Diagnosing and managing canine bacterial pyoderma-parts 1 & 2 (Proceedings)


Diagnosing and managing canine bacterial pyoderma-parts 1 & 2 (Proceedings)

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.
Oct 01, 2011

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 food triggered atopic dermatitis 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 up to 20% of the cases (see reference) 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 unless addressed.  Perpetuating factors include:

  1. Bacteria (cocci most commonly Staphylococcus pseudintermedius [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 (multiple by 2.5 to get per HPF), between normal and abnormal ears range from >1 Malassezia to >4 Malassezia and from >1 cocci shaped bacteria to >10.  It is my opinion that the number of these organisms needed to be present to be considered significant is not just a “number”. I don’t perform cytology on normal ears – I only do them if the ears that are inflamed or have exudate.  In those cases ANY organism seen will be treated as part of the therapy regardless of the number present.   Please note-inflammatory cells and rod shaped bacteria are never normal on ear cytology.

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 and the ear is clinically normal at the recheck examination, 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.

Lastly a recent study comparing the correlation between culture results and clinical response was reported.  In that study they used empirically selected topical antimicrobials and then compared response to treatment vs. what the culture results predicted (susceptible = success and resistant = failure).  They found that there was a poor correlation between in vitro antibiotic resistance and in vivo response to empirically selected therapies for Pseudomonas otitis

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.  Efficacy = MIC + dose+ treatment frequency.  The advantage of the MIC method is that not only does it indicate 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 done by the technician.  It 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.  Because I prefer otic ointments over drops I feel that the ear cleaning with a separate product is not necessary.  It seems that the mineral oil this is in the ear preparations have enough cerumolytic activity that the ear stays clean during treatment (other than ointment remaining in the ears during treatment)

After ear cleaning by the technician, topical agents are dispensed.  As mentioned above,I prefer ointments over drops because of my 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 topical products contain a combination of glucocorticoids, antibacterial and antifungal agents.  Antibacterial agents used topically include:

  1. Broad spectrum agents (gram positive and negative organisms) –
  1. Aminoglycocides
  1. Decreased effectiveness in an acidified ear
  2. Inactivated by purulent debris (so they must be put in a clean ear)
  3. Examples of first line
  • Neomycin 
  • Gentamicin
  1. Silver sulfadiazine - inactivated by purulent debris so they must be put in a clean ear
  1. Spectrum also includes yeast
  1. Narrow spectrum agents (gram negative rods) - reserved for resistant gram negative infections
  1. Polymyxin B - inactivated by purulent material
  2. Fluoroquinolones (enrofloxacin or orbifloxacin) - decreased effectiveness in an acidified ear
  3. Extended-spectrum penicillin’s (anti- Pseudomonas penicillin’s)
  1. Susceptible to beta lactams
  2. Penetrate Pseudomonas cell wall better than other antibiotics
  3. Increase gram negative activity but less activity gram positive and anaerobes compared to other penicillin’s
  4. Carboxypenicllins
  • Ticarcillin
  1. Ureidopenicillins
  • Piperacillin
  • More effective against Pseudomonas than are the carboxypenicllins
  1. Aminoglycocide
  1. Amikacin and tobramycin
  • Gram negative bacteria (including some Pseudomonas) have less resistance to amikacin or tobramycin then gentamicin or neomycin
  • Decreased effectiveness in an acidified ear, also inactivated by purulent debris so they must be put in a clean ear
  1.  Antifungal agents
  1. Thiabendazole (poor efficacy against Malassezia),
  2. Nystatin (mixed efficacy against Malassezia),
  3. Clotrimazole 1%
  4. Miconazole 1 %
  5. Posaconazole – 0.1%
  6. 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. (Figure 1)

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.  Dechra manufactures a commercial veterinary preparation TrizEDTAt. The ear canal should be filled with the solution prior to instilling the topical antibiotic.  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 Dechra contains not only Triz EDTA but also 0.15% chlorhexidene (TrizCHLORTM. Dechra).  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 neither 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 Dechra contains ketoconazole(TrizEDTA ultra 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.  

Lastly Dechra has an ear flush product that contains 0.15% Ketoconazole and 0.15% chlorhexidene in a TrizEDTA base which would be effective for mixed infections (Malassezia, rods and cocci all being present)

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.  This observation was confirmed in a study in which demonstrated the superiority of a mixture of corticosteroids and antifungal agent in comparison with an antifungal agent used alone for the treatment of Malassezia otitis externa.  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> hydrocortisone.  REMEMBER topical steroids are systemically absorbed and can lower thyroid hormone concentrations; elevate liver enzymes even cause pu/pd.

Systemic antibiotics or antifungal agents are used only if there is evidence of otitis media w/bacteria (other than Pseudomonas see below about Pseudomonas) or Malassezia present on cytology or in patients that test positive for bacteria or Malassezia on cytology and that have severe proliferative changes in the ear canals that failed to respond to MY topical treatment.  Empirical choices for cocci include cephalosporins, amoxicillin–clavulanic acid, clindamycin and potentiated sulfas. Empirical choices for rods include cephalosporins, amoxicillin–clavulanic acid (use TID vs. BID for gram positive organisms) and potentiated sulfas.  I reserve fluoroquinolones for culture-proven resistant gram-negative rods.  The antifungal agents I use include ketoconazole (5 to 10 mg/kg sid, given with food to enhance absorption), fluconazole (10 mg/kg sid), and 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 mainstay 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 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 (food trial, intradermal or serum testing for IgE, etc).  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. 
  1. Products that I use for these cases are
  2. If only yeast – miconazole (Conofite lotion1% ® and add 3 cc of dexamethasone SP, Surolan® (Miconazole nitrate 23 mg (=2%) or nystatin (Panolog®, Quadritop®, Animax®
  3. In cases of cocci only or mixed infection (bacteria and yeast) I will use neomycin/nystatin/ thiostrepton/ triamcinolone-containing product (Panolog®, Quadritop®, Animax®) or a miconazole nitrate/polymyxin B/prednisolone containing product.  These are usually effective, especially if it is an acute infection. 
  1. In cases of mixed infection (bacteria and yeast) which has been recently treated I will use a gentamicin containing product (Otomax®).  (2nd line choice)
  2. I consider do not use fluoroquinolone containing products unless the infection has failed to respond to treatment at the follow up examination.  This doesn’t mean the otitis that failed to be rechecked, it means that the patient is re-examined while on treatment and the otitis is still present.  (3rd line choice)
  1. If only rods are present, which is very rare in this scenario, I would use TrisEDTA plus and gentamicin (see below – Pseudomonas)
  2. If the dog is painful, I will add systemic GC +/- analgesics (tramadol and/or Tylenol w/codeine) to the treatment.
  1. 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!). 
  1. 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. 
  2. If the TM is not visible but the swelling has resolved, I will do an ear lavage via FEVO under general anesthesia. 
  3. 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.
  4. If the ear canals are still narrowed at the next recheck, I will consider referring for ear ablation

In cases of chronic (unresolved) otitis externa (not unresolved due to owner compliance issues) 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.  Specific treatment is as follows 

  1. Yeast only
  1. Miconazole 2%
  2. Surolan®
  3. Clotrimazole Solution 1%
  4. Otomax®
  5. Ketoconazole  2% compounded
  6. Posaconazole  0.1%(Posatex®)
  1. Cocci only
  1. Gentamicin- Otomax or EDTA w/gentocin and dexamethasone SP added-see    
  2. below
  3. iii) Amikacin- mixed w/EDTA and dexamethasone SP added- see below
  1. Rods and cocci- TrizEDTA and add/use concurrently (depends on previous antibiotic) as  follows:
  1. Gentamicin – 3-6 mg/ml - added to TrizEDTA and 120 mg dexamethasone 
  2. SP (4 mg/ml)
  3. Polymyxin B (Surolan® otic suspension  (Vétoquinol)
  1. Use concurrently w/EDTA
  1. Amikacin  -10 mg/ml added to TrizEDTA and 120 mg dexamethasone SP (4 mg/ml)
  2. Fluoroquinolone (Posatex, compounded enrofloxacin)
  1. Rods only (probably Pseudomonas)- Triz EDTA – 4 oz and combine w/or use concurrently w/
  1. Gentamicin
  1. 360 mg (720 mg if an intact TM)
  2. 120 mg dexamethasone SP  (4mg/ml)
  3. Final concentration
  • O.26% gentamicin and 0.1% dexamethasone SP
  1. Fluoroquinolones (FQ)
  1. All fluoroquinolones (FQ) should be considered a 3rd line
  2. otic product
  3. Enrofloxacin
  • Avoid mixing w/ Triz Chlor flush (contains CHX) the chlorhexidene component will be active for less       than 14 days
  • Compounded
  • 1200 mg of enrofloxacin (100 mg/ml)
  • 120 mg dexamethasone sodium
  • Phosphate (4mg/ml)      
  1. Orbifloxacin
  • Posatex Otic Suspension (Intervet/Schering-Plough Animal Health)
  • Orbifloxacin 1.0%
  • Mometasone  0.1%
  • Posaconazole 0.1%
  1. Amikacin injectable- 250 mg /ml- final is 10 mg/ml
  1. 4.8 cc of amikacin
  2. 120 mg  dexamethasone  SP
  3. Can add enrofloxacin (1200 mg)
  4. Amikacin and enrofloxacin are synergistic


  1. Polymyxin B - Surolan® otic suspension (Vétoquinol)
  1. Miconazole nitrate
  2. Polymyxin B
  3. Prednisolone acetate
  4. Use concurrently w/EDTA but not combined
  1.  BNT – (BNP compounding pharmacy) contains the following in a lanolin base
  1. Enrofloxacin (0.23%)
  2. Ketoconazole (0.67%)
  3. Triamcinolone (0.1%)
  4. If you need to use this type of product- consider replacing the enrofloxacin w/gentocin.  If there are no bacteria- make the product w/o any antibiotics.  If using enrofloxacin have them make it a 1% concentration and if using it w/ketoconazole have them make it 2%.

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 its 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.


Griffin CE, DeBoer DJ. The ACVD task force on canine atopic dermatitis (XIV): clinical manifestations of canine atopic dermatitis. Veterinary Immunology and Immunopathology 2001; 81: 255–69.

Ginel PJ, Lucena R, Rodriguez JC, et al: A semiquantitative cytological evaluation of normal and pathological samples from the external ear canal of dogs and cats Vet Dermatol 13:151-156, 2002

Robson DC, Burton GG, Bassett RJ Correlation between topical antibiotic selection, in vitro bacterial  antibiotic sensitivity and clinical response in 16 cases of canine otitis externa complicated by Pseudomonas aeruginosa Vet Dermatology 2010, 21: 3 ;245

Bensignor E: Treatment of Malassezia otitis in dogs: a comparative field trial- Vet Dermatology 2004, 15:s1;45