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PubMed2000

Macrolides and clindamycin suppress the release of Shiga-like toxins from Escherichia coli O157:H7 in vitro.

We investigated the effects of antimicrobial agents fosfomycin (FOS), cefdinir (CDIN), levofloxacin (LEVX), rokitamycin (ROK), roxithromycin (ROX), and clindamycin (CLI) on the release of Shiga-like toxins (SLTs) by enterohaemorrhagic Escherichia coli (EHEC). EHEC was cultured for 14 h in the presence of ROX, ROK or CLI at sub-minimum inhibitory concentrations (subMICs) of 1.56-6.25 mg/l, followed by assay of the level of SLTs in the supernatants using cytotoxicity assay and reversed passive latex agglutination method. Exposure to ROX, ROK or CLI reduced the amount of released SLTs compared with untreated control cultures (P<0.05). These agents however, did not decrease the number of viable EHEC, indicating the importance of bactericidal agents. When the bacteria was exposed to CDIN, FOS or LEVX, the level of SLTs in the culture supernatant increased with the destruction of bacterial cells in the order of CDIN, FOS, LEVX. When 0.5 mg/l of LEVX was added to cultures with or without pretreatment using ROX, ROK, or CLI, the release of SLTs was reduced by this pretreatment (P<0.05). These results may have clinical implications for the treatment of EHEC infection.

Animals↗
PubMed2001

Biosynthesis of the orthosomycin antibiotic avilamycin A: deductions from the molecular analysis of the avi biosynthetic gene cluster of Streptomyces viridochromogenes Tü57 and production of new antibiotics.

BACKGROUND: Streptomyces viridochromogenes Tü57 is the producer of avilamycin A. The antibiotic consists of a heptasaccharide side chain and a polyketide-derived dichloroisoeverninic acid as aglycone. Molecular cloning and characterization of the genes governing the avilamycin A biosynthesis is of major interest as this information might set the direction for the development of new antimicrobial agents. RESULTS: A 60-kb section of the S. viridochromogenes Tü57 chromosome containing genes involved in avilamycin biosynthesis was sequenced. Analysis of the DNA sequence revealed 54 open reading frames. Based on the putative function of the gene products a model for avilamycin biosynthesis is proposed. Inactivation of aviG4 and aviH, encoding a methyltransferase and a halogenase, respectively, prevented the mutant strains from producing the complete dichloroisoeverninic acid moiety resulting in the accumulation of new antibiotics named gavibamycins. CONCLUSIONS: The avilamycin A biosynthetic gene cluster represents an interesting system to study the formation and attachment of unusual deoxysugars. Several enzymes putatively responsible for specific steps of this pathway could be assigned. Two genes encoding enzymes involved in post-PKS tailoring reactions were deleted allowing the production of new analogues of avilamycin A.

Anti-Bacterial Agents↗
PubMed2004

Inhibition of Streptococcus suis adhesion by dendritic galabiose compounds at low nanomolar concentration.

A series of mono-, di-, and tetravalent galabiose (Galalpha1-4Gal) compounds were synthesized in good yields by coupling of a general carboxylic acid-bearing sugar building block to dendritic scaffolds based on the 3,5-di-(2-aminoethoxy)benzoic acid branching unit. Furthermore, a poly(amidoamine)- (PAMAM-) based dendritic galabioside was synthesized containing eight galabiose units. All galabiosides were tested in a hemagglutination assay and a surface plasmon resonance (SPR) competition assay in order to establish their potency in the binding to the bacterial Gram-positive pathogen Streptococcus suis. A monovalent galabioside containing a short spacer was used as a reference compound in all the assays. Variations in the scaffold as well as in the spacer arms were introduced to determine their influence on the inhibition. The best inhibitor of hemagglutination was an octavalent galabioside with a minimal inhibitory concentration (MIC) of 0.3 nM, to the best of our knowledge the first example of inhibition of bacterial binding by a soluble carbohydrate at a subnanomolar concentration.

Bacterial Adhesion↗
PubMed2002

Infection rates in surgical neonates and infants receiving parenteral nutrition: a five-year prospective study.

We performed a prospective, observational, cohort study on 208 surgical neonates and infants between 1992 and 1997. Surveillance cultures of the oropharynx and rectum were obtained at the start of parenteral nutrition and thereafter twice weekly. Blood cultures were taken on clinical indication only. Microbial translocation was diagnosed when the micro-organisms in the blood were not distinguishable from those carried in the oropharynx and/or rectum. Liver function was monitored weekly and when septicaemia was suspected. The incidence of septicaemia was 15%. The predominant micro-organisms (86%) were the low-level pathogens, coagulase-negative staphylococci and enterococci. Potential pathogens, including aerobic Gram-negative bacilli, were responsible for the remainder. Microbial translocation was responsible for 84% of septicaemic episodes in 76% of patients. The potential pathogens caused septicaemia significantly later than coagulase-negative staphylococci, at a time when liver function was significantly more impaired. In neonates and infants receiving parenteral nutrition, septicaemia is mainly a gut-derived phenomenon and requires novel strategies for prevention.

Bacteremia↗
PubMed2001

The efficacy and safety of two oral moxifloxacin regimens compared to oral clarithromycin in the treatment of community-acquired pneumonia.

An international multi-centre, randomized, prospective, double-blind study compared oral moxifloxacin (200 mg or 400 mg once daily for 10 days) with oral clarithromycin (500 mg, twice daily for 10 days) in the treatment of community-acquired pneumonia (CAP). The clinical success rate in the evaluable population at the primary efficacy assessment, 3-5 days after the end of study treatment, was 93.9% in patients treated with 200 mg moxifloxacin; 94.4%, with 400 mg moxifloxacin; and 94.3%, with clarithromycin. Clinical success rates were maintained at follow-up, 21-28 days after the end of treatment: 90.7% (200 mg moxifloxacin), 92.8% (400 mg moxifloxacin) and 92.2% (clarithromycin). The 95% confidence intervals indicated that all three treatment regimens were equally effective in treating CAP. At follow-up, the 400 mg moxifloxacin dose had a slightly higher observed cure rate than the 200 mg moxifloxacin dose, but this was not statistically significant. The most frequently isolated pathogens were Streptococcus pneumoniae (42%), Haemophilus influenzae (19%), Haemophilus parainfluenzae (10%), Moraxella catarrhalis (6%), Klebsiella pneumoniae (5%) and Staphylococcus aureus (4%). The bacteriological success rate (eradication and presumed eradication) was 72.5% (29/40) for 200 mg moxifloxacin, 78.7% (37/47) for 400 mg moxifloxacin and 70.7% (29/41) for clarithromycin. The adverse event profile was comparable between the three treatment groups. Most adverse events, possibly or probably related to the study drug, were generally mild or moderate in severity and mostly related to the digestive system: diarrhoea, nausea and abdominal pain in 200 mg moxifloxacin patients; diarrhoea, liver function abnormalities and nausea in 400 mg moxifloxacin patients and liver function abnormalities, diarrhoea, nausea and taste perversion in clarithromycin patients. Study drugs were discontinued because of adverse events in 7/229 (3%) patients treated with 200 mg moxifloxacin, 11/224 (5%) with moxifloxacin 400 mg and 11/222 (5%) with clarithromycin. In all assessments, moxifloxacin was at least as effective clinically, and as well tolerated as clarithromycin in the treatment of CAP. Bacteriological success rates in moxifloxacin-treated patients were greater than those of clarithromycin. Moxifloxacin, given once daily, is free of many drug-drug interactions and requires no dosage adjustments in most renal hepatic deficient patients.

Administration, Oral↗
PubMed1970

Nitrogenaseless mutants of Azotobacter vinelandii.

Mutants of Azotobacter which grow normally on excess ammonia under a variety of conditions and which grow slowly or not at all on atmospheric nitrogen have been isolated. Extracts of these strains have low or no detectable nitrogenase activity. There are three classes of mutants. Cell-free preparations of members of the first class possess an enhancement factor (EF+) which stimulates wild-type nitrogenase in vitro. Homogenates of members of the second class possess an enhanceable factor (EF-) which complements in vitro with extracts of the first class of mutants to give substantial nitrogenase activity. Preparations of members of the third class contain neither EF+ nor EF- activity. EF+ and EF- are repressed by the same conditions that repress nitrogenase. Molybdenum-deficient cells of the second class of mutants do not appear to contain EF- activity, but molybdenum deficient cells of the first class of mutants contain EF+. Because of these observations, EF+ is tentatively equated to azoferredoxin and EF- to molybdoferredoxin.

Azotobacter↗
PubMed1988

Isolation and analysis of ketoconazole resistant mutants of Saccharomyces cerevisiae.

Nine mutants of Saccharomyces cerevisiae which are resistant to ketoconazole, have been isolated and characterized. In each case the mutation is nuclear in origin and allelic to a previously described mutation, erg3, which gives rise to a block in the delta 5-6 desaturation step of ergosterol biosynthesis. The significance of this second site mutation to the point of inhibitory action of ketoconazole, that is the P-450-mediated C-14 demethylation of lanosterol, is discussed.

Cytochrome P-450 Enzyme System↗
PubMed1996

Quinolone resistance mutations in the gyrA gene of clinical isolates of Salmonella.

S. typhimurium AlhR, S. enteritidis OulR, and S. hadar GueR resistant to fluoroquinolones (QR), ciprofloxacin MICs, 0.25 to 1 microgram/ml; norfloxacin MICs, 0.5 to 4 micrograms/ml; nalidixic acid MIC, 256 micrograms/ml were isolated from urinary tract infections (AlhR and OulR) during FQ therapy in immunocompromised patients infected by the parent FQ-susceptible strains (AlhS and OulS) (ciprofloxacin MICs, 0.032-0.063; norfloxacin MICs, 0.125-0.25; nalidixic acid MICs, 4-8) or from intestinal infection (GueR). Transformation of AlhR, OulR, and GueR by plasmid pJSW101 carrying the wild-type gyrA gene of Escherichia coli resulted in complementation (nalidixic acid MICs, 4 to 8), proving that these strains had a gyrA mutation. A 800-bp fragment of gyrA from the five strains was amplified by PCR. Direct DNA sequencing of 252-bp region of this fragment identified a single point mutation leading to a substitution Ser-83 to Tyr in AlhR and to a substitution Ser-83 to Phe in OulR and in GueR. These results emphasize the potential risk of selection of FQ-resistant Salmonella during FQ therapy in immunocompromised patients and suggest that these strains differ from the parent strains at least by one mutation in the gyrA gene. They also confirm the role of substitutions in position 83 of gyrA in FQ-resistant clinical isolates of Salmonella.

Anti-Infective Agents↗
PubMed1983

Ceftazidime as a single agent in the treatment of severe Pseudomonas aeruginosa infections.

Ceftazidime was administered intravenously in doses of 1 to 6 g/day to 21 patients with serious Pseudomonas aeruginosa infections (12 pulmonary, 6 septicaemias, 3 urinary tract infections). Mean MIC was 1.0 mg/l. Eighteen (86%) of the 21 patients responded satisfactorily (cured or improved). The selection or emergence of resistant organisms during treatment (mostly Candida, Staphylococcus aureus, and enterococci) was noted in 6 patients. Toxicity was minimal (eosinophilia and reversible mild liver function abnormalities).

Adolescent↗
PubMed1985

The effect of a range of antimicrobial drugs on the haemagglutination of two clinical isolates from urinary tract infections.

A range of nine common antimicrobial drugs were tested for their effect on adhesion of the mannose-resistant haemagglutination-positive Proteus vulgaris strain BH77 and Escherichia coli strain BH121, isolated from patients with urinary tract infections. Minimum inhibitory concentrations of the antimicrobials for these strains were determined in Mueller-Hinton broth and the effect of each antimicrobial, at the quarter MIC values, on the haemagglutination of the strains was then determined. Haemagglutination could only be prevented by inhibitors of protein synthesis. After the introduction of an R-plasmid into strain BH121 this effect was annihilated. When the new MICs were determined, the inhibition was still observed at the new quarter MIC values.

Anti-Infective Agents, Urinary↗
PubMed1998

Chromobacterium violaceum infection.

Chromobacterium violaceum infection is confined to the tropical and subtropical areas, with almost all reported cases occurring in the Southeast. The most common feature of this infection is sepsis, followed by cutaneous involvement and liver abscesses. Treatment consists of surgical drainage of purulent collections and appropriate antimicrobial therapy, such as chloramphenicol, gentamicin, imipenem, trimethoprim-sulfamethoxazole, or ciprofloxacin. Although C violaceum infection is rare, it is potentially fatal and remains an important entity for clinicians to suspect and treat appropriately.

Anti-Bacterial Agents↗
PubMed2000

Characterisation of isolates of Haemophilus paragallinarum from Indonesia.

OBJECTIVE: To characterise 18 isolates of Haemophilus paragallinarum isolated from chickens in Indonesia. PROCEDURE: The isolates were identified to species level by traditional phenotypic methods. Six of the isolates were also identified by a species-specific polymerase chain reaction. Fourteen of the isolates were examined for resistance to a panel of seven antimicrobial agents using a disc diffusion method. All 18 isolates were serotyped according to the Page scheme using reference antisera in a haemagglutination inhibition test. RESULTS: Four of the 18 isolates were obtained from indigenous (kampung) chickens, with the remainder being from typical intensive poultry production systems. The 18 isolates were obtained from 11 outbreaks that showed the typical clinical signs of infectious coryza and 11 of the isolates were obtained from chickens that had been vaccinated with infectious coryza vaccines. All 18 isolates were confirmed as H paragallinarum by biochemical testing and six isolates were also identified as H paragallinarum by the polymerase chain reaction test. Eleven isolates were resistant to erythromycin and streptomycin, 10 to neomycin, eight to oxytetracycline, five isolates to doxycycline, three to sulphamethoxazoltrimethoprim but only one to ampicillin. Seven isolates were Page serovar A, four were Page serovar B and seven were Page serovar C. CONCLUSION: The presence of all three Page serovars (A, B and C) has been confirmed for the first time in Indonesian chickens. As the majority of the infectious coryza vaccines in use in Indonesia contain only serovar A and C, the presence of serovar B in chickens indicates that the protection by these bivalent vaccines would be reduced. The use of trivalent infectious coryza vaccines that contain serovars A, B and C is recommended for use in Indonesia.

Animals↗
PubMed2006

Reduced susceptibility to polyenes associated with a missense mutation in the ERG6 gene in a clinical isolate of Candida glabrata with pseudohyphal growth.

Little information is available about the molecular mechanisms responsible for polyene resistance in pathogenic yeasts. A clinical isolate of Candida glabrata with a poor susceptibility to polyenes, as determined by disk diffusion method and confirmed by determination of MIC, was recovered from a patient treated with amphotericin B. Quantitative analysis of sterols revealed a lack of ergosterol and an accumulation of late sterol intermediates, suggesting a defect in the final steps of the ergosterol pathway. Sequencing of CgERG11, CgERG6, CgERG5, and CgERG4 genes revealed exclusively a unique missense mutation in CgERG6 leading to the substitution of a cysteine by a phenylalanine in the corresponding protein. In addition, real-time reverse transcription-PCR demonstrated an overexpression of genes encoding enzymes involved in late steps of the ergosterol pathway. Moreover, this isolate exhibited a pseudohyphal growth whatever the culture medium used, and ultrastructural changes of the cell wall of blastoconidia were seen consisting in a thinner inner layer. Cell wall alterations were also suggested by the higher susceptibility of growing cells to Calcofluor white. Additionally, complementation of this isolate with a wild-type copy of the CgERG6 gene restored susceptibility to polyenes and a classical morphology. Together, these results demonstrated that mutation in the CgERG6 gene may lead to a reduced susceptibility to polyenes and to a pseudohyphal growth due to the subsequent changes in sterol content of the plasma membrane.

Antifungal Agents↗
PubMed1989

Influence of fluoroquinolones on expression and function of P fimbriae in uropathogenic Escherichia coli.

P fimbriae are the major adhesins mediating attachment of pyelonephritogenic Escherichia coli to urinary tract tissues, and they therefore constitute a recognized virulence factor. In this work, the effect of fluoroquinolones on P fimbria expression and function in E. coli SS142 and C1212 was assessed. Ciprofloxacin, fleroxacin, and norfloxacin were compared with their precursor nalidixic acid and with trimethoprim in sublethal concentrations ranging from 1/32 to 1/4 of the MIC. Fimbria function was assessed in a standard hemagglutination assay and in a parallel hemagglutination inhibition assay in which the tier of antifimbrial antiserum necessary to inhibit hemagglutination by SS142 was determined. Adhesion of antibiotic-exposed bacteria to human uroma T24 cells in suspension was also measured. Fimbria production was quantitated in an inhibition enzyme-linked immunosorbent assay. Trimethoprim produced a dose-dependent decrease of three to four hemagglutination titers for both strains and a decline in the antiserum titer from 1:16 (control) to 1:128 (1/4 MIC) for E. coli SS142. Adherence exhibited similar decrements from 130 +/- 28 (control) to 16 +/- 3 (1/4 MIC) and from 83 +/- 19 (control) to 30 +/- 11 (1/4 MIC) E. coli cells per uroepithelial cell (mean +/- standard error) for SS142 and C1212, respectively (P less than 0.015). By enzyme-linked immunosorbent assay, the inhibition following exposure decreased in a dose-dependent manner from 31% (control) to 8% (1/4 MIC). By contrast, none of the quinolones produced significant changes in the parameters assessed above. At sublethal concentrations, trimethoprim decreased fimbria production. Following exposure to fluoroquinolones, however, E. coli expressed morphologically and functionally intact P fimbriae.

4-Quinolones↗
PubMed2000

Inactivation of the ampD gene in Pseudomonas aeruginosa leads to moderate-basal-level and hyperinducible AmpC beta-lactamase expression.

It has been shown in enterobacteria that mutations in ampD provoke hyperproduction of chromosomal beta-lactamase, which confers to these organisms high levels of resistance to beta-lactam antibiotics. In this study, we investigated whether this genetic locus was implicated in the altered AmpC beta-lactamase expression of selected clinical isolates and laboratory mutants of Pseudomonas aeruginosa. The sequences of the ampD genes and promoter regions from these strains were determined and compared to that of wild-type ampD from P. aeruginosa PAO1. Although we identified numerous nucleotide substitutions, they resulted in few amino acid changes. The phenotypes produced by these mutations were ascertained by complementation analysis. The data revealed that the ampD genes of the P. aeruginosa mutants transcomplemented Escherichia coli ampD mutants to the same levels of beta-lactam resistance and beta-lactamase expression as wild-type ampD. Furthermore, complementation of the P. aeruginosa mutants with wild-type ampD did not restore the inducibility of beta-lactamase to wild-type levels. This shows that the amino acid substitutions identified in AmpD do not cause the altered phenotype of AmpC beta-lactamase expression in the P. aeruginosa mutants. The effects of AmpD inactivation in P. aeruginosa PAO1 were further investigated by gene replacement. This resulted in moderate-basal-level and hyperinducible expression of beta-lactamase accompanied by high levels of beta-lactam resistance. This differs from the stably derepressed phenotype reported in AmpD-defective enterobacteria and suggests that further change at another unknown genetic locus may be causing total derepressed AmpC production. This genetic locus could also be altered in the P. aeruginosa mutants studied in this work.

Ampicillin↗
PubMed2001

Impact of the order of initiation of fluconazole and amphotericin B in sequential or combination therapy on killing of Candida albicans in vitro and in a rabbit model of endocarditis and pyelonephritis.

In vitro time-kill studies and a rabbit model of endocarditis and pyelonephritis were used to define the impact that the order of exposure of Candida albicans to fluconazole (FLC) and amphotericin B (AMB), as sequential and combination therapies, had on the susceptibility of C. albicans to AMB and on the outcome. The contribution of FLC-induced resistance to AMB for C. albicans also was assessed. In vitro, AMB monotherapy rapidly killed each of four C. albicans strains; FLC alone was fungistatic. Preincubation of these fungi with FLC for 18 h prior to exposure to AMB decreased their susceptibilities to AMB for 8 to >40 h. Induced resistance to AMB was transient, but the duration of resistance increased with the length of FLC preincubation. Yeast sequentially incubated with FLC followed by AMB plus FLC (FLC-->AMB+FLC) showed fungistatic growth kinetics similar to that of fungi that were exposed to FLC alone. This antagonistic effect persisted for at least 24 h. Simultaneous exposure of C. albicans to AMB and FLC [AMB+FLC(simult)] demonstrated activity similar to that with AMB alone for AMB concentrations of > or =1 microg/ml; antagonism was seen using an AMB concentration of 0.5 microg/ml. The in vitro findings accurately predicted outcomes in our rabbit infection model. In vivo, AMB monotherapy and treatment with AMB for 24 h followed by AMB plus FLC (AMB-->AMB+FLC) rapidly sterilized kidneys and cardiac vegetations. AMB+FLC(simult) and FLC-->AMB treatments were slower in clearing fungi from infected tissues. FLC monotherapy and FLC-->AMB+FLC were both fungistatic and were the least active regimens. No adverse interaction was observed between AMB and FLC for the AMB-->FLC regimen. However, FLC-->AMB treatment was slower than AMB alone in clearing fungi from tissues. Thus, our in vitro and in vivo studies both demonstrate that preexposure of C. albicans to FLC reduces fungal susceptibility to AMB. The length of FLC preexposure and whether AMB is subsequently used alone or in combination with FLC determine the duration of induced resistance to AMB.

Amphotericin B↗
PubMed2002

Novel Saccharomyces cerevisiae screen identifies WR99210 analogues that inhibit Mycobacterium tuberculosis dihydrofolate reductase.

The ongoing selection of multidrug-resistant strains of Mycobacterium tuberculosis has markedly reduced the effectiveness of the standard treatment regimens. Thus, there is an urgent need for new drugs that are potent inhibitors of M. tuberculosis, that exhibit favorable resistance profiles, and that are well tolerated by patients. One promising drug target for treatment of mycobacterial infections is dihydrofolate reductase (DHFR; EC 1.5.1.3), a key enzyme in folate utilization. DHFR is an important drug target in many pathogens, but it has not been exploited in the search for drugs effective against M. tuberculosis. The triazine DHFR inhibitor WR99210 has been shown to be effective against other mycobacteria. We show here that WR99210 is also a potent inhibitor of M. tuberculosis and Mycobacterium bovis BCG growth in vitro and that resistance to WR99210 occurred less frequently than resistance to either rifampin or isoniazid. Screening of drugs with M. tuberculosis cultures is slow and requires biosafety level 3 facilities and procedures. We have developed an alternative strategy: initial screening in an engineered strain of the budding yeast Saccharomyces cerevisiae that is dependent on the M. tuberculosis DHFR for its growth. Using this system, we have screened 19 compounds related to WR99210 and found that 7 of these related compounds are also potent inhibitors of the M. tuberculosis DHFR. These studies suggest that compounds of this class are excellent potential leads for further development of drugs effective against M. tuberculosis.

Antibiotics, Antitubercular↗