Owners are often surprised to learn the majority of pyodermas are from a dysbiosis of the normal flora and not an external source. Pyodermas (a.k.a. bacterial skin infections) are common sequela to many primary dermatoses, including allergic disease, endocrinopathies, and other cutaneous immune-mediated diseases. Upon learning a pet has a pyoderma, a common question is, “Where did the bacteria come from?” Owners are often surprised to learn the majority of pyodermas are from a dysbiosis of the normal flora, and not an external or environmental source. For clinicians, an in-depth understanding of the factors that promote the transition from normal flora to a potentially resistant, pathogenic bacteria can help educate the client, direct successful treatment of pyoderma, and decrease the risk of developing antimicrobial resistance in these cases. A look at organisms The normal skin microbiota (a.k.a. normal skin flora) is a mixture of both resident and transient bacterial species working symbiotically to inhibit the colonization of invading organisms or to prevent colonization by resident bacterial species.1 Resident organisms have the ability to successfully multiply on normal skin while transient organisms do not generally multiply on normal skin. Common resident organisms include: Micrococcus spp., Bacillus spp., various Staphylococcal spp., including Staphylococcus pseudintermedius, and many others. Maintenance of the normal microbiota is based on several contributing factors, including skin temperature, pH, moisture levels, fatty acid levels, and salinity.1 Disruption of these factors, often secondary to primary inflammatory skin conditions, can lead to dysbiosis resulting in a shift in the cutaneous environment, which favors overgrowth of certain resident or opportunistic cutaneous pathogens and causes a pyoderma. Staphylococcus pseudintermedius is thought to be the primary cutaneous pathogen resulting in a pyoderma in dogs and cats.1,2 Pyoderma As previously mentioned, a pyoderma is rarely a primary clinical disease and is commonly considered a secondary clinical sign. Primary cutaneous, immunological, or metabolic diseases1 cause a dysbiosis of the normal skin flora, resulting in the secondary bacterial skin infection developing. Pyodermas are commonly classified as superficial or deep based on the layers of skin affected. A superficial pyoderma is the most common form of pyoderma; it affects the epidermis and follicular epithelium.1,2 A deep pyoderma is classified as a bacterial infection that involves tissue below the hair follicle.1 Common clinical signs associated with a superficial pyoderma, include: pruritus, papules/pustules, folliculitis, crusts, epidermal collarettes, alopecia, and erythema. Deeper pyodermas have components of furunculosis, cellulitis, and/or panniculitis. Some deep pyodermas may be both pruritic and painful. Cytology is the most useful in-house diagnostic tool for diagnosing secondary bacterial skin infections. Cytology allows clinicians to easily quantify the number of bacteria present, the size and shape of the bacteria, and note any associated inflammatory cells and whether the bacteria is found intracellularly or extracellularly. Cytology can also be used for monitoring response to treatment and may help guide the need for additional diagnostics, such as a bacterial culture and sensitivity. Confirming infection In order to reduce unnecessary exposure to antibiotics, the presence of bacteria should always be confirmed on cytology before empirical therapy is pursued. When selecting an empirical antibiotic for treatment of a pyoderma, the appropriate class selection, duration of treatment, and dosage of the antibiotic can significantly affect the future risk of developing antimicrobial resistance. Additionally, systemic antimicrobials should be reserved for generalized or more severe pyodermas when possible, while topical antimicrobials should be considered for treating mild or focal pyodermas. As a general rule, empirical therapy should focus on the use of tier-one antibiotic classes. Hiller et al., define tier-one antibiotics as: clindamycin, cephalosporins, amoxicillin-clavulanate, and potentiated sulphonamides2. Notably, the use of fluoroquinolones as first-line antibiotics has been associated with a higher risk of multi-drug resistant pyodermas, and their use should be limited in empirical therapy,.2,3 The duration of treatment depends on the depth of the pyoderma. Although the general rule is to treat at least one week past clinical resolution, superficial pyodermas should be treated for a minimum of three weeks, while deep pyodermas often require at least six weeks of systemic antibiotics.1,2 Finally, the recommended dosages for many of the antibiotics used to treat pyodermas is higher than other common systemic infections, and there have been several papers outlining the recommended doses for treatment of pyoderma, including the 2014 one by Hiller et al.2 Further, topical antimicrobials should be utilized both during the management of a pyoderma, as either a sole therapy, or in combination with systemic antimicrobials, and for long-term maintenance therapy to reduce the risk of recurrent pyodermas in predisposed animals. Over the past decade, there has been a dramatic increase in the rate of methicillin and multi-drug resistant pyodermas diagnosed in veterinary medicine. It is well known Staphylococcus spp. are opportunistic cutaneous pathogens with the ability to become resistant to many antimicrobials.3 Methicillin resistance (MR) in staphylococcal species results from a population of Staphylococcus organisms that has acquired the carriage of the mecA gene. Carriage of the mecA gene results in cellular alteration resulting in bacterial resistance to all beta-lactam antibiotics.3.4,5 Also, many MR strains of Staphylococcus spp. can develop additional resistance mechanisms leading to multi-drug resistant (MDR) populations of Staphylococcus spp., which are resistant to many antibiotic families such as: clindamycin, fluoroquinolones, and sulfonamides.4 Bacterial cultures are considered a cornerstone for diagnosing and managing resistant pyodermas, and should be recommended at any point in treatment if the response to antimicrobial therapy is not as expected. However, it is not uncommon for culture results to have both important cutaneous pathogens and environmental contaminants; culture and sensitivity results should always be interpreted in light of clinical findings and cytological findings to best direct antibiotic therapy. With the emergence of a better understanding of acquired resistance in staphylococcal species, clinicians can play an important role in the management and prevention of resistant bacterial infections in our patient population by reducing patient and clinical risk factors. Nienhoff et al., outlined the most common risk factors for development of resistant bacterial infections in veterinary patients, including: antibiotic therapy within the last six months, corticosteroid treatment within the previous six months, previous recent hospitalization, and/or veterinary contact within the last four weeks.5 When a patient with one or more of these risk factors develops a pyoderma, a culture and sensitivity should be recommended prior to initiating systemic antimicrobials. Even without known patient risk factors, The Antimicrobial Guidelines Working Group of the International Society for Companion Animal Infectious Diseases has recommended clinical guideposts to help clinicians determine when they should be concerned for a potential resistant pyoderma. These include2: Less than 50 percent reduction of lesions within two weeks of initiating appropriate systemic antimicrobials Emergence of new lesions two weeks or more after initiating therapy Presence of lesions after six weeks of an appropriate therapy Rod-shaped bacteria seen cytologically History of previous resistant infection in a pet. Ultimately, the golden rule for treating pyoderma should be when in doubt, culture, culture, culture! The development of both methicillin and multi-drug resistant staphylococcal pyoderma poses both a significant therapeutic challenge and increased health risk to our patients; therefore, it is important to understand the numerous patient and clinical risk factors that can promote development of resistant strains of Staphylococcus spp. in our canine and feline patients. To prevent the good guys from going bad, it is imperative veterinarians work to reduce clinical and patient risk factors through judicious antimicrobial use when treating pyodermas and other cutaneous bacterial infections. Rebecca Mount, DVM, was born and raised in Albuquerque, N.M. She earned her bachelor of science in biology from the University of New Mexico in 2005 and her doctorate of veterinary medicine from Colorado State University College of Veterinary and Biomedical Sciences in 2009. Following graduation, Dr. Mount completed a challenging internship in small animal medicine and surgery at Garden State Veterinary Specialists in New Jersey. Mount began her residency with Dermatology for Animals in 2010 and became a diplomate of the American College of Veterinary Dermatology in 2014. References Miller, WH., Campbell, KL., Griffin, CE. Mueller and Kirk’s Small Animal Dermatology 7th edition (various pages). St. Louis, Missouri: Elsevier. Hillier, A., Lloyd, DH., Weese, JS., Blondeau, JM., et al. Guidelines for the diagnosis and antimicrobial therapy of canine superficial bacterial folliculitis (Antimicrobial Guidelines Working Group of the International Society for Companion Animal Infectious Diseases. Veterinary Dermatology. 2014;25: 163-e43 Weese, JS., van Duijkeren, E. Methicillin-resistant Staphylococcus aureus and Staphylococcus pseudintermeidus in veterinary medicine. Veterinary Microbiology. 2010; 140: 418-429. Beco, L., Guaguere, E., Mendez, CL., Noli, C., et al. Suggested guidelines for using antimicrobials in bacterial skin infections (1): diagnosis based nonclinical presentation, cytology and culture. Veterinary Record. 2013; 172: 72-78. Nienhoff, U., Kadlec, K., Chabern, IF., Verspohl, J., et al. Methicillin-resistant Staphylococcus pseudintermeidus among dogs admitted to a small animal hospital. Veterinary Microbiology. 2011;150: 191-197.
