The 4-quinolones ciprofloxacin, difloxacin, enoxacin, norfloxacin, ofloxacin, and nalidixic acid were found to induce the SOS response in qualitative and quantitative tests on Escherichia coli K12 containing the sfiA::lacZ gene fusion. Maximum induction of the SOS-response was observed with the quinolone concentrations that produced the most killing. There was also a modest increase in the rate of mutation in the lactose and galactose operons in a GalE- background, provided there was a functioning SOS system.

Certain viruses have evolved mechanisms to counteract innate immunity, a host response in which nuclear factor kappaB (NF-kappaB) transcription factors play a central role. African swine fever virus encodes a protein of 28.2 kDa containing ankyrin repeats similar to those of cellular IkappaB proteins, which are inhibitors of NF-kappaB. Transfection of the African swine fever virus IkappaB gene inhibited tumor necrosis factor- or phorbol ester-induced activation of kappaB- but not AP-1-driven reporter genes. Moreover, African swine fever virus IkappaB co-immunoprecipitated with p65 NF-kappaB, and the purified recombinant protein prevented the binding of p65-p50 NF-kappaB proteins to their target sequences in the DNA. NF-kappaB activation induced by tumor necrosis factor, as detected by mobility shift assays or by transfection of kappaB-driven reporter genes, is impaired in African swine fever virus-infected cells. These results indicate that the African swine fever virus IkappaB gene homologue interferes with NF-kappaB activation, likely representing a new mechanism to evade the immune response during viral infection.

To compare the activity of tedizolid (formally known as torezolid and TR-700) with that of 15 agents against a collection of linezolid-resistant staphylococci (164 coagulase-negative staphylococci and 5 Staphylococcus aureus). Antimicrobial susceptibility tests were performed using the broth microdilution method following the recommendations of the CLSI. All isolates were susceptible to vancomycin and tigecycline. Based on the MIC₉₀ values, the potency of tedizolid against coagulase-negative staphylococci was >16-fold greater than that of linezolid. Tedizolid retained activity against most of the linezolid-resistant staphylococci tested, including multidrug-resistant isolates with elevated linezolid MICs (32 to >128 mg/L). Of the isolates, 79.2% and 31.4% were inhibited by tedizolid at ≤4 mg/L and ≤2 mg/L, respectively. The results of this study confirm the activity of tedizolid against linezolid-resistant staphylococci. This new oxazolidinone could have an important role as a potential therapeutic agent against multidrug-resistant staphylococci.

The rates of resistance to erythromycin and clindamycin among Streptococcus agalactiae strains isolated in our hospital increased from 4.2 and 0.8% in 1993 to 17.4 and 12.1%, respectively, in 2001. Erythromycin resistance was mainly due to the presence of an Erm(B) methylase, while the M phenotype was detected in 3.8% of the strains. Telithromycin was very active against erythromycin-resistant strains, irrespective of their mechanisms of macrolide resistance.

Nosocomial pathogens can be associated with a variety of infections, particularly in intensive care units (ICUs) and in immunocompromised patients. Usually these pathogens are resistant to multiple drugs and pose therapeutic challenges. Among these organisms, Acinetobacter baumannii is one of the most frequent being encountered in the clinical setting. Carbapenems are very useful to treat infections caused by these drug-resistant Gram-negative bacilli, but carbapenem resistance is increasing globally. Combination therapy is frequently given empirically for hospital-acquired infections in critically ill patients and is usually composed of an adequate beta-lactam and an aminoglycoside. The purpose of this study was to evaluate the in vitro activity of plazomicin against carbapenem-resistant Acinetobacter baumannii . Amikacin was used as a comparator. The activity of plazomicin in combination with several different antibiotics was tested by disk diffusion, the checkerboard method, and time-kill studies. Synergy was consistently observed with carbapenems (meropenem and/or imipenem) along with plazomicin or amikacin. When the aminoglycosides were combined with other classes of antibiotics, synergy was observed in some cases, depending on the strain and the antibiotic combination; importantly, there was no antagonism observed in any case. These findings indicate the potential utility of plazomicin in combination with other antibiotics (mainly carbapenems) for the treatment of A. baumannii infections, including those caused by carbapenem-resistant isolates.