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Small and Large Animal Dermatology
Environmental Skin Diseases
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Environmental Skin DiseasesSolar Dermatitis – Canine and Feline
A. General Considerations:
1. Solar dermatitis is also called actinic dermatitis or photodermatitis.
2. It is defined as an actinic or photoaggravated reaction that occurs on white, depigmented, or sparsely haired skin.
3. Solar radiation (ultraviolet light waves of 320 to 400 nanometers) and genetic predisposition are thought to play major roles in the cause of solar dermatitis.
4. The exact pathogenesis of solar dermatitis is unknown, although multiple factors are thought to be involved.
5. Some evidence suggests that the ultraviolet rays alter deoxyribonucleic acid (DNA) synthesis and repair in the epidermis.
Important Facts
Solar dermatitis, also called actinic dermatitis or photodermatitis, is defined as an actinic or photoaggravated reaction that occurs on white, depigmented, or sparsely-haired skin.
Solar radiation (ultraviolet light waves of 320 to 400 nanometers) and genetic predisposition are thought to play major roles in the cause of solar dermatitis.
Some evidence suggests that the ultraviolet rays alter DNA synthesis and repair in the epidermis
B. History:
1. The usual history for a dog or cat with solar dermatitis is that the lesions are present on lightly pigmented and sparsely haired areas and are exacerbated with extended exposure to sunlight.
2. The dorsal muzzle is the most common site involved in dogs. The trunk can also be affected in some breeds.
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3. The lesions frequently improve as exposure to direct sunlight is reduced.
4. Solar dermatitis is most frequent in areas with long periods of intense sunlight, although reflection from snow also can result in severe reactions.
5. Solar dermatitis has no sex or age predilection.
6. Light-colored Dalmations, Whippets, American Staffordshire terriers, Beagles, Bulldogs, German shorthaired pointers, and white bull terriers have a higher incidence of solar dermatitis of the trunk.
7. Most affected dogs have a history of being “sunbathers”.
8. Cats usually develop lesions on the pinnae (white cats) or unpigmented noses or eyelids.
9. The drug history often includes either a complete or a partial response to corticosteroids or sunscreens, especially if the lesions are less severe.
10. Animals that show good response to these therapeutic agents should be evaluated for autoimmune disease, especially discoid lupus erythematosus, pemphigus foliaceous, and pemphigus erythematosus.
Important Facts
The usual history for a dog or cat with solar dermatitis is that the lesions are present on lightly pigmented and sparsely haired areas and are exacerbated with extended exposure to sunlight.
The dorsal muzzle is the most common site involved in dogs. The trunk can also be affected in some breeds.
Cats usually develop lesions on the pinnae (white cats) or unpigmented noses or eyelids.
Not only the sunlight but also reflection from snow can result in severe reactions.
C. Clinical Signs:
1. Lesions are initially characterized by erythema, and scaling of nonpigmented, sparsely haired skin.
2. Erosions and ulcerations are frequently present.
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3. Variable degrees of alopecia, crusting, excoriation, depigmentation, and secondary infection are observed.
4. If the lesions are in a healing stage, they are often covered with a thin, dry, alopecic epithelium.
5. Truncal lesions occur on the white skin, usually of the flank and abdomen.
6. The truncal lesions are erythematous initially; with prolonged exposure to sunlight, these areas become thickened, eroded, or ulcerated. Squamous cell carcinoma may develop in the severe, chronic lesion.
7. Actinic keratoses are solar-induced preneoplastic lesions seen in nonpigmented and light-haired skin that is exposed to ultraviolet light.
8. The keratoses are maculopapular eruptions with crusting, indurated plaques and nodules and comedones. The rupture of comedones results in furunculosis and draining tracts.
9. Comedones are formed as a result of the ultraviolet light damage of the upper region of the hair follicles causing dysplasia of this area and comedone formation.
10. Actinic keratoses may progress to squamous cell carcinoma.
Important Facts
Lesions are initially characterized by erythema, and scaling of nonpigmented, sparsely haired skin.
Erosions and ulcerations are frequently present.
Secondary pyoderma may occur.
Healing lesions are often covered with a thin, dry, alopecic epithelium.
Truncal lesions usually occur on the flank and abdomen and are erythematous initially; with prolonged exposure to sunlight, these areas become thickened, eroded, or ulcerated. Squamous cell carcinoma may develop in the severe, chronic lesion.
Actinic keratoses are solar-induced preneoplastic lesions characterized by maculopapular eruptions with crusting, indurated plaques and nodules and comedones. The rupture of comedones results in furunculosis and draining tracts.
Actinic keratoses may progress to squamous cell carcinoma.
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D. Diagnosis:
1. History and clinical findings are suggestive of solar dermatitis.
2. Most of the diagnostic workup is for the purpose of ruling out other primary etiologic factors, which often result in similar lesions.
3. Diagnostic tests include skin scrapings, fungal and bacterial cultures, and skin biopsies.
4. Differentials include: discoid lupus erythematosus, pemphigus foliaceous, pemphigus erythematosus, dermatomyositis, demodicosis, dermatophytosis and nasal pyoderma. Dermatophytosis, demodicosis and nasal pyoderma primarily affect haired areas on the nose versus non-haired nasal planum.
Important Facts
History and clinical findings are suggestive of solar dermatitis.
Skin biopsies are important to rule out other dermatoses that have similar clinical presentation.
Differentials include: discoid lupus erythematosus, pemphigus foliaceous, pemphigus erythematosus, dermatomyositis, demodicosis, dermatophytosis and nasal pyoderma.
Dermatophytosis, demodicosis and nasal pyoderma primarily affect haired areas on the nose versus non-haired nasal planum but skin scrapings and fungal cultures should be performed to rule out these conditions.
E. Treatment:
1. Avoid sunlight from 10 a.m. to 4 p.m..
2. Protect the depigmented light-haired skin with a T-shirt, black felt-tipped markers or tattooing with black ink (allergic reactions occur rarely). Tattooing should be considered when other photoprotection measures are ineffective.
3. Apply topical sunscreens with a SPF of 15 or higher 15 to 30 minutes before sun exposure.
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4. Corticosteroids to decreased the inflammation. Topical hydrocortisone 1% to 2.5% BID. Oral prednisone at the dose of 1 mg/kg q24 for 7 to 10 days can be prescribed for more severe cases.
5. Beta-carotene at the dose of 30 mg given BID. 6. When the solar dermatitis progresses to an actinic keratoses or squamous cell
carcinoma or results in massive destruction of tissue, treatments with retinoids (acitretin (Soritane) 1 mg/kg q12 PO ), hyperthermia (lesions < 5 mm in diameter), cryosurgery, surgical excision, photochemotherapy, or radiation therapy may be of some benefit.
7. Patients requiring these treatments have a poor prognosis.
Important Facts
Avoid sunlight from 10 a.m. to 4 p.m.
Protect the depigmented light-haired skin with a T-shirt, black felt-tipped markers or tattooing with black ink (allergic reactions occur rarely).
Apply topical sunscreens with a SPF of 15 or higher 15 to 30 minutes before sun exposure.
Corticosteroids to decreased the inflammation. Topical hydrocortisone 1% to 2.5% BID. Oral prednisone at the dose of 1 mg/kg q24 for 7 to 10 days can be prescribed for more severe cases.
Beta-carotene at the dose of 30 mg given BID.
When the solar dermatitis progresses to an actinic keratoses or squamous cell carcinoma or results in massive destruction of tissue, treatments with retinoids, hyperthermia, cryosurgery, surgical excision, photochemotherapy, or radiation therapy may be of some benefit.
Patients requiring these treatments have a poor prognosis.
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References
1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Canine Skin Diseases. In: Canine and Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems, Trenton, New Jersey, 1998, p 314-353.
2. Frank LA, Calderwood-Mays MB: Solar dermatitis in dogs. Compend. Contin. Educ. Pract. Vet. 16(4):465-472, 1994.
Learning Objectives
1. Remember! Solar dermatitis develops in depigmented and light-haired skin. Sites more frequently involved in dogs are planum nasal and bridge of the nose. Some breeds with white coat and skin also develop lesions on the flank and abdomen. These dogs usually love to lay in the sun (“sun-bathers”).
2. Sites usually affected in cats are pinnae, bridge of the nose and planum nasal and eyelids.
3. Know the evolution of signs associated with solar dermatitis.
4. Remember! Actinic keratoses are solar-induced preneoplastic lesions characterized by maculopapular eruptions with crusting, indurated plaques and nodules and comedones. The rupture of comedones results in furunculosis and draining tracts. Sunlight damage to the infundibulum (upper region) of the hair follicle causes dysplasia and comedone formation.
5. Remember! Actinic keratoses can progress to squamous cell carcinoma.
6. How do you diagnose actinic dermatosis?
7. Remember! Some autoimmune diseases such as discoid lupus, pemphigus foliaceous, and pemphigus erythematosus will also develop lesions on the planum nasal and bridge of the nose resembling solar dermatitis.
8. Remember! Dermatophytosis, demodicosis and nasal pyoderma have to be included in your list of differentials, however, these conditions involve the haired areas of the nose and face and not the planum nasal. Skin scrapings and fungal cultures have to be part of your diagnostic plan to rule out demodicosis and dermatophytosis.
9. How do you manage solar dermatitis in dogs and cats?
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Environmental Skin DiseasesBurns – Canine and Feline
A. General considerations:
1.Burns are tissue damage resulting from thermal or chemical insult.
Important Facts
Burns are tissue damage resulting from thermal or chemical insult.
B. Etiology:
1. Direct heat burns result from the contact with a hot object or substance.
2. The most common direct heat burn is the “clipper burn” which results from a hot clipper blade contacting the skin.
3. Less frequently, direct burns develop from situations such as cats walking over hot stove burners, contact with hot exhausts parts of cars and wood or coal heaters, poor supervision of paralytic animals on heating pads, hot liquid spilled on animals, and malfunction of hair drying equipment.
4. Flame burns may result from fires in homes or automobile accidents.
5. Electrical burns are often seen in and around the oral cavity when a young dog chews an electrical cord.
Important Facts
The most common direct heat burn is the “clipper burn” which results from a hot clipper blade contacting the skin.
Less frequently, direct burns develop from situations such as cats walking over hot stove burners, contact with hot exhausts parts of cars and wood or coal heaters, poor supervision of paralytic animals on heating pads, hot liquid spilled on animals, and malfunction of hair drying equipment.
Flame burns may result from fires in homes or automobile accidents.
Electrical burns are often seen in and around the oral cavity when a young dog chews an electrical cord.
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C. Pathogenesis and Classification:
1. The severity of burn is related to the maximum temperature the tissue attains and the duration of the overheating.
2. The following variables will influence the severity of the burn: the temperature and mass of the burning agent; the mass, specific heat, and thermal conductivity of the burned body; the temperature of the environment in which post-burning cool takes place; and the amount of heat convection in the surrounding medium.
3. The immediate cooling of the burned area can shorten the duration of tissue overheating, thereby decreasing the tissue damage.
4. Minimal overheating of tissue causes inapparent, reversible cell damage.
5. Finally, when a critical threshold is exceeded, necrosis of the entire tissue occurs.
6. Severe burns may also result in shock as well as hemostatic, liver, kidney, respiratory and immunologic disorders.
7. Depending on the depth of involvement, burns are classified as superficial, partial thickness or full thickness.
Important Facts
The following variables will influence the severity of the burn: the temperature and mass of the burning agent; the mass, specific heat, and thermal conductivity of the burned body; the temperature of the environment in which post-burning cool takes place; and the amount of heat convection in the surrounding medium.
The immediate cooling of the burned area can shorten the duration of tissue overheating, thereby decreasing the tissue damage.
When a critical threshold is exceeded, necrosis of the entire tissue occurs.
Severe burns may also result in shock as well as hemostatic, liver, kidney, respiratory and immunologic disorders.
Depending on the depth of involvement, burns are classified as superficial, partial thickness or full thickness.
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D. Clinical Signs:
1. The clinical appearance of a burn will vary depending on the etiology and severity.
2. The hair coat obscures burns to the skin, which may be more clearly noticed on the sparsely haired regions of the body.
3. As a result, there may be several days delay from the damage until clinical manifestations are evident.
4. Superficial burns involve only the epidermis. Clinically they are characterized by erythematous, painful lesions which heal rapidly. The hair is singed.
5. Partial thickness burns involves the epidermis and the dermis in variable depth. They are characterized clinically by erythema, local edema, occasional small vesicles, and partial sensation to touch.
6. If partial burns involve the epidermis and superficial portions of the dermis (superficial), the lesions will be moist, will blanch with pressure, pain will be present and the healing process will occur in 3 weeks.
7. If partial burns involve the epidermis and deep portions of the dermis (deep), the lesions will be dry, will not blanch with pressure, no pin will be elicited with pin prick and healing process will take place after several months with some scarring.
8. Re-epithelization occurs from hair follicles and sebaceous glands.
9. Full-thickness burns are characterized by complete destruction of all elements of the skin including adnexa and nerves.
10. Clinically, full-thickness burns are distinguished by lack of superficial blood flow, insensitivity to touch, and easy epilation of hair. It may take 10 to 14 days before the skin evidences a color change and separation of necrotic skin begins.
11. Secondary infections and life-threatening sepsis are potential sequela of full-thickness burn.
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Important Facts
There may be several days delay from the damage until clinical manifestations are evident if burn occurs in haired areas.
Superficial burns involve only the epidermis. Clinically they are characterized by erythematous, painful lesions which heal rapidly. The hair is singed .
Partial thickness burns involves the epidermis and the dermis in variable depth.
If partial burns involve the epidermis and superficial portions of the dermis (superficial), the lesions will be moist, will blanch with pressure, pain will be present and the healing process will occur in 3 weeks.
If partial burns involve the epidermis and deep portions of the dermis (deep), the lesions will be dry, will not blanch with pressure, no pin will be elicited with pin prick and healing process will take place after several months with some scarring.
Full-thickness burns are characterized by complete destruction of all elements of the skin including adnexa and nerves.
Clinically, full-thickness burns are distinguished by lack of superficial blood flow, insensitivity to touch, and easy epilation of hair. It may take 10 to 14 days before the skin evidences a color change and separation of necrotic skin begins.
Secondary infections and life-threatening sepsis are potential sequela of full-thickness burn.
E. Diagnosis:
1. History should be an important clue.
2. Biopsies are indicated in the absence of a client history since other considerations would include erythema multiforme, toxic epidermal necrolysis and a variety of immune-mediated skin diseases.
3. Histopathological findings include acute coagulation necrosis of the epidermis, spongiosis, and ulceration.
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Important Facts
History should be an important clue.
Biopsies are indicated in the absence of a client history since other considerations would include erythema multiforme, toxic epidermal necrolysis and a variety of immune-mediated skin diseases.
F. Treatment:
1. Restore and maintain airway.
2. Treat shock.
3. Combat fluid loss.
4. Relieve pain – morphine, oxymorphone, torbugesic, ketamine.
5. Treat skin lesion:
a. Minor burns:
1. Ice packs, soaks, cool isotonic solution (saline, lactated ringer), use in 2 hours after burn. Apply at 3 to 17C for 30 to 45 minutes.
2. Debride devitalized tissue.
3. Topical silver sulfadiazine cream (Silvadene, Marion Laboratories), or chlorhexidine; protects from sepsis; lowers post burn mortality.
4. Sterile bandage.
b. Major burns:
1. Flush with cool isotonic solution at 3 to 17C for 30 to 45 minutes if the burn has occurred within 2 hours.
2. Debride necrotic tissue early and frequently.
3. Subeschar injection of antibiotics based on culture and sensitivity.
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4. Topical antimicrobials:
a. Silver sulfadiazine (Silvadene, Marion Laboratories): expensive, antibacterial, antifungal, nonpainful, not systemically absorbed (best one for young animals).
b. Mafenide (Sulfamylon, Wintrop Laboratories): expensive, antibacterial, painful, absorbed systemically, respiratory alkalosis.
c. Silver nitrate solution 0.5%: inexpensive, antibacterial, may leach NaCl therefore monitor electrolytes; keep gauze dressings soaked.
d. Do not use mupirocin (Bactoderm) ointment: polyethylene glycol base may cause renal failure.
1. Use sterile bandages and change twice daily.
2. Culture wounds twice weekly. Pseudomonas aeruginosa, Staphylococcus sp., Streptococcus sp., Proteus sp., infections are common. Infection is the leading cause of death in-patients surviving the initial injury.
3. Do not put the patient on systemic antibiotics unless septicemia develops: monitor temperature and CBC’s.
4. Early closure: lyophilized pig skin, autografts.
5. Day 5 to 6 to 12 weeks in hypermetabolic state due to increased evaporation, repair process, resetting of thermostat. Animal will need high calorie, high protein diet, and vitamins. May need to administer via nasogastric tube.
6. Blood transfusion may be necessary if persistent anemia.
7. Chemical burns:
a. Remove from source of chemical.
b. Flush affected site with copious water or saline.
c. Volatile solvents and petroleum products may cause pneumonia; apply light oil on coat then wash.
d. Wash with nonalcoholic detergent (Ivory dishwashing liquid).
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e. In cases of burn by hot tar: clip area, coat site with ointment containing emulsifying agent such as polyoxyethylene sorbitan (Neosporin, other antibiotic ointment, polysorbate ointment (Tween 80, Sigma, St. Louis)); then wash.
Important Facts
Restore and maintain airway.
Treat shock.
Combat fluid loss.
Relieve pain – morphine, oxymorphone, torbugesic, ketamine.
Treat the skin lesion according to its severity and depth.
Cooling the affected areas is appropriate if the burn occurred within the past 2 hours. Cooling reduces pain, depth of the burn wound, edema, and mortality.
Clean and debride affected areas early and frequently. Apply topical antibiotics.
In cases of major burns (full-thickness), sterile bandages should be used and changed twice daily.
Infection is the leading cause of death in-patients surviving the initial injury associated with major burns.
Do not put the patient on systemic antibiotics unless septicemia develops: monitor temperature and CBC’s.
Provide adequate nutrition.
Blood transfusion may be necessary if persistent anemia.
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References
1. Scott, Miller, Griffin. Chapter 15, Small Animal Dermatology, 5th ed, 1995.
2. Swaim S.K. Surgery of traumatized skin: Management and reconstruction in the dog and cat. W.B. Saunders, Philadelphia, 1980, pp. 60-62, 199-201, 347, 354.
3. Fox S.M. Management of Thermal Burns – Part I. Compend Cont Education 7:631-642, 1986.
4. Fox S.M. Management of Thermal Burns – Part II. Compend Cont Education 8:439-445, 1986.
Learning Objectives
1. Remember! Most burns are of thermal origin but chemical burns also occur.
2. Know the common causes of thermal burns.
3. Know! According to the tissue depth involved, burns can be classified in superficial, partial-thickness and full-thickness.
4. Know! Superficial burns affect only the epidermis and are characterized by erythematous and painful lesions which heal rapidly. Partial-thickness burns are further divided in superficial and deep. Superficial partial burns involve the epidermis and superficial portions of the dermis and, the lesions are moist, blanch with pressure, pain is present and the healing process occurs in 3 weeks. If partial burns involve the epidermis and deep portions of the dermis (deep), the lesions will be dry, will not blanch with pressure, no pin will be elicited with pin prick and healing process will take place after several months with some scarring. Full-thickness burns are characterized by complete destruction of all elements of the skin including adnexa and nerves. Clinically, full-thickness burns are distinguished by lack of superficial blood flow, insensitivity to touch, and easy epilation of hair. It may take 10 to 14 days before the skin evidences a color change and separation of necrotic skin begins.
5. Remember! Watch for septicemia in cases of full-thickness burns. Monitor temperature and CBC’s, culture wounds twice weekly. Infection is the leading cause of death in-patients with major burns that survived the initial injury.
6. Remember! Do not put the patient on systemic antibiotic unless septicemia develops.
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7. How do you diagnose burn? What are the main differentials?
8. How do you manage a minor and major burn? How do you manage a chemical burn?
9. What is the advantage of cooling the affected areas? When should cooling be applied and for how long?
10. What topical antibiotics are usually used?
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Environmental Skin DiseasesHypothermia and Frostbite
A. General Considerations:
1. Hypothermia is present when body temperature drops and the metabolic processes slow. Blood flow is shunted from surface areas and extremities by extreme vasoconstriction. Cardiac rate and output fall; renal perfusion decreases; mental and neurologic functions diminish. In the terminal stages, ventricular fibrillation can occur.
2. In mild hypothermia, the body temperature reaches 30 to 32C (86 to 90F).
3. In moderate hypothermia, the body temperature reaches 22 to 25C (72 to 77F). Animal succumbs in 4 to 24 hours.
4. In severe hypothermia the body temperatures are lower than 15C (60F).
5. Animal succumbs in 5 to 6 hours. Animal will succumb in 1 to 2 hours if ill.
6. Frostbite occurs with prolonged exposure to freezing temperatures and is more likely to occur if the animal is also exposed to windy conditions or there is wetting of a body area.
7. Body temperatures lower than 34C (93F) decrease blood flow to the skin and extremities resulting in frostbite.
8. Frostbite results from an avascular necrosis with simple freezing of any exposed skin.
9. Necrosis increases with refreezing of thawed skin.
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Important Facts
Hypothermia is present when body temperature drops and the metabolic processes slow.
Cardiac rate and output fall; renal perfusion decreases; mental and neurologic functions diminish.
Mild hypothermia : body temperature reaches 30 to 32C (86 to 90F).
Moderate hypothermia: body temperature reaches 22 to 25C (72 to 77F). Animal succumbs in 4 to 24 hours.
Severe hypothermia: body temperatures are lower than 15C (60F). Animal succumbs in 5 to 6 hours. Animal will succumb in 1 to 2 hours if ill.
Body temperatures lower than 34C (93F) decrease blood flow to the skin and extremities resulting in frostbite.
Frostbite results from an avascular necrosis with simple freezing of any exposed skin.
Necrosis increases with refreezing of thawed skin.
B. Pathogenesis:
1. The pathogenesis of frostbite involves direct cold injury to the cell, indirect cold injury by formation of ice crystals, and impaired circulation with hypoxia as a result of local vasoconstriction and central vasoconstriction to conserve body temperature.
Important Facts
The pathogenesis of frostbite involves direct cold injury to the cell, indirect cold injury by formation of ice crystals, and impaired circulation with hypoxia.
C. Clinical Signs:
1. Hypothermia:
a. Diminished consciousness, low blood pressure, bradycardia, shivering.
b. Respiration is shallow or infrequent.
c. Neurologic reflexes are delayed or decreased.
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d. Increased muscle tone without shivering is observed at body temperatures below 32C (90F).
2. Frostbite:
a. Lesions usually occur in areas where the hair coat is sparse.
b. In cats the tips of the ears, tail, and footpads are most commonly affected.
c. In dogs the scrotum and footpads are most commonly affected.
d. Initially frozen areas are cool to the touch, pale, cyanotic and hypoesthetic.
e. After thawing, the affected areas become erythematous, painful, edematous (2 to 3 days), and eventually may either develop scaling or necrosis (shrinks, discolors; demarcates and sloughs in 20 to 30 days).
f. Cats with mild frostbite may be asymptomatic with the only noticeable feature being a delayed lightening of the hair color on the tip of the ears and curling of the pinna.
Important Facts
If hypothermia develops the following signs are present: diminished consciousness, low blood pressure, bradycardia, shivering, shallow or infrequent respiration, delayed or decreased neurologic reflexes.
Increased muscle tone without shivering is observed at body temperatures below 32C (90F).
The acute phase of frostbite lesions is characterized by lesions being cool to the touch, pale, cyanotic and hypoesthetic.
With thawing, the affected areas become erythematous, edematous, painful, and eventually may either develop scaling or necrosis.
In cats the tips of the ears, tail, and footpads are most commonly affected.
In dogs the scrotum and footpads are most commonly affected.
Cats with mild frostbite may be asymptomatic with the only noticeable feature being a delayed lightening of the hair color on the tip of the ears and curling of the pinna.
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D. Diagnosis:
1. Diagnosis is based on history of exposure to cold, recognition of clinical signs and demonstration of low body temperatures.
E. Treatment:
1. Correct hypothermia: rapid return of body temperature to normal, reversal of shock, correct life-threatening arrhythmias.
2. Rewarming:
a. Mild hypothermia: warm blankets.
b. Moderate to severe hypothermia:
1. External warming : warm water bottles, immersion in warm water, apply water heating pads. Be careful with peripheral vasodilation causing drop in core body temperature. DO NOT USE ELECTRIC HEATING PADS.
2. Internal (core) warming : warmed IV solution (electrolyte or normal saline solutions warmed to 40 to 43C (104 to 109F) IV; IV or oral dextrose to very young animals) warm peritoneal dialysis, colonic/gastric lavage with warm saline solution. Except for warm IV solutions reserve core warming for temperatures lower than 32C (96.8F).
3. Maintain temperature higher than 38C (100 F) for several hours.
3. Skin lesions:
a. Remove source of cold.
b. Apply warm compresses.
c. Next immerse in 39 to 40C (102 to 104 F). Must prevent refreezing as this greatly increases tissue damage. Rewarm rapidly.
d. IV low molecular weight dextran (Dextran 40, Pharmacia Labs) may prevent peripheral sludging.
e. Analgesia if the animal is hemodynamically stable (morphine, oxymorphone, torbugesic, ketamine).
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f. Leave warm, erythematous, edematous areas open to the air.
g. Apply wet dressings for gangrenous areas. Elizabethan collar may be necessary to prevent self-mutilation.
h. Postpone debridement several days. Amputate gangrenous tissues late after well demarcated and mummified (7 to 14 days).
i. Antibiotics should be prescribed if secondary infection occurs. Topical antibacterials, povidone iodine or chlorhexidine are useful.
Important Facts
Correct hypothermia: rapid return of body temperature to normal, reversal of shock, correct life-threatening arrhythmias.
Remove source of cold.
Apply warm compresses.
Must prevent thawing and refreezing as this greatly increases tissue damage.
Leave warm, erythematous, edematous areas open to the air.
Apply wet dressings for gangrenous areas. Elizabethan collar may be necessary to prevent self-mutilation.
Postpone debridement several days. Amputate gangrenous tissues late after well demarcated and mummified.
Antibiotics should be prescribed if secondary infection occurs.
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References
1. Scott, Miller, Griffin. Chapter 15, Small Animal Dermatology, 5th ed, 1995.
2. Morgan R.V. Environmental Injuries. In Hoskins J.D., Veterinary Pediatrics, W.B. Saunders, Philadelphia, 1990.
Learning Objectives
1. Know! Hypothermia is present when body temperature drops and the metabolic processes slow. Body surface and extremities will be cool to the touch and pale due to extreme peripheral vasoconstriction.
2. Remember! Hypothermia should be treated as an emergency! Cardiac rate and output fall; renal perfusion decreases; mental and neurologic functions diminish. In the terminal stages, ventricular fibrillation can occur.
3. Know! In mild hypothermia the body temperature reaches 30 to 32C (86 to 90F). In moderate hypothermia the body temperature reaches 22 to 25C (72 to 77F). Animal succumbs in 4 to 24 hours. In severe hypothermia the body temperatures are lower than 15C (60F). Animal succumbs in 5 to 6 hours. Animal will succumb in 1 to 2 hours if ill.
4. Know! Body temperatures lower than 34C (93F) decrease blood flow to the skin and extremities resulting in frostbite.
5. Remember! Avoid thawing and refreezing as this greatly increases tissue damage.
6. What are the clinical signs associated with hypothermia?
7. What are the clinical signs associated with the acute and late phase of frostbite?
8. What are the sites usually affected in dogs and cats?
9. Cats with mild frostbite may be asymptomatic with the only noticeable feature being a delayed lightening of the hair color on the tip of the ears and curling of the pinna.
10. How do you diagnose hypothermia and frostbite?
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11. How do you manage hypothermia and frostbite?
12. Remember! When managing hypothermia, except for warm IV solutions, reserve core warming for temperatures lower than 32C (96.8F).
13. Remember again! When managing frostbite, must prevent thawing and refreezing as this greatly increases tissue damage.
14. Remember! Postpone debridement until damaged tissue is demarcated and mummified. It may take 7 to 14 days before demarcation occurs.
15. Remember! Necrotic tissue is hypoesthetic or anesthetic. Prescribe an Elizabethan collar to prevent self-mutilation.
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Environmental Skin DiseasesDecubital Ulcers
A. General Considerations:
1. Decubital ulcers (pressure sores) occur mainly over bony prominences because of continual localized pressure to the skin.
Important Facts
Decubital ulcers (pressure sores) occur mainly over bony prominences because of continual localized pressure to the skin.
B. Etiology and Pathogenesis:
1. Compression of the skin and subcutaneous tissue collapses blood vessels resulting in ischemia, necrosis, and subsequent ulceration.
2. Predisposing factors:
a. Neurologic or orthopedic patients: lack of sensory or motor function, patients can not change position.
b. Decreased padding: subcutaneous fat is decreased from weight loss or muscle atrophy due to disease.
c. Loss of tissue elasticity (hyperadrenocorticism).
d. Heating pads burns.
e. Tissue laceration, friction.
f. Fecal and/or urine contamination and scald.
g. Malnutrition: diet, anemia of tissues, hypoproteinemia.
h. Poor circulation: improper bandages or casts.
1. Animals who are recumbent due to neurologic deficits or musculoskeletal problems are predisposed.
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Important Facts
Compression of the skin and subcutaneous tissue collapses blood vessels resulting in ischemia, necrosis, and subsequent ulceration.
Animals who are recumbent due to neurologic deficits or musculoskeletal problems are predisposed.
C. Clinical Signs:
1. Hyperemia that progresses to necrosis and ulceration.
2. Sites: any pressure point.
3. May get secondary infection and osteomyelitis in exposed bones.
Important Facts
Hyperemia is the initial clinical sign.
Hyperemia progresses to necrosis and ulceration.
Any pressure point can develop decubital ulcer.
Secondary infection and osteomyelitis in exposed bones may occur.
D. Diagnosis:
1. Diagnosis is based on history and clinical signs.
Important Facts
Diagnosis of decubital ulcers is based on history and clinical signs
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E. Treatment:
1. Ideally decubital ulcers should be prevented by turning the animal frequently (every 2 hours), providing soft bedding such as water mattress, providing adequate nutrition, keeping the skin clean via twice daily bathing or whirlpool baths, and protecting the skin from contact with urine by using a cage rack and applying petrolatum to areas of the skin that urine is likely to contact.
2. Once developed, ulcers may be managed by either nonsurgical or surgical means.
3. Nonsurgical management consists of wound lavage and topical antibacterials:
a. Protamine zinc insulin and nitrofurantoin.
b. Topical enzyme ointments/sprays.
c. Antibiotic ointments.
1. Doughnut bandages can be placed over the ulcer to avoid direct pressure on the wound.
2. Surgical treatment is accomplished by debridement of necrotic and infected tissue and wound closure to heal by primary intention.
3. The preventative measures previously mentioned must be strictly adhered to following surgery.
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Important Facts
Maximize wound healing.
Provide padded bedding: air, water, mattress, foam, fleece pads.
Change the animal’s position every 2 hours
Keep the coat and skin free of urine and feces.
Provide daily whirlpool soaks: removes feces, urine, necrotic skin, and promotes circulation.
Provide high protein caloric diet.
The ulcers can be managed medically or surgically.
Specific medical therapy involves cleaning and applying topical antibacterials.
Surgical treatment is accomplished by debridement of necrotic and infected tissue and wound closure to heal by primary intention.
Prevention is best!
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References
1. Scott, Miller, Griffin. Chapter 15, Small Animal Dermatology, 5th ed, 1995.
2. Swaim S.K. Surgery of Traumatized Skin: Management and Reconstruction in the Dog and Cat. W.B. Saunders, Philadelphia, 1980. Pp. 60-62, 199-201, 347, 354.
Learning Objectives
1. Remember! Decubital ulcers (pressure sores) occur mainly over bony prominences because of continual localized pressure to the skin.
2. Know! The pathogenesis involves compression of the skin and subcutaneous tissue which collapses blood vessels resulting in ischemia, necrosis, and subsequent ulceration.
3. What are the predisposing factors associated with decubital ulcers?
4. Know! The initial sign is erythema which evolves to necrosis and ulceration. Any body site with bony prominences can develop decubital ulcers if the predisposing conditions are present. Secondary bacterial infections and osteomyelitis can develop in areas of bone exposure.
5. What can you do to prevent pressure ulcers?
6. How do you mange pressure ulcers once they have developed?
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Environmental Skin DiseasesActinic Dermatitis or photodermatitis– Large Animals
A. General Considerations:
1. The ultraviolet spectrum (UV) is of particular importance in dermatology.
2. UV-B (290 to 320 nm) is often referred to as the sunburn, or erythema, spectrum and is about 1000 times more erythemogenic than the UV-A.
3. UV-A (320 to 400 nm) is the spectrum associated with photosensitivity reactions.
4. Photodermatitis is defined as ultraviolet light (UVL)-induced inflammation of the skin.
5. We will discuss two UVL-induced dermatitis: sunburn and photosensitivity.
Important Facts
Photodermatitis is defined as ultraviolet light-induced inflammation of the skin.
UV-B (290 to 320 nm) is often referred to as the sunburn spectrum.
UV-A (320 to 400 nm) is the spectrum associated with photosensitivity reactions.
B. Sunburn:
1. Definition:
a. Sunburn is a phototoxic reaction caused by excessive exposure to UV-B in animals that have lightly pigmented, thinly haired skin.
Important Facts
Sunburn is a phototoxic reaction caused by excessive exposure to UV-B in animals that have lightly pigmented, thinly haired skin.
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2. Clinical Signs:
a. It can be seen in white pigs, goats, llamas, and horses.
b. Goats often develop sunburn on the lateral aspects of the udder and teats.
c. White pigs may develop sunburn, especially along the back and behind the ears. Young pigs and pigs not previously exposed to sustained UV-B are most susceptible.
d. The skin becomes severely erythematous and scaly and if severely burned, may exude, undergo necrose, develop crusting and be painful.
e. White udders often develop darkly pigmented skin after a summer in the sun.
f. Severely affected pigs may slough their ears and tails.
Important Facts
Sunburn can be seen in white pigs, goats, llamas, and horses.
The skin becomes severely erythematous and scaly and if severely burned, may exude, undergo necrose, develop crusting and be painful.
Goats often develop sunburn on the lateral aspects of the udder and teats.
White pigs may develop sunburn, especially along the back and behind the ears.
3. Diagnosis:
a. Diagnosis is based primarily on history and clinical signs.
b. Skin biopsies of affected areas reveal superficial perivascular dermatitis, dyskeratotic keratinocytes in the superficial epidermis, and, in chronic cases, solar elastosis (basophilic degeneration of elastin).
Important Facts
Diagnosis is based on history, clinical signs and histopathologic findings.
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4. Treatment and prevention:
a. Avoid sunlight.
b. Provide symptomatic therapy for the skin lesions.
c. Prevention of sunburn involves moderation of exposure to sunlight for the first few weeks of summer and application of sunscreens with sun protector factors of at least 15.
Important Facts
Avoid sunlight.
Symptomatic therapy for the skin lesions.
Prevent sunburn.
C. Photosensitivity:
1. General Considerations:
a. Photosensitivity is associated with substances that absorb energy from ultraviolet light and transfer it to body cells.
b. Although photosensitized animals seldom die, resultant weight loss, damaged udders, refusal to allow the young to nurse, and the occurrence of secondary infections and fly strike may lead to appreciable economic losses.
c. There are three features basic to all types of photosensitization:
1. The presence of a photodynamic agent within the skin.
2. The concomitant exposure to a sufficient amount of certain wavelengths of UVL.
3. The cutaneous absorption of this UVL, which is greatly facilitated by lack of pigment and hair coat.
a. The substances causing photosensitization can be ingested or acquired via contact with the skin.
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Important Facts
Photosensitivity is associated with substances that absorb energy from ultraviolet light and transfer it to body cells.
Although photosensitized animals seldom die, appreciable economic losses can be associated with photosensitivity.
The substances causing photosensitization can be ingested or acquired via contact with the skin.
2. Classification: according to the source of the photodynamic agent.
a. Primary:
1. The photodynamic agent is either preformed or produced metabolically within the body.
2. The photodynamic agent may be acquired by ingestion, injection, or contact.
3. Examples: St. John’s Wort (hypericin), buckwheat, clover, lucerne, alfalfa, rape, perennial rye, wild carrots, phenothiazine derivatives, tetracycline, sulfonamides.
Important Facts
Primary photosensitization occurs when the preformed or metabolically produced photodynamic agent reaches the skin by ingestion, injection, or contact.
b. Hepatogenous:
1. Due to chronic, severe liver disease and resultant high levels of phylloerythrin (derived from chlorophyll) in the skin.
2. Phylloerythrin, a porphyrin component formed by microbial degradation of chlorophyll in the gut, is normally conjugated in the liver and excreted in the bile.
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3. Liver dysfunction or biliary stasis, or both, result in high levels of phylloerythrin in the blood and body tissues, with resultant photosensitization.
4. Hepatogenous photosensitization is the most common form of photosensitization in large animals, and liver function tests should be run on any animal with photosensitization whether it is showing signs of liver disease or not.
5. Hepatic disease may occur secondary to the ingestion of hepatotoxic plants such as Brassica, Lantana, Nolina, Tribulus, Crotalaria, Senechio.
6. Pithomycotoxicosis (facial eczema) is a mycotoxicosis of sheep and cattle of all breeds, ages, and sexes in Australia, New Zealand, and South Africa.
7. The fungus Pithomyces chartarum produces a hepatotoxin, sporidesmin, when growing on pasture, especially rye grass.
8. The toxin causes an obstructive cholangiohepatitis and hepatogenous photosensitization.
9. Outbreaks usually occur in summer and fall, during warm sunny weather and a week or two after summer rains that follow a dry period.
Important Facts
Hepatogenous photosensitization is associated with chronic, severe liver disease and resultant high levels of phylloerythrin (derived from chlorophyll) in the skin.
Hepatic disease may occur secondary to the ingestion of hepatotoxic plants or the ingestion of the hepatotoxin, sporidesmin, produced by the fungus Pithomyces chartarum which grows on pasture, especially rye grass during summer and fall.
Hepatogenous photosensitization is the most common form of photosensitization in large animals.
c. Congenital:
1. It is caused by aberrant pigment synthesis (porphyrin or heme).
2. Bovine congenital porphyria (erythropoietic porphyria, pink tooth):
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a. It is characterized by reddish brown discoloration of the teeth and bones (fluoresce with Wood’s light) and photodermatitis due to accumulation of porphyrins in the tissue.
b. It is autosomal recessive and is associated with decreased uroporphyrinogen III cosynthetase levels.
c. Many breeds including cross-breeds are affected.
d. Diagnosis is made by the presence of uroporphyrin I and coproporphyrin I in the blood, urine and feces. Skin biopsy reveals subepidermal vesicular dermatitis, festooning, and a homogeneous thickening of the superficial dermal blood vessel walls, associated with the deposition of hyalin-like material.
1. Bovine congenital protoporphyria:
a. It is characterized by extreme photosensitization and photophobia in young calves.
b. It is autosomal recessive and is associated with decreased heme synthetase (ferrochelatase) levels.
c. Increased levels of protoporphyrin accumulate in the blood and tissues.
d. This condition has been reported in crossbred Limousin cattle in the United States.
e. Diagnosis is based on history, physical examination, and levels of protoporphyrin in blood and feces. Teeth and bones do not fluoresce under Wood’s light.
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Important Facts
Congenital photosensitization is caused by aberrant pigment synthesis (porphyrin or heme).
Bovine congenital porphyria is a form of congenital photosensitization characterized by reddish brown discoloration of the teeth and bones (fluoresce with Wood’s light) and photodermatitis due to accumulation of porphyrins in the tissue.
It is autosomal recessive and is associated with the presence of uroporphyrin I and coproporphyrin I in the blood, urine and feces.
Bovine congenital protoporphyria is characterized by extreme photosensitization and photophobia in young calves.
It is autosomal recessive and is associated with increased levels of protoporphyrin in the blood and tissues.
Teeth and bones do not fluoresce under Wood’s light.
3. Clinical Signs:
a. The cutaneous signs of photosensitization are essentially identical, regardless of the cause.
b. Lesions are often restricted to light-skinned, sparsely haired areas but, in severe cases, may extend into the surrounding dark-skinned areas as well.
c. The eyelids, lips, face, ears, perineum, and coronary band region are commonly involved.
d. There is usually an acute onset of erythema, edema, and variable degrees of pruritus and/or pain.
e. Vesicles and bullae may be seen, often progressing to oozing, necrosis, slough, and ulceration.
f. In severe cases, the pinnae, eyelids, tail, teats, and feet may slough.
g. Photodermatitis confined to the distal extremities, muzzle, and ventrum is strongly suggestive of photocontact reactions induced by pasture plants, environmental sprays, or topical medicaments.
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Important Facts
Lesions are often restricted to light-skinned, sparsely haired areas but, in severe cases, may extend into the surrounding dark-skinned areas as well.
The eyelids, lips, face, ears, perineum, and coronary band region are commonly involved.
There is usually an acute onset of erythema, edema, and variable degrees of pruritus and/or pain often progressing to oozing, necrosis, slough, and ulceration.
Photodermatitis confined to the distal extremities, muzzle, and ventrum is strongly suggestive of photocontact reactions induced by pasture plants, environmental sprays, or topical medicaments.
4. Diagnosis:
a. Diagnosis of photosensitization is based on history, physical examination, liver function tests, porphyrin studies, and skin biopsies.
b. Liver function tests should be performed on all animals with photosensitization, whether they are showing clinical signs of liver disease or not.
c. The number of animals at risk compared with the number of animals affected helps to determine whether the photodermatitis is photosensitive (many animals affected) or photoallergic (one animal affected).
d. The distribution of the photodermatitis aids in determining whether the photodynamic agent is systemic or contactant.
e. A thorough examination of the diet, pasture, and drug history is critical.
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Important Facts
Diagnosis of photosensitization is based on history, physical examination, liver function tests, porphyrin studies, and skin biopsies.
Liver function tests should be performed on all animals with photosensitization, whether they are showing clinical signs of liver disease or not.
The number of animals at risk compared with the number of animals affected helps to determine whether the photodermatitis is photosensitive (many animals affected) or photoallergic (one animal affected).
The distribution of the photodermatitis aids in determining whether the photodynamic agent is systemic or contactant.
5. Treatment:
a. Avoidance of sunlight.
b. Identification and elimination of the source of photodynamic agent.
c. Systemic therapy for hepatic disease and other extracutaneous disorders.
d. The photodermatitis may be ameliorated with systemic glucocorticoids, such as prednisone at the dose of 1.1 mg/kg/day and nonsteroidal antiinflammatory agents (e.g. aspirin and phenylbutazone).
e. Systemic antibiotics may be required if secondary pyoderma is present, and surgical debridement may be indicated if necrosis and sloughing are severe.
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Important Facts
Avoid sunlight.
Stop the intake of photosensitizer or hepatotoxin.
Systemic therapy for hepatic disease and other extracutaneous disorders.
The photodermatitis may be ameliorated with systemic glucocorticoids and nonsteroidal antiinflammatory agents.
Systemic antibiotics may be required if secondary pyoderma is present.
Surgical debridement may be indicated if necrosis and sloughing are severe.
6. Prognosis:
a. In general, the prognosis is favorable for primary photosensitization but poor for hepatogenous photosensitization and porphyria.
Important Facts
In general, the prognosis is favorable for primary photosensitization but poor for hepatogenous photosensitization and porphyria.
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References
1. Scott D.W. Environmental Diseases. In: Large Animal Dermatology. W.B. Saunders, Philadelphia, 1988, pp 65-95.
Learning Objectives
1. Know! Photodermatitis is an ultraviolet light-induced inflammation of the skin. Sunburn is induced by UV-B and photosensitization is induced by UV-A.
2. Know! Lesions associated with sunburn or photosensitization occur on lightly pigmented, thinly haired skin.
3. Remember! Goats often develop sunburn on the lateral aspects of the udder and teats. White pigs may develop sunburn, especially along the back and behind the ears.
4. Know! Erythema and scales are the most common signs associated with sunburn but, severe cases may exude and undergo necrosis.
5. How do you diagnose and treat sunburn?
6. Know! Photosensitivity is associated with substances that absorb energy from ultraviolet light and transfer it to body cells.
7. Know! The substances causing photosensitization can be ingested or acquired via contact with the skin.
8. Know! Photosensitization is classified in primary, hepatogenous or congenital, according to the source of the photodynamic agent.
9. Know! Primary photosensitization occurs when the preformed or metabolically produced photodynamic agent reaches the skin by ingestion, injection, or contact.
10. Know! Hepatogenous photosensitization occurs when chronic, severe liver disease results in the accumulation of high levels of phylloerythrin (derived from chlorophyll) in the skin. Phylloerythrin, a porphyrin component formed by microbial degradation of chlorophyll in the gut, is normally conjugated in the liver and excreted in the bile.
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11. Know! Hepatic disease may occur secondary to the ingestion of hepatotoxic plants or the ingestion of the hepatotoxin, sporidesmin, produced by the fungus Pithomyces chartarum which grows on pasture, especially rye grass during summer and fall.
12. Remember! Hepatogenous photosensitization is the most common form of photosensitization in large animals.
13. Know! Liver function tests should be run on any animal with photosensitization whether it is showing signs of liver disease or not.
14. Know! Congenital photosensitization is caused by aberrant pigment synthesis (porphyrin or heme).
15. What are the pathogenesis and clinical signs of bovine congenital porphyria and protoporphyria?
16. How do you diagnose bovine congenital porphyria and protoporphyria?
17. Know! The cutaneous signs of photosensitization are essentially identical, regardless of the cause. Lesions are often restricted to light-skinned, sparsely haired areas but, in severe cases, may extend into the surrounding dark-skinned areas as well.
18. Know! The eyelids, lips, face, ears, perineum, and coronary band region are commonly involved.
19. Know! There is usually an acute onset of erythema, edema, and variable degrees of pruritus and/or pain often progressing to oozing, necrosis, slough, and ulceration.
20. Know! Photodermatitis confined to the distal extremities, muzzle, and ventrum is strongly suggestive of photocontact reactions induced by pasture plants, environmental sprays, or topical medicaments.
21. Know! Diagnosis of photosensitization is based on history, physical examination, liver function tests, porphyrin studies, and skin biopsies.
22. Know! The number of animals at risk compared with the number of animals affected helps to determine whether the photodermatitis is photosensitive (many animals affected) or photoallergic (one animal affected).
23. Know! The distribution of the photodermatitis aids in determining whether the photodynamic agent is systemic or contactant.
24. Remember! A thorough examination of the diet, pasture, and drug history is critical.
25. How do you manage photosensitization?
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Environmental Skin DiseasesOvine Fleece Rot
A. General Considerations:
1. Ovine fleece rot is a superficial dermatitis resulting from bacterial proliferation induced by wetness at skin level and manifested by seropurulent exudation and matting of the wool fiber.
Important Facts
Ovine fleece rot is a superficial dermatitis resulting from bacterial proliferation induced by wetness at skin level and manifested by seropurulent exudation and matting of the wool fiber.
B. Cause and Pathogenesis:
1. Under natural and experimental conditions, continued wetting of sheep will produce fleece rot.
2. Approximately a week of continual skin wetting is sufficient to produce the disease.
3. Temperature itself is not an important factor.
4. Certain sheep show a predisposition to fleece rot, which may be attributed to variations in physical characteristics of the fleece and skin that exist among sheep of different breeds and strains and even among individual sheep.
5. Microanatomically, fleeces with a larger secondary:primary hair follicle ratio are more resistant to fleece rot.
6. Fleeces with a high wax (sebum) content are less susceptible to fleece rot, presumably because of the water-proofing effect of wax.
7. A yellowish fleece color (high suint content) is indicative of susceptibility to fleece rot.
8. Subsequent to wetting of the skin, a marked proliferation of bacteria, almost exclusively Pseudomonas sp., occurs on the skin and in the fleece.
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9. This is followed by an exudation of serum and inflammatory cells, which mats the fleece and attracts blowflies. Fleece discoloration is produced by chromogenic bacteria such as Pseudomonas aeruginosa (green) and P. indigofera (blue).
Important Facts
Approximately a week of continual skin wetting is sufficient to produce fleece rot.
Certain sheep show a predisposition to fleece rot, which may be attributed to variations in physical characteristics of the fleece and skin that exist among sheep of different breeds and strains and even among individual sheep.
Microanatomically, fleeces with a larger secondary:primary hair follicle ratio are more resistant to fleece rot.
Fleeces with a high wax (sebum) content are less susceptible to fleece rot.
A yellowish fleece color is indicative of susceptibility to fleece rot.
Subsequent to wetting of the skin, a marked proliferation of bacteria, almost exclusively Pseudomonas sp., occurs on the skin and in the fleece.
This is followed by an exudation of serum and inflammatory cells, which mats the fleece and attracts blowflies.
C. Clinical Signs:
1. Fleece rot is common in most parts of Australia during wet years and causes considerable economic losses due to depreciation of the value of damaged fleeces.
2. The incidence of fleece rot within a flock varies from 14 to 92%.
3. Lesions are most common over the withers and along the back.
4. Initially, the skin in affected areas assumes a deep purple hue.
5. This is followed by exudation and accumulation of seropurulent material, which causes the characteristic band of matted fleece.
6. The wool in affected areas is always saturated and may be easily epilated.
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7. Discoloration of the wool by green, blue, brown, orange, or pink bands may occur at any level of the staple.
8. Affected sheep are usually otherwise healthy.
Important Facts
The incidence of fleece rot within a flock varies from 14 to 92%.
Lesions are most common over the withers and along the back.
Initially, the skin in affected areas assumes a deep purple hue.
This is followed by exudation and accumulation of seropurulent material, which causes the characteristic band of matted fleece.
The wool in affected areas is always saturated and may be easily epilated.
Affected sheep are usually otherwise healthy.
D. Diagnosis:
1. Diagnosis is based on history and physical examination.
2. The main differential is dermatophylosis, which occurs under similar conditions. However, the characteristic crusting and ulceration of dermatophylosis is not present in fleece rot.
3. Skin biopsy reveals suppurative intraepidermal pustular dermatitis and superficial folliculitis.
4. Affected sheep may have leukocytosis and neutrophilia.
Important Facts
Diagnosis is based on history and physical examination.
The main differential is dermatophylosis, which occurs under similar conditions. However, the characteristic crusting and ulceration of dermatophylosis is not present in fleece rot.
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E. Treatment:
1. Therapy is not usually undertaken and is usually of no benefit.
2. Chemical drying of the fleece decreases wetness and the incidence of fleece rot.
3. A mixture of zinc and aluminum oxides with sterols and fatty acids applied to sheep as a mist was shown to offer protection for 10 to 12 weeks.
4. Immunization of sheep with a cell-free vaccine containing high concentrations of soluble antigens from P. aeruginosa was reported to reduce the severity of fleece rot.
5. Prevention, through selecting sheep for inherent resistance to fleece rot, would appear to be the most logical approach to dealing with the problem.
Important Facts
Therapy is not usually undertaken and is usually of no benefit.
Chemical drying of the fleece decreases wetness and the incidence of fleece rot.
Immunization of sheep with a cell-free vaccine containing high concentrations of soluble antigens from P. aeruginosa was reported to reduce the severity of fleece rot.
Prevention, through selecting sheep for inherent resistance to fleece rot, would appear to be the most logical approach to dealing with the problem.
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References
1. Scott D.W. Environmental Diseases. In: Large Animal Dermatology. W.B. Saunders, Philadelphia, 1988, pp 65-95.
Learning Objectives
1. Know! Ovine fleece rot is a superficial dermatitis resulting from Pseudomonas sp. proliferation induced by wetness at skin level and manifested by seropurulent exudation and matting of the wool fiber.
2. Know! Approximately a week of continual skin wetting is sufficient to produce the disease.
3. Know! Certain sheep show a predisposition to fleece rot, which may be attributed to variations in physical characteristics of the fleece and skin that exist among sheep of different breeds and strains and even among individual sheep.
4. Know! Fleece with a high secondary to primary hair follicle ratio and fleece with high wax content are more resistant to fleece rot.
5. Know! A yellowish fleece color is indicative of susceptibility to fleece rot.
6. Know! Skin moisture results in marked bacteria proliferation (most of the time Pseudomonas sp.) which is followed by an exudation of serum and inflammatory cells, which mats the fleece and attracts blowflies.
7. Know! Fleece discoloration is produced by chromogenic bacteria such as Pseudomonas aeruginosa (green) and P. indigofera (blue).
8. Know! Lesions are most common over the withers and along the back.
9. Know! Initially, the skin in affected areas assumes a deep purple hue, this is followed by exudation and accumulation of seropurulent material, which causes the characteristic band of matted fleece. The affected animals are otherwise healthy.
10. Know! Diagnosis is based on history and physical examination.
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11. Know! The main differential is dermatophylosis, which occurs under similar conditions. However, the characteristic crusting and ulceration of dermatophylosis is not present in fleece rot.
12. How do you manage fleece rot?
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