85 Integumentary Infections

Infectious Diseases of the Dog and Cat, 3rd Edition

CHAPTER 85 Integumentary Infections

BACTERIAL INFECTIONS OF THE SKIN

Peter J. Ihrke

Pyoderma is defined as a pyogenic or pus-producing bacterial infection of the skin. The diversity of clinical syndromes seen with canine pyoderma is enormous, varying from minor annoyances to disease with life-threatening potential.* Pyoderma may affect the surface, creating inflammation without the invasion of living tissue; be superficial, involving the epidermis and hair follicle units; or invade deeper, compromising structures in the dermis and subjacent fatty tissue. This tremendous diversity and pleomorphism is responsible for diagnostic and management difficulties that may be encountered. Misdiagnosis also may result from the continuum of clinical characteristics and severity of the pyoderma, among various dogs, of different anatomic sites, and between acute and chronic disease. The presence of pus cannot be used as a defining diagnostic criterion because pus may not be visible grossly. The aging and rupture of pustules leads to crusted papules that are much more difficult to use for diagnosis. In addition, accumulations of pus in the mid-dermis in deep pyoderma may not be visually obvious.

Globally, pyoderma remains one of the most common causes of canine skin disease. Pyoderma was second only to

flea allergy dermatitis in frequency of diagnosis in a study from North American veterinary colleges.67,134 An additional epidemiologic study performed in a relatively flea-free environment in Canada ranked bacterial folliculitis and furunculosis first among all canine skin diseases, comprising more than one quarter of the

dermatology caseload.133 Conversely, pyoderma is a relatively uncommon cause of skin disease in cats, other domestic animals, and humans. Bacterial skin disease in the cat is rare, with the exception of subcutaneous bite wound abscesses (see Chapter 53).

The reasons for the markedly elevated frequency of bacterial skin disease in the dog in comparison with other mammalian species are unknown. Various host factors that may result in enhanced susceptibility include the comparatively thin, compact canine stratum corneum, the relative lack of intercellular lipids in the canine stratum corneum, the lack of a lipid-squamous epithelial plug in the entrance of canine hair follicles, and the relatively

high pH of canine skin.67,86,98,132

Etiology and Pathogenesis

Normal Microflora of the Skin and Hair

Skin microbial flora is composed of resident and transient bacteria. Resident bacteria are harmless commensals that multiply on the skin surface and in hair follicles and maintain a static, consistent population. Transient bacteria cannot compete long term with the established resident flora and may seed the skin from either mucous membranes, other animals, or the environment. The total number of resident bacteria residing on normal canine skin is not large and may comprise less than 350 organisms per square

centimeter.67 Studies examining the bacterial flora of normal dogs have documented aerobic organisms, including Micrococcus species, β-hemolytic streptococci, and Acinetobacter species, and anaerobic organisms, including Clostridium perfringens and Propionibacterium acnes.*

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Published data have clarified the role of Staphylococcus intermedius in canine pyoderma.† This pathogen is probably not a true cutaneous resident but rather a contaminant on normal canine hair and either a contaminant or a transient, restricted, local colonist on normal canine skin. Mucous membranes such as those of the anus and nares probably play an important role as sources of this potential skin pathogen. Normal grooming in all dogs, and excessive licking in pruritic dogs, may repetitively seed the skin with S. intermedius from the anus and nares.‡

* References 65, 67, 68, 96, 106, 131, 132, 150.

* References 55, 57, 66, 67, 84, 131, 132.

† References 2, 4, 5, 41, 55, 57, 67, 84, 97, 124, 125.

‡ References 2, 3, 4, 5, 67, 84.

Staphylococcus intermedius and Other Canine Cutaneous Pathogens

S. intermedius is the primary canine cutaneous pathogen. This organism is a species separate and distinct

from the human pathogen, Staphylococcus aureus.50,67 Pure cultures of this bacterium are grown from most pustules or draining tracts in dogs with pyoderma. Recently, two subspecies of Staphylococcus schleiferi

were implicated as causing some cases of recurrent canine pyoderma.11,43 It is likely that these subspecies of S. schleiferi formerly were misidentified as S. intermedius. Limited data indicate that methicillin and

fluoroquinolone resistance may be more common in strains of S. schleiferi.43 Methicillin resistance also may

be increasing slightly within the S. intermedius population.47

Pathogenicity of staphylococci in humans correlates with virulence factors such as various proteins and toxins. Evidence does not support virulence factors as the cause of differences in canine susceptibility or

severity of infection.19,25,59,67,68

When potential virulence factors have been examined comparing S. intermedius isolates from normal dogs and dogs with pyoderma, clear differences in toxin profiles, gel electrophoresis of exoproteins, and immunoblotting of concentrated extracellular proteins were not elucidated.* Production of exotoxins does

not appear to play a role in the pathogenicity of S. intermedius for canine skin.19 The role of various other virulence factors such as protein A, leukocidin, hemolysins, epidermolytic toxin, and other soluble products is less clear in the dog. Data suggest that host factors rather than virulence factors appear to be more important in determining susceptibility, severity, and outcome in canine staphylococcal pyoderma.†

Secondary gram-negative invaders such as Proteus species, Pseudomonas species, or Escherichia coli may be isolated in conjunction with S. intermedius, usually from deep pyoderma. However, if gram-negative bacteria are isolated from pyoderma without the concomitant isolation of S. intermedius, the technique used and the results obtained should be questioned, because canine pyoderma caused by gram-negative bacteria without staphylococcal coinfection is exceedingly rare. Primary infection with S. intermedius creates a tissue

milieu that is more conducive to secondary invasion by gram-negative bacteria.66,67

* References 1, 3, 19, 49, 50, 67.

† References 1, 3, 50, 19, 25, 67, 132.

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Microbial Alterations with Skin Disease

The factors that promote the proliferation of S. intermedius on skin leading to pyoderma are poorly understood. However, it is well established that dogs with other skin diseases are more likely to develop secondary pyoderma. Dogs with defects in cornification exhibit a shift in the balance of bacterial species colonizing the skin such that coagulase-positive staphylococci predominate. Clinically, this correlates with an increased frequency of pyoderma in dogs with cornification abnormalities. A shift in the frequency and intensity of staphylococcal colonization has been noted in dogs with atopic dermatitis and contact dermatitis

as well as seborrheic dermatitis.67

Zoonotic Potential of Skin Pathogens

Because S. intermedius is a separate and distinct species from S. aureus, this partially explains why humans with a normally functioning immune system are not at great risk for skin or wound infections contaminated with S. intermedius. Healthy owners of dogs with staphylococcal pyoderma are generally not at risk for zoonotic bacterial infection. However, subclinical transfer of the organism from dogs to people has been

documented.51,140 Many of the isolated strains have been antimicrobial resistant strains. These data indicate that a dog with suppurative pyoderma would be of medical concern if an immunocompromised household member were bitten or exposed to suppurative discharges. Dogs harbor this organism in their mouth; up to

21% of dog bite lesions in people may be infected with S. intermedius.139 Nevertheless, the pathogenicity of other bite-transmitted organisms unassociated with pyoderma is greater. (For additional information on bite transmission of this organism, see Bite Wound Infections, Chapter 53.)

S. schleiferi is a recognized human pathogen, causing nosocomial infections. It has been isolated as a commensal from human skin. Antimicrobial-resistant strains of this organism have been isolated from people, dogs, and cats. In the past, many human and veterinary laboratories have likely confused this organism with S. aureus and S. intermedius, respectively. Although S. schleiferi has been identified in the skin of clinically healthy dogs, the prevalence of carriage has not been determined. Isolations of S. schleiferi in dogs have primarily been from those with otitis externa or recurrent pyoderma, and the majority of isolates

have been methicillin resistant.43 Because S. schleiferi has been both a commensal and pathogen in people, the concern of transferring this potentially drug-resistant pathogen between people and pets is considerable. Additional investigations are needed.

The human pathogen, S. aureus, has also been isolated from animals, including dogs and cats that have close

association with people.63,90 Methicillin-resistant S. aureus strains have also been identified in pets, making them potential sources for infection of people. For an additional discussion of this problem, see Staphylococcal Infections, Chapter 36, and Immunocompromised People and Pets, Chapter 99.

Susceptibility and Host Response to Infection

S. intermedius does not possess the requisite virulence factors to be a potent pathogen. Consequently, most canine pyodermas probably are associated with underlying disease or other host factors. Diseases such as ectoparasitism, cornification defects (seborrhea), allergies (atopic dermatitis, food allergy, flea allergy dermatitis), hereditary skin diseases (genodermatoses)—especially those affecting hair follicles—and endocrinopathies such as hypothyroidism and Cushing's disease frequently predispose animals to

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Infectious Diseases of the Dog and Cat, 3rd Editionpyoderma.35,67,78,131,132 Pyoderma secondary to cornification defects and allergic diseases are best documented. More broadly, pruritus from any underlying disease, cutaneous inflammation from any cause, injudicious use of glucocorticoids (iatrogenic hyperglucocorticoidism), and poor grooming in long-coated dogs all contribute to the likelihood of secondary pyoderma.

Superficial infection of the hair follicle is the most common canine pyoderma. Follicular defects, dysplasia, obstruction, atrophy, inflammation, or degeneration predispose to folliculitis. After pyoderma is initiated, immunologic incompetence, coexisting skin disease, pruritus, inflammation, scar tissue formation, and

improper initial therapy are negative prognostic factors.67

The initiation of staphylococcal pyoderma requires colonization and invasion of host tissues in addition to evasion of host immunity. Host defense mechanisms mobilized to prevent bacterial invasion include immunologic and nonimmunologic processes. Nonimmunologic mechanisms include the desquamation of the stratum corneum (surface and follicular), the lipid intercellular barrier, epithelial proliferation in response to injury, and the antibacterial effect of inorganic salts found in sebum and sweat. Additionally, competition among resident bacteria is a nonimmunologic, “nonhost” defense mechanism. Immunologic host defense mechanisms of the skin include proteins within the intercellular matrix; immunoglobulins within the basement membrane zone; and immunologically active cells such as Langerhans cells, dermal dendrocytes,

lymphocytes, mast cells, and venular endothelial cells present in either the epidermis or dermis.67

Host immunologic response may be deleterious as well as beneficial. Some dogs with chronic or recurrent pyoderma exhibit depression of lymphocyte transformation testing. Exceptionally potent bacterial antigens, termed superantigens, may explain the troublesome nature of pyoderma secondary to canine atopic

dermatitis and the marked inflammation and pruritus seen in some canine pyoderma.67

Bacterial hypersensitivity has long been theorized as a complicating factor in recurrent canine pyoderma. The potential importance of bacterial hypersensitivity has been underscored by work indicating that mast cell

degranulation can initiate enhanced epidermal permeability to bacterial antigens in atopic dogs.67,97 Several studies have verified an association between antistaphylococcal antibodies and various subgroups of canine

pyoderma.67,105

Classification of Pyoderma

Classification based on depth of bacterial involvement is most useful clinically because it provides information on diagnosis, likelihood of underlying disease, prognosis, required duration of therapy and response to therapy. In general, the deeper the infection, the more likely that underlying triggering causes are present. Deeper infections also require that the clinician be more aggressive diagnostically and therapeutically. Using depth of bacterial infection, canine pyoderma can be described as surface, superficial,

or deep (Table 85-1).67

Surface Pyoderma

Surface pyoderma consist of inflammatory processes in the skin without strong evidence of direct bacterial invasion. Bacterial involvement probably is secondary to various factors that encourage surface bacterial overgrowth. Pyotraumatic dermatitis (acute moist dermatitis, hot spots), intertrigo (skinfold pyoderma), mucocutaneous pyoderma, and surface bacterial overgrowth are classified as surface pyoderma. Pyotraumatic dermatitis usually develops secondary to flea allergy dermatitis. Intertrigo occurs

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Infectious Diseases of the Dog and Cat, 3rd Editionin skinfolds secondary to breed-characteristic anatomic defects and is seen in conjunction with friction, poor drainage, and maceration. In mucocutaneous pyoderma, bacterial involvement may become deeper with chronicity. Mucocutaneous pyoderma is a surface disease of unknown cause that predominantly

involves the lips and perioral skin but may involve other mucocutaneous sites such as the anus.67,70 Intertrigo and pyotraumatic dermatitis rarely are diagnostic or therapeutic challenges.

Table 85-1 Classification of Canine Pyoderma Based on Depth of Infection

SURFACE PYODERMA

Pyotraumatic dermatitis (acute moist dermatitis, hot spots)

Intertrigo (skinfold pyoderma): lip-fold, facial-fold, vulvar-fold, tail-fold, obesity-fold

Mucocutaneous pyodermaa

Surface bacterial overgrowtha

SUPERFICIAL PYODERMA

Impetigo (puppy pyoderma)

Superficial bacterial folliculitisa

Superficial spreading pyodermaa (exfoliative pyoderma)

DEEP PYODERMA

Deep bacterial folliculitis and furunculosis

Muzzle folliculitis and furunculosis (canine acne)

Pyotraumatic folliculitisa

Pedal folliculitis and furunculosisa

Callus pyoderma (pressure-point pyoderma)

German shepherd dog pyodermaa

Cellulitis (secondary to demodicosis or immunologic incompetence)

DISEASES FORMERLY CLASSIFIED AS PYODERMA

Juvenile sterile granulomatous dermatitis and lymphadenitis (juvenile cellulitis, puppy strangles, juvenile “pyoderma”)

Hidradenitis suppurativab

a Subgroups of pyoderma in which recurrence or recrudescence is more common.

b These diseases were most likely autoimmune subepidermal blistering diseases or were vesicular cutaneous lupus erythematosus of the Shetland sheepdog or collie.



In the past, the clinical importance of surface overgrowth by staphylococci and other bacteria has not been recognized in the dog. The author feels that secondary surface bacterial overgrowth triggered by underlying, predisposing skin disease is a prime cause and perpetuator of chronic cutaneous inflammation and pruritus in dogs.

Superficial Pyoderma

Superficial pyoderma is the most common type of canine bacterial skin disease. Impetigo is characterized by nonfollicular, intraepidermal pustules involving the superficial layers of the epidermis (Fig. 85-1). Superficial folliculitis affects the ostial portion of the hair follicle and is the most common subgrouping of canine pyoderma. Impetigo and superficial folliculitis may be a diagnostic challenge because pustules rupture readily, giving rise to considerably less diagnostic crusted papules. A third clinical subset of superficial pyoderma, termed superficial spreading pyoderma, is characterized by centrifugally expanding inflammation with characteristic peripheral epidermal collarettes. Superficial spreading pyoderma may be seen alone or in conjunction with superficial folliculitis.

Deep Pyoderma

Deep pyoderma is characterized by infection that proceeds deeper in the hair follicle with or without follicular rupture. The factors that allow infection to proceed from superficial to deep folliculitis are not understood. Deep folliculitis can lead to follicular rupture (furunculosis) with a granulomatous foreign body tissue response (Fig. 85-2). Interconnecting furunculosis involving the interstitium between hair follicles, the dermis, and subcutis is termed cellulitis. Deep pyoderma is much less common than superficial pyoderma. Diagnosis of deep pyoderma usually is not difficult; however, therapy often is problematic.

Clinical Findings

Dermatology has a singular advantage over most other specialty medical disciplines in that skin lesions are visible for careful inspection and available for precise sampling. Excellent lighting is essential for a proper physical examination. A hand lens is beneficial. Severity, extent, and pattern of clinical findings may be clarified additionally by clipping overlying hair from an affected lesion.

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Fig 85-1 Impetigo in young pup with severe intestinal parasitism. (Courtesy University of Georgia, Athens, Ga.)

Fig 85-2 Interdigital pyoderma in dog with draining tracts and a granulomatous inflammatory reaction. (Courtesy University of Georgia, Athens, Ga.)

Primary Skin Lesions

An erythematous papule is the most common primary skin lesion seen in most superficial and milder deep pyoderma. Papules are circumscribed, solid elevations of the skin that usually form in groups. As infection

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Infectious Diseases of the Dog and Cat, 3rd Editionproceeds, pus accumulates in intraepidermal or follicular locations, forming pustules. Small pustules may appear as papules to the unaided eye. Intact pustules often are transient in canine skin. When surface pustules rupture, crusted papules result. In deep pyoderma, more intense inflammation leads to nodule formation. Follicular rupture exacerbates inflammation in the adjacent dermis, resulting in larger nodules with fistulation. Peripheral collarettes, the “footprints” of pyoderma, are composed of detaching stratum corneum at the margins of inflammation. In deep pyoderma, host response is more intense, producing more obvious inflammation and swelling.

Secondary Skin Lesions

Pustules either rupture spontaneously or are obliterated by self-trauma, resulting in crusted papules. Clinically, crusted papules are less useful for diagnosis and may be indistinguishable from the papules seen with many other skin diseases. If crusted papules are grouped, crusts composed of dried pus, exudate, and keratin debris may mimic disorders of cornification. Self-traumatic excoriations may obliterate more diagnostic primary lesions, because pruritus is a feature of many pyodermas.

Alopecia commonly is seen secondary to pyoderma as hair fragments are shed from infected follicles. Transient, patchy (moth-eaten) alopecia probably results from premature telogenization and telogen arrest in a normally mosaic, asynchronous hair replacement pattern. Permanent, scarring alopecia secondary to deep folliculitis and furunculosis is uncommon in the dog, in contrast with pyoderma in people. Cellulitis leads to follicular obliteration.

Follicular rupture in deep pyoderma leads to nodule formation and draining fistulous tracts (see Fig. 85-2). Dermal hemorrhage resulting from follicular rupture with intense inflammation may result in hemorrhagic bullae that appear as dark bluish regions visible in the dermis.

Distribution of Lesions

Acute moist dermatitis, usually secondary to flea allergy dermatitis, is seen most commonly in the dorsal lumbosacral region. Intertrigo, or skinfold pyoderma, is observed at the specific site of the anatomic defect (lip-fold, facial-fold, vulvar-fold, tail-fold) according to breed. Mucocutaneous pyoderma occurs predominantly on and around the lips but may affect other mucocutaneous junctions. Surface bacterial overgrowth most commonly initially affects the intertriginous folds, such as those seen in the groin and axillae, but may become a generalized infection.

Uncomplicated superficial pyoderma occurs predominantly in the moist, intertriginous zones of the groin and axilla and to a lesser extent in the interdigital webs. Impetigo occurs primarily in the groin of prepubescent dogs. Superficial folliculitis and superficial spreading pyoderma are most commonly found in the groin and axilla, but lesions may generalize on the thorax. The attendant patchy, partial alopecia is more visually distinctive in short-coated breeds. Improper use of glucocorticoids may contribute to the spread of any superficial pyoderma while paradoxically decreasing visible inflammation. Bullous impetigo in the adult dog is most commonly secondary to iatrogenic hyperglucocorticoidism but can be associated with other underlying immunosuppressive diseases.

Deep pyoderma usually develop as an extension of superficial pyoderma. A characteristic distribution is seen with interdigital, pressure-point and nasal pyoderma, and canine acne. Because most canine cellulitis occurs secondary to generalized demodicosis, the distribution is similar to that of the primary disease.

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Diagnosis

Differential Diagnoses

Many other skin diseases may mimic canine pyoderma. Differential diagnoses are listed in an approximate

order of importance in Table 85-2. For additional information, see the Suggested Readings.67,131

Various diagnostic procedures may be helpful in diagnosing pyoderma and determining the presence of underlying diseases or other predisposing factors. Skin scrapings, cytologic examination, and skin biopsy

usually are the most useful diagnostic procedures for the evaluation of suspected pyoderma.67 Conversely, bacterial culture and identification and antibiotic susceptibility testing are overused procedures, because bacterial species and susceptibility to antimicrobial therapy commonly can be predicted.

Skin Scrapings

Skin scrapings should be performed in all suspected cases of canine pyoderma, because demodicosis can initiate lesions that mimic uncomplicated pyoderma. It is especially important to scrape any pustular or papular lesion with a follicular orientation. In addition to mimicking pyoderma, demodicosis commonly triggers secondary pyoderma. Pyoderma secondary to demodicosis follows the distribution pattern of demodicosis, aiding diagnosis. Skin scrapings are more likely to yield demodicosis in suspected cases of lip-fold intertrigo, superficial folliculitis, deep folliculitis, furunculosis (canine acne, pedal folliculitis), and cellulitis.

Cytologic Examination

Cytologic examination is a simple, cost-effective, and frequently beneficial diagnostic test for the documentation of canine pyoderma. Material from either direct smears of pustules or draining tracts often yields as much or more useful information than bacterial cultures and is more rapid and cost effective. Cytologic examinations of inflamed skin lacking primary lesions often demonstrates inappropriate surface bacterial overgrowth. Specimens should be air dried and stained with either a modified Romanovsky-type Wright's stain (Diff-Quik) or new methylene blue. Modified Wright's stain is beneficial both for documenting organisms and identifying inflammatory cells. The identification of cocci indicates the probable presence of S. intermedius. The presence of degenerating neutrophils and intracellular cocci supports the diagnosis.

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Table 85-2 Differential Diagnosis of Canine Pyoderma

SURFACE

Pyotraumatic dermatitis (acute moist dermatitis, hot spots): Pyotraumatic folliculitis, demodicosis, neoplasia (especially sweat gland adenocarcinoma), cutaneous metastasis, fixed drug eruption, early necrotizing form of idiopathic nodular panniculitis, early localized vasculitis, focal Malassezia dermatitis, candidiasis

Intertrigo (skin-fold pyoderma)

Lip-fold intertrigo: Localized demodicosis; fixed drug eruption; superficial necrolytic dermatitis, with or without Malassezia dermatitis or candidiasis; zinc-responsive dermatosis; muzzle folliculitis and furunculosis (canine acne); localized pemphigus foliaceus; early pemphigus vulgaris; early autoimmune subepidermal blistering disease

Facial-fold intertrigo: Localized demodicosis, Malassezia dermatitis, dermatophytosis

Vulvar-fold intertrigo: Urinary tract infection with self-trauma, vesicular cutaneous lupus erythematosus, ulcerative dermatosis of the Shetland sheepdog and collie, drug eruption, canine familial dermatomyositis, pemphigus vulgaris, early autoimmune subepidermal blistering disease

Tail-fold intertrigo: Flea allergy dermatitis

Obesity-fold intertrigo: Malassezia dermatitis

Mucocutaneous pyoderma: Lip-fold intertrigo, localized demodicosis, early discoid lupus erythematosus, zinc-responsive dermatosis, generic dog food dermatosis, muzzle folliculitis and furunculosis (canine acne)

Surface bacterial overgrowth: Malassezia dermatitis

SUPERFICIAL

Impetigo (puppy pyoderma): Early flea allergy dermatitis, superficial folliculitis

Superficial bacterial folliculitis: Superficial spreading pyoderma, flea allergy dermatitis, demodicosis, pemphigus foliaceus, sarcoptic acariasis, severe impetigo, drug eruption, erythema multiforme, seborrheic dermatitis, sterile eosinophilic pustulosis

Superficial spreading pyoderma: Superficial bacterial folliculitis, pemphigus foliaceus, erythema multiforme, seborrheic dermatitis

DEEP

Deep folliculitis and furunculosis: Demodicosis, subcutaneous and deep mycoses, opportunistic fungal infections, pythiosis, lagenidiosis, severe maladapted dermatophytosis, sterile granuloma-pyogranuloma, histiocytosis, idiopathic nodular panniculitis, juvenile sterile granulomatous dermatitis and lymphadenitis, vasculitis

Pyotraumatic folliculitis: Pyotraumatic dermatitis, demodicosis, neoplasia (especially sweat gland adenocarcinoma), cutaneous metastasis, fixed drug eruption, early necrotizing form of idiopathic nodular panniculitis, early localized vasculitis, focal Malassezia dermatitis, candidiasis

Muzzle folliculitis and furunculosis (canine acne): Localized demodicosis, early juvenile sterile granulomatous dermatitis and lymphadenitis

Pedal folliculitis and furunculosis: Demodicosis, dermatophytosis, subcutaneous and deep mycoses, opportunistic fungal diseases, pythiosis, lagenidiosis, pelodera dermatitis



Callus pyoderma (pressure-point pyoderma): Acral lick dermatitis, generic dog food skin disease, focal actinic comedones

German shepherd dog pyoderma: Demodicosis with secondary deep pyoderma, subcutaneous and deep mycosis, opportunistic fungal diseases, pythiosis, lagenidiosis

Cellulitis (with or without demodicosis): Juvenile sterile granulomatous dermatitis and lymphadenitis (juvenile cellulitis), subcutaneous and deep mycosis, German shepherd dog, pyoderma, sterile granuloma-pyogranuloma, idiopathic liquefying panniculitis, opportunistic fungal diseases, pythiosis, lagenidiosisModified from Ihrke PJ. 1996. Bacterial skin disease in the dog: a guide to canine pyoderma. Veterinary Learning Systems, Princeton, NJ.

Skin Biopsy

Skin biopsy is an often neglected valuable tool in the diagnosis of canine pyoderma. Increased reliance on skin biopsy has led to the more frequent diagnosis of pyoderma. The benefit of skin biopsy can be maximized if basic principles are followed: timing, lesion selection, method selection, technique, preparation of supportive material, and submission to a dermatopathologist are all important factors.

Bacterial Culture and Identification and Antibiotic Susceptibility

Bacterial culture is overused in the evaluation and management of canine pyoderma. Bacterial culture and identification and antibiotic susceptibility tests are indicated if mixed infection is suspected (as determined by cytologic examination) or if appropriate empiric antibiotic therapy has not been effective. Cultures of intact pustules, furuncles, and nodules are more likely to yield helpful information. Bacterial cultures from open lesions are less likely to yield meaningful results. Bacterial cultures from the skin surface are not recommended.

Evaluation for Immunocompetence

Reliable diagnostic tests to determine immunocompetence in the dog are not available.34,67 Gross information can be derived from a complete blood count (CBC) and serum electrophoresis. An absolute neutrophilia with a lymphocyte count of at least 1000 to 1500 cells per milliliter should be observed in normal dogs with ongoing or recurrent pyoderma. A broad-based elevation in the serum electrophoretic

pattern in the β and γ ranges should be present.66,67 Assays such as in vitro lymphocyte stimulation and bactericidal tests are still primarily research tools because of their expense and lack of availability. The lack of ability to correct any defects that are documented further detracts from the clinical usefulness of these

tests.35,132 Pyoderma, especially when deep, is associated with a high prevalence of circulating immune complexes (CICs). Dogs with chronic deep pyoderma are more likely to be proteinuric, with a predominance

of albuminuria, than dogs with superficial pyoderma.10 The proteinuria is suspected to be a consequence of CICs depositing in glomerular microcapillaries.

Therapy

Systemic antibiotics usually are not needed to treat surface pyodermic infections such as pyotraumatic dermatitis and intertrigo; topical antibacterial therapy usually is sufficient. However, systemic antibiotics are necessary for the management of mucocutaneous pyoderma and surface bacterial overgrowth. Successful

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Infectious Diseases of the Dog and Cat, 3rd Editionmanagement of most superficial and deep pyoderma requires systemic antibiotic therapy. Topical antibacterial shampoo therapy commonly is applied as an adjunct in the management of mucocutaneous pyoderma, surface bacterial overgrowth, and most superficial and deep pyoderma to speed recovery, improve patient well-being, and potentially prevent recurrence. Immunomodulatory therapy is used less frequently, usually in an attempt to prevent or diminish the frequency of recurrent infection. Extended regimens of antibiotics should be considered a last resort in the management of recurrent pyoderma.

Antibiotic Therapy

The basic principles of systemic antibiotic therapy include the selection of an appropriate antibiotic, the establishment of an optimal dosage, and the maintenance of that dosage for enough time to ensure cure rather than transient remission. Although sequestered foci of infection may not be visible, surface lesions in deep pyoderma commonly heal before deeper lesions have resolved, leading to inappropriately early termination of therapy. Antibiotic selection can either be empiric or based on bacterial culture and susceptibility testing. An antibiotic chosen empirically should have a known spectrum of activity directed against S. intermedius and ideally should not be inactivated by β-lactamases, although most β-lactamase–resistant antibiotics are more expensive. Antibiotic therapy should be maintained for at least 1 week after the clinical cure for superficial pyoderma and a minimum of 2 weeks after the clinical cure for all types of deep pyoderma.

An ideal empiric antibiotic should have a narrow spectrum of activity, minimal side effects, and reasonable cost and have been shown to be an effective agent in the management of canine pyoderma. Little clinical evidence exists that bactericidal agents are more effective than bacteriostatic agents in the management of uncomplicated superficial pyoderma. Bactericidal antibiotics are recommended if hair follicle defects are present, in most deep pyoderma cases, and when immunosuppression is suspected or confirmed. If culture is performed, pustules or fistulous tracts should be recultured if S. intermedius was not isolated as the primary pathogen. If multiple isolates are not sensitive to a single oral antibiotic, an antibiotic effective against S. intermedius should be instituted because staphylococci create a tissue milieu favorable to the replication of secondary bacteria invaders. Results of culture and susceptibility studies and detailed information on

individual antibiotics are discussed in greater detail in the Drug Formulary, Appendix 8.67,131,132

Antibiotics effective in the management of pyoderma are listed in Table 85-3. Penicillin, ampicillin, amoxicillin, and tetracycline are poor choices for the treatment of canine pyoderma. Previous and regional usage may alter antibiotic susceptibility.* Not surprisingly, resistant S. intermedius and gram-negative isolates are seen more commonly in referral practices than in general practice, and resistant bacterial

populations are identified most frequently in deep pyoderma.64,67,109 Many clinical trials have shown various antibiotics to be effective in managing canine pyoderma. Erythromycin, tylosin, lincomycin, clindamycin, chloramphenicol, trimethoprim and ormetoprim-potentiated sulfonamides, oxacillin, cephalexin, cefadroxil, fluoroquinolones, amoxicillin-clavulanate, and rifampin have been successful in the treatment of various canine pyoderma.†

Previously, it had been predicted that antibiotic-resistant S. intermedius would preclude the administration of many antibiotics common in dermatology. An examination of similarities and differences in antibiotic

susceptibility patterns published during the past 2 decades indicates remarkably little spp.,67 S. intermedius strains cultured from canine pyoderma in most locales apparently are no more resistant to commonly used antibiotics than they were 25 years ago. Fortunately, in comparison with S. aureus in humans and Pseudomonas spp., S. intermedius appears to lose resistance profiles rather rapidly when antibiotic pressure is removed. Consequently, many of the antibiotics just mentioned are still effective for the management of canine pyoderma. Preferred narrow-spectrum antibiotics include erythromycin, lincomycin, and oxacillin,

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Infectious Diseases of the Dog and Cat, 3rd Editionand preferred broad-spectrum antibiotics include cephalexin, cefadroxil, ormetroprim-potentiated sulfonamides, enrofloxacin, and marbofloxacin.

Owner compliance using different dosing schedule regimens is not well studied in veterinary medicine. Perceived differences in efficacy probably correlate with differences in compliance. Compliance is easier with antibiotics given only once or twice daily than with those that need to be given 3 times daily. Ormetoprim-potentiated sulfadimethoxine and the fluoroquinolones are the only antibiotics useful in canine pyoderma that can be administered once daily. Cephalexin, cefadroxil, and lincomycin require twice-daily dosing. Most other recommended antibiotics require three daily doses.

Table 85-3 Oral Antibiotics Useful for Treating Canine Pyoderma

DRUG NAMEa (DOSE) ADVANTAGES DISADVANTAGES ASSESSMENT

Erythromycin (10–15 mg/kg, 3 times daily)

Inexpensive, narrow spectrum

Cross-resistance with lincomycin, vomiting and diarrhea common, multiple daily dosing

Good first empiric choice

Lincomycin (22 mg/kg, 2 times daily)

Less frequent dosing narrow spectrum, few side effects

Cross-resistance with erythromycin, relatively expensive

Good first empiric choice, especially if need twice-daily drug

Clindamycin (10 mg/kg, 2 times daily, or 11 mg/kg, once daily)

Infrequent dosing Only ∼75% effective, development of resistance during therapy

Only a second-choice therapy for a once-daily drug

Ormetoprim-sulfadimethoxine (27.5 mg/kg, once daily)b

Less frequent dosing broad spectrum

Relatively expensive Good first empiric choice, especially if need once-daily drug

Cephalexin or cefadroxil (22–30 mg/kg, 2 times daily)

Less frequent dosing broad spectrum, rare resistance, good tissue penetration

Cefadroxil expensive, generics moderately expensive

Excellent choice refractory-recurrent deep pyoderma, twice-daily drug

Enrofloxacin (5–15 mg/kg, once daily)

Less frequent dosing broad spectrum, rapidly absorbed, excellent tissue penetration

Expensive, cannot use in growing dogs

Excellent choice for refractory-recurrent deep pyoderma, once-daily drug

Marbofloxacin (2.5–5 mg/kg, once daily)

As above As above As above

Orbifloxacin (7.5 mg/kg, once daily)

As above As above As above

Oxacillin (22 mg/kg, 3 times daily)

Narrow spectrum, rare resistance, side effects rare

Expensive, multiple daily dosing absorption decreased by food

Good choice for refractory-recurrent deep pyoderma

Amoxicillin-clavulanate (12.5–20 mg/kg, 2 or 3 times daily)

Broad spectrum, side effects rare

Expensive, moisture sensitive, in vivo effect may not be as good as would be predicted

Efficacy low, somewhat expensive, for deep pyoderma

Trimethoprim-sulfonamide (22 mg/kg, 2 times daily)

Inexpensive, less frequent dosing broad spectrum

Side effects: keratoconjunctivitis sicca, severe cutaneous drug reactions, hepatic necrosis

Good empiric choice, concern for drug reactions

Modified from Ihrke PJ. 1996. Bacterial skin disease in the dog: a guide to canine pyoderma. Veterinary Learning Systems. Princeton, NJ.

a For additional information on listed drugs, see Drug Formulary, Appendix 8. Treatment generally lasts for a minimum of 21 days.

b Give dose twice daily on the first day.

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Various tiered systems for antibiotic usage have been popularized in the past.35,67,78,131,132 The following recommendations comprise the tiered system recommended by the author. Erythromycin, lincomycin, clindamycin, and ormetoprim-potentiated sulfadimethoxine are useful for the management of uncomplicated, first-occurrence superficial pyoderma. The advantages and disadvantages of these drugs are listed in Table 85-3. Trimethoprim-potentiated sulfonamides are additional possible candidates for uncomplicated, first-occurrence pyoderma. However, the potential side effects of trimethoprim-sulfonamides are of

concern.77

First-generation cephalosporins (cephalexin and cefadroxil), enrofloxacin, marbofloxacin, and oxacillin are recommended for pyoderma refractory to initial antibiotic therapy or recurrent pyoderma. Some veterinary dermatologists use amoxicillin-clavulanate. Chronic, deep pyoderma requires antibiotics with better penetrating ability because sequestered foci of infection and scarring prevent antibiotic access to the site of infection. Cephalexin, enrofloxacin, and marbofloxacin offer better penetrating ability. In the exceedingly rare circumstances when efficacy is not achieved with these drugs alone, rifampin (in conjunction with cephalexin or oxacillin) may be considered.

Enrofloxacin and marbofloxacin and other fluoroquinolones offer the advantages of once-daily dosing, excellent tissue penetration, activity against S. intermedius and gram-negative secondary invaders, and less

likely develop-ment of resistance.39,69,71 Once-daily dosing is recommended because the bactericidal effect

is concentration rather than time dependent.71,103 Uptake of enrofloxacin by macrophages leads to potent

tissue-penetrating abilities.39,71

Oxacillin is a β-lactamase-resistant, narrow-spectrum, synthetic penicillin. Advantages include consistent efficacy in pyoderma and few side effects. Price is the primary disadvantage, even as a generic. Oxacillin must be administered 3 times daily and should be administered at least 1 hour before feeding, because food interferes with absorption.

* References 44, 47, 64, 67, 68, 89.

† References 13, 67-69, 71, 129, 132.

Topical Therapy

Topical therapy is important in the management of pyoderma. Shampoos are the most commonly used delivery system. Antibacterial shampoos may be effective without concurrent antibiotics in some surface pyoderma and are frequently used as adjunctive therapy in the management of superficial and deep pyoderma. Antibacterial shampoos aid in debridement, encourage drainage, and decrease pain and pruritus. Their desired mechanisms of action are to decrease surface bacterial counts and limit recolonizing organisms, thereby diminishing the likelihood of recurrent infections. Improvement in patient attitude and owner encouragement are additional benefits.

Available antibacterial shampoos contain benzoyl peroxide with or without sulfur, chlorhexidine, ethyl lactate, or triclosan. Twice-weekly use of antibacterial shampoos with a minimum of 10 minutes contact time are recommended. Benzoyl peroxide shampoos may decrease recrudescence in susceptible dogs. This compound acts as an antiseborrheic, having antibacterial and degreasing properties.

Dogs with deep pyoderma require more aggressive topical therapy. After clipping, dogs benefit from daily antibacterial shampoos or twice-daily whirlpools or soaks. Chlorhexidine or povidone-iodine are added to

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Infectious Diseases of the Dog and Cat, 3rd Editionwarm water in whirlpools or soaks. Whirlpools remain a seldom used but very beneficial modality of topical therapy for deep pyoderma.

Antibacterial gels, creams, and ointments may be applied in the treatment of limited areas of skin. Cost, messiness, and time required for application limit their usefulness. Benzoyl peroxide is available in a gel vehicle. Mupirocin is a potent antibacterial agent with superior penetrating ability formulated for skin but not mucosal surfaces. Mupirocin should not be used when absorption of large amounts of the polyethylene

glycol vehicle is likely because of the potential for nephrotoxicity.67 Fusidic acid, a topically applied steroid antibiotic, has activity against gram-positive bacteria, such as staphylococci. It is bactericidal at higher concentrations. When applied to canine mucosal sites including the conjunctiva, nostrils, anus, and vulva, populations of S. intermedius were reduced on the mucosal and skin sites within 2 to 4 days after treatment

was instituted and continued for up to 2 weeks after treatment was discontinued.123

Immunomodulatory Therapy

Immunomodulatory therapy remains controversial because of widely varying perceptions of efficacy. If immunomodulation is attempted, it should be an adjunct to antibiotic and topical therapy with the goal of diminishing the frequency or severity of recurrence of infection. Immunomodulatory therapy is most efficacious in dogs with idiopathic recurrent superficial pyoderma that respond completely to appropriate therapy, but recurrence follows within weeks after therapy has been discontinued. Most mentions in the literature referable to immunomodulatory therapy are either highly subjective or anecdotal, because it is often used in conjunction with combined systemic and topical antibacterials. Controlled trials are difficult to perform because immunomodulatory therapy rarely is the sole therapy.

Immunomodulators can be either bacterial or nonbacterial preparations. Commercial products contain either killed Staphylococcus or Propionibacterium species as the antigen. Nonbacterial immunomodulatory drugs include levamisole and cimetidine (see Immunostimulants, Chapter 2).

Staphage Lysate (Delmont Laboratories, Swarthmore, Pa.) is the most common commercial bacterin used in North America and contains bacterial antigens of S. aureus isolated from humans. Staphage Lysate is the only product for which efficacy has been documented (approximately 40% of cases using 0.5 ml twice

weekly37) by double-blinded, placebo-controlled studies. Autogenous bacterins occasionally are made from specific staphylococcal organisms isolated from a dog with pyoderma for use in that dog. Inactivation methodology is crucial because the process must kill the organism without disrupting antigenic determinants.

Nonbacterial immunomodulatory therapy is controversial; most reports are anecdotal. Levamisole, a levo-isomer of tetramisole sold as a vermifuge for large animals, may alter lymphocyte and phagocyte immune function. The recommended dosage of the sheep boluses is 2.2 mg/kg given every other day orally. Cimetidine, an H2-histamine receptor blocker developed for treating gastric ulcers, theoretically could reduce immunosuppression by down-regulating suppressor T lymphocytes, thereby modulating cytokine production. The suggested dosage is 3 to 4 mg/kg orally given twice daily for at least 10 weeks. Controlled studies of

efficacy have not been performed with either product.67 Oral recombinant interferon-a2b has been used to

treat idiopathic recurrent superficial pyoderma in dogs.142 Only transient benefit was noted as compared with placebo.

85.1.4.3



Factors Contributing to Therapeutic Failure and Complicating Management

The most common cause of therapeutic failure in second-opinion cases noted in University of California, Davis Teaching Hospital is failure to adhere to the basic principles of systemic antibiotic therapy. The most common errors are the lack of establishment of an optimal therapeutic dosage and the failure to maintain therapy for long enough to achieve clinical cure.

Treatment failure, disease recrudescence, and disease recurrence also commonly are associated with lack of recognition of factors that can complicate management and influence prognosis. The most common complicating factors include inappropriate initial therapy, unidentified coexisting problems, sequestered foci of infection in deep pyoderma, and external environmental factors such as poor compliance that may not be known to the veterinarian.

Most antibiotic dosages for treatment of pyoderma are largely empiric, because little research has been done in this area. In deep pyoderma, sequestered foci of infection impede antibiotic penetration, and keratin debris from ruptured hair follicles encourages foreign body granulomatous response. Antibiotics that require microbial replication for activity, such as penicillins, are less effective when necrotic tissue and obstructed drainage routes create conditions that are no longer favorable for bacterial multiplication. Consequently, higher dosages usually are warranted in the management of chronic, deep pyoderma. Flexible dosage ranges approved for enrofloxacin and marbofloxacin encourage appropriate dosing.

Concomitant problems such as demodicosis, cornification disorders, hair follicle defects, hypothyroidism, and steroid abuse may hinder successful management. Pruritus, associated with either a pyoderma or an underlying pruritic disease, is an additional complicating factor.

Assessment of Therapy

All dogs receiving systemic antibiotics for pyoderma should be reevaluated within 10 to 14 days. If substantial improvement is not noted, the clinician should consider other factors that can complicate management. The clinician should consider owner compliance to the appropriate dosage regimen, drug loss through vomiting, drug inactivation by food, or malabsorption. Lack of identification of underlying triggering diseases also must be considered as should initial misdiagnosis since other diseases may closely mimic pyoderma. The alternative of referral to a veterinary dermatologist should be considered each time that clinical failure occurs.

Recurrent Pyoderma

Recurrent pyoderma can be defined as bacterial skin infections that respond completely to appropriate therapy, leaving the dog free of clinical signs of infection between episodes of pyoderma. The relatively small but unknown percentage of cases characterized by frequent recurrences is one of the most frustrating aspects of veterinary dermatology. Recurrent superficial pyoderma is the most common subgroup. Underlying skin disease or undiagnosed internal medical abnormalities are the most common causes of

recurrent canine pyoderma.35,67,78,131,132 Possible causes of recurrent pyoderma can be subdivided into persistent underlying skin disease, bacterial hypersensitivity, immunodeficiency, resistant strains of S.

intermedius, and nonstaphylococcal pyoderma.35 Recurrent pyoderma is considered idiopathic only if all appropriate diagnostic procedures have failed to reveal a predisposing cause.

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Recurrent pyoderma triggered by continuing underlying skin disease may alter the clinical appearance of the predisposing condition, making identification of the predisposing trigger difficult. Diagnosis of the underlying disease may be facilitated by first treating with an appropriate course of antibiotics to unmask the symptomatology of the underlying disease.

Pruritus can be an important discriminating feature in evaluating recurrent pyoderma. If pruritus is totally ameliorated by antibiotic therapy, the pruritus probably was caused by the bacterial infection. If pruritus is still present after complete resolution of the pyoderma, the pruritus is most likely being caused by an as yet undiagnosed underlying disease.

Recurrent pyoderma commonly is a lifelong disease requiring extensive client communication and counseling. An informed client is more likely to make the necessary commitment to treatment. Curing underlying diseases may completely prevent recurrent pyoderma. Hypothyroidism is an example of an underlying disease in which pyoderma may be completely eliminated. In contrast, therapy for underlying flea allergy dermatitis seldom completely eliminates secondary pyoderma and requires constant flea control. Many skin diseases that act as triggers for recurrent pyoderma can be controlled but not cured, requiring continuous management. Canine atopic dermatitis and defects in cornification are examples of skin diseases that rarely respond completely to appropriate therapy and therefore continue to trigger occasional secondary

pyoderma.67

Choices in the management of recurrent pyoderma in which successful management of an underlying disease is not possible or the pyoderma is idiopathic include long-term topical antibacterial shampoos, immunomodulatory therapy, and extended regimens of systemic antibiotics. Antibacterial shampoo therapy performed once or twice weekly should be attempted initially. If this therapy prevents recurrence, it can be maintained indefinitely. Adjunctive immunomodulatory therapy should be considered as the next option if shampoo therapy alone is unsuccessful.

Extended regimens of antibiotics using subtherapeutic dosage regimens to prevent recurrence are viewed as a last resort in the long-term management of recurrent canine pyoderma and should be used only after the current episode of the pyoderma has been brought under complete control. Antibiotics most useful for extended regimens include cephalexin, enrofloxacin, marbofloxacin, oxacillin, and amoxicillin-clavulanate.

Risks inherent in the extended administration of systemic antibiotics using subtherapeutic dosage regimens include undesirable effects in the patient, induction of antibiotic resistance, and formation and possible dissemination of resistant strains of bacteria in the environment. The relatively high cost is an additional drawback. The author currently prefers 2 or 3 consecutive days per week at the full daily dosage. Other options include every-other-week dosing at therapeutic levels followed by extending the duration of time off

antibiotics in gradual increments (2 weeks, 3 weeks).67 Long-term therapy must be monitored carefully because of inherent risks.

OTITIS EXTERNA

Craig E. Greene

85.2



Etiology

Otitis externa is inflammation of the external ear canal. The following discussion focuses on microbial factors; reviews should be consulted concerning other causes of this condition. (For a discussion of otitis media-interna, see Musculoskeletal Infections, Chapter 86.) Numerous causative agents have been associated with otitis externa (Table 85-4), and failure to identify and eliminate the underlying cause results in ineffective treatment. Most microbial infections of the external ear canal are secondary to another disease or factor that make it susceptible to colonization by normal or opportunistic microflora. Bacteria, yeasts, parasites, and viruses have all been incriminated as causing otitis externa. In many cases, an underlying disease can be found, and the role of the infectious organism as the primary cause of otitis externa cannot be substantiated. For example, cocker spaniels have ceruminous and sebaceous gland hyperplasia with chronic otitis externa, whereas other breeds

develop fibrosis.6

The normal ear canal is colonized by various microorganisms that can proliferate with damage or inflammation from the primary factors (Table 85-5). Microfloral overgrowth can exacerbate or perpetuate inflammatory reactions. Higher concentrations of bacterial and yeast organisms have been found in the ear secretions of dogs

with otitis externa than in clinically healthy dogs.152 Coagulase-positive S. intermedius is the most common isolate in normal ears and in acute otitis externa, in which it is even more prevalent. β-Hemolytic streptococci are found with equal frequency in normal and diseased ears, so their pathogenic status is uncertain. Other common organisms rarely found in clinically healthy ears and isolated predominantly in cases of chronic otitis

externa are Pseudomonas species and Proteus mirabilis.152 Pseudomonas species have been associated with a severe, virulent form of otitis externa. These organisms are isolated from the ear canal of fewer than 1% of clinically healthy dogs and up to 20% of those with chronic otitis externa. Pseudomonas organisms isolated from the ear canals of dogs are often highly resistant to antibacterial drugs. In one report, Pseudomonas aeruginosa isolated from canine ear cultures were 32% resistant to gentamicin and 100% resistant to ampicillin,

cepthalothin, trimethoprim-sulfonamide, and tetracycline.117 Because of the multidrug resistance pattern of Pseudomonas, empirical therapy is not advised. Mixed infections usually are composed of S. intermedius in conjunction with a gram-negative rod. In cats, Pasteurella multocida may also be isolated.

Bacteria or the broad-based budding yeast Malassezia pachydermatis may proliferate in an ear canal of an animal predisposed to infection because of other underlying diseases or prolonged antibacterial therapy. Microsporum canis is considered to be a secondary invader contributing to or perpetuating and exacerbating inflammation in an already diseased ear canal. In cats the relative importance of M. pachydermatis in disease is less certain because it is found with equal frequency in clinically healthy cats and those with otitis externa. (For additional discussion of M. pachydermatis infections in dogs and cats, see Chapter 58.)

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Table 85-4 Predisposing Factors for Otitis Externa

HOSTAnatomic

Breed German shepherdConformation Long droopy ears (cocker, bassett), stenotic canals (English bulldog, Shar pei,

chow chow), hair in canals (poodle, schnauzer, bichon, Airedale, wirehaired, and fox terriers), ceruminous gland hyperplasia (cocker spaniel)

Otitis media-interna Causing self-inflicted trauma or act as nidusMasses Polyps, squamous cell carcinoma, ceruminous gland tumors, papilloma,

sebaceous adenoma, ceruminous adenoma, fibroma squamous cell carcinoma, basal cell carcinoma, fibrosarcoma

Hyperkeratosis Seborrheic diseases (German and Belgian shepherds), sebaceous gland infection (standard poodles, Akitas, Samoyeds), inflammatory polyp (cats)

Immunologic ConditionsHypersensitivities Atopic dermatitis, juvenile cellulitis (puppy strangles, golden and Labrador

retrievers, dachshunds, pointers, Lhasa apso), contact allergies (propylene glycol), food allergy, drug eruption

Immunodeficiency DebilitationAutoimmune Systemic lupus erythematosus, pemphigus foliaceus

Endocrinopathic Conditions Male-feminizing syndrome, hypothyroidism, Sertoli cell tumor, ovarian imbalance

ENVIRONMENTMoisture Swimming (Labrador retrievers), high environmental temperature and

humidityForeign material Plant material, excessive otic medicants, soil, exudates, dried waxMedicants Yeast infections due to chronic antibiotic and glucocorticoid therapyAstringents Alcohol, cleansing agentsTrauma Iatrogenic or self-induced, lacerations of aural mucosal, excessive cleaning or

medicants, cotton swabsAGENTParasites Otodectes cynotis (ear mite), biting flies, chiggers, ticks, Demodex canis,

Sarcoptes, Notoedres, flea allergyBacteria Staphylococcus intermedius, β-hemolytic streptococci, Proteus, PseudomonasFungi Malassezia canis, Microsporum canis, Candida

The ear mite Otodectes cynotis is believed to be responsible for a majority of feline cases of otitis externa; dogs have a much lower prevalence of infection. Most animals develop a hypersensitivity reaction to the mite that causes the inflammation seen clinically; however, some are nonsymptomatic carriers. In others, the inflammation may lead to a secondary bacterial or yeast infection that can eventually result in the destruction of the mites.

Clinical Findings

A complete history, with special attention to the animal's environment and exposure to vegetation and water, is helpful. Pruritus, a major problem with otitis externa, is manifest by head shaking, scratching, or rubbing the ears along the floor or other objects. On physical examination, pinnal or caudal auricular alopecia, matted hair, broken hairs, excoriations, and occasional areas of acute moist dermatitis are apparent. The external auditory meatus may be erythematous and swollen. In many uncomplicated cases of otitis externa, the clinical findings are limited to erythema and possibly a slight increase in ear wax (ceruminous otitis) (Fig. 85-3). When otitis externa is complicated by secondary bacterial or yeast infections, the character and amount of discharge may become more purulent and moist and may have a foul odor (suppurative otitis). Inflammation may be severe,

85.2.2


Infectious Diseases of the Dog and Cat, 3rd Editionthe ear canals may become painful, and self-inflicted trauma may be apparent. Some animals become head shy; others show evidence of pain only when the canal is palpated. Chronic otitis is characterized by epidermal hyperplasia with thickening of the pinna and narrowing or calcification of the ear canal or both. Fibrosis is observed in most breeds with chronic otitis, although cocker spaniels have the most significant degree of

ceruminous and sebaceous gland hyperplasia (Fig. 85-4).6 A thorough examination of the ear with an otoscope is needed to determine the presence of secondary changes and the extent of the inflammation and discharge as well as the condition of the tympanic membrane. If the canal is very swollen and stenotic, treatment should proceed with a broad-spectrum topical preparation for up to 1 week before performing the otoscopic examination.

Pseudomonas ear infections are highly virulent and characterized by unilateral or bilateral aural pruritus, head shaking, scratching, and rubbing of the ears. A foul-smelling, greenish-yellow discharge is typically found.

Table 85-5 Organisms Isolated from External and Middle Ear Canal of Dogs and Cats

FREQUENCY OF ISOLATION (PERCENTAGE)a

ORGANISM HOST CLINICALLY HEALTHY

OTITIS EXTERNA OTITIS MEDIA PHYSICAL DESCRIPTION

GRAM-POSITIVE BACTERIAStaphylococci (coagulase positive), includes Staphylococcus intermedius

Dog 9–20 22–40 18 Light brown or pale yellow exudates

Streptococci (β-hemolytic)

Dog 16 10 9 Light yellow to light brown exudates

GRAM-NEGATIVE BACTERIAPseudomonas species Dog 0.4 20 26 Painful, copious light

yellow to green exudates, often ulcerated epithelium

Proteus species Dog 0 11 6.5 Light yellow exudates, ulcerated with chronicity

Escherichia coli Dog 0 14 2.6 Light yellow exudatesFUNGIMalassezia species Dog 15–49 50–83 17 Light brown to dark

(chocolate) brown exudatesCat 23 19

METAZOANSOtodectes cynotis Dog 0 5–10 0 Dark brown exudates

Cat 0 50

a Data on animals with otitis media are from Cole LK, Kwochka KW, Kowalski JJ, et al. 1998. Microbial flora and antimicrobial susceptibility patterns of isolated pathogens from the horizontal ear canal and middle ear in dogs with otitis extrerna, J Am Vet Med Assoc 212:534–538. Data on clinically healthy animals and those with otitis externa are from references cited in the text.

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Fig 85-3 Acute otitis externa in dog with erythema and increased ocular discharge. (Courtesy University of Georgia, Athens, Ga.)

Fig 85-4 Chronic proliferative epidermal hyperplasia of ear canal of cocker spaniel dog with otitis externa. (Courtesy University of Georgia, Athens, Ga.)

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Diagnosis

After a complete history and physical otoscopic examination, smears of the ear canal contents should be made. To prevent cross-contamination, a separate, clean otoscope cone must be used for each ear. Sterilized cones should be used if bacterial or fungal culture specimens are taken. The canal should be examined for its diameter, amount and type of exudate, foreign bodies, neoplasms, parasites, condition of the tympanic

membrane, and integrity of the epithelium. As described by others,28 ears can be thoroughly cleaned by placing ceruminolytic ear cleaners within the ear for 10 minutes to emulsify wax and debris. Ears are then flushed with warm sterile isotonic 0.9% saline using a bulb syringe to remove any loosened debris. Some ceruminolytic agents can be irritating and damage the structures of the middle and inner ear if the tympanic membrane is

perforated.92 Because the integrity of the tympanic membrane is not known before cleaning, only mild agents should be used for this purpose.

Additional examination can be done with general anesthesia or sedation. Hand-held or videoendoscopes are used to examine the horizontal canal and deeper structures. Further drying of the cleaned canal may be accomplished using swabs so that the entire canal can be visualized. Deeper irrigation of the canal is accomplished with a syringe attached to an 8 French polypropylene urinary catheter cut to approximately 9 cm,

blunted using a flame, and attached to a 12-ml syringe.28 Swabs should be inserted into the horizontal canal of each ear through a sterilized otoscope cone to recover material for microscopic examination and culture. One swab should be placed in a drop of mineral oil on a slide and examined for ear or Demodex mites. Another swab should be rolled onto microscope slides, and a fast stain based on Giemsa's or Wright's methods is often used. Before staining, the slide should be heat fixed by passing it over an open flame 2 or 3 times. Heat fixing melts some wax and debris, which causes them to adhere better to the glass slide. Without heat fixing, much of the wax, lipid, and associated yeasts may wash away in the staining process. More than 10 yeasts per high-power field are suggestive of their overgrowth.

Cytologic examination of exudate is needed to evaluate the type of inflammatory response and potential underlying cause. Numbers and morphology of leukocytes, neoplastic cells, and bacteria or fungi should be recorded. In one report, mean Malassezia counts per high-dry power (40×) field equal to or greater than 5 in the dog and equal to or greater than 12 in the cat and mean bacterial counts of ≥25 in the dog or equal to or greater

than 15 in the cat were considered indicative of external ear canal infection.45 Because commensals are cultured from normal ears, cytologic enumeration of bacteria provides a means of determining their overgrowth and a hint about their type before culture results become available. When secondary bacterial infections are contributing to the disease, leukocytes and phagocytized bacteria are usually present. When primarily wax and keratin are present, the bacteria observed are most likely incidental but can still contribute to the odor and inflammation by their lipolytic action on waxy debris.

Occasionally, O. cynotis or Demodex can be identified during examination of a smear. Failure to find mites, especially if secondary infection is present, does not rule out their existence.

Bacterial culture and susceptibility testing offer little additional information compared with good basic cytologic evaluation and are costly. Antimicrobial susceptibility can usually be determined on the basis of organism morphology (Table 85-6). Furthermore, the levels achieved by topical application are much higher than the serum levels of sensitivity disks. Bacterial isolation is of more benefit if the tympanic membrane is ruptured with otitis media or interna and the clinician is contemplating systemic antibiotic therapy. Culture and susceptibility testing also are indicated in chronic otitis externa when primarily bacterial rods are found on a smear or when microorganisms persist in spite of apparent appropriate topical medication. Malassezia is better

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Infectious Diseases of the Dog and Cat, 3rd Editionidentified by cytology than by culture (see Fig. 56-4). Repeating cytologic examination on subsequent visits helps evaluate drug resistance or owner compliance. Persistent inflammation in the absence of abundant microorganisms suggests an allergic or ceruminous otitis.

In a prospective study of 23 dogs with chronic bilateral otitis externa, infection was identified in at least one

tympanic bulla in 22 dogs.28 Infection of the middle ear could not be determined by the presence or absence of an intact tympanic membrane. Myringotomy was used to detect infection within the tympanic bulla. Furthermore, organisms isolated from the horizontal ear canal and middle ear were only identical in 10.5% of the ears. Therefore for definitive evaluation, specimens for cultures should be taken from the horizontal ear canal and in the bulla via myringotomy during examination under general anesthesia. Myringotomy is accomplished by passing a sterile culture swab or rubber or polypropylene catheter through a sterilized otoscope cone into the caudoventral portion of the tympanic membrane. Use of a catheter allows for lavage of the bulla should exudate be found on penetration. Duplicate specimens should be taken and submitted for cytologic and cultural examination.

Radiologic imaging should be considered with chronic or recurrent otitis when signs of vestibular dysfunction or other neurologic signs of dysfunction or cranial hyperesthesia are observed. Skull radiography allows for visualizing the tympanic bulla; however, computed tomography and magnetic resonance imaging with contrast enhancement are able to detect meningeal or intracranial involvement.

Therapy

Effective treatment and management of otitis externa are best achieved by combining several principles. If possible, predisposing causes should be identified and eliminated or prophylactically treated. Topical therapy is especially beneficial because drugs attain their highest concentrations with the fewest systemic effects. To obtain owner compliance, the treatment should be specific and simple. Systemic antibacterial or antifungal therapy may be needed if the external canal is occluded or otitis media is present. Systemic therapy can be selected on the basis of culture and susceptibility results. For empiric systemic bacterial therapy, drugs used to treat staphylococcal pyoderma such as erythromycin, first-generation cephalosporins, lincomycin, clindamycin, amoxicillin-clavulanate, ormetoprim- or trimethoprim-sulfonamides, or fluoroquinolones are most effective. For Pseudomonas species, effective drugs have included extended-spectrum penicillins (piperacillin, ticarcillin, carbenicillin), third-generation cephalosporins (ceftazidime, cefoperazone), aminoglycosides, and quinolones. P. aeruginosa is more likely than other organisms to develop resistance to any of these drugs during treatment. For example, isolates of Pseudomonas and Enterococcus species from dogs with otitis externa or urinary tract infection have been shown to develop resistance to enrofloxacin, whereas Klebsiella, Proteus, and

Streptococcus species were less likely to develop resistance.15 In one report, Pseudomonas organisms isolated from chronic canine otitis externa were more susceptible to tobramycin, marbofloxacin, and ceftazidime than to

enrofloxacin, presumably from more extensive use of the latter drug.94 Regardless of which antimicrobial therapy is instituted, treatment usually lasts a minimum of 3 to 4 weeks (see Table 85-6).

Cleaning

Depending on the animal's temperament, sedation or anesthesia may be needed for cleaning the ears, which should be dried before initiating therapy. Initial cleaning and drying of the ear canals are essential to complete the otoscopic examination, determine the integrity of the tympanic membrane, and facilitate the penetration of topically administered drugs. Thorough cleansing of the ear canals removes small secondary foreign bodies as well as degenerated inflammatory cells, free fatty acids, bacterial toxins, wax, and debris.

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Infectious Diseases of the Dog and Cat, 3rd EditionEar cleaning with physical flushing of the canal may be repeated as needed, but it should not be performed more than 2 times weekly because it produces mucosal ulceration. Ear-cleaning solutions may be applied more frequently by the owner, who can instill a few drops just before an otic antimicrobial drug is given. The animal should be allowed to shake its head to disperse the solution, and the excess removed before instilling the desired medication. Cleaning and flushing solutions are generally disinfectants and are listed in Table 85-7. They are used for initial removal of debris or as ceruminolytics. Ceruminolytics are selected when excessive waxy accumulation is present. In most cases, ceruminolytic agents, such as carbamide peroxide and dioctyl sodium sulfosuccinate, are most effective in emulsifying and facilitating the cleaning procedures and are water soluble. Carbamide peroxide has a foaming action that breaks down debris. Ceruminolytic oils such as squalene, lanolin, and mineral oil are more difficult to clean up. Many combination ceruminolytic and drying products contain organic acids with a ceruminolytic agent or alcohol added. They are easier to clean up and can be used as a one-step procedure. These products must be applied with great caution if the tympanum is ruptured. In a study of several ceruminolytic agents, only a solution containing squalene and isopropyl myristate with liquid petrolatum base (Cerumene, Evsco Pharmaceutical, Buena, N.J.) was

nonirritating to the middle ear in the presence of a ruptured tympanum.92 If ceruminolytics are used before the discovery of a ruptured membrane, thorough rinsing with pure water or saline is preferred. Other rinse solutions should not contain detergents or disinfectants because they are ototoxic and contraindicated with a ruptured tympanic membrane.

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Table 85-6 Antimicrobial Selection for Otitis Externaa

ACUTE OTITIS

Cytologic exam: gram-positive cocci; culture; staphylococci, streptococci

Topical

Neomycin (Panolog, Tritop, Quadritop, Tresaderm, Neopredef)

Povidone-iodine (Betadine) dilute 1 : 50 (intact tympanum); 1 : 100 (perforated tympanum)

Chlorhexidine (Nolvasan) dilute 1 : 40 in water

Acetic acid (white vinegar 5%) dilute 1 : 3 in water; concentrations of 2%-5% are irritating (many formulations)

Cytologic exam: gram-negative bacilli; culture; Proteus species, Escherichia coli

Topical

Neomycin (Panolog), polymyxins (Surolan), gentamicin (Gentocin otic)

Acetic acid (white vinegar 5%) dilute 1 : 3 in water (many)

Povidone-iodine (Betadine) dilute 1 : 50 (intact tympanum); 1 : 100 (perforated tympanum)

Cytologic exam: yeasts

Topical

Nystatin (Panolog), thiabendazole (Tresaderm), miconazole (Surolam, Conofite), clotrimazole (Otomax, Genotic B-C, MalOtic Ointment, Otibiotic, Otosoothe, Tri-Otic, Mometamax Otic)

CHRONIC OR RESISTANT OTITIS

Yeasts

Topical

Clotrimazole (Otomax, many formulations), miconazole (Surolam, Conofite), clotrimazole (many), Silvadene

Systemic

Ketaconazole 5 mg/kg twice daily for 2-4 weeks, itraconazole 5-10 mg/kg once daily for 2-4 weeks

Gram-negative species, usually Pseudomonas

Topical

Gentamicin (Gentocin otic, otomax), polymyxin B, colistin or polymyxin E (Coly-Mycin), polymyxin B (Cortisporin)

Polyhydroxidine iodine (Xenodyne, Solvay) diluted 1 : 3 to 1 : 5 in water and apply twice daily

Systemic

Ormetoprim-sulfadimethoxine, trimethoprim-sulfonamide, first-generation cephalosporin



Culture Pseudomonas species

Topical

Ticarcillin (Ticar suspension), add 4 g to 4-oz bottle of Oti-clens

Tobramycin (Tobrex ophthalmic)

Enrofloxacin (Baytril injectable) diluted 50% in water, 3-5 drops twice daily

Amikacin sulfate (Amiglyde-V injectable) undiluted (50 mg/ml) 5-6 drops twice daily

Silver sulfadiazine (Silvadene) diluted 1 : 1 in water, 4-12 drops twice daily

TRIS-edetic acid-gentamicin solution (Wooley's solution) (see Chapter 34, Table 34-12)

Systemic

Enrofloxacin, marbofloxacin, orbofloxacin, gentamicin

a Trade names appear in parentheses.

Table 85-7 Solutions for Management of Otitis Externa

CLASSES AND INDICATIONS INGREDIENTS PRODUCTSFlushing SolutionsPrimary cleaning of canal, have weak antibacterial activity

Cleaning and disinfecting solutions containing dilute acids and disinfectants

Betadine, povidone-iodine 10% (dilute 1:10 to 1:50); Xenodyne, polyhyroxidine iodine 0.5% (dilute 1:1 to 1:15); Nolvasan chlorhexidine 2% (dilute 1:40); vinegar, acetic acid 5% (dilute 1:3); lactic acid 2.5%; salicylic acid 0.1%

CeruminolyticsPermeate and solubilize waxy debris

Squalenes, surfactants, carbamide peroxide, chlorhexidine, dioctyl sodium sulfosuccinate, propylene glycol

Cerumene, Clear X, Veterinary Surfactant, Sebo-o-sol, Otic Chlor-7, Otic Clear, Nolvasan Otic, Adams Pan Otic

Ceruminolytic and Drying AgentWhen combined, dissolve wax and dry out canal

Same as ceruminolytic ingredients, but also includes alcohols and acids such as lactic, salicylic, malic, benzoic, and acetic

Cerbin-otic, Oti-clens, Epi-otic, Chlorhexiderm Otic, Adams Ear Dessicant, Fresh Ear, VPL Otic Cleanser, Chlor-otic-L, Otic-clear

Drying AgentsHave mild antibacterial activity, dry ear canal, act as astringents on exuding lesions

Organic acids, alcohols, silicone dioxide (as listed for previous combinations)

Dermal Dry, Otic Domeboro, Panodry, Otic Calm, acetic acid 5% and isopropyl alcohol in a 3:1 ratio

Rubber bulb ear syringes are a very efficient way to flush the ear. After the initial flushing, loops can be used to remove any remaining material. Cotton swabs should be avoided because they pack exudate and debris down in the ear and may injure the tympanum or epithelial lining. In other cases, especially in animals with a ruptured tympanum, a feeding tube attached to a 12-ml syringe may be used for the final flushing as well as for cleaning out the bulla. In addition, by applying negative pressure, it is a rapid, atraumatic way of removing residual water. Head tilt, ataxia, or both may develop after cleaning as a result of otitis media or interna.



Topical Therapy

Once the ears are clean and dried, topical therapy can be effective in the treatment plan. In general, most ear products contain various combinations of glucocorticoids and antibacterial, antiyeast, and parasiticidal agents in aqueous solution or oil vehicles (Table 85-8). The most appropriate topical drug can be prescribed on the basis of clinical findings, cytology, and diagnosis. Cleaning solutions and disinfectants (antiseptics) are the first preparations that can be used to help remove debris and control overgrowth of microorganisms. Oil vehicles are best applied when the ears are dry, because they tend to moisturize the skin. In moist, exudative ears, water-soluble vehicles are preferred because they are less occlusive. Water-soluble aqueous preparations are most desirable when the tympanic membrane is ruptured. Besides selecting the most appropriate vehicle, the clinician must decide which active ingredients are most appropriate for each case. No single perfect topical ear product exists.

Topical glucocorticoids are most effective when an animal has early, acute inflammation, and high-potency fluocinolone, betamethasone, and dexamethasone are recommended. Although they are generally contraindicated in infectious processes, they do reduce the inflammation in the ear canal, which controls pruritus, swelling, exudation, wax build-up, and tissue proliferation and hyperplasia. It is difficult to find a commercial otic medication that is not formulated with glucocorticoids. Because they may predispose the patient to secondary yeast infections and hyperadrenocorticism, the lowest required potency (e.g., hydrocortisone) and frequency are recommended for long-term (greater than 3 months) treatment. Otic preparations with dexamethasone and triamcinolone have systemic effects and result in signs of hyperadrenalism with iatrogenic pituitary-adrenal suppression. With severely painful or inflamed ears or stenotic canals, systemic prednisone is recommended at a dose of 0.25 to 0.5 mg/kg twice daily for 1 to 2 weeks in dogs and twice this dose for cats.

Bacterial infections should be treated with topical antibiotics or disinfectants. In general, the aminoglycosides (neomycin, polymyxin, gentamicin) and chloramphenicol are frequently effective. Although the aminoglycosides are potentially ototoxic, especially when topically applied to an ear with a ruptured eardrum, this has not been shown to be a problem (see Aminoglycoside Toxicity, Chapter 34). Optimally, drugs that may later be needed for systemic therapy should not be used topically in acute cases because resistance may develop. Disinfectants are an effective alternative to antibiotics. Iodine and chlorhexidine are good choices for treating bacteria and yeasts, respectively, but are ototoxic when put into the middle ear. Acetic acid at 2% is generally effective against Pseudomonas species and at 5% is effective against most bacterial pathogens involved in otitis externa. Other acids that are effective are 2% boric acid,

2.5% lactic acid, and 0.1% salicylic acid.29 For more resistant Pseudomonas infections, otic or ophthalmic medicants containing gentamicin, tobramycin, or polymyxins can be applied, and as a last resort, compounded formulations of ticarcillin or amikacin solutions can be prepared and instilled twice daily. Silver sulfadiazine, a compounded mixture of two antibacterial agents, is highly effective against

Pseudomonas and other bacteria and yeasts in canine otitis externa.110 Silver sulfadiazine ear solution (0.1%) is prepared by mixing 0.1 g of chemical-grade powder into 100 ml distilled water. Alternatively, 1.5 ml of cream is mixed with 13.5 ml distilled water; however, this mixture is more viscous and requires warming above ambient temperature to ease its topical application. TRIS-ethylenediaminetetraacetic acid (EDTA) preparations are also effective against Pseudomonas and other resistant gram-negative bacteria (see Buffered EDTA Solution, Chapter 34, and Table 34-15). Pseudomonas infections may be susceptible to quinolones that have been compounded into topical preparations for treatment of chronic otitis externa. (For specific information on compounding topical enrofloxacin and ticarcillin preparations for treating Pseudomonas described above, see Drug Formulary, Appendix 8.)

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85.2.4.2



Table 85-8 Broad-Spectrum Veterinary Otic Antimicrobial Preparations

PRODUCT (MANUFACTURER)a

FORMULATION/VEHICLE ANTIBACTERIAL ANTIINFLAMMATORY ANTIFUNGAL

Surfacticide (Centaur) DropsNitrofurazone — —Terra-Cortril (Pfizer) Suspension Oxytetracycline Hydrocortisone —Gentocin Otic (Schering) Solution; propylene glycol,

alcohol, glycerineGentamicin Betamethasone —

Betsolan (Janssen) Drops Neomycin Betamethasone —Neo-Predef (Pfizer) Ointment; lanolin,

petrolatum, mineral oilNeomycin Isoflupredone —

Betagen Otic Solution (Med-Pharmex), Garagen Otic Solution (PPC), Gentamicin Otic Solution (Butler), Genta-Otic (Vetus), Gentaved Otic Solution (Vedco)

Solution; alcohol, glycerin, propylene glycol

Gentamicin sulfate

Betamethasone valerate

—

Tritop (Pfizer) Ointment Neomycin sulfate Isoflupredone acetate —Epi-Otic (Virbac), Epi-Otic NF (Virbac), ResiCHLOR Lotion (Virbac)

Solution; propylene glycol Chlorhexidine — Chlorhexidine

Auroto (Kyron) Solution Neomycin — ThiabendazoleBaytril Otic (Bayer) Solution; alcohol, neutral oil Enrofloxacin — Silver

SulfadiazineFungi-Dry-Ear (Q.A. Laboratories)

Gel; alcohol, lanolin oil, acetic acid

— — Zinc undecylenate

Otomax Ointment (Schering), CGB Ointment (PPC), Genotic B-C (Butler), MalOitc Ointment (Vedco), Otibiotic Ointment (RXV), Otosoothe Ointment (Vetus), Tri-Otic (Med-Pharmex)

Ointment; mineral oil, hydrocarbon gel

Gentamicin sulfate

Betamethasone valerate

Clotrimazole

Mometamax Otic Suspensor (Schering-Plough)

Suspension; mineral oil hydrocarbon gel

Gentamicin Momethasone furoate monohydrate

ClotrimazoleSulfate

Panolog (Fort Dodge), Quadritop Cream (Vetus), Oridermyl (Centaur)

Ointment; mineral oil Neomycin Triamcinolone Nystatin

Otospectrine (Phenix) Solution Neomycin Dexamethasone MonosulfiramSurolan (Janssen) Solution Polymixin B Prednisolone MiconazoleTresaderm (Merial) Solution; glycerine, alcohol,

propylene glycolNeomycin Dexamethasone Thiabendazole

Animax Ointment (Pharmaderm)

Ointment; polyethylene, mineral oil

Neomycin sulfate Thiostrepton Nystatin

a Available Internet addresses of manufacturers: Virbac (www.virbac.com), Schering (www.sp-animalhealth.com), Pfizer (www.pfizerah.com), Fort Dodge (www.wyeth.com/divisions/fort_dodge.asp), Merial (www.merial.com), Q.A. Laboratories (see Butler), Bayer (www.bayer-ah.com), Pharmaderm (www.pharaderm.com), PPC, Butler (www.accessbutler.com), Vedco (www.vedco.com), Vetus (www.burnsvet.com), RXV (www.dvmresources.com), Med-Pharmex (www.med-pharmex.com).



Secondary yeast infection may occur when systemic or topical antibacterial therapy is prolonged. Cytologic examination should be performed at repeat visits to check for this complication.

Table 85-9 Culture Results for Specimens Taken During Total Ear Canal Ablation and Bulla Osteotomy in 13 Dogs

BACTERIAL OR FUNGAL SPECIES

INITIAL INCISIONa (MEAN COLONY COUNT PER

GsRAM OF TISSUE)

BULLAb (MEAN COLONY COUNT PER GRAM OF

TISSUE)

SUBCUTANEOUS TISSUE AT CLOSUREc (MEAN COLONY COUNT PER

GRAM OF TISSUE)Streptococcus canis 4.13 >105 >105

Streptococcus bovis 0 53 7Staphylococci (coagulase positive)

15.4 >105 57.66

Staphylococci (coagulase negative)

10 0 18

Proteus mirabilis 0.5 >105 >105

Escherichia coli 0.14 >105 >105

Pseudomonas aeruginosa 0.67 >105 >105

Streptococci (β-hemolytic) 0 2 0Micrococci 0 1 0Malassezia species 1 31 1Alcaligenes dentrificans >105 >105 >105

Enterococci >105 >105 >105

From Vogel et al. 1999. J Am Vet Med Assoc 214:1642-1643.

a Subcutaneous tissue immediately after skin incision.

b Excised epithelium from the bulla ossea.

c Subcutaneous tissue just before skin closure.

When Malassezia organisms are present, the topically applied antiyeast agents such as nystatin and thiabendazole contained in many ear medicants are frequently effective. Thiabendazole can be a contact irritant in some dogs. In more difficult cases, 1% miconazole or clotrimazole lotions usually work. A mixture of 2% boric acid and 2% acetic acid instilled in the ear once daily for 7 weeks was reported to be effective in

treating Malassezia otitis.48 If a Malassezia otitis media is diagnosed, then the systemic antifungal ketoconazole given 5 mg/kg every 12 hours or itraconazole given 5 mg/kg every 24 hours for 4 to 6 weeks is the preferred treatment (see Chapter 58 for further information on Malassezia infections).

O. cynotis is relatively sensitive to most insecticides, including pyrethrins, rotenone, and thiabendazole. In addition to treating the ears, the entire body and other in-contact animals should be treated. Ivermectin at 250 mg/kg, given orally once weekly for 3 to 4 weeks or subcutaneously once every 10 days for two treatments, is effective against Otodectes mites. It also eliminates mites from other areas. However, ivermectin is not approved for use in cats or dogs at this dosage. It is absolutely contraindicated in collies.

Surgical treatment of refractory otitis externa and media is total ear canal ablation and lateral bulla osteotomy. In one study, various bacteria were isolated from the subcutaneous tissues at the time of the

initial skin incision, the tympanic bulla, and the tissues at the time of closure of the incision147 (Table 85-9). In this study, susceptibility of isolates for each drug were as follows: gentamicin (50%), ampicillin (54%),


Infectious Diseases of the Dog and Cat, 3rd Editionamikacin (62.5%), cefazolin (70%), trimethoprim-sulfonamide (87.5%), and greater than 90% showing susceptibility to amoxicillin-clavulanate, ticarcillin, ticarcillin-clavulanate, or ciprofloxacin. Dehiscence from infection is common after this procedure and may also relate to numerous factors, including difficulty of decontaminating the recesses of the ear canal and bulla during surgical preparation and bacterial resistance to surgical preparation solutions such as chlorhexidine that are in many ear remedies. Therefore care should be taken to reduce bacterial contamination before and during otic surgeries, and bacterial culture with antimicrobial susceptibility testing is indicated at the incision site before closure.

Prognosis

The prognosis is generally good in acute (less than 4 weeks’ duration) cases of otitis externa when the tympanic membrane is intact. Early control of the disease is important in preventing secondary changes. A guarded to good prognosis is indicated in chronic cases unless surgical intervention is advised. Whenever the tympanic membrane is ruptured, otitis media is diagnosed, and the prognosis for complete recovery becomes guarded with medical therapy alone. When secondary changes have progressed to marked fibrosis with narrowing of the ear canal or osteomyelitis of the bulla, surgical intervention may be required. In animals with calcified ear canals, surgery is also necessary to achieve good results. Lateral (horizontal) ear resection is indicated to facilitate drainage and administer medicants, but it is usually only palliative because diseased tissue often remains. Total (vertical) canal ablation is needed with tissue proliferation and calcification of the ear canal. When clinical signs of middle or inner ear disease occur and fluid density is apparent within the bulla or thickening of the bulla is seen radiographically, bulla osteotomy is the treatment of choice (see also

Otitis Media/Interna, Chapter 86).143 Total canal ablation and lateral bulla osteotomy can be done

simultaneously.76 Although these procedures may cure the otitis externa and media, postoperative complications include hearing impairment, Horner's syndrome, facial nerve paralysis, and vestibular dysfunction.

Suggested Readings*

* See the CD-ROM for a complete list of references.

6. Angus, JC, Lichtensteiger, C, Campbell, KL, et al.: Breed variations in histopathologic features of chronic severe otitis externa in dogs: 80 cases,1995-2001. J Am Vet Med Assoc. 221, 2002, 1000–1006.

43. Frank, LA, Kania, SA, Hnilica, KA, et al.: Isolation of Staphylococcus schleiferi from dogs with pyoderma. J Am Vet Med Assoc. 222, 2003, 451–454.

51. Guardabassi, L, Loeber, ME, Jacobson, A: Transmission of multiple antimicrobial-resistant Staphylococcus intermedius between dogs affected by deep pyoderma and their owners. Vet Microbiol. 98, 2004, 23–27.

64. Holm, BR, Petersson, U, Morner, A, et al.: Antimicrobial resistance in staphylococci from canine pyoderma: a prospective study of first-time and recurrent cases in Sweden. Vet Rec. 151, 2002, 600–605.

90. Manian, FA: Asymptomatic nasal carriage of mupirocin-resistant, methicillin-resistant Staphlococcus aureus (MSRA) in a pet dog associated with MRSA infection in household contacts. Clin Infect Dis. 36, 2003, e26–e28.

123. Saijonmaa-Koulumies, L, Parsons, E, Lloyd, DH: Elimination of Staphylococcus intermedius in healthy dogs by topical treatment with fusidic acid. J Small Anim Pract. 39, 1998, 341–347.

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85.3


Infectious Diseases of the Dog and Cat, 3rd Edition152. Yoshida, N, Naito, F, Fukata, T: Studies of certain factors affecting the microenvironment and microflora of the external ear of the dog in health and disease. J Vet Med Sci. 64, 2002, 1145–1147.

Uncited references

30. Colombini, S, Merchant, SR, Hosgood, G: Microbial flora and antimicrobial susceptibility patterns from dogs with otitis media. Vet Dermatol. 11, 2000, 235–239.

141. Tejedor Junco, MT, Martín Barrasa, JL: Identification and antimicrobial susceptibility of coagulase positive staphylococci isolated from healthy dogs and dogs suffering from otitis externa. J Vet Med B Infect Dis Vet Public Health. 49, 2002, 419–423.

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85 Integumentary Infections

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