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PubMed1984

Staphylococcus aureus bacteraemia: 400 episodes in St Thomas's Hospital.

Four hundred episodes of Staphylococcus aureus bacteraemia occurred in St Thomas's Hospital from 1969 to 1983, accounting for 17.5% of all episodes of bacteraemia. The mortality was 24%, half attributable to underlying disease, and was highest in patients over 50. Almost 60% of the bacteraemias were acquired in hospital, and the source of the organism was generally obvious, with vascular access sites the most common (37%). Bone and joint infections accounted for 11.5% of episodes and endocarditis for 7%. Most staphylococci were resistant to penicillin only; three isolates were resistant to methicillin and five to fusidic acid. Microbiologists seldom influenced directly the choice of initial antibiotic treatment (though this usually conformed to the hospital's antibiotic prescribing policy) but had considerable influence over definitive treatment, usually cloxacillin or flucloxacillin alone or in combination with fusidic acid. S aureus bacteraemia is easy to identify and treat, though underlying disease may influence the outcome. Efforts should be made to prevent the largely iatrogenic disease.

Adolescent↗

PubMed2002

[Susceptibility of Staphylococcus aureus isolated from blood to 11 antimicrobial agents and a review of the literature].

From November 1998 to February 2000, a total of 91 strains of Staphylococcus aureus isolated from blood were analyzed for their susceptibility to 11 antimicrobial agents using the E-test method. Fifty-two isolates were methicillin-susceptible (MSSA) and 39 were oxacillin-resistant (MRSA). All the MSSA were susceptible to gentamicin, ciprofloxacin, vancomycin, teicoplanin, rifampicin, fusidic acid, quinupristin-dalfopristin and linezolid; 90% were susceptible to erythromycin and 83% to mupirocin. All the MRSA were susceptible to vancomycin, teicoplanin, rifampicin and linezolid; 95% were susceptible to quinupristin-dalfopristin; and 92% to gentamicin, mupirocin, fusidic acid. None of the MRSA were susceptible to erythromycin or ciprofloxacin. The susceptibility of SARM to erythromycin and ciprofloxacin was low, while the susceptibility to the rest of the antimicrobial agents remained active.

Anti-Bacterial Agents↗

PubMed1994

Staphylococcus aureus infection on experimental croton oil-inflamed skin in mice.

Staphylococcus aureus cells were inoculated on the surface of skin inflamed by application of croton oil in cyclophosphamide-treated mice. Skin specimens were taken at 1, 3, 6, 12, and 24 h inoculation and each specimen was examined by microscopy. The S. aureus cells which attached to the surface of the skin immediately after inoculation had invaded the horny layer within 1 h. The cells gradually penetrated deeper into the epidermis. Electron microscopy revealed fibril-like structures around the S. aureus cells and the cells which adhered to the horny layer and fibrin by means of Ruthenium red-positive, fibril-like structures. A combined application of 0.1% gentamicin ointment, 2% fusidic acid ointment, and clobetasol propionate ointment was more effective in decreasing the number of S. aureus cells in the lesions than was an application of clobetasol propionate ointment alone. However, a combined application of 0.1% gentamicin ointment and 2% fusidic acid ointment without clobetasol propionate ointment showed almost the same efficacy as that with clobetasol propionate ointment. Although povidone iodine killed S. aureus in vitro at a concentration of 0.01% (100 micrograms/ml) in 40 s, its in vivo efficacy was limited.

Animals↗

PubMed1978

Determination of antibiotic sensitivities by the Sensititre system.

The Sensititre system provides antibiotics dried in microtitre trays in appropriate concentrations for the determination of minimum inhibitory concentrations (MIC) when organisms are added in liquid culture medium and incubated overnight. Results with a variety of media--for Gram-negative bacilli tested with ampicillin, carbenicillin, cephaloridine, and gentamicin, staphylococci with penicillin, cloxacillin, fusidic acid, and gentamicin, and streptococci with penicillin, ampicillin, cephaloridine, and erythromycin--were usually very similar to those of agar dilution tests. Discrepant results are found in a few situations, and in some cases, especially those involving borderline resistance to fusidic acid and gentamicin among staphylococci and Gram-negative bacilli, we have been unable to suggest modfication to produce the right results. Despite these problems, fortunately few and identifiable, we recommend the system especially for use in laboratories that determine the MICs infrequently.

Anti-Bacterial Agents↗

PubMed1998

Trends in antibiotic resistance of staphylococci over an eight-year period: differences in the emergence of resistance between coagulase positive and coagulase-negative staphylococci.

The antimicrobial susceptibilities of 1058 Staphylococcus aureus and 2,163 coagulase-negative staphylococci (CNS) isolates obtained from clinical specimen between 1988 and 1995, were determined against 13 anti-staphylococcal antibiotics. During the study period the resistance of Staphylococcus aureus to ciprofloxacin, ceftazidime, and norfloxacin increased significantly by 7%, 4%, and 6%, respectively (p < or = 0.001). By comparison, the antibiotic resistance of CNS to ceftazidime, oxacillin, norfloxacin, ciprofloxacin, fusidic acid, and cefoxitin increased by 20%, 17%, 15%, 14%, 12% and 10%, respectively (p < or = 0.001). Invasive and noninvasive S. aureus had similar antibiotic resistance, whereas CNS invasive isolates were more resistant than noninvasive isolates to every antibiotics, except vancomycin and fusidic acid. These differences were significant (p < 0.001) for oxacillin, cefoxitin, and clindamycin. Our observations confirm that staphylococci and particularly CNS isolates show an important rate of increased resistance to the standard antimicrobials used for therapy, and that the rate of emergence of resistance differ considerably between coagulase-positive and coagulase-negative staphylococci.

Anti-Bacterial Agents↗

PubMed1977

Synthesis and properties of nucleoside 5'-phosphoazidates derived from guanosine and adenosine nucleotides: effective on elongation factors G and Tu dependent reactions.

A new type of nucleoside poly (5'-phosphate) analogue, nucleoside 5"-phosphoazidate, with an azido group on the terminal phosphate of GTP, ATP, GDP, GMP, AND AMP, has been synthesized by nucleophilic displacement of the corresponding activated nucleosides by azide ion in yields of 25-45%. Guanosine 5-phosphoazidates is readily photolyzed by ultraviolet light; the corresponding adenosine derivative photolyzes more slowly. Guanosine 5'-O-(2-azidodiphosphate) and guanosine 5"-O-(3-azidotrophosphate) are competitive inhibitors of the formation of the ribosome-EF-G-GDP-fusidic acid complex and of the ribosome-EF-G GTPase. The dissociation constants of the former reaction are calculated to be 27 and 7 micrometer, respectively, or 270 and 73 times that of GDP. In the latter reaction, which is conducted in the absence of fusidic acid, the Ki values are 330 and 28 micrometer, respectively, or 12 and 1 times that of GDP. Guanosine 5"-O-(2-azidodiphosphate) and guanosine 5'-O-(3-azidotriphosphate) also complete with GTP in the formation of the binary complex. EF-Tu-GTP, with respective Kd values of 750 and 75 relative to GTP.

Adenine Nucleotides↗

PubMed1996

Evolution of resistance in Staphylococcus aureus in Australian teaching hospitals. Australian Group on Antimicrobial Resistance (AGAR).

OBJECTIVE: To assess the changes in antibiotic resistances in Staphylococcus aureus, both methicillin-susceptible and methicillin-resistant strains, in Australia. DESIGN: Retrospective review of data collected annually. SETTING: Twenty metropolitan teaching hospitals in the six States of Australia and the Australian Capital Territory from 1988 to 1994. OUTCOME MEASURES: Changes in prevalence and resistance rates of methicillin-resistant S. aureus (MRSA) and methicillin-susceptible strains, based on antibiotic susceptibility testing of clinical isolates of S. aureus. RESULTS: Prevalence of MRSA has remained constant on the eastern seaboard of Australia. A distinctive strain of MRSA emerged in Western Australia which had different antimicrobial susceptibilities. Resistances emerged in MRSA strains from eastern Australia, principally to ciprofloxacin and rifampicin, while resistance to fusidic acid remained stable and resistance to chloramphenicol significantly declined. Resistances in methicillin-susceptible strains remained fairly stable, except for a decline in resistance levels for tetracycline. High levels of resistance were seen to penicillin, moderate levels to erythromycin and low levels to trimethoprim and fusidic acid in methicillin-susceptible strains. CONCLUSIONS: The continued high prevalence of and increasing resistance in MRSA in some Australian hospitals have meant that some strains are now untreatable with oral antibiotics.

Australia↗

PubMed2002

Susceptibility change to antibiotics of Staphylococcus aureus strains isolated from skin infections between July 1994 and November 2000.

We measured the in-vitro susceptibility of 833 Staphylococcus aureus strains, isolated from skin infections at our hospital between July 1994 and November 2000, to 13 antimicrobial agents (ampicillin, methicillin, cephalexin, cefaclor, cefpodoxime proxetil, gentamicin, erythromycin, clindamycin, minocycline, vancomycin, fusidic acid, ofloxacin, and nadifloxacin). The concentrations required to inhibit 50% of the strains (MIC(50)) of all these antimicrobial agents was extremely stable and ranged at levels below 3.13 microg/ml, except for gentamicin; in contrast, the MIC(90) was not uniform. The MIC(90) of vancomycin, fusidic acid, and nadifloxacin was very low and stable. No strain was resistant to vancomycin. The incidence of MRSA was 10%-20%.

Humans↗

PubMed2003

Parental knowledge of topical therapies in the treatment of childhood atopic dermatitis.

Poor adherence with therapy is a major cause of treatment failure in atopic dermatitis. Reasons given are multifactorial, and include fear of real or imaginary side-effects, under-prescribing, failure to renew prescriptions on time, lack of time, and child refusal of therapy. Most important, however, is lack of knowledge about treatment, in particular the use of topical corticosteroid (TCS) therapy. We conducted a questionnaire-based study to determine the level of use and knowledge of commonly prescribed TCS preparations amongst parents or carers of 100 children attending paediatric outpatient clinics. Weakly potent TCSs were the most commonly used (86%), but poorly understood. Only 35 (41%) who had used hydrocortisone were aware that it was weakly potent, and 44% graded it as moderately potent. Of 65 who had used the moderately potent TCS clobetasone butyrate 0.05% (Eumovate); Glaxo Wellcome, Uxbridge, UK), 19 (29%) graded it as potent and eight (12%) as weak. Of 50 who had used betamethasone valerate 0.1% (Betnovate); Glaxo Wellcome, Uxbridge, UK), 42% did not grade it as potent. Understanding of TCS/antimicrobial combinations was generally worse. The hydrocortisone 1%/fusidic acid 2% combination (Fucidin H(R); Leo, Risborough, Bucks, UK) was graded as moderate or strong by 88% of the 74 who had used it. Over half (53%) of the 34 using the combination of clobetasone butyrate 0.05%/nystatin 100000 i.u./g tetracycline 3% (Trimovate); Glaxo Wellcome, Uxbridge, UK) assumed that it was a potent TCS. Forty-nine had used Fucibet (betamethasone valerate 0.1%, fusidic acid 2%; Leo, Risborough, Bucks, UK) but 34.5% did not grade it as potent. There was poor knowledge of the strengths of some of the most commonly used TCSs, and all steroid/antimicrobial combinations were perceived as being of greater potency than the constituent steroid alone. Fusidic acid was thought to be a steroid by almost half (46.9%) of the respondents. The packaging of the different products by some pharmaceutical companies is remarkably similar and labelling contains information on the compound and percentage rather than potency of the TCS. This may be a source of confusion. We recommend that manufacturers clearly label TCS products by potency as mild, moderate, potent or very potent and that packaging is sufficiently different for each strength of TCS or emollient to avoid confusion. In order to achieve optimal topical treatment for atopic dermatitis, patients and their carers must receive adequate information and training in how and when to use topical therapies in conjunction with written care plans.

Administration, Topical↗

PubMed1975

Synthesis of guanosine 5'-di- and -triphosphate derivatives with modified terminal phosphates: effect on ribosome-elongation factor G-dependent reactions.

A series of GTP and GDP analogues modified in the terminal phosphate has been synthesized and their activities were investigated in elongation factor G dependent reactions. All of the analogues, with the exception of guanosine 5'-O-(3-thiotriphosphate), were not hydrolyzed by EF-G and ribosomes, but were competitive inhibitors of the ribosome-dependent EF-G GTPase. The most active inhibitors were P3-fluoro P1-5'-guanosine triphosphate and P3-methyl P1-5'-guanosine triphosphate with a Ki of 1.0 X 10(-6) and 2.5 X 10(-6) M, respectively. The activity of the GTP alkyl ester derivatives decreased with increasing number of carbon atoms in the side chain. GTP analogues were much more effective inhibitors than the corresponding GDP derivatives. This points out the necessity of the presence of at least three negative charges in the phosphate chain of the nucleotide for an effective interaction with the active site of the ribosomal EF-G GTPase. Guanosine 5'-O-(3-thiotriphosphate), which was hydrolyzed at one-third the rate of GTP, was able to support poly(U)-directed poly(phenylalanine) polymerization. Possible mechanisms of ribosome-EF-G GTP hydrolysis that arise from our results are discussed. Activity of the nucleotide analogues in EF-G-ribosome complex formation compared well with their ability to inhibit ribosome-dependent EF-G GTPase, P3-fluoro P1-5'-guanosine triphosphate and P3-methyl P1-5'-guanosine triphosphate being again the most effective ones. The stabilizing action of fusidic acid on the EF-G-ribosome complex formation induced by the various nucleotides could not be correlated to any of the structural modifications of the substrate. Guanylyl methylene diphosphonate was displaced more readily than GDP from the EF-G-ribosome complex by GTP analogues insensitive to fusidic acid.

Escherichia coli↗

PubMed1981

Biosynthesis of vitamin B-12. Part I. Role of the ribosomal proteins in vitamin B-12 biosynthesis.

1. 70 S ribosomes isolated from strains of Escherichia coli 113-3, K12 and B take part in vitamin B-12 biosynthesis from AdoCbi-GDP, NAD and dimethylbenzimidazole in the presence of enzymes of the cytosol fraction. 2. 70 S ribosomes from E.coli 113-3 bind Ado[58Co]Cbi-GDP. This reaction is independent of fusidic acid. 3. Proteins from 5 S RNA complex as well as l3 protein isolated from E.coli 113-3 ribosomes catalyze vitamin B-12 biosynthesis. The main catalytic function in this reaction is preformed by protein L18. 4. Vitamin B-12 biosynthesis proceeding in the presence of isolated ribosomal proteins is inhibited by fusidic acid, chloramphenicol and vernamycin but not by erythromycin. 5. Vitamin B-12 synthesized in the presence of isolated ribosomal proteins is biologically active.

Anti-Bacterial Agents↗

PubMed1977

Interaction of elongation factor 2 from wheat germ with guanosine nucleotides and ribosomes.

1. The amino acid composition of wheat germ EF2 differs to some extent from that of elongation factors from mammals and bacteria. 2. The purified wheat germ EF2, similarly as the factors from other sources, is active in the: EF1-dependent polymerization of phenylalanine; ribosome-dependent GTP hydrolysis; binding of guanosine nucleotides; and ADP-ribosylation in the presence of diphtheria toxin. Fusidic acid at a concentration of 1 mM inhibits all these EF2-dependent reactions. 3. Diphtheria toxin in the presence of NAD+ inhibits polymerization of phenylalanine but does not effect GTP binding to EF2. 4. Binding of GDP to wheat germ EF2 is inhibited by ribosomes. During interaction with ribosomes, GTP in EF2-GTP complex is rapidly hydrolysed to GDP. Both GTP and 5'-guanylmethylenediphosphonate competitively inhibit formation of the ribosome-EF2-GDP complex due to the replacement of GDP from the complex. The latter is stabilized by fusidic acid.

Adenosine Diphosphate↗

PubMed1997

Review article: treatment of Clostridium difficile infection.

AIM: A systematic review of controlled trials of therapy of Clostridium difficile intestinal infection using methodology described by the Cochrane Collaboration. METHODS: Trials were identified by searching computer databases over the years 1978-1996. Trials were included if they were (a) prospective randomized, controlled trials and (b) included patients with symptomatic disease. The primary end-point was clinical resolution of diarrhoea. Secondary end-points were clinical relapse and stool clearance of C. difficile and C. difficile toxin. RESULTS: Nine trials (469 patients) satisfying the inclusion criteria were identified. Two trials were placebo controlled. Six trials compared vancomycin to other antibiotics (fusidic acid, bacitracin, teicoplanin and metronidazole). For clinical resolution response rates ranged from 21 (placebo) to 100% (vancomycin). On pooling the trials, no antibiotic showed clear therapeutic superiority. Rates of clinical relapse ranged from 5 to 42%. Only one trial showed significant advantage of one antibiotic over another for prevention of relapse (teicoplanin vs. fusidic acid). CONCLUSION: The published data are limited, and further studies are required.

Anti-Bacterial Agents↗

PubMed1991

Pharmacologic enhancement or suppression of phagocytosis by bovine neutrophils.

Sixty-three drugs, belonging to 10 chemical classes, were tested in vitro to determine effects on phagocytosis of 32P-labeled Staphylococcus aureus by neutrophils isolated from milk. Within each class, the number of antibiotics tested were: nonsteroidal anti-inflammatory drugs (NSAID; 8), peptolids (2), aminoglycosides (8), tetracyclines and fusidic acid (4), beta-lactam antibiotics (25), secretolytic agents (2), macrolides (5), polypeptides (2), and antibacterial quinolones (8). Percentage of phagocytosis was determined after incubating (2 hours at 37 C) 12.5 x 10(6) viable neutrophils, 200 x 10(6) 32P-labeled S aureus with antibiotics and 5% skimmed milk. Concentrations of antibiotics tested were 1,000, 500, and 10 micrograms/ml of incubation media. When compared with nonantibiotic controls at the highest drug concentration, the NSAID acetylsalicylic acid and centrophenoxine increased phagocytosis 23.2 and 8.8%, respectively, and benzydamine, indomethacin, phenylbutazone, ibuprofen, and acetominophen decreased phagocytosis 22.8, 14.2, 9.8, 27.0, and 18.2%, respectively. The peptolids novobiocin and pristinamycin decreased phagocytosis 24.5 and 22.0%, respectively. The aminoglycosides tobramycin, amikacin, and gentamicin decreased phagocytosis 21.1, 15.4, and 19.2%, respectively. For the tetracyclines and fusidic acid, minocycline and doxycycline decreased phagocytosis 39.8 and 54.2%, respectively. The beta-lactam antibiotics carfecillin, cephapirin sodium, and cephacetrile sodium decreased phagocytosis 11.2, 12.8, and 23.8%, respectively. The secretolytic agent, bromhexin, increased phagocytosis 10.8%. These data indicate that the potential for enhanced phagocytosis exists through use of some NSAID, and for depressed phagocytosis through use of aminoglycosides, peptolids, tetracyclines, and beta-lactams, as well as certain other NSAID.

Animals↗

PubMedDate not supplied

[Sensitivity to antibiotics in coagulase-negative staphylococci isolated from patients with central venous catheters].

We examined 25 coagulase-negative staphylococci isolated from children, of whom 17 with leukaemia and 8 with terminal renal failure. Strain identification performed by api Staph system revealed the presence of S. epidermidis in 21 children, S. hominis in 3 patients and S. haemolyticus in 1 patient. By diffusion method we examined the activity of penicillin, methicillin, cephalexin, cephtriaxon, lincomycin, erythromycin, vancomycin, co-trimoxasol, gentamicin, amikacin, chloramphenicol, rifampicin and fusidic acid. MICs of seven antibiotics were obtained by agar dilution method. MIC50 and MIC90 were as follows: /ml Methicillin 3.13 mg/ml and 50 mg/ml, lincomycin 100 mg/ml and 100 mg/ml, gentamicin 25 mg/ml and 100 mg/ml, chloramphenicol 6.25 mg/ml and 50 mg/ml, amikacin 1.56 mg/ml and 100 mg/ml, rifampicin 0.09 mg/ml and 12.5 mg/ml, fusidic acid 6.25 mg/ml and 12.5 mg/ml, vancomycin 1.56 mg/ml and 3.13 mg/ml. These data show that the examined strains are highly resistant to numerous antibiotics. Thirty six percent of all strains were resistant to methicillin, 88% to lincomycin, 60% to gentamicin, 52% to chloramphenicol, 24% to amikacin, 52% to rifampicin and 56% to fuscidic acid. All the examined strains were sensitive to vancomycin.

Adolescent↗

PubMed2004

Effect of hospitalization and antimicrobial therapy on antimicrobial resistance of colonizing Staphylococcus epidermidis.

Endogenous infections with multi-resistant S. epidermidis are among the leading causes of nosocomial infections. The effect of hospitalization and antimicrobial therapy on antimicrobial resistance of colonizing staphylococci was determined from swabs of the nose, hand, axilla and groin from 157 patients on one day. Hospitalization for >72 hours, compared with <72 hours, was associated with a higher percentage of isolates resistant to oxacillin (56% versus 19%), gentamicin (40% versus 15%), trimethoprim (36% versus 17%), clindamycin (56% versus 17%), and fusidic acid (20% versus 4%; p < 0.01 for all), but not to rifampicin (6% versus 1%) or fosfomycin (43% versus 34%, p > 0.05 for both). Concurrent antimicrobial therapy resulted in increased resistance to oxacillin (61% versus 28%), gentamicin (43% versus 20%), and clindamycin (60% versus 26%; p < 0.01 for all), but not to trimethoprim (39% versus 23%), fusidic acid (19% versus 9%), rifampicin (6% versus 3%), or fosfomycin (46% versus 38%, p > 0.05 for all). The increase in resistant isolates was not independent, since hospitalization and antimicrobial therapy were correlated (p < 0.001). After adjustment for potential risk factors such as diabetes mellitus, central venous catheters, and hemodialysis, the odds ratio for oxacillin resistance was 2.8-3.6. None of the risk factors showed statistically significant results, except for the presence of neoplastic disease, which had a significant interaction (P=0.035). The within-subgroup odds ratios for patients with and without neoplasm were 4.2 (95% CI, 2.3-5.7) and 2.1 (95% CI, 0.78-3.12), respectively. These results show that hospitalization for more than three days, with or without antimicrobial therapy, and the presence of neoplastic disease are associated with increased antimicrobial resistance in colonizing S. epidermidis.

Age Distribution↗

PubMed2006

Effect on infection resistance of a local antiseptic and antibiotic coating on osteosynthesis implants: an in vitro and in vivo study.

The purpose of this study was to acquire information about the effect of an antibacterial and biodegradable poly-L-lactide (PLLA) coated titanium plate osteosynthesis on local infection resistance. For our in vitro and in vivo experiments, we used six-hole AO DC minifragment titanium plates. The implants were coated with biodegradable, semiamorphous PLLA (coating about 30 microm thick). This acted as a carrier substance to which either antibiotics or antiseptics were added. The antibiotic we applied was a combination of Rifampicin and fusidic acid; the antiseptic was a combination of Octenidin and Irgasan. This produced the following groups: Group I: six-hole AO DC minifragment titanium plate without PLLA; Group II: six-hole AO DC minifragment titanium plate with PLLA without antibiotics/antiseptics; Group III: six-hole AO DC minifragment titanium plate with PLLA + 3% Rifampicin and 7% fusidic acid; Group IV: six-hole AO DC minifragment titanium plate with PLLA + 2% Octenidin and 8% Irgasan. In vitro, we investigated the degradation and the release of the PLLA coating over a period of 6 weeks, the bactericidal efficacy of antibiotics/antiseptics after their release from the coating and the bacterial adhesion of Staphylococcus aureus to the implants. In vivo, we compared the infection rates in white New Zealand rabbits after titanium plate osteosynthesis of the tibia with or without antibacterial coating after local percutaneous bacterial inoculations at different concentrations (2 x 10(5)-2 x 10(8)): The plate, the contaminated soft tissues and the underlying bone were removed under sterile conditions after 28 days and quantitatively evaluated for bacterial growth. A stepwise experimental design with an "up-and-down" dosage technique was used to adjust the bacterial challenge in the area of the ID50 (50% infection dose). Statistical evaluation of the differences between the infection rates of both groups was performed using the two-sided Fisher exact test (p < 0.05). Over a period of 6 weeks, a continuous degradation of the PLLA coating of 13%, on average, was seen in vitro in 0.9% NaCl solution. The elution tests on titanium implants with antibiotic or antiseptic coatings produced average release values of 60% of the incorporated antibiotic or 62% of the incorporated antiseptic within the first 60 min. This was followed by a much slower, but nevertheless continuous, release of the incorporated antibiotic and antiseptic over days and weeks. At the end of the test period of 42 days, 20% of the incorporated antibiotic and 15% of the incorporated antiseptic had not yet been released from the coating. The antibacterial effect of the antibiotic/antiseptic is not lost by integrating it into the PLLA coating. The overall infection rate in the in vivo investigation was 50%. For Groups I and II the infection rate was both 83% (10 of 12 animals). In Groups III and IV with antibacterial coating, the infection rate was both 17% (2 of 12 animals). The ID50 in the antibacterial coated Groups III and IV was recorded as 1 x 10(8) CFU, whereas the ID50 values in the Groups I and II without antibacterial coating were a hundred times lower at 1 x 10(6) CFU, respectively. The difference between the groups with and without antibacterial coating was statistically significant (p = 0.033). Using an antibacterial biodegradable PLLA coating on titanium plates, a significant reduction of infection rate in an in vitro and in vivo investigation could be demonstrated. For the first time, to our knowledge, we were able to show, under standardized and reproducible conditions, that an antiseptic coating leads to the same reduction in infection rate as an antibiotic coating. Taking the problem of antibiotic-induced bacterial resistance into consideration, we thus regard the antiseptic coating, which shows the same level of effectiveness, as advantageous.

Absorbable Implants↗

PubMed1996

Delivery of systemic regular insulin via the ocular route in dogs.

Regular porcine insulin was administered as eye drops to eight healthy, euglycemic dogs. Insulin was applied alone and in combination with six different permeation enhancers. Serum glucose and insulin were monitored for four hours following the eye drops. Significant changes in serum glucose and/or insulin occurred when the insulin was administered with 0.5% saponin, 0.5% and 1% BL-9, 0.5% and 1% dodecylmaltoside, and 0.5% and 1% tetradecylmaltoside. Insulin delivered alone and in the presence of 0.5% Brij-78 and 0.5% fusidic acid did not significantly alter glucose and/or insulin concentrations. Solutions containing 0.5% saponin induced signs of ocular irritation for approximately 5 minutes. Transient blinking (1-5 mins.) was encountered with solutions containing 1% BL-9, 1% dodecylmaltoside, and 1% tetradecylmaltoside. No ocular signs occurred with the administration of insulin alone or with 0.5% solutions of Brij-78, fusidic acid, BL-9, dodecylmaltoside, and tetradecylmaltoside. This study demonstrated that short-acting insulin is systemically absorbed in dogs via the ocular route when applied with certain emulsants.

Absorption↗