HOT SPOTS!!!

HOT SPOTS!!!

Also Known As: pyotraumatic dermatitis 

Transmission or cause: Potential underlying causes for hot spots include parasites (especially fleas or scabies mites), allergies (flea, pollen, food), skin infections by bacteria or fungus, or trauma. 

Affected Animals: Hot spots can affect dogs of any age, breed, or gender, but they occur most commonly in thickcoated/longhaired breeds, and in dogs with underlying causes such as parasites or allergies. Hot, humid weather can contribute to the development of hotspots. Hot spots occur rarely in cats. 

Clinical signs: Hot spots start when a dog incessantly licks, chews or scratches a focal area of the body in response to a painful or itchy sensation. The result is a rapidly developing area of redness, hairloss, oozing and eroded skin that is often painful and infected with bacteria. Hot spots occur most frequently on the trunk, base of the tail, outer thigh, neck or face. 

Diagnosis: The diagnosis of hot spot is by clinical presentation and history, and by ruling out other causes of hairloss and red skin such as skin parasites or fungal infection. Diagnostics may include close examination for fleas, skin scrapes for microscopic analysis, or fungal cultures. Additionally, it is important to identify and address the underlying cause of the hot spot, and in recurrent cases diagnostics may also include trial therapy for fleas or scabies, allergy testing, or a hypoallergenic diet trial. 

Prognosis: The prognosis for cure of hot spots is good, although they will tend to recur if the underlying cause is not addressed. 

Treatment: The treatment for hot spots often includes clipping and gently cleaning the affected area (this may necessitate sedation), then application of topical antibacterial and/or steroid-containing products to the area (products that contain alcohol should be avoided). Additionally, many cases need 2-3 weeks of systemic antibiotics for secondary bacterial infection, and/or a short course of oral steroids to stop self-trauma. Some dogs will need an Elizabethan collar to restrict contact with the area for several days. Treatment of the underlying cause is also important, and may include trial therapy for fleas or scabies, a hypoallergenic diet trial, or allergy hyposensitization injections based on allergy testing. 

Prevention: Prevention of hotspots is done by keeping the dog clean and parasite free, and the hair coat brushed and free of mats. It is often helpful to clip long coated dogs down in the warm months. Animals with underlying allergies must have these allergies addressed to avoid hot spot recurrence. 

Sebaceous Adenitis

Sebaceous Adenitis 

Transmission or cause: The cause of sebaceous adenitis is unknown but the end result is inflammation of the sebaceous or oil gland associated with the hair follicles. Loss of the sebaceous gland leads to dysfunction of normal hair growth which results in hair loss. The underlying cause is probably a combination of genetic predisposition and immune-mediated sebaceous gland inflammation.

Affected animals: Sebaceous adenitis is an inflammatory disease that mostly affects young adult to middle aged dogs. Cats are rarely affected. Some breeds of dogs that are prone to sebaceous adenitis include Standard Poodles, Akitas, Vizslas, Samoyeds, and Belgian Sheepdogs. It is believed to be a recessive inherited trait in Standard Poodles.

Clinical signs: Most dogs will show a bilaterally symmetrical hair loss and excessive scaling especially around face, head, ears and trunk. Some dogs may develop a bald “rat-tail”. Many dogs may have a secondary bacterial infection of the skin with pimples, crusting and possible odor. Belgian Shepdogs may have a severe draining ear infection. Vizslas and Dachshunds often have circular areas crusting of hair loss that can spread and eventually merge together. The hairs of affected animals often have adherent surface debris surrounding the base of the hair called ‘hair casts’. Akitas often have more severe disease with red inflamed skin and greasy crusting and matting. Sebaceous adenitis is usually not itchy but can be if there is secondary infection.

Diagnosis: Sebaceous adenitis is suspected when the history and clinical signs are consistent. Microscopic examination of hairs from dogs with sebaceous adenitis often shows obvious hair casting. The definitive diagnosis of sebaceous adenitis is made by taking a skin biopsy which involves removing small pieces of skin after numbing the area with anesthetic and submitting the skin samples to a pathologist.

Prognosis: Some dogs can spontaneously improve but most dogs need lifelong control of their sebaceous adenitis. It is mostly a cosmetic disorder with no internal manifestations of disease.

Treatment: The treatment for sebaceous adenitis may involve anti-inflammatory therapy, retinoid drugs or vitamin A along with anti-scaling shampoos and emollient rinses. Treatment of secondary infections, if present, is also important. Some dogs respond better to some treatments than others, and trying different therapies may be necessary. The goal of therapy is to alleviate and slow progression of symptoms, but only partial improvement may be seen.

Prevention: Prevention of sebaceous adenitis involves not breeding affected animals.

Zinc Responsive Dermatosis

Zinc Responsive Dermatosis

Transmission or Cause: Two distinct syndromes have been recognized: 

Syndrome I zinc-responsive dermatosis: is associated with a defective intestinal absorption of zinc despite being fed a nutritionally well-balanced diet. 


Syndrome II zinc-responsive dermatosis: occurs in rapidly growing puppies / young dogs being fed zinc deficient diets or diets which have high phytates (plant proteins), diets high in minerals, such as calcium, which can interfere with zinc absorption, and/or are fed cereal or soy based diets. Prolonged gastrointestinal disease resulting in chronic enteritis and diarrhea can also interfere with zinc absorption. 


Affected Animals: Syndrome I zinc-responsive dermatosis – This syndrome has been recognized primarily in Alaskan malamutes and Siberian Huskies. Skin lesions typically develop in young adults but onset of disease has been described in older pets. Syndrome II zinc-responsive dermatosis – This syndrome has been described in a plethora of breeds, including the Great Dane, Doberman pinscher, beagle, Boston terrier, German shepherd, and standard Poodle, amongst others. 

Clinical Signs: 

Syndrome I – Skin lesions tend to first occur in September through January and can worsen during estrus or times of stress. Lesions present as red skin with hair loss and crusting around the mouth, chin, eyes and ears. The scrotum, vulva, prepuce and pressure points, such as the elbows and footpads, can also be affected. Lesions are typically itchy.

Syndrome II – Skin lesions typically form on pressure points, nasal planum and footpads and present as thickened, crusted plaques. Fissures can form in thickened, crusted areas. Affected dogs can also have enlarged lymph nodes and develop secondary skin infections. 


Diagnosis: Diagnosis in both syndromes is made through physical examination, a thorough history and biopsy. Hair and serum levels of zinc may also be abnormal; however, analysis of zinc can be difficult and unreliable and so this test is not typically performed.



Treatment: 


Syndrome I – Oral zinc supplementation typically brings rapid resolution of the clinical signs. Some dogs do not achieve clinical resolution with oral zinc supplementation alone; in those cases, low doses of corticosteroids are beneficial. Some dogs also benefit with the addition of fatty acids in addition to zinc. Intact female dogs should be spayed. Treatment is generally lifelong. 


Syndrome II – Treatment is focused on dietary correction and treatment of secondary bacterial and yeast skin infections. Generally lesions should resolve within 2-6 weeks with dietary manipulation, but concurrent zinc supplementation can hasten the resolution. Unlike Syndrome I, zinc supplementation can be discontinued after a few weeks. 


Prognosis: Prognosis is good with response to therapy. 

Pemphigus foliaceus (PF)

Pemphigus foliaceus (PF)

Transmission or Cause: Pemphigus foliaceus is an autoimmune disease whereby antibodies produced by an animal’s own immune system attack the bridges that hold skin cells together. It is the most common autoimmune disease diagnosed in dogs and cats. Affected Animals: Dogs and cats of any age or gender can be affected. In dogs, Akitas, Chow Chows, Doberman Pinschers, Dachshunds, and Newfoundlands may be predisposed. No breed predilections exist with cats. Three forms of Pemphigus foliaceus exist in the dog. The first and most common is the spontaneous form which develops in dogs with no history of skin disease or drug history. The second form of Pemphigus foliaceus is initiated via a drug reaction. The third form occurs in dogs with a history of chronic skin disease (e.g. allergies). 

Clinical Signs: The primary lesion of Pemphigus foliaceus is a pustule. These lesions typically begin along the nasal bridge, around the eyes, and ear pinnae. It is typical for the lesions to spread and occur along the trunk, feet, clawbeds, groin, and footpads. In cats, the nail beds and nipples can also be commonly affected. In most cases, the pustules form and rupture very quickly, so that all that there is left to observe are areas of hair loss, yellow-brown dried crusts, redness and scale. Severely affected animals may become anorexic, depressed and have a fever. The disease itself often displays a waxing/waning course. 

Diagnosis: The diagnosis of Pemphigus foliaceus is made by clinical signs, cytology, and biopsy. Other diseases that can appear similar to Pemphigus foliaceus include infection (bacterial, parasitic, fungal), seborrheic skin disease, and varying forms of lupus. Skin scrapes would be performed to rule out external parasites via microscopic analysis. A fungal culture would be done to rule out ringworm (a type of common fungus). Samples of debris from intact pustules or crusts can allow for a diagnosis of Pemphigus foliaceus. In some cases, multiple skin biopsies are required to confirm the diagnosis of Pemphigu foliaceus. 

Treatment: Localized cases of Pemphigus foliaceus can be treated with varying strengths of topical steroids. The mainstay of therapy for more generalized cases in both dogs and cats Pemphigus Foliaceus are oral glucocorticoids (e.g. Prednisone). In order to minimize the potential side effects of glucocorticoids (e.g. weight gain, excessive drinking and urinating, liver enlargement), nonsteroidal immunosuppressive drugs are added to the regimen. In dogs, azathioprine and/or cyclosporine can be utilized, while in cats leukeran and/or cyclosporine are the most popular supportive drugs. Other nonsteroidal immunosuppressive drugs include gold salts (dogs and cats) and tetracycline/niacinamide (dogs). Affected animals are started at higher dosages initially until remission is achieved (4-12 weeks), and then are tapered to the lowest possible dosages that maintain remission. 

Prognosis: The prognosis is fair to good, but lifelong therapy is usually required to maintain remission. Cases of Pemphigus foliaceus that are induced by a drug reaction, are the most likely to be cured. Regular monitoring of clinical signs, hemograms, serum biochemistry profiles, urinalyses, and urine cultures with treatment adjustments as needed are essential.