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Biomedical subjects

J W Costerton

Publications and source records attributed to J W Costerton.

At least 19 recordsLinked to original sources
PubMed1992

Susceptibility of biofilm cells of Pseudomonas aeruginosa to bactericidal actions of whole blood and serum.

The planktonic and young biofilm cells (harvested on day 2) of mucoid Pseudomonas aeruginosa were susceptible to the bactericidal actions of whole blood and serum. Aging biofilms of this organism (harvested on day 7) were very resistant to the killing effect of whole blood and serum. From this study we propose that the establishment of aging biofilms may contribute to persistence of this organism in biofilm-associated infections.

Environmental Microbiology↗
PubMed1992

Defense system in the biliary tract against bacterial infection.

Bacteria can invade the biliary tract by ascending from the duodenum and via the hematogenous route from the hepatic portal venous blood. The sphincter of Oddi, situated at the junction of the biliary tract and the upper gastrointestinal tract, forms an effective mechanical barrier to duodenal reflex and ascending bacterial infection. Conversely, Kupffer cells and the tight junctions between hepatocytes help prevent bacteria and toxic metabolites from entering the hepatobiliary system from the portal circulation. The continuous flushing action of bile and the bacteriostatic effects of bile salts keeps the biliary tract sterile under normal conditions. Secretory immunoglobulin A (sIgA), the predominant immunoglobulin in the bile, and mucus excreted by the biliary epithelium probably function as antiadherence factors, preventing microbial colonization. When barrier mechanisms break down, as in surgical or endoscopic sphincterotomy and with insertion of biliary stents, pathogenic bacteria enter the biliary system at high concentrations and take up residence on any foreign bodies. Intrabiliary pressure is a key factor in the development of cholangitis. Chronic biliary obstruction raises the intrabiliary pressure. This adversely influences the defensive mechanisms such as the tight junctions, Kupffer cell functions, bile flow, and sIgA production in the system, resulting in a higher incidence of septicemia and endotoxemia in these patients. Knowledge of biliary defense against infection is still quite primitive. Unclear are the roles of sIgA in the bile, mechanism of bacterial adhesion to the biliary epithelium, Kupffer cell function in biliary obstruction, and the antimicrobial activity of bile salts.

Animals↗
PubMed1992

Movement of pseudomonas aeruginosa along catheter surfaces. A mechanism in pathogenesis of catheter-associated infection.

The etiologic mechanism involved in the establishment of catheter-associated bacteriuria is suggested in this in vitro study of the movement of Pseudomonas aeruginosa along a catheter surface against a flowing artificial urine milieu in the presence and absence of antibiotics. Following a lag phase, during which a bacterial biofilm becomes firmly established at a site of contamination, the bacteria ascend the surface of the Foley catheters in a rapidly expanding coherent biofilm. The speed of the bacterial ascent is increased as a result of turbulence-associated planktonic saltatory bacterial movement within the urine column. Bacteriocidal concentrations of antibiotics in the urine can slow down the bacterial ascent, but they do not preclude it.

Catheterization↗
PubMed1992

Coagulase-negative staphylococcus in chronic prostatitis.

Three male patients with a clinical history of prostatitis with coagulase-negative staphylococci localized to the expressed prostatic secretion and who did not respond to antibiotics were studied intensively 4 weeks after cessation of therapy with repeat culture of the prostatic fluid, as well as with culture, and histological and ultrastructural examination of multiple prostatic biopsies. Coagulase-negative staphylococci were cultured in the biopsied prostatic tissue, and gram-positive staphylococci were identified in sparse and focal microcolonies adherent to the prostatic ductal walls. Coagulase-negative staphylococci may be implicated in the pathogenesis of chronic bacterial prostatitis.

Adult↗
PubMed1992

Biofilms on indwelling vascular catheters.

BACKGROUND AND METHODS: Some bacteria have a natural tendency to adhere to available surfaces and to form biofilms. Biofilms have been demonstrated on right heart flow-directed catheters, endocardial pacemaker leads, urinary catheters, and other medical devices. In this study, we examined arterial and central venous catheters that had been in place in ICU patients between 1 and 14 days for the presence of bacterial biofilms by scanning electron microscopy, transmission electron microscopy, and a special scraping/sonication bacterial recovery technique. The data taken from these processes were compared with skin entry site swabs and blood cultures and correlated with patient data on infection, bacterial colonization, and antibiotic use. RESULTS: Extensive biofilm formation was demonstrated by scanning electron microscopy on all 42 arterial and 26 central venous catheters. Bacteria were seen within the biofilms on 69% (29/42) of the arterial and 88% (23/26) of the central venous catheters. These two direct methods for the detection of biofilm bacteria on the catheter surfaces demonstrated the presence of adherent organisms on 81% of devices examined. Some catheters that had been in place for only 1 day were colonized by bacterial biofilms. Biofilm scraped from catheter surfaces and dispersed by mixing and sonication yielded cultures (32% of catheters) of predominantly skin bacteria. In a few instances, the recovery of bacteria from biofilms on vascular catheters coincided with positive cultures from skin entry site swabs and/or from the blood of the patient, but there was no significant correlation between bacterial recovery from the catheter surface, entry site, and/or patients' blood. CONCLUSIONS: Direct microscopic examination of 68 vascular catheters that had been in place 1 to 14 days showed that most (81%) were colonized by bacteria growing in slime-enclosed biofilms. In many cases, this colonization of catheter surfaces could be confirmed by special biofilm culture recovery methods. Although the clinical importance of bacterial biofilms on catheter surfaces is speculative, their presence and potential to serve as a nidus for infection and bacteremia in critically ill immunocompromised hosts are cause for concern.

Alberta↗
PubMed1992

Evaluation of strategies for central venous catheter replacement.

OBJECTIVES: To assess the consequences of leaving a bacterially colonized central venous catheter in place and to compare the effects of three catheter replacement strategies for catheter repair control in an animal model. DESIGN: Prospective study. SETTING: Laboratory and animal facility of a large university. SUBJECTS: Eighteen healthy, female, adult sheep. INTERVENTIONS: Radiopaque-siliconized elastomer central venous catheters were inserted into the jugular veins and colonized with either Escherichia coli or Staphylococcus epidermidis. After 7 days of infection, the catheters were either: a) exchanged using a guidewire; b) removed and replaced with a new catheter in a new jugular vein site after a 48-hr interval; or c) exchanged using a guidewire and antibiotics (tobramycin, cephaloridine) injected into the catheter. Animals were euthanized 7 days after insertion of the new catheter. Quantitative microbiology was performed on blood samples collected daily from the catheters and a peripheral vein, as well as from catheters and tissue recovered from the sheep at the time of autopsy. MEASUREMENTS AND MAIN RESULT: When catheters were changed using a guidewire, they became colonized by bacteria within 48 hrs, and the sheep had embolic pneumonia and vegetative endocarditis at autopsy. Similar consequences were observed when antibiotics were administered into the catheter lumen. If colonized catheters were removed and a new catheter was inserted after a 48-hr interval, recolonization, pneumonia, and endocarditis were not observed. CONCLUSIONS: Replacement of a biofilm-colonized central venous catheter over a guidewire is associated with rapid colonization of the replacement catheter and production of detached, slime-enclosed, antibiotic-resistant aggregates that colonize other catheters or initiate endocarditis or pneumonia by dissemination in the bloodstream.

Animals↗
PubMed1992

Mechanism of persistent infection associated with peritoneal implants.

The ability of rabbits to clear an intraperitoneal injection of Pseudomonas aeruginosa in the presence or absence of a surgically implanted peritoneal device was investigated. Sham-operated rabbits without an implant eliminated a P. aeruginosa challenge of 5 x 10(6) cfu/ml; lavage fluid and peritoneal tissues became culture-negative within 96 h. However, peritonitis developed in rabbits that were given the same number of bacteria in the presence of an implant; high bacterial counts were recovered from the lavage fluid and the device itself. Scanning and transmission electronmicroscopy revealed bacterial biofilms on the surface of the device. Insertion of pre-colonised devices demonstrated a rapid multiplication of sessile organisms within the resulting bacterial biofilm. Counts reached a plateau of about 1 x 10(7) cfu/cm2 of Silastic by day 16 and fluctuated around this level until the end of the study. Pre-immunisation with formalin-killed whole cells of P. aeruginosa did not reduce this bacterial growth despite high levels of specific IgG. The results confirm the failure of peritoneal defences to clear an infection in the presence of an implant following either challenge with planktonic bacteria or insertion of a pre-colonised device, and demonstrate the rapid development of bacterial biofilms on the surface of the implant which appear to protect the bacteria from host defences, even when primed by pre-immunisation.

Animals↗
PubMed1992

Kinetic interaction of biofilm cells of Staphylococcus aureus with cephalexin and tobramycin in a chemostat system.

Planktonic and young biofilm cells were completely eradicated after exposure of these cells to drug levels representing one loading and two maintenance doses of tobramycin and cephalexin. A very different picture was observed when antibiotic exposure was initiated on day 21. Complete eradication of the old biofilm cells was not observed even when the antibiotic exposure was continued for an extra 6 days. Regrowth of the organism was observed when the antibiotic exposure was terminated.

Cell Survival↗
PubMed1992

Dynamic interactions of biofilms of mucoid Pseudomonas aeruginosa with tobramycin and piperacillin.

The dynamic interaction of planktonic and biofilm cells of mucoid Pseudomonas aeruginosa with tobramycin and piperacillin was investigated in a chemostat system. The results indicated that planktonic and young biofilm cells of the 2-day-old chemostat culture of P. aeruginosa were susceptible to killing by chemostat-controlled doses of either 250 micrograms of piperacillin per ml plus 5 micrograms of tobramycin per ml or 500 micrograms of piperacillin per ml plus 5 micrograms of tobramycin per ml. Complete eradication of the planktonic and young biofilm cells was observed after exposure of the cells to six chemostat-controlled doses of these antibiotic at 8-h intervals for 7 days. Regrowth of the organism was not observed after the termination of antibiotic therapy on day 7. A different picture was observed when antibiotic treatment was initiated on day 10 after inoculation. Viable old biofilm cells were reduced to approximately 20% after exposure to the chemostat-controlled doses of 500 micrograms of piperacillin per ml plus 5 micrograms of tobramycin per ml. Complete eradication of old biofilm cells could not be achieved, and regrowth of the organism occurred after the termination of antibiotic therapy. These data suggest that young biofilm cells of mucoid P. aeruginosa can be effectively eradicated with the combination of piperacillin and tobramycin, while old biofilm cells are very resistant to these antibiotics and eradication of old biofilm cells is not achievable with the chemostat-controlled doses of piperacillin and tobramycin used in this study.

Culture Media↗
PubMed1992

Pseudomonas aeruginosa biofilm as a diffusion barrier to piperacillin.

Pseudomonas aeruginosa 579 biofilms formed on dialysis membranes retarded piperacillin diffusion. Treatment of biofilms with 5.0 mM CaCl2.2H2O prevented diffusion. Biofilms permitted equilibration of [14C]glucose. Thin-layer chromatography of fluids distal to untreated (viable and nonviable) and viable Ca(2+)-treated P. aeruginosa 579 biofilms and fluids distal to a viable P. aeruginosa mutant noninducible for the expression of beta-lactamase did not detect piperacillinoic acid.

Chromatography, Thin Layer↗
PubMed1992

Electrical enhancement of biocide efficacy against Pseudomonas aeruginosa biofilms.

When applied within a low-strength electric field (+/- 12 V/cm) with a low current density (+/- 2.1 mA/cm2), several industrial biocides exhibited enhanced killing action against Pseudomonas aeruginosa biofilms grown on stainless steel studs. Biocide concentrations lower than those necessary to kill planktonic cells of P. aeruginosa (1, 5, and 10 ppm of the active ingredients of kathon, glutaraldehyde, and quaternary ammonium compound, respectively) were bactericidal within 24 h when applied within our electrified device.

Dimethylamines↗
PubMed1992

Eradication of biofilm cells of Staphylococcus aureus with tobramycin and cephalexin.

The kinetics of growth and formation of biofilm by Staphylococcus aureus were investigated under iron-limited conditions in the chemostat. The population of planktonic cells reached 5.5 x 10(9) cells/mL 24 h after inoculation (D = 0.05 h-1) and remained constant throughout. The number of biofilm cells of S. aureus colonizing the silicone tubing increased exponentially from 6 x 10(4) to 2.7 x 10(7) cells/cm2 (6 days later) and continued to increase at a reduced rate to 2.7 x 10(8) cells/cm2 on day 13. Planktonic cells of S. aureus were susceptible to tobramycin and cephalexin. The planktonic cells could be successfully eradicated with a combination of 5 micrograms tobramycin plus 100 micrograms cephalexin per millilitre. Exposure of young biofilm cells of S. aureus to 5 micrograms tobramycin plus 100 micrograms cephalexin per millilitre resulted in a rapid loss of cell viability. The percentage of survival dropped to less than 0.0001% after exposure to these concentrations of antibiotics for 3 h. Old biofilm cells of S. aureus were found to be extremely resistant to these antibiotics. The cell viability was reduced to 0.09% after exposure to 10 micrograms tobramycin plus 100 micrograms cephalexin per millilitre. The results suggest that it is possible to eradicate S. aureus infection at the early stage with tobramycin plus cephalexin. Any delay in implementing antibiotic therapy is likely to result in the failure of the treatment. It is important to note that the concentrations of antibiotics required for the eradication of young biofilm cells must be determined for the treatment of device-associated infections.

Bacterial Adhesion↗
PubMed1992

Disparate efficacy of tobramycin on Ca(2+)-, Mg(2+)-, and HEPES-treated Pseudomonas aeruginosa biofilms.

Mucoid exopolysaccharide (MEP) obtained from Pseudomonas aeruginosa 579 was suspended in 10 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) pH 7.2 containing 0.1-10.0 mM of CaCl2.2H2O or MgCl2.4H2O. MEP treated with HEPES or < 5.0 mM of the Ca2+ or Mg2+ salts remained soluble and bound tobramycin in an equilibrium dialysis bioassay. MEP treated with 5.0 or 10.0 mM of the Ca2+ or Mg2+ salts did not bind tobramycin. Five and 10 mM Ca(2+)-treated MEP precipitated but Mg(2+)-treated MEP did not. Pseudomonas aeruginosa 579 biofilms formed using a defined growth medium having < 1 mM Ca2+ or Mg2+ were treated for 1 h with 10 mM HEPES +/- 5.0 mM CaCl2.2H2O or MgCl2.4H2O, prior to an 8-h exposure to HEPES, or the defined growth medium, +/- 125 micrograms/mL of tobramycin. The tobramycin kill kinetics for the HEPES-, Mg(2+)-, and Ca(2+)-treated biofilms were similar and gradual from T = 0-6 h. The viability of the HEPES- and Mg(2+)-treated populations declined sharply (from 6 to 8 h). Bacteria dispersed from the MEP in control biofilms at 0 and 8 h did not grow in the presence of 7.81 micrograms/mL of tobramycin. Thus, binding of tobramycin of P. aeruginosa 579 MEP may not be as influential to the impediment of tobramycin diffusion as is the steric hindrance imposed by the Ca2+ condensation of the polymer.

Binding Sites↗
PubMed1992

Induction and intracellular localization of the 80-kilodalton heat-shock protein of Neurospora crassa.

The most abundant heat-shock protein of Neurospora crassa is a multimeric glycoprotein of 80-kilodaltons (i.e., HSP80), induced strongly by hyperthermia and at a lower level by sodium arsenite, ethanol, and carbon source depletion. Immunoelectron microscopy, using indirect immunogold labelling demonstrated that HSP80 was undetectable in mycelium cultured at the normal growth temperature of 28 degrees C, but it appeared rapidly following the commencement of heat-shock treatment at 48 degrees C. HSP80, visualized by the gold label, was observed almost exclusively in the cytoplasm, exhibiting a uniform distribution. Association of this protein with cellular membranes and (or) targeting to a particular subcellular compartment or organelle was not apparent.

Cytoplasm↗
PubMed1992

Some bacterial parameters influencing the neutrophil oxidative burst response to Pseudomonas aeruginosa biofilms.

Persistence of bacteria in spite of a normal host immune system and relevant antibiotic treatment is a key problem in many chronic infections, such as the bronchopulmonary P. aeruginosa infection in cystic fibrosis patients. The capability of bacteria to establish themselves in microcolonies or biofilms is an important protective mechanism of the microorganisms. We examined the human PMN oxidative burst response to P. aeruginosa in biofilm and in planktonic form. The PMN chemiluminescence response to P. aeruginosa in biofilms was reduced to 30.5-47.5% (p less than 0.04) and the superoxide response to 85.9% (p less than 0.02) of the response to equivalent numbers of planktonic bacteria. Mechanical disruption of the biofilms before the assays elicited a significantly increased response in the chemiluminescence experiments and to nonopsonized biofilms in the superoxide anion experiments. We conclude that biofilm bacteria, although able to stimulate the PMN, result in a reduced, suboptimal response leading to lack of efficient eradication of the bacteria in the chronic infection.

Cystic Fibrosis↗
PubMed1992

Osteomyelitis experimentally induced with Bacteroides thetaiotaomicron and Staphylococcus epidermidis. Influence of a foreign-body implant.

Experimental osteomyelitis was induced in the rabbit tibia with Staphylococcus epidermidis alone, with Bacteroides thetaiotaomicron alone, and with both bacteria as etiologic agents, in the presence or absence of a foreign-body implant. Animals were monitored by clinical observation and roentgenographic, microbiologic, histologic, immunofluorescent microscopic, and electron microscopic methods. Scanning and transmission electron microscopy showed masses of coccoid and rod-shaped bacteria embedded in a matrix of exopolysaccharide and adhered to bone, marrow, and the foreign-body implant (when present). Of the 58 rabbits receiving an implant, osteomyelitis developed in 48 (83%), and bacteria were recovered by culture from 56 (97%). Of the 31 animals without the implant, osteomyelitis developed in 18 (58%), but no bacteria were recovered by culture. Bacterial recovery appeared to be dependent on the presence of the implant. The rate of induction and the severity of osteomyelitis were enhanced by the presence of the foreign-body implant and by the polymicrobic infection.

Animals↗
PubMed1991

An in vivo model to study the pathobiology of infectious biofilms on biomaterial surfaces.

This study examines the morphology, ultrastructure, and microbiology of the intact biofilm developing on an implant surface. Silastic subdermal implant material was colonized with P. aeruginosa and surgically inserted into the peritoneal cavity of adult rabbits. After 4, 8, 28, and 42 days implants were recovered and the intact biofilms examined. P. aeruginosa colonized the implant throughout the entire experimental time. Microcolonies of glycocalyx-coated bacteria were observed within the biofilm. However, the bulk of the biofilm was host-generated and typically contained phagocytes trapped within a thick mesh of fibrin. Polymorphonuclear neutrophils were the predominant cell type. Isolated erythrocytes, macrophages, and fibroblasts were also observed. By day 28, the biofilm was enclosed in a fibrous capsule of vascularized connective tissue. The low numbers of neutrophils seen in biofilms from sterile Silastic sheets implanted into control animals suggested that neutrophilia may represent a specific cellular response to the bacterial colonization. The results indicate that the cell-mediated immune response provides for most of the biofilm mass on colonized implant surfaces. Inactivated phagocytes trapped in fibrin may "wall-off" the embedded bacterial microcolonies and thus shield them from live phagocytic leucocytes. Such a mechanism may play an important role in the pathogenesis of prosthetic device infections.

Animals↗