the prophylaxis of rheumatic fever. cefaclor is generally effective in the eradication of streptococci from the nasopharynx; however, substantial data establishing the efficacy of cefaclor in the subsequent prevention of rheumatic fever are not available at present. urinary tract infections , including pyelonephritis and cystitis, caused by escherichia coli, proteus mirabilis, klebsiella spp., and coagulase-negative staphylococci skin and skin structure infections caused by staphylococcus aureus and streptococcus pyogenes appropriate culture and susceptibility studies should be performed to determine susceptibility of the causative organism to cefaclor. to reduce the development of drug-resistant bacteria and maintain the effectiveness of cefaclor for oral suspension and other antibacterial drugs, cefaclor for oral suspension 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.

as been reported with use of nearly all antibacterial agents, including cefaclor for oral suspension, usp, and may range in severity from mild diarrhea to fatal colitis. treatment with antibacterial agents alters the normal flora of the colon leading to overgrowth of c. difficile. c. difficile produces toxins a and b which contribute to the development of cdad. hypertoxin- producing strains of c. difficile cause increased morbidity and mortality, as these infections can be refractory to antimicrobial therapy and may require colectomy. cdad must be considered in all patients who present with diarrhea following antibiotic use. careful medical history is necessary since cdad has been reported to occur over two months after the administration of antibacterial agents. if cdad is suspected or confirmed, ongoing antibiotic use not directed against c. difficile may need to be discontinued. appropriate fluid and electrolyte management, protein supplementation, antibiotic treatment of c. difficile , and surgical evaluation should be instituted as clinically indicated.

in anuria is 2.3 to 2.8 hours, dosage adjustments for patients with moderate or severe renal impairment are usually not required. clinical experience with cefaclor under such conditions is limited; therefore, careful clinical observation and laboratory studies should be made. as with other β-lactam antibiotics, the renal excretion of cefaclor is inhibited by probenecid. antibiotics, including cephalosporins, should be prescribed with caution in individuals with a history of gastrointestinal disease, particularly colitis.

s media) 9 kg 1/2 tsp b.i.d. 18 kg 1 tsp b.i.d. cefaclor may be administered in the presence of impaired renal function. under such a condition, the dosage usually is unchanged (see precautions ). in the treatment of β -hemolytic streptococcal infections, a therapeutic dosage of cefaclor should be administered for at least 10 days. directions for mixing: add appropriate water volume as indicated in the following table in two portions to dry mixture in the bottle. shake well after each addition. each 5 ml (approximately one teaspoonful) will then contain cefaclor, usp, monohydrate equivalent to 125 mg, 250 mg or 375 mg anhydrous cefaclor, respectively, as shown in the following table. oversize bottle provides extra space for shaking. table 3: cefaclor for oral suspension, usp strength package size (when mixed) water volume to add anhydrous cefaclor/5 ml (approx. one teaspoonful) 125 mg/5 ml 150 ml 106 ml 125 mg 250 mg/5 ml 150 ml 106 ml 250 mg 375 mg/5 ml 100 ml 68 ml 375 mg

econd (or subsequent) course of therapy with cefaclor. such reactions have been reported more frequently in pediatric patients than in adults with an overall occurrence ranging from 1 in 200 (0.5%) in one focused trial to 2 in 8,346 (0.024%) in overall clinical trials (with an incidence in pediatric patients in clinical trials of 0.055%) to 1 in 38,000 (0.003%) in spontaneous event reports. signs and symptoms usually occur a few days after initiation of therapy and subside within a few days after cessation of therapy; occasionally these reactions have resulted in hospitalization, usually of short duration (median hospitalization = 2 to 3 days, based on postmarketing surveillance studies). in those requiring hospitalization, the symptoms have ranged from mild to severe at the time of admission with more of the severe reactions occurring in pediatric patients. antihistamines and glucocorticoids appear to enhance resolution of the signs and symptoms. no serious sequelae have been reported. more severe hypersensitivity reactions, including stevens-johnson syndrome, toxic epidermal necrolysis, and anaphylaxis have been reported rarely. anaphylactoid events may be manifested by solitary symptoms, including angioedema, asthenia, edema (including face and limbs), dyspnea, paresthesias, syncope, hypotension, or vasodilatation. anaphylaxis may be more common in patients with a history of penicillin allergy. rarely, hypersensitivity symptoms may persist for several months. gastrointestinal symptoms occur in about 2.5% of patients and include diarrhea (1 in 70). onset of pseudomembranous colitis symptoms may occur during or after antibiotic treatment (see warnings ). nausea and vomiting have been reported rarely. as with some penicillins and some other cephalosporins, transient hepatitis and cholestatic jaundice have been reported rarely. other effects considered related to therapy included eosinophilia (1 in 50 patients), genital pruritus, moniliasis or vaginitis (about 1 in 50 patients), and, rarely, thrombocytopenia or reversible interstitial nephritis. causal relationship uncertain - cns - rarely, reversible hyperactivity, agitation, nervousness, insomnia, confusion, hypertonia, dizziness, hallucinations, and somnolence have been reported. transitory abnormalities in clinical laboratory test results have been reported. although they were of uncertain etiology, they are listed below to serve as alerting information for the physician. hepatic - slight elevations of ast, alt, or alkaline phosphatase values (1 in 40). hematopoietic - as has also been reported with other β-lactam antibiotics, transient lymphocytosis, leukopenia, and, rarely, hemolytic anemia, aplastic anemia, agranulocytosis, and reversible neutropenia of possible clinical significance. there have been rare reports of increased prothrombin time with or without clinical bleeding in patients receiving cefaclor and coumadin ® concomitantly. renal - slight elevations in bun or serum creatinine (less than 1 in 500) or abnormal urinalysis (less than 1 in 200). cephalosporin-class adverse reactions in addition to the adverse reactions listed above that have been observed in patients treated with cefaclor, the following adverse reactions and altered laboratory tests have been reported for cephalosporin-class antibiotics: fever, abdominal pain, superinfection, renal dysfunction, toxic nephropathy, hemorrhage, false-positive test for urinary glucose, elevated bilirubin, elevated ldh, and pancytopenia. several cephalosporins have been implicated in triggering seizures, particularly in patients with renal impairment when the dosage was not reduced. if seizures associated with drug therapy occur, the drug should be discontinued. anticonvulsant therapy can be given if clinically indicated (see dosage and administration and overdosage sections). to report suspected adverse reactions, contact aytu therapeutics, llc at 855-298-8246 or fda at 1-800-fda-1088 or www.fda.gov/medwatch.

e of cefaclor is slightly prolonged. in those with complete absence of renal function, the plasma half-life of the intact molecule is 2.3 to 2.8 hours. excretion pathways in patients with markedly impaired renal function have not been determined. hemodialysis shortens the half-life by 25% to 30%. microbiology mechanism of action as with other cephalosporins, the bactericidal action of cefaclor results from inhibition of cell-wall synthesis. mechanism of resistance resistance to cefaclor is primarily through hydrolysis of beta-lactamases, alteration of penicillin-binding proteins (pbps) and decreased permeability. pseudomonas spp., acinetobacter calcoaceticus and most strains of enterococci (enterococcus faecalis , group d streptococci), enterobacter spp., indole-positive proteus, morganella morganii (formerly proteus morganii ), providencia rettgeri (formerly proteus rettgeri ), and serratia spp. are resistant to cefaclor. cefaclor is inactive against methicillin-resistant staphylococci. β -lactamase-negative, ampicillin-resistant strains of h. influenzae should be considered resistant to cefaclor despite apparent in vitro susceptibility to this agent. antibacterial activity cefaclor has been shown to be active against most strains of the following microorganisms both in vitro and in clinical infections as described in the indications and usage section. gram-positive bacteria staphylococcus aureus (methicillin susceptible only) coagulase negative staphylococci (methicillin susceptible only) streptococcus pneumoniae streptococcus pyogenes (group a β-hemolytic streptococci) gram-negative bacteria escherichia coli haemophilus influenzae (excluding β-lactamase-negative, ampicillin-resistant strains) klebsiella spp. proteus mirabilis 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 concentrations (mics) less than or equal to the susceptible breakpoint of cefaclor. however, the safety and effectiveness of cefaclor in treating clinical infections due to these bacteria has not been established in adequate and well-controlled trials. gram-negative bacteria citrobacter diversus moraxella catarrhalis neisseria gonorrhoeae anaerobic bacteria bacteroides spp. peptococcus spp. peptostreptococcus spp. propionibacterium acnes susceptibility test methods 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.

even as late as two or more months after having taken the last dose of the antibiotic. if this occurs, patients should contact their physician as soon as possible.