A comparative study of the effects of UVC irradiation on select procaryotic and eucaryotic wound pathogens.

Managing wounds infected with a mixture of several types of microorganisms such as bacteria (procaryotes) and fungi (eucaryotes) is a challenging clinical situation. The purpose of this study was to determine the effectiveness of ultraviolet light (UVC) in eradicating select procaryotic and eucaryotic organisms, in both pure culture and mixed cultures in vitro. Five replications of each organism or mixture of organisms (10(6) organisms/mL singly or 10(15) organisms/mL mixed culture) were plated. The cultures were treated with a UVC light 1 inch from the surface. Irradiation times were 0, 2, 3, 4, 5, 15, 30, 45, 60, 90, 120, and 180 seconds. Bacterial cultures were incubated and colony counts performed. Upon exposure to UVC, a 99.9% kill rate was obtained at 3 to 5 seconds for the procaryotic organisms (Pseudomonas aeruginosa and Mycobacterium abscessus) tested. However, 15 to 30 seconds of UVC treatment was required to obtain 99.9% kill of the eucaryotic organisms (Candida albicans, Aspergillus fumigatus) tested. This study demonstrates a decreasing sensitivity of evolutionarily more complex organisms to UVC. This study also provides further evidence that short exposure times to UVC are detrimental to procaryotic and simple unicellular eucaryotic organisms while sparing more complex multicellular organisms.

The effects of UVC irradiation on group A streptococcus in vitro.

Streptococcus pyogenes (group A streptococcus--GAS) is a common cause of necrotizing fasciitis (NF)--a severe infection of the subcutaneous soft tissue. The purpose of this study was to determine if the topical therapy ultraviolet light C (UVC) is effective in killing GAS in vitro and to evaluate the most effective treatment parameters for use with UVC therapy. Five replications of GAS at 10(8) organisms/mL were plated. The cultures were treated with a UVC light 1 inch from the surface. Irradiation times were as follows: 0, 2, 3, 4, 5, 15, 30, 45, 60, 90, 120, and 180 seconds. Bacterial cultures were incubated and colony counts performed. A second set of GAS cultures were exposed to UVC for 30, 90, and 120 seconds either once daily (qd) or twice daily (bid). Kill rates were 99.9% for GAS at 4 seconds to 180 seconds. Kill rates of 99.9% were also obtained at 30 seconds and 90 seconds when UVC treatment was given either qd or bid. This data indicates that UVC is bactericidal for GAS at times as short as 4 seconds. In addition, UVC treatment was not effective when administered through thin film dressings.

The effects of ultraviolet radiation on antibiotic-resistant bacteria in vitro.

Wound infections produced by antibiotic-resistant bacterial strains are particularly difficult to manage. This study examined the effectiveness of ultraviolet (UV) light treatment in killing antibiotic-resistant strains of Staphylococcus aureus and Enterococcus faecalis in vitro. Between 2 and 5 replications of each organism at 10(8) organisms/ml were prepared and plated on sheep blood agar medium and treated with UV light (254 nm, 15.54 mW/cm2 output). Irradiation times were 0, 2, 5, 8, 15, 30, 45, 60, 90 or 120 seconds. Bacterial cultures were then incubated at 35 degrees C for 24 hours. Kill rates were 99.9 percent for the methicillin-resistant strain of S. aureus (MRSA) at 5, 8, 15, 30, 45, 60 seconds and 100 percent at 90 and 120 seconds. Kill rates were 99.9 percent at 5, 8, 15, 30 seconds for vancomycin-resistant E. faecalis (VRE) and 100 percent at 45, 60, 90, 120 seconds. Similar results were found with UV light treatment of the antibiotic-susceptible strains of S. aureus and E. faecalis. A significant difference in kill rates at 30 seconds of UV exposure was detected between the antibiotic-resistant strain of S. aureus and the antibiotic-resistant strain of E. faecalis (Student's t test, p < 0.01). Significant differences were also detected in the kill rates at 30 second exposure times for the antibiotic-susceptible strains of S. aureus and E. faecalis. These findings suggest that the Enterococcal bacteria is more susceptible to the killing effects of UV. This data also suggests that UV light at 254 nm is bactericidal for antibiotic-resistant strains of S. aureus and E. faecalis at times as short as 5 seconds and that the enterococcal bacteria is more susceptible to the killing effects of UV. With recommended patient treatment times for infected wounds being significantly longer than 5 seconds, this data indicates that patient treatment times need to be re-examined.

Analysis of practice-role perceptions of physical therapy, occupational therapy, and speech-language therapy students.

The purpose of this study was to determine whether physical therapy (PT), occupational therapy (OT), and speech-language therapy (SLP) students shared common perceptions of the practice roles of the three disciplines. The survey instrument used in this study contained 55 questions that addressed practice-role perceptions. The questions were based on a case study. A total of 172 undergraduate students (PT 71, OT 52, SLP 49) from a southeastern university participated. Chi-square test of association was used to analyze the data. Results showed that PT, OT, and SLP students shared common perceptions of administrative and educational practice roles but differed on their perceptions of assessment and physical/mental treatment roles. Practice-role confusion was particularly acute between OT and PT and between OT and SLP students in these areas.

Evidence for the corelease of dynorphin and glutamate from rat hippocampal mossy fiber terminals.

Hippocampal mossy fiber (MF) nerve endings may be isolated in a subcellular fraction (P3) that releases both prodynorphin-derived peptides and glutamate (Glu) in a calcium-dependent manner when depolarized. However, this isolation procedure does not yield a pure preparation of MF synaptosomes. The present study evaluates the proportion of dynorphin (Dyn) and Glu that is released from synaptosomes in the P3 fraction that are of MF origin. We have addressed this issue by determining the degree to which a selective lesion of the dentate granule cell/MF system in vivo concomitantly reduces the exocytosis of Dyn and Glu from the P3 subcellular fraction. Unilateral injections of colchicine into the dentate gyrus resulted in a substantial and selective degeneration of the granule cell/MF pathway in the rat hippocampal formation. The overall integrated density of the Timm-stained band, which corresponds to the position of the MF terminal field, was estimated to be reduced by 75%. After this extensive loss of MF boutons, the K(+)-evoked release of Dyn and Glu from the P3 fraction was reduced by 95 and 51%, respectively. The loss of Timm staining and evoked Dyn release indicate that colchicine effectively eliminated MF synaptosomes from the P3 fraction. Those subcellular entities that were not destroyed by colchicine comprised approximately 50% of the protein and evoked Glu release measured by using the P3 fraction. In addition, the present results demonstrate that the inhibitory potency of the kappa opioid agonist U-50,488H was not altered by the elimination of MF boutons from this synaptosomal preparation. This finding indicates that U-50, 488H is capable of suppressing Glu exocytosis from both MF and non-MF synaptosomes. These results are consistent with the hypothesis that Dyn peptides and Glu are co-released from hippocampal MF terminals.

Inhibition of glutamate release: a potential mechanism of action for the anticonvulsant U-54494A in the guinea pig hippocampus.

U-54494A, a 1,2-diamine, is a potent inhibitor of glutamate release in a synaptosomal preparation that is highly enriched with hippocampal mossy fiber (MF) nerve endings. At a concentration of 100 microM, U-54494A significantly reduced the availability of cytosolic free calcium (Ca2+) in depolarized MF-enriched synaptosomes by 30% and inhibited the K(+)-evoked release of endogenous glutamate by 85%. The extent to which glutamate release was inhibited allows us to conclude that U-54494A acts directly on the MF subpopulation of glutamatergic nerve endings in the guinea pig hippocampus. In addition, this anticonvulsant effectively countered the presynaptic facilitation of K(+)-evoked glutamate release that is induced by kainic acid (KA). Thus, while KA (1 mM) by itself nearly doubled the rate of K(+)-evoked glutamate release, there was no net increase in the presence of both KA and U-54494A (100 microM). However, the opposed effects of these two compounds on glutamate release do not appear to be due to a direct interaction. In the presence of U-54494A (100 microM), KA (1 mM) significantly enhanced the K(+)-evoked release of glutamate. Finally, it is demonstrated that the KA-induced enhancement of glutamate release does not require the depolarization-induced entry of extracellular Ca2+.

Domoic acid enhances the K(+)-evoked release of endogenous glutamate from guinea pig hippocampal mossy fiber synaptosomes.

The presynaptic effects of domoic acid (Dom) on hippocampal mossy fiber synaptic transmission were examined using a subcellular fraction enriched in mossy fiber synaptosomes. Domoic acid significantly increased the K(+)-evoked release of endogenous glutamate from superfused guinea pig mossy fiber synaptosomes. The presynaptic facilitation produced by Dom was dose-dependent and was antagonized by the prior application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). At a concentration of 30 microM, both domoic acid and kainic acid significantly increased the extent to which membrane depolarization augmented the availability of cytosolic free calcium in mossy fiber synaptosomes. These results are consistent with the suggestion that domoic acid enhances the release of mossy fiber neurotransmitters in the guinea pig hippocampus through the activation of a CNQX-sensitive presynaptic receptor.