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Canine and Feline Dermatology and Otology Rod A. W. Rosychuk, DVM, DACVIM Colorado State University Diagnostic Techniques in Dermatology: An Update Dermatology can be frustrating! Part of the dilemma is the fact that many skin diseases look alike. As a result, we routinely perform certain diagnostics on each case. Although we are all quite familiar with many of these tests, it may be of value to not only review some of the "basics", with emphasis on maximizing their benefit, but also to provide a few new "twists" that will be additions to your diagnostic armamentarium. Tips for the evaluation of ectoparasites:
The importance of Malassezia in the pathogenesis of several skin disorders in the dog is now well known (e.g. atopy, food sensitivity, seborrheic disorders). More recently, it has also been noted as a complicating factor in various feline dermatoses (e.g. atopy, food sensitivity). There are many techniques used to document the presence of Malassezia. In our clinic, scrapings, impression smears, swabs and tape impressions are all used with equal frequency but in different scenarios. Superficial scrapings are used on inflamed areas that may have a fair amount of oily/waxy debris (inter-digital spaces, inguinal regions, anterior elbows). Material is squashed on the slide (bread and butter -like application) heat fixed for 2-3 seconds, then stained with Diff Quick. Dry cotton swabs work well in areas that are more difficult to get to (crevices in inter-digital spaces, perivulvar folds, lip folds). The swab is rubbed in the affected area, then rolled on the slide. Impression smears with a slide are best used in an area that is quite oily/waxy and reasonably flat (e.g. inter-digital spaces of larger feet; inguinal area, peri-anal area). The slide should be firmly pressed against the skin; several imprints of the same area are often recommended. Acetate tape preparations are best used when the area is drier (not waxy). It is also a quick, well tolerated procedure that can be done on difficult to restrain individuals. A section of tape just a little shorter than the length of the clear portion of the slide is used. The tape is pressed firmly and repeatedly on the surface of the area examined (e.g. inter-digital spaces, inguinal regions); a drop of Diff Quick is then placed on the slide and the tape is laid over this. The stain is then distributed over the length of the tape by placing pressure on the tape; excess stain is removed by compressing a blotter (e.g. absorbent paper towel) over the slide. Tape preparations do appear to be more difficult to read. This is especially true when evaluating for the presence of bactreria in that they may be difficult to differentiate from debris. In the author's experience, this technique also does not yield as many organisms as other techniques might (with the exception of dryer areas wherein it appears to have an advantage over other techniques). Interpretation of numbers of Malassezia is controversial. In that individuals may develop a hypersensitivity to Malassezia, relatively small numbers may be problematic. Therefore, if 1 or 2 Malssezia per oil immersion field are seen, and the clinical signs suggest that Malassezia may be contributory (inflammation in a an area predisposed to Malassezia; lichenification), then trial treatment for Malssezia should be performed. Diagnostics for Dermatophytes Wood's Lamp Examination: The Wood's lamp should be turned on for 5 - 10 minutes prior to use. Positive fluorescence is yellow-green in color. The hairs themselves should fluoresce. In that some waxy debris adherent to hairs may give the appearance of fluorescence, hairs may be plucked to see if the proximal part of the hair fluoresces. If the hair is infected with a dermatophyte, the proximal portion and root of the hair will fluoresce. If waxy debris is the source of suggestive fluorescence, its fluorescence will not extend lower than the skin surface. Suspected fluorescent hairs are also the best hairs to use when examining for the presence of arthrospores. Recall that only 30 - 40% of M. canis samples will fluoresce. Other dermatophytes will not fluoresce. A positive fluorescence is highly suggestive of dermatophytosis, but negative results do not rule it out. Potassium Hydroxide / Mineral Oil Preparations: Although potassium hydroxide has classically been used to "clear" hair samples to facilitate the identification of arthrospores, we usually do this examination in mineral oil, without KOH. Hair samples are placed in a couple of drops of mineral oil and covered with a cover slip. Under the 10X or 40X lens we look for hairs that have abnormal contours (rotten log appearance) compared to normal hairs. Arthrospores or hyphae are usually seen with the 40X lens, but oil immersion may be necessary. Tip: practice your observational skills on dermatophyte infected hairs that fluoresce with the Woods lamp. These hairs usually have arthropsores that are more predictably observable. If a 20% KOH clearing solution is used, a few drops of KOH are applied to hairs on the slide and this is covered with a cover skip. The slide is read in about 5-20 minutes. Warming the slide will hasten the clearing and time to reading. Fungal Culture: Although there is not much new information regarding culturing for dermatophytes, a few points bear re-visiting. There are now several culture media available. Some have color indicators. These include DTM (Dermatophyte Test Medium; dermatophyte growth produces red color change), Rapid Sporulating Medium (dermatophyte growth produces blue-green color change). Recall that dermatophytes should produce media color change within 24 hours after colony growth. They do this by metabolizing proteins in the media to alkaline by-products which mediate the color change. Saprophytes may also change the media color, but it takes several days after colony growth is noted. Saprophytes metabolize the carbohydrates in the media first, but after they exhaust this, they will then metabolize proteins to produce alkaline by products. We generally circle and date the area immediately over colony growth when it is first noted, to facilitate the interpretation of changes. Colony growth is usually noted within 10 days, although we monitor the media for 3 weeks. There have been some reports of dermatophytes that have not changed the media color. Ideally, all suspect dermatophyte colonies should be speciated to confirm their identification. Noting the type of dermatophyte may offer some epidemiologic insight into the source of the infection. Any colony that grows out white or buff colored should be speciated. Hyphae should be teased away from the colony and placed on a glass slide with a drop of lactophenol cotton blue. The preparation is examined for the characteristic macroconidia of the dermatophyte. Veterinary reference sources such as Scott's Small Animal Dermatology textbook can be used to help in the identification. Colonies have to be quite mature (i.e. 7-10days) before producing macronidia. If these structures are not seen initially, the speciation attempt should be repeated every 2-3 days. Although RSM (rapid sporulating media) has been marketed to enhance sporulation, this has not been proven in one study. Other media available for diagnostic purposes do not have a color indicator included. An example is Mycotec (sabouraud's dextrose). It provides for the development of the classical pigmented colony color and morphology of fungal species. It also provides for more rapid sporulation and the development of macroconidia. In our laboratory, we use Derm-Duets from Bacti-lab, PO Box 1179, Mountain View, California 04042, 1-8000-227-7300 (DTM and RSM - rapid sporulating media) or Sab-Duet (DTM and Mycotec agar). Especially in suspected asymptomatic carrier cats or cats who are on therapy and being re-cultured, sample collection can be facilitated by toothbrush collection. The toothbrush is combed through the coat, gathering up as much hair and debris as possible. The toothbrush is then impressed on the culture media surface or, alternatively, hair and debris is removed from the tines on to the culture media. Cytologic Examination Cytologic examination should be considered in any case wherein one is trying to establish a cause for pustules, erosions, ulcers, draining tracts, plaques, papules, nodules or tumors. Collection techniques include fine needle aspirates, surface impression smears, impression smears of cut surfaces or lanced pustules or papules. Tip: cytologic sample collection for impression smears can often be facilitated by "squeezing" the skin to facilitate exudation. Samples may be distributed over the slide by doing non-traumatic "squash" preparations or brush cytology. In brush cytology, the sample is placed on a clean glass slide and then spread out using a camel hair brush. The brush is then rinsed well and dried for future use. This technique gives single cell layer distribution on the slide, with a minimum of trauma to the sample. Staining is usually done with modified-Wrights stain (Diff-Quck Stain). These slides can be catalogued and used for future reference/teaching etc. Supra-vital stains such as New Methylene Blue are also easy and rapid. Cytologic examination of debris taken from ears should be performed in each examination and re-examination of patients with otitis externa. Material is usually collected by placing a swab down in to the ear as far as it goes comfortably (usually the junction of the horizontal and vertical canal). Debris is then rolled out on a slide and the slide is heat fixed (match or lighter under slide for 2-3 seconds). The slide is then stained with Diff-Quick and examined under 10X, 40X and then oil immersion. Samples are examined primarily for bacteria, Malassezia and neutrophils. A record of relative numbers should be established (e.g. use a scale of 1+ - 4+ with 1+ being a little more than normal, 4+ being full fields of organisms). The observation of an occasional bacterium or Malassezia per oil immersion field would be considered normal. Cytologic examination of debris taken from anal sacs is primarily done to document the presence of anal sacculitis. Debris expressed from the anal sac is placed on a slide and then "squash" prepped and stained with Diff-Quick. The sample is examined under oil immersion. Normal anal sacs should contain pleomorphic bacteria, epithelial debris, and some amorphous, bluish material that often appears about white blood cell size, but has indistinct borders and no nucleus. Patients with anal sacculitis will have large numbers of neutrophils or neutrophils and eosinophils. In some samples, eosinophils may predominate. Trichography Hairs are pulled with the fingers or very carefully with forceps (to minimize trauma to the hairs), placed in mineral oil on a slide and examined under low power. Broken hairs suggest self inflicted alopecia or dermatophytosis, large melanin clumps in hairs may suggest color dilution alopecia, large numbers telogenized hairs (club or spear-shaped) versus anagen hairs (bulbs are rounded, smooth, root is often bent because it is soft) may suggest telogen defluxion or an endocrine disturbance. Hairs that are inappropriately curled, misshapen and malformed suggest nutritional or metabolic disease. Bacterial Culture and Susceptibility Testing: Bacterial C+S testing should be considered in any skin lesion (pustules, abscess, cellulitis, deep or superficial pyoderma or acral lick dermatitis) for which bacteria are considered a differential diagnosis but response to appropriate antibiotic therapy is lacking or any of those suspect bacterial problems which are severe and warrant an accurate antibiotic choice for initial therapy (e.g. severe deep pyoderma in a patient with severe, generalized demodicosis). Ideally, samples should be collected from unbroken pustules, by needle aspirates, or by biopsy (submitting sections of skin for culture). Every attempt should be made to minimize surface contamination of samples. Unbroken pustules are not prepped to prevent false negative cultures. Samples to be taken by biopsy are not cleaned prior to biopsy. Once the sample has been harvested (e.g. 4 mm punch biopsy), the very superficial surface of the sample can be trimmed away with a sharp scalpel blade (to minimize surface contamination). Deep, draining tracts may also be cultured by surgically preparing the surface of the lesion, drying this surface well, then squeezing the tissues and culturing exudates from deeper within the tissue. It has been recently shown that epidermal collarettes (manifestation of superficial bacterial pyoderma) can be cultured by rolling a dry swab over the collarette area 3-4 times (to be considered as an alternative to culturing from unbroken pustules or taking samples by skin biopsy). Skin Biopsies
Atopy is defined as the heritable predisposition to the production of IgE (reaginic antibody) to otherwise ordinary environmental substances such as pollens, molds and house dust mites. It has been hypothesized that atopic individuals tend to produce a T helper 2 cell response to allegens. The Th2 cells produce cytokines which stimulate B cells to produce IgE. In contrast, nonatopic individuals tend to have a Th1 response to environmental allergens. These cells produce cytokines that suppress the proliferation and function of the allergy-promoting Th2 cells, thereby inhibiting IgE production. Allergen exposure is thought to occur both through the respiratory tract and through transcutaneous absorption of allergens. With transcutaneous absorption, epidermal Langerhans cells trap and present allergen to T- lymphocytes which subsequently migrate to regional lymph nodes to culminate in the production of allergen specific IgE (and possibily IgGd) from B lymphocytes. IgE then binds to cutaneous mast cells. Subsequent exposure to allergen (e.g. cutaneous exposure) results in binding of this antigen to IgE, mast cell degranulation and the release of mediators of pruritus and inflammation (e.g. proteolytic enzymes, leukotrienes, prostaglandins, serotonin etc.). The influx of inflammatory cells results in the release of cytokines which may perpetuate inflammation for hours or days after allergen exposure. In human atopy, it is now thought that the disease may also eventually involve an autoimmune component wherein, due to molecular mimicry, IgE is sensitized to self proteins. Incidence: Atopy is thought to affect as many as 15% of the canine population in the U.S. . There is strong breed predilection (e.g. Golden retriever, Labrador retriever, Cocker spaniel, Shar pei, Dalmation, Boxer, Terriers (WHW, Yorkshire, Cairn, Scottish, Wirehaired, Boston), Pug, Irish Setter, Chihuahua, English Bulldog, Lhasa Apso, Miniature Schnauzer, German Shepherd). Although heritability has been strongly suspected for years, it has only recently been confirmed in Labrador and Golden Retrievers (Shaw S et al, AJVR 2004), prompting the recommendation that affected individuals not be used for breeding purposes. Allergic to What? Pollens of weeds, trees, grasses, house dust mites, molds, feathers, animal danders (cat, horse, cow), insects, storage mites (Tyrophagus putrescentiae, Leipidogyphus destructor, Acarus siro), human dander? History and Clinical Signs:
Intradermal testing or serologic testing for atopy are primarily performed to formulate solutions for hyposensitization. They may also provide data to allow for avoidance from some allergens. Due to the potential for both false positives and negatives, these diagnostics should only be performed in patients who are highly suspect to be atopic. Intradermal testing appears to provide more specific data than serologic testing (less false positives). With-drawl times for various medications prior to testing include two weeks for antihistamines, 4-6 weeks for oral glucocorticoids, 8 weeks for "depo" steroids (keeping in mind that with longer term, higher dosage therapy, with- drawl times may be much longer than these) and two to three weeks from relatively short term topical glucocorticoids. Although the author also recommends a two week with-drawl from fatty acid therapy, this point is controversial. It is important to note that "false" negative tests may occur in as many as 20 - 30% of cases. These negatives may be a product of previous medications, off season testing (testing more than two months after the end of the season) and inherent host factors (estrus, pseudopregnancy, stress). In atopics with severe clinical signs it has been suggested that anergy occurs with excessive mast cell degranulation, and that no additional degranulation can be triggered with the skin test injections, giving a false negative result. In man, it is also noted that as many as 20% of atopics will be negative on both skin tests and in vitro serologic testing. These individuals have been said to suffer from "intrinsic" atopy (vs extrinsic atopy) wherein their atopy involves an inherent abnormality in their immunologic responses which are devoid of extrinsic factor influences (allergen exposure etc). In vitro serology is considered less specific than intradermal testing, but is still a reasonable alternative to IDT. Both false positives and/or false negatives may be a trait of any given test. Antihistamines or fatty acids need not be discontinued for this testing. With-drawl times for oral glucocorticoids are controversial and may vary with the test. In general, a two to three week with-drawl time is recommended by the author. The Heska test, however, may require an even much longer with-drawl (weeks to months). It is interesting to note that the success rates of immunotherapy based on the results of IDT compared to those obtained using serologic tests are comparable in several studies (i.e. about 60% success). Some dermatologists are routinely doing both intradermal and serologic testing and utilizing the data from both in establishing hyposensitization protocols. This approach is rationalized on the basis that the two tests measure different things. IDT measures IgE in the skin while serology measures circulating IgE and a direct correlation may not exist between the two. Management of Recurrent Staphylococcal Infections
Glucocorticoids remain the most predictably effective therapies for the management of atopic pruritus and inflammation. Anti-inflammatory dosages are usually used initially (e.g. 0.5 - 1 m/kg/day of prednisone or prednisolone), with dosage tapering indicated by the severity and chronicity of skin changes, to minimize side effects and determine what the lowest dosages required to control symptoms. Glucocorticoids would be an acceptable method of management for shorter term atopic problems (e.g. 4-5 months of each year) - assuming patient tolerance. Alternatives to prednisone /prednisolone include metylprednisolone (reduce incidence of PU/PD) or Temaril-P (5 mg of trimeprazine, an antihistamine and 2 mg of prednisone per tab); may allow for lesser dosages of glucocorticoid because of the antihistamine included. Prior to considering glucocorticoids for longer term maintenance, every effort should be given to provide glucocorticoid alternatives. When this is not possible, the author will usually try to maintain the patient on the lowest, once every other day dose of Temaril-P possible. This is often facilitated by using Temaril-P along with a full, daily dose of another antihistamine such as chlorpheniramine, diphenhydramine, hydroxyzine, amitriptyline, or clemastine. This often allows one to minimize the dose of Temaril-P. Many large breed dogs may be maintained on 1-3 tabs once every other or third day. It is important, even at these low dosages to look for mild signs of iatrogenic hyperadrenocorticism (dry coat / skin; mild hair loss; gradual weight gain; increased propensity to develop bacterial pyoderma; increased propensity to develop urinary tract infections. Fatty Acids Although controversy still exists as to which fatty acids to use in optimizing anti-pruritic effects, products rich in n-3 fatty acids (cold water fish oils and flaxseed) appear to be favored. Using an n-3 fatty acid product (3 V Caps, DVM) at bottle dosages, significant improvement is seen in 10 - 15% of patients (10 - 90% improvement). A very small study showed superior antipruritic effects with very high dose omega 3 fatty acids (180 mg eicosapentaenoic (EPA)acid and 120 mg docosahexanoic acid (DHA) / 10 lb. body weight per day; Logas et al Vet Dermatology, 1994). A study recently completed at CSU appears to support this data. For those dogs receiving 50 - 85 mg/kg of EPA and 35 - 55 mg/kg DHA (equivalent to 1 Giant breed capsule per 5 kg body weight) or 200 - 335 mg/kg of flaxseed oil per day, 40 - 50% improved by greater than 50%. Complete remission was obtained in 10 - 20%. This suggests that higher dosages of omega 3 fatty acids should be used to initiate/assess therapy (e.g. 2-3 times the bottle dosages). Although it has been suggested that fatty acid containing products should be given at least a 12 week trial before they are critically evaluated, it was noted that most individuals had improved within the first 2-3 weeks of therapy in this study. Deleterious side effects are uncommon but include gastrointestinal upsets, increased pruritus and pancreatitis. Although high dose therapy could conceivably result in decreased neutrophil reactivity, decreased clotting and decreased wound healing, this has not been seen in clinical studies nor with clinical use. As fat supplements, it is not uncommon for these products to improve coat luster, softness etc., even though the degree of pruritus is not reduced. Research by Iams has shown that a 5:1 to 10:1 ratio of omega-6 to omega-3 fatty acid in the overall diet may be ideal for management of inflammatory skin disease in the dog. Their diet, formulated to meet these specifications is Eukanuba Veterinary Diets TM Response Formula FpTM for dogs. Our own uncontrolled studies evaluating the efficacy of this diet in 47 atopic dogs showed a greater than 50% reduction in pruritus in 42% of dogs Antihistamines Antihistamines appear to benefit about 20 -30% of our atopic patients. Both first generation H1 blockers (e.g. chlorpheniramine, diphenhydramine) and second generation products that fail to cross the blood brain barrier (e.g. loratidine, ceterizine) appear to have similar success rates. It is felt that one cannot predict which, if any antihistamine, will be of help in a given individual. We generally have the owner try several different antihistamines, each for 2 weeks (3 or 4 weeks if the owner is not very observant). The owner notes which antihistamine is being used and what degree of benefit, if any, it may produce. The following are the antihistamines used most frequently in our practice. Those with an asterisk tend to be most effective/cost effective (unless otherwise marked): * Diphenhydramine (25, 50 mg caps) - 2.2 mg/kg BID or TID;* Hydroxyzine HCl (10, 50mg tabs) - 2.2 mg/kg BID or TID ; * Chlorpheniramine (4, 12mg caps) .4 - .8 mg/kg ( .5 mg ) BID to TID ; *Amitryptyline-(10, 25, 50, 75, 100 mg tabs) 2.2 mg/kg BID; *Clemastine (Tavist or generic) - 1.34 mg tabs, .05 mg/kg BID, for dogs under 10 kg 1/2 tab BID; 10 - 25 kg, 1 tab BID, bigger, 1 1/2 tab BID; Cyproheptadine - (4 mg tabs) .25 - .5 mg/kg TID; Doxepin HCl-(10, 25, 50, 75, 100, 150 mg) .5- 1.0 mg/kg BID; Trimeprazine tartrate - 2.5 - 5 mg/dog TID (expensive). Which is the most effective? Some studies have suggested clemastine; another recent study suggested hydroxyzine and diphenhydramine. The author has best results with chlorpheniramine and hydroxyzine. H 1 blockers that have antihistaminic, antichollinergic, sedative and local anesthetic effects. They must be used with caution, if at all, in the presence of liver disease, glaucoma, urinary retention, gastrointestinal atony and pregnancy. The newer, non-sedating antihistamines include cetirizine ( 10 mg/day/animal < 25 kg and 10 mg BID > 25 kg), loratidine (0.5-1.0 mg/kg/day) and astemazole (.25 mg/kg q24hr). It has been suggested that cetirizine may be the most effective of this group. Combinations of antihistamines may be of benefit when the individual antihistamines themselves appear to have failed. The author has most commonly used chlorpheniramine along with hydroxyzine or amitriptyline or trimeprazine (in Temaril-P). Pentoxifylline Pentoxifylline (a phosphodiesterase inhibitor) has been noted to reduce the pruritus and erythema associated with atopy at a dosage of 10 mg/kg BID, although TID administration at dosages as high as 20 - 25 mg/kg may be more beneficial. The author has, in general, been disappointed with this drug as a monotherapy for atopy. It may help to reduce steroid dosages in patients on glucocorticoids, and may work synergistically with antihistamines. It is therefore usually used as part of a combination therapy, especially when other more conventional therapies have failed. There is some suggestion that some generics may not be as effective and the trade name product (Trental). This may suggest the use of the trade name product, at lest for an initial trial period of one month. If it is effective, the generic can then be tried. The author routinely uses generic products to initiate therapy. Cyclosporine Oral cyclosporine is now available to Veterinarians in the United States as a veterinary product (Atopica, Novartis), specifically marketed as a therapy for canine atopy. Oral cyclosporine has now been used for several years in the management of atopy in the dog. Cyclosporin-A (Neoral ฎ , Sandoz) is most commonly used at a dose of 5mg/kg/day. It has been noted to produce good to excellent results in 70 - 80% of cases. The overall beneficial effects have been shown to be similar to those of prednisolone or methylprednisolone, without the attendant deleterious side effects of the steroid. The major side effect encountered is gastrointestinal upset (vomition, diarrhea, flatulence, abdominal cramping - with vomition being most common). The incidence of vomition may be minimized by gradually working up to the maintenance dose over several days. Cyclosporine should be given on an empty stomach (at least 2 hours before feeding) to enhance absorption. However, if vomition is noted, the drug should be stopped until this side effect has resolved and can be tried again with a small amount of food. Other side effects reported in dogs include gingival hyperplasia, papillomatosis, bacteriuria, bacterial pyoderma, anorexia, nephropathies, bone marrow suppression and a lymphoplasmacytic dermatosis. Trial therapy should be 45 - 60 days. It may take this long to see the maximal benefits of the drug. Once a beneficial effect has been noted, attempts can be made to reduce the daily dosage, or treat once every other day. It has been shown that maintenance may be achieved with either lower daily dosages or less frequent administrations. In this study (Olivry T et al, Proc. AAVD/ACVD, 2003), oral cyclospirne was reduced monthly to 2.5 and 1.25 mg/kg once 50% and 75% reduction of signs were achieved. 12 of 15 dogs were able to be controlled a these dosages. In another group of dogs, a daily dose of 5 mg/kg was reduced to every 2 and 4 days once patients improved by 50% and 75%, respectively. 13 of 15 individuals were able to be controlled. In yet another study of 51 dogs who were treated for 6-30 months, 15% were able to be maintained on 2-3 days per week of cyclosporine, 20% on 4-5 days per week, and 20% required daily therapy (Radowiz S et al, Proc. AAVD/ACVD 2003). It is very interesting to note that in both studies, a significant number of patients were able to have their oral cyclosporine eventually stopped, with a complete remission of disease (no recurrence) (Olivry - 10% of cases; Radowiz - 24%). In that cyclosporine is expensive, it has been used in conjunction with ketoconazole to increase the blood concentrations of the cyclosporine. The mechanism for this decrease in clearance is probably a combination of the inhibition of cytochrome P-450 in the intestine and liver and the inhibition of intestinal p-glycoprotein that would ordinarily pump oral cyclosporine into the intestine. Optimal dosages and frequencies of ketoconazole have yet to be established in atopic dogs. We tend to start with 2.5 mg/kg cyclosporine per day along with 5.0 - 10 mg/kg ketoconazole once per day. A higher dose of ketoconazole (i.e. 10 mg/kg/day) may be associated with higher circulating cyclosporine concentrations and greater anti-pruritic benefits. The ketoconazole is usually given with a small amount of food, but the cyclosporine is usually given 2 hours before or after giving this small amount of food. Behavior Component to Atopic Pruritus? - There has been a suggestion that a subset of both atopic dogs may be pruritic in response to anxiety and/or another central trigger. "These repetitive behaviors are believed to be controlled by endogenous opioid release. Dextromethorphan is an opioid antagonist that does not work by binding and blocking opioid receptors but rather by blocking receptors for N-methyl-d-aspartate, which are found in the brain and spinal cord and mediate various sensations, including pain". Dextromethorphan has been used to significantly benefit some dogs in this fashion (2 mg/kg PO q 12 hours); in one study, 11 of 12 dogs had some degree of improvement. Dextromethorphan use should be reserved for those atopic patients that fail more traditional anti-pruritic therapy and (ideally), where there is suggestion that the behaviors are repetitive and anxiety-induced. Hyposensitization Hyposensitization is noted to benefit 60 - 70% of cases (good to excellent results). "Rush" immunotherarpy, which involves giving all the induction dosages in the hyposensitizing protocol in one day appears to produce a more rapid onset of benefit from hyposensitization and possibly a higher over success rate. Over the long term, 50 - 70% of our patients on hyposensitization require additional medication (antihistamine steroids and/or fatty acids) to control allergic signs during part or all of the year. The majority of our patients on maintenance hyposensitiztion get their shots every 1-2 weeks during the allergy season. For patients who derive only transient benefits from a given shot (2-3 days), we divide our solutions and give .5 cc twice weekly, or even smaller volumes up to three times a week (e.g. .2 cc three times weekly). It is also very important to monitor for increased pruritus following a given shot. Affected individuals may actually have their allergy signs significantly worsened if they react to the hyposensitization solution. If such is the case, we reduce the volume of solution to that which did not produce a reaction. Patients noted to have reactions to shots appear to have an overall better chance of deriving benefit from the shots, assuming the volume and frequency of solution is managed appropriately. It is interesting to note that in one recent study (Power H et al,), 29% of patients who discontinued hyposensitization shots did so because the atopy went in to spontaneous remission. We quote a 20 - 30% chance that individuals with come off hyposensitization after at least 2-3 years on the desensitizing protocol. FELINE ATOPY: AN UPDATE In the older Veterinary literature, it has often been suggested that the incidence of atopy is similar to that of food sensitivity in the cat. However, in our clinic, for cats showing the clinical signs listed below, about 70% are noted to be atopic and 30% food sensitive. Feline atopy is associated with a myriad of clinical signs. These may include: Maracle
Feline atopy is largely diagnosed by rule out. The major differential diagnoses to be considered include flea bite hypersensitivity, food sensitivity, cheyletiella, demodicosis and dermatophytosis. It is not uncommon to see a peripheral eosinophilia and basophilia. Skin biopsies show inflammatory changes that not uncommonly reveal increased numbers of mast cells and eosinophils. The documentation of offending allergens is achieved either with intradermal skin testing, which tends to be more difficult to read than in the dog and in vitro, serologic testing. At present both RAST and ELISA tests are available for use in the cat. In one study, there was poor correlation between IDST and commercial ELISA data. In another study, similar success to hyposensitization was seen based on ELISA or IDT data . Further comments regarding the efficacy of this type of testing awaits controlled studies but it is important to note that many Veterinary Dermatologists have migrated to doing serologic testing in the cat as their choice diagnostic for defining offending allergens. This likely has most to do with its ease of performance compared to doing skin tests. It is important to note that, because of the potential for false positive results, this type of testing should not be done to diagnose atopy in the cat. Therapy The therapy of feline atopy should always include the documentation and treatment of secondary bacterial or Malassezia infections. These are best defined by cytologic examination. Because glucocorticoids are well tolerated in the cat, they tend to be the cornerstone of therapy. However, as the disease becomes more chronic and severe, it is not uncommon to have the patient require higher dosages, more frequent dosage administrations or more potent glucocorticoids to maintain comfort. We are of the impression that prednisolone tends to be more effective than equal dosages of prednisone in some cats, and for this reason, in choosing between these drugs, we would choose to routinely use prednisolone in cats. Cats are often started on 1 - 2 mg/kg/day of prednisolone. "Depo" steroids are acceptable for periodic administration (ideally keep frequency of administration to less than once every 6-8 weeks - methylprednisolone acetate or triamcinolone acetonide). For patients refractory to prednisolone consideration should be given to using the longer acting, more potent oral dexamethasone (.1 - .2 m/kg/day) or triancinolone acetonide (.5 - 1 mg/kg/day). Emphasis should always be placed on reducing dosages to the least frequent administration possible. Fatty acids (omega 3 and 6) such as DVM Derm Caps Liquid or 3V caps (omega 3) benefit approximately 20 - 30% of cases (some quote 30 - 50%). Many cats, however, refuse to eat the fatty acids. The antihistamines that have been of most benefit for in our hands for treating feline atopy are chlorpheniramine (2-4 mg/cat q 12 hrs) or amitriptyline ( 5-10 mg/cat q 12 - 24 hrs. Amitriptyline may cause significant sedation, ataxia etc.; cats may salivate excessively when it is given. The later can be circumvented by using amitriptyline powder mixed in fish/cod liver oil. Other antihistamines to be tried include clemastine fumarate (.34 - .68 mg/cat BID), ceterizine (.5 - 1 mg/kg or 5 mg/cat) or cyproheptadine (2 mg/cat BID; may cause polyphagia and behavioral effects). Each is tried for 3 weeks. Hyposensitization has been reported to benefit anywhere from 45% to 75% of cases. Our success rate has been in the 60 -70% range. Protocols using aqueous allegens are similar to those used for the dog. The author uses the same frequency of administration, but only 1/2 the volumes. One recently published study reported the benefits of hyposensitized based on RAST data. The numbers of patients with various manifestations of atopy and the percentage of patients who improve by greater than 50% included : hair loss - 29cats/53%; military dermatitis - 23cats/76%; eosinophilic plaque - 10 cats/ 73%; indolent ulcer - 6 cats/95%; linear granuloma - 3 cast/100%; otitis externa - 4 cats/65%; Asthma - 4 cats/90% Oral cyclosporine has been noted to work well in the management of atopic dermatitis in the cat. Cats are generally treated with 5 - 7 1/2 mg/kg/day. In one study, eosinophilic plaques and eosinophilic granulomas were put in to remission within 30 - 60 days. 3 cats with indolent ulcers had only partial responses. Cyclosporin at this dosage appears to be tolerated reasonably well . GI upsets (nausea, vomition, anorhexia) are relatively common. If possible, we gradually increase our dosages over several days, prior to getting to our maintenance dose (above). If GI problems are encountered, the drug is stopped until the signs have abated and it is then re-instituted given with a small amount of food. We have seen apparently latent toxoplasmosis exacerbated while on this therapy (likely because of the immunosuppressive effect of cyclosporine .. something to be aware of! Chlorambucil has also been of benefit (usually along with steroids) in treating refractory atopy. Recommended dose is 0.1 - 0.2 mg/kg q 24 hrs until 75% improvement in clinical signs, then this dose every other day. Adverse effects to be monitored for include hepatotoxicity and bone marrow suppression. Megestrol acetate may be considered a "last ditch" alternative for treating feline atopy, in light of potential side effects ( polyphagia / weight gain, PU/PD, personality and behavioral changes, pyometra or stump pyometra, mammary hyperplasia, mammary neoplasia, diabetes mellitus and adrenal suppression). Remission of clinical signs can often be achieved with an oral dose of 2.5 - 5.0 mg/cat every 48 hours for 1-3 weeks. This is followed by weekly maintenance dosages. CANINE AND FELINE FOOD SENSITIVITIES Adverse reactions to foods are generally divided into various subsets based on pathomechanism. Those that are of most significance from a dermatology point of view include food intolerance and food allergy. Food intolerances mimic food allergies, but can occur on first exposure to a dietary ingredient and involve non-immunologic mechanisms. They may be further subdivided into food idiosyncrasy and pharmacologic reactions to foods. Idiosyncratic reactions to various ingredients in foods are often described in human beings. Sulfites, monosodium glutamate, tartrazine, azo and noazo dies, benzoates, parabens and spices have all been incriminated. In the case of azo or nonazo dyes, the mechanism may involve histamine release from leukocytes. Similar reactions are suspected to occur in dogs and cats but are poorly documented. Food ingredients may also be associated with the pharmacologic action of various ingredients in foods (i.e. vasoactive amines such as histamine which can increase in spoiled scombroid fish such as tuna, mackerel, skipjack and bonito). Food allergies are immunologically mediated reactions to water soluble glycoproteins that have molecular weights ranging from 10,000 - 60,000 daltons. This data comes largely from experiences with food sensitivities in man, but appear to be applicable to the dog and cat. CANINE ADVERSE REACTIONS TO FOODS Allergic to what? In the dog, adverse reactions to beef, diary products and wheat account for 2/3 of the reported cases. Reactions to chicken, chicken egg, lamb or soy account for another 25%. Other glycoproteins that have been incriminated include corn, oatmeal, pasta, pork, fish, turkey, potatoes, rabbit, rice flour, rice, artificial food additives (gum carrageenan) and food preservatives . In one study of 25 food allergic dogs, 80% of affected dogs were reactive to 1 or 2 allergens in the diet. 64% were sensitive to two or more allergens. The mean number of allergens reacted to was 2.4. Incidence: controversial: 3-10% of all canine allergic hypersensitivity (excluding parasitic allergy). There does appear to be a significant regional difference in the incidence of food sensitivities across the US (i.e. more common in the east than the southwest etc.). Concurrent flea bite hypersensitivity or atopy may occur in up to 75% of cases. Clinical Signs: In the dog, no age or sex predilections are noted, although many cases tend to occur in younger dogs (33% - 52% less than 1 year of age in reports from various studies). The index of suspicion for food hypersensitivity is above that of atopic disease when pruritus occurs in dogs under six months of age. Breeds predisposed include American cocker spaniel, English Springer spaniel, Labrador retriever, collies, miniature schnauzer, Chinese Shar pei, poodle, west highland white terrier, Wheaten terrier, Boxer, dachshund, Dalmation, lhasa apso, German shepherd and Golden retriever. Pruritus is nonseasonal, although it may wax and wane if exposure to the offending allergen is episodic. The hallmark clinical manifestation is pruritus (most commonly ears, rump, distal limbs, axillae, and groin). Secondary seborrheic, bacterial and Malassezia problems are common. Symptoms may be restricted to just an otitis externa in as many as 20-25% of cases. Food colorants and other additives have been suggested to cause erythema multiforme and other "drug-like" skin eruptions. Lesions include erythematous macules, and papules that spread to produce annular target and arciform lesions. Involvement of the oral and nasal mucosa, pinnae, axilla and groin are common. Other associations include recurrent bacterial pyoderma (with or without pruritus), eosinophilic vasculitis (presenting as urticaria or any of the various lesions associated with vasculitis), malaise, dullness and rarely seizures. Gastrointestinal signs (vomiting, diarrhea, colic) are noted in 10-15%. Gastrointestinal signs may be characterized by only an increased frequency of bowel movements. Diagnosis and Therapy: The histologic changes associated with food sensitivity in the dog are relatively nonspecific and consist of a superficial perivascular dermatitis with mononuclear cells or neutrophils predominating. Increased eosinophils are occasionally present. There is one report which suggests that the presence of eosinophilic infiltrates is more closely associated with a diagnosis of food sensitivity than atopy in the dog (when evaluated in a flea free environment). Serologic testing for food allergies (radioallergosorbent RAST or ELISA testing) and intradermal skin testing have shown poor predicatability and poor correlation with response to provocative challenge and are not recommended for diagnostic purposes. Home prepared diets appear to be closest to 100% effective in determining the presence of food sensitivity. There are several reports in the literature of both dogs and cats who have manifest signs of food sensitivity when fed a commercial diet consisting of the same ingredients offered in a home prepared form. Home prepared diets that the author favors include a single, novel carbohydrate (potato, yams, pinto bean) combined with a single, novel protein (venison, duck, rabbit, ostrich, kangaroo). We generally feed one cup per ten pounds body weight of the mix per day; _ - 1/3 of this mix is usually the protein component. It is recognized that these diets are nutritionally inadequate for growth and maintenance. Homemade foods lack a source of calcium, essential fatty acids, certain vitamins and various micronutrients. These homemade diets are not recommended for trial purposes in growing animals for any longer than three weeks unless they have been balanced with a non-flavored, additive free vitamin, calcium/phosporous and a source of essential fatty acids such as vegetable oil. Vegetable oils are not likely to contribute to allergic symptoms. Because of the inconvenience factor required in home formulating balanced diets, the author tends to use commercial restrictive diets for most growing animals. Commercial diets currently available are quite good, but it is well known that no commercial diet works for all food allergic individuals. An estimate of about an 80% - 85% chance of success with any given diet seems reasonable based on data available to date. Commercial restrictive diets can generally be divided into two categories:
The signs associated with food sensitivities are variably responsive to glucocorticoids (some may be resistant to anti-inflammatory dosages; some may be very responsive to even low dosages). Antihistamine therapy appears to be less successful when compared to treating atopy in the dog. FELINE ADVERSE REACTIONS TO FOODS Allergic to What? Adverse reactions to beef, dairy products (milk, cheese) and fish have accounted for nearly 90% of the reported cases in cats. Others include pork, chicken, rabbit, horse meat, lamb, eggs, cam juice and cod liver oil. Incidence: In one group of 25 allergic cats, flea bite hypersensitivity was seen in 70%, food sensitivity in 17% and atopy in 13%. In our practice, we feel that food sensitivity and atopy are of about equal incidence. Siamese or Siamese crosses may be at increased risk. Clinical Signs: Pruritus is present in 100% of cases. Pruritus most commonly affects the face, head, pinnae and neck or combinations thereof. Pruritus may also be generalized or restricted to other areas of the body (e.g. racing stripe down the back). Other manifestations include self induced alopecia, military dermatitis and any of the manifestations of the eosinophilic granuloma complex (indolent ulcer, eosinophilic plaque, eosinophilic granuloma). There are rare reports of an exfoliative dermatitis characterized histologically by a lymphocytic mural folliculitis and an erythematous papulopustular eruption characterized by eosinophilic folliculitis and furunculosis related to food sensitivities in the cat. Angioedema, urticaria and conjunctivitis, sneezing, malaise, dullness and a peripheral lymphadenopathy have also been noted. Gastrointestinal signs (vomition, diarrhea) are noted in 10 - 15% of cases. Up to 25% of cases have concurrent hypersensitivities (atopy or flea bite hypersensitivity). Diagnosis and Therapy: The histopathology of food sensitivity most commonly involves a superficial and/or deep perivascular dermatitis wherein eosinophils are the dominant inflammatory cell type. Mast cells are commonly increased and may be the prominent cell type noted. A peripheral eosinophilia may be seen in as many as 50% of cases. The diagnosis is confirmed by assessing response to a restrictive diet. Home prepared diets are again most predictably effective. Single, novel protein sources include lamb or ham baby food, ham, ostrich, rabbit, venison, duck. The protein source may be fed alone or blended with potato or rice. For the purposes of a diet trial (8 weeks), balancing the diet may not be necessary. For long term feeding, however, supplementation with taurine tablets, dicalcium phosphate, safflower oil and a multiple vitamin is recommended. Alternatively, commercial restrictive diets may also be fed. As for the dog, no commercial diet will likely be beneficial for all food allergic cats. Novel protein diets such as the Innovative Veterinary Diets (lamb, rabbit, duck, venison) are used by the author. They have the advantage of coming as both dry and canned foods to help satisfy picky appetites. Hydrolysate diets are also available (Prescrition Diet Feline a/d low allergen (rice, hydrolyzed chicken liver, hydrolyzed chicken). Cats with food sensitivities are noted to be variably responsive to glucocorticoids (50% may not respond). Response to antihistamines also appears to be generally poor. A "MINI" COURSE IN OTOLOGY Rod A.W. Rosychuk DVM, DACVIM Colorado State University NORMAL ANATOMY AND PHYSIOLOGY OF THE EAR The ear canal in the dog and cat is divided into a vertical segment that is contiguous with the pinna and a horizontal segment that extends to the tympanic membrane. The horizontal and vertical canals are largely surrounded by cartilage. However, adjacent to the tympanum, the horizontal canal is supported by bone. The ear canals are lined by skin containing hair follicles, sebaceous glands in the superficial dermis and fewer small modified apocrine (ceruminous) glands in the deeper dermis. The number of hair follicles, sebaceous glands and apocrine glands are more numerous in the vertical than horizontal canal in the dog. Hair follicle density in the horizontal canal varies with breed. Hairs may be seen growing just adjacent to the TM in normal dogs. Cerumen consists of desquamated cornocytes, apocrine secretions, and sebaceous secretions. It is a mixture of proteins, lipids, amino acids and mineral ions. Normal ceruminous secretions facilitate trapping foreign material in the ear and have inherent antibacterial and antifungal activity. The self cleaning function of the canals is achieved through a process of epithelial migration. Epithelial cells are noted to grow laterally from the tympanum (area around the manubrium of the malleus). The tympanic membrane of the dog is made up of the pars flaccida, a small area of the dorsolateral tympanum which is relatively flaccid, vascular and appears to heal rapidly after perforation and the large pars tensa which is under considerable tension and, once perforated, takes longer to heal. Following complete destruction of the pars tensa in normal dogs, complete regrowth is noted within 21-35 days. The periphery of the tympanum attaches to the annulus fibrocartilagenous which is a fibrocartilagenous ring that attaches to the surrounding bone. The manubrium of the malleus is situated within the fibrous layer of the tympanum. It is white and reverse"C" shaped with the open end of the reverse "C" pointed towards the nose. Tension on this structure gives the tympanum a mildly concave outer contour. The tympanum is oriented at about a 30 - 45 degree angle from perpendicular (dorsal to ventral). The middle ear of the dog and cat is separated in to three sections: the epitympanic bulla, which is the most dorsal space in the middle ear, housing the ossicles; the tympanic cavity which is that area immediately medial to the tympanum and the tympanic bulla which is immediately ventral to this and is partially separated from the tympanic cavity in the dog by a ridge of bone (variable width from individual to individual) . In the cat, the tymapic bulla is separated from the tympanic cavity by a bony plate that is essentially complete but for a small hole in the center of the plate (allowing for communication between the bulla and the tympanic cavity). The middle ear is lined by a respiratory -like epithelium (ciliated columnar cells with some mucous producing goblet cells). The middle ear has a normal bacterial flora. The middle ear communicates with the back of the pharynx through the auditory canal (originates in the anterior medial aspect of the epitympanic recess) which allows for equalization of air pressure across the tympanum. Normal Canine Tympanic Membrane  THE PATHOGENESIS OF OTITIS EXTERNA AND OTITIS MEDIA PATHOGENESIS OF OTITIS EXTERNA The successful management of otitis externa is very dependent on an understanding of the pathogenesis of the disease. Primary factors are those which are capable of initiating inflammation within ears (e.g. allergies). Predisposing factors are those which make the ear more prone to the development of inflammation (e.g. pendulous pinna, excessive moisture in ears) and perpetuating factors are those which are capable of perpetuating the otitis even if the primary factors have been removed/resolved (e.g. opportunistic infections with bacteria and/or yeast). It is true that with the majority of acute cases of otitis externa seen in practice, symptomatic therapy (cleansing and the use of a broad spectrum topical preparation containing a glucocorticoid, antibiotic and antifungal) will often resolve the otitis and the primary factor/factors responsible for initiating the inflammation will never be known. However, when dealing with chronic or recurrent cases of otitis externa, it becomes imperative to return to the list of primary factors and make sure each is considered. Only through the delineation of these underlying pathologic states can rational therapies be established to resolve or control these particularly difficult cases. Primary Factors Factors capable of initiating inflammation within ears.
These are factors that are capable of perpetuating the otitis even if the primary factor has been removed/resolved:
Inflammation within the middle ear (epitympanic recess, tympanic cavity and/or bulla) may be infectious (bacterial, fungal) or noninfectious (foreign body, neoplasia, polyps in cats, trauma, cholesteatoma). Otitis media is most commonly an extension of otitis externa in the dog. In the cat, while this is still the most common association, there appears to be a higher incidence on retrograde problems that involve the auditory canal. Obstruction of the auditory canal may result in the accumulation of mucoid secretions within the middle ear. Otherwise normal microflora of the middle ear may then produce infection. This pathogenesis is also uncommon. Middle-ear involvement via hematogenous spread of infection is rare. In the dog, it has been estimated that otitis media is present in 50% or more of the ears associated with chronic otitis externa. A higher incidence is noted in those ears in which the horizontal canal is stenotic and when inflammation/purulent exudation is severe (e.g. Pseudomonas infection). However, especially in chronic allergic otitis externa, it would appear that perforation of the tympanum is much less common than the 50% quoted above. It is more common to see the tympanum partially forced in to the tympanic cavity and bulla (the so called "false middle ear) than it is to see actual perforation. The bacteria associated with otitis media, in roughly decreasing order of occurrence include Staphylococcus intermedius, Malassezia pachydermatis, Pseudomonas spp., Corynebacterium spp., Enterococcus spp., Proteus spp., B-hemolytic streptococcus, alpha-hemolytic streptococcus, Citrobacter spp. E. Coli, and Anaerobes. It is important to note that, with chronicity, the epithelial lining of the middle will potentially become markedly hyperplastic and may be responsible for much of the soft tissue density seen within the bulla on radiographic or CT/MRI examination. These changes may require prolonged times, with therapy, to regress. Cholesteatoma are formed when the tympanum is pushed into the bulla by usually dry concretions. Epithelial debris continues to accumulate within this "pouch" until it fills the entire bulla. With time, pressure may be placed on the bulla wall to result in thinning of the bone and an actual expansion of the bulla. Clinical Signs: In most cases, the signs of otitis media mimic those of otitis externa (pruritus, head shaking, pain, exudation). Neurologic signs are less commonly encountered (approx. 25% of cases). They include facial paresis and paralysis, Horners syndrome, KCS and xeromycteria (unilateral drying and hyperkeratosis of the planum nasale on the affected side). In that otitis media may extend to also involve the inner ear, other neurologic signs that may be present include e deafness, head tilt, asymmetric ataxia and horizontal nystagmus. MANAGEMENT OF OTITIS EXTERNA IN THE DOG AND CAT EAR CLEANING A clean ear must be achieved at some point in the work-up of every case of otitis externa: Debris serves as a potential source of irritation; may serve as a nidus of infections; may prevent the access of topical medications to their targeted area of need and may inactivate some of the ingredients in topical medications. Ear Cleansers
In a predominantly referral practice, the author is commonly presented with cases of chronic otitis externa wherein the otitis is significantly perpetuated by a "wad" of debris (waxy concretion; ceruminolith) that has accumulated within the horizontal canal adjacent to the tympanum. The horizontal canal often becomes hyperplastic, narrowing the canal in this area. With chronicity, the tympanum is also commonly "pushed" in to the tympanic cavity to variable degrees. This scenario is most commonly encountered in cases of canine allergic otitis externa (atopy, food sensitivity) complicated by secondary Malassezia infections. A similar situation is seen in cats, most commonly as a sequel to ear mite infestations or as a complication of allergic otitis. In cats, the horizontal canal epithelium is less likely to become hyperplastic and the tympanum is usually not significantly pushed in to the tympanic cavity as it is in the dog. The "at home" use of topical cleansers is usually not able to remove this debris. To resolve, or at least significantly improve the otitis, the debris must be removed. This is most effectively and a-traumatically achieved through deep ear cleaning under general anesthesia (flushing and suctioning through an operating otoscope or through a video-otoscope). If, at presentation ears severely inflamed, usually elect to treat topically +/- systemically for several days to one to two weeks to reduce inflammation prior to more in- depth cleaning. For actual deep ear cleaning: Once in to the ear, the author routinely uses an open ended tomcat catheter on a 12 cc syringe to obtain exudates from deep within the horizontal canal of the ear. Samples are used for cytologic examination and possibly culture. If the middle ear is entered during the cleaning, samples are again obtained as soon as this occurs (for both cytology and culture). For effective, safer deep ear cleaning, the author prefers flushing and the use of a suction apparatus. The suctioning is of paramount importance. Flush under direct visualization through surgical ototscope head with an open ended TomCat catheter attached to a 12 cc syringe. Ideally, suction through vacuum system (e.g. suction hose attached to a 14 guage, 5.5. inch teflon catheter (Abbott Hospital Incorporated, North Chicago, IL 60064, No. 4535-84). It is important that the operator be able to control the intensity of the vacuum used. Particular care must be taken to reduce suction when working on or around the tympanum while greater suction settings can be used to remove larger, more tenacious material away from the tympanum. The author routinely uses only saline to initiate cleaning. However, if debris appears to be quite tenacious, a ceruminolytic (e.g. EipOtic or Cerumene) can be used to facilitate cleaning. An alternative to the use of suction would be a 3.5 to 5 Fr feeding tube attached to a syringe. -Alligator forceps - to remove large particulate material. -Ear curettes - for removing larger amounts of material in vertical and horizontal canal; concern for using adjacent to the tympanum. If the tympanum is found to be perforated or is intentionally perforated, debris should be flushed out with copious amounts of saline. Visualization of the middle ear may be facilitated through the use of a 1.9 mm or 2.7 mm arthroscope. Cleaning Through the Video-Otoscope Video-Otoscope: procedures are usually begun with a thorough examination of the ear. A picture may be taken at the initiation of the cleaning to document before and after improvement. A sample of debris is aspirated from the depths of the ear for both cytolgic examination and possibly for culture and sensitivity testing. If the culture is not deemed necessary at the end of the procedure (i.e. in light of cytologic findings; assessment of integrity of the tympanum), it can simply be discarded. If the tympanum is noted to be perforated, then samples should always be taken from both the horizontal canal and the middle ear for both cytologic examination and culture and sensitivity testing. It has been noted that the organisms from horizontal canal and middle ear may differ and that the sensitivity patterns of the same organism may also differ from one area to the other. Samples taken from the middle ear should always be submitted for culture (both aerobic and anaerobic) even if they do not show cytologic evidence of organisms. The administration of saline through the working channel will facilitate expansion of the canals, further magnification of images, prevents fogging of the lens and lessens debris accumulation around the tip. The pressure of gravity flow is usually sufficient. Loosening and flushing of debris is often facilitated by this maneuver alone. Flushing and suctioning can be done through the working channel utilizing a 16 gage, 5.5 Inch teflon catheter (Abbot Hospital Incorporated) or a 4 1/2 inch, open ended tomcat catheter. The channel can be used for passage of biopsy or grabbing forceps or an appropriately modified ear curette. Debris can be grasped and removed, masses can be biopsied or removed, cysts "popped" or removed and polyps removed in cats. When utilizing the Storz double port adapter, fluids may be administered while biopsy forceps or grabbers are simultaneously used (Fig ). A home made flushing and suction apparatus may be created that allows for alternating flushing and suctioning action through one catheter in the operating port. A 16 guage, 5.5 inch teflon jugular catheter (Abbot Hospital Incorporated, North Chicago, IL 60064) or a 5.5 inch, open-ended tomcat catheter can be attached via an extension set to a three way stopcock. For flushing purposes, a 60 cc syringe is also attached to the stopcock. The hose from a suction apparatus is the attached to the remaining portal of the 3 way stopcock. The "trick" to the use of this apparatus is control of suction. Excessive suction, will result in collapse of the canal. Minimal amounts of suction should be used when working deep within the canal, adjacent to the tympanum. It is possible to perforate the tympanum when suction is excessive. The more rapid removal of debris from the canals is often facilitated by utilizing a combination of cleaning techniques. Alligator forceps and ear curretts can be utilized through a conventional operating otoscope head to remove larger debris. Flushing, utilizing a 12 cc syringe attached to an open ended tomcat catheter, then suctioning through a 14 gage teflon catheter (Abbot Hospital Incorporated) attached to a suction hose and controlled suction apparatus can allow for rapid debris removal with quicker directional changes within the canal. One shortcoming of the video-otoscope is the fact that the exit point of the operating channel is fixed. Any instrumentation coming out of this channel is fixed in its range of motion. The camera tip must be manipulated to assure access to various areas. This can be cumbersome and time consuming. ROUTINE TREATMENT OF ACUTE AND INFREQUENTLY RECURRENT OTITIS EXTERNA In many cases seen in clinical practice, such cases are often readily managed with topical products that contain a combination of an antibiotic, anti-fungal and glucocorticoid. The neomycin in products such as Tresaderm and Panalog provide reasonable gram positive and gram negative coverage; the thiabendazole in Tresaderm and the nystatin in Panalog provide reasonable anti-Malassezia therapy; and the dexamethasone in Tresaderm and triamcinolone acetonide in Panalog provide a relatively potent anti-inflammatory effect. When rods predominate in our Diff-Quick stained cytology, we often reach for the gentamicin in Otomax or if large numbers of Malassezia are noted, we may look for the superior antifungal effect of clotrimazole in Otomax. The betamethasone in an ointment base (Otomax) also appears to give us a more potent anti-inflammatory effect. Systemic Antibiotics Recommended when bacteria are seen on cytologic examination or culture and sensitivity testing and the problem is chronic and proliferative or when the otitis is severe and inflammatory changes are seen on cytologic examination (i.e. large numbers of neutrophils) or when there is a significant peri-aural dermatitis or if the tympanic membrane is perforated. Antibiotics are best chosen by culture and sensitivity testing but empiric choices include first generation cephalosporins when cocci are seen cytologically (e.g. cephalexin, cefadroxil) or enrofloxacin or marbofloxacin if rods are seen cytologically. Systemic Glucocorticoids Systemic glucocorticoids are an invaluable adjunctive therapy used to quickly reduce inflammation associated with more severe otitis externa (especially if allergic in origin). They are also the most effective therapy for reducing proliferative change secondary to inflammation within the ears. Generally start therapy with oral prednisone/prednisolone at .5 to 1.0 mg/kg/day (use higher range for more severe inflammatory changes). Systemic Antifungals Oral ketoconazole or itraconazole are generally excellent choices for treating more refractory Malassezia infections - especially where the owners are unable to do as good a job as we would desire for topical treatment or if the ears are quite proliferative and it is questionable as to what topical treatments alone will achieve. These drugs are also indicated for cases of otitis media wherein Malassezia are involved. Client Education and Follow-up It is very important to provide the client with instructions (medication application technique, frequencies, amounts etc.). The use of a "take home" instruction sheet may also be of value. For difficult to medicate dogs or cats, the owner may try placing the appropriate number of drops for a given treatment in a syringe (e.g. tuberculin) then rapidly squirting this in the ear. Follow-up: the initial recheck for most cases of otitis externa is usually done two weeks after initiating therapy. Subsequent rechecks are dictated by response to therapy. Each follow-up examination should involve an otoscopic examination, cytologic examination of exudates and an accurate recording of findings. Routine rechecks should be maintained until the problem is either resolved or controlled. ALLERGIC OTITIS EXTERNA Routine Treatment of Acute and Infrequently Recurrent Allergic Otitis Externa In many cases seen in clinical practice, such cases are often readily managed with topical products that contain a combination of an antibiotic, anti-fungal and glucocorticoid. The neomycin in products such as Tresaderm and Panalog provide reasonable gram positive and gram negative coverage; the thiabendazole in Tresaderm and the nystatin in Panalog provide reasonable anti-Malassezia therapy; and the dexamethasone in Tresaderm and triamcinolone acetonide in Panalog provide a relatively potent anti-inflammatory effect. When rods predominate in our Diff-Quick stained cytology, we often reach for the gentamicin in Otomax or if large numbers of Malassezia are noted, we may look for the superior antifungal effect of clotrimazole in Otomax. The betamethasone in an ointment base (Otomax) also appears to give us a more potent anti-inflammatory effect. Long Term Management of Allergic Otitis Externa
Once secondary bacterial infections have been controlled and proliferative changes have been significantly improved, then potential primary factors can be further worked up and treated (e.g. document and treat food sensitivity; atopy management etc.). Note: As part of our aggressive initial management of those chronic/proliferative ears - we will often start a restrictive diet at the outset of topical/systemic otic therapy. We prefer a commercial, balanced restrictive diet because it will likely be fed long term (several months) before a more definitive decision can be made about the actual role dietary hypersensitivity may be playing in the pathogenesis of the disease. Once more intensive topical/systemic therapy is completed and the ears doing well, see if diet alone is able to keep the otitis from recurring. To prove the benefit of restrictive diet, challenge with the previous diet to see if problem exacerbated and to document the future need of feeding special diets. APPARENTLY REFRACTORY MALASSEZIA ASSOCIATED WITH OTITIS EXTERNA True refractory infections with Malassezia appear to be uncommon. Recurrent infections, however, are frequently encountered (i.e. secondary to atopy). When Malassezia appears to be refractory, factors that may affect the efficacy of conventional therapies include:
Resistance is suspected if:
Current options for managing resistant Pseudomonas infections Pseudomonas infections are quite commonly encountered as complicating factors in chronic otitis externa/media in the dog and, on occasion, may be very resistant to routine anti-microbial therapy. The following are important points to consider in establishing a successful therapeutic protocol for such cases:
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