterinary
medicine as the
intermediate host
for the canine
heartworm,Dirofilari
aimmitis, and as the
vectors of the
equine viral
encephalitides,
including West Nile
virus.
Anopheles
quadrimaculatus is
the intermediate
host for malaria
(Plasmodium spp) in
people and other
primates. Aedesaegy
pti is the yellow
fever mosquito,
transmitting this
virus among
people. Psorophorac
olumbiae is a severe
pest of both
livestock and people
in the rice fields of
Louisiana and
Arkansas.Culextarsal
is is an important
vector of Western
equine encephalitis
and is found in the
western, central,
and southern
USA. Aedesvexans is
an important
nuisance species
found in the
midwest.Aedesalbop
ictus is a recently
introduced Asian
species that also
spreads yellow fever,
dengue, and equine
encephalitis.
Certain Mansonia sp
p are severe pests of
livestock in Florida.
In Central and South
America, the adult
female bot
fly Dermatobiahomi
nis fastens her eggs
to a species
pupal stages) is
probably best left to
an entomologist.

9. of Psorophoramosq
uito, which then
transmits them to
the mammalian host
during feeding.
Stable Flies *The stable
fly, Stomoxyscalcitrans, is often
called the biting house fly. It is
about the same in size and
general appearance
as Muscadomestica, the house
fly. It is brownish gray, the outer
of four thoracic stripes is broken,
and the abdomen has a
checkered appearance. It has a
bayonet-like, needle-sharp
proboscis that, when at rest,
protrudes forward from the
head. The wings, when at rest,
are widely spread at the tips.
* Stable flies are mechanical
vectors of anthrax, surra, and
equine infectious anemia. They
are the intermediate host
for Habronemamuscae, a
nematode found in the stomach
of horses.
*These flies are
found throughout
the world. In the
USA, they are found
in the midwestern
and southeastern
states.
The larval and pupal
forms develop in
decaying organic
matter, including
grass clippings and
seaweed along
beaches. In the
midwestern USA,
larvae can be found
in wet areas around
the edges of hay
stacks and silage
pits. Where cattle
are fed hay,
breeding can occur
at the edge of the
feeding area where
hay has become
mixed with urine
and feces. The life
cycle in the field can
be completed in 2–3
wk, and adults may
live ≥3–4 wk.
*Both male and
female stable flies
are avid blood
feeders, feeding on
any warm-blooded
animal. Stable flies
stay on the host for
short periods of
time, during which
they obtain blood
meals. This is an
outdoor fly;
however, in the late
fall and during rainy
weather, it may
enter barns.
Horses are the
preferred hosts. The
fly usually lands on
the host with its
head and proboscis
pointed upward and
inflicts painful bites
that puncture the
skin and bleed
freely. It is a
sedentary fly, not
moving on the host.
Stable flies usually
attack the legs and
ventral abdomen
and may also bite
the ears. They can
be a problem in
cattle feedlots in the
midwestern USA.
The damage
inflicted to cattle is
caused by the
painful bite and
blood loss, and the
irritation results in a
reduced efficiency in
converting feed to
meat or milk. In
pets, stable flies
prefer to feed on the
tips of the ears of
dogs with pointed
*Stable flies are
easily identified by
their size (about the
same as that of the
house fly),
coloration, and
bayonet-like
proboscis that
protrudes forward
from the head.
* Sanitation
*A combination of
two compounds,
imidacloprid and
permethrin, works
to repel S calcitrans.
Monthly application
of this product
repels these flies
and prevents their
blood feeding on
dogs, but the
product does not kill
this type of biting
fly.

10. ears, especially
German Shepherds.
Tse-Tse flies *The tsetse flies, Glossina spp,
are important blood-feeding
flies found in Africa (latitude 5°N
to 20°S). Tsetse flies are narrow
bodied, yellow to dark brown,
and 6–13.5 mm long. When
resting, their wings are held over
the back in a scissor-like
configuration. The thorax has a
dull greenish color with
inconspicuous spots or stripes.
The abdomen is light to dark
brown.
* Both sexes are avid blood
feeders. One copulation renders
a female fly fertile for her
lifetime, during which she can
produce as many as 12 larvae.
She produces one larva at a
time, retaining it within her
uterus; after ~10 days, the larva
is deposited on loose, sandy soil,
where it digs in and begins
pupation within 60–90 min. This
pupation period averages ~35
days, after which the adult
emerges. Adult flies feed avidly
on vertebrate blood
approximately every 3 days.
*Tsetse flies serve as
the intermediate
hosts for several
species of
trypanosomes that
cause fatal diseases
of both domestic
animals (nagana)
and people (African
sleeping sickness).
Trypanosomes
invade the blood,
lymph, CSF, and
various organs of
the body, such as
the liver and spleen.
Nagana, a related
complex in cattle
caused
by Trypanosomabru
cei, has occurred
throughout
enormous areas
estimated to be as
great as one quarter
of the African
continent. The
disease is fatal to
horses, mules,
camels, and dogs.
Cattle, sheep, and
goats usually
survive, except
when parasitized by
certain strains.
Many wild ungulates
native to Africa
show no evidence of
harm.
*Tsetse flies can be
identified by their
honeybee-like
appearance, the
long proboscis with
its onion-shaped
bulb at the base,
and the unique wing
venation with the
characteristic
cleaver- or hatchet-
shaped cell in the
center of the wing.
*Catching and
trapping (tsetse
traps), bush
clearing, fly screens,
repellents,
insecticides, and
sterile male release
techniques.
Lice *Horses and donkeys may be
infested by 2
species oflice,Haematopinusasin
i, the horse sucking louse,
and Damaliniaequi, the horse
biting louse. Both species are
worldwide in distribution.
Normally, H asini is found at the
roots of the forelock and mane,
around the base of the tail, and
on the hairs just above the
hoof. D equi prefers to oviposit
on the finer hairs of the body
*Lice live within the
microenvironment
provided by the skin
and its hair or
feathers, and are
transmitted
primarily by contact
between hosts.
In temperate
regions, lice are
most abundant
during the colder
months and often
*Pediculosis is
manifest by pruritus
and dermal irritation
with resultant
scratching, rubbing,
and
biting of infested
areas.
*A generally
unthrifty
appearance, rough
coat
*Skin lesions due to
rubbing,fleces have
tufts protruding and
lose their brightness
*Separate from
allergic dermatitis
*Based on the
presence of lice. The
hair should be
parted, and the skin
and proximal
portion of the coat
examined with the
aid of light if
indoors. The
hair of large animals
should be parted on
the face, neck, ears,
topline, dewlap,
*Organophosphates,
syntheticpyrethroids
and macrocylic
lactones
*Premises recently
vacated by infested
stock should be
disinfected before
being used for clean
stock.
* Wipe-on
formulations of per
methrin, permethrin
plus diflubenzuron,
and pyrethrins are
available
for lice control

11. and is found on the sides of the
neck, the flanks, and the
base of the tail.
are difficult to find
in the
summer. Lice are
largely host-specific,
living on one species
or several closely
related species.
Anoplura are
parasites of mamma
ls. However,
Mallophaga infest
both mammals and
birds.
*Transmission
usually occurs by
host
contact. Lice droppe
d or pulled from the
host die in a few
days, but
disengaged ova may
continue to hatch
over 2–3 wk in
warm weather.
*Lowered
production in farm
animals are
common.
* In severe
infestations, there
may be loss of hair
and local
scarification.
Extreme infestation
with sucking lice can
cause anemia.
escutcheon, tail
base, and tail
switch. The head,
legs, feet, and
scrotum should not
be overlooked.
on horses.
* Horses may also
be dusted with
coumaphos.
MANGE IN HORSES
Sarcoptic Mange *Sarcoptesscabieivarequi is rare
in the USA but is the most
severe type of mange in horses
*Female mites from shallow
burrow in the lower stratum
corneum of the skin in which
they deposit eggs.Development
for both sexes includes the larval
stage,two nymphal stages prior
to the molting to the adult
*Later papules and
vesicles occur and
the skin becomes
thickened,coveredwi
h pale scabs and the
hair is lost
*The first sign is
intense pruritus due
to hypersensitivity
to mite products.
Regions protected
by long hair and
lower parts of the
extremities are
usually not involved.
*Early lesions
appear on the head,
neck, and shoulders.
*Lesions start as
small papules and
vesicles that later
develop into crusts.
Alopecia and
crusting spread, and
the skin becomes
lichenified, forming
folds. If untreated,
lesions may extend
over the whole
body, leading to
emaciation, general
weakness, and
anorexia.
*The horses may be
affected by
psoropticor
chorioptic mange
but the lesions are
most common at
the base of the
mane and tail and at
the back of the
pastern respectively
*Skin scrapings
*Biopsy
*Macrocylic lactone
endectocides are
preffered products
*Prefarrowing
treatment with
Ivermectin to
prevent
transmission
*Organophosphate
insecticides or lime-
sulfur solution can
be used by spraying,
sponging, or
dipping. Treatment
should be repeated
at 12- to 14-day
intervals at least 3–4
times. Alternatively,
the oral
administration of ive
rmectin or
moxidectinat 200
μg/kg can be
attempted. Several
treatments are
required 2–3 wk
apart. It is important
to treat all contact
animals.
Psoroptic Mange *Pruritus is characteristic.
*Psoroptesequi rare in horses;
Pcuniculi can sometimes cause
*Spread of ear mite
in the horses can
occur by grooming
*The mites migrates
to all parts of the
skinand prefers
*Production of a
large,thick crust on
the part of the body
*It produces lesions
on thickly haired
regions of the body,
*Lesions start as
papules and
alopecia and
-ELISA test has been
developed
Treatment is as
for sarcoptic mange
*Affected ears
should be cleaned of
all wax and ear

12. otitis externa in horses and may
cause head shaking.
or by the use of
infected harness
areas coveredwith
hair or foal.Salivary
secretions and mite
excreta contain
proteinases that
result in a severe
allergic pruritis
carrying long
hair,the base of the
hair and hairless
areas such as the
udder, prepuce and
axilla
*Severe irritation in
the ear,shaking of
the head,rubbing of
the head,
tenderness of the
poll
such as under the
forelock and mane,
at the base of the
tail, under the chin,
between the
hindlegs, and in the
axillae.
develop into thick,
hemorrhagic crusts.
Mites are more
easily recovered
from skin scrapings
compared
with sarcoptic
mange.
drawn to the
condition because of
the horse rubbing its
head,by swelling
around the base of
the ear,or by
resentment to the
bridle passing over
the ears.In some
horses the affected
ear may droop
preparations
containing benzene
hexachloride should
be used a weekly
intervals
Chorioptic Mange (Leg Mange) *Chorioptic mange is common in
heavy breeds of horses.
*Widespread
*Mostly draft and
other working horse
*Most horses in
group affected
*Causes an allergic,
exudative dermatitis
*The yellowish
serous exudates
coagulates and
breaks as the hair
grows so that the
small scabby
lessons are seen on
the hair
*Papules are seen
first, followed by
alopecia, crusting,
and
thickening of the
skin. A moist
dermatitis of the
fetlock develops in
chronic cases.
*Lesions caused
by Chorioptesequi st
art as a pruritic
dermatitis affecting
the distal limbs
around the foot and
fetlock.
*Greasy heel *“Greasy heel” in
draft horses
-washing encrusted
areas with oil of
salicylic acid and
later removal of
crust with a stiff
brush,eradication
was achieved
Topical treatments
recommended for
other manges are
effective
Demodectic Mange *Demodexequi is rare in horses.
The mites live in the hair follicles
and sebaceous glands; D
equi lives on the body, and D
caballi in the eyelids and muzzle
*Spread via
grooming tools and
rugs
*Rare
*Invasion of hair
follicles and
sebaceous gland
leads to chronic
inflammation,loss of
the hair fiber and
many instances the
development if
secondary
staphyloccocal
*Patchy alopecia
and scaling or as
nodules.
*Lesions appear on
the face, neck,
shoulders, and
forelimbs. Pruritus is
absent. This disease
has been reported in
association with
chronic
corticosteroid
treatment.
*The commonest
error is to diagnose
the disease as a
non-specific
staphyloccocal
infection
*Deep-seated
ringworm in horses
has much common
with demodicosis
*Unknown *This disease has
been reported in
association with
*Chronic
corticosteroid
treatment
*No effective
treatment regimens
have been
developed. Amitraz,
used in other
species, is
contraindicated in
horses because it
can cause severe
colic and death.
Trombiculidiasis (Chiggers,
Harvest Mite)
*Trombiculid mites can
parasitize the skin of horses,
especially during the late
summer and fall. The adult mites
live on invertebrates and plants;
the larvae normally feed on
small rodents, but they can
opportunistically feed on
humans and domestic animals
including horses.
*Lesions
consist of severely
pruritic papules and
wheals.
*Specific treatment
is not required
*The pruritus can be
controlled with
glucocorticoids.
Repellents may help
prevent infestation.
Straw Itch Mite (Forage Mite) *These mites usually feed on
organic material in straw and
grain and can opportunistically
infest the skin of horses.
*Papules and wheals
appear on the face
and neck if horses
are fed from a hay
*Pruritus is variable
and can be
controlled with
glucocorticoids.

13. rack, and on the
muzzle and legs if
fed from the ground.
URTICARIA
*Hives
*Nettle rash
*It is an allergic condition
characterized by the appearance
of wheals on the skin surface
Caused by:
Exogenous hives
>Toxic irritating substance of the
stinging nettle
>Stings or bites of insects
>Medications/Chemicals
(Carbolic acid, Turpentine,
Carbon disulfide or Crude oil)
Endogenous/
Symptomatic hives
>Young horses
>Inhalation or absorption of
ingested allergens
>May be associated with
intestinal parasite
*Though they can
occur during any
season, it is a
common problem
during the summer
months.
Immunologic causes
include insect bite
hypersensitivity
caused by stable
flies, mosquitoes,
culicoides (biting
midges), horse flies,
and chiggers.
*The lesions of
urticaria are
characteristic of an
allergic reaction. A
primary dilatation of
capillaries causes
erythema of the
skin. Exudation from
the damaged
capillary walls
results in local
edema of the
dermis, which
swelling and pallor
due to compression
of the capillaries.
The lesion usually
remains red in the
edges. Only the
dermis, and
sometimes the
epidermis, is
involved.
*Wheals or plaques
appear within a few
minutes or hours of
exposure to the
causative agent
*Cutaneous
eruptions are
preceded by fever,
anorexia, or dullness
in severe cases
*Often become
excited and restless
*Elevated, round,
flat-topped, and 0.5-
8in (1-20cm) in
diameter, may be
slightly depressed in
the center
*Develop on any
part of the body but
occur mainly on the
back, flanks, neck,
eyelids and legs. In
advance cases, they
may be found on the
mucous membranes
of the mouth, nose,
conjunctiva, rectum
and vagina.
*Angioneurotic
edema
-involves
subcutaneous tissue
rather than the skin
and the lesions are
much larger and
more diffuse
-In urticaria, the
lesions can be
palpated in the skin
itself
*Based on clinical
signs
*Acute Urticaria
>Glucocorticosteroid
s
(Hydrocortisone
sodium succinate;
Prednisolone
sodium succinate or
Hemisuccinate
>Dexamethasone
(0.1mg/kg)
>Epinephrine: may
be given in life-
threatening
situations
*Chronic
Urticaria
>Antihistamine
hydroxyzine (0.4-0.8
mg/kg, bid, or the
tricyclic
antidepressant
doxepin (which have
antihistaminic
properties) at
3mg/5kg, bid
*Eradication of the
causal
Insect and plants
*Keeping horses
stalled
at dawn and dusk
when
insects are at their
peak
Dermatophilosis
*Dematophilus infection
*Cutaneous streptothricosis
****erroneously called Mycotic
Dermatitis
*The infection is caused by a
species of actinomycete, a
microorganism that
resembles bacteria and
funguses. Factors such as
prolonged wetting by rain, high
humidity, and high temperature,
increase the occurrence of
dermatophilosis. The organism
can live in the skin quietly
until infection is stimulated by
climatic conditions. High
humidity and moisture increases
the release of spores and
spreads the infection. Epidemics
usually occur during the rainy
season.
*It is seen
worldwide but is
more prevalent in
tropical
environments where
rain is frequent and
humidity is high.
* Seen in all ages
but most prevalent
to young, in animals
chronically exposed
to moisture and in
immune-suppressed
host
Transmission:
>Direct contact
between animals
through
contaminate
environments or
*In chronic
infections, scabs and
crusts can spread
over a large portion
of the body,
particularly along
the back. Itching is
variable. Some
wounds may be
painful.
*Lameness and loss
of performance may
occur in horses that
are severely
affected around the
pasterns.
*Horses with long
Winter hair coats:
=Developing matted
hair and paint brush
lesions leading to
crust or scab
formation with
yellow green pus
present under can
larger scabs
Short Summer Hair:
=matting and scab
formation is
uncommon; loss of
hair with fine paint
brush effect can be
extensive
*Depends on the
appearance of
wounds in diseased
animals and the
finding of the
actinomycete in skin
smears or culture
*Diagnostic test is
microscopic
examination of
scabs or impression
smears of the
underside of fresh
wounds.
*Infected horses
should be isolated
from other animals
to reduce spread of
the disease.
*Careful attention to
the cleanliness of
living areas, tack,
blankets, grooming
tools, and other
accessories is
required and can
help control spread
of the disease.
* Control insects

14. possibly via biting
insects
Reservoir:
>Asymptomatic
chronically infected
animals
Equine eosinophilic granuloma
*Nodular necrobiosis or
collagenolytic granuloma with
collagen degeneration
*It is the most common nodular
skin disease in horses. There are
many proposed causes;
however, insect bite reactions
are the most likely. Trauma and
other environmental allergies
may also be involved. Many
collagenolytic granulomas occur
during the warmer months of
the year and may recur
seasonally. Some may persist
year round or distinctively occur
under tack and saddle areas
where pressure and trauma
occur.
*Lesions vary in size
and number from
less than ¼ inch (0.5
centimeter) to larger
than 2 inches (5
centimeters) and
usually occur over
the neck, trunk and
back. Some horses
can develop a
generalized form
with hundreds of
pea-sized nodules
over most of the
body. The overlying
skin is usually
normal but on
occasion may open
and ulcerate. More
chronic lesions may
calcify and become
“rock hard;” such
lesions are often the
most difficult to
treat effectively.
BENIGN, NONVIRUS-ASSOCIATED PAPILLOMATOUS LESIONS
Epidermal hamartomas (nevi) *Are rare proliferations
identified only in dogs, most
often in the young.
*They are benign,
but their
appearance is
unpleasant, and the
extensive
hyperkeratosis is
prone to secondary
bacterial
infection.Some
forms are associated
with pustules and
acantholytic cells.
*Epidermal nevi
appear as
pigmented,
hyperkeratotic,
vaguely papillated
papules and plaques
that are occasionally
arranged in a linear
pattern.
*Localized lesions
can be excised; dogs
with multiple lesions
or lesions too large
to be surgically
removed may be
responsive to
isotretinoin or
etretinate.
*Use of topical
keratolytic
shampoos and
emollients.
HELMINTHS OF THE SKIN
CUTANEOUS HABRONEMIASIS
*Summer sores
*Jack sores
*Bursatti
*Is a skin disease of
Equidaeaused in part of by the
larvae of the spirurid stomach
worm
*When the larvae
emerge from flies
feeding on pre-
existing wounds or
on moisture of the
genitalia or
eyes,they migrate
*Non healing,
reddish brown,
greasy skin
granulomas that
contain yellow
calcified material
the size of rice
*The lesions
become chronic and
healing is protracted
*Skin scraping of the
lesions
*Based on finding
nonhealing, reddish
brown,
greasy skin granulo
*Symptomatic
treatment,
including;
>use of insect
repellents, may
be of benefit, and
organophosphates
*Control of fly host
and regular stacking
Of manure, together
with anthelminthic
therapy

15. into and irritate the
tissue
grains mas that contain
yellow, calcified
material the size of r
ice grains.
applied topically
to the abraded
surface may
kill the larvae.
*Surgical removal or
cauterization ofthe e
xcessive granulation
tissue may be
necessary.
>Ivermectin (200
μg/kg) has been
effective, and
although there may
be temporary
exacerbation of
the lesions
(presumably in react
ion to the dying
larvae),
spontaneous healing
may be expected.
*Moxidectinat 400
μg/kg also appears
to be active
against Habronemas
ppinthe stomach.
Onchocerciasis *O cervicalis is found in the
ligamentumnuchae and possibly
other sites in Equidae
*Adults are associated with
connective tissues; they are very
thin and 3–60 cm long.
Microfilariae are found in the
dermis and on rare occasions
circulating in peripheral blood.
The microfilariae lack a sheath
and are 200–250 μm long with a
short, sharply pointed tail.
*Culicoidessppare
the intermediate
hosts for O
cervicalis,
and Simuliumspp for
O gutturosaand O
lienalis
*O cervicalis has
been associated
with fistulous
withers, poll evil,
dermatitis, and
uveitis in horses.
*Adults in the
ligamentumnuchae
induce inflammatory
reactions ranging
from acute
edematous necrosis
to chronic
granulomatous
changes, resulting in
marked fibrosis and
mineralization.
Mineralized nodules
are more common
in older horses.
Although lesions are
found in these
areas, presumably
associated with
dead parasites, it is
generally agreed
that fistulous
withers and poll evil
are not caused by O
cervicalis infections.
*These lesions may
*Full thickness Skin
biopsy >6mm
*No treatment is
effective against the
adults
>Ivermectin,
Moxidectin is
efficacious against
microfilariae

16. be pruritic and often
include areas of
scale, crusts,
ulceration, alopecia,
and
depigmentation.
PARAFILARIA MULTIPAPILLOSA *P multipapillosa is found in the
subcutaneous tissues of horses
in various parts of the world
*It is similar in size, appearance,
life cycle, and development to P
bovicola. Blood-
sucking Haematobiaspp are
thought to be the invertebrate
hosts.
*It is especially
common in the
Russian steppes and
eastern Europe.
*Skin nodules,
particularly on the
head and upper
forequarters.
*These bleed
transiently but often
profusely (“summer
bleeding”) and then
resolve; other
hemorrhaging
nodules develop as
the parasite moves
to a different site.
*Occasionally, the
nodules suppurate.
The nodules and
bleeding are
unsightly and
interfere with
harnesses of
working horses but
generally are of little
consequence. The
clinical signs are
pathognomonic.
*Carcass lesions can
be differentiated
from bruising by the
presence of
numerous
eosinophils in
Giemsa-stained
impression smears
made from the
lesions.
*In addition,
affected tissue has a
characteristic,
disagreeable,
metallic smell.
Usually, only small
numbers of worms
are present in
affected carcasses
and are often
difficult to find
because of their
color and the
accompanying
inflammatory
reaction.
*Microscopic
examination of the
sediment
*Affected tissues
can be incubated in
warm saline to
facilitate the
recovery of
parasites.
*An ELISA for the
detection of
antibodies against P
bovicola has been
developed.
*No satisfactory
treatment has been
reported
Ivermectin (200
μg/kg) or nitroxynil
(20 mg/kg) given by
SC injection reduces
the number and
surface area
of Parafilaria lesions
.
Animals should be
treated at least 70–
90 days before
slaughter to provide
sufficient time for
lesions to resolve.
The treatment-to-
slaughter interval
should not be >120
days because
unaffected larval
forms of the
parasite may induce
fresh lesions as they
mature.
*Fly control may
reduce the
incidence.
PHOTOSENSITIZATION *Photosensitization occurs when
skin (especially areas exposed to
light and lacking significant
protective hair, wool, or
pigmentation) becomes more
susceptible to ultraviolet light
due to the presence of
photodynamic
agents. Photosensitization differ
s from sunburn and
photodermatitis, as both of
these conditions
result in pathologic skin changes
without the presence of a
photodynamic agent.
*Most compounds that are
important causes of
photosensitivity in veterinary
medicine are plant-derived.
*Photosensitization
occurs worldwide
and can affect any
species, but is most
commonly
seen in cattle,
sheep, goats
and horses.
*Inphotosensitizatio
n, unstable high-
energy molecules
are formed when
photons react with a
photodynamic
agent. These high-
energy molecules
initiate reactions
with substrate
molecules of the
skin, causing the
release of free
radicals that in turn
result in increased
permeability of
outer cell and
lysosomalmembrane
s. Damage to outer
cell membranes
*Dermatologic signs
associated with
photosensitivity are
similar regardless of
the cause.
Photosensitive
animals are
photophobic
immediately when
exposed to sunlight
and appear agitated
and uncomfortable.
They may scratch or
rub lightly
pigmented, exposed
areas of skin (eg,
ears, eyelids,
muzzle). Lesions
initially
appear in white-
*Severe
phylloerythrinemia
and bright sunlight
can induce typical
lesions even in
black-coated
animals
*Evaluation of
serum liver enzymes
and liver biopsies
*Examination of
blood,feces and
urine for porphines
*Diagnosis
of photosensitizatio
n is based on clinical
signs, evidence or
history of exposure
to photosensitizing
agents or
hepatotoxins, and
characteristic
lesions.
Photophobia in com
bination with
erythema and
edema of hairless,
nonpigmented areas
of skin is strongly
suggestive of the
disease. The period
from exposure to
photodynamic or
*The prognosis for
animals with
hepatogenous photo
sensitization and
porphyria is poor,
however the
prognosis for
animals with
primary photosensiti
zation is generally
good. Treatment
involves mostly
palliative measures.
While
photosensitivity
continues, animals
should be shaded
fully or, preferably,
housed and allowed
to graze only during
*Unknown

17. Primary Photosensitization
Primary photosensitization occur
s when the photodynamic agent
is either ingested, injected, or
absorbed through the skin. The
agent enters the systemic
circulation in its native form
where it results inskin cell
membrane damage after the
animal is exposed to ultraviolet
light. Examples of primary
photosensitizing agents include
hypericin
(from Hypericumperforatum [St.
John's wort]) and fagopyrin
(fromFagopyrumesculentum [bu
ckwheat]). Plants in the families
Umbelliferae and Rutaceae
contain photoactive
furocoumarins (psoralens),
which
cause photosensitizationin livest
ock and
poultry.Ammimajus (bishop's
weed)
and Cymopteruswatsonii (spring
parsley) have
produced photosensitizationin c
attle and sheep, respectively.
Ingestion of A majus and A
visnaga seeds has produced
severephotosensitizationin poult
ry. Species
of Trifolium, Medicago (clovers
and
alfalfa), Erodium, Polygonum,
and Brassica have been
incriminated as primary
photosensitizing agents. Many
other plants have been
suspected, but the toxins
responsible have not been
identified
(eg, Cynodondactylon [bermuda
grass]). Additionally, coal tar
derivatives such as polycyclic
aromatic hydrocarbons,
tetracyclines, and some
sulfonamides have been
reported to cause
primary photosensitization.
Phenothiazine anthelmintics
allows for leakage of
cellular potassium
and cytoplasmic
extrusion. Lysosomal
membrane damage
releases lytic
enzymes into the
cell. This can lead to
skin ulceration,
necrosis, and
edema. The time
interval between
exposure to the
photodynamic agent
and the onset of
clinical signs
depends on the type
of agent, its dose,
and the exposure to
sunlight.
haired,
nonpigmented, or
hairless areas such
as the nose and
udder. However,
severe
phylloerythrinemia
and bright sunlight
can induce typical
skin lesions,
evenin black-coated
animals. Erythema
develops rapidly and
is soon followed by
edema. If exposure
to light stops at this
stage, the lesions
soon resolve. When
exposure is
prolonged, lesions
may progress to
include vesicle and
bulla formation,
serum exudation,
ulceration, scab
formation, and skin
necrosis. The final
stage involves skin
sloughing. In cattle,
and
especially in deer,
exposure of the
tongue while licking
may
result in glossitis,
characterized by
ulceration and deep
necrosis.
Irrespective of coat
color, cattle may
develop epiphora,
corneal edema, and
blindness.
Depending on the
initial cause of the
accumulation of the
photosensitizing
agent, other clinical
signs may be seen.
For example, if the
photosensitivity is
hepatogenous,
icterus may be
present. In bovine
congenital
hepatotoxic agents
to the onset of
clinical signs can
vary from several
hours up to 10 days.
Clinical signs;
elevated serum
biochemical
measurements
including sorbitol
dehydrogenase,
gamma
glutamyltransferase,
alkaline
phosphatase, and
direct bilirubin; and
gross or histologic
signs of liver disease
help support a
diagnosis of
hepatogenous photo
sensitization. A
presumptive
diagnosis of
porphyria is based
on signalment (sex,
breed, age)
combined with
clinical signs, and a
definitive diagnosis
can be made by
measuring
porphyrin
levels in blood,
feces, and urine.
darkness. The
severe stress
of photosensitizatio
n and extensive skin
necrosis can be
highly debilitating
and increase
mortality.
Corticosteroids,
given
parenterally in the
early stages, may be
helpful. Secondary
skin infections and
suppurations should
be treated with
basic wound
management
techniques, and fly
strike prevented.
The skin lesions heal
remarkably well,
even after extensive
necrosis.

18. have been reported to cause
primary
photosensitivity in cattle, sheep,
goats, and swine.
Aberrant Pigment Metabolism
Type II photosensitivity due to
aberrant pigment metabolism is
known to occur in both cattle
and cats.In this syndrome, the
photosensitizing porphyrin
agents are endogenous
pigments that arise from
inherited or acquired defective
functions of enzymes
involved in heme synthesis.
Bovine congenital erythropoietic
porphyria and bovine
erythropoieticprotoporphyriaare
the most commonly reported
diseases in this category.
Secondary (Hepatogenous)
Photosensitization
Secondary or type
III photosensitization is by far
the most frequent type of
photosensitivity
observed inlivestock. The
photosensitizing agent,
phylloerythrin (a porphyrin),
accumulates in plasma due to
impaired hepatobiliary
excretion. Phylloerythrin is
derived from the breakdown of
chlorophyll by microorganisms
present in the GI tract.
Phylloerythrin, but not
chlorophyll, is normally
absorbed into the circulation
and is effectively excreted by the
liver into the bile. Failure to
excrete phylloerythrin due to
hepatic dysfunction or bile duct
lesions increases the
amount in the circulation. Thus,
when it reaches the skin, it can
absorb and release light energy,
initiating a phototoxic reaction.
Phylloerythrin has been
incriminated as the phototoxic
agent in the following
conditions: common bile duct
occlusion; facial eczema;
lupinosis; congenital
erythropoietic
porphyria,
discoloration of
dentin, bone (and
other tissues), and
urine often
accompanies the
skin lesions.
Photodermatitis is
the sole
manifestation
observed in bovine
erythropoieticproto
porphyria.

19. photosensitivity of Southdown
and Corriedale sheep and
poisoning by numerous plants
including Tribulisterrestris (punct
ure
vine), Lippiarehmanni, Lantana
camara,
several Panicumspp (kleingrass,
broomcorn millet, witch
grass), Cynodondactylon,Myopor
umlaetum (ngaio),
and Nartheciumossifragum (bog
asphodel).
Photosensitization also has been
reported in animals that have
liver damage associated with
various poisonings: pyrrolizidine
alkaloid
(eg, Seneciospp, Cynoglossumsp
p, Heliotropiumspp, Echiumspp;
cyanobacteria
(Microcystisspp, Oscillatoriaspp),
Nolinaspp (bunch grass), Agave
lechuguilla (lechuguilla), Holocal
yxglaziovii, Kochiascoparia, Tetra
dymiaspp (horse brush or rabbit
brush), Brachiariabrizantha, Bras
sica
napus, Trifoliumpratense and T
hybridum (red and alsike
clover), Medicago
sativa, Ranunculus spp,
phosphorus, and carbon
tetrachloride. Phylloerythrin is
likely the phototoxic
agent in many of these
poisonings.
Type IV Photosensitivity
Photosensitivity where the
pathogenesis is unknown or the
photodynamic agent is not
identified is classified as type IV.
One such example involves a
case of primary
photosensitivity in cattle
presumed to be caused
by Thlaspiarvense (field
pennycress) even though field
pennycress had not been
reported to
cause photosensitization.
Outbreaks
of photosensitization have been
reported in cattle exposed to

20. water-damaged alfalfa hay,
moldy straw, and foxtail-
orchardgrass hay. These cases
were suspected to be
hepatogenous in origin. Ranuncu
lus bulbosus (buttercup) has also
been presumed to be a cause of
hepatogenous photosensitizatio
n. Other plants associated
with photosensitizationinclude
winter wheat
(cattle), Medicagospp (alfalfa), B
rassica spp (mustards),
and Kochiascoparia(fireweed).
Many of these plants are
believed to be type I
photosensitizers. Forages such
as oats, wheat, and red clover
have been suspected in cases
of photosensitization and may
be associated with specific
environmental conditions such
as heavy rainfall.
DERMATOPHYTOSIS
*Ringworm
*It is an infection of keratinized
tissue (skin, hair, claws)
*The agents
>Trichophytonequinum ; T.
mentagrophytes-main
>Microsporumgypseum; M.
canis; T.verrucosum
Are zoonotic
*Transmission:
>Direct contact
>Contaminated
fomites
>Grooming
implements
>Tack
*Dermatophytes can
survive solely on
outer cornified
layers of the skin.
Natural infection is
acquired by the
deposition of viable
arthrospores or
hyphae on the
surface of the
susceptible
individual. After the
inoculation in the
host skin, suitable
conditions favor the
infection to progress
through the stages
of adherence and
penetration.
Development of
host response is
mostly by a T-cell
mediated response
of delayed-type
hypersensitivity.
Antibody formation
does not seem to be
protective. Natural
defenses against
dermatophytes
depend on both
*Consist of one or
more patches of
alopecia
-Erythema
-Scaling
-Crusting
*EARLY:
- May resemble
papularurticaria but
progress with
crusting and hair
loss within a few
days
*Most lesions are
seen in the saddle
and girth areas
(“girth itch”)
*Dermatophilosis
*Pemphigus
foliaceus
*Bacterial Folliculitis
*Fungal culture-
most accurate
*Wood’s lamp
examination
*Direct microscopy
of hair or skin
*Topical (because
systemic therapy is
expensive and of
unproven efficacy)
*Whole body rinses
*Individual lesions:
Clotrimoxazole/Mico
nazole preparations
*Grooming
implements
and tack should be
disinfected, and
affectedhose should
be isolated.

21. immunological and
nonimmunological
mechanisms
SADDLE SORES COLLAR GALLS *The area of riding horses that is
under saddle, or the shoulder
area of those driven in harness,
is frequently the site of injuries
to the skin and deeper soft and
bony tissues.
*Absolute rest of the affected
parts is necessary. During the
early or acute stages, astringent
packs (Burow solution) are
indicated. Chronic lesions and
those superficially infected may
be treated by warm applications
and topical or systemic
antibiotics. Hematomas should
be aspirated or incised. Necrotic
tissue should be removed
surgically. In severe folliculitis
and furunculosis, antibiotics,
ideally chosen on the basis of
culture and sensitivity, are
always indicated. Scars and/or
leukotrichia (white hairs) are
common sequelae of healed
areas. Recurrence of
hematomas, seromas, and/or
sloughing skin upon initial
saddlings of a young Quarter
horse or Paint horse should elicit
suspicion of the genetic disease
hereditary equine dermal
asthenia.
*Emaciated horses
are at increased
risk. Chronic saddle
sores are
characterized by a
deep
folliculitis/furunculo
sis (boils) with
fibrosis or a
localized indurative
and proliferative
dermatitis. Lesions
are usually caused
by poorly fitting
tack.
*Sores affecting only
the skin are
characterized by
inflammatory
changes that range
from erythematous
to papular, vesicular,
pustular, and finally
necrotic.
*Frequently, the
condition starts as
an acute
inflammation of the
hair follicles and
progresses to a
purulent folliculitis.
*Affected areas
show hair loss and
are swollen, warm,
and painful. The
serous or purulent
exudate dries and
forms crust. or moist
necrosis.
*Clinical signs vary
according to the
depth of injury and
the complications
*Advanced lesions
are termed “galls.”
When the skin and
underlying tissues
are more severely
damaged, abscesses
may develop.
*These are
characterized as
warm, fluctuating,
painful swellings
from which purulent
and
serosanguineous
fluid can be
aspirated.
Severe damage to
the skin and
subcutis or deeper
tissues results in dry
*A simple DNA test,
performed on the
hair bulbs of the tail,
will confirm this
diagnosis.
*Identification and
elimination of the
offending portion of
tack is more
important than any
other treatment.
*Excoriations and
inflammation of the
skin of the
saddles and harness
regions are treated
as any other
dermatosis.
*Absolute rest of
the affected parts is
necessary.
*During the early or
acute stages,
astringent packs
(Burow solution) are
indicated.
*Chronic lesions and
those superficially
infected may be
treated by warm
applications and
topical or systemic
antibiotics.
*Hematomas should
be aspirated or
incised. Necrotic
tissue should be
removed surgically.
*In severe folliculitis
and furunculosis,
antibiotics, ideally
chosen on the basis
of culture and
sensitivity, are
always indicated.
A simple DNA test,
performed on the
hair bulbs of the tail,
will confirm this
diagnosis.

22. SCRATCHES
*Greasy heel
*Dermatitis verrucosa
*Often associated with poor
stable hygiene, but no specific
cause is known.
*Standardbreds :
frequently affected
in the spring when
tacks are wet
*Skin is itchy,
sensitive and
swollen in acute
stages; later it
becomes thickened
and most of the hair
is lost.
*Surface of the skin
is soft, and the
grayish exudate
commonly has a
fetid odor
*Chronic: with
vegetative
granulomas
*Lameness may or
may not be present ;
it can be severe and
associated
generalized cellulitis
of the limb. As the
condition
progresses, there is
thickening and
hardening of the
skin of the affected
regions, with rapid
hypertrophy of
subcutaneous
fibrous tissue
*Removing of the
hair
Regular washing and
cleansing with warm
water and soap to
remove all soft
exudates, drying and
applying an
astringent dressing.
If granulomas
appear, they can be
cauterized
Cellulitis require
systemic antibiotic
therapy and tetanus
prophylaxis
DERMATOPHILOSIS
*Dematophilus infection
*Cutaneous streptothricosis
****erroneously called Mycotic
Dermatitis
*Dermatophiluscongolensis *More prevalent in
the tropics
Transmission:
>Direct contact
between animals
through
contaminate
environments or
possibly via biting
insects
Reservoir:
>Asymptomatic
chronically infected
animals
*Seen in all ages but
most prevalent to
young, in animals
chronically exposed
to moisture and in
immune-suppressed
host
*Horses with long
Winter hair coats:
=Developing matted
hair and paint brush
lesions leading to
crust or scab
formation with
yellow green pus
present under can
larger scabs
Short Summer Hair:
=matting and scab
formation is
uncommon; loss of
hair with fine paint
brush effect can be
extensive
*Dermatomycosis
Dermatophytosis
Immune-mediated
scaling diseases oh
horse
*Presumptive
Diagnosis:
Appearance of
lesions in clinically
diseased animals
Definitive Diagnosis:
demonstration of
organism in
cytologic
preparations
isolation via culture
skin biopsy
*Lesion should be
gently soaked and
removed
Topical antibacterial
shampoo therapy is
Antimicrobials
(erythromycin,
spiamycin, penicillin
G, ampicillin,
chloamphenicol,
streptomycin,
amoxicillin,
tetracycline,
novobiocin
Wart infection *Infection with papilloma virus
is relatively common in young
horses kept in a large grot. Warts
are usually self-limiting
condition lasting 2-6 months,
however warts are contagious to
other horses sharing feeders and
*Infectious to horses
only and can be
transmitted to or
from man or other
species
*Small, single or
multiple,
cauliflower-like,
raised, rough lumps
especially on the
muzzle, eyelids and
inner surface of the

23. tack. ears, jowl and chest
(rarely on the belly
and hindlegs)
Equine Sarcoids *Most commonly diagnosed
tumor of the equids
*No significant
gender or age is
predisposition
*6 distinct clinical
entities are
recognized:
Occult-flat, gray,
hairless and
persistent
Verrucous-gray,
scabby or warty in
appearance and may
contain small, solid
nodules; possibly
surface ulceration;
well-defined or
cover large, ill-
defined areas.
Nodular-multiple,
discrete, solid
nodules of variable
size; may ulcerate
and bleed
Fibroblastic fleshy
masses, either with
a thin pedicle or a
wide flat base, that
commonly bleed
easily; may have a
wet, hemorrhagic
surface
Mixed variable
mixtures of 2 or
more types
Malevolent-are
extremely rare,
aggressive tumor
that spreads
extensively through
skin; cords of tumor
tissue intersperse
with nodules and
ulcerating
fibroblastic lesion
*The lesions are
characteristically
nodular growths of
viable tissue and if
there is no traumatic
injury,with
nodiscontinuity of
the covering
epidermis
*Can occur in single
or multiple lesions
in different forms;
can occur anywhere
on the body
TICKS OF HORSES *Are importance in the
production of animal diseases
*Life cycles vary
widely both in the
number of hosts
required and the
hostsspecificity.Ani
mals are infested by
larval or nymphal
states on the
ground.
*The definitive sign
of tick infestation is
the presence of a
tick on the animal.
Ticks that have been
on an animal only a
short time (an hour
to a few days)
appear flat. Ticks
that have been on
*Skin damage due
to biting and
rubbing anemia
*Ticks easily
found,should be
identified to species
*Dipping,pour-ons
and injectable
acaricides
*Regular treatment
at intervals
dependenton the
life cycle of the
tick,pasture spelling
to destroyfree living
stages,(Kahn,
2010)the use of
resistant and
vaccination all play a

24. an animal for several
hours or days
appear much more
rounded due to the
blood they have
consumed.
Diagnosis is by
appearance of tick
bite marks on the
animal and the
presence of the
offending pest.
part
References:
Kahn, C. M. (2010). THE MERCK VETERINARY MANUAL 10th Edition. WhiteHouse Station.N.J.,USA: Merck & Co.,Inc.,.
Radostits, O. (n.d.). Veterinary Medicine Diseases of Cattle, Horses, Sheep, Pigs, and Goats.

25. In Partial Fulfillment of the Requirements in
Equine Medicine
Urinary Diseases of Horses
Submitted to: Dr. Karen B. Gaerlan
Submitted by: Dongga-as, Chester N.
Payad, Bellamy