{"id":1597,"date":"2012-01-01T15:57:42","date_gmt":"2012-01-01T15:57:42","guid":{"rendered":"http:\/\/phosdev.com\/todaysveterinarypractice\/?p=1597"},"modified":"2022-02-18T18:08:31","modified_gmt":"2022-02-18T18:08:31","slug":"challenges-new-developments-in-canine-pyoderma-disease-overview-diagnosis-2","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/dermatology\/challenges-new-developments-in-canine-pyoderma-disease-overview-diagnosis-2\/","title":{"rendered":"Challenges & New Developments in Canine Pyoderma: Disease Overview & Diagnosis"},"content":{"rendered":"

Kimberly S. Coyner, DVM, Diplomate ACVD<\/em><\/p>\n

This is the first article in a 3-part series discussing the latest information available regarding canine pyoderma. Future articles will discuss treatment as well as methicillin-resistant infection.<\/p>\n

\u2022 Canine pyoderma is a bacterial skin disease usually caused by Staphylococcus pseudintermedius (previously known as Staphylococcus intermedius).1<\/sup>
\n\u2022 S pseudintermedius is a gram-positive, coagulase-positive cocci bacteria, which is considered part of the normal canine mucosal flora and cultured from 37% to 41% of normal dogs.2,3<\/sup>
\n\u2022 Less common bacterial species found in canine pyodermas include S aureus (4.7%\u20138.3% of cases, usually human origin) and S schleiferi (19%\u201328% of cases).4-6<\/sup><\/p>\n

The Three Ms: MIC, MPC, & MSW<\/span><\/h2>\n

Mean inhibitory concentration (MIC)<\/strong> is usually based on blood levels of an antibiotic, and is the minimal antibiotic concentration needed to inhibit bacterial growth. When the MIC exceeds the concentration of drug that can be safely achieved in the bloodstream, then the organism is deemed resistant.Bacterial Mutation & Resistance<\/span>
\nMIC is based on standardized bacterial inoculums (105<\/sup>\u00a0CFU\/mL) exposed to varying drug concentrations in a test tube, and it varies with both the drug and the bacterial species targeted.
\n\u2022 Since MIC does not equal complete killing of all bacteria, bacterial mutation and resistance is a concern.
\n\u2022 Patients with normal intact immune systems: Inhibition of the susceptible bacterial population allows immune clearance of infection, including resistant mutants.
\n\u2022 Immunocompromised patients, those with prior infection or previous exposure to antibiotics, or those in which therapy for acute infection fails: Continued proliferation of resistant mutants may occur.
\n\u2022 When a high-density bacterial population is exposed to an antimicrobial agent, it only requires one spontaneous mutation to the exposed agent for the culture to become a > 1012<\/sup>\u00a0population of resistant bacteria following overnight incubation.1<\/sup><\/p>\n

Measuring Mutant Prevention<\/span><\/strong>
\nRecently, the mutant prevention concentration (MPC) has been described as a novel measurement of in vitro bacterial susceptibility or resistance. MPC defines the lowest drug concentration required to block the growth of the least susceptible bacterium present in the tested population.
\nMPC is based on the testing of a larger bacterial inoculum (>= 109<\/sup>\u00a0CFU\/mL), which:
\n\u2022 More closely approximates bacterial load in actual infections
\n\u2022 Takes into account the probability of mutant subpopulations being present in high-density bacterial populations.1,2<\/sup>
\nDosing based on MPC drug concentration may reduce overall bacterial numbers as well as prevent the selective amplification of the resistant subpopulation. As with MIC, MPC varies with both the antimicrobial and bacterial species targeted.<\/p>\n

Minimizing Mutation Development<\/span><\/strong>
\nThe mutant selection window (MSW) defines the danger zone for therapeutic drug concentrations, and is bordered by the MIC and the MPC values. Minimizing the length of time that an antibiotic concentration remains in the MSW may reduce the likelihood for development of resistance during therapy.<\/p>\n

Achieving Optimal Antibiotic Dosing<\/span><\/strong>
\nMPC values, when considered with antimicrobial pharmacology, may allow more accurate prediction of probability of resistance when bacteria are exposed to antibiotics during therapy for infectious diseases. With the increasing emergence of resistant infections, resistance prevention should be an important goal of antimicrobial therapy.1-3<\/sup>
\nHopefully, MPC and MSW values may eventually become more widely available from reference laboratories and allow for optimal antibiotic dosing, reducing antimicrobial resistance.<\/p>\n

CFU = colony forming units; MIC = mean inhibitory concentration; MPC = mutant prevention concentration; MSW = mutant selection window<\/p>\n

1. Blondeau J. New concepts in antimicrobial susceptibility testing: The mutant prevention concentration and mutant selection window approach. Vet Derm 2009; 20:383-396.
\n2. Xilin Zhao X, Drlica K. Restricting the selection of antibiotic-resistant mutants: A general strategy derived from fluoroquinolone studies. Clin Infect Dis 2001; 33(3):S147\u2013S156.
\n3. White SD. Review article: Systemic treatment of bacterial skin infections of dogs and cats. Vet Derm 1996; 7:133-143.<\/p>\n

DISEASE PROFILE<\/span><\/h2>\n

Transmission<\/span><\/strong>
\nThe perineum and nasal mucosa are primary colonization sites, and bacteria can be transferred to other body sites via licking and grooming.2<\/sup>
\n\u2022 S pseudintermedius can be an opportunistic pathogen and create infection in dogs with underlying conditions that compromise the normal skin barrier or immune function.
\n\u2022 Similar to S aureus, S pseudintermedius produces virulence factors to enhance infection, such as coagulase, proteases, thermonuclease, and toxins (ie, haemolysins, exfoliative toxins, enterotoxins). It also has the ability to bind to fibrinogen, fibronectin, and cytokeratin, as well as form biofilms.1<\/sup><\/p>\n

Types of Conditions<\/span><\/h2>\n

Underlying Conditions<\/strong><\/p>\n

Chronic or recurrent canine pyoderma is usually associated with an underlying cause; idiopathic pyoderma is rare. The most common underlying conditions include (Table 1, page 33):7<\/sup>
\n\u2022 Hypersensitivity dermatitis
\n\u2022 Parasitic skin infestations
\n\u2022 Endocrinopathies
\n\u2022 Follicular dysplasia
\n\u2022 Keratinization disorders.<\/p>\n

In one prospective study of 30 cases of canine recurrent pyoderma:8<\/sup>
\n\u2022 Atopic dermatitis was found in 60% of cases. Atopic dogs are prone to recurrent skin infections due to increased adherence of staphylococcal bacteria to atopic canine skin cells,9-11<\/sup>\u00a0alterations in normal skin barrier function,12<\/sup>\u00a0and altered skin immune system function.13,14<\/sup>
\n\u2022 Food allergy, flea allergy, and hypothyroidism each accounted for 7% of cases.
\n\u2022 Hyperestrogenism, demodicosis, and zinc-responsive dermatosis each accounted for 4% of cases.
\n\u2022 In only 2 dogs were underlying causes unidentified.<\/p>\n

Identification of Conditions<\/span><\/strong>
\nDepending on clinical presentation, age of onset, seasonality, and other clinical signs, identification of underlying disorders includes:
\n\u2022 Stringent flea control
\n\u2022 Deep skin scrapings for Demodex
\n\u2022 Trial treatment for scabies
\n\u2022 Hypoallergenic diet trial
\n\u2022 Intradermal allergy testing and desensitization
\n\u2022 Screening for endocrinopathies
\n\u2022 Skin biopsy for keratinization disorders.<\/p>\n

Outcomes<\/span><\/strong>
\n\u2022 In dogs without compromising disease, treatment of pyoderma will likely result in complete cure.
\n\u2022 In patients with relapsing infection (recurs within 1\u20132 weeks), inadequate duration of treatment or bacterial resistance is likely.
\n\u2022 In patients with recurrent infection (recurs within 3 months), identification\/treatment of underlying disorders must be undertaken.7<\/sup><\/p>\n

Differential Diagnosis<\/span><\/strong>
\nThe following differential diagnoses should be considered for any dog presenting with signs of pyoderma:
\n\u2022 Demodicosis (Figure 1, page 34)
\n\u2022 Dermatophytosis
\n\u2022 Malassezia dermatitis
\n\u2022 Noninfectious skin diseases (Figures 2 through 4), such as sebaceous adenitis, cutaneous lymphoma, and pemphigus foliaceus.<\/p>\n

\"Screen<\/a><\/p>\n

\"Screen<\/a><\/p>\n

Clinical Signs<\/span><\/strong>
\nCanine pyoderma can be nonpruritic or minimally to markedly pruritic. Clinical signs can vary with the:
\n\u2022 Depth of infection (superficial versus deep)
\n\u2022 Location of infection (ie, haired versus nonhaired skin, mucocutaneous junctions, skin folds)
\n\u2022 Breed of dog (in some cases).
\nThe variable manifestations of pyoderma are listed in Tables 2, page 33, and 3, page 35. These tables will be repeated in the next article and will include figures and treatment recommendations.<\/p>\n

Lesion Distribution & Appearance<\/span><\/strong>
\nLesion distribution in cases of canine pyoderma:
\n\u2022 May be localized or generalized
\n\u2022 Can depend on the underlying cause
\nIn pruritic dogs, lesions commonly occur in areas of self trauma and then spread
\nIn dogs with endocrinopathies, lesions commonly begin on the trunk, then spread and become pruritic after development of infection.7<\/sup>
\nClinical recognition of pyoderma can be complicated by differences in disease presentation, including area of the body affected and variations in coat length and breed of dog.<\/p>\n

Identification<\/span><\/strong>
\n\u2022 Mucocutaneous or nasal pyoderma can present as a crusting inflammatory disease similar to discoid lupus erythematosus (Figures 5\u20137, page 36).<\/p>\n

\"Figure<\/a><\/p>\n

\"Figure<\/a><\/p>\n

\"Figure<\/a>
\n\u2022 Pyoderma on the thinly haired inguinal area may be easy to identify, but the same lesions on the thickly haired dorsal and lateral trunk may be harder to notice.
\n\u2022 Short-coated dogs with folliculitis can present with raised tufts of hair on the trunk that can be confused with urticaria; however, lesions are not evanescent as occurs in urticarial lesions, and eventually hair is lost, leaving a moth-eaten appearance of the hair coat (Figure 8, page 36).<\/p>\n

\"Figure<\/a>
\n\u2022 Long-coated dogs with pyoderma may initially demonstrate a dull coat with scaling +\/- odor, easily epilated hair, and pruritus (Figure 9, page 36).<\/p>\n

\"Figure<\/a>
\n\u2022 In chronic lesions of pyoderma, lichenification can develop that may appear identical to Malassezia infection (Figure 10, page 36).<\/p>\n

\"Figure<\/a><\/p>\n

Dog Breeds<\/span><\/strong>
\nBreed differences with regard to pyoderma manifestations are not uncommon (Figures 11\u201313, page 37).
\n\u2022 Bulldogs often develop localized areas of plaque-like hyperkeratosis or papillomatous appearing dermatitis (Figure 11).<\/p>\n

\"Figure<\/a>
\n\u2022 Dalmatians can develop small areas of brownish, discolored fur associated with papules (“dalmatian bronzing syndrome,” Figures 12 and 13).<\/p>\n

\"Figure<\/a><\/p>\n

\"Figure<\/a>
\n\u2022 Shar-peis often diffusely lose hair due to folliculitis, with minimal to no associated skin inflammation or visible papules.
\n\u2022 Cocker spaniels may present with crusted plaques and follicular casting as a manifestation of pyoderma that can be mistaken for idiopathic or primary seborrhea (a far rarer diagnosis) and lead to inappropriate diagnosis and therapy.
\n\u2022 Shetland sheep dogs often develop large superficial spreading areas of alopecia, erythema, and scaling.<\/p>\n

DIAGNOSIS<\/span><\/h2>\n

Consideration of clinical signs and lesions is taken together with evaluation of microscopic cytology, skin scrapings, and possibly dermatophyte culture to eliminate other possible causes of folliculitis.<\/p>\n

Cytology<\/span><\/strong>
\nCollection<\/span>
\n\u2022 Impression cytology: Impression cytology of an exudative or lichenified lesion or a ruptured pustule directly onto a slide is easy to obtain.
\n\u2022 Skin scrapings: Drier lesions, such as scaly areas or epidermal collarettes, can be sampled by collecting skin debris on a dull dry scalpel blade or spatula, smearing the debris on a slide, and then staining it with Diff-Quik or similar stain.
\n\u2022 Tape preparation: Clear acetate tape preparation of an affected area can be applied onto a slide over a drop of blue stain.<\/p>\n

Microscopic Evaluation<\/span><\/strong>
\n\u2022 Slides are first scanned under 10\u00d7 to identify areas of interest; then examined under 40\u00d7 to 100\u00d7 to evaluate inflammatory cells and organisms.
\n\u2022 Bacterial folliculitis can be confirmed by identification of inflammatory cells and intracellular cocci (Figure 14).<\/p>\n

\"Figure<\/a><\/p>\n

\"Figure<\/a><\/p>\n

\"Figure<\/a>
\n\u2022 In bacterial overgrowth syndrome, numerous extracellular bacteria are seen, which can include mixed flora with rod-shaped bacteria with or without Malassezia (Figures 15\u201316).<\/p>\n

\"Figure<\/a><\/p>\n

\"Figure<\/a><\/p>\n

\"Figure<\/a>
\n\u2022 In cases of deep pyoderma, marked pyogranulomatous inflammation is usually seen, and organisms may be few in number (Figure 17).<\/p>\n

\"Figure<\/a><\/p>\n

Culture & Sensitivity<\/span><\/strong>
\nWhen to Culture<\/span>
\nCulture and sensitivity of skin lesions associated with pyoderma is recommended if:
\n\u2022 There is no clinical response and bacteria persist cytologically despite empiric antibiotic therapy (especially if a patient with recurrent pyoderma has been treated with multiple antibiotics) or if there is a history of multidrug- or methicillin-resistant infections
\n\u2022 If primarily rod-shaped bacteria are found on cytology of lesions
\n\u2022 In cases of deep pyoderma.7<\/sup><\/p>\n

Culture Techniques<\/span><\/strong>
\nCulture can be obtained with a sterile culturette via:
\n\u2022 Swabbing contents of a freshly ruptured pustule
\n\u2022 Swabbing debris or exudate under an intact crust or under the rim of an epidermal collarette
\n\u2022 Obtaining a 4- to 6-mm punch biopsy of a papule or pustule for macerated aerobic tissue culture (the biopsy sample is placed in a red top tube with 0.25 mL sterile saline).
\nSince lidocaine has antibacterial activity, biopsies for culture should ideally be collected under sedation or general anesthesia.7<\/sup><\/p>\n

Sensitivity Testing<\/span><\/strong>
\nSensitivity is usually tested by either:
\n\u2022 Agar diffusion and disk process (ie, Kirby Bauer, which may be more indicative of topical antibiotic concentrations achievable at surface infections, such as otitis)
\n\u2022 Broth diffusion technique, resulting in determination of the mean inhibitory concentration (MIC).
\nAntimicrobial susceptibility or resistance is then determined by comparing the measured MIC value to previously established breakpoints that take into account the drug’s in vitro activity, achievable and sustainable drug concentrations in the host, drug pharmacokinetics, and drug toxicity.15<\/sup>\u00a0See The Three Ms: MIC, MCP, & MSW (page 32) for further information.<\/p>\n

Histopathology<\/span><\/strong>
\nBiopsy of lesions is recommended if:
\n\u2022 There is a poor response to antibiotics based on culture
\n\u2022 No organisms are identified on cytology or culture
\n\u2022 There is an unusual distribution (ie, facial, pinnal, or footpad lesions are suggestive of immune-mediated disease) or appearance of skin lesions.
\nCanine demodicosis can sometimes be difficult to find in very scarred, fibrotic areas, such as the feet or in the shar-pei breed, and may require biopsy for diagnosis.<\/p>\n

The second article in this series will be published in our next issue and will focus on topical and systemic treatment of canine pyoderma.<\/p>\n

Kimberly S. Coyner,<\/strong> DVM, Diplomate ACVD, received her DVM from Colorado State University. After a private referral practice internship and a year practicing emergency medicine, she completed a 2-year teaching position and then a 3-year residency position in dermatology at the University of Georgia. Dr. Coyner has authored several book chapters in the field of dermatology\u2014<\/span>Morgan’s Handbook of Small Animal Practice, 4th edition (2002) and Sma<\/span>ll Animal Dermatology Color Atlas and Therapeutic Guide\u00a0(2001 and 2006)\u2014as well as articles in Veterinary\u00a0<\/span>Dermatology, Veterinary Medicine, and\u00a0<\/span>The Compendium on Continuing Education for the Practicing Veterinarian. She is currently in private practice at the Dermatology Clinic for Animals of Las Vegas.<\/span><\/em>
\nMIC = mean inhibitory concentration<\/p>\n

References<\/p>\n

1. Fitzgerald JR. The Staphylococcus intermedius group of bacterial pathogens: Species re-classification, pathogenesis and the emergence of methicillin resistance. Vet Derm 2009; 20:490-495.
\n2. Frank LA, Kania SA, Hnilica KA, et al. Isolation of Staphylococcus schleiferi from dogs with pyoderma. JAVMA 2003; 222(4):451-454.
\n3. May ER, Hnilica KA, Frank LA, et al. Isolation of Staphylococcus schleiferi from healthy dogs and dogs with otitis, pyoderma, or both. JAVMA 2005; 227(6): 928-931.
\n4. Fazakerley J, Nuttall T, Sales D, et al. Staphylococcal colonization of mucosal and lesional skin sites in atopic and healthy dogs. Vet Derm 2009; 20:179-184.
\n5. Harvey RG, Lloyd DH. Aspects of nasal, oropharyngeal and anal carriage of in normal dogs and dogs with pyoderma. Vet Derm 1998; 9(2):99-104.
\n6. Griffeth GC, Morris DO, Abraham JL. Screening of skin carriage of methicillin-resistant coagulase-positive Staphylococci and Staphylococcus schleiferi in dogs with healthy and inflamed skin. Vet Derm 2008; 19(3):142-149.
\n7. Scott DW, Miller WH, Griffin CE. Muller and Kirk’s Small Animal Dermatology, 6th ed. Philadelphia: WB Saunders, 2001, pp 291-296.
\n8. Bensignor E, Germain PA. Canine recurrent pyoderma: A multicenter prospective study. Vet Derm 2004; 15(supp):42.
\n9. McEwan NA. Adherence by Staphylococcus intermedius to canine keratinocytes in atopic dermatitis. Res Vet Sci 2000; 68:279-283.
\n10. McEwan NA, Mellor D, Kalna G. Adherence by Staphylococcus intermedius to canine corneocytes: A preliminary study comparing noninflamed and inflamed atopic skin. Vet Derm 2006; 17:151-154.
\n11. Simou C, Thoday KL, Forsyth PJ, et al. Adherence of Staphylococci to canine and human corneocytes: A preliminary study. Vet Derm 2005; 16:156-161.
\n12. Olivry T. Is the skin barrier abnormal in dogs with atopic dermatitis? Vet Immunol Immunopath 2011; 144:11-16.
\n13. McGirt LY, Beck LA. Innate immune defects in atopic dermatitis. J Allergy Clin Immunol 2006; 118:202-208.
\n14. De Benedetto A, Agnihothri R, McGirt LY, et al. Atopic dermatitis: A disease caused by innate immune defects? J Invest Derm 2009; 129:14-30.
\n15. White SD. Review article: Systemic treatment of bacterial skin infections of dogs and cats. Vet Derm 1996; 7:133-143.<\/p>\n","protected":false},"excerpt":{"rendered":"

Kimberly S.<\/p>\n","protected":false},"author":1,"featured_media":2395,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"iawp_total_views":1467,"footnotes":""},"categories":[378],"tags":[13],"class_list":["post-1597","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-january-february-2012","tag-peer-reviewed","column-features","clinical_topics-dermatology"],"acf":{"hide_sidebar":false,"hide_sidebar_ad":false,"hide_all_ads":false},"yoast_head":"\nChallenges & New Developments in Canine Pyoderma: Disease Overview & Diagnosis | Today's Veterinary Practice<\/title>\n<meta name=\"robots\" content=\"noindex, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Challenges & New Developments in Canine Pyoderma: 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