The discovery, commercialization, and regular administration of antimicrobial agents have revolutionized the therapeutic paradigm, making it possible to treat previously untreatable and fatal infections. However, the excessive use of antibiotics has led to develop resistance soon after their use in clinical practice, to the point of becoming a global emergency. The mechanisms of bacterial resistance to antibiotics are manifold, including mechanisms of destruction or inactivation, target site modification, or active efflux, and represent the main examples of evolutionary adaptation for the survival of bacterial species. The acquirement of new resistance mechanisms is a consequence of the great genetic plasticity of bacteria, which triggers specific responses that result in mutational adaptation, acquisition of genetic material, or alteration of gene expression, virtually producing resistance to all currently available antibiotics. Understanding resistance processes is critical to the development of new antimicrobial agents to counteract drug-resistant microorganisms. In this review, both the mechanisms of action of antibiotic resistance (AMR) and the antibiotic resistance genes (ARGs) mainly found in clinical and environmental bacteria will be reviewed. Furthermore, the evolutionary background of multidrug-resistant bacteria will be examined, and some promising elements to control or reduce the emergence and spread of AMR will be proposed.

The spread of extended-spectrum β-lactamase-producing Escherichia coli and methicillin-resistant Staphylococcus aureus has caused a reduction in antibiotic effectiveness and an increase in mortality rates. Essential oils (EOs), known for their therapeutic efficacy, can be configured as novel broad-spectrum biocides. Accordingly, the bacteriostatic–bactericidal activity of Citrus Lemon (LEO), Pinus Sylvestris (PEO), Foeniculum Vulgaris (FEO), Ocimum Basilicum (BEO), Melissa Officinalis (MEO), Thymus Vulgaris (TEO), and Zingiber Officinalis Rosc. (GEO), at concentrations ranging from 1.25 to 40% (v/v), were tested in vitro against different E. coli and S. aureus strains using minimal inhibitory concentrations (MICs) and minimum bactericidal concentrations (MBCs). The chemical compositions of the EOs were analyzed using GC/MS. The major components of all seven tested oils were limonene, α-pinene, anethole, estragole, citral, thymol, and zingiberene, respectively. We found that the bacteriostatic–bactericidal activity of the EOs was related to their chemotypes and concentrations, as well as the strain of the bacteria. A dose–effect correlation was found when testing GEO against S. aureus strains, whilst FEO was found to have no activity regardless of concentration. PEO, MEO, and BEO were found to have bactericidal effect with a MIC and MBC of 1.25% (v/v) against S. aureus strains, and LEO was found to have values of 1.25% (v/v) and 5% (v/v) against ATCC and clinical isolate, respectively. Interestingly, the antimicrobial activity of TEO was not related to oil concentration and the complete inhibition of growth across all E. coli and S. aureus was observed. Although preliminary, our data demonstrate the efficacy of EOs and pave the way for further investigations on their potential synergistic use with traditional drugs in the human and veterinary fields.

Canine parvovirus type 2 (CPV2) emerged in 1978 as causative agent of a new disease of dogs. New antigenic variants (biotypes), designated CPV2a and CPV2b, became widespread during 1979 to 1980 and 1984, respectively. At the present time the original CPV2 has disappeared in the dog population and has been replaced by the two new viruses. In the present study the comparison of neutralizing antibody titers in two groups of pups (18 pups in each group) inoculated with CPV2 and CPV2b modified live virus vaccines is reported. Using the hemagglutination inhibition (HI) test, relevant differences between antibody titers, against either the homologous or the heterologous virus, were not constantly observed. Using the neutralization (Nt) test, however, the pups inoculated with CPV2 had antibody titers which were approximately 30 times higher to the homologous virus (mean, 4,732) than to the heterologous virus (CPV2b) (mean, 162). The results of these experiments support two conclusions: (i) the HI test may not always accurately evaluate the true immune status of dogs with respect to CPV, and (ii) dogs inoculated with CPV2 vaccine develop relatively low Nt antibody titers against the heterologous virus (CPV2b). These data may suggest an advantage for new vaccines, considering that most presently licensed vaccines are produced with CPV2, which no longer exists in the dog population.