pelvis and genital tract such as endometritis, nongonococcal tubo-ovarian abscess, pelvic cellulitis and postsurgical vaginal cuff infection. streptococci serious respiratory tract infections; serious skin and soft tissue infections. staphylococci serious respiratory tract infections; serious skin and soft tissue infections. pneumococci serious respiratory tract infections. bacteriologic studies should be performed to determine the causative organisms and their susceptibility to clindamycin. to reduce the development of drug-resistant bacteria and maintain the effectiveness of clindamycin hydrochloride and other antibacterial drugs, clindamycin hydrochloride should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. when culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. in the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.

ontinued. appropriate fluid and electrolyte management, protein supplementation, antibiotic treatment of c. difficile , and surgical evaluation should be instituted as clinically indicated. anaphylactic and severe hypersensitivity reactions anaphylactic shock and anaphylactic reactions have been reported (see adverse reactions ). severe hypersensitivity reactions, including severe skin reactions such as toxic epidermal necrolysis (ten), drug reaction with eosinophilia and systemic symptoms (dress), and stevens-johnson syndrome (sjs), some with fatal outcome, have been reported (see adverse reactions ). in case of such an anaphylactic or severe hypersensitivity reaction, discontinue treatment permanently and institute appropriate therapy. a careful inquiry should be made concerning previous sensitivities to drugs and other allergens. usage in meningitis since clindamycin does not diffuse adequately into the cerebrospinal fluid, the drug should not be used in the treatment of meningitis.

ally appropriate circumstances, the physician may elect to initiate treatment or continue treatment with clindamycin hydrochloride capsules. in cases of b-hemolytic streptococcal infections, treatment should continue for at least 10 days.

, anaphylactic reactions and hypersensitivity have also been reported. skin and mucous membranes pruritus, vaginitis, angioedema and rare instances of exfoliative dermatitis have been reported (see hypersensitivity reactions ). liver jaundice and abnormalities in liver function tests have been observed during clindamycin therapy. renal although no direct relationship of clindamycin to renal damage has been established, renal dysfunction as evidenced by azotemia, oliguria, and/or proteinuria has been observed. hematopoietic transient neutropenia (leukopenia) and eosinophilia have been reported. reports of agranulocytosis and thrombocytopenia have been made. no direct etiologic relationship to concurrent clindamycin therapy could be made in any of the foregoing. immune system drug reaction with eosinophilia and systemic symptoms (dress) cases have been reported. musculoskeletal cases of polyarthritis have been reported.

oses. distribution concentrations of clindamycin in the serum increased linearly with increased dose. serum concentrations exceed the mic (minimum inhibitory concentration) for most indicated organisms for at least six hours following administration of the usually recommended doses. clindamycin is widely distributed in body fluids and tissues (including bones). no significant concentrations of clindamycin are attained in the cerebrospinal fluid, even in the presence of inflamed meninges. metabolism in vitro studies in human liver and intestinal microsomes indicated that clindamycin is predominantly metabolized by cytochrome p450 3a4 (cyp3a4), with minor contribution from cyp3a5, to form clindamycin sulfoxide and a minor metabolite, n-desmethylclindamycin. excretion the average biological half-life is 2.4 hours. approximately 10 % of the bioactivity is excreted in the urine and 3.6 % in the feces; the remainder is excreted as bioinactive metabolites. specific populations patients with renal impairment serum half-life of clindamycin is increased slightly in patients with markedly reduced renal function. hemodialysis and peritoneal dialysis are not effective in removing clindamycin from the serum. elderly patients pharmacokinetic studies in elderly volunteers (61 to 79 years) and younger adults (18 to 39 years) indicate that age alone does not alter clindamycin pharmacokinetics (clearance, elimination half-life, volume of distribution, and area under the serum concentration-time curve) after iv administration of clindamycin phosphate. after oral administration of clindamycin hydrochloride, the average elimination half-life is increased to approximately 4 hours (range 3.4 to 5.1 h) in the elderly compared to 3.2 hours (range 2.1 to 4.2 h) in younger adults. the extent of absorption, however, is not different between age groups and no dosage alteration is necessary for the elderly with normal hepatic function and normal (age-adjusted) renal function 1 . microbiology mechanism of action clindamycin inhibits bacterial protein synthesis by binding to the 23s rna of the 50s subunit of the ribosome. clindamycin is bacteriostatic. resistance resistance to clindamycin is most often caused by modification of specific bases of the 23s ribosomal rna. cross-resistance between clindamycin and lincomycin is complete. because the binding sites for these antibacterial drugs overlap, cross-resistance is sometimes observed among lincosamides, macrolides and streptogramin b. macrolide-inducible resistance to clindamycin occurs in some isolates of macrolide-resistant bacteria. macrolide-resistant isolates of staphylococci and beta-hemolytic streptococci should be screened for induction of clindamycin resistance using the d-zone test. antimicrobial activity clindamycin has been shown to be active against most of the isolates of the following microorganisms, both in vitro and in clinical infections [see indications and usage ( 1 )]: gram-positive bacteria staphylococcus aureus (methicillin-susceptible strains) streptococcus pneumoniae (penicillin-susceptible strains) streptococcus pyogenes anaerobic bacteria clostridium perfringens fusobacterium necrophorum fusobacterium nucleatum peptostreptococcus anaerobius prevotella melaninogenica the following in vitro data are available, but their clinical significance is unknown. at least 90 percent of the following bacteria exhibit an in vitro minimum inhibitory concentration (mic) less than or equal to the susceptible breakpoint for clindamycin against isolates of a similar genus or organism group. however, the efficacy of clindamycin in treating clinical infections due to these bacteria has not been established in adequate and well-controlled clinical trials. gram-positive bacteria staphylococcus epidermidis (methicillin-susceptible strains) streptococcus agalactiae streptococcus anginosus streptococcus mitis streptococcus oralis anaerobic bacteria actinomyces israelii clostridium clostridioforme eggerthella lenta finegoldia (peptostreptococcus) magna micromonas (peptostreptococcus) micros prevotella bivia prevotella intermedia propionibacterium acnes susceptibility testing for specific information regarding susceptibility test interpretive criteria and associated test methods and quality control standards recognized by fda for this drug, please see: https://www.fda.gov/stic.

s, usp equivalent to 300 mg of clindamycin are white to off white granular powder filled in size '0' hard gelatin capsules with blue colored cap printed with "z-91" in black ink and blue colored body printed with "300 mg" in black ink and are supplied as follows. ndc 68382-236-08 in bottles of 16 capsules ndc 68382-236-01 in bottles of 100 capsules ndc 68382-236-05 in bottles of 500 capsules store at 20° to 25°c (68° to 77°f) [see usp controlled room temperature].