Re: Radiology

[Ryder1234]

To the contrary!  and we know much more now.  Heparin is recognized as having potential to support microbial (biofilm) growth.  One very good example of this is in the following report.

Centers for Disease Control and Prevention (CDC).
Update: Delayed onset Pseudomonas fluorescens bloodstream infections after
exposure to contaminated heparin flush--Michigan and South Dakota, MMWR Morb Mortal Wkly Rep. 2006 Sep 8;55(35):961-3 2005-2006.

This is a classic example of biofilm behavior.  The growth potential of heparin is also multi-species including gram positive, gram negative and fungal. Another example:

Shanks RM, Donegan NP, Graber ML, Buckingham SE, Zegans ME, Cheung AL, O'Toole
GA.Heparin stimulates Staphylococcus aureus biofilm formation.
Infect Immun. 2005 Aug;73(8):4596-606.
Heparin, known for its anticoagulant activity, is commonly used in catheter
locks. Staphylococcus aureus, a versatile human and animal pathogen, is commonly
associated with catheter-related bloodstream infections and has evolved a number
of mechanisms through which it adheres to biotic and abiotic surfaces. We
demonstrate that heparin increased biofilm formation by several S. aureus
strains. Surface coverage and the kinetics of biofilm formation were stimulated,
but primary attachment to the surface was not affected. Heparin increased S.
aureus cell-cell interactions in a protein synthesis-dependent manner. The
addition of heparin rescued biofilm formation of hla, ica, and sarA mutants. Our
data further suggest that heparin stimulation of biofilm formation occurs
neither through an increase in sigB activity nor through an increase in
polysaccharide intracellular adhesin levels. These finding suggests that heparin
stimulates S. aureus biofilm formation via a novel pathway.

This is why so much work is ongoing to find alternatives as demonstrated below:

Shanks RM, Sargent JL, Martinez RM, Graber ML, O'Toole GA.
Catheter lock solutions influence staphylococcal biofilm formation on abiotic
surfaces.Nephrol Dial Transplant. 2006 Aug;21(8):2247-55. Epub 2006 Apr 20.

BACKGROUND: Microbial biofilms form on central venous catheters and may be
associated with systemic infections as well as decreased dialysis efficiency due
to catheter thrombosis. The most widely used anticoagulant catheter lock
solution in the US is sodium heparin. We have previously shown that sodium
heparin in clinically relevant concentrations enhances Staphylococcus aureus
biofilm formation. In the present study, we examine the effect of several
alternative catheter lock solutions on in vitro biofilm formation by laboratory
and clinical isolates of S. aureus and coagulase-negative staphylococci (CNS).
METHODS: Lepirudin, low molecular weight heparin, tissue plasminogen activator,
sodium citrate, sodium citrate with gentamicin and sodium ethylene diamine
tetra-acetic acid (EDTA) were assessed for their effect on biofilm formation on
polystyrene, polyurethane and silicon elastomer. RESULTS: Sodium citrate at
concentrations above 0.5% efficiently inhibits biofilm formation and cell growth
of S. aureus and Staphylococcus epidermidis. Subinhibitory concentrations of
sodium citrate significantly stimulate biofilm formation in most tested S.
aureus strains, but not in CNS strains. Sodium EDTA was effective in prevention
of biofilm formation as was a combination of sodium citrate and gentamicin. Low
molecular weight heparin stimulated biofilm formation of S. aureus, while
lepirudin and tissue plasminogen activator had little effect on S. aureus
biofilm formation. CONCLUSIONS: This in vitro study demonstrates that heparin
alternatives, sodium citrate and sodium EDTA, can prevent the formation of S.
aureus biofilms, suggesting that they may reduce the risk of biofilm-associated
complications in indwelling catheters. This finding suggests a biological
mechanism for the observed improvement in catheter-related outcomes in recent
clinical comparisons of heparin and trisodium citrate as catheter locking
solutions. A novel and potential clinically relevant finding of the present
study is the observation that citrate at low levels strongly stimulates biofilm
formation by S. aureus.

However, tetrasodium EDTA appears to be the most promising.

Percival SL, Kite P, Eastwood K, Murga R, Carr J, Arduino MJ, Donlan RM.Tetrasodium EDTA as a novel central venous catheter lock solution against biofilm.Infect Control Hosp Epidemiol. 2005 Jun;26(6):515-9.
BACKGROUND: Central venous catheter (CVC)-related bloodstream infections (BSIs)
are known to increase rates of morbidity and mortality in both inpatients and
outpatients, including hematology-oncology patients and those undergoing
hemodialysis or home infusion therapy. Biofilm-associated organisms on the
lumens of these catheters have reduced susceptibility to antimicrobial
chemotherapy. This study tested the efficacy of tetrasodium EDTA as a catheter
lock solution on biofilms of several clinically relevant microorganisms.
METHODS: Biofilms of Staphylococcus epidermidis, methicillin-resistant S.
aureus, Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and
Candida albicans were grown to levels of approximately 1 x 10(5) colony-forming
units (CFU)/cm(-1) on CVC segments in a model system, then subjected to the
tetrasodium EDTA lock treatment. RESULTS: Comparisons of biofilms before and
after exposure to the 40-mg/mL(-1) tetrasodium EDTA lock for 21 hours showed
that the biofilm viable cell counts of all organisms tested were significantly
reduced (P < .05) after exposure to the treatment. CONCLUSION: Antimicrobial
lock treatment using 40 mg/mL(-1) of tetrasodium EDTA for at least 21 hours
could significantly reduce or potentially eradicate CVC-associated biofilms of
clinically relevant microorganisms.

As for the Schilling abstract. There is only a trend identified towards the heparin group and does not differentiate whether these were intra or extraluminal infections from the information provided. The information in abstract is non-conclusive.  I have not read the full article as yet.

I hope this clarifies the issue for you. Any questions?
Marcia Ryder