Ulcerative Dermatosis of Sheep

Ulcerative dermatosis is an infectious disease of sheep caused by a virus similar to the ecthyma virus. It manifests in 2 somewhat distinct forms, one characterized by formation of ulcers around the mouth and nose or on the legs (lip and leg ulceration), and the other as a venereally transmitted ulceration of the prepuce and penis or vulva.

Contagious Ecthyma -Orf

Contagious ecthyma is an infectious dermatitis of sheep and goats that affects primarily the lips of young animals. The disease is usually more severe in goats than in sheep. Humans are occasionally affected, and the disease has been reported in dogs that have eaten infected carcasses.

Pyoderma

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Pyoderma literally means “pus in the skin” and can be caused by infectious, inflammatory, and/or neoplastic etiologies; any condition that results in the accumulation of neutrophilic exudate can be termed a pyoderma. Most commonly, however, pyoderma refers to bacterial infections of the skin. Pyodermas are common in dogs and less common in cats.

Interdigital Furunculosis

Etiology:

The most common cause is a deep bacterial infection. Many dog breeds (eg, Shar-Pei, Labrador Retriever, English Bulldog) are predisposed to bacterial interdigital furunculosis because of the short bristly hairs located on the webbing between the toes, prominent interdigital webbing, or both. The short shafts of hairs are easily forced backward into the hair follicles during locomotion (traumatic implantation). Hair, ie, keratin, is very inflammatory in the skin, and secondary bacterial infections are common. Less commonly, foreign material is traumatically embedded in the skin. Demodicosis ( Mange in Sheep and Goats) may be a primary cause of interdigital furunculosis. Canine atopy ( Allergic Inhalant Dermatitis: Introduction) is also a common cause of recurrent interdigital furunculosis.

Exudative Epidermitis

• Lesions are caused by Staphylococcus hyicus (hyos) , which can produce an exfoliative toxin but seems unable to penetrate intact skin. Both virulent and avirulent strains exist. Abrasions on the feet and legs or lacerations on the body precede infection. Such injuries are usually caused by fighting or by abrasive surfaces such as new concrete. Other predisposing factors that may affect the severity and progress of the disease include immunity, hygiene, nutrition, and the presence of mange mites or anything that damages the skin. Mature sows that have acquired a high level of immunity from previous exposure will provide protection to piglets via their colostrum. The incidence is often higher in gilt litters and in newly established SPF herds in which the majority of breeders are gilts.

Pigs develop resistance with age, but S hyicus may be recovered from the skin of older pigs, the vagina of sows, and the preputial diverticulum of boars. These inapparent carriers serve as a source of contamination for naive herds. Suckling pigs are usually infected by their dams, in some cases during birth from sows with vaginal infections, or from contamination in the farrowing unit. Suckling piglets are the most commonly and severely affected, but cross-infection occurs after mixing at weaning with a morbidity of up to 80%. However, mortality is usually low in this age group. The incidence appears to have increased due to pig production units with high stocking densities and possibly earlier weaning.

Dermatophilosis

Etiology, Transmission, and Epidemiology:

D congolensis is a gram-positive, non-acid-fast, facultative anaerobic actinomycete. It is the only species in the genus, but a variety of strains can be present within a group of animals during an outbreak. It has 2 characteristic morphologic forms—filamentous hyphae and motile zoospores. The hyphae are characterized by branching filaments (1-5 µm in diameter) that ultimately fragment by both transverse and longitudinal septation into packets of coccoid cells. The coccoid cells mature into flagellated ovoid zoospores (0.6-1 µm in diameter). The natural habitat of D congolensis is unknown. Attempts to isolate it from soil have been unsuccessful, although it is probably a saprophyte in the soil. It has been isolated only from the integument of various animals and is restricted to the living layers of the epidermis. Asymptomatic chronically infected animals are considered the primary reservoir. Factors such as prolonged wetting by rain, high humidity, high temperature, and various ectoparasites that reduce or permeate the natural barriers of the integument influence the development, prevalence, seasonal incidence, and transmission of dermatophilosis. The organism can exist in a quiescent form within the epidermis until infection is exacerbated by climatic conditions. Epidemics usually occur during the rainy season. Moisture facilitates release of zoospores from preexisting lesions and their subsequent penetration of the epidermis and establishment of new foci of infection. High humidity also contributes indirectly to the spread of lesions by allowing increases in the number of biting insects, particularly flies and ticks, that act as mechanical vectors. Shearing, dipping, or introducing an infected animal into a herd or flock can spread infection. Dermatophilosis is contagious only in that any reduction in systemic or local skin resistance favors establishment of infection and subsequent disease.

Urticaria

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Urticaria, horse Urticaria is characterized by multiple plaque-like eruptions that are formed by localized edema in the dermis and that often develop and disappear suddenly. It occurs in all domestic animals but most often in horses (see also sweet itch, Biting Midges). Allergic urticaria may be exogenous or endogenous. Exogenous hives may be produced by toxic irritating products of the stinging nettle, the stings or bites of insects, medications, or chemicals (eg, carbolic acid, turpentine, carbon disulfide, or crude oil). Nonimmunologic factors such as pressure, sunlight, heat, exercise, psychologic stress, and genetic abnormalities may precipitate or intensify urticaria. Pruritus is not always present.

Sensitive animals, particularly shorthaired dogs and purebred horses, also may exhibit dermographism, a phenomenon wherein rubbing or whipping produces urticaria-like skin lesions. It is of no clinical significance.

Endogenous or “symptomatic” urticaria may develop after inhalation or absorption of ingested allergens; it has been seen mostly in horses and dogs. In horses, it has been noted in the course of GI conditions, particularly severe constipation or inflammation of the intestinal mucosa. A unique form of urticaria has been described chiefly in the Channel Island breeds of cattle (Jersey, Guernsey), which become sensitized to the casein in their own milk (see also Localized Anaphylactic Reactions); it occurs in cases of milk retention or unusual engorgement of the udder with milk. Urticaria has been seen in bitches during estrus. In young horses, dogs, and pigs, urticaria may be associated with intestinal parasites. Angioneurotic edema is a life-threatening variant of urticaria in which there is diffuse subcutaneous edema, often localized to the head, limbs, or perineum. In horses, dermatophytosis (ringworm) and pemphigus foliaceus may present as urticaria early in the disease.

مقدمة أمراض الجلد لدى الحيوانات في المزارع

تحدث أمراض الجلد إما أولياً _ حيث تكون الآفات محصورة في الجلد أو الكسوة وأما ثانوياً حيث تكون هناك إصابة أولية في عضو أو نسيج آخر . ويتم تحديد ذلك بالفحص الدقيق والحصول على تاريخ مفصل للحالة وتدرج الأعراض زمنياً . وفي حالة وجود أعراض أو آفات منسوبة لإصابة أعضاء أخرى فيجب تحديد ما إذا كانت لاحقة أو سابقة للآفة الجلدية وعليه فإن المعرفة الدقيقة بالإصابات المحتملة حسب الأعراض المعينة يشكل حجر الزاوية في تشخيص المرض الجلدي وتحديد ما إذا كان أولياً أو ثانوياً .
الفحص الخاص بالجلد :
يتم أولاً الكشف العام على الحيوان والذي يتمخص عنه بالاشتباه أو بالتحديد ما يدل على الإصابة الجلدية ، مما يقود للتركيز على هذا النسيج وملحقاته . ويجب أن يتم قص دقيق للجلد بحيث يشمل ذلك الكشف النظري والجس ، بالإضافة إلى الحصول على عينات مناسبة تشمل الحكة ( Skin Scraping ) والمسحة (Swab ) والخزعة ( Biopsy ) وعينات من الصوف أو الشعر أو الريش ، مع ضرورة أن تشمل العينات ( الحكة أو المسحة .. الخ ) أجزاء حيه وأخرى متنخره من الآفة . كما يمكن استخدام مصباح وود( Wood’s Lamp) الفحص الخاص بالفطريات الجلدية .
يجب وصف الآفات وصفاً دقيقاً يشمل حجمها وشكلها وعمقها الجلدي وانتشارها على سطح الجلد ( المناطق المصابة ) كما يجب ملاحظة أي اضطراب في وظائف الغدد العرقية ( Sweat glands ) وأي خلل في لون الكسوة وملمسها .

فيما يلي الأعراض الرئيسية للإصابات الجلدية والتي تتراوح درجة قسوتها (ووجودها ) من مرض لآخر ومن حالة لأخرى في المرض الواحد :

Alopecia

Etiology:

There are many causes of alopecia; any disease that can affect hair follicles can cause hair loss. There are 2 broad etiologic categories of alopecia— congenital or hereditary and acquired. Acquired alopecia is further divided into 2 categories: inflammatory and noninflammatory. Congenital or hereditary alopecia ( Hereditary Alopecia and Hypotrichosis) has been described in cows, horses, dogs, cats, and pigs. Hairless breeds of mice, rats, cats, and dogs have been bred and developed for personal and research interests. Congenital alopecia may or may not be hereditary; it is caused by a lack of development of hair follicles and is apparent at or shortly after birth. Animals with tardive alopecias are born with normal coats, and focal or generalized hair loss occurs when the animal sheds its juvenile coat or when it becomes a young adult. Examples of this include pattern baldness of Dachshunds, color dilution alopecia (most commonly seen in Doberman Pinschers), and certain types of follicular dysplasias. Acquired alopecia encompasses all other causes of hair loss. In this type of alopecia, the animal is born with a normal hair coat, has or had normal hair follicles at one time, and is or was capable of producing structurally normal hairs. Acquired alopecia may be noninflammatory, as is seen in endocrine alopecia or some types of immune-mediated alopecia, or inflammatory. Inflammatory acquired alopecia is the most common cause of alopecia. Acquired alopecia develops because a disease destroys the hair follicle or shaft, interferes with the growth of hair or wool, or causes the animal discomfort (eg, pain, pruritus) leading to self-trauma and loss of hair. Diseases that can directly cause destruction or damage to the hair shaft or follicle include bacterial skin diseases, dermatophytosis, demodicosis, severe inflammatory diseases of the dermis (eg, juvenile cellulitis, deep pyoderma), traumatic episodes (eg, burns, radiation), and (rarely) poisonings caused by mercury, thallium, and iodine. These diseases tend to be inflammatory. Diseases that can directly inhibit or slow hair follicle growth include nutritional deficiencies ( particularly protein deficiencies), hypothyroidism, hyperadrenocorticism, and excessive estrogen production or administration (hyperestrogenism, Sertoli cell tumors, estrogen injections for mismating). Temporary alopecia in horses, sheep, and dogs can occur during pregnancy, lactation, or several weeks after a severe illness or fever. These types of alopecia tend to be noninflammatory unless a secondary infection of the skin develops. Pruritus or pain is a common cause of acquired inflammatory alopecia in animals. Diseases that commonly cause pruritus or pain include infectious skin diseases (eg, bacterial pyoderma and dermatophytosis), ectoparasites, allergic skin diseases (eg, atopy, food allergy, contact, insect hypersensitivity), and less commonly neoplastic skin diseases. Friction may cause local hair loss, eg, poorly fitted halters or collars. Rarely, excessive grooming may be the cause of hair loss in some animals, particularly cats. Feline endocrine alopecia is no longer recognized as a bona fide syndrome; the new name is feline acquired symmetric alopecia. To date, there is no documented evidence of an endocrine disease in these cats, and the symmetric alopecia seen is a clinical sign of an underlying disease, most commonly a pruritic disease.