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               Bacterial Pyodermas
               Jennifer R. Schissler, DVM, MS, DACVD

               College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA



                 Etiology/Pathophysiology                           Pyoderma Classifications
                                                                  and Presentations
               Pyodermas are bacterial infections of the skin and com-
               monly involve coagulase‐positive staphylococci. Indeed,   Pyodermas are often categorized based on the depth of
               staphylococcal pyoderma is one of the most common   infection (surface, superficial or deep) and the site
               conditions treated in clinical practice. For this reason,   involved, particularly when describing a pyoderma
               this chapter is focused exclusively on staphylococcal   that affects a specific body region (e.g., interdigital
               pyodermas. Staphylococcal  infection  opportunistically   pyoderma, nasal pyoderma). These categorizations are
               arises secondary to dermatologic or systemic diseases   useful, particularly the depth of infection because
               that prompt cutaneous physical or immunologic func-  it  dictates  the  methods  and  duration  of  therapeutic
               tion insults. These may include hypersensitivity, endo-  interventions.
               crine, conformational, and keratinization disorders, as
               well as an immunocompromised status. Clinical presen-  Surface Pyodermas
               tations are diverse, and mimic a multitude of other
                 dermatopathies. In the current era of antimicrobial   Acute Moist Dermatitis
               resistance, optimal outcomes for staphylococcal pyo-  Acute moist dermatitis, also known as pyotraumatic der-
               derma are achieved via correct diagnosis, rational treat-  matitis and commonly referred to as a “hot spot,” is charac-
               ment and follow‐up, and management of the inciting   terized by the rapid development of a focal, erythematous,
               cause(s).                                          erosive, and exudative lesion that develops due to intense
                 Staphylococcus pseudintermedius, previously identi-  pruritus and self‐trauma (Figure 166.1).
               fied as Staphylococcus intermedius, is the most common   Acute moist dermatitis is typically initiated by hyper-
               etiologic agent in canine pyoderma.  Staphylococcus   sensitivity disorders, including cutaneous adverse food
               aureus, Staphylococcus schleiferi subsp. coagulans, and   reaction, atopic dermatitis, and flea bite hypersensitivity,
               coagulase‐negative staphylococci such as Staphylococcus   or pruritogenic parasitic diseases such as pediculosis,
               schleiferi subsp.  schleiferi are isolated at a lesser fre-  sarcoptic mange, and cheyletiellosis. Surface staphylo-
               quency on healthy or inflamed skin.                coccal overgrowth is concurrently present in nearly all
                 Staphylococcal pyoderma is less prevalent in cats   cases of acute moist dermatitis. Cytology of exudate
               than dogs. Feline keratinocyte adhesion of  S. aureus   obtained via surface impression smear reveals neutro-
               and S. pseudintermedius is inferior compared to human   phils and intracellular and extracellular cocci. Superficial
               and dog keratinocytes, perhaps a reflection of inferior   bacterial folliculitis lesions (see “Superficial bacterial fol-
               host adaptation. S. pseudintermedius, S. schleiferi, and   liculitis” section below) observed at the periphery of the
               S. aureus are most frequently isolated; S. aureus is iso-  self‐trauma suggest a longer duration of staphylococcal
               lated at a higher frequency than in dogs.          involvement and that the staphylococcal folliculitis itself








               Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
               © 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
               Companion website: www.wiley.com/go/bruyette/clinical
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