Due to the mechanism of their attack on bacterial cell wall synthesis, β-lactams are considered to be bactericidal.Unlike β-lactams such as penicillin and amoxicillin, which are highly susceptible to degradation by β-lactamase enzymes (produced, for example, nearly universally by S. aureus), cefotaxime boasts the additional benefit of resistance to β-lactamase degradation due to the structural configuration of the cefotaxime molecule. The syn-configuration of the methoxyimino moiety confers stability against β-lactamases. Consequently, the spectrum of activity is broadened to include several β-lactamase-producing organisms (which would otherwise be resistant to β-lactam antibiotics), as outlined below. Cefotaxime, like other β-lactam antibiotics, does not only block the division of bacteria, including cyanobacteria, but also the division of cyanelles, the photosynthetic organelles of the glaucophytes, and the division of chloroplasts of bryophytes. In contrast, it has no effect on the plastids of the vascular plants. This supports the endosymbiotic theory and indicates an evolution of plastid division in land plants. Administration
Cefotaxime is administered by intramuscular injection or intravenous infusion. As cefotaxime is metabolized to both active and inactive metabolites by the liver and largely excreted in the urine, dose adjustments may be appropriate in people with renal or hepatic impairment. Plant tissue culture
Cefotaxime is the only cephalosporin which has very low toxicity in plants, even at higher concentration (up to 500 mg/L). It is widely used to treat plant tissue infections with Gram-negative bacteria, while vancomycin is used to treat the plant tissue infections with Gram-positive bacteria. See also
Ceftazidime

References
External links
"Cefotaxime". Drug Information Portal. U.S. National Library of Medicine.
Sometimes the pain is well localized, and the individual is able to determine the exact tooth from which the symptoms are originating, but not always.If the crack propagates into the pulp, irreversible pulpitis, pulpal necrosis and periapical periodontitis may develop, with the respective associated symptoms. Pathophysiology
CTS is typically characterized by pain when releasing biting pressure on an object. This is because when biting down the segments are usually moving apart and thereby reducing the pressure in the nerves in the dentin of the tooth. When the bite is released the "segments" snap back together sharply increasing the pressure in the intradentin nerves causing pain. The pain is often inconsistent, and frequently hard to reproduce. Pain associated with CTS has been reported to occur more commonly on biting, rather than on release of pressure after biting. If untreated, CTS can lead to severe pain, possible pulpal death, abscess, and even the loss of the tooth. If the fracture propagates into the pulp, this is termed a complete fracture, and pulpitis and pulp death may occur. If the crack propagates further into the root, a periodontal defect may develop, or even a vertical root fracture.According to one theory, the pain on biting is caused by the 2 fractured sections of the tooth moving independently of each other, triggering sudden movement of fluid within the dentinal tubules. This activates A-type nociceptors in the dentin-pulp complex, reported by the pulp-dentin complex as pain.