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PubMed2000

Lincomycin-induced endotoxin release in Escherichia coli sepsis: evidence for release in vitro and in vivo.

OBJECTIVE: To evaluate the propensity of lincomycin and clindamycin to induce release of endotoxin, the authors investigated endotoxin release in Escherichia coli isolated from a patient who developed septic shock following lincomycin treatment. METHODS: Endotoxin release from the E. coli isolate exposed to lincomycin, clindamycin, and ceftazidime were determined in vitro and in vivo. RESULTS: In vitro, this E. coli released significantly larger amounts of endotoxin after exposure for 6 hours to lincomycin or clindamycin versus no antibiotic; however, endotoxin release with these antibiotics was significantly less than with ceftazidime. There was no significant difference in in vitro endotoxin release between small (8 mg/L) and large (0.5 minimum inhibitory concentration [MIC]) doses of these antibiotics, and 0.5 MICs of lincomycin and clindamycin were 1024 and 256 mg/L, respectively. These results were supported by scanning electron microscopic observations, which demonstrated that lincomycin, clindamycin, and ceftazidime induced formation of filamentous cells. In addition, plasma endotoxin concentrations after treatment for 4 hours with lincomycin, clindamycin, and ceftazidime (5 mg/kg) were at least 20-fold higher than with no antibiotic in an E. coli sepsis rat model. CONCLUSION: Results of this study suggest that the bacteriostatic antibiotics, lincomycin and clindamycin, induce endotoxin release in the treatment of E. coli infections.

Animals↗

PubMed1998

Bioavailability of spiramycin and lincomycin after oral administration to fed and fasted pigs.

The disposition of spiramycin and lincomycin was measured after intravenous (i.v.) and oral (p.o.) administration to pigs. Twelve healthy pigs (six for each compound) weighing 16-43 kg received a dose of 10 mg/kg intravenously, and 55 mg/kg (spiramycin) or 33 mg/kg (lincomycin) orally in both a fasted and a fed condition in a three-way cross-over design. Spiramycin was detectable in plasma up to 30 h after intravenous and oral administration to both fasted and fed pigs, whereas lincomycin was detected for only 12 h after intravenous administration and up to 15 h after oral administration. The volume of distribution was 5.6 +/- 1.5 and 1.1 +/- 0.2 L/kg body weight for spiramycin and lincomycin, respectively. For both compounds the bioavailability was strongly dependent on the presence of food in the gastrointestinal tract. For spiramycin the bioavailability was determined to be 60% and 24% in fasted and fed pigs, respectively, whereas the corresponding figures for lincomycin were 73% and 41%. The maximum plasma concentration of spiramycin (Cmax) was estimated to be 5 microg/mL in fasted pigs and 1 microg/mL only in fed pigs. It is concluded that an oral dose of 55 mg/kg body weight is not enough to give a therapeutically effective plasma concentration of spiramycin against species of Mycoplasma, Streptococcus, Staphylococcus and Pasteurella multocida. The maximum plasma concentration of lincomycin was estimated to be 8 microg/mL in fasted pigs and 5 microg/mL in fed pigs, but as the minimum inhibitory concentration for lincomycin against Actinobacillus pleuropneumoniae and P. multocida is higher than 32 microg/mL a therapeutically effective plasma concentration could not be obtained following oral administration of the drug. For Mycoplasma the MIC90 is below 1 microg/mL and a therapeutically effective plasma concentration of lincomycin was thus obtained after oral administration to both fed and fasted pigs.

Administration, Oral↗

PubMed1994

New aspects of the kinetics of inhibition by lincomycin of peptide bond formation.

We have investigated the inhibition of peptide bond formation by the antibiotic lincomycin, at 150 mM NH4Cl. We have used an in vitro system in which a ribosomal ternary complex, the acetyl[3H] phenylalanine-tRNA-70 S ribosome-poly(U) complex (complex C), reacts with puromycin, forming peptide bonds. Complex C can be considered an analog of the elongating ribosomal complex and puromycin an analog of aminoacyl-tRNA. In a previous study we reported on the kinetics of inhibition by lincomycin at 100 mM NH4Cl. In the present investigation, we find that an increase of the ammonium ion concentration to 150 mM causes profound changes in the kinetic behavior of the system, which can be summarized as follows. First, the association rate for complex C and lincomycin is increased. At a lincomycin concentration of 10 microM the apparent equilibration rate constant is 4.3 min-1 at 100 mM NH4Cl, whereas it becomes 6.7 min-1 at 150 mM. Second, at 150 mM NH4Cl, with increasing concentrations of lincomycin, there is a transition from competitive to mixed-noncompetitive inhibition. The prevailing notion is that lincomycin acts at the ribosomal A-site, a mechanism that agrees only with competitive kinetics (mutually exclusive binding between puromycin and lincomycin). At the molecular level, the change in the kinetics of inhibition that we observe may mean that the mutually exclusive binding between aminoacyl-tRNA and lincomycin is converted to simultaneous binding, as a result of conformational changes occurring in the elongating ribosomal complex.

Binding, Competitive↗

PubMed1975

Microbial kinetics of drug action against gram-positive and gram-negative organisms. III: Effect of lincomycin and clindamycin combinations on Staphylococcus aureus and Escherichia coli.

The functional dependencies of apparent first-order generation rate constants kapp, of drug-affected cultures on drug concentrations indicate that lincomycin and clindamycin possess the same mechanism of action, which is bacteriostatic, against Staphylococcus aureus. Clindamycin also possesses another mechanism of action, which is bactericidal, at high concentration levels. However, clindamycin possesses only one of the two mechanisms of lincomycin action, which is bacteriostatic, against Escherichia coli. The relative potency of action of a clindamycin-lincomycin combination against Staph. aureus is variable, and the effective ratio ranges between 5:1 and 9:1; the effective ratio against E. coli is fixed at 6:1 over a wide concentration range. This difference is attributed to differences in bioavailability and/or binding characteristics of the drugs for bioreceptors, as a consequence of structural modifications in the drug molecules, and to differences in modes of action in the respective organisms. Mixtures containing equipotent fractions of clindamycin and lincomycin show "equivalence" or "indifference" of effects on Staph. aureus. The combined action of the mixtures can be quantitatively predicted from the separate dose-response curves of either component drug alone. Therefore, it is concluded that clindamycin and lincomycin may bind to the same receptor site that is engaged in microbial protein synthesis to inhibit the generation of Staph. aureus. However, combinations of clindamycin and lincomycin are less active than the a priori equipotent concentration of either drug alone in their action against E. coli, demonstrating unequivocally an antagonism of effects. Furthermore, the degree of antagonism is dependent on the order of addition of the drugs, which is attributed to the possibility that clindamycin and lincomycin bind differently on active and allosteric loci of the same receptor site functionally engaged in protein synthesis in E. coli. A rational approach to the quantification and prediction of combined antibiotic action must, therefore, be based not only on the kinetics and mechanisms of action as well as on the dose-response relationship over a wide concentration range for the separate antibiotics but also on the strain and species of the test organism.

Clindamycin↗

PubMed1993

Subcellular location of lincomycin resistance in Nicotiana mutants.

Lincomycin-resistant Nicotiana plumbaginifolia plastid mutants were considered also to carry mitochondrial mutations on the basis of their ability to grow in the dark under selective conditions. To clarify the role of mitochondria, individual protoplasts of the green, lincomycin-resistant N. plumbaginifolia mutant LR400 were microfused with protoplasts of the N. tabacum plastid albino line 92V37, which possesses N. undulata cytoplasm. the production of lincomycin-resistant albino cybrid lines, with N. undulata plastids and recombinant mitochondria, strongly indicated a determining role for mitochondria in the lincomycin resistance. Sequence analysis of the region encompassing putative mutation sites in the 26S rRNA genes from the LR400 and several other lincomycin-resistant N. plumbaginifolia mutants revealed, however, no differences from the wild-type sequence. As an alternative source of the resistance of the fusion products, the N. tabacum fusion partner was also taken into account. Surprisingly, a natural lincomycin resistance of tobacco was detected, which was inherited as a dominant nuclear trait. This result compromises the interpretation of the fusion data suggested above. Thus, to answer the original question definitively, the mutant LR400 was crossed as a female parent with a N. plumbaginifolia line carrying streptomycin-resistant N. tabacum plastids. Calli were then induced from the seedlings. Occasional paternal plastid transmissions were selected as streptomycin-resistant calli on selective medium. These cell lines were shown by restriction enzyme analysis to contain paternal plastids and maternal mitochondria. They were tested for greening and growing ability in the presence of lincomycin. These resistance traits proved to be genetically linked and exclusively located in the plastids.

Base Sequence↗

PubMed2006

Electrochemical study of lincomycin on a multi-wall carbon nanotubes modified glassy carbon electrode and its determination in tablets.

Multi-wall carbon nanotubes (MWNTs) were dispersed in dihexadecylphosphate (DHP), sodium dodecylbenzenesulfonate (SDBS), and Nafion to give a homogeneous and stable suspension, respectively. MWNTs film in different solvents was fabricated onto a glassy carbon electrode (GCE) with an easy and convenient method. It was found that on MWNTs-DHP film lincomycin exhibited a well-defined oxidation peak. The electrochemical behavior of lincomycin at coated GCE was investigated by cyclic voltammetry and chronocoulometry. The MWNTs-DHP film modified glassy carbon electrode shows obvious electrocatalytic activity to the oxidation of lincomycin, since it greatly enhances the oxidation peak current of lincomycin as well as lowers its oxidation overpotential. Based on this, a very sensitive and simple voltammetric method was developed for the measurement of lincomycin. A sensitive linear voltammetric response for lincomycin was obtained in the concentration range of 4.5x10(-7) to 1.5x10(-4) mol/l, and the detection limit is 2.0x10(-7) mol/l using linear sweep voltammetry. Compared with other methods, this proposed method possesses many advantages such as very low detection limit, fast response, low cost and simplicity. The practical application was demonstrated to determine lincomycin in tablets with good result.

Adsorption↗

PubMed1986

Lincomycin stimulates synthesis of TEM-2 beta-lactamase by Escherichia coli.

Lincomycin increased the TEM-2 beta-lactamase activity of Escherichia coli K-12 cells carrying plasmid RP4 at a concentration which slightly inhibited cell growth. In a control culture beta-lactamase activity reached its maximal level in late log phase, whereas when lincomycin was present beta-lactamase activity continued to increase into the stationary phase. Lincomycin (100 micrograms/ml) inhibited both cell growth and protein synthesis by about 35% but stimulated beta-lactamase activity 2.5-fold per ml of culture and about 4-fold per cell after 20 h of growth. The amount of beta-lactamase produced in each culture was also compared by densitophotometry of a stained sodium dodecyl sulfate-polyacrylamide gel. The relative values were in good agreement with the relative enzyme activities, indicating that the stimulatory effect of lincomycin was due to an increase in the amount of beta-lactamase protein. Inactivation of beta-lactamase appeared to be faster when lincomycin was present. This was determined by measuring the decrease in beta-lactamase activity when phenethyl alcohol was present to prevent maturation of the enzyme. There was no significant difference in plasmid copy number between the cells grown in the presence or absence of lincomycin. These results indicate that lincomycin stimulates transcription, translation, or translocation of beta-lactamase.

Electrophoresis, Polyacrylamide Gel↗

PubMed1976

[Biosynthesis of 14C- and 35S-lincomycin using different sources for the label].

The sources of radioactive labels were chosen for biosynthesis of labeled lincomycin. The levels of the label incorporation into lincomycin were high with all the sources used when the lincomycin-producing organism was cultivated on the synthetic medium as compared to the complex medium. Incorporation of the label into lincomycin was most effective when I14C- or 214C-thyrosine was used as the precursors. These precursors were effective in both the complex and the synthetic media. In production of significant amounts of the labeled lincomycin I14C- or 214C-sodium propionate, I14C- or 142C-sodium acetate and 14C-protein hydrolysate may be used as the sources of the radioactive carbon. In production of 35S-lincomycin K235SO4 may be used as the source of the label. The optimal conditions for biosynthesis of 14C- and 35S-lincomycin were developed (concentration of some components of the medium, time of the label addition and others).

Acetates↗

PubMedDate not supplied

Ecophylaxis: preventive treatment with gentamicin of rabbit lincomycin-associated diarrhea.

In rabbits the oral or parenteral administration of lincomycin result in a severe and usually fatal form of diarrhea. The rabbits treated simultaneously with lincomycin and gentamicin do not present any sign of disease and behave exactly, therefore, as the control subjects. The same occurs in subjects treated with gentamicin alone. In all the subjects which died with diarrhea there was a marked alteration of the intestinal bacterial flora. Among the aerobic bacteria there was an overgrowth of coliforms and less frequently of enterococci, while bacilli were reduced and lactobacilli completely disappeared. Among the anaerobic bacteria, bacteroides and bifidobacteria disappeared and there was an overgrowth of clostridia instead. In rabbits treated contemporaneously with lincomycin and gentamicin, coliforms were absent and the mean number of clostridia was at least one hundred times lower; as in rabbits treated only with lincomycin, enterococci were present in greater number, while lactobacilli, bifidobacteria and bacteroides completely disappeared. Some of the bacteria which are able to overgrow in lincomycin treated subjects, in particular coliforms and clostridia, can be considered potentially pathogenic and their overgrowth could therefore explain the onset of diarrhea. Actually in faecal specimens of rabbits with lincomycin-associated diarrhea, together with the overgrowth of E. coli and clostridia, there is an absence of lactobacilli, bifidobacteria and bacteroides. It is known that these last bacteria contribute, in normal conditions, to maintaining the ecological equilibrium of the intestinal microbial flora. The diarrhea itself can be attributed most likely to the ecological alteration of intestinal microbial flora, with an overgrowth of some potentially pathogenic bacteria and the suppression of others which normally exert an inhibiting effect on the former. It has been suggested to call this form of gentamicin prophylaxis of lincomycin-associated diarrhea 'ecophylaxis', in the sense that it prevents or corrects certain types of ecological alteration of the intestinal microbial flora which lead to diarrhea.

Animals↗

PubMed2001

Oxidation of lincomycin by hydrogen peroxide restricts its potential biotransformation with haloperoxidases.

Lincomycin biotransformation was conducted by using Streptomyces venezuelae and Streptomyces phaeochromogenes cell-free extracts. Reaction products were isolated and identified by MS and NMR spectroscopy as lincomycin sulfoxide and lincomycin sulfone. Both compounds arise also by chemical oxidation with hydrogen peroxide; this reaction represents a new efficient way for the preparation of lincomycin sulfoxide and lincomycin sulfone and simultaneously excludes the biotransformation of lincomycin using haloperoxidases.

Hydrogen Peroxide↗

PubMed2006

Development of a hydrophilic interaction chromatography-mass spectrometry assay for spectinomycin and lincomycin in liquid hog manure supernatant and run-off from cropland.

A specific and sensitive analytical method was developed to extract and quantify spectinomycin and lincomycin in liquid hog manure supernatant and simulated rainfall run-off from manure-treated cropland. Sample extracts were prepared using solid-phase extraction (SPE) employing a weak cation-exchange resin (Oasis WCX) for extraction of spectinomycin. An Oasis HLB cartridge was used for extraction of lincomycin. Hydrophilic interaction chromatography (HILIC) was used to obtain the necessary separation of the two antibiotics from interfering compounds and to provide baseline separation. Analytes were detected using atmospheric pressure chemical ionization tandem mass spectrometry. Extraction recoveries were 77% for lincomycin and 84% for spectinomycin in liquid hog manure supernatant, and 89% for lincomycin and 95% for spectinomycin in run-off water. The corresponding limits of quantitation were 6.0 and 0.040 microg l(-1) for spectinomycin and lincomycin, respectively, in liquid hog manure supernatant and 0.2 and 0.008 microg l(-1) for spectinomycin and lincomycin, respectively, in run-off from manure treated cropland. The method is suitable for monitoring the environmental fate and transport of these two antibiotics in both liquid hog manure and agricultural field run-off.

Animals↗

PubMed2004

Electrochemiluminescence detection with integrated indium tin oxide electrode on electrophoretic microchip for direct bioanalysis of lincomycin in the urine.

In this article, an antibiotic, lincomycin was determined in the urine sample by microchip capillary electrophoresis (CE) with integrated indium tin oxide (ITO) working electrode based on electrochemiluminescence (ECL) detection. This microchip CE-ECL system can be used for the rapid analysis of lincomycin within 40s. Under the optimized conditions, the linear range was obtained from 5 to 100 microM with correlation coefficient of 0.998. The limit of detection (LOD) of 3.1 microM was obtained for lincomycin in the standard solution. We also applied this method to analyzing lincomycin in the urine matrix. The limit of detection of 9.0 microM was obtained. This method can determine lincomycin in the urine sample without pretreatment, which demonstrated that it is a promising method of detection of lincomycin in clinical and pharmaceutical area.

Anti-Bacterial Agents↗

PubMed1990

Effect of lincomycin as a growth promoter for broiler chicks.

1. The effects of adding lincomycin to either the food (2.2 mg/kg) or drinking water (equivalent or 0.5 equivalent amount) of male broiler chicks were examined. 2. There were four treatments: control (no lincomycin), diet containing 2.2 mg lincomycin/kg, control diet plus drinking water containing lincomycin at concentrations calculated to provide an intake equivalent to treatment 2, and treatment 14 with lincomycin concentration reduced by half. 3. There was no significant effect of any treatment upon mortality, efficiency of food utilisation at 42 d of age, final body weights or monetary indices. 4. Analyses of breast, thigh and liver tissues, using a method with a sensitivity of 1.0 mg/kg, failed to reveal any evidence of lincomycin residues. 5. It is concluded that the use of lincomycin at 2.2 mg/kg may not be effective in improving either the biological or economic performance of the broiler chicken.

Animal Feed↗

PubMed1972

Resistance of group A beta-hemolytic streptococci to lincomycin and erythromycin.

Ten (0.05%) of 18,628 strains of Streptococcus pyogenes isolated from clinical specimens in the 3 years 1968 to 1970 were resistant to lincomycin and erythromycin. All 10 strains were highly resistant to lincomycin, having minimal inhibitory concentration (MIC) values of 200 mug/ml. There were two degrees of resistance to erythromycin: four strains were highly resistant, having MIC values of 200 mug or more/ml; and six strains showed slight resistance, MIC values being 0.78 to 1.56 mug/ml. There was no known epidemiological relationship between any of the patients infected with the resistant strains, which belonged to a variety of T serotypes. A zonal pattern of resistance to lincomycin occurred in four strains, all of which were only slightly resistant to erythromycin. After incubation for 24 hr in a twofold dilution series of lincomycin in broth, the strains grew in 0.05 mug or less/ml and in 50 and 100 mug/ml, but not in intermediate concentrations. Tests in agar indicated that the bacterial population of one strain, but not of the other three, was homogeneous in respect to its ability to grow readily in low and high, but not in intermediate, concentrations. The zone phenomenon is of significance in the clinical laboratory, since unawareness of it might result in a highly resistant strain being regarded as susceptible to lincomycin in tube or plate MIC tests that do not include sufficiently high concentrations of lincomycin.

Drug Resistance, Microbial↗

PubMedDate not supplied

Neostigmine and 4-aminopyridine antagonism of lincomycin-pancuronium neuromuscular blockade in man.

Seven anesthetized patients were studied to determine the interaction between pancuronium and lincomycin and the ability of neostigmine and 4-aminopyridine to antagonize the block. Lincomycin 600 mg given IV alone did not decrease twitch tension. An 8 to 10% decrease in twitch tension occurred when lincomycin was given after neostigmine antagonism of pancuronium. Lincomycin augmented a partial pancuronium neuromuscular blockade. The combined lincomycin-pancuronium neuromuscular blockade was effectively antagonized by both neostigmine and 4-aminopyridine although the latter produced a slower rate of antagonism. The authros conclude that lincomycin, 600 mg IV, augments a pancuronium neurovascular blockade. 4-Aminopyridine offers no advantage over neostigmine and, in fact, may offer a disadvantage because of a slower rate of antagonism.

Adolescent↗

PubMed1983

Comparative effects of clindamycin and lincomycin on end-plate currents and quantal content at the neuromuscular junction.

The pre- and postjunctional effects of the lincosamide antibiotics, clindamycin and lincomycin, were studied in voltage-clamped transected twitch fibers of costocutaneous muscles of garter snakes (species Thamnophis). Miniature end-plate currents and end-plate currents (EPCs) were recorded over a wide voltage range for each antibiotic. The amplitude and kinetics of these currents were studied and estimates of the quantal content of evoked transmitter release determined. High concentrations of clindamycin (2 X 10(-4) M) and lincomycin (2 X 10(-3) M) produced significant depression of EPC amplitude and a nonlinearity in the EPC-voltage relationships. The time constant of EPC decay was accelerated in clindamycin and the relationship between the time constant of EPC decay and membrane potential remained a single exponential function with a concentration-dependent loss of the voltage dependence. In contrast to clindamycin, lincomycin produced biphasic EPCs which consisted of two components, one faster and one slower than the control decay rate. The relative amplitude and decay rate of each component was both concentration and voltage dependent. Either increasing the concentration of lincomycin or membrane hyperpolarization decreased the amplitude ratio, iota slow/iota fast, and increased the ratio of the respective time constants, tau slow/tau fast. Clindamycin affected EPC decay amplitude and quantal content in the same concentration range, whereas lincomycin affected EPC decay at concentrations 20 times less than those required to reduce EPC amplitude and quantal content. These results suggest that the neuromuscular blocking effects of clindamycin involve both pre-and postjunctional sites, whereas the effects of lincomycin are primarily on the postjunctional receptor-channel complex.

Animals↗

PubMed1984

Possible role of lincomycin-therapy in the genetic alteration of a staphylococcus epidemic population.

In a staphylococcosis epidemic occurring in a child community, the proportion of inducible lincomycin resistance has risen significantly in the bacterium population. This conveyed the possibility that lincomycin or its derivatives may induce a lincomycin resistance in Staphylococcus aureus as it is already known in streptococci. Examination of human and animal samples obtained during lincomycin treatment showed that lincomycin had no role in the induction of resistance; the agent can effectively be applied against pathogens of the above-mentioned phenotype. Immunological examination of serum samples provided opportunity for a more exact localization of the protein-linkage of lincomycin.

Animals↗

PubMed1981

[Therapeutic action of proteolytic enzymes and antibiotics in experimental staphylococcal infection. The effect of lincomycin, chymotrypsin and their combinations on the level of autoplaque-forming cells in the blood and the immune adherence reaction of staphylococci].

The effect of lincomycin, chymotrypsin and their combination on the blood count of the plaque-autoforming cells (PAFC) and immune adhesion (IA) of staphylococci was studied on mice with staphylococcal infection. The infected mice were divided into 4 groups: nontreated, lincomycin treated, chymotrypsin treated, and lincomycin + chymotrypsin treated. The doses of lincomycin and chymotrypsin were 150 and 2 mg/kg, respectively. The mice were decapitated by the 3rd, 7th, 14th or 21st day of the infection and treatment and the blood was collected for the count of the PAFC and IA. A decrease in the rate of IA with a simultaneous increase in the PAFC count was found in the untreated mice and the mice treated with lincomycin alone. The use of chymotrypsin and its combination with lincomycin stimulated IA and lowered the level of autosensibilization.

Animals↗