Tetracyclines bacteriostatic action

Doxycydine (Adoxa, Periostal-, Oracea, Vibramycin, Vibra-Tabs) [Anribiotic/Tetracycline] Uses Broad-spectrum antibiotic acne vulgaris, uncomplicated GC, Chlamydia sp, PID, Lyme Dz, skin Infxns, anthrax, malaria prophylaxis Action Tetracycline bacteriostatic X- protein synth Dose Adults. 100 mg PO ql2h on 1st d, then 100 mg PO daily bid or 100 mg IV ql2h acne daily dosing, Chlamydia 7d, Lyme Dz 14—21 d, PID 14 d Peds >8 y 5 mg/kg/24 h PO, to a max of 200 mg/d - daily-bid Caution [D, +] Hepatic impair Contra Children <8 y, severe hepatic dysfxn Disp Tabs, caps, syrup, susp, inj SE D, GI disturbance, photosens Interactions T Effects OF digoxin, warfarin 1 effects W/ antacids, Fe, barbiturates, carbamazepine, phenytoins, food 4-effects OF penicillins EMS Monitor for signs of electrolyte disturbances and hypovolemia d/t D monitor for S/Sxs of super Infxn T risk of photosensitivity Rxns antibiotic of choice for the Tx and prophylaxis of anthrax exposure expired tetracyclines have been known to cause nephrotox OD May cause adverse GI effects symptomatic and supportive... 

Minocycline (Solodyn) [Anribiotic/Tetracycline] Uses Acne Action Tetracycline, bacteriostatic Dose Adults Peds >12y. 1 mg/kg PO daily x l2wk w/ food to X- irritation Caution [C, ] assoc w/ pseudomembranous colitis w/ renal impair Contra Allergy, women of childbearing potential Disp Tabs SE D, HA, fever, rash, joint pain, fatigue, dizziness Interactions T Effects OF digoxin, oral anticoagulants T risk of nephrotox W/ methoxyflurane X- effects W/... 

Tetracyclines may antagonize the bactericidal effects of penicillin, inhibiting cell growth through bacteriostatic action. 

The tetracyclines exert their effect by inhibiting bacterial protein syndiesis, which is a process necessary for reproduction of die microorganism. The ultimate effect of diis action is tiiat the bacteria are either destroyed or dieir multiplication rate is slowed. The tetracyclines are bacteriostatic (capable of slowing or retarding die multiplication of bacteria), whereas die macrolides and lincosamides may be bacteriostatic or bactericidal (capable of destroying bacteria). 

Mechanism of Action A tetracycline antibacterial that inhibits bacterial protein synthesis by binding to ribosomal receptor sites also inhibits ADH-induced water reabsorption. Therapeutic Effect Bacteriostatic also produces water diuresis. Pharmacokinetics Food and dairy products interfere with absorption. Protein binding 41 %-91%. Metabolized in liver. Excreted in urine. Removed by hemodialysis. Half-life 10-15 hr. 

Mechanism of Action A tetracycline antibacterial that inhibits bacterial protein synthesis by binding to ribosomes. Therapeutic Effect Bacteriostatic. 

The tetracyclines were discovered towards the end of the 1940 s (structure of oxytetracycline shown in Figure 5), They have a broader spectrum of activity than the early penicillins. In addition effects on bacteria are different. The penicillins are bactericidal whereas the tetracyclines are bacteriostatic, reflecting differing modes of action. Tetracyclines disrupt protein synthesis by binding to the bacterial ribosome whilst the P-lactams inhibit bacterial cell wall biosynthesis. During the 60 s, 70 s and early 80 s, tetracycline-based products made the biggest commercial impact in the animal health industry. 

Mode of action. Tetracyclines interfere with protein synthesis by binding to bacterial ribosomes and their selective action is due to higher uptake by bacterial than by human cells. They are bacteriostatic. 

MOA Tetracyclines inhibit protein synthesis by binding with the 305 and SOS ribosomal subunits of bacteria. The antibacterial action of the tetracyclines is bacteriostatic. 

Unwanted interactions at the site of action classically include the highly undesirable concomitant use of tetracyclines and penicillins. The latter are bacteriocidal when the organism is dividing because they obstruct cell wall manufacture, and thus expose the new bacterial membrane to osmotic destruction. Bacteriostatic compounds, such as tetracyclines, reduce the rate of bacterial division and thus reduce the effectiveness of penicillins. 

Early explanations of the mechanism of action of tetracyclines involved their demonstrated ability to inhibit various bacterial enzymes that catalyzed such biochemically essential reactions as glucose oxidation and oxidative phosphorylations. Their ability effectively to chelate di- and trivalent metallic ions was also invoked in the theorization. However, at clinically achievable serum levels the bacteriostatic effects of tetracyclines are now accepted to involve primarily direct inhibition of protein synthesis. 

The aminoglycosides are bacteriocidal. Other antibiotics whose mechanism of action involves inhibition of protein synthesis (tetracycline, the macrolides, lincomycin, etc.) are invariably bacteriostatic. The reason for this difference is not known. In fact, the reason that protein inhibition by aminoglycosides should be a cell-killing process has not been satisfactorily addressed. The accumulation of nonsense proteins due to misreading of mRNA has been shown not to be the reason. If ribosomal binding were an irreversible process, lethality might be comprehensible SM does not bind irreversibly. 

Antibiotic tetracycline prototype bacteriostatic inhibitor of protein synthesis (SOS). Broad spectnun, but many resistant organisms. Used for mycoplasmal, chlamydial, rickettsial infections, chronic bronchitis, acne, cholera a backup drug in syphilis. Tox GI upset and superinfections, antianaboUc actions. Fan-coni s syndrome, photosensitivity, dental enamel dysplasia. 

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