Cleocin
Stability of clindamycin phosphate with aztreonam, ceftazidime sodium, ceftriaxone sodium, or piperacillin sodium in two intravenous solutions.

Marble DA, Bosso JA, Townsend RJ.

In admixtures containing clindamycin and either aztreonam, ceftazidime, ceftriaxone, or piperacillin in either 5% dextrose injection (D5W) or 0.9% sodium chloride injection (NS), the stability of each drug was studied. Each of the following combinations of drugs was added to 100-mL glass bottles of base solution: clindamycin phosphate 0.9 g and aztreonam 2.0 g, clindamycin phosphate 0.9 g and ceftazidime sodium 2.0 g, clindamycin phosphate 1.2 g and ceftriaxone sodium 2.0 g, and clindamycin phosphate 0.9 g and piperacillin sodium 4.0 g. Duplicate samples were prepared. Admixtures containing each single drug were also tested. Samples were visually inspected and tested for pH and drug concentration immediately after mixing and at 1, 4, 8, 12, 24, and 48 hours of storage in room temperature and light. Drug concentrations were determined by high-performance liquid chromatographic assay methods. Ceftriaxone retained greater than 90% of its original concentration for 24 hours in single-drug admixtures in NS, for eight hours with clindamycin in NS, and for one hour with clindamycin in D5W. Ceftazidime retained greater than 90% potency for 24 hours with clindamycin in D5W. In all other test admixtures, all drugs were stable for 48 hours. Under the conditions studied, clindamycin is compatible in the admixtures tested with aztreonam and piperacillin. Admixtures of clindamycin and ceftazidime in D5W should be used within 24 hours at room temperature. Clindamycin and ceftriaxone can be mixed in NS if administered within eight hours, but ceftriaxone is stable for only one hour in combination with clindamycin in D5W.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3529949&dopt=Abstract clindamycin antibiotic Cleocin-T



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Interactions of clindamycin with antibacterial defenses of the lung.

Astry CL, Nelson S, Karam GH, Summer WR.

Clindamycin is speculated to have select advantages in the treatment of certain infections because biologically active antibiotic is internalized by macrophages and PMNs in vitro. By challenging pulmonary host defenses with various bacterial species as probes, we were able to evaluate clindamycin-phagocyte interaction in vivo. A murine model was developed using an implanted mini-osmotic pump to maintain constant clindamycin blood levels at 1/4 MIC (1 microgram/ml). Mice pretreated for 24 h with clindamycin killed a significantly greater percentage of intratracheally inoculated Bacteroides thetaiotaomicron in 4 h than did control animals (37 +/- 2% versus 7 +/- 5%). The enhancing effects of clindamycin on pulmonary defenses could not be duplicated by a 1-h preincubation of B. theta in 1/4 MIC of clindamycin before inoculation into untreated mice. Clindamycin blood levels of 1 microgram/ml did not alter the rate at which Pseudomonas aeruginosa (clindamycin-resistant) was killed by pulmonary defenses, suggesting that clindamycin did not cause nonspecific activation of phagocytic defenses. Both PMNs and alveolar macrophages lavaged from the lungs of clindamycin-treated mice contained bioassayable concentrated intracellular antibiotic. The presence of intracellular antibiotic was further supported by experiments in which the intrapulmonary killing of large numbers of Staphylococcus aureus (sensitive, but not resistant organisms) was significantly enhanced (89 +/- 5 versus 70 +/- 5%) by clindamycin pretreatment. In contrast, phagocytes lavaged from mice with constant 1/4 MIC (4 micrograms/ml) blood levels of penicillin G had no detectable intracellular antibiotic activity and did not augment the intrapulmonary killing of B. theta.(ABSTRACT TRUNCATED AT 250 WORDS)

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3579002&dopt=Abstract clindamycin antibiotic Cleocin-T



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In-vivo effects of clindamycin on polymorphonuclear leucocyte phagocytosis and killing of gram-negative organisms.

Bassaris HP, Lianou PE, Skoutelis AT, Papavassiliou JT.

Polymorphonuclear leucocyte (PMNL) phagocytosis and killing were evaluated in ten healthy volunteers who had received 600 mg of clindamycin intramuscularly. Serum obtained 3 h after the administration of clindamycin significantly increased PMNL phagocytosis and killing of Gram-negative aerobic organisms. Serum obtained at 12 and 24 h after the administration of the drug did not induce a significant increase in PMNL phagocytosis and killing. The administration of clindamycin had no direct effect on the PMNLs in terms of their phagocytic and bactericidal function. These results demonstrate serum-associated augmentation of PMNL function by clindamycin in vivo which may be of potential clinical benefit in the outcome of infections.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3583968&dopt=Abstract clindamycin antibiotic Cleocin-T



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Clindamycin in a murine model of toxoplasmic encephalitis.

Hofflin JM, Remington JS.

We investigated the efficacy of clindamycin in a murine model of toxoplasmic encephalitis using direct intracerebral inoculation. Clindamycin reduced mortality from 40% in normal mice and 100% in cortisone-treated mice to 0% in both groups. Although we were unable to document appreciable levels of clindamycin in the brains of infected mice, the histological features of cerebral infection were markedly altered. The formation of large numbers of cysts and the intense inflammatory response seen in the brains of normal mice and the unchecked infection and tissue necrosis in the brains of cortisone-treated mice were absent in the brains of clindamycin-treated mice. Enumeration of cysts in the brains of mice 10 weeks after infection revealed a significantly lower number in the clindamycin-treated mice. Spread of infection to other organs was also decreased during clindamycin administration. These observations suggest that clindamycin may have a role in the therapy of toxoplasmic encephalitis.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3606059&dopt=Abstract clindamycin antibiotic Cleocin-T



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Antimicrobial management of surgically treated gangrenous or perforated appendicitis: comparison of cefoxitin and clindamycin-gentamicin.

Sirinek KR, Levine BA.

Patients with gangrenous or perforated appendicitis were treated with cefoxitin or a combination of clindamycin and gentamicin for a minimum of five post-operative days. Septic complications developed in four of the 54 patients receiving cefoxitin: one was an intraabdominal abscess requiring surgery and three were wound infections. Of the 51 patients receiving clindamycin-gentamicin, two had septic complications: one was an intra-abdominal abscess requiring surgery and one was a wound abscess requiring drainage. The differences in the septic complications in the two treatment groups were not statistically significant. The cost to the patient of combined therapy with clindamycin and gentamicin was 36% higher than the cost of cefoxitin alone. The results demonstrate that cefoxitin alone is comparable to the "gold standard" of clindamycin-gentamicin in the treatment of patients with gangrenous or perforated appendicitis.

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Clindamycin at subinhibitory concentrations enhances antibody- and complement-dependent phagocytosis by human polymorphonuclear leukocytes of Staphylococcus aureus.

Veringa EM, Verhoef J.

The influence of subinhibitory concentrations of clindamycin on opsonization and phagocytosis of Staphylococcus aureus was studied. S. aureus was grown overnight in the presence or absence of one half or one quarter of the minimal inhibitory concentration (MIC) of clindamycin. Radioactively labeled S. aureus was opsonized for various periods of time in different concentrations of normal serum, heated antiserum and serum of patients with agammaglobulinaemia or C3 deficiency. Complement- as well as antibody-dependent phagocytosis of the antibiotic treated S. aureus was significantly enhanced, compared to phagocytosis of the untreated control. Killing experiments showed that clindamycin-treated S. aureus was also better killed by the granulocytes than untreated S. aureus. The mechanism of action is likely to be an increased susceptibility of clindamycin-treated bacteria to antibody- and complement-dependent phagocytosis.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3608624&dopt=Abstract clindamycin antibiotic Cleocin-T