Staphylococcus pseudintermedius is often associated with pyoderma, which can turn into a life-threatening disease. The dissemination of highly resistant isolates has occurred in the last 10 years and has challenged antimicrobial treatment of these infections considerably. We have compared the carriage of virulence genes and biofilm formation between methicillin-resistant and methicillin-susceptible S. pseudintermedius (MRSP and MSSP, respectively) isolates and their in vitro gene expression profiles by transcriptome sequencing (RNA-seq). Isolates were relatively unevenly distributed among the four agr groups, and agr type III predominated in MRSP. Five virulence genes were detected in all isolates. Only the spsO gene was significantly associated with MSSP isolates (P ؍ 0.04). All isolates produced biofilm in brain heart infusion broth (BHIB)-4% NaCl. MSSP isolates produced more biofilm on BHIB and BHIB-1% glucose media than MRSP isolates (P ؍ 0.03 and P ؍ 0.02, respectively). Virulence genes encoding surface proteins and toxins (spsA, spsB, spsD, spsK, spsL, spsN, nucC, coa, and luk-I) and also prophage genes (encoding phage capsid protein, phage infection protein, two phage portal proteins, and a phage-like protein) were highly expressed in the MRSP isolate (compared with the MSSP isolate), suggesting they may play a role in the rapid and widespread dissemination of MRSP. This study indicates that MRSP may upregulate surface proteins, which may increase the adherence of MRSP isolates (especially sequence type 71 [ST71]) to corneocytes. MSSP isolates may have an increased ability to form biofilm under acidic circumstances, through upregulation of the entire arc operon. Complete understanding of S. pseudintermedius pathogenesis and host-pathogen signal interaction during infections is critical for the treatment and prevention of S. pseudintermedius infections.
M ethicillin-resistant Staphylococcus pseudintermedius (MRSP)isolates have emerged as one of the leading causes of infectious diseases (including pyoderma, otitis and urinary tract infections) in companion animals, accounting for 20% to 47% of all clinical S. pseudintermedius isolates from dogs and cats (1). Moreover, some MRSP isolates are resistant to the antimicrobials regularly used for treatment (-lactams, fluoroquinolones, tetracyclines, lincosamides, and potentiated sulfonamides) in small animal practice (1, 2). The mecA gene, encoding resistance to -lactams, has been acquired by several S. pseudintermedius clonal lineages on independent occasions; however, two clones, MRSP ST68-SCCmec V and MRSP ST71-SCCmec II-III, are the dominant ones and have spread globally (1, 3, 4). This dissemination was rapid, but the reasons for the fast emergence and success of these lineages are not fully understood (2). Genomic and proteomic studies conducted in the last few years are giving the first clues on the pathways by which MRSP isolates have become successful. A recent genomic report suggested that multidrug resistance evolved rapidly in MRSP due to the ...