Abstract
AIM: To describe clinically overt infections with methicillinresistant Staphylococcus aureus (MRSA) in animals in New Zealand, characterise clinical isolates, and track their sources.
METHODS: MRSA isolates identified in 2005 and 2006 by a veterinary diagnostic laboratory were referred to Massey University for confirmation and characterisation. Clinical information was extracted from the laboratory records or obtained from referring clinicians.
RESULTS: Seven MRSA isolates from animals and contact persons were characterised. All the isolates belonged to the British epidemic MRSA 15 strain (EMRSA-15). Three EMRSA-15 were isolated from post-operative infections in two dogs. An EMRSA-15 indistinguishable from the isolate recovered from one dog was isolated from the anterior nares of a healthy hospital staff member involved in the care of the animal, suggesting nosocomial transmission. Other EMRSA-15 isolates of uncertain clinical significance were isolated from the femoral head of a cat, and from a sample of cow's milk. All EMRSA-15 isolates were resistant to ciprofloxacin, and four were resistant to erythromycin; the latter four isolates also exhibited inducible resistance to clindamycin.
CONCLUSIONS: MRSA can cause clinically overt and difficult-to-treat infections in animals in New Zealand. The rapid emergence of EMRSA-15 as the dominant MRSA strain in humans has resulted in infection spillover to animals.
CLINICAL RELEVANCE: Little is known about the incidence of clinically overt infections with MRSA in animals. The cases described here illustrate the complexities involved in the pharmacological management of EMRSA-15 infections, which is compounded by the universal resistance to β-lactams, and by the strain's fluoroquinolone resistance and frequent inducible resistance to clindamycin. Such complexities indicate there is a need to develop specific empirical antimicrobial treatment strategies and antibiotic susceptibility testing protocols in countries where EMRSA-15 is dominant.
Acknowledgements
The authors are grateful to the veterinarians who provided clinical information, and to Helen Heffernan and Luella Wheeler from the Institute of Environmental Science and Research (Porirua, Wellington) for performing the phage-typing and PFGE. Financial support from the McGeorge Research Fund and Lewis Fitch Research Fund is acknowledged.