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At least 19 recordsLinked to original sources
PubMed1978

High-pressure liquid chromatographic assays for clindamycin, clindamycin phosphate, and clindamycin palmitate.

High-pressure liquid chromatographic procedures are described for clindamycin, clindamycin palmitate, and clindamycin phosphate as bulk drugs and in formulations. All three procedures utilize a C18 reversed-phase chromatographic column with refractive index detection. The mobile phases are hydroalcoholic solutions containing dioctyl sodium sulfosuccinate or disodium ethylenediaminetetraacetate. Separations of related impurities or degradation products also are discussed. The relative standard deviations of the methods range from 0.8 to 1.8%.

Chromatography, High Pressure Liquid↗
PubMed1978

Intraocular penetration of topical clindamycin in rabbits. II. Clindamycin phosphate.

We have obtained comparative data for the intraocular absorption of topically administered clindamycin hydrochloride hydrate and clindamycin phosphate, made feasible with a new gas chromatographic method of analysis. Results indicated that clindamycin phosphate underwent hydrolysis in the eye, liberating the biologically active clindamycin. However, topical clindamycin hydrochloride produced higher levels (two to six times more) of the antibiotic than those achievable with the phosphates ester in the uvea, aqueous humor, and cornea, presumably due to clindamycin hydrochloride's higher lipid solubility. Based on this data, clindamycin hydrochloride appears to be the preferred form of the antibiotic for topical ocular applications.

Administration, Topical↗
PubMed1978

Serum and plasma concentrations of clindamycin following a single intramuscular injection of clindamycin phosphate in maintenance haemodialysis patients and normal subjects.

Serum levels of clindamycin bioactivity and total clindamycin were studied after single intramuscular injections of 300 mg of clindamycin phosphate in a group of 6 normal subjects and a group of 6 maintenance haemodialysis patients. The patients were studied during a non-dialysis period and then again during haemodialysis. Peak levels tended to be higher and elimination half-lives shorter in the patients than in the normal subjects. Possible reasons for these differences are discussed. There was no evidence that haemodialysis per se influenced the pharmacokinetics of clindamycin phosphate. The proportion of unhydrolysed clindamycin phosphate tended to be higher in the renal failure patients and the reason for this is not apparent. Little, if any, dosage modification is necessary in severe renal fialure although there is probably little point in exceeding a dose of 300 mg intramuscularly every 5 h even in severe infections in patients with severe renal failure. The higher peak levels in patients with advanced renal failure indicate the need for further studies with repeated doses.

Adult↗
PubMed1975

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

Clindamycin-affected Staphylococcus aureus cultures show biphasic steady-state generation curves. An initial (phase I) generation of the clindamycin-affected Staph. aureus is followed by an ultimate (phase II) generation at the same dose level. The phase I apparent generation rate constant is greater than the phase II apparent generation rate constant and suggests the development of resistant Staph. aureus mutants to clindamycin action after a finite period of drug-bacteria contact at any subcompletely inhibitory concentration level. It is rationalized that the increased resistance to drug action in mutant strains is due to a comparatively reduced ribosomal binding affinity for clindamycin. In contrast, clindamycin-affected Escherichia coli cultures show monophasic steady-state generation curves at all concentration levels; E. coli cultures do not develop resistance to clindamycin action. The dependence of the apparent generation rate constant on drug concentration yields a sigmoidal curve, which is coincident by a potency factor for the phase I and phase II generations of clindamycin-affected Staph. aureus and suggests a common mechanism of action for both generation phases. That of clindamycin-affected E. coli yields an asymptote curve, which indicates a different mechanism of action. Clindamycin possesses both a bacteriostatic and a bactericidal action on initial and mutant resistant strains of Staph. aureus, whereas its action on E. coli is only bacteriostatic. Consequently, clindamycin has a minimum inhibitory concentration (MIC) against E. coli that is about 1000 times the MIC value against Staph. aureus at 37.5 degrees. The effect of pH changes in broth media on generation inhibition of both Staph. aureus and E. coli by clindamycin action indicates that the unprotonated fraction of drug concentration contributes to the activity, possibly because of its ready penetration through cell membranes.

Clindamycin↗
PubMed1977

Microbial transformation of antibiotics. Clindamycin ribonucleotides.

Addition of clindamycin to whole-cell cultures of Streptomyces coelicolor Müller resulted in the loss of in vitro activity against organisms sensitive to clindamycin. Incubation of such culture filtrates with crude alkaline phosphatase generated a biologically active material identified as clindamycin. Fermentation broths containing inactivated clindamycin yielded clindamycin 3-ribonucleotides and clindamycin 3-phosphate the structure of which was established by physicochemical and enzymatic means. Attempts to transform clindamycin to clindamycin 3-ribonucleotides by lysates or partially purified enzyme preparations from S. coelicolor have failed.

Animals↗
PubMed1977

[Bacteriological evaluation of clindamycin-2-phosphate (author's transl)].

Clindamycin-2-phosphate, a newly developed injectable antibiotic, was bacteriologically evaluated in comparison with the parent compound, clindamycin. Clindamycin-2-phosphate has a rather weak antibacterial activity. However, it is metabolized into clindamycin in vivo. And this parent compound shows strong activity against both gram-positive bacteria and gram-negative cocci. In vitro studies demonstrated that clindamycin-2-phosphate and clindamycin are affected by the pH of the medium used--the antibacterial activity becomes stronger as the medium is made more alkaline--while they are little affected by the size of the inoculum. In mice with experimental infections, clindamycin-2-phosphate showed about the same therapeutical effect as clindamycin in contrast with the former's inferior in vitro activity as compared with the latter.

Animals↗
PubMed1977

Endocarditis treated with clindamycin: relapse and liver dysfunction.

Clindamycin was used to treat six patients with endocarditis because of allergy to penicillin in five, and an unfavorable clinical response to methicillin in one. Only one patient had an uneventful cure with clindamycin. Two had hepatotoxicity which resolved rapidly after clindamycin was stopped. Two patients, one of whom had an aortic prosthesis, had completed four to six weeks of clindamycin therapy when clinical relapse occurred and blood cultures were again positive for a clindamycin-sensitive isolate. A fifth patient had peptostreptococcal endocarditis. Despite a favorable initial clinical and bacteriologic response, blood cultures taken on the 20th day of therapy again grew the Peptostreptococcus. This relapse pathogen had become resistant to clindamycin and was 100-fold less sensitive than the initial isolate. The few conditions in which clindamycin is indicated for therapy of bacterial endocarditis are outlined.

Adult↗
PubMed1977

[Preclinical and clinical studies of clindamycin-2-phosphate (author's transl)].

Preclinical and clinical studies of clindamycin-2-phosphate developed as an infectable were conducted, and the following results were obtained: 1) Clindamycin-2-phosphate administered by the intravenous drip in a dose of 600 mg over one hour showed a peak blood clindamycin level of 10.5 mcg/ml at the end of administration. Though the blood level then decreased rapidly, it stayed at 0.7 mcg/ml at 8 hours later. 2) The blood level of clindamycin following intramuscular injection of 300 mg of clindamycin-2-phosphate reached a peak of 3.3 mcg/ml at one hour later. The blood level of 6 hours after injection was 1.0 mcg/ml. 3) Clindamycin-2-phosphate 300 mg was given intramuscularly 2 to 4 times daily for 5 approximately 14 days in 4 cases of pneumonia. The drug proved effective in two cases of pneumonia due to Mycoplasma; fairly effective in another case of mixed infection caused by pneumococci, Hemophilus and N. meningitidis; and ineffective in the fourth case of infection due to Hemophilus parainfluenzae. 4) No such adverse reactions as hepatic disorder, renal disorder and colitis were noted following administration of clindamycin-2-phosphate.

Adult↗
PubMed1979

Prophylaxis of streptococcal infections and rheumatic fever: a comparison of orally administered clindamycin and penicillin.

Orally administered clindamycin and penicillin were compared for effectiveness in preventing streptococcal infections in 202 randomly assigned patients with previous rheumatic fever (RF). Among 143 patients aged 21 years or younger observed for 537 patient-years, the number of streptococcal infections (and number per patient-year) was 23 (0.084) in the penicillin group and 12 (0.045) in the clindamycin group. Excluding uncooperative patients, the rate of streptococcal infection remained less, though not statistically significant, in the clindamycin group than in the penicillin group. Two RF recurrences occurred in the penicillin group, and no recurrence occurred in the clindamycin group. Clindamycin was well tolerated except for possible mild gastrointestinal symptoms in six patients. Clindamycin can be substituted for penicillin for RF prophylaxis when there is allergy to penicillin or concern about the development of penicillin-resistant mouth organisms.

Administration, Oral↗
PubMed1977

Diarrhea associated with clindamycin and ampicillin therapy: preliminary results of a cooperative study.

Patients treated with clindamycin were monitored for development of diarrhea and colitis in a cooperative study at three hospitals in Edmonton, Toronto, and Winnipeg, Canada. Ampicillin-treated patients were matched with clindamycin-treated patients. Diarrhea occurred in 62 (18%) of 343 clindamycin-treated patients compared with 16 (5%) of 315 ampicillin-treated patients (P less than 0.001). Among the three hospitals, the rate of diarrhea associated with clindamycin therapy ranged from 10% to 23% compared with 0 to 10% for ampicillin therapy. The only identified risk factor in the development of diarrhea was increased age; clindamycin-associated diarrhea occurred in 18 (46%) of 39 patients greater than or equal to 60 years old. No correlation was observed between the risk of diarrhea and the duration of treatment, total dosage of drug, route of administration, or type of underlying disease. Pseudomembranous colitis was diagnosed in seven (2%) of 343 patients treated with clindamycin and in one (0.3%) of 315 patients treated with ampicillin.

Administration, Oral↗
PubMed1977

Gastrointestinal side effects of clindamycin and ampicillin therapy.

Hospitalized patients who received clindamycin or ampicillin were evaluated for gastrointestinal side effects for a period of up to six weeks after therapy was discontinued. Of 104 patients receiving clindamycin therapy, 31 (29.8%) developed diarrhea, and two (1.9%) developed pseudomembranous colitis (PMC). Of 138 patients receiving ampicillin, 24 (17.3%) developed diarrhea, and one (0.7%) developed PMC. Diarrhea persisting for three days or more was noted in 13 (12.5%) of the patients receiving clindamycin and in seven (5.1%) of those receiving ampicillin. The tendency to develop diarrhea was positively correlated with serious illness, abdominal or pelvic sepsis, and total dosage of clindamycin. Examination of stools from a patient with PMC that was associated with clindamycin therapy showed a decrease in the number of anaerobic bacteria from the numbers found in stool cultures of normal controls. Those patients who did not develop diarrhea also had fewer anaerobic bacteria and coliform organisms. Lymphocytes from the patient with PMC were hyporeactive to phytohemagglutinin and hyperreactive to clindamycin.

Adult↗
PubMed1977

In vitro activity and clinical efficacy of clindamycin in the treatment of infections due to anaerobic bacteria.

Clindamycin, rosamicin, josamycin, and metronidazole had similar inhibitory activity against 29 clinical isolates of Bacteroides fragilis, i.e., 100% of strains were inhibited by 0.8 microng of metronidazole or josamycin/ml and 100% by 1.6 microng of clindamycin or rosamicin/ml. Metronidazole was bactericidal against 97% of the isolates, and clindamycin or rosamicin (in concentrations of 1.6 microng/ml) was bactericidal against 80%. Erythromycin and josamicin were the least bactericidal agents in vitro. Thirty-two patients with pleuropulmonary and intraabdominal or pelvic infections caused by anaerobic bacteria were treated with clindamycin. Cure was achieved in 27 patients. In another group of 37 patients treated with parenteral clindamycin, diarrhea developed in 30% and was significantly more common in those patients with abdominal or pelvic infection. Only one patient developed pseudomembranous colitis. These observations suggest that clindamycin is an excellent and relatively safe antibiotic for treatment of infections caused by anaerobes when combined with surgery or with other antibiotics selected for activity against aerobic gram-negative bacilli.

Aminoglycosides↗
PubMed1977

Clindamycin-associated colitis due to a toxin-producing species of Clostridium in hamsters.

Clindamycin-associated enterocolitis in hamsters was studied to detect and characterize a transmissible agent. It was found that the disease could be transferred by cecal contents and filtrates of cecal contents (pore size of filter, 0.02 micron) obtained from animals after administration of clindamycin. Subsequent work showed that enterocolitis could be produced with broth cultures of a species of Clostridium recovered from cecal contents of animals with clindamycin-induced disease. The cell-free supernatant of this strain also caused enterocolitis. Cecal contents from animals with clindamycin-induced disease incubated with gas gangrene antitoxin failed to cause intestinal lesions. These experiments indicate that clindamycin-associated colitis in hamsters is due to a clindamycin-resistant, toxin-producing strain of Clostridium.

Animals↗
PubMed1976

Clindamycin enhances a nondepolarizing neuromuscular blockade.

Neuromuscular blockades induced by clindamycin alone and with d-tubocurarine or pancuronium were examined in the in-vitro guinea pig lumbrical muscle-nerve preparation. Clindamycin, 80-240 mug/ml, initially increased twitch tension. With higher concentrations (180-240 mug/ml) twitch tension subsequently decreased. With 15 to 20 per cent depression of twitch tension by clindamycin, neostigmine (5-20 ng/ml) or calcium (81 mug/ml) slightly but not completely antagonized the blockade. Clindamycin, 40 mug/ml, a dose that did not depress twitch tension, potentiated d-tubocurarine- or pancuronium-induced neuromuscular bloackade. Plasma concentrations of clindamycin of 10-40 mug/ml were recommended for treating serious infections. The authors conclude that the administration of clindamycin may augment nondepolarizing blockade in man, and antagonism by neostigmine and calcium may be incomplete.

Adjuvants, Anesthesia↗
PubMed1976

Effect of clindamycin on aminoglycoside activity in a murine model of invasive Escherichia coli infection.

Previous studies have demonstrated that the early in vitro bactericidal activity of gentamicin and amikacin is inhibited by clindamycin. To investigate the possible clinical implications of these findings, the effect of clindamycin in combination with gentamicin or amikacin was compared with that of the aminoglycoside alone in the treatment of normal and neutropenic mice with Escherichia coli peritonitis and bacteremia. Mice treated with saline or clindamycin alone experienced rapid multiplication of bacteria in the peritoneal cavity, bacteremia, and subsequent death. Gentamicin or amikacin given 2 h after E. coli inoculation significantly reduced the mortality and peritoneal bacterial counts in normal and neutropenic mice in comparison with untreated controls. Prior or simultaneous administration of clindamycin with either aminoglycoside did not inhibit survival or bacterial clearance from the peritoneum. The only clindamycin effect was slight enhancement of survival of neutropenic mice treated with multiple doses of amikacin and clindamycin in comparison to those treated with amikacin alone.

Aminoglycosides↗