Introduction

Bacterial pyoderma is one of the most common diagnoses in canine dermatology. A wide spectrum of clinical lesions may be caused by bacterial pyoderma. None of those lesions is pathognomonic for infection, although a clinician playing the odds can presume bacterial pyoderma particularly with follicular papules and pustules and be right in the majority of cases.

In the majority of dogs and cats with bacterial pyoderma, the offenders are staphylococci, either Staphylococcus (S.) pseudintermedius in the dog or S. aureus or S. pseudintermedius in the cat. In the past, most pyodermas were suspected due to appropriate clinical signs and confirmed by trial therapy with oral antibiotics. Very conscientious clinicians would use cutaneous cytology in an attempt to find out which type of microorganism was involved (cocci, rods or possibly even yeast organisms). Pyoderma was a common disease that was easily treated and not considered a problem. Culture and sensitivity were used to further identify the species involved and aid in the selection of antibiotics used only in very rare cases not responding to treatment. In some areas of the world, this still holds true. In others, however, bacterial pyodermas have become a difficult condition to treat due to the increased prevalence of multiresistant staphylococci.

Multiresistant Bacteria

Multiresistant bacteria are bacteria that can survive the exposure to several antibiotics of different classes. With staphylococci that typically means dealing with either methicillin-resistant S. aureus (MRSA) or methicillin-resistant S. pseudintermedius (MRSP). Both of those have developed a resistance to beta-lactam antibiotics (penicillins and cephalosporins). These bacteria are not more pathogenic than methicillin-sensitive strains, but harder to treat, particularly since the methicillin resistance often goes along with resistance to antibiotics other than penicillins and cephalosporins. In general, resistance can either occur through a spontaneous mutation (which is transmitted only vertically through proliferation) or through acquisition of extrachromosomal genetic elements containing the genes responsible for the resistance (which can be transmitted via horizontal gene transfer). The gene responsible for the methicillin resistance is the mecA gene that encodes the penicillin-binding protein 2a. This penicillin-binding protein does not bind beta-lactam antibiotics and thus enables normal cell wall synthesis in the presence of those antibiotics. This mecA gene is contained in a staphylococcal cassette chromosome mec (SCCmec), a genomic island that in some genotypes (types I–III) also contains additional resistance genes.

For MRSA, different strains exist; the first ones occurred in a hospital setting with severely affected patients and high antibiotic use and thus were named hospital-acquired MRSA. In humans, the genotypes I–III are typically associated with hospital-acquired MRSA. In contrast, type IV and V are smaller, lack other resistance genes and are associated with community-acquired MRSA that occurred later and infected healthy people not in contact with healthcare facilities. Different strains exist and the predominant strains are different in North America compared to Australia or Europe, but overall a highly clonal population structure exists for MRSA in contrast to MSSA, which is genetically extremely diverse.

MRSP strains also show a highly clonal population structure. Their mecA gene is highly homologous to the mecA gene of MRSA (95–100%). MRSP was first described in 2007, a recent PubMed search revealed 23 papers about MRSP in 2012, indicating a clear increase. This problem will not go away quickly but will become more prominent for all of us in the next years. When dogs with MRSP and MSSP infections were treated and recultured after clinical remission, 26 of 42 dogs initially infected with MRSP still were positive for that microorganism on culture, and, more disturbing, 23 of 60 dogs initially infected with MSSP showed an MRSP on culture after clinical remission (Beck 2012). In another study, it was shown that simply culturing the nares of dogs previously diagnosed with bacterial pyoderma due to MRSP and successfully treated will not identify carrier animals and that pharynx, perineum and mouth should be cultured to minimize the number of false-negative cultures (Windahl 2012). This study also showed that affected dogs carried MRSP for more than a year after clinically apparent infection. Dogs that were treated with an antibiotic to which the MRSP was resistant to carried the organism for a significantly longer time period, a fact that points out the potential dangers of empirical therapy in areas where such MRSP are regularly diagnosed.

Diagnosis of Multiresistant Staphylococci

With this increase of infections with multiresistant bacteria and the problem to eliminate them from our patients, we should recommend culture and sensitivity to every patient with a bacterial infection based on history, clinical examination and cutaneous cytology, which we plan to treat with systemic antibiotics. I am aware that this is a challenge, as most owners in practice are not willing to spend the money, but the veterinary profession should at least push for the ideal approach and if clients refuse it, we at least tried.

Antibacterial Treatment Options

In general, we have the choice of topical antiseptic agents such as wipes, sprays, rinses and shampoos, topical antibacterial agents and systemic antibiotics. The animal's general condition, severity of infection, duration of disease and previous treatments will dictate the choice as much as the owner's financial and personal situation. Antibiotic use is increasingly implicated in the development of multiresistant bacteria. In some countries, active steps have been taken to limit the use of antibiotics in small animal practice, apparently without a detectable decrease in treatment success. For example, a recent randomized study has shown that dogs with generalized demodicosis and pyoderma respond just as fast with miticidal and topical antiseptic therapy as when additionally treated with oral antibiotics. So whenever possible, we should focus on the use of topical antiseptics rather than systemic antibiotics; studies have shown the successful use of topical therapy for treatment of bacterial pyoderma in the dog.

When dogs with MRSP and MSSP infections were treated and recultured after clinical remission, 26 of 42 dogs initially infected with MRSP still were positive for that microorganism on culture, and, more disturbing, 23 of 60 dogs initially infected with MSSP showed an MRSP on culture after clinical remission. When treating dogs infected with MRSP, the most frequently used antibiotics included chloramphenicol and doxycycline, and the percentage of dogs achieving clinical remission was as high as that of dogs treated for MSSP. Topical treatment alone was also shown to be effective in MRSP as well as MSSP.

A number of antibiotic choices are available to the small animal practitioner. Which antibiotic is chosen should ideally depend on the results of culture and sensitivity testing. Further factors influencing the decision in practice are the cost, the tolerance of the patient for the antibiotic, the finances and the previous history. If a dog never had a health problem, was not hospitalised in the past, and did not receive antibiotics previously, then empirical therapy with an antibiotic known to be effective in the majority of staphylococcal infections may be attempted, if the owner does not want to pay for a culture and sensitivity. If the dog, however, has a previous history of health problems and antibiotic therapies, culture and sensitivity should be imperative.

Some dermatologists and microbiologists support the notion of first-line, second-line and third-line antibiotics. First-line antibiotics are preferably narrow-spectrum antibiotics with good activity against staphylococci. Some broad-spectrum antibiotics with anti-staphylococcal activity are also recommended. Those antibiotics include first-generation cephalosporins and are suitable for empirical therapy in most countries. Second-line antibiotics are considered important for human and animal health and should not be used empirically but only when a culture shows that the organisms are sensitive to the antibiotic in question and there is no first-line antibiotic with identical efficacy. Examples for such second-line antibiotics are fluoroquinolones and third-generation cephalosporins. Third-line antibiotics are important in the treatment of infections with multiresistant organisms and often not approved for veterinary use. Examples include aminoglycosides. They should only be used when first- and second-line antibiotics are not effective and topical therapy is not possible. In my opinion, we as veterinarians should only use those third-line antibiotics approved for the use in veterinary medicine. Human reserve antibiotics such as vancomycin or linezolid should not be used in veterinary medicine.