Antibiotic-resistant status and pathogenic clonal complex of canine Streptococcus canis-associated deep pyoderma

Abstract

Background: Streptococcus canis causes deep pyoderma in canines, which raises concerns about the risk of isolates from lesions acquiring an antibiotic-resistant phenotype. It is necessary to identify effective antibiotics and the characteristics of the pathogenic cluster for S. canis-associated deep pyoderma.

Results: The signalment, molecular typing, and antibiotic-resistant status of S. canis isolated from deep pyoderma lesions (27 strains) and oral cavities (26 strains) were analyzed. Older dogs tended to have S. canis-associated deep pyoderma (15 of 27 dogs over 10 years old). Veterinarians chose quinolones for 10/16 cases (63%), even though the rate of quinolone-resistant strains of S. canis is 38-59%. Although 70% of the strains showed resistance to three or more antibiotic classes (37/53), 94% (50/53) strains showed sensitivity for penicillins. We also identified β-lactamase activity among penicillin-resistant strains of S. canis. Clonal complex 13 (CC13) was detected only in lesions and formed independent clusters in the phylogenetic tree. One strain of CC13 was resistant to the anti-methicillin-resistant Staphylococcus aureus drugs, vancomycin and linezolid.

Conclusion: Although antibiotic-resistant strains of S. canis are isolated at a high rate, they can currently be treated with β-lactamase-inhibiting penicillins. CC13 may be a pathogenic cluster with high levels of antibiotics resistance.

Keywords: Antibiotic resistance; Beta-lactamase; Dogs; Multilocus sequence typing; Opportunistic infections; Oral cavity; Pyoderma; Streptococcus.

Fig. 1

Antibiotic resistance profile of deep pyoderma cases and control isolates. A neighbor-joint tree of 53 isolates (27 cases of deep pyoderma, 26 oral controls) was built with multilocus sequence typing data. The strains indicated in bold italics produced a minimum inhibition concentration to penicillin, cephems, and anti-methicillin-resistant Staphylococcus aureus drugs, and β-lactamase activity. The status of each isolate is indicated by the colored cell (red, deep pyoderma; blue, oral control). Colored cells then indicate the presence of resistance to the antibiotic agent, namely penicillin G (PCG), amoxicillin (ABPC), amoxicillin/clavulanic acid (ACV), cephalexin (CEX), cefovecin (CFV), fosfomycin (FOM), enrofloxacin (ERFX), marbofloxacin (MFLX), levofloxacin (LVX), gatifloxacin (GFLX), clindamycin (CLM), lincomycin (LCM), doxycycline (DOT), minocycline (MNO), tetracycline (TC), gentamicin (GM), sulfamethoxazole and trimethoprim (SXT), erythromycin (EM), kanamycin (CAM), and the anti-methicillin-resistant Staphylococcus aureus (MRSA) drugs linezolid (LZD) and vancomycin (VCM) in a disk diffusion test (resistant, pink; intermediate, yellow; sensitive, green). Antibiotic resistance status was determined based on clinical and laboratory standards institute criteria

Fig. 2

β-Lactamase activity profile in five strains of S. canis. Penicillin-resistant strains (P03, P23, 014) and penicillin-sensitive strains genetically close to P03 and P23 (P02, P05) were grown aerobically, and β-lactamase enzyme activity units were measured. P23 and O14 produced higher β-lactamase than the other strains (*p < 0.05, ***p < 0.005). No significant differences were observed among strains other than those bars shown in the figure (p > 0.05)