Biofilms on shoulder implant metals - can topical adjuncts help impede them?

Effectiveness of topical adjuvants in reducing biofilm formation on orthopedic implants: an in vitro analysis

Biofilms form on surfaces of shoulder arthroplasty implants where they interfere with host defenses and the action of antibiotics; thus they form, a "safe harbor" in which bacteria can persist for long periods of time. Resolution of a shoulder periprosthetic infection associated with a prosthetic biofilm usually requires implant removal and exchange.

These authors compared three topical agents,  Bactisure (Zimmer Biomet, Warsaw, IN, USA), povidone-iodine (Betadine), and chlorhexidine gluconate solution (Irrisept; Irrimax, Gainesville, FL, USA) with respect to their ability in vitro to reduce biofilm formation by Staphylococcus aureus  (ATCC 35556), Staphylococcus epidermidis (ATCC 35984), and Cutibacterium acnes (LMG 16711) inoculated on cobalt-chrome, titanium, and stainless steel disks.

For each bacterial strain, disks were divided into 4 groups: (1) control, (2) povidone-iodine (Betadine), (3) chlorhexidine gluconate (Irrisept), and (4) Bactisure. Bacteria were grown on 5% sheep blood agar plates. 

At 48 and 72 hours after implementation of the topical adjuvant, reduction in colony forming units (measured using adenosine triphosphate bioluminescence) was observed for all topical adjuvants across all tested metals, as compared with their respective control. In most cases the number of colony forming units were reduced by over 90% as shown below

48 h

72 h

The authors concluded that through the use of topical adjuvants on S aureus–, S epidermidis–, and C acnes–inoculated disks of various implant metals, a significant reduction in biofilm production was observed. 

Comment: Among the three agents included in this in vitro study, Betadine has been the most investigated in vivo. In prior reports Betadine has been shown to reduce the rate of clinical infections in  primary total hip arthroplasties and total knee arthroplasties as well as in spine surgery and other surgical fields.

When determining the value (benefit/cost) of the three topical adjuncts, two factors merit consideration:

(1) While there may be statistically significant differences among the three agents, all are quite effective in reducing the colony forming units by >90% on the three metals; it is unclear whether the differences in benefit among them would be clinically significant. (2) While the costs of the proprietary preparations (Irrisept and Bactisure) are not presented in the article, they are likely to be greater than generic povidone-iodine or Betadine. 

Because of our concern that Cutibacterium are routinely inoculated into shoulder arthroplasty wounds when the pilosebaceous units are severed during the skin incision, we routinely use dilute povidone-iodine lavage prior to the placement of the arthroplasty implants. 

How you can support research in shoulder surgery Click on this link.

Here are some videos that are of shoulder interest

Shoulder arthritis - what you need to know (see this link)

The smooth and move for irreparable cuff tears (see this link)

The total shoulder arthroplasty (see this link).

The ream and run technique is shown in this link.

The cuff tear arthropathy arthroplasty (see this link).

The reverse total shoulder arthroplasty (see this link).

Shoulder rehabilitation exercises (see this link).

Follow on twitter: Frederick Matsen (@shoulderarth)

Shoulder joint infections and biofilms

Cutibacterium is recognized as the most common organism recovered from failed shoulder joint replacements. Shoulder arthroplasty wounds are often inoculated by Cutibacterium released from the dermal pilocebaceous units when the skin is incised. When these planktonic (free floating) bacteria come in contact with prosthetic joint surfaces, they can form a biofilm that protects them from antibiotics and host defenses. Efforts to minimize the risk of periprosthetic infections focus on minimizing the size of the inoculum and on killing the introduced organisms before they have an opportunity to form a durable biofilm. 

Here are a few relevant articles

Biofilm formation by Propionibacterium acnes is a characteristic of invasive isolates

Propionibacterium acnes (Cutibacterium) has been shown to form biofilm both in vitro and

in vivo. These authors analyzed biofilm formation by 93 P. acnes isolates, either from invasive infections (n = 45) or from the skin of healthy people (n = 48). The majority of isolates from deep infections produced biofilm in a microtitre model of biofilm formation, whereas the skin isolates were poor biofilm producers (p <0.001 for a difference). They concluded that there was a role for biofilm formation in P. acnes virulence. The type distribution, as determined by sequencing of recA, was similar among isolates isolated from skin and from deep infections, demonstrating that P. acnes isolates with different genetic backgrounds have pathogenic potential. The biofilm formed on plastic and on bone cement was analysed by scanning electron microscopy (EM) and by transmission EM. The biofilm was seen as a 10-lm-thick layer covering the bacteria and was composed of filamentous as well as more amorphous structures. Interestingly, the presence of human plasma in solution or at the plastic surface inhibits biofilm formation, which could explain why P. acnes primarily infect plasma-poor environments

of, for example, joint prostheses and cerebrospinal shunts. This work underlines the importance of biofilm formation in P. acnes pathogenesis, and shows that biofilm formation should be considered in the diagnosis and treatment of invasive P. acnes infections.

Delayed Propionibacterium acnes surgical site infections occur only in the presence of an implant

These authors used a mouse model to compare the effects of P. acnes inoculation with an implant into the mouse femur to a control group with the bacteria but no implant. They observed the animals over a 6-month period using optical imaging system. During the first 2 weeks, bacterial signals were detected in the femur in the both groups. The bacterial signal completely disappeared in the control group within 28 days. Interestingly, in the implant group, bacterial signals were still present 6 months after inoculation. Histological and scanning electron-microscope analyses confirmed that P. acnes was absent from the control group 6 months after inoculation, but in the implant group, the bacteria had survived in a biofilm around the implant. PCR analysis also identified P. acnes in the purulent effusion from the infected femurs in the implant group. 

A Comparison of Bacterial Adhesion and Biofilm Formation on Commonly Used Orthopaedic Metal Implant Materials: An In vitro Study

These authors conducted an in vitro study is to evaluate the ability of Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa to adhere to and to form biofilms on the surface of five orthopaedic biomaterials: cobalt and chromium, highly cross-linked polyethylene, stainless steel, trabecular metal, and titanium alloy. While Cutibacterium was not included, they did include the second most common infecting organism for shoulder periprosthetic infections, S. epidermidis. They found that the highest level of adherence was observed on highly cross-linked polyethylene, followed by titanium, stainless steel, and trabecular metal, with the lowest occurring on the cobalt-chromium alloy. Among the bacterial strains tested, the ability for high adherence was observed with S. epidermidis and K. pneumoniaefollowed by P. aeruginosa and E. coli, whereas S. aureus showed the least adherence.

Cutibacterium acnes Biofilm Study during Bone Cells Interaction

These authors point out that Cutibacterium acnes can exist internally with osteoblast-like cells. For commensal strains, less than 1% of the bacteria were internalized.  C. acnes infection seems to have no cytotoxic effect on the bone cells. Commensal C. acnes showed a significant increase in biofilm formation after osteoblast-like internalization for 50% of the strains (2.8-fold increase). This phenomenon is exacerbated on a titanium, the material commonly used for shoulder implants. 

For the  strains associated with bone and prosthesis infections, they observed a similar internalization rate, but  did not notice any increase in biofilm formation. Fluorescent staining revealed more live bacteria within the biofilm after osteoblast-like cell interaction for all strains. They did not find any link between clinical origin and phylotype. 

Comparative analyses of biofilm formation among different Cutibacterium acnes isolates

These authors point out that Cutibacterium isolates exhibit marked heterogeneity and can be divided into at least 6 phylotypes by multilocus sequence typing and that biofilm formation may well be a relevant factor for Cutibacterium virulence. They performed a first comparative analysis of 58 diverse skin- or implant-isolates covering all six C. acnes phylotypes to investigate biofilm formation dynamics, biofilm morphology and attachment properties to abiotic surfaces. 

Their results suggest that biofilm formation correlates with the phylotype, rather than the anatomical isolation site. IA1 isolates, particularly SLST sub-types A1 and A2, showed highest biofilm amounts in the microtiter plate assays, followed by isolates of the IC, IA2 and II phylotypes.

Microscopic evaluation revealed well-structured three-dimensional biofilms and relatively high adhesive properties to abiotic surfaces for phylotypes IA1, IA2 and IC. 

Representatives of phylotype III formed biofilms with comparable biomass, but with less defined structures, whereas IB as well as II isolates showed the least complex three-dimensional morphology. 

Proteinase K- and DNase I-treatment reduced attachment rates of all phylotypes, therefore, indicating that extracellular DNA and proteins are critical for adhesion to abiotic surfaces. Moreover, proteins seem to be pivotal structural biofilm components as mature biofilms of all phylotypes were proteinase

K-sensitive, whereas the sensitivity to DNase I-treatment varied depending on the phylotype.

How you can support research in shoulder surgery Click on this link.

Here are some videos that are of shoulder interest

Shoulder arthritis - what you need to know (see this link).

How to x-ray the shoulder (see this link).

The total shoulder arthroplasty (see this link).

The ream and run technique is shown in this link.

The cuff tear arthropathy arthroplasty (see this link).

The reverse total shoulder arthroplasty (see this link).

The smooth and move procedure for irreparable rotator cuff tears (see this link).

Shoulder rehabilitation exercises (see this link).

Follow on twitter: Frederick Matsen (@shoulderarth)

Biofilms on titanium - the race to the surface

Strategies to Prevent Biofilm Infections on Biomaterials: Effect of Novel Naturally-Derived Biofilm Inhibitors on a Competitive Colonization Model of Titanium by Staphylococcus aureus and Human Cells

This is a very interesting article that points out that bacteria love to form biofilms on the material we love to use in arthroplasty: titanium and that there is competitive colonization of the surface, either by  host cells or by bacteria = 'the race for the surface'.

Since this article appeared in a journal that shoulder surgeons may not read regularly, we summarize a bit of the article here.

"Antimicrobial resistance is one of the major healthcare challenges that is currently faced by mankind. By switching into the biofilm state, bacteria can withstand antibiotic chemotherapy, and this is increasingly regarded as the most important nonspecific mechanism of antimicrobial resistance. Biofilms are defined as a community of cells encased within a self-produced matrix that adhere to biological or non-biological surfaces. Because implanted medical devices can be ideal substrates for bacteria to attach, biofilm-mediated infections are one of the leading causes of prosthesis implantation failures.

When implanting a biomaterial, the desired outcome is the correct integration of such material with the host tissue. However, this ideal outcome is often impacted by the presence of bacterial cells at the moment of implantation. According to the concept of “race for the surface”, if host cells are able to colonize the surface of the device first, the chances of bacterial cells to adhere to such surface are lower, therefore lowering the risk of implant infection. A frequent route of infection for implants occurs during surgery, as microorganisms can be introduced on the implant surface, providing them with an advantage to colonize the unprotected surface and create a biofilm.

Taking this in consideration, a reasonable approach would be to design an antimicrobial material or coating, which promotes tissue integration. In that direction, it would be advantageous to precondition the material with host cells. Staphylococcus aureus is found asymptomatically on the skin and its presence there enhances the risk of infection in the surgical site, which is why it is egarded as a frequent causative agent of implant-related infections, especially in orthopaedics."

The authors assessed the potential applicability of three anti-biofilm compounds (based on natural compounds) as part of implanted medical devices by testing them on in a competition model based on the co-culture of SaOS-2 mammalian cells and Staphylococcus aureus (collection and clinical strains) on a titanium surface. 

Comment: The search for non-antibiotic approaches to the prevention and treatment of prosthetic infections is of great importance in that it is apparent that antibiotics cannot do the job alone.

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What non-antibiotic treatments may be effective against Propionibacterium?

N-acetylcysteine inhibits growth, adhesion and biofilm formation of Gram-positive skin pathogens

Propionibacterium are increasingly acquiring resistance to the antibiotics commonly used to kill them, such as tetracyclines and Clindamycin.

These authors investigated the antimicrobial efficacy of N-Acetylcysteine (NAC) against biofilm phenotypes of Gram-positive and Gram-negative bacteria. 

Although, no clinical isolate of P. acnes has been reported resistant to rifampicin so far, these authors observed that rifampicin resistance emerged rapidly and this strain can form stronger biofilm than the parent strain. Thus, they selected P. acnes VKM Ac-1450 Rifr strain with total resistance to rifampicin and used this microorganism for a multispecies P. acnes and S. epidermidis biofilm model.

The biofilm formation and growth of mixed culture of P. acnes and S. epidermidis was significantly slowed at 12.5 mg/ml of NAC. NAC also has a high disruptive effect on mature P. acnes and S. epidermidis biofilm.

Here's a plot of the growth (solid circles) and biofilm formation of Propionibacterium with different concentrations of NAC

Here's a plot of the relationship of growth (A) and biofilm formation (B) for Staph Epi, Rifampin resistant Propi and a mixture of the two.

In summary, they found that the bacterial growth and biofilm formation of P. acnes was slowed at sub-MIC of NAC (1.56 mg/ml). NAC prevented growth of plantonic cells of P. acnes VKM Ac-1450 Rifr as well as their biofilm formation. This sensitivity of P. acnes to NAC persisted even in the multispecies P. acnes plus S. epidermidis model.

They concluded that NAC appears to be a promising, non-antibiotic alternative to prevent biofilm-associated infections.

They suggest that long-term treatment with NAC might change of the skin microflora composition, in particular a reduction of propionic acid bacteria in comparison with staphylococci. 

Comment: We do not know if modification of the skin micro biome by reducing the Propi prevalence would be beneficial or harmful. However, we are interested in continuing to observe the efficacy of non-antibiotic measures to prevent and remove biofilms. See this related post: Prevention and treatment of propionibacterium biofilms

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Anaerobic biofilm conditions optimize Propionibacterium growth

Propionibacterium acnes biofilm - A sanctuary for Staphylococcus aureus?

These authors measured planktonic growth and biofilm formation of Propionibacterium acnes and Staphylococcus aureus alone and together under aerobic and anaerobic conditions.

Both P. acnes and S. aureus grew under anaerobic conditions. 

When grown under anaerobic conditions, P. acnes alone or with S. aureus formed a biofilm denser than that of S. aureus alone. 

Viable S. aureus was recovered from a 16- day old combined P. acnes and S. aureus biofilm, but not a monomicrobial S. aureus biofilm, suggesting that P. acnes biofilms may provide an ideal growth site for S. aureus.

Comment: 

Some key findings from our standpoint:

(1) planktonic growth of Propionibacterium was poor under aerobic conditions 

 (2) biofilm growth of Propionibacterium was poor under aerobic conditions

 (3) planktonic growth of Propionibacterium was slowed under anaerobic conditions

  (4) biofilm growth of Propionibacterium was robust under anaerobic conditions

These data demonstrate that anaerobic biofilm conditions optimize Propionibacterium growth.

Does a titanium implant in a relatively anaerobic medullary canal produce these conditions? See:

Infections with Propionibacterium - the necessity of a surgical implant

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Use the "Search" box to the right to find other topics of interest to you.

You may be interested in some of our most visited web pages including:shoulder arthritis, total shoulder, ream and run, reverse total shoulder, CTA arthroplasty, and rotator cuff surgery as well as the 'ream and run essentials'

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Biofilms and prosthetic joint infections - the news is mostly bad

What's New in Musculoskeletal Infection: Update on Biofilms.

Here we try to summarize this interesting article for those of us in the shoulder world. 

A biofilm is a complex structure formed by bacteria adherent to our favorite materials:  cobalt-chromium, titanium, polyethylene, and polymethylmethacrylate cement. These bacteria (one or several different species) surround themselves with an extracellular polymeric matrix consisting of proteins, polysaccharides, lipids and nucleic acids.  The bacteria in a biofilm communicate via quorum sensing leading them to team up in the establishment of virulence, antibiotic resistance, and the formation of an enhanced extracellular matrix that only anchors the bugs to the implant surface, but also provides a physical barrier against host defenses and antibiotics. This barrier also slows the flow of nutrients to the bacteria, causing them to enter a 'dormant' stage reminiscent of Rip Van Winkle or Sleeping Beauty (take your choice).

  

 

In this dormant state the bacteria can resist antimicrobials that are effective against actively growing bugs. Cells in a biofilm can also develop inherent resistance to antibiotics and hang around as 'persister' cells in spite of vigorous therapy. The term 'minimum biofilm eradicate concentration (MBEC)' has been used to refer to the concentration of an antimicrobial necessary to kill all the persister cells - n.b. the battle against infection is not won if the number of bacteria is reduced, only if they're all dead. If persisters persist, the infection is still present.

Several factors make it difficult to recover and grow bacteria in biofilm infections. (1) there may be no free floating (planktonic) bacteria, so that culturing fluid or surfaces is unproductive, (2) without vortexing or sonicating implants, biofilm bacteria may not be recoverable, and (3) bacteria from biofilms may have become genetically altered so that they may not grow well in the laboratory setting. 

Comment: While our understanding of biofilms is increasing, the foundation was presented by our late friend Tony Gristina over 25 years ago, in his largely forgotten article "Infections from biomaterials and implants: a race for the surface" (see this link). 

From the abstract to that article, we can see that he got it right, "Microorganisms in nature and disease are dependent on substratum attachment for optimal growth and development. Similarly, implanted biomaterials tend to potentiate bacteria on their surfaces so that normally friendly special or opportunistic organisms become virulent pathogens. Virulence is also enhanced because both bacteria and biomaterials interfere with host defense mechanisms. Infections centered on biomaterials are most difficult to eliminate and usually require removal of the device. The consequences of device failure are catastrophic and costly. It is the specific nature of the biomaterial surface, which is indirectly a reflection of bulk features, that causes and directs the changes in bacterial behavior which result in virulence. "

The recognition that biofilms are the problem in shoulder prothetic infections, causes us to move from the conventional presentation of infections (which we refer to as 'obvious') to the current recognition of 'stealth' infections. Both can contribute to prosthetic failure, just as both fire and carpenter ants can lead to failure of a house, but the presentation is different.

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Use the "Search" box to the right to find other topics of interest to you.

You may be interested in some of our most visited web pages including:shoulder arthritis, total shoulder, ream and run, reverse total shoulder, CTA arthroplasty, and rotator cuff surgery as well as the 'ream and run essentials'

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Why prosthesis exchange is important: biofilms protect bacteria from antibiotics

Antibiotic-tolerant Staphylococcus aureus Biofilm Persists on Arthroplasty Materials.

These authors cultured methicillin-sensitive Staphylococcus aureus biofilm on total knee arthroplasty materials and exposed these biofilms to increasing concentrations of cefazolin (control, 0.5, 1.0, 10.0, 100.0 μg/mL) to determine if the biofilm could be treated with antibiotics.

Quantitative confocal microscopy and quantitative culture were used to measure viable biofilm cell density.

At the highest concentration tested (100 µg/mL), residual viable biofilm was present on all three materials, and there were no differences in percent biofilm survival among cobalt-chromium (18.5% ± 15.1%), polymethylmethacrylate (22.8% ± 20.2%), and polyethylene (14.7% ± 10.4%). They found that tolerance was a phenotypic phenomenon, because increasing cefazolin exposure did not result in changes in minimum inhibitory concentration as compared with controls.

They concluded that antibiotics are inadequate at complete removal of the biofilm from the surface of arthroplasty materials.

Comment: Biofilms provide a protective niche for bacteria. The biofilms impede antibiotic access by providing a barrier to diffusion. They also allow bacteria to persist at a lower metabolic rate, again making them less susceptible to the effects of antibiotics. 

These results help explain the ineffectiveness of washout and partial prosthesis exchange in managing  colonized implants.

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Hyperglycemia may facilitate biofilm formation

Biofilm growth has a threshold response to glucose in vitro.

These authors used an in vitro model of biofilm formation to investigate the relationship between the amount of biofilm formed by Staphylococcus epidermidis and Staphylococcus aureus and the glucose concentration in the clinically important range of 20 to 300 mg/dL.

They found increased biofilm growth by S aureus and S epidermidis in the clinically important range of 20 to 300 mg/dL.

They concluded that postoperative hyperglycemia may increase the risk for implant infection through increased pathogenicity of intraoperative wound contaminants in addition to compromising host immune status.

Comment: This is an example of how a change in the host environment may increase the pathogenicity of bacteria.

Optimizing the blood glucose after shoulder surgery may reduce the chances of biofilm formation.

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Propionibacterium is orthopaedically different from staphylococcus and can be a cause of 'aseptic' failure

Propionibacterium acnes and Staphylococcus   Cause Pyogenic Osteomyelitis in an Intramedullary Nail Model in the Rabbit

Both Propionibacterium acnes and coagulase-negative staphylococci are opportunistic pathogens implicated in prosthetic joint and fracture fixation device-related infection.

These authors isolated Propionibacterium and coagulase-negative staphylococci from ‘aseptically failed’ prosthetic hip joints and attempted to produce osteomyelitis in an established implant-related osteomyelitis model in the rabbit, in the absence of implant material wear debris.

The Propionibacterium LED2 was isolated after ultrasound treatment of a retrieved prosthetic hip joint, due to a supposed aseptic joint failure. Bacterial biofilm was also detected in the sonicate fluid by immunofluorescence microscopy (IFM) after labeling with a P. acnes-specific antibody.

This isolate belonged to the ST5 lineage within the type IB phylogenetic grouping. Isolates from this 

phylogroup are associated with healthy skin, and rarely recovered from acne vulgaris lesions. They
 have, however, been associated with soft tissue and medical device-related infections, although their
exact clinical importance in these cases has remained unclear.

The histological features of Propionibacterium infection in the in vivo rabbit model were consistent with localized pyogenic osteomyelitis, and biofilm was present on all explanted IM nails. The animals displayed no outward signs of infection, such as swelling, lameness, weight loss, or elevated white cell count. 

In contrast, infection with coagulase-negative staphylococci resulted in histological features consistent with both pyogenic osteomyelitis and septic arthritis, and all coagulase-negative staphylococci animals displayed weight loss and an elevated white cell count despite biofilm detection in only two out six rabbits.

The differences in the histological and bacteriological profiles of the two species in this rabbit model of infection are reflective of their different clinical presentations; low-grade infection in the case of Propionibacterium and acute infection for coagulase-negative staphylococci. 

These results are especially important in relation to the growing recognition of chronic Propionibacterium  biofilm infections in prosthetic joint failure and non-union of fracture fixations, which may be currently reported as ‘aseptic’ failure.

The authors conclude that: Propionibacterium has the potential to cause prosthetic joint infection and fracture non-union, in the absence of signs of classical infection and patient morbidity. Propionibacterium should therefore no longer be dismissed as an insignificant pathogen in the setting of failed retrieved implants; clinical diagnostic practice should be tailored to enable the efficient detection of P. acnes. Without this there is the risk of  an incorrect diagnosis of aseptic loosening and subsequent patient treatment may be misinformed. If a failed prosthetic joint with a mis-diagnosis of aseptic loosening is removed, and a new sterile device placed in the underlying infected site it is very possible that higher numbers of bacteria will be present, particularly if adjacent bone has been colonized.

Comment: This animal model of Propionibacterium infection nicely replicates many of the features encountered in revision arthroplasty, where the preoperative impression of 'aseptic' failure is disproven by positive cultures for Propionibacterium.

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Infections in shoulder arthroplasty - the role of biofilms

The term 'biofilm' refers to bacteria embedded in an extracellular slime layer consisting of polysaccharides, extracellular DNA, proteins and lipids. Biofilms can develop channels allowing for diffusion of nutrients to the embedded bacteria. Because of the limited ability of oxygen to enter, the biofilm provides a range of environments from aerobic on the surface to anaerobic at the depth. Spatial separation of metabolic environments allows for niches for different types of bacteria. Bacteria in biofilms behave differently from those in the free-floating (planktonic) form.

Biofilms can form on all orthopaedic implants, including metal, plastic, and cement. They can be found in fibrous membranes surrounding implants. Because they are viscoelastic liquids, they can resist detachment and can flow across surfaces.

Biofilms protect bacteria from host defenses (1) forming conglomerates too large for phagocytosis by inflammatory cells and  (2) blocking antibodies from diffusing in to reach the bacteria. They also protect the bacteria from antibiotics such that the levels a 1000 times greater concentration is required to kill bacteria in biofilms in comparison to planktonic bacteria.

Biofilms make bacteria difficult to recover. Even though a prosthesis has a bacteria-ladened biofilm, joint fluid aspiration may well be negative because the bacteria are not present in the fluid. Bacteria in biofilms are not easily recovered because conventional culturing methods may not dislodge the biofilm. Even if the biofilm is recovered, host factors such as endonucleases may prevent the bacteria from growing. Bacteria in biofilms may enter a dormant or slow growing phenotype that grows slowly or not at all in cultures.

Essentially all periprosthetic infections involve biofilms. These can progress very slowly and may be non-symptomatic for years. Biofilm infections may exert their pathological effects by triggering insidious tissue damage (such as bone resorption) rather than by creating the usual signs of inflammation. Thus it may be very difficult to differentiate prosthetic loosening from the chronic effects of a biofilm from 'aseptic' mechanical loosening. These infections do not resolve spontaneously and usually require surgical debridement and antibiotics.

Biofilms may serve as sources of more obvious planktonic infection if the biofilm is stimulated or if the host is weakened.

These observations regarding biofilms have informed our current approach to failed shoulder arthroplasty.

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Bacterial Biofilms and Periprosthetic Infections - how do we know if a failure is 'aseptic'?

Bacterial Biofilms and Periprosthetic Infections

This is an important article because it emphasizes that low-virulence infections sheltered in biofilms may underlie many apparently ‘aseptic’ failures of prosthetic joint arthroplasty.

The authors point out that in nature most bacteria in nature grow as biofilms rather than as isolated or ‘planktonic’ colonies. Interestingly, the biofilm matrix has a structure and function analogous to the extracellular matrix that is the hallmark of higher-order multicellular organisms. As with the extracellular matrix, the biofilm matrix is produced by cells but, in this case, bacterial cells. The biofilm matrix offers protection as well as provides an organizing scaffold, which can facilitate the metabolic activity and even communication among the bacteria. Bacteria in biofilms are relative protected from immune system attack and are less susceptible to antibiotics. In a biofilm, bacteria can be tolerant to antibiotics at concentrations that are several hundredfold greater than that needed to kill planktonic bacteria. While in biofilms, bacteria seem to exist in a more quiescent, less virulent state; however, they can still elicit a host inflammatory response that contributes to continual adjacent tissue destruction that results ultimately in the clinical symptoms of pain and implant loosening seen in longstanding chronic periprosthetic infection.

It can be difficult to culture biofilm bacteria. Special methods may be necessary, including polymerase chain reaction methodologies and mass spectrometry. These methods have been successful in identifying organisms in culture-negative periprosthetic infection as well as in cases of revision arthroplasty thought to be due to aseptic loosening. The authors suggest that many ‘aseptic’ failures of arthroplasty components may actually involve low-grade chronic infections that simply present as chronic pain, which may be the only clinical symptom.

It can be difficult to resolve such infections. The authors suggest that any surgical treatment will ultimately fail if that treatment does not adequately remove the biofilm at the infection site.

A single-stage exchange can be successful if it adequately removes the biofilm at the infection site: that on the prosthesis as well as that in surrounding tissues.

While the authors do not discuss chronic low grade shoulder infections, it is well recognized that the commonly recovered Priopionibacterium is an excellent former of biofilms

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