Diseases Caused by Food Borne Microorganisms

Topics: Bacteria, DNA, Penicillin Pages: 8 (2782 words) Published: April 13, 2013
Name of diseases| antibiotics| pharmacokinetics| Mechanism of action| Listeriosis and e.coli enteritis | AmpicillinGentamicin| Half-Life: 1-1.8 hrProtein Bound: 15-25%Absorption: oral 50%Distribution: bile, blister & tissue fluids, CSF with inflamed meningesMetabolism: liverExcretion: urineHalf-Life: 2-3 hr (NRF)Protein Bound: <30%Peak Plasma Time: IM 30-90 min; IV 30 min after 30 min infusionDistribution: crosses placenta, relative diffusion from blood into CSF: minimal even with inflammation, CSF: blood level ratio: normal meninges: nil; inflamed meninges: 10-30%Vd: increased by edema, ascites, fluid overload; decreased w/ dehydration, neonates: 0.4-0.6 L/kg children: 0.3-0.35 L/kg adults: 0.2-0.3 L/kgExcretion: urine (as unchanged drug), clearance: directly related to renal function| Ampicillin, a beta-lactam semi-synthetic aminopenicillin, acts as a bactericidal agent against microorganisms by inhibiting cell wall synthesis during active multiplication Inhibits bacterial cell wall synthesis by binding to one or more of the penicillin binding proteins (PBPs); which in turn inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell walls, thus inhibiting cell wall biosynthesis. Bacteria eventually lyse due to ongoing activity of cell wall autolytic enzymes (autolysins and murein hydrolases) while cell wall assembly is arrested.Gentamicin is ineffective against anaerobic bacteria because its transport across bacterial cell membranes is dependent upon the presence of oxygen. Gentamicin works by inhibiting protein synthesis in susceptible bacteria by binding strongly to the bacterial ribosome at the 30S-50S interface and preventing ribosomal activity. It is bacteriocidal, meaning it causes bacterial cell death rather than just stopping bacterial growth. 

Cholera| Tetracyclinechloramphenicol| Tetracycline:Absorption in GItract.Distribution-Volume of distribution is 1.3 L/kg or 108 L Metabolised to Δ-epitetracyclineUnchanged drugs are excreted by renal and bilary routes.Excretion:30 % in urineand 20-60% in feaces.half life:6-11 hours.Chloramphenicol:Absorption:GI tract.Chloramphenicol palmitateis hydrolyzed in GI tract and rapidly absorbed as free chloramphenicol.Distribution:60% bound to serum proteins Metabolized by the liver to chloramphenicol glucuronateMetabolized by the liver to chloramphenicol glucuronate.Excreted in urine.Half life is1.5 to 4 hours | Tetracycline is bacteriostatic. Inhibits protein synthesis.It binds to 30s subunit of 70s ribosome at A site and prevent attachment of aminoacyltRNA.Chloramphenicol is bacteriostatic. It prevents protein chain elongation by inhibiting peptidyltransferase activity of bacterial ribosome.in short prevent peptide bond formation.| Ameobicdystentry caused by Entameobahistolytica| METRONIDAZOLE| ROUTES:ORAL, INTRAVENOUS, TOPICAL, RECTAL, VAGINAL BIOAVAILABILITY:100% ( ORAL )59 – 94 % ( RECTAL) HALF LIFE :6 – 7 HOURS EXCRETION :60 – 80 % RENAL | * Entry into the microorganism — Metronidazole is a low molecular weight compound that diffuses across the cell membranes of anaerobic and aerobic microorganisms. However, antimicrobial activity is limited to anaerobes. * Reductive activation by intracellular transport proteins —Metronidazole is reduced by the pyruvate:ferredoxinoxidoreductase system in the mitochondria of obligate anaerobes, which alters its chemical structure. Reduction of metronidazole creates a concentration gradient that drives uptake of more drug, and promotes formation of intermediate compounds and free radicals that are toxic to the cell . * Reduced intermediate particle interacts with intracellular targets — Cytotoxic intermediate particles interact with host cell DNA, resulting in DNA strand breakage and fatal destabilization of the DNA helix . * Breakdown of cytotoxic intermediate products — The toxic intermediate particles decay into inactive end products .| Shigellosis|...
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