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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, -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 folliclesand
endocrinopathies such as hypothyroidism and Cushing's disease frequently predispose animals to
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pyoderma.
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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in 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 pyoderma
a
Surface bacterial overgrowth
a
SUPERFICIAL PYODERMA
Impetigo (puppy pyoderma)
Superficial bacterial folliculitis
a
Superficial spreading pyoderma
a
(exfoliative pyoderma)
DEEP PYODERMA
Deep bacterial folliculitis and furunculosis
Muzzle folliculitis and furunculosis (canine acne)
Pyotraumatic folliculitis
a
Pedal folliculitis and furunculosis
a
Callus pyoderma (pressure-point pyoderma)
German shepherd dog pyoderma
a
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 suppurativa
b
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.
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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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proceeds, 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
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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, lagenidiosis
Modified 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 and 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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management 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 -lactamases, although most -lactamaseresistant 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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and 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 NAME
a
(DOSE)
ADVANTAGES DISADVANTAGES ASSESSMENT
Erythromycin (1015 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
(2230 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 (515 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 (2.55 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
(12.520 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.
812
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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 -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
813
814
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warm 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
weekly
37
) 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 H
2
-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.
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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.
814
815
85.1.4.4
85.1.4.5
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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
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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. -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.)
815
816
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Table 85-4 Predisposing Factors for Otitis Externa
HOST
Anatomic
Breed German shepherd
Conformation 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 nidus
Masses 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 Conditions
Hypersensitivities Atopic dermatitis, juvenile cellulitis (puppy strangles, golden and Labrador
retrievers, dachshunds, pointers, Lhasa apso), contact allergies (propylene
glycol), food allergy, drug eruption
Immunodeficiency Debilitation
Autoimmune Systemic lupus erythematosus, pemphigus foliaceus
Endocrinopathic Conditions Male-feminizing syndrome, hypothyroidism, Sertoli cell tumor, ovarian
imbalance
ENVIRONMENT
Moisture Swimming (Labrador retrievers), high environmental temperature and
humidity
Foreign material Plant material, excessive otic medicants, soil, exudates, dried wax
Medicants Yeast infections due to chronic antibiotic and glucocorticoid therapy
Astringents Alcohol, cleansing agents
Trauma Iatrogenic or self-induced, lacerations of aural mucosal, excessive cleaning or
medicants, cotton swabs
AGENT
Parasites Otodectes cynotis (ear mite), biting flies, chiggers, ticks, Demodex canis,
Sarcoptes, Notoedres, flea allergy
Bacteria Staphylococcus intermedius, -hemolytic streptococci, Proteus, Pseudomonas
Fungi 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
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the 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 BACTERIA
Staphylococci
(coagulase positive),
includes
Staphylococcus
intermedius
Dog 920 2240 18 Light brown or pale
yellow exudates
Streptococci
(-hemolytic)
Dog 16 10 9 Light yellow to light
brown exudates
GRAM-NEGATIVE BACTERIA
Pseudomonas 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 exudates
FUNGI
Malassezia species Dog 1549 5083 17 Light brown to dark
(chocolate) brown
exudates
Cat 23 19
METAZOANS
Otodectes cynotis Dog 0 510 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 212:534538. Data on
clinically healthy animals and those with otitis externa are from references cited in the text.
816
817
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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.)
817
CHAPTER 85 Integumentary Infections Page 21 of 31
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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
817
818
85.2.3
CHAPTER 85 Integumentary Infections Page 22 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
identified 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.
818
819
85.2.4
85.2.4.1
CHAPTER 85 Integumentary Infections Page 23 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
Ear 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.
819
820
CHAPTER 85 Integumentary Infections Page 24 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
Table 85-6 Antimicrobial Selection for Otitis Externa
a
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
CHAPTER 85 Integumentary Infections Page 25 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
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 PRODUCTS
Flushing Solutions
Primary 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%
Ceruminolytics
Permeate 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 Agent
When 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 Agents
Have 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.
CHAPTER 85 Integumentary Infections Page 26 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
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.)
820
822
85.2.4.2
CHAPTER 85 Integumentary Infections Page 27 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
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, glycerine
Gentamicin Betamethasone
Betsolan (Janssen) Drops Neomycin Betamethasone
Neo-Predef (Pfizer) Ointment; lanolin,
petrolatum, mineral oil
Neomycin 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 Thiabendazole
Baytril Otic (Bayer) Solution; alcohol, neutral oil Enrofloxacin Silver
Sulfadiazine
Fungi-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
Clotrimazole
Sulfate
Panolog (Fort Dodge),
Quadritop Cream (Vetus),
Oridermyl (Centaur)
Ointment; mineral oil Neomycin Triamcinolone Nystatin
Otospectrine (Phenix) Solution Neomycin Dexamethasone Monosulfiram
Surolan (Janssen) Solution Polymixin B Prednisolone Miconazole
Tresaderm (Merial) Solution; glycerine, alcohol,
propylene glycol
Neomycin 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).
CHAPTER 85 Integumentary Infections Page 28 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
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 INCISION
a
(MEAN
COLONY COUNT PER
GsRAM OF TISSUE)
BULLA
b
(MEAN COLONY
COUNT PER GRAM OF
TISSUE)
SUBCUTANEOUS TISSUE
AT CLOSURE
c
(MEAN
COLONY COUNT PER
GRAM OF TISSUE)
Streptococcus canis 4.13
>10
5
>10
5
Streptococcus bovis 0 53 7
Staphylococci (coagulase
positive)
15.4
>10
5
57.66
Staphylococci (coagulase
negative)
10 0 18
Proteus mirabilis 0.5
>10
5
>10
5
Escherichia coli 0.14
>10
5
>10
5
Pseudomonas aeruginosa 0.67
>10
5
>10
5
Streptococci (-hemolytic) 0 2 0
Micrococci 0 1 0
Malassezia species 1 31 1
Alcaligenes dentrificans
>10
5
>10
5
>10
5
Enterococci
>10
5
>10
5
>10
5
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 incision
147
(Table 85-9).
In this study, susceptibility of isolates for each drug were as follows: gentamicin (50%), ampicillin (54%),
CHAPTER 85 Integumentary Infections Page 29 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
amikacin (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, 10001006.
43. Frank, LA, Kania, SA, Hnilica, KA, et al.: Isolation of Staphylococcus schleiferi from dogs with
pyoderma. J Am Vet Med Assoc. 222, 2003, 451454.
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, 2327.
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, 600605.
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, e26e28.
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, 341347.
822
823
85.2.4.3
85.3
CHAPTER 85 Integumentary Infections Page 30 of 31
Infectious Diseases of the Dog and Cat, 3rd Edition
152. 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, 11451147.
Uncited references
30. Colombini, S, Merchant, SR, Hosgood, G: Microbial flora and antimicrobial susceptibility patterns from
dogs with otitis media. Vet Dermatol. 11, 2000, 235239.
141. Tejedor Junco, MT, Martn 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, 419423.
85.4
CHAPTER 85 Integumentary Infections Page 31 of 31

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