## 1 Introduction  
Diabetic foot ulcers are the most serious complication of diabetes mellitus and the most common lower extremity injuries that are ended by amputation. The non-traumatic amputations are mainly observed among diabetics. For instance, the rate of amputations in diabetics is 30 to 40 times higher than in non-diabetics. The diabetic foot ulceration risk is considerably high among diabetics and may reach 25%; the majority will suffer from amputation within few years after first diagnosis [1]. Unfortunately, mortality rate within five years after amputation is predicted to be 40% to 70% [2]. There are several risk factors account for the increase in the incidence of diabetic foot. Neuropathy and peripheral arterial occlusive disease are considered among the major causes of diabetic foot according to epidemiological studies [3]. The management of ulcerations in diabetic foots requires a professional management emphasizing the interdisciplinary cooperation between various medical health care providers [2]. The worst could happen when minor trauma or any breakdown in the skin integrity that leads to chronic diabetic foot wounds. Neuropathy, low vascularity and compromised immunity increase the chance to the flourishment of microbial infection especially bacterial infections [4; 5]. The diabetic foot bacterial infections are very parlous and if not controlled may spread deeper in underlying tissues and bones. The necessity to an efficient anti-bacterial therapy is mandatory to control infections in early stages and to minimize the necessity to surgical interventions in later stages. Frequently, the diabetic foot ulcers can be infected by diverse Gram-positive or -negative bacteria that are characterized by high resistance to antibiotics [2; 4]. Infection with _Proteus mirabilis_ is recognized among the most serious diabetic foot ulcers infections. _Proteus mirabilis_ is a motile and non-lactose fermenter member of Gram-negative Enterobacteriaceae family. To describe _Proteus_ species shapeshifting, [PERSON] (1885) named it after the sea-God [PERSON] in [PERSON]'s Odyssey. _P. mirabilis_ is characterized by its dimorphic short rods and elongated swarmer cells that express a lot of flagella [6]. _P. mirabilis_ causes a broad range of pathogenesis, it causes more than 3% of all nosocomial infections and up to 44% of catheter-associated urinary tract infections [7]. _P. mirabilis_ is one of the most serious diabetic foot ulcers infectious agents that isolated in percentage about 18% [8; 9; 10]. The _P. mirabilis_ virulence factors are encoded on chromosomally integrated or even extra-chromosomally imported genes [11]. Theses virulence factors are widely assorted from constitutional organelles as flagella swarming motility and adhesive fimbia to production of various extracellular enzymes and toxins as protease, urease and hemolysis [6; 7]. Quorum sensing (QS) system is a signaling system to regulate the bacterial pathogenesis, QS plays crucial roles in organization of _P. mirabilis_ infection, colonization and biofilm formation [12]. Furthermore, _P. mirabilis_ incessantly develops a resistance to various antibiotics [13; 14]. The infectious ability of _P. mirabilis_ is mostly related to the biofilm formation, that constitutes an additional difficulty in treatment by conventional antibiotics [7; 12; 14]. Critically, resistance development beside biofilm formation worsens the _P. mirabilis_ infections to diabetic foot ulcers and impede the therapeutic treatment towards favoring surgical interventions [9; 13]. In such aggressive bacterial infections as those in diabetic foot ulcers, it is essential to invent new strategies to guarantee an effective treatment by antibiotics. One of these strategies is crippling bacterial virulence and targeting its QS [15; 16; 17; 18]. Without affecting the bacterial growth, this strategy decreases the possibility of the bacterial resistance development [19; 20; 21].