Pyoderma literally means “pus in the skin” and can be caused by infectious, inflammatory, and/or neoplastic etiologies; any condition that results in the accumulation of neutrophilic exudate can be termed a pyoderma. Most commonly, however, pyoderma refers to bacterial infections of the skin. Pyodermas are common in dogs and less common in cats.
Bacterial pyodermas are classified by depth of infection, etiology, and whether or not they are primary or secondary. Bacterial pyodermas limited to the epidermis and hair follicles are referred to as superficial, whereas those that involve the dermis, deep dermis, or cause furunculosis are referred to as deep. Etiologic classification refers to the pathogenic organism involved in the infection (eg, staphylococci, streptococci, etc). Most skin infections are superficial and secondary to a variety of other conditions, most notably allergies (flea allergy, atopic dermatitis, food allergy), internal diseases (particularly endocrinopathies such as hypothyroidism or hyperadrenocorticism), seborrheic conditions (including follicular or sebaceous gland diseases), parasitic diseases (eg, Demodex canis), or anatomic predispositions (eg, skin folds). Primary pyoderma occurs in otherwise healthy animals, without an identifiable predisposing cause, resolves completely with appropriate antibiotics, and is usually due to Staphylococcus intermedius or other staphylococci.
Bacterial pyoderma is usually triggered by an overgrowth/overcolonization of normal resident or transient flora. S intermedius is the most common etiologic agent isolated from clinical infections. However, classification is changing and recent phenotypic testing has found that S pseudintermedius is the most common pathogen of dogs.
Normal resident bacteria in canine skin also include coagulase-negative staphylococci, streptococci, Micrococcus sp, and Acinetobacter. Transient bacteria in canine skin include Bacillus sp, Corynebacterium sp, Escherichia coli, Proteus mirabilis, and Pseudomonas sp. These organisms may play a role as secondary pathogens, but often S pseudintermedius is required for a pathologic process to ensue. Normal resident bacteria in feline skin include Acinetobacter sp, Micrococcus sp, coagulase-negative staphylococci, and α-hemolytic streptococci. Transient bacteria in feline skin include Alcaligenes sp, Bacillus sp, Escherichia coli, Proteus mirabilis, Pseudomonas sp, coagulase-positive and coagulase-negative staphylococci, and α-hemolytic streptococci.
The most important factor in superficial pyodermas that allows a bacteria to colonize the skin surface is bacterial adherence or “stickiness” to the keratinocytes. Warm, moist areas on the skin, such as lip folds, facial folds, neck folds, axillary areas, dorsal or plantar interdigital areas, vulvar folds, and tail folds, often have higher bacterial counts than other areas of skin and are at an increased risk for infection. Pressure points, such as elbows and hocks, are prone to infections, possibly due to follicular irritation and rupture due to chronic repeated pressure. Any skin disease that changes the normally dry, desert-like environment to a more humid environment can predispose the host to overcolonization of the skin with resident and transient bacteria.
Clinical Findings and Lesions
The most common clinical sign of bacterial pyoderma in both dogs and cats is excessive scaling; scales are often pierced by hairs. Pruritus is variable. In dogs, superficial pyoderma commonly appears as multifocal areas of alopecia, follicular papules or pustules, epidermal collarettes, and serous crusts. The trunk, head, and proximal extremities are most often affected. Shorthaired breeds often present with multiple superficial papules that look similar to urticaria because the inflammation in and around the follicles causes the hairs to stand more erect. These hairs are often easily epilated, an important feature that helps to distinguish superficial pyoderma from true urticaria, in which hairs do not epilate. In bacterial pyoderma, affected hairs epilate and progress to form focal areas of alopecia 0.5–2 cm in diameter. At the margins of the hair loss, mild epidermal collarette formation may be present, but follicular pustules and erythema are often absent in shorthaired breeds, making diagnosis difficult. Collies and Shetland Sheepdogs often have diffuse areas of widespread alopecia with mild erythema and epidermal collarette formation at the leading edge of the expanding area, often mimicking an endocrinopathy. Pustules and crusts are infrequently found.
The hallmarks of deep pyoderma in dogs are pain, crusting, odor, and exudation of blood and pus. Erythema, swelling, ulcerations, hemorrhagic crusts and bullae, hair loss, and draining tracts with serohemorrhagic or purulent exudate may also be seen. The bridge of the muzzle, chin, elbows, hocks, interdigital areas, and lateral stifles are more prone to deep infections, but any area may be involved. Acral lick granulomas and areas of pyotraumatic dermatitis are also clinical manifestations of deep pyoderma. Interdigital furunculosis (see Interdigital Furunculosis) is another manifestation of deep pyoderma. Plant awns, naked keratin from hair shafts or ruptured hair follicles, and other foreign bodies play a significant role in the inflammatory process associated with deep pyodermas.
Superficial pyoderma in cats is usually due to Staphylococcus intermedius It is often overlooked and underdiagnosed. The most common clinical finding is scaling, particularly over the lumbosacral area; scales pierced by hairs are a common finding. Intact pustules are almost never found. Feline pyoderma is most common in allergic skin diseases, parasitic diseases, and feline chin acne.
Miliary dermatitis can be a clinical manifestation of superficial pyoderma. Cats with deep pyodermas often present with alopecia, ulcerations, hemorrhagic crusts, and draining tracts. Eosinophilic plaques are a common clinical presentation of deep pyoderma secondary to an allergic disease. Recurrent nonhealing deep pyoderma in cats can be associated with systemic disease, such as feline immunodeficiency virus or feline leukemia virus, or atypical mycobacteria.
The diagnosis of superficial pyoderma is usually based on clinical signs—hair loss, scaling, erythema, papules, pustules, and epidermal collarettes. Differential diagnoses for superficial pyoderma include demodicosis, Malassezia dermatitis, dermatophytosis, and other causes of folliculitis as well as uncommon crusting diseases such as pemphigus foliaceus. Diagnosis of pyoderma should also include steps to identify any predisposing causes.
Identification of the dermatologic lesions described above allows a tentative diagnosis of superficial pyoderma. Direct impression smears of intact pustules, areas underlying crusts or epidermal collarettes, or moist erythematous areas may reveal cocci, rods, or inflammatory cell infiltrates. Impression smears of areas of hair loss and scaling may only reveal large numbers of exfoliative keratinocytes. One of the most important reasons to do impressions is to determine whether a concurrent Malassezia infection or overcolonization is present; there is a symbiotic relationship between Staphylococcus and Malassezia, and both are found in ~50% of cases. The infection will not resolve without concurrent systemic antimicrobial therapy. Multiple deep skin scrapings are needed to rule out parasitic infections, particularly Demodex canis. Dermatophyte cultures should be done to rule out dermatophytosis. Bacterial culture and sensitivity testing is mandatory in cases of deep pyoderma and recurrent superficial pyoderma.
Accurate test results are most likely obtained from intact pustules or induced rupture of deep lesions. Caution should be exercised in interpreting culture results from samples submitted from crusted lesions, papules, epidermal collarettes, and fistulous tracts because contamination of the sample is more likely than with samples obtained from a closed lesion. Empiric antibiotic therapy is appropriate in mild, first-time superficial pyodermas with no complicating factors.
The most common underlying triggers of superficial pyoderma include fleas, flea allergy dermatitis, atopic dermatitis, food allergy, hypothyroidism, hyperadrenocorticism, and poor grooming. Appropriate diagnostic testing and treatment of underlying triggers is mandatory. The most common causes of recurrent bacterial pyoderma include failure to identify an underlying trigger, antibiotic undertreatment (dose too low or duration of therapy too short), concurrent use of glucocorticoids, wrong antibiotic, or wrong dose.
The primary treatment of superficial pyoderma is with appropriate antibiotics for ≥21 and preferably 30 days. All clinical lesions (except for complete regrowth of alopecic areas and resolution of hyperpigmented areas) should be resolved for at least 7 days before antibiotics are discontinued. Chronic, recurrent, or deep pyodermas typically require 8–12 wk or longer to resolve completely.
First-time bacterial pyoderma can be treated with empiric antibiotic therapy such as lincomycin, clindamycin, erythromycin, trimethoprim-sulfamethoxazole, trimethoprim-sulfadiazine, chloramphenicol, cephalosporins, amoxicillin trihydrate-clavulanic acid, or ormetoprim-sulfadimethoxine.
Amoxicillin, penicillin, and tetracycline are inappropriate choices for treating superficial or deep pyodermas because they are ineffective in 90% of these cases. Fluoroquinolones should not be used for empiric therapy. Severe deep pyoderma, recurrent pyoderma, or first-time bacterial pyodermas that do not respond to therapy should be treated based on culture and sensitivity.
Topical antibiotics may be helpful in focal superficial pyoderma. A 2% mupiricin ointment penetrates skin well and is helpful in deep pyoderma, is not systemically absorbed, has no known contact sensitization, and is not used as a systemic antibiotic that would increase the likelihood of cross-resistance. It is not very effective against gram-negative bacteria. This ointment should not be used in cats with any known or suspected history of renal disease because the preparation contains propylene glycol. Neomycin is more likely to cause a contact allergy than other topicals and has variable efficacy against gram-negative bacteria. Bacitracin and polymyxin B are more effective against gram-negative bacteria than other topical antibiotics but are inactivated in purulent exudates.
Attention to grooming is often overlooked in the treatment of both superficial and deep pyoderma. The hair coat should be clipped in patients with deep pyoderma and a professional grooming is recommended in medium- to longhaired dogs with generalized superficial pyoderma. This will remove excessive hair that can trap debris and bacteria and will facilitate grooming. Longhaired cats usually benefit most from having the hair coat clipped.
Dogs with superficial pyoderma should be bathed 2–3 times/wk during the first 2 wk of therapy and then 1–2 times until the infection has resolved. Dogs with deep pyoderma may require daily hydrotherapy. Medicated shampoos should be prediluted 1:2 to 1:4 prior to application to facilitate lathering, dispersal, and rinsing. Appropriate antibacterial shampoos include benzoyl peroxide, chlorhexidine, chlorhexidine-ketoconazole, ethyl lactate, and triclosan. Shampooing will remove bacteria, crusts, and scales, as well as reduce the pruritus, odor, and oiliness associated with the pyoderma. Clinical improvement in superficial pyodermas may not be evident for a least 14–21 days, and recovery may not be as rapid as expected.
Of increasing concern is the development methicillin-resistant staphylococci (MRS). In order to minimize the development of MRS, narrow-spectrum antibiotics should be used in the treatment of pyoderma. Recurrent bacterial pyoderma, deep pyoderma, and/or patients with a history of extensive antibiotic use are best treated based on culture and sensitivity. Concurrent aggressive topical antimicrobial therapy is helpful. Avoidance of fluoroquinolones and second- and third-generation cephalosporins as empirical therapy is important to minimize the development of multistrain-resistant staphylococci.
Last full review/revision July 2011 by Karen A. Moriello, DVM, DACVD