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PubMed1988

Moxalactam vs tobramycin-clindamycin. A randomized trial in secondary peritonitis.

One hundred five patients with peritonitis were randomized to receive either tobramycin sulfate plus clindamycin phosphate or moxalactam alone before surgical intervention. Fifty-nine patients were evaluable. A mean of 3.1 (moxalactam) and 3.5 (tobramycin-clindamycin) pathogens per patient were identified. Overall success rate was 85% (tobramycin-clindamycin, 24/30; moxalactam, 26/29). When patients with appendicitis were excluded, there was an observed but not statistically significant advantage of moxalactam over tobramycin-clindamycin (85% vs 67%). There were five deaths (tobramycin-clindamycin, four; moxalactam, one). Other complications included hypoprothrombinemia (tobramycin-clindamycin, five; moxalactam, five), renal dysfunction (tobramycin-clindamycin, three; moxalactam, one), and superinfection (tobramycin-clindamycin, nine; moxalactam, six). More wound infections were noted in the group given tobramycin-clindamycin. These data suggest that moxalactam is as safe and efficacious as tobramycin plus clindamycin. The observed benefits of this agent warrant study in a larger sample to verify advantages of moxalactam over combination therapy.

Abscess↗

PubMed2006

Dose-independent pharmacokinetics of clindamycin after intravenous and oral administration to rats: contribution of gastric first-pass effect to low bioavailability.

The pharmacokinetic parameters of clindamycin were evaluated after intravenous (at doses of 50, 100, and 200mg/kg) and oral (at doses of 75, 150, and 300mg/kg) administration of the drug to rats. The first-pass effect of clindamycin was also evaluated after intraportal, intragastric, and intraduodenal administration of the drug at a dose of 150mg/kg to rats. After both intravenous and oral administration of clindamycin, the pharmacokinetic parameters of the drug were dose-independent. Hence, the extent of absolute oral bioavailability (F) was also independent of oral doses. After oral administration of clindamycin (150mg/kg), 7.68% of oral dose was not absorbed up to 24h and F value was 28.2%. The gastric first-pass effect of clindamycin was 60.7% of oral dose. The first-pass effects of clindamycin in the lung, heart, intestine, and liver were almost negligible, if any, in rats. The low F of clindamycin in rats was mainly due to considerable gastric first-pass effect. Clindamycin was stable in rat gastric juice and various buffer solutions having pHs ranging from 1 to 13. The plasma-to-blood cells partition ratio of clindamycin was 7.59 in rat blood. The plasma protein binding of clindamycin in rats was 67.5%.

Administration, Oral↗

PubMed1999

Clindamycin hypersensitivity appears to be rare.

BACKGROUND: A patient developed a generalized confluent erythematous papular rash after a single injection of clindamycin preoperatively. The literature from two small studies suggested a 10% incidence of cutaneous eruptions to clindamycin which seemed too high. OBJECTIVE: Describe a patient with clindamycin hypersensitivity and determine the incidence of hospital-wide adverse drug reactions from clindamycin from 1995-1997. METHODS: At a tertiary care center, utilizing the Department of Pharmacy records, the incidence of adverse drug reactions was determined with (1) voluntary physician reporting, (2) Health Information Management chart reviews and adverse drug reaction coding, and (3) chart reviews by the Pharmacy and Therapeutics Committee of adverse drug reactions. RESULTS: (I) A 50-year-old patient developed a generalized raised, erythematous rash that worsened over 3.5 days until hydrocortisone was administered. Immediate skin tests with clindamycin were negative. (2) From 3,896 administrations of clindamycin from April 1995 to October 1997, 14 (0.47%) adverse drug reactions occurred but 7 were confounded by other medications also being administered. CONCLUSION: (1) Adverse drug reactions to clindamycin are much lower than reported 25 years ago with an incidence < 1%. (2) A patient who previously had experienced facial edema and a generalized rash after receiving clindamycin and a cephalosporin 6 years ago and who was considered allergic to cephalosporins, was found to be clindamycin allergic when she received a preoperative dose of clindamycin.

Antibiotic Prophylaxis↗

PubMed1999

Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals.

BACKGROUND: Large outbreaks of diarrhea caused by a newly recognized strain of Clostridium difficile occurred in four hospitals located in different parts of the United States between 1989 and 1992. Since frequent use of clindamycin was associated with the outbreak in one of the hospitals, we examined the resistance genes of the epidemic-strain isolates and studied the role of clindamycin use in these outbreaks. METHODS: Case-control studies were performed at three of the four hospitals to assess the relation of the use of clindamycin to C. difficile-associated diarrhea. All isolates of the epidemic strain and representative isolates of other strains identified during each outbreak were tested for susceptibility to clindamycin. Chromosomal DNA from these representative isolates was also analyzed by dot blot hybridization and amplification with the polymerase chain reaction (PCR) with the use of probes and primers from a previously described determinant of erythromycin resistance - the erythromycin ribosomal methylase B (ermB) gene - found in C. perfringens and C. difficile. RESULTS: In a stratified analysis of the case-control studies with pooling of the results according to the Mantel-Haenszel method, we found that the use of clindamycin was significantly increased among patients with diarrhea due to the epidemic strain of C. difficile, as compared with patients whose diarrhea was due to nonepidemic strains (pooled odds ratio, 4.35; 95 percent confidence interval, 2.02 to 9.38; P<0.001). Exposure to other types of antibiotics or hospitalization in a surgical ward was not significantly associated with the risk of C. difficile-associated diarrhea due to the epidemic strain. All epidemic-strain isolates were highly resistant to clindamycin (minimal inhibitory concentration, >256 microg per milliliter). DNA hybridization and PCR analysis showed that all these isolates had an ermB gene, which encodes a 23S ribosomal RNA methylase that mediates resistance to macrolide, lincosamide, and streptogramin antibiotics. Only 15 percent of the nonepidemic strains were resistant to clindamycin. CONCLUSIONS: A strain of C. difficile that is highly resistant to clindamycin was responsible for large outbreaks of diarrhea in four hospitals in different states. The use of clindamycin is a specific risk factor for diarrhea due to this strain. Resistance to clindamycin further increases the risk of C. difficile-associated diarrhea, an established complication of antimicrobial use.

Anti-Bacterial Agents↗

PubMed1988

In-vitro and in-vivo bacterocodal interactions of clindamycin and ceftazidime, by non-beta-lactamase mechanisms, in experimental Pseudomonas aeruginosa endocarditis caused by a constitutive beta-lactamase overproducing strain.

We studied a ceftazidime-resistant strain of Pseudomonas aeruginosa (PA-48) stably-derepressed for constitutive beta-lactamase overproduction, and its ceftazidime-susceptible parent (PA-96) in order to characterize the ability of clindamycin to: (1) enhance the in-vitro and in-vivo bactericidal activities of ceftazidime for PA-48; and (2) prevent beta-lactamase induction and spontaneous mutation to the derepressed state by the parental strain (PA-96). In vitro, clindamycin synergistically enhanced the bactericidal activity of ceftazidime vs PA-48. In the experimental aortic endocarditis model, the combination of clindamycin with ceftazidime significantly reduced mean intravegetation bacterial densities of PA-48 versus ceftazidime monotherapy and untreated controls at therapy days 6 and 11 (P less than 0.05). Exposure of growing PA-48 cells to clindamycin did not interfere with the hydrolytic function of extracted periplasmic beta-lactamase. Moreover, clindamycin did not suppress cefoxitin-mediated beta-lactamase induction in the parental strain (PA-96). In vitro, clindamycin prevented spontaneous mutation of PA-96 to the stably-derepressed state for beta-lactamase overproduction and also enhanced reversion of derepressed cells of PA-48 to the ceftazidime-susceptible parental phenotype by approximately 2 log10 cfu/ml. This latter effect was mirrored in vivo during clindamycin+ ceftazidime therapy of experimental endocarditis due to strain PA-48, as the proportion of ceftazidime-susceptible cells with vegetations increased by approximately 1-1.5 log10 cfu/g, versus untreated controls or ceftazidime monotherapy recipients. After clindamycin treatment ceased, vegetations contained predominantly ceftazidime-resistant variants. Clindamycin appeared to enhance bactericidal effects of ceftazidime vs PA-48 through non-beta-lactamase mechanisms probably involving promotion and maintenance of spontaneous reversion to the fully-repressed state. However, the concentrations of clindamycin required to achieve these effects are unlikely to be sustained at normal therapeutic dosage.

Animals↗

PubMed2005

Clindamycin and quinolone therapy for Bacillus anthracis Sterne infection in 60Co-gamma-photon-irradiated and sham-irradiated mice.

OBJECTIVES: Sublethal ionizing doses of radiation increase the susceptibility of mice to Bacillus anthracis Sterne infection. In this study, we investigated the efficacy of clindamycin in 60Co-gamma-photon-irradiated and sham-irradiated mice after intratracheal challenge with B. anthracis Sterne spores. Clindamycin has in vitro activity against B. anthracis and inhibits the production of toxin from other species, although no direct evidence exists that production of B. anthracis toxin is inhibited. METHODS: Ten-week-old B6D2F1/J female mice were either sham-irradiated or given a sublethal 7 Gy dose of 60Co-gamma-photon radiation 4 days prior to an intratracheal challenge with toxigenic B. anthracis Sterne spores. Mice were treated twice daily with 200 mg/kg clindamycin (subcutaneous or oral), 100 mg/kg moxifloxacin (oral), 50 mg/kg ciprofloxacin (subcutaneous) or a combination therapy (clindamycin + ciprofloxacin). Bacteria were isolated and identified from lung, liver and heart blood at five timed intervals after irradiation. Survival was recorded twice daily following intratracheal challenge. RESULTS: The use of clindamycin increased survival in gamma-irradiated and sham-irradiated animals challenged with B. anthracis Sterne in comparison with control mice (P < 0.001). Ciprofloxacin-treated animals had higher survival compared with clindamycin-treated animals in two experiments, and less survival in a third experiment, although differences were not statistically significant. Moxifloxacin was just as effective as clindamycin. Combination therapy did not improve survival of sham-irradiated animals and significantly decreased survival among gamma-irradiated animals (P = 0.01) in comparison with clindamycin-treated animals. B. anthracis Sterne was isolated from lung, liver and heart blood, irrespective of the antimicrobial treatment. CONCLUSIONS: Treatment with clindamycin, ciprofloxacin or moxifloxacin increased survival in sham-irradiated and gamma-irradiated animals challenged intratracheally with B. anthracis Sterne spores. However, the combination of clindamycin and ciprofloxacin increased mortality associated with B. anthracis Sterne infection, particularly in gamma-irradiated animals.

Administration, Oral↗

PubMed2002

Clindamycin treatment of methicillin-resistant Staphylococcus aureus infections in children.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) with a narrower antibiotic resistance pattern have emerged. There is a risk for the appearance of resistance during clindamycin therapy of erythromycin-resistant MRSA infections because of the linked resistance mechanisms. METHODS: We analyzed clindamycin-susceptible MRSA organisms from children (1987 to 2000) along with clinical data. Antibiotic susceptibilities of organisms were tested, pulsed field gel electrophoresis (PFGE) was done and the linked resistance mechanism was detected by the D test. RESULTS: An average of 11 clindamycin-susceptible MRSA per year were obtained from children since 1993. Of 88 isolates 33 (38%) were erythromycin-resistant. The latter were less often community-acquired (45% vs. 69%), more often from infants <1 month of age (24% vs. 4%) and less likely to be in the community acquisition-associated PFGE Group 1 (62% vs. 87%) than those that were susceptible. The D test was positive in 31 of 33 erythromycin-resistant isolates. A 9-month-old boy with pneumonia/empyema caused by a clindamycin-susceptible, erythromycin-resistant, D test-positive MRSA developed a PFGE-identical clindamycin-resistant isolate and clinical relapse during clindamycin treatment. In contrast a 12-year-old girl with abscesses caused by a similar MRSA developed another abscess after clindamycin therapy, but the organism was unchanged in susceptibility. CONCLUSIONS: Erythromycin resistance was present in 38% of clindamycin-susceptible MRSA in children, and clindamycin resistance was detected during treatment in one child. Clindamycin remains a treatment option if the clinician is notified of the risk by the microbiology laboratory and the clinical situation is suitable.

Abscess↗

PubMed2006

Growth phase-dependent effect of clindamycin on production of exoproteins by Streptococcus pyogenes.

The administration of high-dose clindamycin plus benzylpenicillin has been recommended for the treatment of streptococcal toxic shock-like syndrome caused by Streptococcus pyogenes, and clindamycin has been found to be more effective than beta-lactams in retrospective analyses of human cases. Although therapeutic doses of clindamycin have also been shown to be effective against experimental infections and clindamycin has great efficacy against the production of bacterial exoproteins, we recently reported that the level of production of some exoproteins was unchanged or even increased by a subinhibitory dose of clindamycin when it is added upon the initiation of bacterial culture and the treated cultures were analyzed by two-dimensional gel electrophoresis. In this study we further examined the effect of clindamycin on the production of exoproteins by adding it to Streptococcus pyogenes cultures during various growth phases. We found that the levels of production of some proteins, NAD+ glycohydrolase, streptolysin O, and streptococcal inhibitor of complement, were increased when clindamycin was added at early-log-phase growth, which was the result that was seen when clindamycin was added at the beginning of culture. However, clindamycin inhibited the production of most types of proteins when it was administered to Streptococcus pyogenes cultures at mid-log-phase growth. In csrS- or mga-knockout bacterial strains, the increase in exoproteins seen in parental strains was considerably inhibited. Our study indicates that the in vitro effect of clindamycin on the production of exoproteins greatly depends on the growth phase of bacteria and some regulatory factors of Streptococcus pyogenes that are involved in this phenomenon.

Anti-Bacterial Agents↗

PubMed1990

Pharmacokinetics and serum bactericidal activities of quinolones in combination with clindamycin, metronidazole, and ornidazole.

To enhance the antimicrobial spectrum of the quinolones against anaerobic organisms and gram-positive bacteria, we investigated in two studies the parenteral combinations of ciprofloxacin (200 mg) and ofloxacin (200 mg) with metronidazole (500 mg) or clindamycin (600 mg) and the oral combinations of enoxacin (400 mg) and fleroxacin (400 mg) with metronidazole (400 mg), clindamycin (300 mg), or ornidazole (500 mg) (only with fleroxacin). The pharmacokinetics and serum bactericidal activities (SBAs) against 5 aerobic and 2 anaerobic species (total, 58 strains) were determined in two groups of 10 healthy volunteers by using a randomized crossover study design. The additions of metronidazole, clindamycin, and ornidazole did not affect the pharmacokinetics of the quinolones. The combination of clindamycin with ciprofloxacin, ofloxacin, and, to a lesser extent, fleroxacin resulted in an increase of the SBA against gram-positive strains (mean peak titers): Staphylococcus aureus, ciprofloxacin alone, 1:5.5; ciprofloxacin-clindamycin, 1:19.9; ofloxacin alone, 1:3.6; ofloxacin-clindamycin, 1:17.5; fleroxacin alone, 1:4.3; fleroxacin-clindamycin, 1:8.1; Streptococcus pneumoniae (fleroxacin and enoxacin were not tested), ciprofloxacin alone, 1:2.0; ciprofloxacin-clindamycin, 1:53; ofloxacin alone, 1:2.6; and ofloxacin-clindamycin, 1:49.2. The high SBA of quinolones against gram-negative bacteria was not affected by the combinations; however, relatively low activities against Pseudomonas aeruginosa were detected. In general, against anaerobic bacteria, low bactericidal activities were determined in both studies (mean peak titers ranged from 1:2.1 to 1:3.1; mean trough titers range from 1:2.0 to 1:2.9). In clinical settings with severe mixed infections, a parenteral therapy consisting of modern quinolones together with clindamycin or imidazole derivatives seems to be active and offers no obvious interactions.

4-Quinolones↗

PubMed1987

Compatibility and stability of clindamycin phosphate-aminoglycoside combinations within polypropylene syringes.

The stability and compatibility of clindamycin phosphate admixed separately with gentamicin sulfate, tobramycin sulfate, and amikacin sulfate in polypropylene syringes under specific storage conditions were studied. In duplicate syringes, clindamycin phosphate 900 mg was admixed with sterile NaCl 0.9% l ml and with either gentamicin sulfate 120 mg, tobramycin sulfate 120 mg, or amikacin sulfate 750 mg. In duplicate polypropylene syringes, control solutions of clindamycin phosphate and each aminoglycoside were prepared separately and stored under the same conditions. The clindamycin control consisted of clindamycin phosphate 900 mg in 6 ml. The gentamicin and tobramycin controls consisted of gentamicin sulfate and tobramycin sulfate 120 mg in 3 ml plus 1 ml of sterile NaCl 0.9%. The amikacin control consisted of amikacin sulfate 750 mg in 3 ml plus 1 ml of sterile NaCl 0.9%. Drug concentrations were determined at the time of preparation and 1, 4, 8, 12, 24, and 48 hours thereafter. Aminoglycosides were assayed by fluorescence polarization immunoassay and clindamycin was assayed by high performance liquid chromatography. Visual inspections and pH determinations of each combination and control solution were performed at each assay time. For the clindamycin, gentamicin, tobramycin, and amikacin control solutions, changes in concentration were within ten percent of the original concentration. Concentrations of clindamycin and gentamicin when admixed together also remained within ten percent of the original concentration. Similar results were found with concentrations of clindamycin and amikacin when admixed together. Tobramycin and clindamycin formed a lasting precipitate upon initial contact when admixed under the study conditions.

Amikacin↗

PubMed1981

Effect of clindamycin on intestinal water and glucose transport in the rat.

Clindamycin therapy occasionally results in pseudomembranous colitis but more often results in a watery diarrheal syndrome which usually stops on cessation of clindamycin. This study was done to determine whether clindamycin itself might alter intestinal water, electrolyte, and glucose transport in the rat. The in vivo single-pass perfusion method was used. Perfusion with clindamycin altered intestinal water and electrolyte transport in a dose-related manner. Glucose transport was unaffected. Different segments of the intestine revealed a varying sensitivity to clindamycin: ileum greater than jejunum greater than colon. The transport defect was reversible on cessation of clindamycin perfusion. Chronic exposure of the intestine to clindamycin did not result in any alterations in water transport. The mechanism by which clindamycin causes these transport defects is unknown but did not involve the cyclic AMP or cyclic GMP systems, increased mucosal permeability, or alterations of mucosal morphology. The findings that clindamycin markedly inhibits intestinal water transport and induces net secretion in the ileum may explain the reversible watery diarrhea that many patients experience when treated with clindamycin.

Animals↗

PubMed1988

Clindamycin-induced alteration of ganglionic function. I. Direct effects on ganglion cell properties.

The influence of the lincosamide antibiotic, clindamycin, on the properties of bullfrog sympathetic ganglion B cells has been determined in vitro using conventional voltage recording methods or single microelectrode voltage-clamp recording techniques. Individual neurons were depolarized with both bath application or local perfusion of clindamycin. The amplitude of the depolarization was not altered by pretreatment with 50 microM (+)-tubocurarine, 10-microM atropine, or 1.5 microM tetrodotoxin (TTX), indicating that the clindamycin-induced depolarization does not result from either the activation of (1) nicotinic receptors, (2) muscarinic receptors, or (3) voltage-gated sodium channels. Clindamycin partially inhibited IM, an action which accounts for part of the clindamycin-induced depolarization. The duration of the hyperpolarizing afterpotential (HAP) following the action potential was decreased in the presence of clindamycin. Clindamycin decreased the amplitude and maximum rate of rise (MRR) of TTX-insensitive action potentials. As calcium influx is thought to contribute to the depolarizing phase of the TTX-insensitive spikes, we suggest that the decrease in HAP duration by clindamycin results from a decrease in the somal calcium current. Further, it is suggested that a decrease in IM and HAP duration may be responsible for the increased excitability exhibited during exposure to clindamycin.

Action Potentials↗

PubMed2006

Oral clindamycin 300 mg BID compared with oral amoxicillin/clavulanic acid 1 g BID in the outpatient treatment of acute recurrent pharyngotonsillitis caused by group a beta-hemolytic streptococci: an international, multicenter, randomized, investigator-blinded, prospective trial in patients between the ages of 12 and 60 years.

BACKGROUND: The increasing rate of treatment failure with penicillin and other beta-lactam antibiotics in pharyngotonsillitis caused by group A beta-hemolytic streptococci (GABHS) has prompted the search for alternative antimicrobials. Both clindamycin and amoxicillin/clavulanic acid have excellent clinical activity in pharyngotonsillitis. OBJECTIVE: This study compared the clinical and bacteriologic efficacy and tolerability of oral clindamycin with those of oral amoxicillin/clavulanic acid in the outpatient treatment of acute recurrent GABHS pharyngotonsillitis. METHODS: This was an international, multicenter, randomized, investigator-blinded, prospective study in patients with acute recurrent pharyngotonsillitis. Recurrence was defined as > or =2 episodes of documented pharyngeal and/or tonsillar infection within the 12 months before the study. A rapid diagnostic test for GABHS was performed before initiating therapy, and positive results were confirmed by pharyngotonsillar culture. Patients were randomly assigned to receive oral clindamycin 300 mg BID or oral amoxicillin/clavulanic acid 1 g BID for 10 days. Culture was repeated on day 12. The primary study end points were clinical and bacteriologic efficacy assessed on day 12, and clinical and bacteriologic recurrence rates assessed at a visit taking place up to 3 months after the completion of treatment. Tolerability was the secondary end point. RESULTS: Seven hundred seventy-four patients with acute, recurrent GABHS pharyngotonsillitis were enrolled in the study (mean age, 28 years; age range, 12-60 years). Five hundred forty-two patients (272 clindamycin, 270 amoxicillin/clavulanic acid) were clinically evaluable at day 12. Four hundred ninety-four patients were bacteriologically evaluable, and the safety population included 772 patients. There were no significant differences between groups at baseline. In terms of clinical efficacy at day 12, 252/272 (92.6%) patients in the clindamycin group and 230/270 (85.2%) patients in the amoxicillin/clavulanic acid group were considered cured (P < 0.003). At day 12, bacteriologic eradication was achieved in 237/242 (97.9%) and 238/252 (94.4%) patients in the respective treatment groups (P = NS). No clinical response was observed in the absence of bacteriologic eradication. At 3-month follow-up, clinical cure was achieved in 267/280 (95.4%) patients in the clindamycin group and 267/280 (95.7%) patients in the amoxicillin/clavulanic acid group (P = NS); bacteriologic eradication was observed in 235 (99.2%) and 237 (99.6%) of the respective treatment groups (P = NS). Both treatments were well tolerated. Adverse events were reported in 53/384 (13.8%) patients in the clindamycin group and 41/390 (10.5%) patients in the amoxicillin/clavulanic acid group. The most commonly reported adverse events involved the digestive system (mainly diarrhea), occurring in 33 (8.6%) and 22 (5.6%) patients in the respective treatment groups. CONCLUSIONS: In this study in patients with acute recurrent GABHS pharyngotonsillitis, oral clindamycin 300 mg BID and oral amoxicillin/clavulanic acid 1 g BID achieved comparable rates of bacteriologic eradication at 12 days and 3 months and comparable clinical cure rates at 3 months. Patients who received clindamycin had significantly greater clinical cure rates at 12 days. Both regimens were well tolerated.

Acute Disease↗

PubMed1988

Activity of clindamycin with primaquine against Pneumocystis carinii in vitro and in vivo.

The combination of primaquine with clindamycin is effective in both in vitro and in vivo models of Pneumocystis infection. Primaquine alone at concentrations from 10 to 300 micrograms/ml reduced the numbers of organisms in cultures to less than 7% of control. Significant inhibition was observed down to 0.1 microgram/ml. Clindamycin at 5 micrograms/ml was ineffective alone. Combinations of clindamycin and primaquine in culture at various concentrations were effective, but there was no evidence of true synergy. In rats with established Pneumocystis pneumonia, clindamycin alone at 5 or 225 mg/kg was ineffective. Primaquine alone at 0.5 or 2 mg/kg did not significantly affect the numbers of organisms remaining. The combination of 0.5 mg of primaquine per kg and 225 mg of clindamycin per kg was effective for therapy, lowering the numbers of organisms in the lungs by about 90%. The combination of 2 mg of primaquine per kg and 225 mg of clindamycin per kg was more effective, lowering the numbers of organisms by almost 98%. In the in vivo prophylaxis model, primaquine at 0.1 or 0.2 mg/kg did not prevent the development of Pneumocystis pneumonia in immune-suppressed rats. Clindamycin at 50 mg/kg had a modest effect alone, but at 5 mg/kg all animals became heavily infected. At 0.5 mg/kg, primaquine alone reduced the severity of infection, but seven of eight rats were still infected. In contrast, the combination of 5 mg of clindamycin per kg and 0.5 mg of primaquine per kg prevented infection in 8 of 10 rats; 2 rats had minimal infection. These studies suggest that the combination of clindamycin and primaquine should be tested in therapy or prophylaxis of Pneumocystis infections in humans.

Animals↗

PubMed1992

Inducible expression of ribosomal clindamycin resistance in Bacteroides vulgatus.

The abilities of erythromycin and clindamycin to act as inducers of clindamycin resistance in the strain Bacteroides vulgatus RYC18F6 is evaluated in vivo (efficiency of plating of inhibitory clindamycin concentrations) and in vitro [efficiency of poly(U)-directed polypeptide synthesis by ribosomes]. Uninduced cells failed to grow during the first 72 h, even at a very low clindamycin concentration (0.1 microgram/ml); after induction with erythromycin or clindamycin, cells were able to form colonies at 32 micrograms/ml after 48 h. The in vitro polymerization test with B. vulgatus RYC18F6 ribosomes (S-30 extract) showed that ribosomes from uninduced cells were fully sensitive to the inhibitory effect of clindamycin. Ribosomes obtained from erythromycin- or clindamycin-induced cells presented a reduced sensitivity to clindamycin inhibition. These results show that resistance to clindamycin in B. vulgatus RYC18F6 is an inducible phenomenon involving a ribosomal modification, probably similar to that previously described for gram-positive bacteria.

Bacteroides↗

PubMed1993

Placebo-controlled trial of intravaginal clindamycin 2% cream for the treatment of bacterial vaginosis.

OBJECTIVE: To compare the safety and efficacy of intravaginal clindamycin 2% cream with placebo in nonpregnant women with bacterial vaginosis. DESIGN: A randomized, double-blind, placebo-controlled clinical trial. SETTING: Ambulatory patients in the general community. PATIENTS: Two hundred fifteen nonpregnant outpatients with a diagnosis of bacterial vaginosis were entered into this study. Of the 134 evaluable patients, 65 received clindamycin and 69 placebo. Demographic parameters were comparable between the two treatment groups. INTERVENTION: Study subjects were equally randomized to receive either 5 g of clindamycin 2% vaginal cream or placebo cream for seven nights. MAIN OUTCOME MEASURES: Clinical and microbiologic follow-up evaluations were scheduled for 5-10 days and 25-39 days posttreatment. Patients were interviewed about signs and symptoms, adverse events, and compliance. Diagnostic examinations were performed. RESULTS: Clinical success rates (cure and improvement) occurred in 50 of 65 patients who received clindamycin (77 percent) and 17 of 69 patients who received placebo (25 percent) by the first posttreatment visit (p < 0.001). Microbiologic cures or improvement were observed in 59 of the 65 patients treated with clindamycin (91 percent) compared with 20 of 69 placebo-treated patients (29 percent) (p < 0.001). At the end of the study, clinical and microbiologic cures or improvement were evident in 45 of 57 (79 percent) and 37 of 57 clindamycin-treated patients (65 percent), respectively, and 18 of 51 (35 percent) and 14 of 51 (28 percent) of the placebo-treated patients, respectively. The success rates with clindamycin 2% cream were statistically higher than those with placebo. The adverse-effect profiles in the two groups were similar and no serious adverse effects were reported. Patients who received clindamycin had a statistically higher incidence of nonbacterial vaginitis/cervicitis (18.5 vs. 7.5 percent, p = 0.003). CONCLUSIONS: Intravaginal clindamycin 2% cream appears to be an effective and safe treatment of symptomatic bacterial vaginosis in nonpregnant women.

Administration, Intravaginal↗

PubMed2000

Therapeutic effect of clindamycin and tetracycline on Babesia rodhaini infection in mouse model.

In order to identify the alternative effective chemotherapeutic agents for murine babesiosis, some selected drugs were examined for their efficacy against protozoan infection in the mouse-Babesia rodhaini (B. rodhaini) model. Clindamycin was not completely effective for elimination of parasites in a dose of 50 mg or 100 mg/kg BW/day b.i.d. but effective to prolong the life span of hosts, while it completely cured B. rodhaini infections in a dose of 200 mg. On the other hand, a double therapy consisting of 2 treatments with 100 mg clindamycin and 100 mg clindamycin and with 100 mg clindamycin and 100 mg tetracycline; respectively, and a single therapy with 100 mg tetracycline or 200 mg clindamycin, had a possibility to clear away B. rodhaini organisms from hosts. However, almost all the treatment groups, had a relapse of the infection within 10 days post treatment or re-treatment. Cured mice by treatment with clindamycin and clindamycin, or clindamycin and tetracycline showed complete resistance against challenge with B. rodhaini, while mice cured by administration of clindamycin at 200 mg or tetracycline at 100 mg showed incomplete resistance to challenge infection. The present data suggest that the two former chemotherapies can induce effective protective immunity (premunization), but the latter two chemotherapies induce incomplete premunization.

Animals↗

PubMed2005

[In vitro activity of linezolid, moxifloxacin, levofloxacin, clindamycin and rifampin, alone and in combination, against Staphylococcus aureus and Staphylococcus epidermidis].

Information about the in vitro effect of combinations of anti-staphylococcal agents on staphylococci is scarce. The aim of the study was to evaluate the in vitro activity of linezolid, moxifloxacin, levofloxacin, clindamycin and rifampin, alone or in combination, against Staphylococcus spp. Two Staphylococcus aureus and two Staphylococcus epidermidis strains isolated from blood cultures were studied using the killing curve method. The combinations analyzed were linezolid+moxifloxacin, linezolid+levofloxacin, linezolid+clindamycin, linezolid+rifampin, moxifloxacin+rifampin, moxifloxacin+clindamycin, levofloxacin+rifampin and levofloxacin+clindamycin. The following concentrations (mg/l) were used: 8 and 16 for linezolid, 2 for moxifloxacin, 3 for levofloxacin, 2 for clindamycin and 2 and 5 for rifampin. The activity was considered synergistic when a reduction in growth of at least 2 log(10) was produced with the combination in comparison to the most active antibiotic alone; antagonistic when a growth of at least 2 log(10) was produced with the combination in comparison to the most active antibiotic alone; and indifferent if the variation was less than 1 log(10). Linezolid and clindamycin were bacteriostatic, while moxifloxacin and levofloxacin were bactericidal. Rifampin was bacteriostatic against S. aureus and bactericidal against S. epidermidis. Linezolid and clindamycin reduced the bactericidal activity of levofloxacin and moxifloxacin, however an antagonistic effect was only observed against S. aureus. Other combinations of linezolid, rifampin, clindamycin, levofloxacin or moxifloxacin were indifferent. Linezolid and clindamycin antagonize the bactericidal activity of fluorquinolones against staphylococci. There was no difference between any other combinations against either S. aureus or S. epidermidis.

Acetamides↗