How does bacteria enter bloodstream




















Now, researchers have discovered that an additional mouth microbe, Streptococcus gordonni, can damage your health in a different way. Studies have shown that bacteria within your mouth can escape into your bloodstream and cause trouble. Understanding this phenomena and its link to systemic diseases may facilitate an effective treatment for such diseases.

If allowed into the bloodstream, this microbe is able to produce a molecule on its surface that mimics fibrinogen, a human protein that is also a blood-clotting factor. These clots can cause formations on the heart valve endocarditis , as well as block blood flow to vital organs. Malicious bacteria in your mouth begin attacking your oral health almost immediately. By brushing and flossing your teeth at least twice a day, you are able to remove bacteria before it can accumulate enough to effectively attack.

At Modern Dentistry, Todd A. To schedule your next appointment, contact our office by calling today. Your Name required.

Your Email required. Home Phone Number required. Enter the letters in the box below:. Voted Best Dental Office By:. Schedule Your Appointment. The Deceptive Mouth Germ Studies have shown that bacteria within your mouth can escape into your bloodstream and cause trouble.

People with chronic diseases are at a higher risk of sepsis. One complication of septicemia is a serious drop in blood pressure. This is called septic shock.

Toxins released by the bacteria in the bloodstream can cause extremely low blood flow, which may result in organ or tissue damage. Septic shock is a medical emergency. A third complication of septicemia is acute respiratory distress syndrome ARDS. This is a life-threatening condition that prevents enough oxygen from reaching your lungs and blood. It often results in some level of permanent lung damage.

It can also damage your brain, leading to memory problems. Diagnosing septicemia and sepsis are some of the biggest challenges facing doctors.

It can be difficult to find the exact cause of the infection. Diagnosis will usually involve a wide range of tests. Your doctor will evaluate your symptoms and ask your medical history. The doctor may also look for signs of conditions that more commonly occur along with septicemia, including:. Your doctor may want to perform tests on multiple types of fluids to help confirm a bacterial infection.

These may include the following:. Your doctor may check your cell and platelet counts and also order tests to analyze your blood clotting. Your doctor may also look at the oxygen and carbon dioxide levels in your blood if septicemia is causing you to have breathing issues. Septicemia that has started to affect your organs or tissue function is a medical emergency.

It must be treated at a hospital. Many people with septicemia are admitted for treatment and recovery. These are designed to work against a wide range of bacteria at once. A more focused antibiotic may be used if the specific bacteria is identified. You may get fluids and other medications intravenously to maintain your blood pressure or to prevent blood clots from forming. You may also get oxygen through a mask or ventilator if you experience breathing issues as a result of septicemia.

Bacterial infections are the underlying cause of septicemia. See a doctor right away if you think you have this condition. If your infection can be effectively treated with antibiotics in the early stages, you may be able to prevent the bacteria from entering your bloodstream. Parents can help protect children from septicemia by ensuring they stay up to date with their vaccinations.

If you already have a compromised immune system, the following precautions can help prevent septicemia:. When diagnosed very early, septicemia can be treated effectively with antibiotics. Research efforts are focused on finding out better ways to diagnose the condition earlier. This is especially true for people with preexisting conditions that affect their immune systems.

There have been many medical developments in diagnosis, treatment, monitoring, and training for septicemia. This has helped reduce mortality rates. It includes the use of bacteriophage, Bdellovibrio like organisms and Saccharomyces therapy.

The use of bacteriophages as a replacement for antibiotics in sepsis is an attractive option. Bacteriophages may be useful in the treatment of sepsis caused by antibiotic resistant bacterial infections. They have some advantages over antibiotics being more effective in treating certain infections in humans [ — ]. Phage therapy is safe and can be given intravenously in systemic infections.

Bacterial isolates from septicemia patients spontaneously secrete phages active against other isolates of the same bacterial strain, but not to the strain causing the disease [ ]. Such phages were also detected in the initial blood cultures, indicating that phages are circulating in the blood at the onset of sepsis.

The fact that most of the septicemic bacterial isolates carry functional prophages suggests an active role of phages in bacterial infections [ ]. Prophages present in sepsis-causing bacterial clones play a role in clonal selection during bacterial invasion [ ]. The major problem of bacteriophage usage is their exquisite specificity; bacteriophages are much more specific than antibiotics. They attack only specific for them strains of bacteria, thereby precluding their use as empiric therapy in sepsis.

Phage therapy is possible after identification of sepsis causing bacterium and selection of appropriate phage from existing stocks. Stocking a hospital laboratory with a complete library of phage for every conceivable bacterial pathogen is a major challenge [ ]. Bdellovibrio and like organisms prey on other bacteria. They can be used as medical microbiological settings [ , ]. Bdellovibrio bacteriovorus attacks a wide range of pathogens: Escherichia coli , Salmonella enteric , Pseudomonas aeruginosa , S.

It invades and grows within the periplasm. Bdellovibrio bacteriovorus is highly motile, flagellated, Gram-negative and measures 0. It uses a single polar flagellum to stalk other bacteria; it burrows through the surface of its prey by secreting enzymes and consumes its host from the inside out [ , ].

Bdellovibrio bacteriovorus has dual probiotic and antibiotic nature [ , ] and it is perspective to try it in the therapy of sepsis. Saccharomyces boulardii SB is a non-pathogenic yeast used in the prevention or the treatment of diarrheas [ , ]. SB directly inhibits the growth of Candida albicans , E. SB exerts direct anti-toxin effects and inhibits the growth of pathogens.

SB also produces a phosphatase that dephosphorylates endotoxins such as lipopolysaccharide of E. SB maintains epithelial barrier integrity during bacterial infection [ ]. SB affects the immune response of host cells and stimulates the secretion of secretory immunoglobulin A [ ]. Probably, the antimicrobial and antifungal products, produced by SB may be studied as a possible therapeutic option in sepsis.

Bacteria removal from the bloodstream by technical devices has a good perspective: it is effective in case of all bacterial species and does not need bacteria identification before the procedure. Plaktonic bacteria and biofilm fragments may be easily removed from the bloodstream whereas encapsulated bacteria, pathogens inside erythrocytes and bacterial L-forms may escape removal.

The technical devices should be used as soon as sepsis is suspected and it should be done before empiric use of antibiotics because the latter may cause bacterial encapsulation and formation of L-forms. On the other hand, the devices provide removal and accumulation of removed bacteria in devices facilitating precise identification of pathogens. Bacteria were removed by matrix of micro-encapsulated albumin activated charcoal ACAC. The bacteria adhered to the ACAC, but the charcoal was not bactericidal.

It includes hollow fiber that removes lipopolysaccharides LPS and lipoteichoic acids LTA from blood or plasma in an extracorporeal perfusion system. Some years ago, for bacteria and endotoxin removing from the blood magnetic nanoparticles MNPs modified with bis-Zn-DPA, a synthetic ligand that binds to bacteria, was used [ ].

Recently an external device that mimics the structure of a spleen and cleanses the blood in acute sepsis has been tested [ ]. In this device the blood is mixed with magnetic nanobeads coated with an engineered human opsonin—mannose-binding lectin MBL. Magnets pull the opsonin-bound pathogens and toxins from the blood then the cleansed blood is returned back to the individual.

Mechanical devices can remove from the bloodstream not only bacteria, but also toxins and cytokines. For example, a mechanical devices has been developed to remove a variety of cytokines, lipopolysaccharide, or C5a from plasma [ ]. A cytokine adsorption device CAD filled with porous polymer beads efficiently depletes middle-molecular weight cytokines from a circulating solution [ ]. At present mechanical removal of pathogens and their toxins from the bloodstream by mechanical devices is the most promising clinical application that rapidly may be seen in the near future.

It is most effective in case of planktonic bacteria and less effective in the removing of encapsulated bacteria and bacterial L-forms. Antimicrobial actions needed for increasing the effectiveness of antibacterial therapy in sepsis are summarized in Table 3. In sepsis planktonic bacteria cause abundant release of oxygen from erythrocytes [ 22 , 23 ]. Oxygen oxidizes and inactivates plasma hormones and other biologically active substances. As a result, a severe endocrine dysregulation occurs in septic patients and so the replacement of hormones, peptides and other active substances in sepsis is indispensable.

Corticosteroids were the first drugs tested in randomized controlled trials [ — ], then catecholamines, anti-diuretic hormone, thyroxin, insulin, adrenocorticotropin, growth hormone, estrogens, androgens, etc. The results of separate and combined use of hormones are controversial and the positive effect is not convincing. Hormonal replacement therapy protocol should include simultaneous use of a combination of hormones that takes into account their synergism and antagonism, anabolic and catabolic properties, half-life, resistance to oxidation, pharmacokinetics, pharmacodynamics, etc.

The profile and proportions of most important hormones and regulatory substances for support of vital functions should be established and the replacement of all indispensable hormonal and other regulatory components should be performed. Injected components may be oxidized and inactivated so constant control of their concentrations is necessary. Central venous catheters CVC are an integral part in medical management of sepsis, particularly, they are indispensable for antibiotic therapy.

In sepsis catheters can be placed in veins in the neck internal jugular vein , chest subclavian vein or axillary vein , groin femoral vein , or through veins in the arms a PICC line, or peripherally inserted central catheters. Three anatomical sites the subclavian, jugular, or femoral vein are commonly used to insert central venous catheters, but insertion at each site has the potential for major complications.

Subclavian-vein catheterization is associated with a lower risk of bloodstream infection and symptomatic thrombosis and a higher risk of pneumothorax than jugular-vein or femoral-vein catheterization [ ].

Subclavian and internal jugular CVC have similar risks for catheter-related complications in long-term catheterization. Subclavian CVC is preferable to femoral CVC in short-term catheterization because of lower risks of catheter colonization and thrombotic complications. In short-term catheterization, femoral and internal jugular CVA routes have similar risks for catheter-related complications; internal jugular CVA routes are associated with higher risks of mechanical complications [ ].

In sepsis pathogens circulate in the bloodstream. Catheters themselves can introduce bacteria into the bloodstream. Catheter-related bloodstream infections CRBSIs may deteriorate the condition of patients with sepsis. Although earlier studies showed a lower risk of catheter-related bloodstream infections when the internal jugular was compared to the femoral site, recent studies show no difference in the rate of catheter-related bloodstream infections between the sites [ ].

If a central line infection is suspected in a person, blood cultures are taken from both the catheter and a vein elsewhere in the body. Quantative blood culture is more accurate, but it is not widely available [ ]. To prevent infection, stringent cleaning of the catheter insertion site is advised. Povidone-iodine solution is often used for such cleaning, but chlorhexidine is twice as effective as iodine [ ].

Routine replacement of lines makes no difference in preventing infection [ ]. Recommendations regarding risk reduction for infection of CVCs, include antibiotic lock therapy - a method for sterilizing the catheter lumen that involves instilling high concentrations of antibiotics into the catheter lumen for extended periods of time.

Results from in vitro studies demonstrate stability of antibiotics while maintaining high concentrations for prolonged periods of time. In vivo studies show antibiotic lock technique as an effective and safe option for both prevention and treatment of CRBSIs [ ].

Recently, non-antibiotic antimicrobial catheter lock solutions also are used [ ]. Sepsis starts when infection enters the bloodstream and overcomes the host mechanisms of blood clearing from bacteria.

The most common primary sites of infection include the lungs, urinary tract, abdominal organs, and pelvis. Early source identification is important if sepsis is to be treated adequately.

Before giving antibiotics, blood cultures should be taken. Blood culture provides information regarding the infection and bacteria sensitivity to antibiotics. Revealing the source of infection is necessary for targeting of antibiotics. The primary site of infection may be the source of constant bacteremia during the course of sepsis. The blood culture may help to choose appropriate antibiotics and de-escalate from broad spectrum to narrow spectrum antimicrobials.

Although blood cultures are the gold standard in identifying infections, other interventions may be also needed. Current guidelines recommend starting antibiotic therapy in sepsis as early as possible and within one hour of identification of septic shock [ 7 ]. Updated versions were published in [ ], [ 11 ] and most recently in [ ] and [ ]. Applying the sepsis bundle simplifies the complex processes of the care of patients with sepsis.

Updates to clinical management guidelines precede the updates to the sepsis bundles. The Hour-1 bundle should be viewed as a quality improvement opportunity moving toward an ideal state. For critically ill patients with sepsis or septic shock, time is of the essence. Although the starting time for the Hour-1 bundle is recognition of sepsis, both sepsis and septic shock should be viewed as medical emergencies requiring rapid diagnosis and immediate intervention [ ]. The Hour-1 bundle encourages clinicians to act as quickly as possible to obtain blood cultures, administer broad spectrum antibiotics, start appropriate fluid resuscitation, measure lactate, and begin vasopressors if clinically indicated.

Ideally these interventions would all begin in the first hour from sepsis recognition but may not necessarily be completed in the first hour. Minimizing the time to treatment acknowledges the urgency that exists for patients with sepsis and septic shock. It is understood that the interventions may not be completed within the hour. The guidelines recommend administering empiric broad-spectrum antimicrobials that cover all likely pathogens [ ].

The initial empiric antibiotic regimen for patients in septic shock should include at least two antibiotics from different classes combination therapy directed toward the most likely pathogens. Treatment should be narrowed once the pathogen and its antimicrobial sensitivities are ascertained or when the patient demonstrates clinical improvement. With respect to antibiotic duration, combination therapy in patients with septic shock should be de-escalated to monotherapy within a few days if clinical improvement or with evidence of infection resolution [ ].

Bacteria cause sepsis being in different forms: planktonic, encapsulated, L-form and biofilm fragments.

Antibacterial therapy is most effective when infection is in the tissues. If infection enters the bloodstream and starts to occupy erythrocytes, the effectiveness of antibacterial therapy dramatically decreases.

So the most effective approach to sepsis treatment is prevention of bacteremia. Sublethal effect of antibacterial drugs in the tissues may provoke bacterial encapsulation, biofilm growth, switching to L-form. Early detection of infection in the tissues and selection of appropriate antibacterial medication in adequate doses is of great importance. Inhibition of the production of bacterial antioxidant enzymes catalase, superoxide dismutase, glutathione peroxidase may increase the effectiveness of phagocytosis in the tissues and oxycytosis in the bloodstream.

Inactivation of bacterial hemolysins may prevent bacterial penetration through erythrocyte membranes and forming of infection reservoir inside erythrocytes. Acceleration of bacterial respiration may increase the effectiveness of bactericidal drugs. Dispersion of bacterial exopolymers is indispensible in antibacterial therapy of infection caused by encapsulated bacteria and biofilm. Inhibition, inactivation or binding of bacterial LPS and SAgs is necessary for preventing of host intoxication and decreasing of infection virulence.

Sepsis therapy should include the use of antibacterial medications, modulation of bacterial respiration, inhibition of bacterial antioxidant enzymes and hemolysins, neutralization of exo- and endotoxins, dispersion of bacterial capsule and biofilm, increasing of host tolerance to bacterial products, facilitation of host bactericidal mechanisms, support of host vital functions and restore of homeostasis.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. National Center for Biotechnology Information , U. Published online Feb Hayk Minasyan. Author information Article notes Copyright and License information Disclaimer. Yerevan, Armenia. Corresponding author. Received Oct 24; Accepted Feb 1.

This article has been cited by other articles in PMC. Associated Data Data Availability Statement Data sharing not applicable to this article as no datasets were generated or analyzed during the current study. Abstract In bacteremia the majority of bacterial species are killed by oxidation on the surface of erythrocytes and digested by local phagocytes in the liver and the spleen.

Human innate immunity in sepsis The pathogenesis of the sepsis syndrome is dependent on activation of the innate immune response. The mechanisms of bacterial survival in the tissues and the effectiveness of antibacterials Host tissues are a hostile environment for bacterial pathogens. Capsule production Capsular polysaccharide CPS plays important biological role in nutrient uptake [ 26 ], protection against environmental stresses [ 27 ], biofilm formation [ 28 ], survival against phagocytosis or antibiotics; it is also an important virulence factor [ 29 , 30 ].

Switching into the L-form The majority of antibacterials, particularly, bactericidal antibiotics, kill bacteria by inhibiting the growth of bacterial wall. Biofilm formation The formation of biofilm is an adaptation of microbes to hostile environments [ 44 ].

Planktonic bacteria in the tissues Bacterial cell exhibit two types of growth mode: planktonic cell and sessile aggregate which is known as the biofilm. Bacteria in the bloodstream Bacteria may circulate in the bloodstream as planktonic free-floating and inside erythrocytes bacteria, encapsulated bacteria, biofilm fragments and L-form free-floating and inside leukocytes.

Planktonic bacteria in the bloodstream Planktonic bacteria usually enter the bloodstream from the tissues. Table 1 Microbiological features of sepsis causing bacteria that cause problems to host defense. Open in a separate window.

Encapsulated bacteria in the bloodstream Bacterial capsule provides physical, chemical and immunologic shielding of bacteria [ 64 ]. Biofilm fragments in the bloodstream Biofilm is the natural mode of bacterial growth in nature [ 46 ].

L-form bacteria in the bloodstream L-form bacteria enter the bloodstream from the tissues after surviving treatment by wall-targeting antibacterials. The effectiveness of antibacterials in the bloodstream In sepsis the effectiveness of antibacterials in the bloodstream is limited by different factors.

Table 2 bacterial forms of sepsis-causing bacteria, types of sepsis and the optimal strategies of antibacterial treatment. Different types of sepsis When an infection surpasses local tissue containment, bacteria enter the bloodstream and cause bacteremia. The problems of antibacterial therapy in sepsis Bacterial toxins The mechanisms by which bacteria cause sepsis and septic shock involve bacterial factors cell wall, secreted products and host factors susceptibility, primary immune response, secondary tissue response, etc.

Bacterial antioxidant enzymes, hemolysins and respiration Oxycytosis is the main mechanism of planktonic bacteria clearing from the bloodstream [ 22 ]. Bacterial exopolymers Encapsulated bacteria and biofilm fragments survive in the tissues and the bloodstream because of exopolymers [ 23 ]. Overcoming the problems of antibacterial therapy in sepsis Development of new antimicrobials Search for new antibacterials, in particular, new antibiotics, is indispensable.

Early detection of pathogens Early detection of pathogens and their sensitivity to bactericidal medications remain indispensable. Managing intoxication caused by exotoxins A variety of gram-positive organisms are capable of causing sepsis. Affecting bacterial capsule Planktonic bacteria grow and proliferate because their thin capsule does not interfere respiration and metabolic exchange.

Inhibition and neutralization of hemolysins Iron is an essential nutrient for nearly all known life forms. Inhibition of antioxidant enzymes Antioxidant enzymes of sepsis-causing bacteria provide bacterial survival during phagocytosis in the tissues and oxycytosis oxidation on the surface and inside erythrocytes in the bloodstream.

Inhibition of catalase production Inhibition of bacterial catalase production increases the effectiveness of bacteria killing by phagocytes and erythrocytes.

Inhibition of superoxide dismutase production The manganese and zinc binding protein calprotectin CP reduces bacterial superoxide dismutase activity resulting in increased sensitivity of pathogens to oxidative stress. Inhibition of glutathione peroxidase production Glutathione peroxidase makes an important contribution to bacterial virulence [ — ]. Modulation of respiration Sepsis-causing bacteria have flexible respiration.

Bacteria killing by non-antibiotic agents Bacterial resistance to carbapenems [ ] and colistin [ ] indicate that the post-antibiotic era has arrived and common infections will not be treatable with the current arsenal of antibiotics. Bacteriophage therapy The use of bacteriophages as a replacement for antibiotics in sepsis is an attractive option.

Therapy by Bdellovibrio like organisms Bdellovibrio and like organisms prey on other bacteria. Saccharomyces therapy Saccharomyces boulardii SB is a non-pathogenic yeast used in the prevention or the treatment of diarrheas [ , ]. Bacteria clearing from the bloodstream by technical devices Bacteria removal from the bloodstream by technical devices has a good perspective: it is effective in case of all bacterial species and does not need bacteria identification before the procedure.

Table 3 Antimicrobial actions needed for increasing of sepsis therapy effectiveness. Antimicrobials Needed actions and available agents and technologies New antibiotics Should be able to: a. Exotoxin neutralizing compounds Should be able to: a. Endotoxin neutralizing compounds Should be able to: a.

Bacterial capsule affecting agents Should be able to: inhibit tyrosine phosphatase PTP and a protein tyrosine kinase available agent: Fascioquinol E.

Bacterial biofilm affecting agents Should be able to: a. Agents that inhibit and neutralize hemolysins Should be able to: a. Agents that inhibie antioxidantenzymes Should be able to: a. Non-antimicrobial solutions for managing sepsis In sepsis planktonic bacteria cause abundant release of oxygen from erythrocytes [ 22 , 23 ]. Optimal route and timing of antibiotic administration in sepsis Central venous catheters CVC are an integral part in medical management of sepsis, particularly, they are indispensable for antibiotic therapy.

Table 4 Surviving sepsis campaign hour-1 bundle of care elements. Conclusion Bacteria cause sepsis being in different forms: planktonic, encapsulated, L-form and biofilm fragments. Acknowledgements Not applicable. Funding No funding. Availability of data and materials Data sharing not applicable to this article as no datasets were generated or analyzed during the current study. Notes Ethics approval and consent to participate Not applicable. Consent for publication Not applicable.

Competing interests The author declares that he has no competing interests. References 1. WHA adopts resolution on sepsis.

Global dissemination of Carbapenemase-producing Klebsiella pneumoniae: epidemiology, genetic context, treatment options, and detection methods. Front Microbiol. Li XZ, Nikaido H. Efflux-mediated drug resistance in Bacteria: an update. Inhibition of mutation and combating the evolution of antibiotic resistance. PLoS Biol.

The worldwide emergence of plasmid-mediated quinolone resistance. Lancet Infect Dis. Assessment of global incidence and mortality of hospital-treated sepsis: current estimates and limitations.

N Engl J Med. Surviving sepsis: campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. Assessment of the worldwide burden of critical illness: the intensive care over nations ICON audit. Lancet Respir Med. Opal SM. The evolution of the understanding of Sepsis, infection, and the host response: A brief history. Crit Care Clin.

Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: Soong J, Soni N. Sepsis: recognition and treatment. Clin Med.

Siddiqui S, Razzak J. Early versus late pre-intensive care unit admission broad spectrum antibiotics for severe sepsis in adults. Cochrane Database Syst Rev. Overview of antimicrobial therapy in intensive care units. Expert Rev Anti-Infect Ther. Mortality and morbidity attributable to inadequate empirical antimicrobial therapy in patients admitted to the ICU with sepsis: a matched cohort study.

J Antimicrob Chemother. Alanis AJ. Resistance to antibiotics: are we in the post-antibiotic era? Arch Med Res. The future of antibiotics and resistance. Antibiotic resistance is prevalent in an isolated cave microbiome. PLoS One. Mechanisms of Innate Immunity in Sepsis. In: Baudouin SV, editor. The interface between innate and adaptive immunity.

Nat Immunol. Mackaness GB. The immunological basis of acquired cellular resistance. J Exp Med. Mynasyan H. Phagocytosis and oxycytosis: two arms of human innate immunity.

Immunol Res. Minasyan H. Mechanisms and pathways for the clearance of bacteria from blood circulation in health and disease. Sepsis and septic shock: pathogenesis and treatment perspectives. J Crit Care. Erythrocyte and leukocyte: two Partners in Bacteria Killing. Int Rev Immunol. Roberts IS. The biochemistry and genetics of capsular polysaccharide production in bacteria. Annu Rev Microbiol.

Ophir T, Gutnick DL. A role for exopolysaccharides in the protection of microorganisms from desiccation. Appl Environ Microbiol. Role of bacterial cell surface structures in Escherichia coli biofilm formation. Res Microbiol. Capsule polysaccharide mediates bacterial resistance to antimicrobial peptides. Infect Immun. Identification and characterization of the cps locus of Streptococcus suis serotype 2: the capsule protects against phagocytosis and is an important virulence factor. Kumar A, Schweizer HP.

Bacterial resistance to antibiotics: active efflux and reduced uptake. Adv Drug Deliv Rev. Delcour AH. Outer membrane permeability and antibiotic resistance. Biochim Biophys Acta. Concentration of kanamycin in the presence of ppGpp synthase RelA confer protection against subsequent lethal antibiotic assaults in E. J Exp Microbiol Immunol. Effect of growth at sublethal concentrations of kanamycin on the cell membrane integrity and amount of capsular glucaronic acid in wild-type Escherichia coli and strain with a cpsB mutation.

The role of wza in extracellular capsular polysaccharide levels during exposure to sublethal doses of streptomycin. Fischer E, Braun V. Permeability barrier of bacterial cell envelopes as cause of resistance to antibiotics. Immun Infekt. Innate immune recognition of microbial cell wall components and microbial strategies to evade such recognitions. Microbiol Res. Adams DW, Errington J. Bacterial cell division: assembly, maintenance and disassembly of the Z ring.

Nat Rev Microbiol. Bacterial L-forms. Adv Appl Microbiol. General principles for the formation and proliferation of a wall-free L-form state in bacteria. Roberts RB.

Production of L forms of Neisseria meningitidis by antibiotics. Exp Biol Med. Yamamoto A, Homma JY. L-form of Pseudomonas aeruginosa. II antibiotic sensitivity of L-forms and their parent forms. Jpn J Exp Med. Cell wall-deficient bacteria as a cause of infections: a review of the clinical significance. J Int Med Res. Bacterial biofilms: from the natural environment to infectious diseases. Biofilms as complex differentiated communities.

Biofilm vs. Biochemical and biophysical research. Davies D. Understanding biofilm resistance to antibacterial agents. Nat Rev Drug Discov. Costerton JW. Introduction to biofilm. Int J Antimicrob Agents. Antibiotic resistance of bacterial biofilms.

Antimicrob Agents Chemother. Curr Microbiol. Ryan GB, Majno G. Acute inflammation. A Review. Am J Pathol. Antagonism between bacteriostatic and bactericidal antibiotics is prevalent. Clinical relevance of bacteriostatic versus bactericidal mechanisms of action in the treatment of gram-positive bacterial infections.

Clin Infect Dis. Antibiotic resistance in Sepsis patients: evaluation and recommendation of antibiotic use. N Am J Med Sci. Five years of nosocomial gram-negative bacteremia in a general intensive care unit: epidemiology, antimicrobial susceptibility patterns, and outcomes. Int J Infect Dis. Bacteremia of oral origin. Rev Stomatol Chir Maxillofac. World Health Organization. Injection safety, fact sheet No.

Endocarditis in intravenous drug users. In: Kaye D, editor. Infective Endocarditis. New York City: Raven Press; Human immunodeficiency virus infection and other risk factors for skin abscesses and endocarditis among injection drug users. J Clin Epidemiol. Bacteremia in narcotic addicts at the Detroit medical center. Infectious endocarditis: a prospective comparative study. Rev Infect Dis. Staphylococcus aureus bicomponent gamma-hemolysins, HlgA, HlgB, and HlgC, can form mixed pores containing all components.

J Chem Inf Model. Capsule shields the function of short bacterial Adhesins. J Bacteriol. Enhanced vulnerability for Streptococcus pneumoniae sepsis during asplenia is determined by the bacterial capsule. Acute septic arthritis. Clin Microbiol Rev. Growth and detachment of cell clusters from mature mixed species biofilms.

Stickler DJ. Bacterial biofilms and the encrustation of urethral catheters. Susceptibility of Pseudomonas aeruginosa and Escherichia coli biofilms towards ciprofloxacin: effect of specific growth rate.

Investigation of ciprofloxacin penetration into Pseudomonas aeruginosa biofilms. Persistence of Staphylococcus aureus L-form during experimental lung infection in rats. Devine KM. Bacterial L-forms on tap: an improved methodology to generate Bacillus subtilis L-forms heralds a new era of research. Mol Microbiol. Presence of mycobacterial L-forms in human blood: challenge of BCG vaccination.

Hum Vaccin Immunother. Domingue GJ. Demystifying pleomorphic forms in persistence and expression of disease: are they bacteria, and is peptidoglycan the solution? Discov Med. Pease P. Morphological appearances of a bacterial L-form growing in association with the erythrocytes of arthritic subjects. Ann Rheum Dis. Unstable L-forms of micrococci in human platelets. Microbial Ultrastructure: the Use of the Electron Microscope. London: Appl Bact Tech;



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