Staphylococcus pseudintermedius and Other Canine Cutaneous Pathogens

The most common canine cutaneous bacterial pathogen, formerly identified as Staphylococcus intermedius, is in fact a closely related species, Staphylococcus pseudintermedius.50,167 Although many prior published works and cited references use the former terminology, for clarity and accuracy the correct term, S. pseudintermedius, is substituted throughout this chapter (see Chapter 34).

The role of S. pseudintermedius on canine skin is better understood.^† This facultative pathogen is a resident primarily in the nares and perianal region, a transient, restricted, local colonist on clinically healthy canine skin, and a contaminant on canine hair. Seeding of the skin from the perianal region and nares probably occurs during both normal grooming and excessive licking by pruritic and especially allergic dogs.^3–5,89,111

Considerably less frequently than S. pseudintermedius, Staphylococcus aureus and Staphylococcus schleiferi can cause skin infection in dogs.65,71,130,139 Most likely the novel awareness of these two species is explained because they are grouped generically with S. pseudintermedius or simply not speciated in the past.

Methicillin-resistant (MR) staphylococci (MRS) and especially MR S. aureus (MRSA) have been a “hot button” issue in human medicine for more than a decade. The identification of MRS and especially MRSA in dogs, cats, and horses also has focused scrutiny on their prevalence in animals.¹¹⁰ Carriage and infection with MR S. pseudintermedius (MRSP), MR S. schleiferi, and MRSA are being identified globally in dogs and cats with seemingly increased prevalence. It is important to emphasize that MRS do not possess any greater virulence than methicillin-sensitive staphylococci. However, effective treatment is more problematic. Because of escalating concern for MRS and multidrug-resistant staphylococci, bacterial culture and susceptibility testing are being performed much more frequently than in the past. More frequent culture has led to heightened awareness that other species of staphylococci may cause pyoderma in animals.

Pure cultures of S. pseudintermedius are grown from most pustules or draining tracts in dogs with pyoderma. Infection with S. aureus may actually be more common in cats than in dogs. Further details on the ecology and epidemiology of staphylococcus in animals and humans are found elsewhere in this book (see Chapter 34).

Pathogenicity of S. aureus in humans can correlate with virulence factors such as adhesins (protein A); secreted enzymes such as proteases, hyaluronidase, and lipases; clumping factors; various other binding proteins; leukocidin; and toxins. S. pseudintermedius exfoliative toxin has been identified, but a role in disease has not been proven. When potential virulence factors have been examined comparing S. pseudintermedius 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 noted.2,4,24,64,67 Production of exotoxins does not appear to play a role in the pathogenicity of S. pseudintermedius for canine skin.²⁴ Evidence does not support virulence factors as the cause of differences in canine susceptibility or severity of infection.^{24,32,80,89,90} Data suggest that host factors rather than virulence factors appear to be more important in determining susceptibility, severity, and clinical 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. pseudintermedius, usually from deep pyoderma. However, if gram-negative bacteria are isolated from pyoderma without the concomitant isolation of gram-positive staphylococcus, the technique used and the results obtained should be questioned, because canine pyoderma caused by gram-negative bacteria without staphylococcal co-infection is uncommon. Infection with S. pseudintermedius creates a tissue milieu that is more conducive to secondary invasion by gram-negative bacteria.88,89

Microbial Alterations with Skin Disease

The factors that promote the proliferation of S. pseudintermedius 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 allergic skin diseases such as atopic dermatitis or defects in cornification exhibit a shift in the balance of bacterial species colonizing the skin such that coagulase-positive staphylococci can predominate.⁸⁹ Clinically, this correlates with an increased frequency of pyoderma.

Biofilms, aggregates of organisms that form on interfaces, protect bacteria from the toxicity of antimicrobials or the host immune response and hence lead to difficulties in killing the offending organisms. This concept probably has importance for the understanding of pyoderma, especially when tenacious mucus films form on the surface of infected lesions.

Zoonotic Potential of Skin Pathogens

Most public health concerns regarding dogs and cats and staphylococci are linked to MRSA. Colonization or infection in dogs or cats living in households with owners colonized with MRSA has been widely reported.* According to compilations by others,¹⁹⁴ it is likely that human-to-animal transmission occurs as least as commonly, if not more often, than animal-to-human transmission (see Chapter 34). S. schleiferi also is of potential public health concern, because this organism can be equally pathogenic in either humans or animals. The zoonotic potential for MRSP in humans is substantially less, because S. pseudintermedius has low pathogenicity for humans and opportunistic infection by MRSP in humans is rare. Humans with a normally functioning immune system are not at great risk for skin infections caused by S. pseudintermedius. Dogs also harbor S. pseudintermedius in their oral cavities; up to 21% of dog-bite lesions in humans may be contaminated with this organism.¹⁸⁴ (For an additional discussion see Staphylococcal Infections, Chapter 34, Bite Wound Infections, Chapter 51, and Zoonotic Infections of Medical Importance in Immunocompromised People, Chapter 99).

Susceptibility and Host Response to Infection

In comparison with S. aureus, S. pseudintermedius does not possess the requisite virulence factors to be a potent pathogen. Consequently, most cases of canine pyoderma probably are associated with underlying disease or other host immune factors. Diseases such as allergies (atopic dermatitis, food allergy, flea-allergy dermatitis), ectoparasitism, cornification defects (seborrhea), hereditary skin diseases (genodermatoses)—especially those affecting hair follicles—and endocrinopathies such as hypothyroidism and Cushing’s disease frequently predispose dogs to secondary pyoderma.46,89,103,175,176 Pyoderma secondary to allergic diseases and cornification defects are best documented. More broadly, pruritus from any underlying disease, cutaneous inflammation from any cause, injudicious excessive 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, or folliculitis, 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.⁸⁹

The initiation of staphylococcal pyoderma requires colonization (bacterial overgrowth) and frequently 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.⁸⁹

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.⁸⁹

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.89,125 Several studies have verified an association between anti-staphylococcal antibodies and various subgroups of canine pyoderma.^89,140

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 specific 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 (Box 84-1).⁸⁹

Superficial Pyoderma

Superficial pyodermas are the most common canine bacterial skin diseases. Impetigo is characterized by nonfollicular, intraepidermal pustules involving the superficial layers of the epidermis (Fig. 84-1). Superficial folliculitis affecting the ostial portion of the hair follicle is the most common canine pyoderma. Impetigo and superficial folliculitis may be diagnostically challenging 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 peeling epidermal collarettes. Superficial spreading pyoderma may be seen alone or in conjunction with superficial folliculitis.

Deep Pyoderma

Deep pyodermas proceed deeper in the hair follicle with or without follicular rupture. 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. 84-2). Interconnecting furunculosis involving the interstitium between hair follicles, the dermis, and subcutis is termed cellulitis. Cellulitis commonly initiates sepsis. Deep pyoderma is much less common than superficial pyoderma. Although diagnosis of deep pyoderma usually is not difficult, therapy often is problematic.

Primary Skin Lesions

An erythematous papule often is the initial lesion noted in superficial and milder deep pyoderma. Papules are circumscribed, solid elevations of the skin that form in groups. As infection proceeds, pus accumulates in intraepidermal or follicular locations, forming pustules. Small pustules may be mistaken for papules by the unaided eye. Intact pustules often are transient in canine skin. When pustules rupture, crusted papules result. In deep pyoderma, more intense inflammation leads to nodule formation. Follicular rupture and attendant foreign body tissue response 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 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. In the past, markedly exfoliative pyodermas probably were misdiagnosed as seborrhea. 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 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 canine pyodermas, in contrast with pyoderma in humans.

Cellulitis results in follicular obliteration. Follicular rupture in deep pyoderma leads to nodule formation and draining fistulous tracts (see Fig. 84-2). Dermal hemorrhage resulting from follicular rupture may result in hemorrhagic bullae visible as dark bluish regions in the dermis.

Distribution of Lesions

Acute moist dermatitis, usually secondary to flea-allergy dermatitis, is seen most commonly in the dorsal lumbosacral region and lateral thighs. Intertrigo, or skin-fold pyoderma, is observed at the specific site of the anatomic defect (lip-fold, facial-fold, vulvar-fold, tail-fold, obesity-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, axillae, neck, and interdigital regions, but may generalize.

Uncomplicated superficial pyodermas occur 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 groins of prepubescent dogs. Superficial folliculitis and superficial spreading pyoderma also occur most commonly in the groin and axilla, but lesions may generalize on the trunk. 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 develops as an extension of superficial pyoderma. A characteristic distribution is seen with interdigital and pressure-point pyoderma and canine acne. Because most canine cellulitis occurs secondary to generalized demodicosis, the distribution pattern mirrors that of demodicosis.

Skin Scrapings

Skin scrapings should be performed in all dogs with canine pyoderma, because demodicosis can mimic uncomplicated pyoderma and induce secondary pyoderma. It is especially important to scrape any pustular or papular lesion with a follicular orientation. 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 rapid diagnostic test for the diagnosis of pyoderma. Specimens are harvested by direct smears of pustules, draining tracts, or the surface of inflamed skin. Specimens should be air-dried and stained with either a modified Romanowsky-type Wright’s stain (Diff Quik) or new methylene blue. Modified Wright’s stain is beneficial both for documenting organisms and for identifying inflammatory cells. The identification of cocci indicates the probable presence of S. pseudintermedius. Finding degenerating neutrophils and intracellular cocci supports the diagnosis.

Skin Biopsy

Skin biopsy is a valuable but often-neglected tool in the diagnosis of canine pyoderma. Increased use of skin biopsy has led to the more frequent diagnosis of pyoderma. The benefit of skin biopsy can be maximized if basic principles are followed: early biopsy, correct lesion selection, proper technique, documentation of the history and clinical features, and submission to a pathologist with interest and experience in veterinary dermatology.

Bacterial Culture and Identification and Antibacterial Drug Susceptibility

Bacterial culture is indicated if cytology reveals mixed infection, if appropriate empiric antibacterial therapy was not effective, or if bacterial resistance is suspected. 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 because contaminants may be cultured.

Evaluation for Immunocompetence

Reliable diagnostic tests to determine immunocompetence in the dog are not available.45,89 Gross information can be derived from a complete blood (cell) count (CBC) and serum protein electrophoresis. An absolute neutrophilia with a lymphocyte count of at least 1000 to 1500 cells/mL should be observed in normal dogs with ongoing or recurrent pyoderma. A broad-based elevation in the serum protein electrophoretic pattern in the β and γ ranges should be present.^88,89 Assays such as in vitro lymphocyte stimulation and bactericidal tests remain research tools because of their expense, lack of reproducibility and lack of availability. The lack of ability to correct any defects that are documented further detracts from the clinical usefulness of these tests.^46,176 Pyoderma, especially when deep, is associated with a high prevalence of circulating immune complexes. Dogs with chronic deep pyoderma are more likely to be proteinuric, with a predominance of albuminuria, than dogs with superficial pyoderma.¹³ Proteinuria is suspected to be a consequence of circulating immune complexes depositing in glomerular microcapillaries.

Antibacterial Therapy

The basic principles of systemic antibacterial therapy include the selection of an appropriate antibacterial, the establishment of an optimal dosage based on weight and depth of infection, and the maintenance of therapy for enough time to ensure cure rather than transient remission. After use of antibacterials, sequestered foci of deep infection may not be obvious because surface lesions in deep pyoderma commonly heal before deeper lesions have resolved, leading to inappropriately early termination of therapy. Antibacterial selection can be either empiric or based on bacterial culture and susceptibility testing. An antibacterial chosen empirically should have a known spectrum of activity directed against S. pseudintermedius and should not be inactivated by β-lactamases. Antibacterial therapy should be maintained for at least 1 week after clinical cure for superficial pyoderma and a minimum of 2 weeks after the clinical cure for all deep pyoderma.

An ideal empiric antibacterial should have a narrow spectrum of activity, minimal side effects, and reasonable cost and should have been shown to be effective 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 antibacterials 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 gram-positive staphylococci are not isolated as the primary pathogen. If multiple isolates are not sensitive to a single oral antibacterial, an antibacterial effective against staphylococci should be instituted because staphylococci create a tissue milieu favorable to the replication of secondary bacterial invaders. Results of culture and susceptibility studies and detailed information on individual antibacterials are discussed in greater detail in the Drug Formulary in the Appendix.89,175,175

Antibacterials useful in the management of canine pyoderma are listed in Table 84-1. Penicillin, ampicillin, amoxicillin, and tetracycline are poor choices for the treatment of canine pyoderma. Previous and regional use may alter antibacterial susceptibility.^{59,62,86,89,116} Not surprisingly, resistant S. pseudintermedius 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.^86,89,89 Clinical trials have shown multiple antibacterials to be effective in managing canine pyoderma. Erythromycin, tylosin, lincomycin, clindamycin, chloramphenicol, trimethoprim and ormetoprim-potentiated sulfonamides, oxacillin, cephalexin, cefadroxil, cefpodoxime, quinolones, and amoxicillin-clavulanate have been successful in the treatment of various forms of canine pyoderma.* Preferred narrow-spectrum antibacterials still include erythromycin, lincomycin, and oxacillin, and preferred broad-spectrum antibacterials include cephalexin, cefadroxil, cefpodoxime, trimethoprim and ormetroprim-potentiated sulfonamides, and quinolones such as enrofloxacin and marbofloxacin.

For many years, it had been predicted that antibacterial-resistant S. pseudintermedius would preclude the administration of many antibacterials common in dermatology. Similarities and differences in antibacterial susceptibility patterns published during the 2 decades before the late 1990s indicated very little change.⁸⁹ Unfortunately, a rise in staphylococcal resistance has occurred over the past decade and more rapidly during that interval (see Chapter 34).

Owner compliance using different dosing schedule regimens is not well studied in veterinary medicine. Some perceived differences in efficacy may correlate with differences in compliance. Compliance is more likely to be achieved with antibacterials requiring dosing only once or twice daily than with those that need to be given three times daily. Cefpodoxime, ormetoprim-potentiated sulfadimethoxine, and the quinolones are the only antibacterials useful in canine pyoderma that can be administered once daily.³⁴ Cephalexin, cefadroxil, and lincomycin require twice-daily dosing. Other suggested antibacterials require three daily doses.

Various tiered systems for antibacterial use have been popularized.46,89,103,175,176 Cephalexin, cefadroxil, erythromycin, lincomycin, clindamycin, and ormetoprim-potentiated sulfadimethoxine are useful for the management of uncomplicated, first-occurrence surface and superficial pyoderma. The advantages and disadvantages of these drugs are listed in Table 84-1. Trimethoprim-potentiated sulfonamides, chloramphenicol, veterinary quinolones, and amoxicillin-clavulanate are possible alternative candidates for use in pyoderma. However, the potential side effects of trimethoprim sulfonamides are of concern.¹⁰²

Chronic, deep pyoderma requires antibacterials with better penetrating ability because sequestered foci of infection and scarring prevent antibacterial access to the site of infection. Cephalexin, cefadroxil, cefpodoxime, clindamycin, enrofloxacin, and marbofloxacin offer better penetrating ability. In circumstances when efficacy is not achieved with these drugs alone, rifampin (in conjunction with cephalexin) may be considered.

Quinolones offer the advantages of once-daily dosing, excellent tissue penetration, activity against S. pseudintermedius and gram-negative secondary invaders.53,89,89 Once-daily dosing is recommended because the bactericidal effect is concentration rather than time dependent.^93,137 Uptake of enrofloxacin by macrophages leads to potent tissue-penetrating and concentrating abilities.^53,93

Oxacillin and other isoxazolyl penicillins are β-lactamase-resistant, narrow-spectrum, synthetic penicillins. Advantages include consistent efficacy in pyoderma and few side effects. Price and current availability are the primary disadvantages. Oxacillin must be administered three times daily and should be administered at least 1 hour before feeding, because food interferes with absorption.

Empiric treatment of staphylococcal skin infection has been the norm in veterinary dermatology. Cultures have only been routinely performed in refractory disease. This probably has led to the lack of identification of MRS strains. However, MRS causing skin disease in dogs and cats is still not common in most general small animal practices. Unfortunately, methicillin resistance is being seen with increased prevalence in university referral centers and in dermatology specialty practices. The day may be coming when bacterial culture should be recommended for all pyoderma that has not responded to appropriate initial empiric antibacterial therapy. Systemic antibacterials useful for the management of MR skin infection include chloramphenicol, ormetoprim-potentiated sulfadimethoxine, and trimethoprim-potentiated sulfonamides.

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 systemic antibacterials in some surface pyoderma and are frequently used as adjunctive therapy in the management of superficial and deep pyoderma. Antibacterial shampoos aid in debridement, remove infectious and inflammatory debris, 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. Active ingredients in antibacterial shampoos include chlorhexidine, ethyl lactate, triclosan, and benzoyl peroxide with or without sulfur. Twice-weekly antibacterial shampoos with a minimum of 10 minutes of contact time are recommended.

An important use of topical antibacterial therapy is in the treatment of MR skin infections. Surface and superficial pyoderma caused by MRS may respond to antibacterial shampoo used daily or every other day as sole therapy in circumstances when one does not have a good choice for systemic therapy. Antibacterial shampoos also may be used as an adjunct to systemic therapy.

Dogs with deep pyoderma can benefit from more aggressive topical therapy. After clipping, daily antibacterial shampoos or twice-daily whirlpool immersion baths or soaks may be used. Chlorhexidine or povidone-iodine is added to warm water in whirlpools or soaks. Whirlpools remain a seldom-used but beneficial modality of topical therapy for deep pyoderma. Unfortunately, shampoos, soaks, or whirlpools all diminish efficacy of topical “spot-on” flea control products. Soaks and whirlpools also are labor intensive.

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.⁸⁹ Fusidic acid, a topically applied steroidal antibacterial not available in the United States, has activity against gram-positive bacteria, such as staphylococci.¹⁶³

Immunomodulatory Therapy

Immunomodulatory therapy remains controversial because of widely varying perceptions of efficacy. If immunomodulation is attempted, it should be as an adjunct to antibacterial and topical therapy with the goal of diminishing the frequency or severity of recurrent 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 publications advocating immunomodulatory therapy are subjective, because products often are used in conjunction with systemic and topical antibacterials. Controlled trials are difficult to perform because immunomodulatory therapy rarely is used as sole therapy.

Immunomodulators can be either bacterial or nonbacterial preparations. Commercial bacterial preparations contain either killed Staphylococcus or Propionibacterium species as the antigen. 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 weekly⁴⁸) 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 has been used in an attempt to stimulate lymphocyte and phagocyte immune function. Cimetidine theoretically could reduce immunosuppression by downregulating suppressor T lymphocytes, thereby modulating cytokine production.