Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Diseases of the epidermis and dermis
 Pityriasis:
 Primary pityriasis,
Excessive bran-like scales on the skin, characterized by overproduction of
keratinized epithelial cells, Primary pityriasis scales are superficial,
accumulate where the coat is long, and are usually associated with a dry,
lusterless coat. Itching or other skin lesions are not features. can be
caused by:
 Hypovitaminosis A
 Nutritional deficiency of B vitamins, especially of riboflavin and
nicotinic acid, in pigs, or linolenic acid, and probably other
essential unsaturated fatty acids.
 Poisoning by iodine
Secondary pityriasis, is usually accompanied by the lesions of the
primary disease and characterized by excessive desquamation of
epithelial cells is usually associated with:
 Scratching in flea, louse and mange infestations
 Keratolytic infection, e.g. with ringworm fungus.
Pityriasis scales are accumulations of keratinized epithelial cells,
sometimes softened and made greasy by the exudation of serum or
sebum. Overproduction, when it occurs, begins around the orifices of the
hair follicles and spreads to the surrounding stratum corneum.
Diagnosis
Pityriasis is identified by the absence of parasites and fungi from skin
scrapings.
Differential diagnosis
Hyperkeratosis and Parakeratosis
Treatment:
Primary treatment requires correction of the primary cause. Supportive
treatment commences with a thorough washing, followed by alternating
applications of a bland, emollient ointment and an alcoholic lotion.
Salicylic acid is frequently incorporated into a lotion or ointment with a
lanolin base.
1
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 Hyperkeratosis
Epithelial cells accumulate on the skin as a result of excessive
keratinization of epithelial cells and intercellular bridges, interference
with normal cell division in the granular layer of the epidermis and
hypertrophy of the stratum corneum.
 local hyperkeratosis the lesion at pressure points as elbows, when
animals lie habitually on hard surfaces.
 Generalized hyperkeratosis may be caused by:
 Poisoning with highly chlorinated naphthalene compounds.
 Chronic arsenic poisoning.
 Inherited congenital ichthyosis.
 Inherited dyserythropoiesis dyskeratosis.
The skin is dry, scaly, thicker than normal, usually corrugated, hairless
and fissured in a grid like pattern. Secondary infection of deep fissures
may occur if the area is continually wet. However, the lesion is usually
dry and the plugs of hyperkeratotic material can be removed, leaving the
underlying skin intact.
Diagnosis
by the demonstration of the characteristically thickened stratum corneum
in a biopsy section.
Differential diagnosis parakeratosis and inherited ichthyosis.
Treatment Primary treatment depends on correction of the cause.
Supportive treatment is by the application of a keratolytic agent (e.g.
salicylic acid ointment) .
 Parakeratosis:
Parakeratosis, a skin condition characterized by incomplete keratinization
of epithelial cells. It is a nutritional deficiency disease of 6- to 16-wk-old
pigs characterized by lesions of the superficial layers of the epidermis. It
is a metabolic disturbance resulting from a deficiency of zinc or
inadequate absorption of zinc due to an excess of calcium, phytates, or
other chelating agents in the diet. Predisposing factors include rapid
growth, deficiency of essential fatty acids, or malabsorption due to GI
diseases.
Caused by:
 Nonspecific chronic ,
 Inflammation of cellular epidermis,
2
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 Associated with dietary deficiency.
Pathogenesis:- The initial lesion comprises edema of the prickle cell
layer, dilatation of the inter cellular lymphatic's, and leukocyte
infiltration. Imperfect keratinization of epithelial cells at the granular
layer of the epidermis follows, and the horn cells produced are sticky and
soft, retain their nuclei and stick together to form large masses, which
stay fixed to the underlying tissues or are shed as thick scales.
The main signs:The lesions may be extensive and diffuse but are often confined to the
flexor aspects of joints (referred to historically in horses as mallenders
and sallenders) . Initially the skin is reddened, followed by thickening and
gray discoloration. Large, soft scales accumulate, are often held in place
by hairs and usually crack and fissure, and their removal leaves a raw, red
surface. Hyperkeratosis scales are thin, dry and accompany an intact,
normal skin.
Diagnosis:Confirmation of a diagnosis of parakeratosis is by the identification of
imperfect keratinization in a histopathological examination of a biopsy or
a skin section at necropsy.
Differential diagnosis
1- Hyperkeratosis .2- Pachyderma .3- Ringworm .4-Inherited
ichthyosis .5- Inherited Adema disease in cattle .6-Inherited
dermatosis vegetans in pigs .7-Inherited epidermal dysplasia.
Treatment
Primary treatment requires correction of any nutritional deficiency.
Supportive treatment includes removal of the crusts by the use of
keratolytic agent (e.g. salicylic acid ointment) or by vigorous scrubbing
with soapy water, followed by application of an astringent (e.g. white
lotion paste), which must be applied frequently and for some time after
the lesions have disappeared.
Pachyderma
Pachyderma including scleroderma, is thickening of the skin affecting all
layers, often including subcutaneous tissue, and usually localized but
often extensive as in lymphangitis and greasy heel in horses.
3
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Causes :-There are no specific causes, most cases being due to
nonspecific chronic or recurrent inflammation.
Pathogenesis :- In affected areas the hair coat is thin or absent and the
skin is thicker and tougher than usual. It appears tight and, because of its
thickness and reduced volume of subcutaneous tissue, cannot be picked
into folds or moved easily over underlying tissue.
The main signs: The skin surface is unbroken
 No lesions
 No crusts or scabs as in parakeratosis and hyperkeratosis.
Diagnosis:Confirmation of the diagnosis depends cells in all layers are usually on
histopathological examination of a biopsy. The normal but the individual
layers are increased in thickness. There is hypertrophy of the prickle cell
layer of the epidermis and enlargement of the interpapillary processes.
Differential diagnosis
1- Parakeratosis 2- Cutaneous neoplasia 3- Papillomatosis
Treatment
Primary treatment requires removal of the causal irritation but in wellestablished cases little improvement can be anticipated, and surgical
removal may be a practical solution when the area is small. In early cases
local or systemic corticosteroids may effect a recovery.
Impetigo
superficial eruption of thin -walled, small vesicles, surrounded by a zone
of erythema, that develop into pustules, then rupture to form scabs.
Causes :- a staphylococcus: The only specific examples of impetigo in
large animals are:
 Udder impetigo of cows .
 Infectious dermatitis or' contagious pyoderma' of baby pigs
associated with unspecified streptococci and staphylococci. .
Pathogenesis:The causative organism and appears to gain entry through minor
abrasions, with spread resulting from rupture of lesions causing
4
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
contamination of surrounding skin and the development of secondary
lesions.
Clinical feature: Small (3-6 mm) vesicles appear chiefly on the relatively hairless
parts of the body and do not become confluent.
 In the early stages each vesicle is surrounded by a narrow zone
of erythema.
 No irritation is evident.
 Vesicle rupture occurs readily but some persist as yellow scabs.
 Involvement of hair follicles is common and leads to the
development of acne and deeper, more extensive lesions.
 Individual lesions heal rapidly in about a week but successive
crops of vesicles may prolong the duration of the disease.
Diagnosis:Confirmation of the diagnosis is by culture of vesicular fluid and
identification of the causative bacterium and its sensitivity.
Differential diagnosis
 Cowpox, (the lesions occur a lmost exclusively on the teats and
pass through the characteristic stages of pox).
 Pseudocowpox.
Treatment: Primary treatment
Antibiotic topically is usually all that is required because individual
lesions heal so rapidly.
 Supportive treatment is aimed at preventing the occurrence of
secondary lesions and spread of the disease to other animals.
Twice daily bathing with an efficient germicidal skin wash is
usually adequate.
URTICARIA
An allergic condition characterized by cutaneous wheals. It is most
common in horses.
Etiology
 Primary urticaria
 Results directly from the effect of the pathogen, e.g.:
5
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )









Insect stings
Contact with stinging plants
Ingestion of unusual food, with the allergen, usually a protein.
Occasionally an unusual feed item, e.g. garlic to a horse After a
recent change of diet .
Administration of a particular drug,
e.g. penicillin; possibly
guaifenesin or other anesthetic agent .
Allergic reaction in cattle 8 days following vaccination for footand mouth diseases.
Death of warble fly larvae in tissue .
Milk allergy when Jersey cows are dried off Transfusion reaction.
Secondary urticaria
occurs as part of a syndrome, e.g.:
 Respiratory tract infections in horses, including strangles and the
upper respiratory tract viral infections
Pathogenesis:An allergic reaction.
degranulation of mast cells
liberation of
chemical mediators inflammation,
resulting in the subsequent
development of dermal edema.
A primary dilatation of capillaries
causes cutaneous erythema.
Exudation from the damaged capillary
walls causes local edema in the dermis and a wheal develops. Dermis,
and sometimes the epidermis, is involved.
(Note) :In extreme cases the wheals may expand to become seromas,
when they may ulcerate and discharge. The lesions of urticaria usually
resolve in 12-24 hours but in recurrent urticaria an affected horse may
have persistent and chronic eruption of lesions over a period of days or
months.
Clinical feature: Wheals, mostly circular, well delineated, steep-sided, easily
visible elevations in the skin, appear very rapidly and often
in large numbers, commencing usually on the neck but
being most numerous on the body.
 They vary from 0.5-5 cm in diameter, with a flat top, and
are tense to the touch.
 There is often no itching, except with plant or insect stings,
nor discontinuity of the epithelial surface, exudation or
weeping.
6
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 Pallor of the skin in wheals can be observed only in un
pigmented skin.
 The affected areas become hairless and the wheals exude
serum and become scabbed over.
 Edema of the legs is common and vesicles occur on the
teats. The lesions appear 8-12 weeks postvaccination and
may persist for 3-5 weeks.
 Loss of body weight and lymphadenopathy.
Clinical pathology
 Intradennal skin tests to detect the presence of hypersensitivity are
of little value because many normal horses. as well as those with
urticaria, will respond positively to injected or topically applied
allergens. Also, reactions usually occur within the first 24 hours
after the injection, but the interval is very erratic.
 Intrademal tests in horses without atopy and horses with atopic
dennatitis or recurrent urticaria using environmental allergens
indicate a greater number of positive reactions for intradennal tests
in horses with atopic dennatitis or recurrent urticaria, compared
with horses without atopy.
 Biopsies show that tissue histamine levels are increased and there
is a local accumulation of eosinophils.
 Blood histamine levels and eosinophil counts may also show
transient elevation.
TREATM E NT
 Primary treatment A change of diet and environment, especially
exposure to the causal insects or plants, is standard practice.
Spontaneous recovery is common.
 Supportive treatment Corticosteroids, antihistamines, or
epinephrine by parenteral injection provide the best and most
rational treahnent, especially in the relief of the pruritus, which can
be atmoying in some cases.
 The local application of cooling astringent lotions such as
calamine or white lotion or a dilute solution of sodium bicarbonate
is favored.
 In large animal practice parenteral injections of calcium salts are
used with apparently good results. Long-term medical management
of persistent urticaria involves the administration of corticosteroids
and or antihistamines.
 Oral administration or prednisone or prednisolone at the lowest
possible dose on alternate days is the method of choice. The
7
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
antihistamine of choice is oral hydroxyzine hydrochloride initially
at 600 mg three times daily, followed by gradual reduction to a
minimum maintenance dose required to keep the horse free of
lesions.
Dermatitis and dermatosis
Etiology:Any disease of skin, including those characterized by inflammation. All
pathogens, infectious, chemical, physical, allergic, and autoimmune.
Special local dermatitides: These include dermatitis of the teats and
udder, the bovine muzzle and coronet, and flexural seborrhea, and are
dealt with under their respective headings.
Epidemiology:Sporadic or outbreak, acute or chronic course, cosmetic to lethal, but of
most importance as constraints on movement, sale or exhibition
Pathogenesis :
 Dermatitis is basically an inflammation of the deeper layers of the
skin involving the blood vessels and lymphatics. The purely
cellular layers of the epidermis are involved only secondarily. It
may be acute or chronic, suppurative, weeping, seborrheic,
ulcerative or gangrenous.
 In all cases there is increased thickness and increased temperature
of the part.
 Pain or itching is present and erythema is evident in un pigmented
skin. Histologically there is vasodilatation and infiltration with
leukocytes and cellular necrosis. These changes are much less
marked in chronic dermatitis.
Clinical signs:Primarily localized to skin, including lesions varying from parakeratosis
and pachyderm a to weeping, through necrosis, vesicles and edema.
Secondarily signs of shock, toxemia, anaphylaxis
Clinical pathology: Examination of skin scrapings or swabs for parasitic, bacterial or
other agents is essential.
 Culture and sensitivity tests for bacteria are advisable to enable
the best treatment to be selected.
 Skin biopsy maybe of value in determining the causal agent.
8
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )

In allergic or parasitic states there is usually an accumulation of
eosinophilsin the inflamed area.
 In mycotic dermatitis organisms are usually detectable in the deep
skin layers although they may not be cultivable from superficial
specimens.
Necropsy lesions Inflammatory, degenerative or vascular lesions in skin
biopsy
Treatment
 Primary is removal of the pathogen
 supportive includes treatment for shock, toxemia or fluid and
electrolyte loss .
PHOTOSENSITIZATION
Etiology
Caused by the sensitization of dorsally situated, lightly pigmented skin,
mucosa and cornea to light. Dermatitis develops when the sensitized skin
is exposed to sunlight. Photodynamic agents are substances that are
activated by light and may be ingested preformed (and cause primary
photosensitization) or be products of abnormal metabolism (and cause
photosensitization due to aberrant synthesis of pigment) or be normal
metabolic products that accumulate in tissues because of faulty excretion
through the liver (and cause hepatogenous photosensitization) .
 Intake of primary photodynamic agents (PDAs)
 Faulty excretion of phylloerythrin (metabolic product of
chlorophyll and a PDA) due to liver damage.
 Inherited defects of porphyrin metabolism, producing PDAs.
 Many unexplained cases and outbreaks in pastured or housed
animals
Epidemiology
Exposure to photosensitizing substances and sunlight .Similar incidence
of sporadic cases a n d outbreaks. Always life-threatening unless
exposure to sunlight can be avoided.
Pathogenesis
Penetration of light rays to sensitized tissues causes local cell death and
tissue edema. Irritation is intense because of the edema of the lower skin
level, and loss of skin by necrosis or gangrene and sloughing is common
in the terminal stages. Nervous signs may occur and are caused either by
9
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
the photodynamic agent, as in buckwheat poisoning, or by liver
dysfunction. Hepatogenous photosensitization involves production of a
toxin, by a higher plant, fungus or cyanobacterium (algae),that causes
liver damage or dysfunction, resulting in the retention of the
photosensitizing agent phylloerythrin.
Clinical signs
General signs
 These commence with intense irritation and the animal rubs the
affected parts, often lacerating the face by rubbing it in bushes.
When the teats are affected the cow may kick at them and walk
into ponds to immerse the teats in water, sometimes rocking
backwards and forwards as if to cool the affected parts.
 In nursing ewes there may be resentment towards the lambs
sucking, and heavy lamb mortalities due to starvation may result.
 Local edema is often severe and may cause drooping of the ears,
closure of the eyelids and nostrils, causing dyspnea, and dysphagia
due to swelling of the lips.
 An early sign is increased lacrimation, with the initially watery
discharge developing into a thicker, serous discharge accompanied
by blepharospasm and swelling of the eyelids.
 Initial erythema of the muzzle is followed by fissuring, then
sloughing of the thick skin.
Skin lesions
 Primary cases have cutaneous signs only (erythema, edema,
necrosis, gangrene of light colored skin or mucosae exposed to
sunlight).
 Restricted to the un pigmented areas of the skin and to those parts
which are exposed to solar rays.
 They are most pronounced on the dorsum of the body, diminishing
in degree down the sides and are absent from the ventral surface.
Predilection sites for lesions are the ears, conjunctiva, causing
opacity of the lateral aspect of the cornea, eyelids, muzzle, face, the
lateral aspects of the teats and, to a lesser extent, the vulva and
perineum.
 In solid black cattle dermatitis will be seen at the lips of the vulva
and on the edges of the eyelids, and on the cornea.
 In severe cases the exudation and matting of the hair and local
edema causes closure of the eyelids and nostrils.
10
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 In the late stages necrosis or dry gangrene of affected areas leads
to sloughing of large areas of skin.
Systemic signs
These include shock in the early stages, due to extensive tissue damage.
There is an increase in the pulse rate with ataxia and weakness.
Subsequently a considerable elevation of temperature (41-42°C, 106107°F) may occur.
Nervous signs
 These including ataxia, posterior paralysis and blindness;
depression or excitement are often observed.
 A peculiar sensitivity to water is sometimes seen in sheep with
facial eczema: when driven through water they may lie down in it
and have a convulsion.
 Liver insufficiency Signs are described elsewhere and may
accompany photosensitive dermatitis when it is secondary to liver
damage.
Clinical pathology
Nil for evidence of photosensitivity. In secondary cases there is evidence
of the primary disease
Necropsy lesions
Only skin lesions in primary cases. Secondary cases show liver
lesions or evidence of porphyrin accumulation
Differentia l diagnosis
Clinical evidence of restriction of damage to white, wool-less skin on
body dorsum and lateral aspects of limbs, teats, corneas and tongue and
lips.
Treatment
 Primary treatment includes immediate removal from direct
sunlight, prevention of ingestion of further toxic material and the
administration of laxatives to eliminate toxic materials already
eaten. In areas where the disease is enzootic the use of darkskinned breeds may make it possible to utilize pastures that would
otherwise be too dangerous.
11
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Local treatment will be governed by the stage of the lesions. Nonsteroidal
anti-inflammatory drugs (NSAIDs), corticosteroids or antihistamine can
be administered parenterally and adequate doses maintained. To avoid
septicemia the prophylactic administration of antibiotics may be
worthwhile in some instances.
Diseases of the hair, wool, follicles, skin glands, horns, and hooves
Alopecia and Hypotrichosis
Etiology
Alopecia is complete absence of the hair or wool coat; hypotrichosis is
less than the normal amount of hair or wool. Both may be caused by the
following conditions.
Failure of follicles to develop Congenital hypotrichosis.
Loss of follicles
 Cicatricial alopecia due to scarring after deep skin wounds
that destroy follicles.
 Cicatricial alopecia occurs following permanent destruction
of the hair follicles, and regrowth of hair will not occur.
Examples include physical, chemical or thermal injury,
Failure of the follicle to produce a fiber
 Inherited symmetrical alopecia
 Congenital hypotrichosis
 Hair- coat-color-linked follicle dysplasia.
Loss of preformed fibers
 Dermatomycoses – ringworm.
 Mycotic dermatitis in all species.
 Metabolic alopecia subsequent to a period of malnutrition or
severe illness -'a break in the wool', e.g. excessive whale,
palm or soya oil in milk replacers to calves; the fibers grown
during the period of nutritional or metabolic stress have a
zone of weakness and are easily broken ,tick or itch-mite
infestations; Poisoning by thallium, selenium.
PATHOGENESIS
 Normal shedding of hair fibers is a constant but largely
unexplained process, especially during significant changes in
environmental temperature.
 The long winter coat is shed in response to warmer spring
temperatures and increased hours of sunlight, and rapidly regrows
as environmental temperatures fall in the autumn.
12
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 In inherited hair defects there may be a reduction in follicle
numbers or a reduced capacity of each follicle to produce fibers.
 Chemical depilation produced by cytotoxic agents, such as
cyclophosphamide, occurs as a result of induced cytoplasmic
degeneration in some of the germinative cells of the bulb of the
wool follicle.
 The alteration in cell function is temporary, so that regrowth of the
fiber should follow.
Clinical Finding
o When alopecia is due to breakage of the fiber, the stumps of old
fibers or developing new ones may be seen. When fibers fail to
grow the skin is shiny and in most cases is thinner than normal.
o In cases of congenital follicular aplasia, the ordinary covering hairs
are absent but the coarser tactile hairs about the eyes, lips and
extremities are often present.
o Absence of the hair coat makes the animal more susceptible to
sudden changes of environmental temperature. There may be
manifestations of a primary disease and evidence of scratching or
rubbing.
o Congenital hypotrichosis results in alopecia which is apparent at
birth or develops within the neonatal period.
Clinical Pathology
If the cause of the alopecia is not apparent after the examination of skin
scrapings or swabs, a skin biopsy will reveal the status of the follicular
epithelium.
Differential Diagnosis
Diagnostic confirmation of alopecia is by visual recognition, the
diagnostic problem being to determine the primary cause of the hair or
fiber loss. Hypotrichosis is a reduction in numbers of fibers instead of a
complete absence.
TREATMENT
Primary treatment consists of removing the causes of trauma or other
damage to fibers. In cases of faulty follicle or fiber development
treatment is not usually attempted.
13
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
ACHROMOTRICHIA
Deficient pigmentation in hair or wool fiber as follows: Bands of
depigmentation in an otherwise black wool fleece are the result of a
transitory deficiency of copper in the diet Cattle on diets containing
excess molybdenum and deficient copper show a peculiar speckling of
the coat caused by an absence of pigment in a proportion of hair fibers.
The speckling is often most marked around the eyes, giving the animal
the appearance of wearing spectacles General loss of density of
pigmentation in all coat colors, e.g. Hereford cattle shade off from their
normal deep red to a washed-out orange.
Leukoderma and Leukotrichia
Several skin diseases of the horse are characterized by an acquired loss of
melanin pigment in the epidermis of hair. Melanocytes in the epidermis
and those in the hair bulbs are frequently affected independently.
Leukotrichia occurs when the melanocytes in the hair bulbs lose their
normal amount of melanin pigment. When the melanocytes in the
epidermis are affected and the skin loses normal pigmentation, the
abnormality is leukoderma.
The etiology and pathogenesis
leukoderma are unknown. Reticulated leukotrichia, spotted leukotrichia
and juvenile Arabian leukoderma have been described.
VITILIGO
Patchy depigmentation of the skin with premature graying of the local
hair is not uncommon in cattle and horses.
Etiology
A genetic etiology is suspected in Arabian horses and Holstein-Friesian
cattle.
 Application of' supercooled' instruments that selectively destroy
melanocytes, the basis for freeze branding.
 Prolonged pressure, e.g. by poorly fitting harness. X-irradiation.
Clinical Feature :
 The usual manifestation is the appearance of patches of gray or
white hair -'snowflakes' in an otherwise pigmented coat.
 The defect is esthetic only.
14
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 An idiopathic state in horses, usually during a debilitating disease,
with patchy depigmentation of skin appearing on the prepuce,
perineum, underneath the tail, and on the face.
 There is no discontinuity of the skin.
Clinical Pathology
Histopathological examination reveals a complete absence of
melanocytes from affected areas but the cause is unknown in most cases.
15
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
SEBORRHEA
Etiology:- Seborrhea is an excessive secretion of sebum on to the skin
surface. In large animals it is always secondary to dermatitis or other skin
irritation.
Pathogenesis:- Increased blood supply to the skin and increased hair
growth appear to stimulate the production of sebum, but why seborrhea is
provoked in some individuals and not in others is unknown.
Clinical finding
 In primary seborrhea there are no lesions, only excessive
greasiness of the skin.
 The sebum may be spread over the body surface like a film of oil
or be dried into crusts, which can be removed easily. Sebaceous
glands may be hypertrophied.
 In Flexure seborrhea the extensive skin necrosis follows, causing a
pronounced odor of decay, which may be the first sign observed by
the owner. Irritation may cause lameness and the cow may attempt
to lick the part. Shedding of the Oily, malodorous skin leaves a raw
surface beneath; healing follows in 3-4 weeks.
Greasy heel of cows
Cause :- Cows grazing constantly irrigated, wet pastures, or in very
muddy conditions in tropical areas .
Symptoms : Swelling, with deep fissuring of the skin and an outpouring of evilsmelling exudate, on the back of the pastern of all four feet but
most severely in the hind limbs.
 Affected animals are badly lame and their milk yield declines
sharply.
Treatment:- Removing the cows to dry land and treating systemically
with a broad spectrum antibiotic effects a rapid recovery.
Greasy Heel of horse
Greasy Heel is a condition affecting the pastern and lower leg of horses.
It is especially common in horses with white socks or pasterns and in
certain breeds such as draft Horses. The condition is a type of dermatitis
resulting in inflammation, ulceration and crusting. There are varying
degrees of the condition ranging from short term infections through to
16
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
chronic granulomatous (excessive skin growth) lesions that are almost
impossible to cure.
Causes :- There are numerous causes, most commonly exposure to wet or
muddy areas, such as coastal regions or housing in stables for extended
periods of time.
 Solar exposure – sun burn.
 Can be infectious (bacterial or fungal) or non-infectious(mites or
allergic).
 Chemical or physical irritants are involved.
 Contact allergies to grass or other plants.
 Mange is more common in certain breeds eg, Draft horses.
 Bacteria involved are quite often Staphylococcus or Dermatophilus
(similar to rainscald).
 Fungal infections are usually Dermatophytes similar to ringworm
in other animals.
Symptoms of Greasy Heel of horse.
 Dermatitis (inflammation of the skin) of the lower limbs – hind
limbs more often affected.
 Unpigmented (white) skin becomes red, oedematous (swollen),
itchy and painful.
 The lesions start as a mild scab which continues to thicken with a
moist surface underneath.
 In severe cases the scabs crack and cause pain which may result in
lameness as the pastern flexes e.g. with exercise.
 The lesions normally start at the back of the leg on the heels and
progress up the pastern and around towards the front of the leg and
can be seen on one to all four legs.
Clinical Pathology:The primary cause of the seborrhea may be diagnosed by a suitable
examination for the presence of parasitic or bacterial pathogens.
Treatment



The skin must be kept clean and dry.
Affected areas should be defatted with hot soap and water washes,
then properly dried, and an astringent lotion, e.g. white lotion,
should be applied daily.
In acute cases of greasy heel the application at 5-day intervals of an
ointment made up of five parts salicylic acid, three parts boric acid,
17
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
two parts phenol, two parts mineral oil and two parts petroleum
jelly is recommended.
Long-standing cases profit from the twice-daily washing of the part
and covering with an ointment containing an antibiotic, a
fungistat and a corticosteroid, e.g. gentamicin, clotrimazole,
betametasone.

FOLLICULITIS
Etiology:Infection and inflammation of hair follicles associated with suppurative
organisms, including staphylococci. Identifiable forms of folliculitis as
individual diseases include:





Staphylococcal dermatitis of horses .
Contagious acne of horses .
Benign facial folliculitis of sucking lambs.
Demodectic mange.
Bovine sterile eosinophilic folliculitis.
Pathogenesis :Sebaceous gland ducts blocked by inspissated secretion and epithelial
debris or by pressure become infected. Folliculitis is also a sequel to
seborrhea, with hypertrophy of sebaceous glands and dilatation of their
ducts.
Clinical Finding : The sequence of lesion development is: nodules around the base of
the hair, then pustules, then crusts, finally hair fiber loss.
 Itching may occur, but pain and rupture of pustules under pressure
are more common .
 Pustule rupture leads to contamination of the surrounding skin and
development of further lesions.
Clinical Pathology
Swabs should be taken for bacteriological and parasitological
examination. Diagnostic confirmation is by demonstration of infection of
hair follicles in a biopsy specimen.
18
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Treatment: Primary treatment commences with cleaning the skin by washing
followed by a disinfectant rinse.
 Affected areas should be treated with antibacterial ointments or
lotions. If the lesions are extensive the parenteral administration of
antibiotics is recommended.
 The course of treatment should last 1 week; in chronic cases this
may need to be at least 1 month; a broad-spectrum preparation such
as trimethoprim-sulfadiazine is recommended. In stubborn cases an
autogenous vaccine may be helpful.
 Supportive treatment infected animals should be isolated and
grooming tools and blankets disinfected.
Subcutaneous edema (Anasarca)
Extensive accumulation of edema fluid in the subcutaneous tissue is part
of general edema
Etiology :- Caused by the same diseases, as follows.
 Increased hydrostatic pressure
 Congestive heart failure.
 Vascular compression by tumor, e.g. anterior mediastinal
lymphosarcoma, udder engorgement in heifer about to calve.
 Hypoproteinemic edema .
 In liver damage with reduced albumin production due to liver
insufficiency, especially fascioliasis.
 Renal damage with protein loss into urine occurs rarely in animals.
Pathogenesis
Alteration to the balance between the hydrostatic pressure of
intravascular fluids, the blood and lymph, to the osmotic pressure of those
fluids or to the integrity of the filtering mechanism of the capillary
endothelium leads to a positive advantage by the hydrostatic pressure of
the system and causes a flow of fluid out of the vessels into the tissues.
This results in anasarca and, coincidentally, in fluid accumulations in the
body cavities.
19
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Clinical Finding : There is visible swelling, either local or diffuse.
 The skin is puffy and pits on pressure; there is no pain unless
inflammation is also present.
 In large animals the edema is usually confined to the ventral
aspects of the head, neck and trunk and is seldom seen on the
limbs.
Clinical Pathology
Anasarca is a clinical diagnosis but many estimates, for example of
arterial blood pressure, serum and urine protein levels, provide
contributory evidence.
Differentiation between obstructive and inflammatory edema can be
made by cytological and bacteriological examination of the fluid.
Differential diagnosis
Diagnostic confirmation is by clinical detection of serous fluid in a
subcutaneous site.
1. Extravasation of urine as a result of urethral obstruction and
perforation.
2. Ventral hernia, usually unilateral and does not pit on pressure .
3. Cellulitis, usually asymmetric, hot, often painful, does not pit on
pressure and can be sampled by needle puncture.
Treatment
Primary treatment requires correction of the causal abnormality.
Supportive treatment includes removal of the fluid by drainage methods
such as intubation or multiple incision, both likely to result in damaging
infection in animals in the average farmyard situation, or by the use of a
diuretic.
Angioedema (Angioneurotic edema)
Etiology:Transient, localized subcutaneous edema due to an allergic reaction and
caused by endogenous and exogenous allergens provokes either local or
diffuse lesions. Angioedema occurs most frequently in cattle and horses
on pasture, especially during the period when the pasture is in flower.
This suggests that the allergen is a plant protein. Fish meal may also
provoke an attack. Recurrence in individual animals is common.
20
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Pathogenesis
After an initial erythema, local vascular dilatation is followed by leakage
of plasma through damaged vessels.
Clinical Finding
 Local lesions most commonly affect the head with diffuse edema
of the muzzle, eyelids, conjunctiva and cheeks.
 Occasionally only the conjunctiva is affected, so that the eyelids
are puffy, the nictitating membrane swollen and protruding, and
lacrimation is profuse.
 Affected parts are not painful to touch but shaking the head and
rubbing against objects suggest irritation.
 Salivation and nasal discharge may be accompanying signs.
 Perineal involvement includes vulvar swelling, often asymmetrical,
and the perianal skin, and sometimes the skin of the udder, is
swollen and edematous.
 When the udder is affected, the teats and base of the udder are
edematous and cows may paddle with the hind limbs, suggesting
irritation in the teats.
 Edemaof the lower limbs, usually from the knees or hocks down to
the coronets, is a rare sign.
 Systemic signs are absent, except in those rare cases where
angioedema is part of a wider allergic response, when bloat,
diarrhea and dyspnea may occur, often with sufficient severity to
require urgent treatment.
Clinical Pathology
The blood eosinophil count is often within the normal range, but may be
elevated from a normal level of 4-5% up to 12-15%.
Treatment
Primary treatment to remove the specific cause is usually impossible
but affected animals should be removed from the suspected source of
allergens. Cattle running at pasture should be confined and fed on dry
feed for at least a week.
Supportive treatment to relieve the vascular lesion is always
administered even though spontaneous recovery is the rule.
21
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
In acute cases with severe dyspnea epinephrine can be administered
parenterally, but cautious intravenous injection is recommended.
For subacute cases corticosteroids or other anti-inflammatories are
preferred over antihistamines or epinephrine; usually only one injection is
required.
Subcutaneous Emphysema
Emphysema, free gas in the subcutaneous tissue, occurs when air or gas
accumulates in the subcutaneous tissue
Etiology
 Air entering through a cutaneous wound made surgically or
accidentally
 Air entering tissues through a discontinuity in the respiratory tract
lining, e.g. in fracture of nasal bones; trauma to pharyngeal,
laryngeal, tracheal mucosa caused by external or internal trauma
as in lung puncture by a fractured rib; a foreign body, as in
traumatic reticulitis
 Rumen gases migrating from a rumenotomy or ruminal
trocharization.
 Extension from a pulmonary emphysema Gas gangrene infection.
Pathogenesis
Air moves very quickly through fascial planes, especially when there is
local muscular movement. For example when a lung is punctured, or in
cases of severe interstitial pulmonary edema, air escapes under the
visceral pleura and passes to the hilus of the lung, hence to beneath the
parietal pleura, between the muscles and into the subcutis.
Clinical Finding
 Visible subcutaneous swellings are soft, painless, fluctuating and
grossly crepitant to the touch, but there is no external skin lesion.
 In gas gangrene, discoloration, coldness and oozing of serum may
be evident.
 Emphysema may be sufficiently severe and widespread to cause
stiffness of the gait and interference with feeding and respiration.
Clinical Pathology
None is necessary except in cases of gas gangrene, when a bacteriological
examination of fluid from the swelling should be carried out to identify
the organism present.
22
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Differential Diagnosis
Diagnostic confirmation is based on the observation of crepitus and the
extreme mobility of the swelling; these distinguish emphysema from
other superficial swellings.
o Anasarca, dependent and pits on pressure.
o Hematoma, seroma at injury sites, confirmed by needle puncture.
o Cellulitis is accompanied by toxemia, confirmed by needle
puncture.
TREATMENT
Primary treatment is to close the entry point for the gas but this is usually
impossible to locate or to close. Supportive treatment is only necessary
when the emphysema is extensive and incapacitating, when multiple skin
incisions may be necessary. Gas gangrene requires immediate and drastic
treatment with antibiotics.
LYMPHANGITIS
This is characterized by inflammation and enlargement of the lymph
vessels and is usually associated with lymphadenitis .
Etiology
Lymphangitis is due in most cases to local skin infection with subsequent
spread to the lymphatic system. Common causes are as follows.
Diseases of the subcutis
Horse :Glanders,
epizootic lymphangitis,
sporadic lymphangitis,
ulcerative lymphangitis due to C. pseudotuberculosis.
Strangles in cases where bizarre location sites occur In foals
ulcerative
lymphangitis
associated
with
Streptococcus
zooepidemicus.
Cattle
Skin farcy associated with Nocardia jarcinica, Rhodococcus equi
Cutaneous tuberculosis associated with atypical mycobacteria,
rarely
Mycobacterium bovis.
23
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Pathogenesis
Spread of infection along the lymphatic vessels causes chronic
inflammation and thickening of the vessel walls. Abscesses often
develop, with discharge to the skin surface through sinuses.
Clinical Finding
An indolent ulcer usually exists at the original site of infection. The
lymph vessels leaving this ulcer are enlarged, thickened and tortuous and
often have secondary ulcers or sinuses along their course.
Local edema may result from lymphatic obstruction.
In chronic cases much fibrous tissue may be laid down in the subcutis and
chronic thickening of the skin may follow. The medial surface of the hind
limb is the most frequent site, particularly in horses.
Clinical Pathology
Bacteriological examination of discharges for the presence of the specific
bacteria or fungi is common practice.
Treatment
Primary treatment requires vigorous, early surgical excision or specific
antibiotic therapy. Supportive treatment is directed toward removal of
fluid and inflammatory exudate and relief of pain.
Necrosis and Gangrene
Necrosis is tissue death; gangrene is sloughing of dead tissue. When
either change occurs in the skin it involves the dermis, epidermis and
subcutaneous tissue.
Cutaneous cysts
Cysts contained by an epithelial wall enclosing amorphous contents or
living tissue may be congenital, inherited defects or acquired
Cause:- as a result of inappropriate healing of accidental wounds.
Clinical feature : They are smooth, painless, about 1.5-2.5 cm in diameter, round and
usually fluctuating, although inspissated contents may make them
feel quite hard.
 The skin and hair coat over them is usually nonl1al, although some
may leak mucoid contents on to the skin.
24
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
Melanoma :- Superficially situated melanomas occur most commonly
at the tail root in aged, gray horses and rarely in dark-skinned cattle,
sheep and goats.
Diseases of the conjunctiva
Conjunctivitis and Keratoconjunctivitis:- This is inflammation of
the covering membrane of the eye, including the orbit and the inner
surface of the eyelids. The inflammation commonly extends to layers
below the conjunctiva, hence keratoconjunctivitis.
Etiology
Specific conjunctivitis
Cattle:- Infectious bovine keratoconjunctivitis is associated with:
Moraxella bovis, the only significant cause
M. bovis with infectious bovine rhinotracheitis virus
Neisseria catarrhalis , Mycoplasma spp. And Chlamydophila spp.
Sheep and Goats :- Rickettsia conjunctivae is the important infection
N. catarrhalis, and Mycoplasma conjunctivae
Pigs :- Rickettsia spp.
Horses:- Moraxella equi and Thelazia spp. and Habronema spp.
Nonspecific conjunctivitis
Inflammation caused by foreign bodies or chemicals, or secondarily as
exposure keratitis, and conjunctivitis keratitis in paralysis of eyelids as
in listeriosis. Ant-bite conjunctivitis occurs in similar circumstances
Clinical Finding : Blepharospasm and weeping from the affected eye are the initial
signs.
 Watery tears are followed by mucopurulent, then purulent
ocular discharge if the lesion extends below the conjunctiva.
 Varying degrees of opacity of the conjunctiva may develop,
depending on the severity of the inflammation.
 In the severest lesions there is underrunning of the conjunctiva
with pus accompanied by vascularization of the cornea.
25
Diyala University
Stage : 4th Stage
Faculty of Veterinary Medicine
Subject: Internal Medicine
By: Dr. TAREQ RIFAAHT MINNAT (No. )
 During the recovery stage there is often long-lasting, diffuse
opacity of the eye and terminally a chronic white scar in some
cases.
Congenital defects of the eyelids and cornea
Dermoid cysts
Ocular dermoid cysts are solid, skin-like masses of tissue, adherent
usually to the anterior surface of the eye, causing irritation and
interfering with vision. The eyelid, the third eyelid and the canthus
may also be involved, and the lesions may be unilateral or bilateral.
Surgical ablation is recommended.
Diseases of the external ear
Otitis Externa :- It isinflammation of the skin and external auditory
canal, can affect cattle of all ages, in isolated cases, an entire herd or in
entire regions. Arthropod parasites, foreign bodies and sporadic
miscellaneous infections may cause irritation in the ear, accompanied by
rubbing of the head against objects and frequent head-shaking.
The mites Raillietia auris and Dermanyssus avium, the tick Otobius
magnini, larvae (Stephanofilaria zahaeeri), free-living nematodes
(Rhabditis bovis) and the blue fly (Chrysomia bezziano). Malassezia spp.,
Candida spp., Rhodotorula mucilaginosa, Aspergillus spp. are common
causes of otitis in cattle
OTITIS MEDIA
Otitis media (middle ear infection) occurs in milk-fed calves from a few
days of age up to 10 weeks and in weaned calves from 4-8 months and
from 12-18 months of age.
The major bacteria that cause otitis media in calves include Actinomyces
spp., C. pseudotuberculosis, Escherichia coli, Histophilus somni
(formerly Haemophilus somnus), Pasteurella multocida, Mannheimia
(formerly Pasteurella) haemolytica, Pseudomonas spp., Streptococcus
spp. And M. bovis.
26