Practical approach to diagnosing and managing ear disease in the dog (Proceedings)


It is important to understand that ear disease is only a symptom (no more specific than "pruritus").

It is important to understand that ear disease is only a symptom (no more specific than "pruritus"). As Dr Flemming Kristensen stated "A patient showing ear problems is a dermatology case until proven otherwise". It is appropriate therefore to approach the diagnosis of ear disease just as you would for any other skin disease.

Obtaining the signalment is the first step that must be taken when a dog is presented w/clinical signs of ear disease. Age, breed and sex can help point you in the right directions. For example, it has been reported that Labrador retrievers have a higher incidence of cutaneous adverse food reactions then does the general population. A puppy w/ear disease should have Otodectes, dermatophytosis and juvenile cellulitis ("puppy strangles") on the list of differential diagnosis while a young adult dog would typically have environmental allergen induced atopic dermatitis and cutaneous adverse food reactions high on the differential diagnosis. A geriatric dog, w/o prior ear disease, would have neoplasia (eg adenoma, adenocarcinoma) or an endocrinopathy as important rule outs.

The next step may be the most important one, obtaining a detailed history! This starts by getting a copy of the dog's medical record. If the dog has had previous skin or ear disease, getting a copy of the medical records may help tremendously in developing a differential diagnosis list. The very first thing I tell owners with a dog w/ear disease is that many ear diseases look the same; it is the underlying causes that vary. Therefore, just like a good detective novel, we need to begin at the start and retrace the "footsteps" looking for clues along the way. Specific questions that I feel should be asked include:

1. When did the symptoms first occur? This is an important question, because many owners will only tell you when this current episode of symptoms occurred, not the very first time it occurred;

2. Other than the problem the owner presents the patient for, you must ask all owners if the dog has EVER had problems with excessive licking, scratching, chewing, biting or rubbing. Has the dog ever had ear problems before this episode? If so, when, with what medication and what was the response to treatment;

3. Where does the dog live—indoor, outdoors, both? Describe the environment, especially the outdoor environment;

4. Is she on heartworm and flea preventative? If so, what product, how often is it administered and is it year round or seasonal?

5. Are there any other pets in the household? If so, what kind and are they symptomatic. If they are cats, do they go outside?

6. Are any of the humans in the household showing "new" skin problems? If so, what kind;

7. Do they board the dog, take him to obedience school, training or to the groomers? If so, when was the last time?;

8. Do they know if the parents of the dog or any siblings have pruritic skin problems? If so, what was done and what was the response?;

9. What does the dog eat?

10. How do the ears seem today- is today's presentation the best, worse or average since the problem began?

11. Do you notice if the symptoms were better, worse or no different or not sure between the different seasons.

After reviewing signalment and thoroughly questioning the owner, the next step is to do a complete do a complete physical examination – be sure to aware of any constitutional signs (i.e. pot belly, fever) that may be present.

This is followed by a complete dermatologic examination. This is especially important to remember when a dog is presented only for otic pruritus- frequently practitioners fail to examine the rest of the body. Please note- when a dog is presented for truncal pruritus be sure to do an otic examination.

Following the dermatologic examination, examining the ear is next. In order not to miss an abnormality, you should do this otic exam in a systematic manner beginning w/the pinna. You should note any alopecia, erythema, ulceration, crusting, scaling or swelling. Then palpate the canals for pain, calcification or thickening. This is followed by an otoscopic examination of the ear canals. To evaluate the ear canals and the tympanic membrane, the tip of the cone of the otoscope should be placed in the opening of the external ear canal. The cone is advanced proximally by initially pulling straight up on the pinna. Due to the curve in the external ear canal, the ear canal must be straightened in order to see the horizontal canal and the tympanic membrane. This is done by pulling the pinna laterally (outward). By "stretching" the pinna laterally into a straight line horizontally the ear canal becomes straight. The otoscope is advanced into the horizontal ear canal as the canal is straightened.

The presence, degree and location of inflammation, ulceration & proliferative changes should be noted (i.e. cobblestone hyperplasia). Describing the size of both the vertical and horizontal canals along w/the type, location and quantity of debris or exudate should also be included in the medical record. Next you need to report if you can visualize the tympanic membrane or not. If you are not able to do so, is it because of swelling, the presence of a ceruminolith or is there just debris in the proximal horizontal canal obstructing your view?

Sometimes it is because the animal is too painful to allow deep examination of the ear canal. If you can visualize the tympanic membrane (TM) you need describe if it is normal in appearance or not. Changes noted may include discoloration or bulging.

It is important to then evaluate for concurrent middle or inner ear disease. This is because dogs with chronic recurrent otitis externa (OE) may have concurrent otitis media (OM). This step may require heavy sedation or general anesthesia. Evidence of middle ear involvement include a ruptured TM or an abnormal appearing TM (i.e. thickened, change in lucency (opaque), bulging or discolored. Even though it is stated that an intact TM DOESN'T rule out otitis media it is important to follow that statement with "but the TM is usually NOT normal in appearance". Supporting this statement is a study by Little, Lane and Pearson in 1991 in which they diagnosed OM in 42 dogs via biopsy or necropsy of the middle ear. In this group of dogs they reported that the TM was rarely torn. (However this was before fiberoptic video enhanced otoscopy (FVEO) was used. It is possible that some of the dogs (many?) may have had tears in the TM that could not be appreciated w/o FVEO). The authors went on to state that the TM was often thickened, supporting my contention that having OM w/an intact NORMAL TM is very rare.

Horner's syndrome; keratoconjunctivitis sicca (parasympathetic) and facial nerve paralysis may be present in cases of OM due to the close association of the sympathetic innervation to the eye (sympathetic, the parasympathetic innervation to the lacrimal glands (branch of the facial nerve) and facial nerve, respectively, to the middle ear. Deafness may also be present w/OM.

I know that some veterinarians will have their staff collect ear cytology samples prior to the examination (as a time saver) but I feel that it makes it difficult to evaluate the true appearance of the ear canal. Debris may be pushed into the horizontal canal thereby limiting visualization of the tympanic membrane due to the compacting of debris in the canals.

Now we move on to diagnostics and treatment. The first step is to identify and treat the primary (underlying) cause(s) of the ear disease. These would include:

1. Parasitic (including Demodex, Otodectes, Sarcoptes);

2. Foreign bodies;

3. Hypersensitivities (atopy- NOTE OE may be the ONLY symptom in 3-5% of the atopic cases and it may be UNILATERAL!!; cutaneous adverse food reaction where it too may be the ONLY symptom in 20% of the cases and also may be unilateral; flea allergy dermatitis (but should have skin disease in addition to the OE);

4. Allergic or irritant contact dermatitis;

5. Endocrinopathies, keratinization or sebaceous gland disorders leading to an altered lipid layer in the epidermis, alteration in normal keratinization or glandular function; idiopathic seborrhea (is there such a disease?);

6. Autoimmune or immune mediated diseases (eg pemphigus complex, vasculitis- note these diseases involve the pinna >>> canals);

7. Zinc responsive dermatosis (not typically just pinna disease);

8. Juvenile cellulitis;

9. Immunosuppressive diseases (distemper, FeLV, FIV, parvo virus); neoplasias (adenomas, adenocarcinomas) and

10. Dermatophytosis (affects the pinna rather than the ear canal).

In addition to identifying the primary cause, secondary factors must be addressed if possible. Secondary factors don't cause ear disease but increases the risk of developing ear disease and may make successful treatment more difficult. Secondary factors are: anatomical factors (eg- long pendulous ears in the Basset Hound or stenotic ear canals in Shar Peis); excessive moisture in ears (swimming); and iatrogenic trauma (plucking hairs from the ear canals, cleaning ear canals with cotton tip applicators).

Lastly perpetuating factors must be identified and treated. These factors don't initiate the problem, but will cause the disease to continue, even w/the elimination of the primary factor, once it has been established until these factors have also been addressed. Perpetuating factors include:

1. Bacteria (cocci most commonly Staphylococcus intermedius (acute infections), beta hemolytic streptococci and rods most commonly E. coli, Pseudomonas spp (chronic infections); Proteus spp, Klebsiella spp and Corynebacterium spp);

2. Fungi (Malassezia pachydermatis (which may cause a hypersensitivity reaction so that small numbers may be significant);

3. Progressive pathological changes;

4. Otitis media;

5. Contact hypersensitivity/irritant;

6. Treatment errors (most commonly under treating).

Laboratory tests are a necessary component to the proper workup of a case of canine ear disease. CBC, serum chemistry profile, urinalysis, skin scrapings, fungal culture, endocrine testing and skin biopsies may be necessary depending on what the differential diagnoses are for that patient.

Cytologic examination of a roll swab sample should be performed on any exudate being sure to quantitate numbers & type of bacteria, yeast and inflammatory cells. The question of what is an abnormal number of organisms, per oil field, in cases of OE has not been settled. Depending on the study, cutoff numbers, per oil immersion field (divide by 2.5 to get per HPF), between normal and abnormal ears range from >1 Malassezia to >4 Malassezia and from >1 bacteria to >10 bacteria. It is my opinion that the number of organisms needed to present to be considered significant is not just a "number". I don't perform a cytology on normal ears – I only do them if the ears that are inflamed or have exudate, ANY organism seen will be treated as part of the therapy regardless of the number present. The only time I do perform a cytology during therapy is when the ear is not improving clinically OR if a cytology had primarily or exclusively rods on the initial cytology. If there is a mixed population of organisms present at the initial examination w/o rods, follow-up cytology is not performed.

Bacterial culture and susceptibility (c/s) is rarely performed in cases of OE and when performed it is done in conjunction w/cytology. One reason I don't perform cultures in cases of otitis externa is that with a culture the susceptibility is based on antibiotic levels measured in microgram/mL. When applied topically you are delivering milligrams/mL concentrations, a 1,000 fold (at least) higher level. Another reason is that recent studies have reported poor reproducibility of c/s results when culturing the ear. In a study where two samples were taken for bacterial c/s from the same location in the external ear canal of dogs who had otitis externa, there were different bacterial isolates identified 20% of the time and the same isolate with different susceptibility patterns another 20% of the time. Eleven percent of the P. aeruginosa isolates had different susceptibility patterns. In addition, the cytopathology and the culture results only agreed 68% of the time. A second study took triplicate samples and sent one of the samples to 3 different laboratories. There were 18 samples that had identified Pseudomonas spp but none of the samples had identical patterns of antibiotic susceptibility. All three laboratories agreed on the presence of Pseudomonas in 15 (83.35) of the ears while 2 agreed on 2 (11.1%) of the samples and on one occasion (5.5%) only 1 lab identified Pseudomonas. A 3rd study was performed in which duplicate samples were sent to the same lab. Seventy percent of the Pseudomonas aeruginosa had different susceptibility profiles.

To help understand why these studies reported discordant results let's use Staphylococcus as an example of why discordant results may occur.

1. The presence of a single strain of bacteria w/2 subpopulations – 1 susceptible and 1 resistant (heteroresistance) for example that occurs w/MRSA

a. Expression of methicillin resistance is often heterogeneous in that the subpopulations of one strain will express resistance at different concentration of methicillin.

  • With most MRSA the majority of the cells express resistance to low concentrations of methicillin, and a minority of the cells express resistance to much higher concentrations.

2. Multiple strains of the same bacteria species

a. Strain differences - A strain is a subset of a bacterial species differing from other bacteria of the same species by some minor but identifiable difference

  • Virulence factors (toxins, surface proteins, etc)

  • Enzyme production (eg glucuronidase)

  • Utilization of substances in vitro (eg urea)

  • Acid production from mannose, etc

b. Example

  • CA- MRSA produces Panton-Valentine leukocidin (PVL) toxin while HA MRSA doesn't

3. Small # of bacteria so that the colonies are not properly identified on the culture plate

These results should give you great pause as to the reliability of cultures. I only cultures cases of OE when there are proliferative changes present AND there are numerous rods present on cytology AND the dog has failed to respond to my empirical antimicrobial therapy.

The MIC (broth microdilution technique) method is the "gold standard" for culture technique therefore if a c/s is submitted, the MIC method should be used to determine the susceptibility of the organism(s) rather than the disc diffusion method (Kirby-Bauer). This is because the disk-diffusion susceptibility test (DDST) is only semi quantitative. This means that the drug concentration achieved in the agar surrounding the disc can be roughly correlated w/the concentration achieved in the patient's serum. It will only report the organism's susceptibility (susceptible, intermediate or resistant) based on an approximation of the effect of an antibiotic on bacterial growth on a solid medium. Tube dilution (MIC) is quantitative, not only reporting SIR but also the amount of drug necessary to inhibit microbial growth. This allows you to not only decide susceptible or resistant but also the proper dosage and frequency of administration of the antibiotic. Please be aware that a susceptible designation alone does not necessarily imply efficacy. The advantage of the MIC method is that not only does it indicates susceptibility, but it also implies the relative risk of emerging resistance and thus the need for a high dose.

The other limitation to the Kirby-Bauer results in regards to Pseudomonas susceptibility is the discrepancy between it and MIC. In two studies, Kirby-Bauer underestimated P. aeruginosa sensitivity to enrofloxacin (when compared with MIC) whereas in 2 other studies Kirby-Bauer overestimated enrofloxacin susceptibility. Since Pseudomonas infections is one of the most common reasons cultures are performed in cases of otitis externa, and enrofloxacin is a commonly used antibiotic for this infection, this inability to properly identify susceptible vs resistance to enrofloxacin is an important limitation to using Kirby-Bauer testing.

With the information gathered above the treatment is directed toward the primary causes (eg parasiticidal treatment, food trial, intradermal testing and allergen specific immunotherapy, etc) and perpetuating factors. Ear cleaning is performed in the clinic w/a bulb syringe, AuriFlushTM system or by retrograde tube flushing (under anesthesia). I may not do a cleaning on the first visit if the ears are very swollen, preferring to use topical glucocorticoids (GC) +/- systemic GC for 10-14 days to decrease the swelling. Once the swelling has decreased it will be much easier to visualize the TM.

Cleaning agents contain substances that soften and emulsify wax and lipids. This initial cleaning is necessary in order to remove debris that may interfere with the effectiveness of topical agents and reduce inflammatory debris (bacterial toxins). I don't usually have the owner do cleaning after the initial exam since it seems that many owners have trouble with just medicating the ear, let alone do cleaning too. Many of the cleaners have a low pH leading to discomfort if used in an inflamed ear. A study comparing 2 ear cleaners (original formulation and then a new formulation) noted that in 38% of the cases w/the old formulation and 37.5% of the cases w/the new formulation dogs had a moderate to marked avoidance to having the cleaner instilled. This behavior was believed to be due to either a reaction to the ear cleaner or just overall animal irritability. Also the base in the otic ointments (mineral oil) acts as a ceruminolytic agent. Lastly a recent study calls into question whether any of the ear cleaners have any ceruminolytic activity. In this study the ceruminolytic activity of 13 ear cleansers was evaluated using a standardized synthetic cerumen (SSC) that mimics the composition and texture of canine cerumen. Of the tested products only Cerumene®, Epiotic® and VET ear cleaning solution are available in the US. The test products were incubated with mild agitation for 20 min with 500 mg of SSC previously compacted at the bottom of a test tube. Ceruminolytic activity was then assessed by quantifying the SSC removed by decantation. Overall, Otoclean® (OT) was most efficacious, reaching an activity of 86–90% followed by Netaural® (NET) with a 39%, Specicare® (SP) with a 23% and Cerumene® (CE) with an 8% ceruminolytic activity. None of the other products displayed any ceruminolytic activity. It was concluded that, in the experimental conditions used in this study, only 1/13 products had significant ceruminolytic activity. Please note that the company that manufactures OT funded this study.

There is frequently discussion of the ototoxicity of agents put into ears. In humans because ofloxacin otic solution (Floxin Otic) is the only topical agent to be labeled by the U.S. Food and Drug Administration (FDA) for use when the tympanic membrane is perforated, oral antibiotics have traditionally been used in this situation. However, because the risk of cochlear damage with the use of other topical medications seems quite small, perforation alone is not an indication for oral antibiotics. I have only once seen what was believed to be ototoxicity to a topical agent and in that case the TM was intact! Therefore, the agents are chosen more for their effectiveness than the concern about ototoxicity, especially since there are very few agents that have been proven to be safe in cases of a ruptured TM. It is more important to get rid of the infection than to avoid effective drugs because of ototoxicity concerns. Also, just because the TM is intact doesn't mean that the barrier function is complete, therefore, even in the presence of an intact TM it is possible to get drugs into the middle ear.

After ear cleaning topical agents are dispensed. I prefer ointments over drops because of the impression that ointments get the drugs to the region of the tympanic membrane better than drops do (this may be a volume issue more than the formulation- it has been reported that it takes 1.0 cc of medication to get down to the TM in a medium sized (40 pound) sized dog respectively- personal communication) and also the base in the otic ointments (mineral oil) acts as a ceruminolytic agent.

Most topicals contain a combination of glucocorticoids, antibacterial and antifungal agents. Antibacterial agents used topically include:

1. Broad spectrum agents (gram positive and negative organisms) –

a. Aminoglycocides which have a decreased effectiveness in an acidified ear, also inactivated by purulent debris so they must be put in a clean ear

  • Neomycin

  • Gentamicin

b. Silver sulfadiazine - inactivated by purulent debris so they must be put in a clean ear

  • Spectrum also includes yeast

2. Narrow spectrum agents (gram negative rods)- reserved for resistant gram negative infections

a. Polymyxin B - inactivated by purulent material

b. Enrofloxacin - decreased effectiveness in an acidified ear

c. Extended-spectrum penicillins (anti- Pseudomonas penicillins)

  • Susceptible to beta lactamase

  • Penetrate Pseudomonas cell wall better than other antibiotics

  • Increase gram negative activity but less activity gram positive and anaerobes compared to other penicillins

  • Carboxypenicillin

o Ticarcillin

  • Ureidopenicillins

o Piperacillin

o More effective against


than are the carboxypenicllins

a. Aminoglycocide

  • Amikacin and tobramycin

o Gram negative bacteria (including some


) have less resistance to amikacin or tobramycin then gentamicin or neomycin

o Decreased effectiveness in an acidified ear, also inactivated by purulent debris so they must be put in a clean ear

Antifungal agents used include thiabendazole (poor efficacy against Malassezia), nystatin (mixed efficacy against Malassezia), iodine based (Xenodine®)- avoid in cats- reports of renal failure associated w/its use), clotrimazole 1%, miconazole 1 % and ketoconazole 2%.

When gram negative organisms are present in cases of OE, EDTA should be used. To understand the action of ethylenediaminetetraacetic acid (EDTA) solution we need to review some microbiology. A capsule surrounds bacteria. Under the capsule is the cell wall that contains peptidoglycans. Under the cell wall is the cytoplasmic membrane (plasma membrane, cell membrane). The cytoplasmic membrane surrounds the cytoplasm and nuclear body. Gram negative have 2 additional layers. The outer most is the outer cell membrane that lies between the capsule and the cell wall. The outer cell membrane is composed of lipopolysaccharides. The other additional layer is between the cell wall and cytoplasmic membrane, called the periplasmic space. This space contains a variety of enzymes and other proteins that help digest and move nutrients into the cell. Gram positives do not have the outer cell membrane (and therefore no lipopolysaccharides) or a periplasmic space but do have a thick layer of peptidoglycans in the cell wall (vs. gram negatives which only have a thin layer). Note the peptidoglycans are the site of action for beta-lactam antibiotics.

Topical EDTA solution has a direct bactericidal action against bacteria by chelating metal ions important for the integrity of the bacterial cell wall. EDTA also stimulates the release of outer cell membrane lipopolysaccharides (LPS), proteins, and other cell contents. The end result of these actions is the leakage of cell solutes leading to cell death and better drug penetration and antimicrobial activity. Note - since EDTA stimulates the release of LPS from the outer membrane it is less effective at inhibiting gram-positive than gram-negative bacteria because gram-positive bacteria lack an outer membrane.

Pseudomonas bacteria have an efflux pump that is mediated by the MEX gene. This protein pumps the drugs out the bacteria, rendering the antibiotic ineffective. EDTA also blocks this pump thereby allowing the antibiotic to accumulate in the bacteria.

To maximize its bactericidal activity it is essential for EDTA to be in an environment w/an alkaline pH. Appropriate pH (8.0) is maintained by combining it with buffers such as tromethamine (TRIS) hydrochloride. This alkaline pH also decreases the bacterial MIC for aminoglycocides and fluoroquinolones. It is therefore useful to use TrisEDTA prior to instilling either of these antibiotics. Two commercial veterinary preparations are available - T8 Solution, DVM Pharmaceuticals and TrizEDTA, DermaPet. The ear canal should be filled with the solution prior to instilling the topical antibiotic (15-30 minutes is ideal). This is done q 8-12 hrs. EDTA is used primarily for treatment of otitis externa caused by gram-negative organisms especially Pseudomonas.

A product made by Dermapet, Triz EDTA plus contains 0.15% chlorhexidene. There is potentially a synergistic effect between EDTA and chlorhexidene. Recently there was a study that revealed that chlorhexidene at concentrations of 0.2% concentrations or less was safe to put in the middle ear. In this study, 0.2% chlorhexidine was instilled in greyhound's ears bid who had experimentally ruptured tympanic membranes. After 21 days there were no clinical vestibular signs nor BAER changes noted. Please note that Nolvasan Otic doesn't contain chlorhexidine as it had in the past.

A product made by DVM Pharmaceuticals, Inc. contains EDTA with 0.1% ketoconazole – called T8 + keto. Dermapet has a similar product called TrizEDTA plus keto. My concern is whether 0.1% will be effective in vivo and whether we will get resistance to the ketoconazole if used chronically. Also acidifying the ear canal is one of the best treatments for Malassezia otitis and these products alkalinize the ear.

GC's are an essential component of topical treatment. Successful treatment of OE frequently requires topical GC and in fact I have seen cases resolve where the only change in therapy was the addition of topical GC. GC are antipruritic, anti-inflammatory, decreases glandular secretions (cerumen), decreases pain and swelling and decreases hyperplasia- all properties that can help restore the normal barrier function to the epithelium of the ear canal. When using topical GC it is best to begin with the most potent form and if you need to use it long term, go to less potent forms (mematsone>betamethasone> fluocinolone> triamcinolone>dexamethasone> prednisolone> hydro-cortisone. REMEMBER topical steroids are systemically absorbed and can lower thyroid hormone concentrations; elevate liver enzymes even cause pu/pd.

Ear wicks are used to keep medication in contact with the ear canal during the treatment of otitis externa and or media especially when the owners just can't medicate the ear because the dog is too painful or their schedule prevents frequent dosing. It has also been used when there is a middle ear infection that can't control well. It is a unique medical grade sponge constructed with specially formulated polyvinyl acetate material. The wicks are supplied fully compressed for ease of insertion and will expand as fluid is introduced. The wicks absorb the medication and act as a reservoir slowly releasing the drugs. Antimicrobial agents and/or steroids solutions are applied bid to weekly depending on owner's ability to treat the dog/cat. They are changed (or removed) in 2 weeks. (conversation w/Dr Gotthelf).

Systemic antibiotics or antifungal agents are used only if there is evidence of otitis media w/bacteria (see below about Pseudomonas) or Malassezia present on cytology, OR there are severe proliferative changes and there are bacteria (or Malassezia) found on cytology. Empirical choices for cocci include cephalosporins, amoxicillin-clavulanate or clindamycin while for rods cephalosporins are selected, reserving fluoroquinolones for culture proven resistant gram-negative rods. Antifungal agents used include ketaconazole- 5-10 mg/kg sid-bid given w/food to enhance absorption or itraconazole 5 mg/kg –sid.

If the OM infection is due to Pseudomonas it is unlikely that systemic antibiotics would be useful. This is because systemic administration of antibiotics, including the fluoroquinolones, can't exceed the MIC for P. aeruginosa. Since P. aeruginosa is the most common pathogen associated w/OM in dogs, systemic administration of antibiotics will only encourage more resistant organisms. Since it has been documented in humans that high drug concentration may be achieved in the middle ear when treated with topical antibiotic, in cases of OM topical treatment is my mainstain therapy.

Systemic glucocorticoids are used if the ear canals are edematous and/or stenotic. Even proliferative changes may decrease due to the secondary edema that may be present. Prednisone at 0.25-.50 mg/# bid for 7-14 days is dispensed. Reassessment at that time dictates whether the dose is maintained for another 7-14 days, decreased or the drug just stopped.

Specific scenarios

1. Acute otitis (and/or infrequent) externa treatment overview. Be sure to differentiate whether this is a first time occurrence, a recurrence or an unresolved previous infection. The only way to know this is to do follow-up examinations on ALL your OE cases. Absence of symptoms vs. resolution of disease is not synonymous. If this is the first episode, explain the possible predisposing, primary and perpetuating causes and foreshadow the possible workups that may be necessary. Eliminate easily diagnosed primary causes (foreign bodies, parasites, masses, etc). Be sure to evaluate the status of the tympanic membrane. Diagnosis and treat secondary infection and inflammation, treat for 7-14 days & then recheck!! Be sure to treat for 7 days past clinical cure. Unless contraindicated I will always put some type of GC containing product into the ear as part of the therapy.

a. Products that I use for these cases are – if only yeast – miconazole 2%-Conofite cream®, Resizole® or Conofite lotion1% ® - I will either mix w/3 cc of dexamethasone SP if it is a lotion or I will treat w/synotic first and then follow w/the creams.

b. In cases of mixed infection (bacteria and yeast) I will use nystatin-containing products (Panolog®, Quadritop®, Animax®). These are frequently effective, especially if it is an acute infection.

c. If cocci or cocci/rods are present I will use neomycin or gentamicin containing products (Otomax®).

d. If only rods are present, which is very rare in this scenario, I would use TrisEDTA and either gentamicin or polymyxin B or E. (see below – Pseudomonas)

e. If the dog is painful, I will add systemic GC +/- analgesics (tramadol and/or Tylenol w/codeine) to the treatment.

2. If initially I am unable to visualize the TM due to swelling of the ear canals I will add to my topical treatment, oral glucocorticoids -prednisone ½-1mg/#/day for 10-14 days and topical Synotic or Mometamax. Many times I will add an analgesic as previously described (NO NSAID!).

a. I will recheck the dog in 10-14 days. If the TM is visible and the swelling resolved, I will stop the prednisone but continue all other treatment and diagnostics.

b. If the TM is not visible but the swelling has resolved, I will do an ear lavage via FEVO under general anesthesia.

c. If at the 10-14 day recheck the TM is not visible and the swelling has NOT resolved, I will continue prednisone for another 10-14 days and then recheck.

d. If the ear canals are still narrowed at the next recheck, I will consider referring for ear ablation

3. In cases of chronic (recurrent and/or unresolved) otitis externa in addition to the above I will be very aggressive about identifying and treating primary, perpetuating and secondary factors and I will treat for a minimum of 30 days. As above, GC will be an important component of therapy. I will treat the dog for a minimum of 30 days. As above, GC will be an important component of therapy.

a. If there is only yeast, then the depending on what products have already been used, I will use clotrimazole 1%, miconazole 1% or will make a 2% ketaconazole lotion (take 600 mg ketaconazole tabs, crush and add to 1 oz of Burotic HC) w/steroids added as described previously. Sometimes I use an acetic acid/boric acid cleaner (Malacetic otic) depending on how inflamed the ear is (if it is inflamed I avoid the cleaner).

b. If cocci are the only organism present then I will use gentamicin or mupirocin.

c. If rods +/- cocci are present then I will use-Triz-Edta (+/- chlorhexidene if cocci are present) mixed w/ gentamicin or use concurrently, but not mixed in vitro, with polymyxin B containing products depending on which antibiotics had been used in the past.

d. I rarely use enrofloxacin in these cases unless the infection fails to respond to my aggressive therapy.

Pseudomonas infections are especially challenging because of Pseudomonas' intrinsic multidrug resistance (MDR). Many of the clinically relevant resistance mechanisms in Pseudomonas aeruginosa are attributed to synergy between it's outer membrane that has a very low permeability to drugs and the presence of an active drug efflux pump (MEX). Because of the MDR we must be aggressive in our treatment of Pseudomonas infections. This will be discussed in more detail in the lecture on otitis media.


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