Compositions for treating biofilm

Abstract

A two component composition comprises an anchor enzyme complex to degrade biofilm structures and a second anchor enzyme component having the capability to act directly upon the bacteria for a bactericidal effect.

Description

[0001] This application is a continuation of U.S. application Ser. No. 09 / 587,818 filed Jun. 6, 2000, which is a continuation-in-part of U.S. application Ser. No. 09 / 249,674 filed Feb. 12, 1999, which is a continuation-in-part of U.S. application Ser. No. 08 / 951,393 filed Oct. 16, 1997 (issued as U.S. Pat. No. 5,871,714 on Feb. 16, 1999), all of which are incorporated herein by reference.FIELD AND BACKGROUND OF THE INVENTION[0002] Standard chemical analyses, traditional microscopic methods as well as digital imaging techniques such as confocal scanning laser microscopy, have transformed the structural and functional understanding of biofilms. Investigators, with these techniques have a clearer understanding of biofilm-associated microorganism cell morphology and cellular functions. The heightened awareness of metabolic biochemistry and the events associated with them have led to a better understanding, not only of individual cells and their varying environments, but also collections...

AI Technical Summary

Problems solved by technology

Industrial biofilms are an important cause of economic inefficiency in industrial processing systems.

Antibiotic resistance and persistent infections that are refractory to treatments are a major problem in bacteriological transmissions, resistance to eradication and ultimately pathogenesis.

However, the lack of consistency in results and the inability to retain the enzymes at the site where their action is required has prohibited their widespread use.

There are conditions, however, where these non-enzymatic approaches cannot be used e.g., caustic- and acidic-sensitive environments, temperature or abrasion sensitive components that are associated with the biofilm and dynamic fluid action.

In these circumstances, the lack of demonstrated efficacy of enzymes to control biofilms is not related exclusively to their lack of ability to be retained at the site of the biofilm.

Rather, the choice of enzyme to degrade the biofilm was inappropriate.

However, not infrequently in an open system, the same forces that flush or sweep away the biofilm degrading enzymes also flush bactericidal agents so that they cannot act directly upon bacteria unless there is a chance meeting between the agent and a planktonic bacterium.

Unless the biofilm is removed or disrupted, complete cellular kill within the biofilm structure is not achieved by chemical or physical agents.

Furthermore, removal or disruption of the biofilm will free cells from a sessile state to make them planktonic which also increases their susceptibility to chemical and physical agents.

However, for the majority of situations when fouling by biofilms occurs, these strategies are not practical or at best have limited utility.

There are obvious drawbacks to any one method, precluding a universal method or approach.

However, the common trait of all of these methods lies in their focus on the biofilm structure and not the living cells within the biofilm.

As the biofilm is removed, some cells within the biofilm are liberated and become planktonic; others, however, remain sessile but are more vulnerable to being killed because the protective quality of the biofilm is reduced.

Without the capability to keep the appropriate active agents at or near the biofilm structure, they may be swept away in the fluid flow.

Contact lens use, particularly extended wear soft lenses, may exacerbate corneal ulcers.

The lens itself or even the lens solution may introduce P. aeruginosa into the eye, while minor lens induced damage to the eye provides the opportunity of infection.

Patients exposed to intensive care environment, have serious burns or have undergone ocular irradiation are especially susceptible to P. aeruginosa infections.

The colonization of P. aeruginosa accelerates disease pathology resulting in increased mucus production, airway obstruction, bronchiectasis and fibrosis in the lungs.

These conditions eventually lead to pulmonary disease leading to hypertension and hypoxemia.

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