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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↗
PubMed1976

Sensitivity of Escherichia coli after exposure to lincomycin in vitro and in vivo.

Exposure of 10 Escherichia coli isolates in vitro to a concentration of lincomycin found in the intestine of swine fed the maximun concentration recommended in feed did not significantly affect sensitivity to 8 antibiotics, 1 nitrofuran, and 1 sulfonamide when compared with sensitivity of E coli isolates not exposed to lincomycin. Changes in sensitivity, on the basis of Kirby-Bauer interpretation, did occasionally occur; however, these alterations were in zonal sizes, which were marginal for designation as sensitive, intermediate, or resistant. These same fluctuations were observed in E coli not exposed to lincomycin. Exposure of E coli to lincomycin in the intestinal tract of swine for 34 days did not alter sensitivity of E coli to tetracycline, dihydrostreptomycin, spectinomycin, lincomycin, or triple sulfa. The results indicated that addition of lincomycin to the feed did not appear to promote resistance transfer in E coli.

Ampicillin↗
PubMed1985

Evaluation of lincomycin as a cholesterol gallstone dissolution rate accelerator.

These studies were undertaken to test the hypothesis that interfacial resistance may be an important rate-limiting factor in cholesterol gallstone dissolution. The addition of lincomycin hydrochloride to the gallbladder bile of dogs in an in vitro bath system resulted in an acceleration in the rate of dissolution of a compressed cholesterol monohydrate pellet incubating in the bile. However, the constant infusion of lincomycin for 13 d directly into the gallbladders of conscious, unrestrained dogs, which resulted in biliary lincomycin concentrations comparable to that of the in vitro tests, did not alter the dissolution rate of a compressed cholesterol monohydrate pellet which had been surgically placed into the gallbladder. We therefore conclude that the interfacial resistance between the cholesterol monohydrate pellet and the bile may be reduced by the addition of lincomycin to the gallbladder bile which, in the in vitro environment, results in an acceleration in the rate of dissolution of compressed cholesterol pellets. However, the ineffectiveness of lincomycin in accelerating the dissolution of cholesterol pellets in vivo suggests that interfacial resistance is not the only rate-limiting factor in gallstone dissolution. Other factors, such as mixing, may also be critical.

Animals↗
PubMed1977

Plasma, bone, hip capsule, synovial and drain fluid concentrations of lincomycin during total hip replacement.

1 Lincomycin (600 mg) was given 6 h preoperatively by intramuscular injection, as an intravenous infusion over 30 min and for 72 h postoperatively in twelve patients having total hip replacement. 2 The plasma, bone, hip capsule, synovial and drain fluid concentrations of lincomycin were almost always above the M.I.C. of lincomycin against penicillinase producing Staphylococcus aureus. 3 There was a good correlation between the estimated concentrations of lincomycin in bone by the grinding and agitation methods of analysis. 4 Two patients developed pseudomembranous colitis after parenteral lincomycin.

Adult↗
PubMed1989

Lincomycin increases the half-life of beta-lactamase mRNA.

Escherichia coli K-12 strains isolates carrying plasmid pBR322 were grown in the presence of subinhibitory concentrations of lincomycin, which stimulated beta-lactamase synthesis about 2.5-fold, and the effects of the drug on the synthesis and degradation of bla mRNA were studied. The bla mRNA levels determined by 1-min pulse-labeling with [3H]uridine were significantly higher in a lincomycin-containing culture than in the control culture, indicating that stimulation of beta-lactamase synthesis is caused by an increase in the amount of bla mRNA. The enhancing effect of lincomycin was observed in strains harboring pBR322 delta P1 and pBR322 delta P3, which lacked the P1 or P3 promoter, respectively, as well as in the strain harboring pBR322. S1 nuclease analysis showed that the half-life of bla mRNA increased about 2.7-fold when lincomycin was present. These results indicate that the increase in beta-lactamase synthesis caused by lincomycin is due to an increase in the stability of bla mRNA rather than activation of its synthesis.

Coliphages↗
PubMed1976

Characterization of the neuromuscular block produced by clindamycin and lincomycin.

The site of neuromuscular blockade induced by clindamycin and lincomycin was studied on isolated nerve and nerve-muscle preparations. Clindamycin (3.6 X 10(-3) M) but not lincomycin (up to 1.5 X 10(-2) M) had a local anaesthetic effect on a frog desheathed nerve preparation. Clindamycin (8 X 10(-4) M) and lincomycin (4 X 10(-3) M) depressed the response of the rat diaphragm to nerve stimulation and to direct muscle stimulation in parallel. This indicated that the predominant neuromuscular blocking effect of these antibiotics was due to an effect on the muscle. Clindamycin was fivefold more potent than lincomycin in this effect, and the unionized form of both drugs was the active form. Lincomycin (4 X 10(-3) M) but not clindamycin (8 X 10(-4) M) also had some depressant effect on nerve-muscle transmission as indicated by the interaction of the effects of the antibiotics and d-tubocurarine. The significance of these findings is discussed in relation to the acute clinical toxicity of these antibiotics.

Animals↗
PubMed1977

Efficacy of lincomycin feed medication for the control of necrotic enteritis in broiler-type chickens.

Necrotic enteritis was reproduced in two trials, conducted in a penned research-type broiler facility, by growing broiler-type chickens on litter obtained from a commercial poultry house which had experienced a chronic necrotic enteritis mortality problem. In each trial, various concentrations of lincomycin in feed were evaluated for effectiveness in controlling necrotic enteritis. Lincomycin was evaluated at concentrations of 2 to 100 g./ton in Trial 1 and at concentrations of 2 and 4 g./ton in Trial 2. In each trial, non-lincomycin medicated control groups were also included. Each trial included six treatment groups each consisting of four 60-bird replicates. The coccidiostat used in all groups in Trial 1 and in four of the six treatment groups of Trial 2 was the same as had been used on the farm which the litter had been obtained. No other medications were used in any groups. Clinical coccidiosis due to Eimeria brunetti and E. maxima was prevalent in both trials. Birds receiving lincomycin at a concentration of 2 g./ton, or higher, showed a significant reduction in mortality from necrotic enteritis when compared to birds in coccidiostat-control pens not receiving lincomycin medication. Clostridium perfringens was isolated from the litter in all pens and from the livers of birds dying from necrotic enteritis.

Animals↗
PubMed1992

Lincomycin-induced severe colitis in ponies: association with Clostridium cadaveris.

Four groups of two ponies, free of fecal Salmonella and Clostridium cadaveris, were treated as follows: Group A, control group; B, single nasogastrically administered dose of lincomycin (25 mg/kg) followed 48 h later by 3 L of C. cadaveris (10(9) organisms/mL); C, the same dose of lincomycin as group B; D, the same dose of C. cadaveris as group B on each of three occasions at 12 h intervals. Groups A and D remained healthy, but groups B and C developed severe colitis 48-56 h (B) or 72 h (C) after administration of lincomycin. Three ponies were euthanized and one in group B died. Clostridium cadaveris was isolated at about 10(6)/mL of colonic contents from these ponies, but one pony in group B also yielded Salmonella typhimurium from the colon. Subsequent challenge of group A ponies (3 L of C. cadaveris 10(9)/mL, three times at 12 h intervals) did not produce colitis. Nasogastric administration of lincomycin (25 mg/kg) to group A and D ponies, 20 days after administration of C. cadaveris, resulted in severe colitis in all ponies within 48-72 h. Salmonella agona was isolated from the colonic contents of one pony and C. cadaveris (10(6)/mL) from all four ponies. Clostridium cadaveris was not isolated from the colonic content of 45 healthy horses examined immediately after death. These studies confirm the potential for lincomycin to induce severe enterocolitis in ponies and implicate C. cadaveris further as a cause of "idiopathic colitis" in ponies.

Animals↗
PubMed1974

Therapeutic effect of lincomycin and spectinomycin water medication on swine dysentery.

The therapeutic effects of various water medications on swine dysentery were determined in 223 pigs under controlled conditions. Carrier pigs were mixed with test animals until the disease was established. Lincomycin (22 mg/liter), spectinomycin (44 mg/liter) alone and lincomycin and spectinomycin in combination (66 mg/liter) and sodium arsanilate (161 mg/liter) in drinking water for seven days were the drugs evaluated. Negative and positive controls were also included. The experiment was terminated 41 to 43 days after initial medication. Mortality, mean value for stool consistency, incidence of dysenteric days and gross lesions of swine dysentery were the parameters measured for each treatment group.The lincomycin-spectinomycin water medication was effective for the treatment of swine dysentery. Pigs treated with lincomycin-spectinomycin had a higher survival rate, a lower incidence of dysenteric days and fewer gross lesions of swine dysentery than pigs treated with sodium arsanilate, lincomycin or spectinomycin alone or the infected controls (P < 0.05).

Animals↗
PubMed1979

[Serum concentration and kinetics after i.v.-infusion of 3 g lincomycin (author's transl)].

The pharmacokinetics of lincomycin (Albiotic) were studied in ten healthy male and female volunteers after administration of 1 X 3 g and 2 X 3 g lincomycin i.v., respectively, infused over 60 min. After discontinuing the infusion a mean serum value of lincomycin of 97.5 microgram/ml was measurable. 5 h later the mean serum values were 13.5 microgram/ml and 24 h later 1.6 microgram/ml. After 24 h 72.5% of the drug had been eliminated in the urine of 4 volunteers. The mean serum half-life was 286.3 min with the one-compartment model. The volume of distribution was 78.7 l with the one-compartment model and 25.9 l with the two-compartment model. The area under the curve has the value of 14 805.39 microgram . min . ml-1 and 44 418.9 microgram . min. ml-1 with the one- and two-compartment model, respectively. The mean values for the total renal clearance with the two models were 204.8 and 75.5 ml/min. The importance of high-dose therapy with lincomycin is discussed with respect to the tissue penetration of the substance and possible bactericidal effects, whereas lincomycin in general only acts bacteriostatic.

Adult↗
PubMed1978

[Action of lincomycin, chymotrypsin and their combinations on the course of experimental staphylococcal infection].

The culture of Staphylococcus aureus was administered intraperitoneally in a dose of LD30 to albino mice. The animals of the 1st, 2nd and 3rd groups were treated with lincomycin, chymotripsin and combination of lincomycin with chymotripsin respectively. The animals of the 4th group were used as control and were not subjected to the treatment with the drugs. A part of the animals from every group was killed on the 3rd, 7th, 14th, 21st and subsequent days and their organs were investigated microscopically and bacteriologically. It was found that staphylococci was isolated from the control mice during a 50-day period after inoculation. Complete liberation of the organs from the causative agent within 25 days from the beginning of the experiment was registered in the animals treated with lincomycin. Isolation of the staphylococci was over by the 27th day in the animals treated with chymotrypsin. Liberation of the organs from the causative agent by the 17th day was observed in the albino mice treated with the combination of lincomycin with chymotrypsin. The combined use of lincomycin with chymotrypsin proved to be most effective: no death was registered among the albino mice, the levels of the pathogenicity and antibiotic resistance in the pathogenic staphylococci decreased.

Animals↗
PubMed1978

Use of gentamicin to prevent intestinal side effects of lincomycin therapy.

Mild to severe and persisting diarrhea and even colitis have been reported as a side effect of therapy with lincomycin and clindamycin. An alteration in the normal bowel flora with an overgrowth of coliforms and other antibiotic-resistant bacteria has been postulated as a mechanism for the development of diarrhea. Investigations were undertaken in men to observe whether the simultaneous administration of gentamicin was capable of preventing lincomycin-associated intestinal disturbances. Of the 30 subjects treated only with lincomycin 11 (36.6%) developed diarrhea. Of the 18 subjects treated with lincomycin and simultaneously with oral gentamicine, none developed diarrhea. Results of bacteriological examinations indicate that in subjects treated with lincomycin, some potentially pathogenic bacteria, like coliforms and clostridia, are still present in intestinal flora; the simultaneous absence of bifidobacteria and bacteriodes could result in the abolishment of the host resistance to the noxious activity of these endogenous bacteria, as some reported data of the literature suggest. Coliforms and the majority of clostridia strains are not present in subjects treated simultaneously with gentamicin.

Adult↗
PubMed1976

Unfavorable effect of atropine-diphenoxylate (Lomotil) therapy in lincomycin-caused diarrhea.

In this double-blind, randomized study, 200 normal subjects received a three-day course of one of five treatment regimens: lincomycin hydrochloride monohydrate injection (sterile solution, 300 mg/ml) with two tablets of either placebo, a mixture of atropine sulfate and diphenoxylate hydrochloride (Lomotil), an aspirin-phenacetin-caffeine (APC) combination or the latter with codeine, or an injection of saline with two placebo tablets. Gastrointestinal irritation was most prominent in subjects receiving lincomycin with atropine-diphenoxylate and lincomycin with APC plus codeine (P less than .05). Decreased intestinal motility from atropine-diphenoxylate or codeine may increase the contact time between the lincomycin (or its metabolites) or some developing toxic substances and the mucosal epithelium. The use of atropine-diphenoxylate or codeine in treating lincomycin-induced diarrhea may be questionable.

Administration, Oral↗
PubMed1977

[Optimal regime of intravenous administration of lincomycin in osteomyelitis].

The pharmacokinetics of lincomycin in the blood of 8 patients with osteomyelitis was studied on the drug single and uninterrupted intravenous administration in therapeutic doses. It was found that when the antibiotic was administered continuously according to the routine scheme, its therapeutic blood levels were attained only 1.5 hours after the drug infusion. The optimal regimen of lincomycin uninterrupted infusion providing its constant rate in combination with the single intravenous administration was estimated with the help of the constants of the two-compartment model of lincomycin pharmacokinetics. According to the calculations the rate of the antibiotic administration necessary for providing therapeutic levels should be 2.2 mg/kg in complex with the loading dose equal to 5.4 mg/kg. Practical trials showed that intravenous administration of lincomycin with the above regimen remained within therapeutic range already 10 to 20 minutes after the beginning of the drug infusion. Therefore, from the pharmacokinetic point of view the recommended regimen for lincomycin infusion should be considered preferable to that used presently.

Adolescent↗
PubMed1976

[Pharmacokinetics and enzymatic transformations of 35S-lincomycin in the tissues of certain organs].

Pharmacokinetics of 35S-lincomycin was studied with the microbiological and radiometric methods of the antibiotic determination. Significant deviations in the results obtained with the two methods in determination of lincomycin levels in the liver and kidneys were observed. The values obtained with the radiometric method were 10 times higher than those obtained with the microbiological method. Paper radiochromatography of the extracts from the liver and kidneys of the animals treated with 35S-lincomycin revealed the presence of not only 35S-lincomycin, but also a number of the label containing substances, the products of the antibiotic enzymatic transformation. Radiochromatography of the extracts from the brain of the animals treated with 35S-lincomycin revealed several peaks of radioactivity against the back ground of low levels of the label.

Animals↗
PubMedDate not supplied

[Antibacterial activity of clindamycin and lincomycin in broth, serum, and in combination with polymorphonuclear leukocytes against Staphylococcus aureus and Staphylococcus epidermidis].

We investigated the antibacterial activity of clindamycin and lincomycin at 1/4 X minimum inhibitory concentration (MIC), 1 X MIC and 4 X MIC against a serum-resistant Staphylococcus aureus and a serum-resistant Staphylococcus epidermidis strain in broth, in serum with and without the presence of leukocytes and in Hank's medium in combination with leukocytes alone. Against both test strains, lincomycin in broth and serum was similarly effective, whereas against S. aureus clindamycin in broth was somewhat more active. In the combined test mixture of serum with leukocytes, even a 1/4 X MIC of clindamycin or lincomycin markedly improved leukocyte killing of S. aureus, whereas both compounds could not further enhance the marked leukocyte killing of S. epidermidis, even at inhibitory concentrations. In Hank's medium with leukocytes alone, clindamycin and lincomycin had at the most only a bacteriostatic effect against both test strains.

Blood↗
PubMed1992

Slow-onset inhibition of ribosomal peptidyltransferase by lincomycin.

In a system derived from Escherichia coli, we carried out a detailed kinetic analysis of the inhibition of the puromycin reaction by lincomycin. N-Acetylphenylalanyl-tRNA (Ac-Phe-tRNA; the donor) reacts with excess puromycin (S) according to reaction [1], C+S Ks <--> CS k3 --> C'+P, where C is the Ac-Phe-tRNA-poly(U)-ribosome ternary complex (complex C). The entire course of reaction [1] appears as a straight line when the reaction is analyzed as pseudo-first-order and the data are plotted in a logarithmic form (logarithmic time plot). The slope of this straight line gives the apparent ksobs = k3[S]/(Ks + [S]). In the presence of lincomycin the logarithmic time plot is not a straight line, but becomes biphasic, giving an early slope (ke = k3[S]/(Ks(1 + [I]/Ki) + [S])) and a late slope (k1 = k3[S]/(Ks(1 + [I]/K'i + [S])). Kinetic analysis of the early slopes at various concentrations of S and I shows competitive inhibition with Ki = 10.0 microM. The late slopes also give competitive inhibition with a distinct inhibition constant K'i = 2.0 microM. Excluding alternative models, the two phases of inhibition are compatible with a model in which reaction [1] is coupled with reaction [2], C+I k4 <--> k5 CI k6 <--> k7 C*I, where the isomerization step CI <--> CI* is slower than the first step C+I <--> CI, Ki = k5/k4 and K'i = Ki [k7/(k6 + k7)]. Corroborative evidence for this model comes from the examination of reaction [2] alone in the absence of S. This reaction is analyzed as pseudo-first-order going toward equilibrium with kIeq = k7 + (k6 [I]/(Ki + [I])). The plot of kIeq versus [I] is not linear. This plot supports the two-step mechanism of reaction [2] in which k6 = 5.2 min-1 and k7 = 1.3 min-1. This is the first example of slow-onset inhibition of ribosomal peptidyltransferase which follows a simple model leading to the determination of the isomerization constants k6 and k7. We suggest that lincomycin inhibits protein synthesis by binding initially to the ribosome in competition with aminoacyl-tRNA. Subsequently, as a result of a conformational change, an isomerization occurs (CI <--> C*I), after which lincomycin continues to interfere with the binding of aminoacyl-tRNA to the isomerized complex.

Binding, Competitive↗
PubMed1979

Clindamycin and lincomycin alter miniature endplate current decay.

Antibiotic-induced muscle paralysis has frequently been found in both experimental animals and man with three distinct classes of antibiotic: (1) streptomycin and related aminoglycoside compounds, (2) polymyxins and (3) tetracyclines. Recently lincomycin and its chemical congener, clindamycin, have been reported to produce muscle paralysis which has different characteristics from those seen with other classes of antibiotic. Although closely related in chemical structure, lincomycin and clindamycin also seem to produce muscle paralysis by different mechanisms. Clindamycin is considered to exert a direct depressant action on muscle contractility whereas the action of lincomycin is considered to be primarily a depression of neuromuscular transmission. We report here that each of these antibiotics had a significant but different influence on endplate channel behaviour. Clindamycin increased the rate of miniature endplate current (m.e.p.c.) decay and reduced its voltage sensitivity without altering its exponential nature. Lincomycin split m.e.p.c. decay into an initial rapid phase followed by a prolonged phase.

Animals↗