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Q: What is an extended-spectrum β-lactamases?
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What is Beta-lactamase positive?

Beta-lactamases are enzymes produced by bacteria. Gram-positive bacteria can produce beta-lactamases. This type of bacteria takes up the crystal violet stain in gram staining.


Mode of action amoxicillin and clavulanic acid?

A. Amoxicillin inhibits the synthesis of the cross-linkage of the peptidoglycan in the cell wall.


How can penicillin be structurally modified to overcome bacterial resistance?

In the bicyclic system, a bulky group can be added to position 6. This creates a steric shield which leads to steric hindrance. The beta-lactam ring is hence more protected and the drug can become more resistant to beta-lactamases of bacteria.


Are there any published data for Cefixime and clavulanic acid?

Yes, we have complete data for our new brand Sifixim - CV (Combination of Cefixime with Clavulanic acid).In which we have given the complete rational of combination, some important points of the same are as follows:-Journal of Antimicrob Chemotherapy - "Resistance to cephalosporins due to Class A beta-lactamases was reversed by clavulanate."Classical TEM and SHV beta-lactamases is exceptional for a cephalosporin, but was reversible with clavulanate,Clin Microbiol Infect. 2008 - Clavulanate is a highly effective inhibitor of extended-spectrum beta-lactamases (ESBLs) in detection tests, but the commercial amoxycillin-clavulanate and ticarcillin-clavulanate combinations have borderline activity, at best, against most ESBL producersCombinations of clavulanate with modern anti-methicillin-resistant Staphylococcus aureus cephalosporins also deserve investigation, as these compounds remain labile to ESBLs.• HA-MRSA Since HA-MRSA strains are multidrug-resistant organisms (MDRO), final therapy should be guided by results of susceptibility testing from cultures obtained before the initiation of empirical therapy.11,13,15,25 For initial empirical antibiotic therapy for HA-MRSA, Grayson25 has suggested vancomycin, , 3rd / 4th generation cephalosporins plus clavulanate, linezolid, daptomycin or rifampin plus trimethoprim-sulfamethoxazole.For further detail you can contact the undersignedAmit VyasMarketing ManagerSvizera Healthcare Ltd.amitvyas@svizerahealth.com


How well does bacteria spread?

Bacteria initiate infection by making use of virulence factors which are; 1. pilli: These are small hairs that enable some pathogens to attach easily to cell surfaces, particularly mucous membranes. bacteria possessing pilli include Neisseria gonorrheae and some strains of Escherichia coli, Salmonella and Shigella species 2. Production of enzymes that help pathogens to spread: for example, hyaluronidase produced by Clostridium perfringes and some Streptococci and Staphylococci,helps organisms to spread through the body by breaking down the hyaluronic acid of connective tissue. 3. production of beta-lactamases: These penicillin-destroying enzymes are produced by many bacteria including some strains of Staphylococcus aureus and Neisseria gonorrhoeae. 4. Mechanisms that interfere with phagocytosis: Bacteria such as Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, and Neisseria meningitidis secrete a capsule around their cell wall which helps to prevent opsonization and phagocytosis. 5. production of exotoxin: several gram positive and a few gram negative bacteria secrete powerful poisons called exotoxins that are capable of destroying or injuring host cells. They tend to be specific in their action, e.g. the exotoxin of Clostridium tetani is neurotoxin. 6. Release of endotoxin: The cell walls of Gram negative organisms contain endotoxin ( O antigen ). When endotoxin is released into the blood circulation, the resulting toxaemia may cause shock, rigor, chills. 7. Mechanisms that destroy or neutralize antibodies: For e.g., the destructive IgA protease of Pseudomonas aeruginosa.