May 2000

Dermatology: Diagnosis, Problems and Therapy

John M. MacDonald, D.V.M.
Diplomate ACVD
College of Veterinary Medicine
Auburn University, Auburn, AL 36849

Juvenile Dermatoses

Skin diseases that effect the juvenile animals are variable and extensive. This presentation is only a partial listing of common problems encountered. It is beyond the limitations of the proceedings to include all the pertinent information regarding each condition. The intent is to present clinical examples with a method of differentiating the condition and emphasis on clinical management.


Canine atopy is an inherited predisposition to produce excessive immunoglobulin (IgE or IgGd) against substances that would be considered quite harmless and usually proteins called allergens. The exact mode of inheritance of this condition is unknown, and attempts to demonstrate specific genotypes have not been achieved. The other factors involved with development of canine atopy include presentation of allergen and the degree of allergen exposure. In one study the occurrence of canine atopy was shown to have a high correlation with the month of birth. Dogs born around the time of plant pollination had a higher chance of developing the disease. The presence of pollens at the critical time of immunological development appears to have a relationship to the tendency to develop allergen specific antibody against those substances. There appears to be an optimal window of sensitization that is seen in the neonate although atopy may occur without the high allergen effect observed during the pollen season. Other factors may come into play as well. Th2 cells are recognized for the production and release of a variety of interleukins (IL-4, IL-5, IL-9, IL-10 and IL-13) which lead to the activation of B lymphocytes which in turn favors the production of IgE as well as the activation and proliferation of mast cells and eosinophils. IL-5 stimulates the differentiation & proliferation of eosinophils while IL-10 causes proliferation of mast cells and B lymphocytes. IL-4 is one of the most important cytokines since it is the lymphokine that is involved with the switching to IgE production. Once the mechanism for the allergic reaction is in place and the exposure to the allergen occurs, the resulting inflammation further stimulates the production of more Th2 cells which tends to amplify the reaction and induce an even greater inflammatory response. Since this usually occurs at such an early age, the chronic allergic patient is well endowed with the necessary immunological mechanisms to induce severe and perpetuating clinical disease.

It has been estimated that up to 10 or 15 % of the canine population is afflicted with atopy. It is the second most common allergy in the dog next to flea allergy in most parts of the United States. Demonstration that canine atopy is a genetically programmed disease has been accomplished by observation of strong breed predilections, familial involvement and limited breeding trials. There is however, a strong influence of environmental factors (quantity of allergen) and the individual tolerances of allergenic load. Bitches are affected approximately 2.5 times more frequently than males. Breeds with strong predispositions include: Terrier breeds (West Highland White, Scottish, Wire Haired Fox Terrier, Cairn, and Wheaton), Shar Pei, Golden Retriever, Irish Setter, Cocker and Springer Spaniels, Dalmatians, Lhasa Apsos, Pugs, Boston Terriers, English Bulldogs and Miniature Schnauzers. Despite the predilection of certain breeds, any breed may develop the condition. Onset usually occurs between 6 months & 3 years (75%) although cases have been observed as early as 3-4 months or as late as 7 years.

Pruritus is the most prevalent clinical sign of canine atopy. Scratching, biting, licking, chewing or rubbing are the common signs of the disease although few will demonstrate respiratory problems (wheezing, coughing or sneezing). Distribution of lesions classically occur on the feet, face, ears, forearm, axillary region and/or groin. Some cases will become generalized with time. Lesions include erythema, excoriations, often with secondary hyperpigmentation & lichenification in the chronic case. Scaling may also be observed particularly if there is a concurrent bacterial pyoderma. Concurrent flea allergy dermatitis &/or food allergy are frequent complicating factors in addition to the already mentioned pyoderma, malassezia dermatitis and dry, scaly/crusty skin.

The symptoms of canine atopy and the severity of allergic disease depends upon: 1) the individual's reactivity to allergens; 2) the allergen load; 3) exposure factors and concurrent nonallergic pruritic disease and 4) the individual pruritic threshold.

The diagnosis of canine atopy is predominantly made through the history and clinical features. Allergy testing or other laboratory procedures are not intended to achieve the diagnosis. Allergy testing is used with the specific purpose of formulating an allergen solution for immunotherapy and therefore considerations of immunotherapy must first be encountered. Consideration for immunotherapy should include several aspects of the clinical case. They include 1) a tentative diagnosis of atopy; 2) an age greater than twelve months; 3) poor response to nonsteroidal therapy; 4) duration of pruritus greater than three months per year; and 5) other prospects of immunotherapy.

Most cases of canine atopy will be treated symptomatically because pet owners do not have an interest in or cannot afford allergy testing and hyposensitization therapy. Symptomatic therapy can be categorized into nonsteroidal medication and glucocorticoid medication. Combination therapy is often used for optimal results. The principle philosophy of medication is to minimize the amount of steroid treatment. This is much easier to do when the symptoms are mild, as in the early stage of the disease or if hyposensitization therapy is being used. The combination of nonsteroidal antipruritic medication like antihistamines is also helpful. The best choice of antipruritic therapy cannot be determined empirically. The variability of drug tolerance, drug effectiveness, client expectations, medication administration regimens, and cost factors all influence the choice for a given case. The best choice must have no risk of worsening the condition and a low rate of side effects, and be the best suited for the individual animal and the pet owner. The main concept is to use steroid-sparing drugs as the first choice, rather than when it's determined that other therapy isn't helpful. The importance of considering side effects of drugs cannot be over stated. Potentiation of infection or complications from infection may be a result of glucocorticoid therapy, which may be avoided with the incorporation of nonsteroidal treatment.

Food Allergy

Food allergy should be strongly considered in any dog which develops pruritus prior to six months of age, and in any dog which develops pruritus after six years of age with no previous history of cutaneous disease. Non-seasonal pruritus is the most common clinical manifestation of food allergy and the reason for seeking veterinary attention in most cases. Food allergy is often associated with other pruritic dermatopathies including canine atopy, flea allergy and superficial staphylococcal pyoderma. Simultaneous occurrence of food allergy with canine atopy or flea allergy may cause a seasonal intensification of the pruritus although most food allergic cases are intensely pruritic throughout the year. The response of food allergic dogs to conventional anti-inflammatory doses of glucocorticoids is minimal in most cases.

Historical questions may be helpful to establish a presumptive or tentative diagnosis of food allergy, although clinical features of the disease are comparable to other pruritic dermatoses. The association of abrupt dietary change with onset of pruritus is not a valid factor. A list of commercial dog foods, table foods, snacks, treats and digestible chew toys should be part of the historical database.

Episodic food hypersensitivity may occur following intermittent exposure to the offensive diet from the table, from predation, or eating garbage. This is especially true of cats since owners tend to buy more variety of canned cat foods. Copraphagic dogs may obtain undigested material that could effect a food allergy.

Although the most common clinical sign of food allergy is pruritus, it is not present in every case. Erythema with a papular eruption is also commonly observed. Urticaria and angioedema are less common clinical signs. There is much variation in the appearance and distribution of lesions, and any portion of the body may be involved. Young dogs may show generalized pruritus with no specific areas of involvement. Secondary scale and crust is often present and may be a primary owner complaint. Malodor is typically noticed when oiliness is present.

Most commonly, clinical signs mimic those of canine atopy with facial, ear, extremity and ventral distribution. In a recent study, the ear region was most consistently involved (80%) followed by the feet (61%) and the inguinal region (53%). The axillary, anterior foreleg and periorbital regions were nearly equal in occurrence (31-37%). The ear was the only area affected in 12 dogs (24%).

Certain breeds of dogs may have a higher incidence of food allergy. They include Labrador retrievers, cocker spaniels, golden retriever, German shepherd dog, Shar Pei, dalmatian, schnauzer, Boxer and Poodle. The primary differentials of food allergy are canine scabies and atopy.

There are a variety of proposed methods of diagnostic testing for food allergy. Laboratory test procedures have the convenience of rapid and easily acquired information regarding potential allergens. The use of either a RAST (radioallergosorbent test) or an ELISA (enzyme linked immunsorbent assay) technique for evaluating circulating IgE levels for food allergens is unreliable in the authors experience.

Confirmation of food allergy can only be determined by an elimination trial. The diet is restricted to specific food determined by the animal's previous exposure and known reactions. The preferred diet is home prepared and simplified to include a protein source and a carbohydrate source. The primary objective is to select a food combination that has minimal or no history of previous exposure. This may require reviewing the list of ingredients of commercial dog foods and treats. Although lamb and rice has been in vogue for dietary trials for some time the prevalence of these substances in commercial feed is limiting its usefulness and dietary related skin disease has been associated with lamb & rice based foods. Protein sources currently available include fish, venison, rabbit, duck, whole chicken egg as well as lamb. Rice has conventionally been the carbohydrate source of choice although potato is now substituted for rice in several commercial foods. The restricted diet must exclude all other food sources including table scraps, chew toys, treats, and access to other animals' food. Predation is a primary concern with cats. Dogs that have coprophagic activity must be carefully monitored to eliminate the source of undigested protein from cat litter or other dog feces. Although some veterinary allergists suggest the use of distilled water, it is my experience that this factor has minimal effect on the large percentage of food allergic dogs. Chewable heartworm preventative should be replaced with diethylcarbamazine (in an unchewable form), ivermectin or milbemycin. Chewable vitamins should likewise be avoided.

Supplementation with a multivitamin from a pharmacy may be used during the elimination trial although it probably is not necessary for the length of the trial. Concern is often expressed about young growing dogs placed on a home prepared elimination diet. An option to balancing a home prepared diet is to select one of the commercial foods. Any vitamin/mineral supplement during an elimination trial should be the non-chewable variety and not derived from plant source. Consulting with nutritionists for advice about specific breed requirements may be helpful. I have not experienced any problems with a limited trial period of 6 - 12 weeks with home prepared diets supplemented with a multiple vitamin/mineral.

The confirmation of food allergy can only be made following optimal improvement of the case and conducting dietary challenge. Challenge most often uses the single most common diet fed prior to the elimination trial. Some owners may be reluctant to institute a dietary challenge particularly if the improvement has been great. It is important to follow through with careful monitoring of the dietary challenge even when the owners may feel the improvement has been minimal. When the animal is challenged there may be a pronounced increase in the pruritic intensity which is often a significant recognition of allergy to that food. Reversal of manifestations following return to the elimination diet provides further evidence of causal relationship.

The treatment of choice is avoidance of offending food antigens. The ideal diet would be commercially available, contain a simplified ingredient list, be readily accessible, nutritionally complete, and not costly. The feasibility of satisfying all factors is unlikely in most cases. The ingredients used in these foods is quite variable. Confusion occurs when different food sources are used in products with the same name. Most food allergic dogs are allergic to multiple foods. This makes formulating an ideal diet more difficult. The following tables provide a source of commercial diets and their ingredient list.

Flea Allergy Dermatitis

Flea allergy dermatitis may occur in young animals as early as 6-8 weeks of age provided there is an optimal exposure to fleas. This liability is further accentuated if the animal has a tendency to develop atopy which places the risk factor at about 80 %. Flea allergy is not always classical in the young dog at the beginning of the clinical symptoms. The classical pattern of tailhead dermatitis may not be seen initially. The animal may show more generalized signs of pruritus combined with slight to moderate scaliness. Flea allergy is definitely on of the major considerations of any young animal in the geographic region where fleas are found.

The diagnosis of flea allergy may vary in ease depending on how classical the clinical symptoms are. Confirmation can be attained by allergy testing which serves several virtues particularly in the young dog. First, it proclaims a diagnosis early on so the owner can have acceptance rather than denial and focus with greater confidence on flea control. The second is confirmation of a problem for the medical record. Intradermal allergy testing with whole flea extract is still a worthwhile procedure with the expectation of 90 % of the flea allergic animals demonstrating positive reaction in 15-30 minutes. A small percent will show a delayed reaction in 24 - 48 hours. Greer Laboratories, Lenoir, NC produce a test kit at a nominal fee for this purpose. In vitro testing has been met with variable results and reliability. Many tests appear to have false positives or false negatives. The test provided by the Heska Corp. uses a purified flea saliva allergen using a modified ELISA test with excellent correlation to flea allergy.

Treatment should be directed at rapid reduction of fleas on the animal with observation intervals established for determining the treatment response. Products with safety should be considered in the young animal. Imidacloprid (Advantage, Bayer Inc.) has both safety and acute plus residual efficacy. It can be used every 7, 14, 21 or 30 days and in animals as young as 6 weeks. A standard treatment regimen I use is the application of imidacloprid every 14 days for four applications to assess response. Adjunctive therapy may be considered depending upon circumstances.

Canine Juvenile Cellulitis

Juvenile cellulitis has a number of aliases including juvenile pyoderma, puppy strangles, juvenile sterile granulomatous dermatitis and is a relatively uncommon problem affecting puppies typically between 4 weeks and 6 months of age. Hereditability has been supported by breed predilection (Golden retriever) and by familial histories. This disease is poorly understood but is not related to an infection. The condition represents a severe non-septic inflammatory response resulting in tissue swelling (cellulitis), lymphadenitis, pustular dermatitis, blepharitis and nodular dermatitis. Occasionally sterile nodular panniculitis may be seen concurrently. Affected dogs may be febrile, depressed and inappetent. Facial swelling is a consistent finding. Swelling of the pinnae accompanied by purulent discharge is commonly found. Joint pain and swelling may be present.

Skin scrapings and fungal culture should always be performed. Cytology of purulent material from the skin or from fine needle aspirate of the lymph nodes reveals a predominant representation of neutrophils and macrophages without evidence of infective agents. Biopsies reveal granulomas and pyogranulomas with inflammatory cells (neutrophils & macrophages) with evidence of infective organisms. Treatment should be started early to resolve the systemic effects of the disease and limit cutaneous scarring. Prednisolone or prednisone at high doses is administered until the disease is quiescent and beyond. A dosage of 2.2 mg /kg daily orally is administered for 14 days with reevaluation and dose reduction and gradual withdrawal. Topical therapy may be helpful with water therapy and moist soaks and mild astringents and antipruritic products. Dogs with intercurrent panniculitis may require more protracted therapy.

Infectious Skin Diseases

Impetigo is a bacterial disease causes by staphylococcal bacteria seen in young dogs usually before puberty. Impetigo differs from most staph pyodermas from the aspect is does not have an underlying disease relationship. Relationships may exist with other factors such as poor hygiene, malnourishment, parasitism, systemic infection or other debilitating disease. The lesions are pustules located on the glabrous area of the caudal abdomen an are easily resolved with conservative therapy. The pustules typically are large, superficial and do not involve the hair follicles. Upon rupturing there is debris left behind consisting of honey colored crust.

Clinical management may only require topical therapy with an antimicrobial shampoo such as chlorhexidine, ethyl lactate or benzoyl peroxide. Systemic antibiotics may be included and should be selected from the "first round" antibiotic choices.

Superficial Crusting Staphylococcal Pyoderma in Young Dogs

Occasionally neonatal dogs may develop an crusting dermatitis that tends to have a predilection for the extremities although there may be more generalized lesions affecting the truncal area and face. This may be seen in several puppies in a litter and may be progressive. Contagious characteristics has not been established. Differential diagnosis includes dermatophytosis, demodicosis and keratinization disorders because of its crusting characteristics and fungal cultures should invariably be evaluated along with skin scraping. Systemic antibiotics are almost always necessary to resolve the lesions. Affected dogs may develop anorexia and become febrile. Topical therapy is almost always used as adjunctive therapy.

Antibiotics for treating juvenile staphylococcal pyoderma:

Amoxicillin trihydrate with clavulanate potassium14-22 mg /kg bid
Lincomycin22 mg/kg bid
Clindamycin5.5-11.0 mg/kg bid
Trimethoprim-sulfadiazine or
trimethopirm sulfamethoxizole
20-30 mg/kg qd-bid
Ormetoprim-sulfadimethoxine28 mg/kg qd
Erythromycin10-15 mg/kg tid
Cephadroxil22 mg/kg bid

Mycotic Dermatoses

Dermatophytosis is an infectious disease caused by a fungal agent that effects the keratin of the epidermis and the hair follicle. The most common genera of organisms are Microsporum and Trichophyton. Microsporum canis is the most common caus of dermatophytosis in the dog and the cat. Although exposure to the infective arthrospores of the fungal element may lead to an active infection, normal host defenses often will prevent the establishment of clinical disease. A number of factors may come into play during this process. It is well recognized that the immaturity of the host immune system in the neonate or juvenile may play a prominent role in the susceptibility of infection in the young animal. The ability of the host to mount an inflammatory response is critical to the course of the infection. Asymptomatic carrier states of M. Canis is well recognized and demonstrates the balance between host and potential pathogen. Suppression of immunomechanisms may also lead to infection or be associated with chronic persistent disease. Conditions such as feline leukemia virus infection, FIV or neoplasia may be underlying reasons. Chronic or aggressive steroid therapy has been associated with protracted disease in some situations.

Clinical signs of dermatophytosis may be variable depending upon the extent of host response. The classical lesion is the one characterized as a circumscribed, circular alopecic, erythemic macule or patch with superficial scale. Although the classical "ringworm" lesion may be caused by a dermatophyte, it is most often associated with bacterial pyoderma. Dermatophytosis results in folliculitis and is one of the three main causes (staphylococcal folliculitis & demodicosis are the others) often associated with papular dermatitis particularly in the short coated dog. Folliculitis may progress to furunculosis resulting in a fibrosing pyogranulomatous dermatitis. Cicatricial alopecia may be the consequence of the deeper inflammation and destruction of the hair follicle. Nodular dermatitis may be seen in the dog with a kerion reaction or in the cat with pseudomycetomas or Majochii's granuloma. Cats tend to have more variability in lesions associated with dermatophytosis. Miliary dermatitis conveys a mandatory rule out of dermatophytosis although there are other diseases more commonly seen with that presentation. Cats tend to be more pruritic than dogs with dermatophytosis and may be a major cause of persistent self mutilation with generalized or regionalized lesions. Misdiagnosis under these circumstances may be common as they are often confused with allergic dermatitis. For more details on the diagnosis and treatment of dermatophytosis refer to notes related to Infectious Skin Diseases, Part 2 in these proceedings.

Cutaneous Malasssezia

Malassezia pachydermatis is a yeast organism most commonly recognized as an associated cause of otitis externa. Cutaneous malassezia is a condition more commonly recognized now and most often encountered in geographic areas characterized by high humidity or non-arid climates. The disease is considered to be a secondary problem to an underlying disease in almost all cases. Recognition of this component is necessary for acceptable control of the accumulative problem. Local factors that contribute to the proliferation of the yeast include wax and sebum production, moisture and disruption of the epidermal barrier. Greasy skin secondary to pruritic dermatoses such as allergy are often associated with the condition. It has also been shown that staphylococci will enhance the growth of malassezia in culture. Combinations of underlying diseases in addition to the individuals tendency to develop oily skin and hair are important in the development of cutaneous malassezia. The organism is categorized as a facultative pathogen with opportunistic characteristics.

Clinical Disease:

The clinical manifestations of cutaneous malassezia is often overshadowed by the primary disease or by the similar manifestations of other conditions. Malassezia has most often been seen in conjunction with allergic dermatoses, in particular atopy and food allergy although it may be associated with any condition. Metabolic/endocrine dysfunctions are another group of associated problems. Keratinization defects (West Highland White Terrier) have been the underlying problem in some cases. Breeds recognized with possible predilection include the West Highland white terrier, basset hound, cocker or springer spaniel, poodles, silkie terriers, maltese, Australian terrier and Shetland sheepdog.

Bacterial pyoderma is also a very important differential diagnosis for malassezia dermatitis and often the two have such similar appearances as to lead to a misdiagnosis. Antibiotic failure has been interpreted in cases with persistent dermatitis when in actuality the dermatitis was due to malassezia. Enrofloxacin is often used in the case of a perceived failure of other antibiotics such as cephalosporins. It is important not to blame an antibiotic for poor response when the perceived failure is actually another problem.

The clinical features include dermatitis in either a regionalized pattern or may be generalized. The hallmark of the disease is usually pruritus that typically has a limited response to standard antiinflammatory doses of glucocorticoids. Clinical symptoms may mimic canine scabies or food allergy with convincing similarities. The lesions observed may be variable but usually includes erythroderma with a variability of scale and/or greasy buildup. The scale may have characteristic plaques appearing grey to white in color. A papular dermatitis is often seen but may represent the co-existence of bacterial pyoderma. Distribution areas often include the face, pinnae, head, ventrum and extremities of the animal.


The diagnosis of cutaneous malassezia is accomplished by cytological examination of material collected from the surface of the skin. This is best accomplished by using a dry scalpel blade or spatula to collect from affected areas particularly those with more oiliness. Some cases are characterized by dry crusty lesions making it more difficult to obtain specimens. The use of a cotton applicator stick may facilitate the acquisition of material from this type of lesion. Rolling the cotton over a slide after it has been rubbed on the skin surface will often provide sufficient specimen to evaluate. Other alternatives include using an acetate tape to collect scale/crust from the skin surface.

For more detailed information on the clinical treatment of this condition please refer to notes pertaining to Infectious Skin Diseases, Part 2 in these proceedings.

Selected Parasitic Dermatoses of the Juvenile Dog
Canine Demodicosis

Conservative therapy continues to represent the preferred approach to localized demodicosis in the juvenile. Benzoyl peroxide gel or cream is often selected as an initial choice. Application is performed daily for 30 days then reassessed. Total body acaricidal therapy is not warranted or recommended for the localized form in most cases. Providing adequate opportunity for spontaneous remission should be encouraged. Use of benzoyl peroxide shampoos is recommended. The majority of localized cases will self limit, while others may progress to a generalized form.

Treatment of the generalized case often necessitates total body demodicidal therapy, although spontaneous recovery is observed. This is more likely in young dogs with multifocal lesions than those with diffuse generalized areas of involvement. Initiation of systemic or generalized demodicidal therapy is accompanied by the recommendation for neutering since spontaneous remission cannot be evaluated. Treatment options are influenced by previous therapy and response.

Acaricidal treatment of uncomplicated generalized demodicosis in the juvenile is amitraz (Mitaban(R) - Upjohn) applied very two weeks at a concentration of 250 ppm with evaluation following 3-6 applications. Agricultural amitraz pour-on products have been used as a less expensive amitraz source with demonstrable efficacy . Tactik is a brand used at a dilution of 10cc/gal providing .125 % solution. This is an extra label use on dogs. Treatment should be continued as long as positive skin scrapings are found. One or preferably two treatments should be used following the evaluation with multiple negative skin scrapings obtained from previously affected areas. Yohimbine has demonstrated effectiveness in reversing the intoxicating signs of amitraz therapy. It is used at one half the dosage recommended for tranquilization reversal. Usually .25 ml/20lbs. or less is effective. This may be used as a pretreatment in animals of know sensitivity to amitraz.

Localized treatment is usually restricted to feet and facial areas where persistent demodicosis is likely to be found. Mitaban(R) and mineral oil may be used daily or every other day. Mitaban(R) 0.5-1.0 ml is mixed with 1 oz. of mineral oil. Stability of this combination is unknown. It is best to place the mixture in a dark or amber bottle and place in a protective bag in the refrigerator. An optional treatment approach for more rapid recovery in cases with heavy infestation or in cases with refractory demodicosis is the application of amitraz to ONE HALF the body daily.

Another option for regional treatment is using an aqueous preparation which should be made fresh with each application. Smaller volume of solution can be made by proportional dilution. Remaining Mitaban(R) can be stored in the freezer in a protective bag (Zip Loc(R)). Affected feet can be soaked daily or every other day as required. Tactik can be used at the dilution of 1 ml/100ml water for regional therapy or 1.5 ml added to 8.5 ml of mineral oil for spot therapy or treatment of the ears.

Systemic Therapy:

  1. Ivermectin has shown efficacy when used daily by oral administration at a dosage of 300 - 600 ug/kg. but has not demonstrated efficacy when used intermittently (weekly). Duration of therapy is to effect.
  2. Milbemycin (Interceptor) therapy has shown variable efficacy for demodicosis but is decidedly more expensive than ivermectin and probably not as efficacious. The dosage required is 1.0 - 2.0 mg/kg and must be administered daily. This is expensive and usually requires prolonged treatment.

Maintenance Therapy:

Maintenance therapy is customized to each animal. The objective is to suppress the proliferation of mites to a minimum and to attain an asymptomatic state. This therapy is not satisfactory if a substantial population of mites is present. It is necessary to treat more aggressively in the initial phase then modify to a maintenance regimen based upon the individual response. Topical applications are typically performed on a 2-4 week interval. The manufacturers recommendation of dilution is followed although the animal is allowed to maintain a normal coat. Systemic therapy may also be used in a maintenance program. This is accomplished by the administration of ivermectin or milbemycin on a schedule sufficient to control clinical signs. This may be an alternate day or every third day dosage. Less frequent treatment will unlikely be effective in controlling the refractory or frequent relapsing case.

Canine Scabies

Canine scabies is most often confused with either canine atopy or food allergy +/- flea allergy. Distribution patterns can be comparable. The facial area, ears, ventrum, and extremities are classical involved although early cases may have generalized pruritus without a classical pattern. Response to glucocorticoid is partial, much like the responsiveness of food allergy. Complicating superficial pyoderma may also be a factor. The characteristic scaling and crusting may resemble cutaneous malassezia which may also be a complicating disease and therefore should be evaluated, Treatment with typical flea control products (pyrethrins, pyerethroids, carbamates, and some organophosphates) may modify the disease features but not be sufficient to eliminate the scabies mite. From an historical perspective, not all in-contact dogs or humans will develop lesions or clinical signs restricting the interpretation of this information in leading to disease confirmation. Skin scrapings are the most reliable method of diagnosis but are only positive in 50% of the clinical cases if 25 skin scrapings are performed per case. Ear margins and extremities are the most yielding areas to scrape particularly in heavily crusted regions. Identification of a single mite or egg is diagnostic.

Relevant clinical points concerning Sarcoptes scabei infestation are:

  1. Clinical features resembling other pruritic dermatopathies particularly atopy and food allergy.
  2. Limited reliability of diagnostic testing for disease confirmation;
  3. Variable dependability of acaricidal products;
  4. Contagiousness/asymptomatic carrier state and zoonotic significance of the disease.


If scabies is suspected, treatment should be instituted. This is a curable disease unlike so many dermatoses that are only controllable. All topical therapy should be applied at a regular interval (weekly) for a minimum of 4-6 weeks. The dog should be kept absolutely dry between applications with exception of a cleansing or anti-seborrheic bath just prior to the next treatment. The acaricidal product should not be rinsed from the dog following the treatment. All medium to long haired dogs should have coats removed with a #10 or #40 clipper if topical treatment is elected. This procedure should be repeated every 2 weeks during the treatment regimen.

Acaricidal products:

  1. Lime sulfur is a smelly but an effective scabicide at 3- 4% concentration for topical application. Scented products are commercially available (Lym Dyp, DVM Inc.) although horticultural lime sulfur may be substituted if a veterinary product is not available. Weekly application is sufficient but should be continued for a minimum of 4 -6 weeks. Sulfur is quite soothing, antibacterial, and antifungal. A complicated case of canine atopy with secondary pyoderma will improve with this treatment, thereby leading to a false conclusion when diagnostic confirmation has not been attained. Monitoring lesions and intensity of pruritus is essential. Lime sulfur may stain materials (porcelain tubs) and tarnish metal (particularly gold) in addition to having a pungent odor thereby restricting its use.
  2. Ivermectin is the creme de la creme treatment for canine scabies. It is highly efficacious, inexpensive, convenient to use BUT NOT APPROVED for small animal application: It is nearly 100% effective with 2-3 treatments and may be administered parenterally (S.Q. injection) or orally. Adverse reactions have been observed, particularly collies where this ivermectin therapy should be avoided. The dosage is 250 - 300 ug/kg S.Q. or P.O. and repeated in weekly for three treatments or administered every 2 weeks for 2-3 treatments. Ivermectin should never be used in sensitive breeds unless test doses are used to determine tolerance. It should also not be administered until the animal has been checked for heartworms if living in an endemic area of the country.
  3. Amitraz (Mitaban, Upjohn) has shown regional efficacy but is not totally reliable. The effectiveness is variable with respect to different geographical regions. There are minimal side effects and the cost is reasonable. It is also approved for canine application nut not labeled for scabicidal activity. Multiple treatments are necessary. Application weekly for 4-6 weeks should be curative if there is no mite resistance and the provisional diagnosis was totally correct. Limitations include long hair coats and poor client compliance.
  4. Organophosphates may be effective but are variable depending upon region of the country (parasite susceptibility) and type of organophosphate used. Phosmet has regional effectiveness as a scabicide although it is not considered as reliable as malathion.
  5. Fipronil spray (Frontline, Merial) has acaracidal properties and has been used successfully in a limited number of scabies cases. There have been other reports of limited efficacy thereby limiting usefulness as a reliable demodicide. If fipronil spray is used it most be applied at the recommended dosage based upon body weight to attain maximal efficacy.

Miscellaneous Diseases Affecting the Skin

Familial Canine Dermatomyositis is a hereditary, idiopathic condition of the skin and muscles resulting from an idiopathic inflammatory process observed in young collies, Shetland sheepdogs and various crosses. Other breeds have also been recognized. An immune-mediated mechanism is postulated. Lesions occur early in life and may appear as young as 7-11 weeks of age. The progression of the disease is variable but usually reaches maximum severity by one year of age. Lesions are most prevalent on the face, extremities over bony prominence, the tail tip and ear tips. Alopecia, erythema, scaling, crust formation, vesicles, erosions, ulcers and scars may be seen. Diagnosis is by history, clinical findings, rule out of other dermatoses and supportive evidence from dermatohistopathology. Treatment has been symptomatic with vitamin E therapy (200-800 IU/day) and glucocorticoid therapy (1mg/kg qd) during exacerbations. Steroid therapy should be used cautiously because of the muscle atrophy and the secondary problems such as demodicosis and pyoderma. Newer therapeutic modalities are being investigated.

Epidermal Dysplasia in West Highland White Terriers is a condition that tends to occur in families and is typically seen in animals between 6 and 12 months although it may occur much younger (5-6 weeks). It is characterized by pruritus with erythema and increased greasiness predominantly affecting the face, ventrum and extremities. Secondary complications are common including cutaneous malassezia, demodicosis and staphylococcal pyoderma. Clinical features may closely resemble atopy, food allergy, scabies or cutaneous drug reaction. Diagnosis is by history & clinical examination and should be toward evaluating and ruling out complicating diseases. Biopsies are helpful and may demonstrate some of the characteristic findings of this disease. Treatment includes identification and elimination of intercurrent diseases and specific therapy of the epidermal dysplasia. Cyclosporine has become the treatment of choice for the epidermal dysplasia using 10 mg/kg once daily until remission then modifying to a maintenance dose. Many of these dogs may have concurrent atopy or food allergy requiring additional therapy. Since cyclosporine is relatively expensive the pet owner may choose conservative therapy which is predominantly symptomatic and with variable response. Frustration is commonly observed in these circumstances.

Psoriasiform-Lichenoid Dermatosis in Springer Spaniels is an uncommon (rare) condition observed in young dogs. The disease is characterized by lichenoid papules and plaques predominantly on the pinnae but subsequently located elsewhere on the body usually the ventral truncal region. The lesions progress to hyperkeratotic lesions with adherent crust and keratinaceous debris. Follicular casts may be observed. Chronic cases resemble severe seborrhea with malodor a definite part of the history. Staphylococcal pyoderma may be seen as a secondary factor. The disease may take a convoluted course of exacerbations with minimal response to most conventional therapeutics.

Primary Seborrhea in Dogs is used to describe animals with an inherited disorder of keratinization or cornification more commonly seen in the American Cocker spaniel, English Springer spaniel, West Highland white terrier and Basset hound. Other breeds may be affected. The disease is characterized by scaling, greasy dermatitis with adherent crusts developing. Lesions may affect the skin of the body, ear canals, claws or foot pads and is characterized with hyperkeratosis. More prominent distribution includes the ventral neck, face, feet, perineum, and ventral body. Lesions usually start between 12 -18 months of age and are progressive throughout life. Secondary malassezia is frequently observed as is staphylococcal pyoderma. Intermittent skin scrapings for demodex should be included. The diagnosis is by history, clinical examination, rule out of common dermatopathies and skin biopsy. Clinical management includes aggressive topical treatment with antiseborrheic shampoos and treatment of the coexisting diseases. Retinoic acids have been used extensively with varying results. Most favorable results has been with the use of etritinate 1mg/kg qd for 2-3 months then reduction to a maintenance dose. Side effects of this and related drugs should be reviewed with owner education paramount. Human contact hazards should be made aware due to potent teratogenic effects of the drug.

Canine Acquired Alopecias

Canine Pinnal Alopecia is a condition most commonly seen in the dachshund but also observed in other breeds including Boston terriers, Whippets, Italian Greyhounds and Chihuahuas. The alopecia is characterized by its name and begins in animals less than one year of age with gradual loss of hair from the pinnae. The hair loss may become more progressive but usually does not extend to the rest of the body. Small villous hairs may be seen in the alopecic areas. The alopecia may also be accompanied by vasculitis eventually leading to ulceration or fissures at the ear margin.

Color Dilution Alopecia occurs in dogs with blue or fawn coat colors but does not occur in all dogs of these coat colors. Although the coat color gene plays a role in the disease, there is no known mechanism established. The condition is most commonly recognized in the blue Doberman but may be seen in other breeds including dachshunds, whippets, Italian greyhounds, Chowchows, standard poodles, Min. Pins. And others. The coat is usually normal until 4-6 months of age and then gradual loss of hair is observed with the development of bacterial folliculitis as a secondary complication. The diagnosis is usually by history and clinical examination although biopsies usually provide the necessary confirmational criteria. Treatment is restricted to treating the secondary complications and providing good topical management with regular shampooing and moisturizing rinses.

Black Hair Follicle Alopecia is in many ways similar clinically to color dilution alopecia since it is predominantly a single pigmentary hair that is affected. Black hair follicular dysplasia by name indicates that the dark (black) pigmented hairs are affected with minimal effect of other remaining hair colors. The striking contrast of the clinical presentation is usually sufficient to make a tentative diagnosis although biopsies may contribute to a confirmation. Treatment is limited as with other causes of follicular dysplasia. Hair loss is typically seen in the young dog.

Congenital Hypotrichosis or Alopecia is hair loss observed at birth or develops during the first 2-4 weeks of life. The hair may not be the only defect present with other morphological components of the skin affected. Minimal diagnostic intervention is usually indicated. There is no treatment for this condition.

Antihistamine Therapy

Antihistamines or antihistamine like compounds are certainly less reliable than glucocorticoids but recently have resurfaced in popularity for symptomatic treatment of the pruritic patient. They are particularly useful in conjunction with hyposensitization therapy or to decrease the requirement of glucocorticoids. Synergism has been demonstrated between some antihistamines and prednisone as well as essential fatty acids. In general, approximately 30% response rate is observed with the treatment of an antihistamine. Some guidelines concerning the use of antihistamines include the following:

  1. Antihistamines should be used at the recommended dosage and for a period of 10-14 days to adequately evaluate response. Each antihistamine requires individual evaluation to determine response.
  2. Antihistamine therapy is only expected to partially control pruritus unless the intensity is mild as in the early symptoms of an atopic patient.
  3. The presence of coexistent pruritogenic conditions dramatically influence the response observed to antihistamines. Elimination of as many of these factors as possible (fleas, food, pyoderma, malassezia etc.) is necessary for representative evaluation.
  4. Antihistamine therapy should be trialed at different times of the year when there is a difference of allergen load and the summation of pruritogenic factors.
  5. Side effects of antihistamines are variable but usually not a major concern. They include somnolence, CNS excitation, teratogenic, anti-cholinergic-atropine actions and agranulocytosis (rare).

The following drugs are commonly available and may be used to evaluate responsiveness. It usually takes some experimentation to determine the most beneficial product or in some instances combination of drugs.

Commonly Used Non-Steroidal Drugs for the Treatment of Canine Atopy

1. Diphenhydramine (Benadryl)2.2 mg/kg TID
2. Hydroxyzine HCl (Atarax)2.2 mg/kg TID
3. Chlorpheniramine (Chlortrimeton)4-12 mg two - three times daily.
4. Trimeprazine (Temaril)1-2 mg/kg, three times daily.
5. Doxepin Hcl2-5 mg/kg twice daily.
6. Fluoxetine (Prozac)1 mg/kg once daily X 4 weeks then adjust
7. Amitryptyline1-2 mg/kg BID
8. Cyproheptadine0.3-2.0 mg/kg, BID
9. Astemizole, (Hismanal)0.25 mg/kg, BID
10. Clemastine (Tavist)1.0 mg/kg, BID
11. Clomipramine1-2 mg/kg, BID
12. Cetrizine (Zyrtec)5 mg q 24h < 7.5 kg
10 mg q 24 h >7.5 kg
13. Loratidine (Clariton).5-1.0 mg/kg/day

Selected Pharmaceuticals

  1. Cyclosporine
    1. General background
      1. A polypeptide product from a fungus Tolypoladium inflatum.
      2. Used in organ transplant patients to produce immunosuppression
      3. Used commonly to increase tear production in dogs with KCS (Optimune)
    2. Immunological Effects
      1. Inhibits lymphocytes & affects T-helper lymphocytes
      2. Depresses induction of cytotoxic T-lymphocytes
      3. Suppression of IL-1 & IL-2, macrophage activating factor & gamma interferon
      4. Blocks proliferation of T-lymphocytes
      5. Less affect on B-lymphocytes
    3. Indications for use
      1. West Highland white terriers with cornification/follicular dysplasia ("Westie Disease")
      2. Contact allergy
      3. Autoimmune dermatoses ( pemphigus complex, lupus, bullous pemphigoid) with limited response
      4. Auto-immune hemolytic anemia (AIHA)
      5. Canine atopy
    4. Treatment regimen
      1. Man: 5-10 mg/kg qd
      2. Vet. Med.: various protocols
        1. 5-10 mg/kg qd; 12-17 mg/kg qd for AIHA; 20 mg/kg divided bid
        2. In man the dosage is adjusted to obtain blood levels of 400-600 ng/ml (toxicity > 600). Dosage is adjusted to an optimum trough level of 100-250 ng/ml
    5. Adverse Effects
      1. Minimal myelosuppression compared to other drugs
      2. Vomiting, diarrhea, anorexia, gingival hyperplasia and secondary infections observed.
      3. Nephrotoxicity is observed in humans with chronic treatment
      4. Hepatotoxicity is rare .
      5. Secondary infections seen most commonly in man but not as apparent in the dog.
    6. Drug Availability and Interactions
      1. Ketoconazole will decrease the metabolism.
      2. Cimetidine & erythromycin inhibit metabolism
      3. Drug produced in 25, 50 & 100 mg tab; 100 mg/tsp. oral soln & 50 mg/ml injectable (Sandimmune)
  2. Pentoxifylline
    1. General background
      1. Pentoxifylline is a methylxanthine derivative with properties similar to theobromine, caffeine & theophylline
      2. It is absorbed through the intestines & metabolized by RBC's and liver
      3. Excretion is predominantly through the urine
    2. Mechanisms of action
      1. Red blood cells and vasculature
        1. Increased or restored deformability
        2. increased RBC membrane ATP
        3. Influences membrane fluidity (enzymatic methylation of phospholipid)
        4. Inhibits microvascular constriction & decreases RBC & platelet aggregation
        5. Stimulates fibrinolysis & decreases plasma fibrinogen levels
      2. Effect on white blood cells
        1. Decreases neutrophil adherence & prevents neutrophil priming by platelet PAF
        2. Inhibits neutrophil degranulation without affecting phagocytosis
        3. Increases PMN motility & chemotaxis
        4. Selected inhibition of T- & B- lymphocyte activation (superantigens)
      3. Effect of pentoxifylline on collagen
        1. Decreases collagen production
        2. Increases activity of collagenases in dermis
        3. Inhibits fibroblast hyperactivity (reduces excessive fibrosis in scleroderma, keloids and morphea)
        4. Down regulatesadhesion molecules on keratinocytes & decreases cytosine release by keratinocytes & inhibits T-cell adherence
    3. Indications for use
      1. Vaso-occlusive disorders, infectious diseases (septic shock), polycythemia, hyper coagulable states, acute respiratory distress syndromes, immuno deficiencies from chemotaxis dysfunction
      2. Cachexia of cancer improved by affect on TNF-alpha.
      3. Decrease incidence of graft vs. Host disease after B.M. transplant
    4. Applications in veterinary dermatology
      1. Canine familial dermatomyositis
      2. Contact allergic dermatitis (Commelinceae family)
      3. Vasculitis & vasculopathies
    5. Dosage of pentoxifylline
      1. Dosage is variable but generally administered at 10mg/kg qd - tid
      2. Pentoxifylline is supplied as 400 mg controlled release caplets
    6. Adverse reactions
      1. Gastrointestinal irritant and must be taken with food
      2. CNS
      3. Cardiovascular (arrhythmia or tachycardia)
      4. Hematologic (leukopenia, thrombocytopenia)
    7. Metabolism & excretion
      1. Enhances activity of cisplatin
      2. Reduces nephrotoxicity of cyclosporine and amphotericin B.
      3. Decreased metabolism by cimetidine.
      4. Combination with fluoroquinolones may further reduce activity of TNF-alpha

  1. Mupirocin
    1. General background.
      1. Product produced by the fermentation of Pseudomonas fluorescens.
      2. Inhibits protein synthesis by specific and reversible binding to bacteria isoleucyl transfer RNA synthtase.
      3. Inhibits growth of both gram positive & Gram negative bacteria.
    2. Indications
      1. Bacteria susceptibility includes staphylococcal varieties including methicillin resistant & beta-lactimase producers.
      2. Used to treat focal areas of staphylococcal dermatitis: chin, muzzle, pressure point pyoderma and early acral lick dermatitis.
      3. Particularly effective in treatment of feline acne.
    3. Mupirocin administration
      1. Apply to affected area(s) twice daily.
      2. Limit treatment of open wounds or areas where excessive licking is possible. Avoid in these circumstances or use mechanical devises to limit ingestion.
      3. Reevaluate intermittently. Do no forget to skin scrap and perform fungal culture.
    4. Drug availability
      1. 2 % mupirocin available as an ointment with an ethylene glycol base (Bactoderm[SKB/Pfizer] on Veterinary side and Bactoban on human side)
      2. Maximum treatment recommended is 30 days.

Antipruritic glucocorticoid therapy

Induction therapy of an oral glucocorticoid is usually 1.1 mg prednisolone or prednisone per kg per day. This may be given sid or divided bid for 5-7 days. The antiinflammatory maintenance dosage is usually 0.55 to 1.1 mg per kg every other day but may be administered to a maximum of 2.2 mg/kg every other day. In general, cats usually require 2-3 times the glucocorticoid dose for both induction and maintenance regimen of antipruritic/ antiinflammatory therapy. Methylprednisolone (Medrol, Upjohn Co., Kalamazoo, MI) provides effective control of the pruritic dog at a dosage of 1 mg / 10-20 pounds body weight and can be given daily for induction with conversion to alternate day for maintenance. There appears to be less polydipsia and polyuria with methylprednisilone compare to prednisone or prednisolone. Oral triamcinolone has also been used to treat pruritus and may be effective at a dosage of 0.2 mg/kg. Since triamcinolone is rated as an intermediate glucocorticoid it has been advised to use every three days for maintenance regimens.


Diseases of the ear represent a majority of cases observed in practice and often with accompanying integumentary involvement. The causes of the otitis have previously been classified according to anatomical location or etiological association. Other criteria of classification have been used to relate to ear disease. One such scheme categorizes conditions affecting ear disease by predisposing factors, primary causes and the perpetuating factors. The following list of factors represent the main concerns for disease identification and treatment.

Predisposing Factors
Stenotic canals
Hair in canals
Pendulous pinnae
Canal obstruction
neoplastic growth
Systemic disease
Systemic infection
Liver failure
Treatment effects
Microflora imbalances

Perpetuating Factors
Bacteria: Staphylococcus intermedius, Proteus spp., Pseudomonas spp., Escherichia coli & Klebsiella spp.
Yeasts: Malassezia pachydermatis, Candida albicans, etc.
Otitis media

Primary Causes
Foreign Bodies: plant awns, foxtails, hairs, etc. Glandular disorders: apocrine hyperplasia, Parasites: ear mites, demodicosis, scabies mites Microorganisms: dermatophytes/intermediate mycoses
Hypersensitivities: atopy, food, contact, drugs. Keratinization disorders: Primary idiopathic & endocrinopathies, abnormal cerumen production.
Autoimmune Diseases: Pemphigus copmlex, bullous pemphigoid and lupus.
Viral diseases: Canine distemper
Glandular disorders: apocrine hyperplasia, sebaceous hyperplasia, altered secretions. Systemic metabolic disease

Perpetuating Factors (cont.)
Progressive pathologic changes

Epithelial folds/hyperplasia
Apocrine gland hypertrophy

An important aspect of treating otitis externa is determining the primary cause of the otitis. The accentuation of the perpetuating factors may lead to inadequate recognition of the predisposing factors or primary causes. The establishment of chronic infections often obscures the clinical features of primary casuses observed in the ear because of the over abundance of the pathology related to the infectious complications and also because it may be difficult to resolve or control that component of the problem. There is also a strong liklihood of progression of the infection to otitis media. While culturing the chronic otitis externa is indicated, in some instances it focuses all the attention to the perpetuating factors to the exclusion of the primary causes. The bacterial culture and susceptability testing is also incorporated in the diagnostic plan with the exclusion of direct microscopic examination of material collected from the ear canal in many cases. Smears should always be included in the appraisal of otits externa. Infectious agents are the predominant perpetuating factors causing chronic otitis externa particularly in the early stages of the disease. The progressive pathological changes are potentiated by the infectious agents and further complicates the therapy as well as becoming yet another perpetuating factor.

The most common primary cause of otitis externa in the dog in Southeastern U.S. is allergy (atopy, food allergy or contact allergy to mediactions). Many other primary causes do occur and likelise eventually develop an infectious component. Treating only the infectious aspect and ignoring the underlying problem results in partial control of the problem. Suffice it to say that in some cases dealing with the infectious agent alone is a major challenge. A complete dermatological examination and history should be included to assist in the recognition of the primary cause since the integumentary disease is so often observed in association with ear disease.

Principles of Assesment

There are several major principles of clinical assesment for routine otitis externa that are often overlooked. Some of the relevant points are as follows:

  1. Perform a complete examination of both the pinnae (often a signficant component of the ear disease) as well as the ear canal. Evaluate both ears even if the primary complaint is relevent to only one ear. Look for signs of skin disease.
  2. Use sedation when possible particularly in the initial visits when there is apt to be abundant exudate and sensitive ear pathology making adequate visualization impossible.
  3. Always perform ear cytology even if culture & susceptability testing is to be performed. Rapid stains make this procedure very simple. Utilize the Gram's stain kits for more precise recogntion of bacteria.
  4. Reevaluate the ear canal after it has been adequately flushed and cleaned. You are not always going to be in a position of seeing the tympanic membrane at the initial examination.
  5. Repeat the first four steps on reevaluations.

Principles of Treatment

Treatment principles are often overlooked in the management of otitis externa. Instead we look for that one medication that will solve the problem (at least for an appropriate period of time). Most cases of otitis require more than exam room evaluation and treatment. Outpatient admission is often excluded because of time or financial constraints and may represent a major limitation to satisfactory control. The ideal therapeutic approach is dependent on the results of both the direct inspection of the ear(s) (gross and otoscopic) and direct microscopic examination of otic material. The following list presents the order in which to approach the treatment of otitis.

  1. Direct smear of material collected from the ear canal as well as the inside of the pinna if suspicious lesions are present. Do not forget to "heat fix" the specimens before staining.
  2. Perform otoscopic examination. If unable to accomplish, it may be necessary to wait for sedation. If the canal is full of debris and exudate, it may be necessary to continue through the cleaning procedure and attempt later.
  3. Cerumenolytic application is necessary partiularly if there is a ceruminous otitis with waxy build up in the canal/pinnae. Be familiar with products that have good cerumenolytic activity but also be aware of potential irritancy and restrictions. Allow at least 10 minutes for adequate time for drug action.
  4. Cleaning and flushing should always follow cerumenolytic application.
  5. Drying.
  6. Treatment based on results of direct microscopy of otic material and culture results if performed.

Unfortunately, steps 3 - 5 are often ommited and therapy is initiated prematurly limiting the liklihood of resolution of the problem. If response is not noted with conservative treatment (ie. minimal or no ear cleaning) the animal should then be hospitalized for more thorough ear cleansing and examination. Modifications of the approach to individual cases depends upon previous history and response to treatment, understanding all factors relevent to the disease, temperment of the animal and financial factors.


There a several important reasons that cleansing of the diseased ear is essential for optimal therapeutic response. The most obvious is merely the removal of barriers that do not allow proper penetration of the epithelial lining of the ear canal by the medication or produce the desired effect on the infective organisms or to have an antiinflammatory effect. Many antimicrobials such as aminoglycocoides are inactivated in presence of pus making its removal essential. The accumulation of exudate can further potentiate the irritation by the effect of toxins, degenerating cellular debris and metabolic by-products. Removal of foreign bodies are also a major reason for complete cleansing. Cleaning can be subcategorized in three areas: 1. mechanical 2. ceruminolytic 3. aqueous flushing

Mechanical cleansing

Removal of large accumulations of material with the aid of ear loops or cotton swabs help facilitate cleansing but should not replace it. Cotton swab applicator sticks are probably over used and can actually cause epidermal irritation and abrasion in the inflamed ear. Application of a ceruminolytic helps solubilize the material for easier removal and allows the use of products containing topical anesthetics if utilized. Cleaning soutions may include 2-4 % lidocaine solution. Cleaning the ear also removes the end products of inflammation including toxins, enzymes and other irritating substances.


Many products carrying labels suggseting claims of cleansing properties are no more than alcohol or pH adjusters (malic, acetic, lactic or other type acid) The active ingredients in these products have little to no activity on emulsifying waxes or lipids. Active ingredients with excellent ceruminolytic actitivity include dioctyl sodium/calcium sulfosuccinate , carbamide peroxide, urea peroxide, squalene, triethanolamine polypeptide elit condensate, and hexamethyltetracosane . Less effective, but certainly not to be overlooked, ingredients include propylene glycol, glycerin, and other oils. Ceruminolytics should not be used if the tympanum is not intact although squalene has least adversity in this situation. Some cerumenolytics may be very effective but if left in the ear cause irritancy. Unfortunately, many times, visualizaiton of the tympanum cannot be accomplished until adequate cleaning has been performed. Removal of debris is important for proper examination. Ceruminolytics require time to work, usually 10 - 15 minutes. Unless used properly, their attributes are limited. Removal of as much exudate/solubilized wax as possible provides more effective flushing with an acqueous solution.

Aqueous Flushing

Flushing the ear canal is the next step toward complete cleansing. The easiest method is an ear bulb syringe or the use of a 12-20 ml syringe attached to either a tom cat catheter or pediatric feeding tube. Antiseptic solutions such as chlorhexidine may be included but may cause some irritation. Warmed physiological saline is the best alternative for ulcerative or extremely irritated ears. Following repeated flushes, removal of all fluid should be performed to allow otoscopic exam of the canal and the tympanum. Suction devices with a Frazier suction tip or the more simplistic version consisting of a catheter (tom cat) and syringe. Application of drying agents containing organic acids (acetic, malic, salicylic, lactic, boric or benzoic) +/- alcohol may be used to help dry the ear. If much irritation/ulceration is observed, strong alcohol products should be avoided. Otic products with Burrow's solution (BurOtic & BurOtic HC, Allerderm-Virbac) combines burrow's solution with acetic acid and provides both an astringent/drying and antibacterial activity. There are a number of products with combination of ingredients for cleaning such as propylene glycol, lanolin, glycerin, lactic acid, parametaxylenol and different drying agentsand pH adjusters (acetic, malic, ascorbic or other weak organic acid. Many of these products can be used for the maintenance treatment of chronic cases but may not be effective in the initial treatment because of lack of antiinflammatory ingredients such as glucocorticoids. Some may contain alcohol which aggrevates an aready irritated ear.

Some Otic Cleansing Products

DrugManufacturerActive Ingredients
Adams pan-oticPfizeralcohol, aloe vera, diasolidinyl urea, methylparaben, propylparaben, DSS, octoxyl, sodium laurel sulfate, para- chlorometaxylenol, PPG
CerulyticAllerdermbenzyl alcohol, butylated hydroxytoluene, Propylene glycoldicaprylate/dicaprate base
CerumeneEvscoCerumene (Squalene) in isopropyl myristate
CleaRxDVM Pharm.DSS, urea peroxide
DermaPet CleanserDermaPetacetic acid, boric acid with surfactants
Ear-Oxide CleanerTomlyncarbamide peroxide
Epiotic Ear CleanerAllerdermlactic acid, salicylic acid, chitosanide, parachlorometaxylenol, PPG & sodium docusate

Treatment products for infectious and inflammatory conditions are also variable. Most of these products contain glucocorticoid which has a distinct advantage in the treatment of the inflamed ear canal/pinna. In addition antimicrobials (antibiotic(s) &/or antifungals) are usually added. The vehicle may be either an oil base or aqueous. Crusty or dry, scaly ears are best treated with an oil base where moist lesions are best treated with solutions. The use of creams or other occlusive medications should not be used in ears that are moist and exudative. Glucocorticoid containing products will result in systemic absorption. Liver enzyme elevations, adrenocortical suppression and inhibition of intradermal allergy testing results have been observed as a consequence of otic glucocorticoid therapy. Examination of product labels should be done routinely to recognize the type/concentration of steroid present. Excessive use of glucocoritcoid/antibitoic preparations can result in the superinfection by yeast.

Selected Therapeutic Otic Products

DrugManufacturerActive Ingredients
BaytrilBayerenrofloxacin injectable
Cipro HCBayerciprofloxacin HCl, hydrocortisone
CleaRx Drying Soln.DVM Pharm.acetic acid, colloidal sulfur, hydrocortisone
Coly-mycin S oticParke-Daviscolistin, neomycin, hydrocortisone acetate, thonzonium bromide, acetic acid
Conofite soln.Mallinckrodt1% miconazole nitrate
CortAstrinVedcoBurrow's soln., hydrocortisone & PPG
Cortisporin Otic Soln.Glaxco-Wellcomepolymyxin B, neomycin, hydrocortisone
Decadron Phosphate 1%Merckdexamethasone phosphate
Forte TopicalUpJohn/Pharmacianeomycin, penicillin G, polymyxin B, hydrocortisone acetate, hydrocortisone sodium succinate, chlorbutanol
Gentocin OticSchering-Ploughgentamycin, betamethasone
LiquichlorEvscochloramphenicol, prednisolone, tetracaine, Squalene
LotrisoneSchering-Ploughclotrimazole, betamethasone
Miconazole SprayEvsco2% miconazole nitrate
NeoPredefUpJohn/Pharmaciaisoflupredone acetate, neomycin, lanolin, mineral oil, white petrolatum
OtomaxScherring-Ploughclotrimazole, gentamycin, betamethasone
PanalogSolvaynystatin, neomycin, thiostrepton
Silvadene CremeMarionsilver sulfadiazine
SynoticFt. Dodgefluocinolone & DMSO
TresadermMerialthiabendazole, dexamethasone, neomycin
Tobradex OphthalmicAlcontobramycin
TicarSmith-Kline Beachamticarcillin 1 gram; mix with 2 ml of water to reconstitute then add 5 ml to 15 ml saline
Tri- OticMed-Pharmexgentamycin, betamethasone, clotrimazole triamcinolone
TriTopUpJohn/Pharmaciaisoflupredone acetate, neomycin, tetracaine HCl

Antibiotics used in otic preparations are quite variable. There is a tendency of many clinicians to utilize those with the greatest amount of antibiotic potential, such as aminoglycocides without trying more conservative approach first. Aminoglycides may actually cause ototoxicity and should not be used extensively. Common antibiotics used include: chloramphenicol, neomycin, polymyxin B & gentamycin. Systemic antibiotics are usually reserved for cases of confirmed or suspected otitis media or interna and are usually required for a prolonged period. Total regimens have required 45-90 consecutive days or longer. Determination of treatment endpoint may be very difficult even with the most sophisticated methods. Antifungal drugs are most important in the control of Malassezia pachdermatis or Candida species. The infection of dermatophytes may occassionaly involve the pinnae or the canal.

Compounding Otic Medications

Compounding otic mediactions is a common practice and is often helpful to get resolution of the perpetuating infectious agents present in the otitis externa. There are many formulations that are currently in vogue and this list is not meant to be a treatise on all the versions but to represent several that have been helpful in routine therapy.

Malassezia otitis: There are several products available that are manufactured for this condition but I have found a compounded otic solution to be more precise in the treatment and provide better results. Miconazole nitrate is a very effective antifungal and is available in two products useful in making formulations. Conofite is a 1% soution whereas Miconazole Spray (Evsco) is a 2%. Compounding either with a vehicle or other solution in a 1:1 ratio provides a very effective treatment. EpiOtic (Allerderm/Virbac) provides a good base for the combination of either miconazole solutions. The use of CortAstrin (Vedco) adds the additional enhancement of hydrocortisone and Burrow's solution. Some use Conofite directly but limits the volume available to treat with. The spray may also be used for application to the inside of the pinnae which usually have demonstrable lesions of malassezia and is important to include in the treatment. Yet another formulation uses 5 ml of epiotic, 2 mls of miconazole spray and 2 mls of dexamethasone (2mg/ml).

Gram Negative bacterial otitis: Fluroquinolones are commonly compounded for this problem usually incorporating injectable enrofloxacin. One simple formulation consists of 6.6 ms of Baytril with 23.4 ml of water or propylene glycol to make a .5 % solution. Another formulation uses 6.6 cc of Baytril with 15-20 ml of propylene glycol and a 30 gram tube of clotrimazole for combined antibiotic and antifungal properties. Another formula includes 2 ml of enrofloxacin, 12 ml of an acetic acid/boric acid ear cleanser with 6 mg. of dexamethasone.

The use of TrisEDTA is always helpful as a pre-rinse before the administration of antimicrobials to enhance their efficacy when dealing with a gram negative organisms. This product is commercially available and can be purchased from compounding pharmacies in 500 ml or liter quantities.

Silver sulfadiazine (Silvadene) has shown both in vivo & in vitro efficacy against Pseudomonas aeroginosa and may be mixed with water in a 1:1 ratio or up to a 1:10 ratio.


Diagnosis and treatment of ear disease can be a real challenge particularly if the condition has been chronic. The following basic principles should be used.

  1. Look for an underlying or co-existent problem in all cases of chronic recurrent otitis.
  2. Thoroughly clean and dry the ear canal before commencing therapy.
  3. Topical therapy should be used; systemic therapy is usually only used in otitis media/interna cases.
  4. Treat specific otitic diseases with appropriate medication based on etiological considerations. Always base therapy upon results of otic smears
  5. Treat or eliminate predisposing or perpetuating factors when possible.

Reevaluations are key to success. Initially plan on weekly revisits with smears for microscopic evaluation and cleaning of the ears (sedation will often be necessary for optimal cleaning). Home rinses may be used in the event that cleansing cannot be performed in the clinic. Most treatment should be performed twice to three times daily for a minimum of two weeks. More protracted therapy may be needed. Consider the use of systemic antimicrobials if otitis media is present or suspected. Systemic glucocorticoids may be helpful to reduce some of the inflammation and discomfort of the problem. Prednisone or prednisolone are preferred as an oral therapy on a daily basis for 7-14 days with the initial dosage for the first week at 1.5 mg/kg and then 1.0 mg/kg.

The best choice for chronic pseudomonas infection is Polymyxin B or silversulfadiazine although enrofloxacin may have appropriate efficacy. Repeated cultures may be necessary if persistence of Gram negative bacteria persist on the otic smears.

Recognition of underlying disease is often overlooked with the result of major surgical expenses and persistence of the otitis externa. Many conditions will not be cured. Maintenance therapy may be necessary. Home flushing can be helpful especially for cases with ceruminous otitis externa, keratinization defects or allergic diseases. Proper instruction and determination of intact tympanum are essential. Reduction of the inflammation and discomfort is usually necessary before the owner will be able to utilize the flushing procedure. Flushing is best done at bath time. Many of the products that have mild cleaning activity but are predominantly used for acidifying the ear canal work well as a maintenance regimen for routine use.

Some Home Maintenance Ear Products

DrugManufacturerActive Ingredients
Aloacetic Ear RinseDVM Pharm.acetic acid, methylparaben, DMDM hydantoin, aloe vera
BurOticAllerdermPPG, Burrow's soln., acetic acid
DermaPet CleanserDermaPetacetic acid, boric acid with surfactants
Gent-L-ClensSchering-Ploughlactic acid, salicylic acid, PPG & PCMX
OtiCalmDVM Pharm.benzoic acid, malic acid, salicylic acid, oil of eucalyptus
Otic ClearButleralcohol, PPG, glycerine, salicylic acid, lanolin oil, lidocaine Hcl, boric acid, acetic acid
OticlensPfizerPPG, malic acid, benzoic acid & salicylic acid
OtiRinseDVM Pharm.PPG, DSS, glycerin, salicylic acid, lactic acid, benzoic acid, benzyl alcohol, aloe vera
OtiFoamDVM Pharm.cocaminidopropyl betaine, salicylic acid, oil of eucalyptus

Surgical therapy should be reserved for cases that have significant conformational changes to their ear canal or requires exposure for more appropriate medical therapy. An aggressive medical approach should always precede the decision for surgery.

Selected Skin Infections: Pyoderma & Dermatophytosis

Factors Related to Pyoderma

In general, canine pyodermas are secondary. Factors that are probably involved with the development or recurrence/perpetuation of the infection are multifactorial. They include the following: 1. the bacterial characteristics and pathogenic properties 2. the underlying disease and its relationship towards decreasing the protective mechanisms of the skin and the permissive effects on host defense 3. the inflammatory response (or lack of) by the host. The identification of the underlying/predisposing disease(s) become a predominant focus point in the treatment of the clinical case since this is an area of major concern in the evolvement of the disease but also it is one of the few areas we can do sometihing about. Changing the bacterial characteristics is not possible and modifying the howt response has proven to be of little value leaving the underlying disease(s) the most logical emphasis although the problem may not always be easily determined and in some cases cannot be identified.

In the southeastern United States (and other geographic regions) pruritic, allergic dermatitis is the most common predisposing factor. Atopy, flea allergy, food allergy and less commonly allergic contact allergy are represented. This is further complicataed by the length of coat, amount of oiliness, scaliness or crusts (seborrhea) and the pets habits (environmental factors). Other disease considerations include ectoparasites (demodex, scabies, cheyletiella, fleas, etc.), and endocrinopathies (hypothyrodism, hyperglucocorticoidism or sex hormone disturbance), metabolic abnormalities (keratnization defects, idiopathic seborrheic dermatitis), hair follicle dysplasias and immunological incompetencies. A major predisposing factor of recurrent pyoderma in the dog is the administration of glucocorticoid compounds, particularly when given chronically or when long acting products are used. Therapeutic failures are most often a result of incomplete recognition and treatment of underlying factors. A chronic relapsing pyoderma is most likely secondary. The most common reason for therapeutic ineffectiveness or chronic/recurrent pyodermas is a failure to eliminate or control predisposing factors or the inability to identify co-existing disease (idiopathic pyoderma).

Recognizing lesions associated with bacterial pyoderma

Active lesions"Footprint" lesions
Pustules"Moth eaten" alopecia
Papules"Epidermal collarettes"
ErythrodermaPost-inflammatory hyperpigmentation

Coat Association of Pyoderma Lesions

Short coat
Active lesions:

Papule (folliculitis)
Nodule (folliculitis/furunculosis)
Resolving lesion:
Multifocal alopecia
Long coat
Active lesions:

Erythemic macule
Resolving lesions:
hyperpigmented macule
"epidermal collarettes"

Etiologies of Pustules

Staphylococcal spp.
Pemphigus foliaceous
Subcorneal pustular dermatosis
Sterile eosinophilic pustulosis

Etiologies of Papules

Bacteria (staphylcoccus)
Mycotic (dermatophytosis)
Parasitic (demodicosis)
Flea allergy dermatitis
Food allergy
Contact dermatitis (allergic/irritant)
Cutaenous drug reaction (erythema multiforme)
Pemphigus foliaceous
Cutaneous malassezia

Distribution Patterns

Axilla & inguinal regions
Extremities (pressure points)
Tailhead region
Nasal region

Most Common Underlying Diseases

Pruritic PyodermaNon-pruritic Pyoderma
Flea allergyCushing's syndrome
Food allergyCornification disorders
Scabies(primary or secondary)

Primary folliculopathies

Endocrine Dysfunctions Associated With Recurrent Pyoderma
Hyperglucocorticoidsim (iatrogenic!)
Reproductive Hormone Imbalance

Diagnostic Procedures for Evaluating Pyoderma

All cases with lesions suggestive of bacterial pyoderma should be skin scraped for evidence of ectoparasites (demodicosis). Lesions with suspicion of cutaneous malassezia should be should be evaluated by microscopic inspection of specimens obtained from the surface of the skin for the presence of yeast. Pustules should be evaluated by microscopic inspection of the pus carefully obtained from the lesion placed on a microscopic slide and stained. Bacterial cultures are not routinely performed on superficial pyoderma but may be indicated in the evaluation of deep pyoderma. Bacterial cultures should never be obtained without performing susceptability testing. Cultures are best acquired from unruptured pustule or hemorrhagic bullae. Biopsies may be indicated for further histopathologic evaluation of antibiotic refractory or recurrent pyoderma.


Specific therapy should be directed at treating the underlying disease(s) in addition to systemic antibiotics. Antibiotics chosen for the management of canine pyodermas should have a known spectrum of activity against S. intermedius. Selection on the basis of cidal versus static activity is not as important as once postulated. In situations of known immune incompetency, bactericidal antibiotics should be used. Antibiotics that should never be used include penicillin, ampicillin, amoxicillin, tetracycline and sulfa drugs without trimethoprim potentiation. All antibiotics should be dosed on the basis of actual body weight determination. Antibiotics should be administered for a minimum of 21-30 consecutive days or 10 days beyond apparent remission. Deep pyodermas may require 8-12 weeks or even longer. Pyogranulomatous lesions (acral lick dermatitis) have taken as long as 4-6 months of continuous antibiotic treatment. It is not necessary to change antibiotics if they are still effective. One should watch for discrepency between in vivo responsiveness and in vitro susceptability. It is the response of the tissue dwelling bacteria that is significant in the treatment process not those on the culture plate. Antibiotic responsiveness will change. Recognition of resistance patterns is essential. Proper dosing may make the difference between response and failure. Enrofloxacin, for example, had the perception of being only partially effective in staphylococcal pyoderma at 2.5 mg/kg but has demonstrated excellent efficacy at 5 mg/kg.

Problems associated with antibiotic therapy:

The response is obviously predicated on the proper identification of a bacterial pyoderma realizing there are a number of non-bacterial and non-septic conditions that will mimic the clinical appearance of pyoderma. Co-existing or underlying diseases will effect the responsiveness to antibiotic therapy but are more likely to have the most dramatic influence on the relapse rate and remission interval. Recurrence of the pyoderma may be observed within several days of the cessation of antibiotic therapy. The effectiveness of an antibiotic is related to the previous use of that particular antibiotic and the chronicity of the problem and therapy. "First round" antibiotics such as used early in the treatement regimen (lincomycin, clindamycin, clavuanic acid potentiated amoxicillin, potentiated sulfas, etc.) May have limited or minimal effect on the chronic case typically seen at a dermatology referral clinic. Increased observaations of refractoriness of the pyoderma to antibiotics previously considered the "second round" or the highly effective drugs (cephalosporins) are being reported. Seeking an alternative in these in these instances may be more difficult and predictably more expensive, The use of cephalosporins has conventionally been used in the event of failure recognized with more conservative antibiotics. Failure of cehpalexin leaves in fewer realistc choices. Administration of enrofloxacin has become a routine approach in instances of perceived cephalexin failure. It is critical, however to use the effective dose of 5 mg/kg qd (once daily).

Initial Troubleshooting the Relapsing Pyoderma

The following questions should represent a check list for evaluation of the dog with chronic recurrent pyoderma. Was the proper antibiotic selected? Was the drug dosed & administered properly? Was the animal reevaluated during treatment to determine the end point? Was the antibiotic used for sufficient duration? Were skin scrapings acquired? Was the animal pruritic and did the pruritus persist after the pyoderma had cleared? The approach to the clinical management of these cases include several objectives. The first is to acquire a detailed history and perform a com;ete clinical examination to lead toward the development of a differential diagnosis and diagnostic plan for the underlying disease as well as the symptoms of the pyoderma. The second is to formulate a plan to treat the underlying disease and also eliminate the current active infection. The final objective is to develop a plan that will reduce the recurrence of the pyoderma until the underlying/predisposing factors can be maximally controlled.

Antibiotics used for the Treatment of Pyoderma in the Dog

Antibiotic choices for first-occurrence pyoderma:

Amoxicillin trihydrate with clavulanate potassium14-22 mg /kg bid
Lincomycin22 mg/kg bid
Trimethoprim-sulfadiazine or
trimethopirm sulfamethoxizole
20-30 mg/kg qd-bid
Erythromycin10-15 mg/kg tid

Antibiotic choices for refractory, recurrent or resistant pyoderma:

Ormetoprim-sulfadimethoxine28 mg/kg qd
22 mg/kg tid or 33 mg/kg bid
22 - 33 mg/kg bid
22 mg/kg bid
Clindamycin5.5-11.0 mg/kg bid
Oxacillin22 mg/kg tid
Superficial pyoderma
5 mg/kg qd - bid
Deep pyoderma/otitis
10 - 20 mg/kg qd
Orbifloxacin2.5 - 7.5 mg/kg bid
Marbofloxacin2.5 mg/kg bid
Ciprofloxacin5.0 - 20.0 mg/kg bid

Failure of antibiotic therapy should be followed by more aggressive diagnostics and attempt to discover underlying or co-existing diseases. Treat for the Staphylococcus organisms when a mixed culture is obtained even at the exclusion of some gram negatives. Many times it will result in resolution of opportunistic bacteria since they appear to be somewhat dependent upon the favorable environment created by staphylococcus organism.

Treatment of the chronic relapsing case may result in the utilization of combined therapy or more aggressive treatment techniques. Among the options include chronic use of antibiotics, pulse therapy, sub-inhibitory antibiotic therapy and immunotherapy. Persistent use of antibiotics is tolerated well by most dogs but poses heavy financial burdens to the owner. Gastrointestinal disorders may occur. Cutaneous malassezia has been a concern as a sequela to antibiotic therapy although recent observations do not support this.

Maintenance Antibiotic Therapy

An alternative to continuous antibiotic therapy is to use intermittent therapy (pulse treatment). Selection of a proven antibiotic is used intermittently (eg. One week on followed by one week off; then one week on followed by two weeks off, one week on three weeks off, etc.). This may reduce the chance of relapse and control the pyoderma so it does not reach a level of clinical significance. Another alternative is sub-optimal therapy which utilizes a chronic regimen (daily therapy) but uses an altered dosage/frequency schedule than routinely employed. Cephalexin used at a low dose once daily would be an example. Enrofloxacin has also been used in pulse treatment protocol for prolonged intervals.

The predominant factors associated with the outcome of antibiotic therapy include:

  1. Proper diagnosis
  2. Recognition of co-existing or underlying conditions
  3. The choice of antibiotic used
  4. Adequate dosage
  5. Frequency of administration
  6. Duration of treatment

Immunotherapy has limited efficacy in most cases. It is usually selected as an option for the "last chance case".

Some Immunomodulating Drugs

Levamisole2.2mg/kg TID
Thiabendazole (MintezolR)5 - 10 mg/kg. TID
Nizoral10 - 15 mg/kg QD
Cimetadine6- 8 mg/kg TID
Hydroxyzine2.2 mg/kg BID

Two products most often used are Staph Phage Lysate and Immunoregulin. The first is more specific since it is derived from staphylococcus bacteria while the latter is a bacterial cell antigen (Propionibacterium acnes) that provides non-specific immunoenhancement. A major reason why neither of these products are more effective may be the normal immunoresponsiveness of most dogs with pyodermas.

Staphylococcus Aureus Phage Lysate (SPL) is a bacteriologically sterile staphylococcal vaccine for use as a therapeutic aid in the treatment of recurrent staphyloccal pyodermas or staphylococcal hypersensitivities. There are a variety of protocols used. The following are three representations.

1. Most often a subcutaneous injection of 0.5 ml is administered twice weekly (every 3-4 days) for 10-18 weeks then decreased to every 2-4 weeks for maintenance (usually .75-1.0 ml every 14-21 days). Larger dogs >50 -60 pounds may be treated with 1.0-2.0 ml. Staphage Lysate may be purchased from: Delmont Laboratories, Swarthmore, PA

Miscellaneous Therapy for the Chronic Relapsing Pyoderma

Routine shampooing may be very helpful in the control of a chronic relapsing pyoderma. The use of chlorhexidine, benzoyl peroxide or ethyl lactate containing shampoos are recommended. The choice is somewhat empirical and based on factors such as breed and extent of dryness of the skin. Moisturizing shampoos may also be used. In dogs with greater greasiness (e.g. cocker spaniel) a more potent degreasing agent such as a tar shampoo may be useful. Weekly bathing as a preventative has demonstrated usefulness in avoiding ( most likely postponing) the relapsing pyoderma.

Avoidance of glucocorticoid therapy is an important objective in the management of the chronic recurrent pyoderma. Use of nonsteroidal topicals and systemics should be included in the management of the allergic animal. Essential fatty acids and antihistamines are advocated even if their individual effect does not eliminate the pruritus.


Dermatophytosis is an infectious disease caused by a fungal agent that effects the keratin of the epidermis and the hair follicle. The most common genera of organisms are Microsporum and Trichophyton. Microsporum canis is the most common caus of dermatophytosis in the dog and the cat. Although exposure to the infective arthospores of the fungal element may lead to an active infection, normal host defenses often will prevent the establishment of clinical disease. A number of factors may come into play during this process. It is well recognized that the immaturity of the host immune system in the neonate or juvenile may play a prominent role in the susceptibility of infection in the young animal. The ability of the host to mount an inflammatory response is critical to the course of the infection. Asymptomatic carrier states of M. Canis is well recognized and demonstrates the balance between host and potential pathogen. Suppression of immunomechanisms may also lead to infection or be associated with chronic persistent disease. Conditions such as feline leukemia virus infection, FIV or neoplasia may be underlying reasons. Chronic or aggressive steroid therapy has been associated with protracted disease in some situations.

Clinical signs of dermatophytosis may be variable depending upon the extent of host response. The classical lesion is the one characterized as a circumscribed, circular alopecic, erythemic macule or patch with superficial scale. Although the classical "ringworm" lesion may be caused by a dermatophyte, it is most often associated with bacterial pyoderma. Dermatophytosis results in folliculitis and is one of the three main causes (staphylococcal folliculitis & demodicosis are the others) often associated with papular dermatitis particularly in the short coated dog. Folliculitis may progress to furunculosis resulting in a fibrosing pyogranulomatous dermatitis. Cicatricial alopecia may be the consequence of the deeper inflammation and destruction of the hair follicle. Nodular dermatitis may be seen in the dog with a kerion reaction or in the cat with pseudomycetomas or Majochii's granuloma. Cats tend to have more variability in lesions associated with dermatophytosis. Miliary dermatitis conveys a mandatory rule out of dermatophytosis although there are other diseases more commonly seen with that presentation. Cats tend to be more pruritic than dogs with dermatophytosis and may be a major cause of persistent self mutilation with generalized or regionalized lesions. Misdiagnosis under these circumstances may be common as they are often confused with allergic dermatitis.

The diagnosis of dermatophytosis is best accomplished by dermatophyte test medium culture. Inoculation of scale an hair from affected lesions will usually be positive within 3-15 days. Some organisims may be slow growers (Trichophyton spp.). Colony morphology and other characteristics should be determined in addition to color change of the medium. False positives are often associated with saprophytic fungal growth and the accompanying color change when the medium has aged and there is colony overgrowth. The reader is referred to other resources for information that is beyond the scope limited by the length of the proceeding notes. Wood's lamp examination may be used but is not reliable in many cases and should not be used for diagnostic confirmation. The inclusion of biopsy should be performed in the event of negative culture findings in the face of lesions with high suspect or in the event of a nodular dermatitis with other major differentials where dermatohistopathology may be helpful. The MacKenzie brush technique is often helpful in cases where there are minimal lesions as in the asymptomatic carrier or to reevaluate by fungal culture during the treatment of a case. This procedure uses a new or sterile toothbrush which has been used to groom the animal. The bristles are pushed slightly down into the media and existing scale and hair removed.

Treatment: Systemic treatment is the treatment of choice to efficiently resolve the active infection. It should be noted however in mature dogs with concurrent dermatopathies, spontaneous resolution will occur if the co-existing/underlying problem is alleviated. Topical therapy has limitations as the only treatment although it is often included as adjunctive therapy for decontamination of the infected hair/skin. Topical therapy will not reach the deeper follicles potentially containing infective agents and it isn't always possible to recognize the borders of the infective lesions. Lime sulfur, 4oz/gal, (LymDyp, DVM Pharmaceuticals, Inc.) Appears to be the most effective topical available. Miconazole nitrate shampoos are also available (Dermazole, Allerderm-Virbac; Miconazole Shampoo, Evsco) for adjunctive use to decontaminate the animal. Zoonotic significance of this disease should not be overlooked.

Conventional systemic therapy for dermatophytosis is griseofulvin, a fungistatic drug with excellent binding properties to the keratin and accumulation in the keratinocytes. The dosage is variable and depends on the particle size and whether it is formulated for enhanced absorption with polyethelene glycol (PEG). Dosage of the microsize formulation (Fulvicin V/F, Schering/ Plough) is 25-50 mg/kg/day. The ultramicrosize combined with PEG is 5-10 mg/kg/day (Gris-PEG, Allergan). Dosages may be divided into a bid regime and should be administered with a fatty meal to enhance absorption. Due to the terratogenicity of the drug, it should not be used in a pergnant or breeding female. Other side effects include vomiting, diarrhea, & anorexia. An idiosyncratic reaction in FIV positive cats results in irreversible myelosuppression which is often fatal. Use in cats should include screening tests for FIV & FeLV and cautious monitoring during therapy. Other alternatives should be considered.

Ketoconazole (Nizoral, Janssen) is an alternative to be considered for use in the dog although it should be eliminated from feline therapy because of adverse reactions. Ketoconazole is an imidazole and should be dosed at 5mg/kg bid or 10 mg/kg once daily. Antacids and H2 blockers should be avoided and it should be mediated with a meal to enhance absorption. Side effects most commonly seen is inappetence and depression. Lower dosage may help alleviate some of the symptoms. Monitoring liver enzymes should be considered particularly if systemic signs of intolerance is observed. Ketoconazole may have limited activity in some cases of dermatophytosis.

Itraconazole (Sopranox, Janssen) is a triazole that is better tolerated than ketoconazole though more expensive. It appears to have a faster cure time than griseofulvin and much safer. As with ketoconazole, itraconazole can be hepatotoxic and at higher dosages may be teratogenic. Itraconazole is available in only 100 mg size capsules but can easily be compounded for use in smaller animals. The dosage is 10mg/kg once daily although doses of 2.5mg/kg and 5.0 mg/kg have demonstrted efficacy.

Terbinafine (Lamisil) is a recent systemic antifungal which may be safer than ketoconazole or even itraconazole. The dosage is 10-30 mg/kg every 24 hours. Treatment principles are same for other systemic antifungals. ALT & SAP should be monitored in situations of chronic therapy (6-8 weeks or greater). Although this drug may be hepatotoxic it is used in human medicine with less concern compared to ketoconazole & itraconazole. More common adversities include vomiting, inappetence & lethargy often times without abnormal blood parameters. This drug provides another option for systemic antifungal therapy.

Fungal vaccine is commercially prepared and introduced as Fel-o-Vax MC-K by Fort Dodge. This vacine is intended to be used as an adjunct to treatment rather than a prophylaxis. It will improve the resolution of dermatophytic lesions although it will not eliminate the infection. It may be helpful to decrease the environmental contamination. Side effects include sterile abscess at the injection site but otherwise well tolerated. Over expectation of this form of treatment should be emphasized.

© 2000 John M. MacDonald, DVM - All rights reserved