Small Animal Dermatology, 3rd edition

CHAPTER 7 ANTIBIOTIC STEWARDSHIP AND EMERGING RESISTANT BACTERIAL INFECTIONS 143

ETIOLOGY

 Emerging infections include methicillin-resistantStaphylococcus,Pseudomonassp.,

Enterococcussp., andCorynebacteriumsp., with staphylococcal infections being the

most widespread and problematic at this time.

 The most frequently noted problematic bacterial infections include the methicillin-

resistant staphylococci: MRSP (pseudintermedius), MRSS (schleiferi), and MRSA

(aureus).

 “Methicillin resistance” implies a resistance to other antibiotics in the same beta-

lactam class of drugs such as penicillin, amoxicillin, oxacillin, and cephalosporins.

 Staphylococci are gram-positive cocci that exist as part of the normal cutaneous and

mucosal microflora of mammals.

 Numerous species of staphylococcus can be detected on canine skin, with the most

common species beingS. pseudintermedius.

 Coagulase-positive species have been considered to be more pathogenic than

coagulase-negative species, recent data suggest that coagulase-negative species may

also be pathogenic (S. schleiferissp.schleiferiin dogs).

 MRSA/MRSP/MRSS emergence is suspected to be associated with overuse of antibi-

otics; broad-spectrum antibiotics such as cephalexin, cefazolin, cefadroxil, amox-

icillin, penicillin, and fluoroquinolones may hasten the development of oxacillin/

methicillin resistance.

 Unnecessary prescriptions, poor client compliance in the use of antibiotics, and feed

additives in livestock production are also suspect.

 Four proposed mechanisms of resistance in methicillin-resistant Staphylococcus

organisms:

Penicillin-binding proteins (PBP) and the mecA gene

Cell wall thickening noted in all MRS organisms

Efflux pump

Biofilm production.

 PBP and mecA:
Transmission of the mecA gene encodes for an altered defective penicillin-

binding protein (PBP2a) which is involved in cell wall peptidoglycan synthesis

All penicillins and cephalosporins (beta-lactams) require binding to the PBP in

the bacterial cell wall to initiate the drug’s activity

MRSA produces a defective PBP due to the presence and activation of the mecA

gene

The mecA gene comes from a mobile genetic component called a staphyloccal

chromosomal cassette (SCCmec)

The spread of MRSA is usually through clonal expansion rather than the normal

process of mutation or plasmid transfer

All MRSA strains can be traced back to a single clone found in Europe in the

mid-1960s.

 Cell wall thickening:
Increased synthesis of peptidoglycan in the cell wall of vancomycin-resistant

staphylococci