Disease relevance of Cefodizime

• The concentrations of non-protein-bound cefodizime in blister fluid already exceeded the MIC for 90% of Neisseria gonorrhoeae strains 10 min after i.v. injection and 20 to 30 min after the i.m. dose [1].
• The aim of the present study was to explore some of the new opportunities offered by AFM by studying the morphological and surface alterations induced in Escherichia coli by supra-MICs and sub-MICs of a beta-lactam antibiotic (cefodizime) [2].
• Influence of cefodizime on pulmonary inflammatory response to heat-killed Klebsiella pneumoniae in mice [3].
• Cefodizime concentrations of 2 micrograms/ml inhibited about 90% of Enterobacteriaceae studied [4].
• Among gram-positive cocci, 50% of strains were inhibited by 2 micrograms/ml of cefodizime (including methicillin-resistant Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus faecalis, and penicillin-resistant Streptococcus pneumoniae) [4].

High impact information on Cefodizime

• One day after surgery E. coli- and S. aureus-driven neutrophil ROI production was not different from the preoperative values (-2 and +12%, respectively, for the cefodizime group and +7 and +15%, respectively, for the cefuroxime group; P > 0.15 for all) [5].
• In both groups the mean phagocytic ability for E. coli and S. aureus decreased during surgery (-21 and -8%, respectively, for the cefodizime group and -39 and -38%, respectively, for the cefuroxime group; P < 0.05 for all) [5].
• The effects of cefodizime and cefuroxime on neutrophil phagocytosis and reactive oxygen production in 54 patients undergoing elective coronary artery bypass grafting were studied [5].
• The study was carried out to determine the concentrations of cefodizime (single 2-g intravenous [i.v.] dose) and ceftriaxone (single 2-g i.v. dose) in the sera and bones of 42 patients (18 women and 24 men) undergoing hip arthroplasty [6].
• Pharmacokinetics of cefodizime following single doses of 0.5, 1.0, 2.0, and 3.0 grams administered intravenously to healthy volunteers [7].

Chemical compound and disease context of Cefodizime

• The MICs of cefodizime and cefotaxime for the isolate of Neisseria gonorrhoeae ranged from 0.004 to 0.06 micrograms/ml [8].
• The in vitro effect of three cephalosporins (cefodizime, cefotaxime, and ceftizoxime) on the growth of the following lymphocytes or their derivatives was tested: L 5178y mouse lymphoma cells, Molt-4 cells, and murine splenic lymphocytes [9].
• Pseudomonas aeruginosa was employed as the bacterial target for cefodizime and cefotaxime (MICs greater than 128 mg/l), cefsulodin (MIC 16 mg/l) and ceftazidime (MIC 32 mg/l) [10].
• The electrophoretic mobility of Staphylococcus aureus 209P treated with cefodizime or cefotiam was examined by microscopic electrophoresis, and the production of oxygen-derived radicals by human polymorphonuclear leucocytes (PMN) was measured by a luminol-chemiluminescence assay [11].
• In order to clarify the mechanisms of the in vivo antibacterial activity of a cephalosporin, cefodizime (CDZM), the effect of this antibiotic on Pseudomonas aeruginosa E7 infection was examined in rats whose neutrophils had been selectively depleted by monoclonal antibody RP-3 [12].

Biological context of Cefodizime

• Cefodizime was very stable to hydrolysis by Richmond-Sykes type I, II, III, and IV beta-lactamases, as well as the enzyme derived from Bacillus cereus [13].
• Cefodizime was not hydrolyzed by common plasmid or chromosomal beta-lactamases, and it inhibited type I beta-lactamases [14].
• Determinations of the extractable activities of DNA-synthesizing enzymes from cefodizime-treated Molt-4 cells showed a direct correlation between cell growth and DNA polymerase alpha as well as terminal deoxynucleotidyl transferase activity; the DNA polymerase beta activity remained unchanged [9].
• Furthermore, increased non-opsonin dependent stimulation of the PMN oxidative burst was obtained; the strongest response was observed with cefodizime-treated P. aeruginosa in the case of low responder PMN, which displayed a deficient response after stimulation by control bacteria [10].
• Conversely, cefodizime at 100 mg/l had no enhancing effect on diabetic neutrophil chemotaxis, but decreased the chemotactic activity of healthy neutrophils (1.1 +/- 0.2 vs 3.6 +/- 0.7, P less than 0.01) [15].

Anatomical context of Cefodizime

• Cefodizime (0.15 to 50 microM) which was added to mouse spleen cell cultures significantly increased [3H]thymidine incorporation into lymphocytes [9].
• A single dose of cefodizime 1 or 2 g is also useful in treating lower urinary tract infections, particularly uncomplicated infections, with a rate of clinical success of 72 to 88% [16].
• Data obtained both in vivo and ex vivo show that cefodizime enhances various immune parameters such as phagocyte function, B lymphocyte responsiveness and delayed hypersensitivity; it may restore natural killer (NK) and phagocyte activity, as well as interleukin 1 (IL-1) and interferon production, in immunocompromised patients and animals [17].
• Effects of cefotaxime and cefodizime on human granulocyte functions in vitro [18].
• Cefodizime penetrates into several tissues and body fluids such as lung, sputum, pleural and ascitic fluids, prostate, kidney, and urine to give concentrations often exceeding the MICs of susceptible pathogens [19].

Associations of Cefodizime with other chemical compounds

• In vitro antimicrobial activity evaluation of cefodizime (HR221), a new semisynthetic cephalosporin [13].
• In vitro activity of cefodizime (HR-221) [4].
• The reference PADAC and nitrocefin substrate hydrolysis by a type I beta-lactamase was markedly inhibited (greater than 80%) by cefodizime at concentrations 0.4 to 4% of substrate concentration [13].
• The enhanced bactericidal activity of human neutrophils induced by cefotaxime and cefodizime, two methoxy-imino-amino- 2-thiazolyl cephalosporins, is linked to the cell stimulation of oxygen-dependent and oxygen-independent killing systems, respectively [20].
• On the contrary, cefodizime enhances killing of opsonized and non-opsonized bacteria by neutrophils regardless of treatment with phenylbutazone which blocks neutrophil oxidative metabolism [20].

Gene context of Cefodizime

• Cefodizime modulates in vitro tumor necrosis factor-alpha, interleukin-6 and interleukin-8 release from human peripheral monocytes [21].
• No additive effect of cefodizime with TNF alpha was observed [22].
• The influence of cefodizime (CDZ) on CD4 and CD8 lymphocytes was investigated in patients with lower respiratory tract infection and underlying respiratory diseases [23].
• Cefodizime induced a significant (p < 0.05), dose-dependent increase in GM-CSF release [22].
• Feedsidewards in vivo were seen in the chronomodulation of tumor-host balance occurring after melatonin, IL-2, cefodizime, and cyclosporine treatments that enhanced or delayed tumor growth and survival time of tumor-bearing mice [24].

Analytical, diagnostic and therapeutic context of Cefodizime

• Concentrations of cefodizime in the serum and urine were determined by high-performance liquid chromatography [7].
• Single doses of 1 g of cefodizime were injected i.v. and i.m. according to a randomized crossover design [1].
• Atomic force microscopy: application to investigation of Escherichia coli morphology before and after exposure to cefodizime [2].
• An open multicentre study of the efficacy and tolerance of cefodizime 1 g bd intravenously or intramuscularly in lower respiratory tract infections [25].
• Concentrations of cefodizime were measured by HPLC in blood and dialysate samples collected during an 8-h dwell period and in additional dialysate samples collected up to 48 h after drug administration [26].

References