Phenol-Soluble Modelins In Synovial Flu-Sb Case Study

“Bacterial illness is a result of complex interactions between bacteria and the host. During evolution, humans developed many ways to protect themselves against bacterial pathogens. On the other hand, bacteria have developed strategies to evade, subvert or circumvent these defenses” (Sousa, 2003) “One of the most important characteristics of bacterial pathogenicity is the various strategies developed by prokaryotic organisms to use host molecules for their own benefit” (Sousa, 2003). “To accomplish this, bacteria have evolved elaborate control mechanisms to turn genes on and off, varying the transcriptional activator or

Biofilms play a crucial role in the persistence of lung infections in CF patients due to the protective extracellular matrix that is formed by the bacterial community (5). This barrier limits the penetration of antibiotics and results in varying nutrient gradients, allowing for a diverse range of bacteria (5). Bacteria inside this biofilm are able to sense the presence of other cells, and alter their properties accordingly to suit the environment. This is particularly interesting as the bacterial communities within a biofilm may compete with each other for dominance in the biofilm (6). Therefore, bacterial competition may impact the treatment and actions needed to treat biofilms in the lungs of CF patients

The effectiveness of disease treatment is often presented by the challenge of antimicrobial resistance. Cystic Fibrosis (CF) for example, is a pulmonary infection characterized by the poly-microbial growth of bacteria within biofilms, in the pulmonary tract of humans. For children suffering from CF, Staphylococcus aureus (S. aureus) initially colonizes their airways, which with age, becomes replaced by Pseudomonas Aeruginosa (P. aeruginosa). The eradication of P. aeruginosa by antibiotics fails in 10-40% of CF patients. In the article, it was proven that there existed an interaction between the staphylococcal protein A (SpA) from S. aureus filtrates (SaF, a bacterial supernatant of S. aureus), and an exopolysaccharide (Psl) of P. aeruginosa. This interaction lead to the aggregation and increased resistance to tobramycin¬ – an antibiotic used to eradicate P. aeruginosa, to prevent chronic colonization of the bacteria. The study conducted involved 7 samples of P. aeruginosa that were taken from individuals who underwent successful eradication treatment, and 7 samples from individuals who still had persistent isolates. These P. aeruginosa samples were cultured for 24 hours in media. When SaF was added to the overnight preformed biofilms, the eradicated isolates were not affected by the SaF; however, the persistent isolates showed significant reduction is surface coverage due to densely packed cellular aggregation, without affecting the biomass or viability of persistent isolates. The

The most common pathogenic strains that cause wound infection is Staphylococcus aureus (35%), Escherichia coli (15%), Pseudomonas aeruginosa (13%) and other bacteria (37%) (Amit Kumar Gupta et al., 2015). In another study, Staphylococcus aureus has been reported as the major cause of wound infection with (24.2%), followed by Pseudomonas aeruginosa (21.4 %), Escherichia coli (14.8 %) and another different organism (39.6 %) (Jyoti Sangwan et al., 2016). Staphylococcus aureus (Methicillin Resistant Staphylococcus aureus) is gram positive bacteria and can be a lethally opportunistic pathogen or human commensal, it is one of the leading organisms causing a variety of hospital-acquired infection and community acquired infection (Brown et al., 2014). S. aureus has

Microorganisms that are cultured from the wounds have two types that exist. Type 1 necrotizing fasciitis is a polymicrobial infection which consist of infection with aerobic and anaerobic bacteria. Which consists of clostridium and bacteroides species, these work synergistically in the progression of necrotizing fasciitis. Type 2 necrotizing fasciitis consists of group A streptococcus and with or without a coexisting staphylococcal infection. The Type 2 also consists of staphylococcus aureus, clostridium perfringens, bacteroides fragilis, and aeromonas hydrophila. The microscopic level would include the laboratory of necrotizing fasciitis the bacteria that is seen with a microscope. “The micrograph of necrotizing fasciitis shows necrosis of the dense connective tissues and fascia interposed between fat lobules”. The gross anatomy is the structures visible to the naked eye, such as the

Thus we sought to determine whether those bacteria that produced coaggregation were associated with cohesion in contact lens case biofilm formation. Cohesion can also occur when a pioneer species modifies the substratum to encourage adhesion of successor species. As, Staphylococcus spp are the most commonly isolated from the lens cases, could be considered as pioneer species, but 10% of the lens cases also showed the contamination of Gram negative bacteria. Based on recent in vivo data we found Staphylococcus spp often isolated with Acinetobacter spp. There is other literature which also showed the isolation of P. aeruginosa and S. marcescens from lens cases. The present study showed cohesion between Staphylococcus spp and Acinetobacter spp/ Micrococcus spp, where Staphylococcus spp can be considered as pioneer species and Acinetobacter and Micrococcus as successor. Whist this study did not investigate the facilitating factor for the cohesion, will be worth to consider in future study. The next step will be to see whether the elimination of Micrococcus and Acinetobacter contamination from lens cases will reduce the adhesion of Staphylococcus spp which may reduce the overall rate of contact lens case

It is very difficult to treat bacterial biofilm infection. Antibiotic treatment by itself is not enough to destroy biofilm infections adequately. Overall, the approaches to combat biofilms can be categorized into two groups depending if the infection involves a foreign body or not. If the biofilm infection does not involving a foreign body (such as indwelling implants), continuing treatment using high doses of combination of several antibiotics with different mode of action toward the bacteria is used to combat the infection. On the other hand, if a foreign body is involved in the biofilm infection, extraction of the implant is needed for positive result. In some cases, only physical reduction of the biofilm is possible (using mechanical methods)

In the United States, the fourth most leading cause of death are hospital-acquired infections. Furthermore, it is estimated that greater than 65 percent of all bacterial infections are associated with biofilms. A greater understanding of biofilms is essential if we are to find effective methods to combat their formation in order to promote public health. Unfortunately, with bacteria in space behaving widely different than on Earth, this can cause a huge problem when it comes to health in space. First of all, biofilms could contaminate and bio-deteriorate the space habitats, the health of the crew, and the function of waste recycling or food production systems in extremely different ways then handled before on Earth. All of these issues would

Most common among them are extracellular polymeric, biofilms production by bacteria that may lead to multidrug resistance in pathogens. The Biofilms formation in foot ulcer leads to ineffective penetration of antibiotics due to render of leukocytes into the ulcers by developing antiphagocytic properties inside the biofilm matrix. The matrices formed by bacteria in the biofilms can facilitate altered gene expression, intercellular communication and horizontal gene transfer. Furthermore, peripheral arterial diseases are often present in patients with foot ulcers infection and may lead to poor penetration of antibiotics into the lower limb tissues, thereby promoting selection of resistant bacteria strains. More than 90% strains in Acinetobacter baumannii were resistant to all beta-lactams, fluoroquinolones, aminoglycosides antibiotics [11]. Alternatively, treatment to heal foot ulcer antibiotic were colistin, polymyxin B, tigecycline [12]. Therefore, the present investigation was done in order to study the prevalence, and antibiotic resistance pattern and biofilm formation of Acinetobacter baumannii strains in Diabetic and non-diabetic foot ulcer

Biofilms are a major concern to the public health since they can be highly resistant to antimicrobial agents. They provide a basis for chronic infections such as cystic fibrosis. The bacteria responsible for chronic lung infection in cystic fibrosis patients is Pseuomonas Aeruginosa (P.Aeruginosa) and is the most commonly studied biofilm infection (Høiby, 2017). This causes a major health problem that occurs when a thick mucus causes obstruction of the airway as the aggregation of cells are colonized. As the biofilm infection progresses, this can lead to damage of the lung tissue causing respiratory problems. Since biofilms are associated with opportunistic infections such as P.Aeruginosa, they can be harder to treat due to their tolerance

T6SS is believed to resemble the tail of a bacteriophage. TssJ, TssL and TssM proteins combine to form a complex which anchors it to the cell membrane, stretching from outer to inner membrane. A baseplate, created by TssA, E, F, G and K resides within the inner membrane. VgrG resides within the baseplate and supports the tube of Hcp hexamers extending into the cytoplasm. TssB and TssC combine to form a sheath-like structure supporting the Hcp hexamer tube. Their interlacing construction provides strength to the barrel during contraction and effector release. At the tip PAAR and VgrG combine to create the “spike” at the end of the tube, which serves to puncture the membrane of the target cell, so that the effector proteins can be delivered. PAAR repeat containing proteins have been found to play an important role in the formation of the puncturing structure at the top of the tube, as their omission in certain bacteria result in loss of virulence. Once the effector proteins have been successfully delivered to the target cell, ClpV attaches to TssC to promote disassembly of the TssBC sheath. A specific defensive strategy, termed ‘Tit for tat’ has been described in Pseudomonas aeruginosa. This is made possible by TPP (threonine phosphorylation pathway) accessory proteins during cell to cell connection. PpkA and PppA act upon Fha1. Accessory proteins TagQ, R, S and T lead to a change in conformation and a firing event. All accessory proteins are necessary for activation. This strategy is activated in response to aggression from another cell. Not all P. aeruginosa organisms contain the necessary components for this defense

Biofilms are hard to treat for many reasons. The main reason is because they are highly resistant to antibiotics. This is because the outer cells protect the inner cells from the antibiotic. Therefore, a long-term treatment of antibiotics is required to help the biofilm related infection. Living in groups, give bacteria properties they didn't have when living alone. Another reason they're hard to treat is because they are undefeatable by the body's natural immune defense system. Biofilms avoid chemical disinfection in two different ways. The first is that a gel-like polysaccharide layer provides a physical barrier against any outside agent, biological or chemical. The second is that even if a biocidal agent is introduced in a large enough quantity to eliminate the living bacteria, then

Virulence Factors: The most important virulence factor of S. aureus is the specific surface proteins that allow the organism to attach to host proteins. The surface proteins of this bacterium allow it to attach to host proteins such as laminin and fibronectin, which form the extracellular matrix of epithelial and endothelial cells. S. aureus also produces a number of membrane damaging toxins that allow the organism to further invade and harm the host, of which the alpha- toxin is the most well studied and is the protein responsible for septic shock. The alpha- toxin is a protein that binds to a specific receptor in platelets and monocytes in humans, forming pores that eventually destroy the cell.

Treatment of the disease is currently based on antimicrobial susceptibility tests according to Clinical and Laboratory Standards Institute (CLSI) [5]. Standard therapy designed for bacteria isolates at planktonic state continues to be applied. However, the pathogenic profile and the antimicrobial resistance are totally different from biofilms, causing reduced cure rates. Furthermore, the ability to form biofilm is important both from the pathogenicity to the animal as for the manufacturing milk industries, where the pathogen can adhere to abiotic food processing structures and persist in adverse conditions through biofilms. The development and establishment of the biofilm depend on the ability of pathogen to adhere to bovine mammary epithelial cells. S. dysgalactiae have many virulence factors including the capacity to bind to the host's cells surface by a protein called GFBA, which is involved in adherence and internalization, by its linking to lactoferrin [6]. It was demonstrated that the S. dysgalactiae isolated from mastitis cows was able to produce biofilm [7]. Economic negative effects in the milk production around the world and the possible involvement of biofilms in S. dysgalactiae mastitis infections, address the research to the study of factors that may contribute for the biofilm production in order to establish more effective treatment strategies. Different studies report that environmental conditions influence the capacity to form biofilm in

Every wound poses a risk for infection and since chronic wounds have a delayed wound healing response already, the risk for bacterial growth is much higher in these wounds. If microorganisms continue to multiple, and proliferate within the wound bed, critical colonization and infection can occur (3). Therefore, it is important for clinicians to be able recognize and distinguish between critical colonization and deep surrounding infection to guide them with an appropriate treatment plan.