Pharmacotherapeutic group: Other antibiotics for topical use
ATCvet code: QD06AX
Pharmacodynamic properties
Mode of action
Clindamycin is a semi-synthetic antibiotic produced by 7(S)-chloro substitution of the 7(R)-hydroxy group of the natural antibiotic produced by Streptomyces lincolnensis var. lincolnensis.
Clindamycin, a mainly time-dependent acting antibiotic, acts by a bacteriostatic mechanism where the drug interferes with protein synthesis within the bacterial cell, thus inhibiting the growth and multiplication of the bacteria.
Clindamycin binds to the 23S ribosomal RNA component of the 50S subunit. This prevents amino acids binding on these ribosomes, and therefore inhibits peptide bond formation. The ribosomal sites are close to those bound by macrolides, streptogramins or chloramphenicol.
Antibacterial spectrum
The spectrum of activity of lincosamides is similar to the macrolide antibiotics and includes streptococcus spp., staphylococcus spp. (including ß-lactamase-forming Staphylococcus aureus).
MIC data
CLSI clindamycin veterinary breakpoints are available for dogs in Staphylococcus spp. and Streptococci-β-haemolytic group in skin and soft tissue infections: S≤0.5μg/ml; I=1-2µg/ml; R≥4μg/ml (CLSI February 2018). These breakpoints are established for systemic treatment and should be considered as indicative for topical treatment only.
Type and mechanism of resistance
Clindamycin belongs to the lincosamide group of antibiotics. Resistance can develop to the lincosamides alone, but more commonly cross-resistance occurs among macrolides, lincosamides and streptogramin B antibiotics (MLSB group). Resistance is the result of methylation of adenine residues in the 23S RNA of the 50S ribosomal subunit, which prevents drug binding to the target site. Different bacterial species are able to synthesize an enzyme, encoded by a series of structurally related erythromycin ribosomal methylase (erm) genes. In pathogenic bacteria, these determinants are mostly borne by plasmids and transposons that are self-transferable. The erm genes occur predominantly as variants erm(A) and erm(C) in Staphylococcus aureus and as variant erm(B) in Staphylococcus pseudintermedius, streptococci and enterococci.
MLSB inducible resistance is not detected by standard in vitro susceptibility testing methods. The CLSI recommends the D-zone test to be routinely performed in veterinary diagnostic laboratories in order to detect clinical isolates with inducible resistance phenotype. Clindamycin use should be discouraged in these patients. The incidence of resistance to lincosamides in Staphylococcus spp. appears to be wide-ranging in Europe. Studies (2010) report an incidence between 25-40%.
Pharmacokinetic properties
No data is available for clindamycin plasma levels or clindamycin levels in the inflamed area after application of the formulation.
All other information indicates that clindamycin is hardly absorbed through the skin.
In case clindamycin will be absorbed through the skin, distribution will be high due to the basic nature of the substance, and accumulation will occur in tissues with a lower pH than plasma.