**8.5 Cystic fibrosis**

Cystic Fibrosis is a chronic bacterial infection of intrapulmonary airways with *P. aeruginosa* [19]. Its consequences include thickening of mucus in many body systems which results in impaired mucociliary clearance of microorganisms and chronic infection in lungs. The infection gets punctuated by acute aggravation of disease and inflammation which will lead to lung failure and premature death [20]. According to the genetic etiology, one out of more than 1500 potential mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene results in its malfunction, as a result sodium absorption is inhibited through epithelial sodium channel. And due to hyper-absorption of water, airway surface liquid gets depleted, mucociliary clearance get depleted and inhaled bacteria are allowed to remain within airway [20, 21].

Microscopic studies of sputum samples and lung tissue section have shown the presence of biofilm or micro-colonies in the airways. These biofilms are able to grow larger than 100 μm in diameter [22]. Some common cystic fibrosis pathogens include *S. aureus, H. influenzae* and ultimately predominant one *P. aeruginosa* [20, 21]. *P. aeruginosa* has some adaptive mechanisms which make it survive and persist for several decades in CF patient's respiratory tract. Biofilm adaptation of *P. aeruginosa* makes it resistant to antibiotic therapy and inflammatory defense

**159**

*Microbial Biofilms*

oxygen [15].

**8.6 Periodontitis**

**8.7 Osteomyelitis**

*DOI: http://dx.doi.org/10.5772/intechopen.90790*

mechanism. This also makes it survive in different conditions like whether it is aerobic respiratory zone or the conductive zone of the lungs which have anaerobic sputum or the paranasal sinuses where mucus too has a lower concentration of

by giving an early treatment with ciprofloxacin and colistin [5, 22].

which dental carries and periodontal diseases occurs [5].

coated with PLL-g-PEG in comparison to uncoated surfaces [25].

flora via oral hygiene methods [6, 23].

Early antimicrobial treatment (i.e. during early colonization period of microbes) for preventing chronic infection of *P. aeruginosa* may give a possibility for successful treatment of cystic fibrosis, as this chronic infection may postpone for several years

Periodontitis is the infection of supporting tissues of teeth, gums (gingiva) and periodontal tissues (gingiva, alveolar bone, and periodontal ligament). Its chronic form may lead to exfoliation of teeth. The primary site of periodontitis is sub gingival crevice which is the channel between the tooth root and the gum. Organisms responsible for this infection are *Fusobacterium nucleatum*, *Peptostreptococcus micros*, *Eubacterium timidum*, *E. brachy*, *Pseudomonas anerobicus,* and predominate one *P. gingivalis.* They can easily colonize the surface of the oral cavity which helps them in invading mucosal cells, altering calcium flux in epithelial cells and in releasing toxins. As a result, plaque (a climax biofilm community) is formed within 2–3 weeks. Calculus or tartar is the mineralized plaque which acts as a resistance against the antimicrobial activity of saliva in protecting tooth enamel, as a consequence of

Dental plaque or biofilm cannot be eliminated, only their pathogenic nature can be minimized by minimizing the bioburden and effectively maintain a normal oral

Osteomyelitis is an inflammatory bone disorder characterized by infection in bone/bone marrow which leads to necrosis and bone destruction [24, 25]. When complex multi-resistant biofilm has established, treatment of osteomyelitis becomes more challenging. Due to increased bacterial resistance to antibiotics in biofilm mode, they cause persistent infections. It has been found that in more than 50% osteomyelitis cases, causative organisms are *S. aureus* and *S. epidermidis* [24]. Although, endoprostheses which are found to be an increasingly common source of infection, surgically implanted devices or other implants like orthopedic internal fixation devices also represents a remarkable risk factor for the development of osteomyelitis. Stainless steel, titanium, titanium alloys are most commonly used materials in implants in which stainless steel is found to be associated with greater infection rate as compared to titanium. A possible reason of this is might be that soft tissues get firmly adhered to a titanium-implant surface while a fibrous capsule is formed enclosing a liquid filled space around the steel implants. This unvascularized space is less accessible to host defense mechanisms where bacteria can multiply and freely spread. Studies showed that *S. aureus* and *S. epidermidis* adhesion to the surface can be reduced by the use of coatings based on human proteins such as albumin or human serum. Coatings of poly(1-lysine)-grafted-poly(ethylene glycol) (PLL-g-PEG) when extensively studied for use in biomedical applications, it has been found to be highly effective in reducing the absorption of blood serum, blood plasma and single proteins like fibrinogen and albumin. Fibroblast and osteoblast cell adhesion get remarkably reduced by spreading of metal oxide surface

### *Microbial Biofilms DOI: http://dx.doi.org/10.5772/intechopen.90790*

mechanism. This also makes it survive in different conditions like whether it is aerobic respiratory zone or the conductive zone of the lungs which have anaerobic sputum or the paranasal sinuses where mucus too has a lower concentration of oxygen [15].

Early antimicrobial treatment (i.e. during early colonization period of microbes) for preventing chronic infection of *P. aeruginosa* may give a possibility for successful treatment of cystic fibrosis, as this chronic infection may postpone for several years by giving an early treatment with ciprofloxacin and colistin [5, 22].

### **8.6 Periodontitis**

*Bacterial Biofilms*

*Streptococcus* [5]*.*

**8.3 Otitis media**

for combating otitis media [5].

**8.5 Cystic fibrosis**

**8.4 Chronic bacterial prostatitis**

terminate the effect of *Candida endocarditis* [5].

adhered to it and as a result nonbacterial endocarditis (NBTE) develops at the site of injury and thrombus (accumulation of platelets, fibrin, and red blood cells) formed [13]. Fibronectin which has been found as a thrombotic lesion of the heart valve can simultaneously bind to fibrin, collagen, human cell and bacteria. Fibronectin receptors are found in many bacterial species like *Staphylococcus and* 

Many antibiotic therapies are suggested depending on the organisms involved as Penicillin is recommended for normal treatment of *Streptococcal endocarditis* and for synergistic killing gentamycin may be supplemented. Fluconazole can successfully

It is a condition of chronic ear infection caused due to inflammation of mucoperiosteal lining [5]. In the middle ear cavity, fluid gets accumulated which ultimately affects speech development and learning capability of the patient. However, its complete etiology is still under research [7]. Various organisms responsible for otitis media include *S. pneumoniae, H. influenzae, Moraxella catarrhalis, S. epidermidis, P. aeruginosa,* etc. As due to limited penetration of antibiotic, its low concentration is present in middle ear fluid, hence strong antibiotics like amoxicillin, cefaclor, erythromycin, and clarithromycin are needed

Prostatitis is the inflammation of the prostate gland which possibly occurs due to the microorganisms that have ascended from the urethra or by the reflux of infected urine into prostatic ducts which vacates into the posterior urethra. Once the microbe gets entered in the prostatic duct, they start multiplying rapidly and can form sporadic micro-colonies and biofilms which gets adhered to the epithelial cells of the system of ducts. Microbes responsible for this infection are *E. coli,* 

Cystic Fibrosis is a chronic bacterial infection of intrapulmonary airways with *P. aeruginosa* [19]. Its consequences include thickening of mucus in many body systems which results in impaired mucociliary clearance of microorganisms and chronic infection in lungs. The infection gets punctuated by acute aggravation of disease and inflammation which will lead to lung failure and premature death [20]. According to the genetic etiology, one out of more than 1500 potential mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene results in its malfunction, as a result sodium absorption is inhibited through epithelial sodium channel. And due to hyper-absorption of water, airway surface liquid gets depleted, mucociliary clearance get depleted and inhaled bacteria are allowed to remain within airway [20, 21].

Microscopic studies of sputum samples and lung tissue section have shown the presence of biofilm or micro-colonies in the airways. These biofilms are able to grow larger than 100 μm in diameter [22]. Some common cystic fibrosis pathogens include *S. aureus, H. influenzae* and ultimately predominant one *P. aeruginosa* [20, 21]. *P. aeruginosa* has some adaptive mechanisms which make it survive and persist for several decades in CF patient's respiratory tract. Biofilm adaptation of *P. aeruginosa* makes it resistant to antibiotic therapy and inflammatory defense

*P. aeruginosa*, species of *Klebsiella*, *Proteus, Serratia*, *Bacteroides,* etc. [5].

**158**

Periodontitis is the infection of supporting tissues of teeth, gums (gingiva) and periodontal tissues (gingiva, alveolar bone, and periodontal ligament). Its chronic form may lead to exfoliation of teeth. The primary site of periodontitis is sub gingival crevice which is the channel between the tooth root and the gum. Organisms responsible for this infection are *Fusobacterium nucleatum*, *Peptostreptococcus micros*, *Eubacterium timidum*, *E. brachy*, *Pseudomonas anerobicus,* and predominate one *P. gingivalis.* They can easily colonize the surface of the oral cavity which helps them in invading mucosal cells, altering calcium flux in epithelial cells and in releasing toxins. As a result, plaque (a climax biofilm community) is formed within 2–3 weeks. Calculus or tartar is the mineralized plaque which acts as a resistance against the antimicrobial activity of saliva in protecting tooth enamel, as a consequence of which dental carries and periodontal diseases occurs [5].

Dental plaque or biofilm cannot be eliminated, only their pathogenic nature can be minimized by minimizing the bioburden and effectively maintain a normal oral flora via oral hygiene methods [6, 23].

### **8.7 Osteomyelitis**

Osteomyelitis is an inflammatory bone disorder characterized by infection in bone/bone marrow which leads to necrosis and bone destruction [24, 25]. When complex multi-resistant biofilm has established, treatment of osteomyelitis becomes more challenging. Due to increased bacterial resistance to antibiotics in biofilm mode, they cause persistent infections. It has been found that in more than 50% osteomyelitis cases, causative organisms are *S. aureus* and *S. epidermidis* [24].

Although, endoprostheses which are found to be an increasingly common source of infection, surgically implanted devices or other implants like orthopedic internal fixation devices also represents a remarkable risk factor for the development of osteomyelitis. Stainless steel, titanium, titanium alloys are most commonly used materials in implants in which stainless steel is found to be associated with greater infection rate as compared to titanium. A possible reason of this is might be that soft tissues get firmly adhered to a titanium-implant surface while a fibrous capsule is formed enclosing a liquid filled space around the steel implants. This unvascularized space is less accessible to host defense mechanisms where bacteria can multiply and freely spread. Studies showed that *S. aureus* and *S. epidermidis* adhesion to the surface can be reduced by the use of coatings based on human proteins such as albumin or human serum. Coatings of poly(1-lysine)-grafted-poly(ethylene glycol) (PLL-g-PEG) when extensively studied for use in biomedical applications, it has been found to be highly effective in reducing the absorption of blood serum, blood plasma and single proteins like fibrinogen and albumin. Fibroblast and osteoblast cell adhesion get remarkably reduced by spreading of metal oxide surface coated with PLL-g-PEG in comparison to uncoated surfaces [25].

*Bacterial Biofilms*
