A variety of pharmaceutical preparations, which are applied in the management of non-infectious diseases, have shown in vitro some antimicrobial activity. These drugs are called “non-antibiotics”. So far, a lot of attention has been focused on phenothiazines, thioxanthenes and other agents with affinities to cellular transport systems or agents showing other inhibition mechanism. Several authors confirmed that some non-antibiotics are “helper compounds”, which enhance the in vitro activity of certain antibiotics against specific bacteria (ex. omeprazole and nizatidine enhance the effect of metronidazole on Helicobacter pylori). The aim of this study was to detect and characterise the antimicrobial activity of non-antibiotic drugs, selected from the pharmaceutical products analysed during the state control performed in National Medicines Institute in Warsaw. Over 100 pharmaceutical preparations were randomly chosen from different groups of drugs. The surveillance study was performed on standard ATCC microbial strains used for drug control: Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, Candida albicans and Aspergillus brasiliensis. It was shown that the drugs listed below inhibited growth of at least one of the examined strains: Cyclaid 100 mg cap. (ciclosporine), Heminevrin 300 mg cap. (clomethiazole edisylate), Hydroxycarbamid Teva 500 mg caps. (hydroxycarbamide), Ibandronat Apotex 150 mg tab., Ossica 150 mg tab. (ibandronic acid), Lazivir 150 mg + 300 mg tab. (lamivudyne, zydovudine), No-Spa Max 80 mg tab. (drotaverine HCl) and Rupafin 10 mg tab. (rupatadine). The MIC values of active substances of above drugs were evaluated. The broad spectrum of activity was found in case of clomethiazole which inhibited growth of all tested strains ( MIC: 1.6 – 3.2 mg/ml ). All tested bacterial strains were inhibited by hydroxycarbamide (MIC: 0.8 - 1.6 mg/ml). The high activity against Gram-positive strains was found for drotaverine and rupatadine (MIC: 0.4 mg/ml). Mould strain A. brasiliensis was inhibited by ibandronic acid (MIC 3.2 mg/ml), clomethiazole (MIC 1.6 mg/ml) and cyclosporine (MIC 0.8 mg/ml). Moreover ibandronic acid was active against P. aeruginosa in relatively low concentration (MIC: 0.2 mg/ml). In case of antiviral tablets Lazivir (two active substance: lamivudine and zidovudine) only zidovudine inhibited growth of E. coli in very low concentration 0.00125 mg/ml whereas lamivudine to concentration 1.6 mg/ml did not show any inhibition towards tested strains. The antimicrobial activity of the drugs emphasize a necessity of neutralization of their activity during microbial purity assays of pharmaceutical products.

BackgroundMost patients with bacterial infections suffer from fever and various pains that require complex treatments with antibiotics, antipyretics, and analgaesics. The most common drugs used to relieve these symptoms are non-steroidal anti-inflammatory drugs (NSAIDs), which are not typically considered antibiotics. Here, we investigate the effects of NSAIDs on bacterial susceptibility to antibiotics and the modulation of bacterial efflux pumps.MethodologyThe activity of 12 NSAID active substances, paracetamol (acetaminophen), and eight relevant medicinal products was analyzed with or without pump inhibitors against 89 strains of Gram-negative rods by determining the MICs. Furthermore, the effects of NSAIDs on the susceptibility of clinical strains to antimicrobial agents with or without PAβN (Phe-Arg-β-naphtylamide) were measured.ResultsThe MICs of diclofenac, mefenamic acid, ibuprofen, and naproxen, in the presence of PAβN, were significantly (≥4-fold) reduced, decreasing to 25–1600 mg/L, against the majority of the studied strains. In the case of acetylsalicylic acid only for 5 and 7 out of 12 strains of P. mirabilis and E. coli, respectively, a 4-fold increase in susceptibility in the presence of PAβN was observed. The presence of Aspirin resulted in a 4-fold increase in the MIC of ofloxacin against only two strains of E. coli among 48 tested clinical strains, which included species such as E. coli, K. pneumoniae, P. aeruginosa, and S. maltophilia. Besides, the medicinal products containing the following NSAIDs, diclofenac, mefenamic acid, ibuprofen, and naproxen, did not cause the decrease of clinical strains’ susceptibility to antibiotics.ConclusionsThe effects of PAβN on the susceptibility of bacteria to NSAIDs indicate that some NSAIDs are substrates for efflux pumps in Gram-negative rods. Morever, Aspirin probably induced efflux-mediated resistance to fluoroquinolones in a few E. coli strains.

Peri-implant infective diseases (PIIDs) in oral implantology are commonly known as peri-implant mucositis (PIM) and periimplantitis (PI). While PIM is restricted to the peri-implant mucosa and is reversible, PI also affects implant-supporting bone and, therefore, is very difficult to eradicate. PIIDs in clinical outcome may resemble gingivitis and periodontitis, as they share similar risk factors. However, recent study in the field of proteomics and other molecular studies indicate that PIIDs exhibit significant differences when compared to periodontal diseases. This review aims to elucidate the current knowledge of PIIDs, their etiopathology and diversified microbiology as well as the role of molecular studies, which may be a key to personalized diagnostic and treatment protocols of peri-implant infections in the near future.