More and more frequently, clinicians are raising the alarm about the ever increasing therapy resistance of bacteria as one of the major clinical challenges in the 21st century. The renowned New England Journal of Medicine (NEJM) reported such antibiotic resistances even have the potential to jeopardize important achievements of modern medicine like chemotherapy or organ transplants.

Treatment of antibiotic resistant bacteria with broadband antibiotics offers no real alternative: they still have limited effectiveness, typically have a higher toxicity, are expensive, and are one of the prime causes of the increasing incidence of antibiotic resistance.

Combating antibiotic resistant strains of bacteria for example by an antibiotic resistant variant of the most common cause of Staphyloccocus infections is putting an increasing strain on clinical outcomes and hospital budgets. For instance, MRSA is prevalent in 30% of Staphylococcus cases in France, England, Italy or Belgium, and as high as 70% of cases in some institutions in the US.

For patients who develop an MRSA infection, the KISS (a German hospital infection surveillance system) in Germany for 2005 shows the mortality rate doubles, with around 15 % to 20 % of infected patients dying. The extra treatment costs averaged € 5,700 for each patient, or roughly € 600 a day.

In the 1950s, strains of S. aureus rapidly accumulated resistance to tetracycline, macrolides and aminoglycosides, posing considerable problems in the management of nosocomial infections.

The rapid rise of resistance to ampicillin in the early 1960s turned out to be due to a beta-lactamase. The industry responded by developing a more sophisticated beta-lactam compound, the so-called third-generation cephalosporins.

The further selection of resistant mutants and the acquisition of novel antibiotic resistance genes, in turn, led to the appearance of extended-spectrum beta-lactamases (ESBLs) in the late 1980s and 1990s, which now compromise the use of third-generation cephalosporins for the treatment.

The introduction carbapenems throughout the 1990s seemed to be the answer. However, the spread of a variety of beta-lactamases capable of hydrolyzing carbapenems are seen increasingly in clinical isolates of Gram-negative bacteria.