beauty and health

m? mechanism mol? dicular to the r? resistance to m? cines r? resistance to m? cines is r? reduce the effectiveness? a m? medicament for the treatment of a disease or the continued improvement of the symptoms? my patient. If the m? Medicament is not destiny? ? t? ? States or inhibit a pathogenic agent? Does the term is synonymous with strength? Failed or representation? Representatives? Possibility? drugs. H? The term is most often caustic? S in disease caus? Are by pathogenic? Ties. Patho? Ties are said r? Sistent treatment when m? Cines mean less to neutralize its effect. If an organization is r? Tants? several m? cines, it is its multi-r? resistant. R? Resistance to m? Cines is an example f? R? Evolution of micro-organisms. People who are not NFA? Lliga f? The effects of R m? Cines are able to survive? Medikament? With treatment, and therefore a gr? Fitness Era that ANF? Lligen people. Gr? This process nat?-S? Natural selection, are more r? Tants Z? In sp GE? Teren descendants in a Bev? Lkerung, the r? Tants handselected s number of cr? Is called. The r? Multiple resistance or multi? Resistance is a condition for an organism pathogenic? Do? r? sister? various m? tion or chemicals? from a varieties is structure and function? the? elimination of the target organism?. R? Organizations that display multiple resistance k? pathological cells can einschlie? Lich bact? riennes and n? oplasiques (tumor) cells. The r? Strength believe? E is the tol? Rancid?? About the one? G? The re Extraordinary toxic substance? Following the exhibition?? About it? Similar-looking substance. This is a Ph? Flag? Pending, for example, pesticides and antibiotics. For example, rifabutin and rifapin r? Action think? E in the treatment of tuberculosis. various micro-organisms are f? Appendix A thousand? Are? survive by adapting their power to antimicrobial agents. They are spontaneous mutation? E or transfer of DNA. This process m? Me who can? certain bacterial? ries r? sister? the attack of certain antibiotics, making antibiotics ineffective. These micro-organisms from? Scribed? Ftig several m? Nisms for r? Alisea multi? Resistance: Zellwandpermeabilit increasingly no longer a cell glycoprotein? Ine wall enzymatic inactivation of antibiotics? T Remove obtained antibiotic Altered destinations m? Nisms efflux of antibiotics against antibiotics? Mutation rate? Lev? r? response to stress, many bacterial? ries diff? annuities, now show multi einschlie? resistance? staphylococci Lich ent? rocoques, gonococci, streptococci, salmonella, Mycobacterium tuberculosis and others. Dar? More Ber, some bacterial? Ries r? Sistas are able to make copies of the DNA code, the f? A R m? Mechanism of r? Resistance? other bacterial? ries, which cr? e a r? resistance against their neighbors, who then? also? be able to transmit the g? do r? resistance? Transferable. To ensure the d? Development of the r? Resistance to antibiotics, you must: Use antibiotics only for bacterial infections? Riennes caus? Are the pathogenic agent? Only if m? Possible, use the right antibiotic, and not on a broad? Ventail antibiotics Tzen-st? No antibiotics Cancel s? d? s that am? improves the symptom? my, arr? tez NAT? Natural antibiotics do f full? Dr. Erk more? ltung, cough, bronchitis, anyway? hlenentz? births and eye infections caus? are by viruses. He argues that the? State legislations is Aufkl? Tion of the public is it? ? About the importance of the restrictive use of antibiotics, not only f? A human clinical use, but also f? R f is the treatment of animals? A human consumption is obtained? Help ht. Causes and risk factors, such as the chart available to the antibiotic produced by nat? The s? Natural selection. The upper part? Interior repr? Feel a bacterial population? Ries before exposure? About an antibiotic. The middle section shows the Bev? Lkerung directly after? S exposure, the phase that took place in the s? Election. The last? First section pr? Feel the r? Partition of the r? Resistance? a new g? n? ration bact? ries. The l? Legend indicates the levels of r? Strength of the individual. k r? resistance to antibiotics? Can by horizontal transfer of g? Ties, and connectivity? S? Pfung between mutations in the g? Nome pathogenic agent? Do and a rate of about 1108 by the r? Cation chromosome. The activity? antibiotic against pathogenic agent? can? be whatever they want r? e as pollution of the environment, the bacterial? ries that a mutation, so they survive? Can live to reproduce k?. You will then be on the properties? T? ? their descendants, who have compl? ment in one? Lead constantly r? Tants colony f?. Many? Studies have shown? that the sch? mas antibiotic use influence whatever they want Saddle on the number of bodies r? tants? d? develops some. ? Berm? Force the use of antibiotics? wide spectrum, such as c? phalosporines of second? me and third? me g? n? rations, greatly acc? l? r? the d? development of the r? resistance? the m? ticilline. Other factors involved? S in the r? Resistance unn contain misdiagnosis?? Stem requirements, irr? Guli? Res? use of antibiotics in patients S Impr? Print? M ination articles? Swim toys with low concentrations of antibiotics and administration of antibiotics in farm animals by mouth? Wachstumsf promotion?. So unhealthy practices in the pharmaceutical industry can contribute? the probability? of Sch? Pfung r? Tants St antibiotic? Ms. Researchers r? Of recently? Show? the prot? bacterial ine? k LexA Saharan Africa? Then a cl?? Sselrolle play in the acquisition of bacterial mutations? Riennes. The r? Resistance to m? Cines occurs in several classes of patho? Nes: bact? Ries, viruses, parasites are r? Antibiotic resistance to antiviral m? Nisms mushrooms cancer, the top four m? Nisms by which micro-organisms pr? feel a r? resistance to antimicrobial agents: drug inactivation or modification: E. g. enzymatic inactivation of p? nicilline G bact? ries r? tants? p? nicilline by the production of?-lactamases. Antibiotic? The change is most known: the bacterial? Rie r? Sistent retain m? Me sensitive to antibiotics sensitive target St mounds, but antibiotics can not reach. This occurs for example with the lactamase enzyme cleaves lactamase cycle? four chapters? NONS lactam, which inactivates antibiotics. Over 200 varieties will lactamase from? T? d? criteria (Table). Most lactamases act to some extent against the p? Nicillines and c? Phalosporines, while others are more sp? Cific, N? C? Phalosporinases Mlich (that is, for example, an enzyme AmpC? Enterobacter spp) or p? Nicillinases (such as Staphylococcus aureus p? Nicillinase). Lactamases are many types of bacterial? Ries (? Time? Gram positive and Gram-n? Ative) and diff? Ent degree? S inhibition by-lactamase inhibitors like clavulanic? Ure g? N? RALIS? E. ? Change the target site: E. g. PBP site change a binding target of p? nicillines? MRSA and other bacterial? Ries r? Tants? p? nicilline. Ver changes? In the site s? privilege? gi? s action may mean that the antibiotic p? No? be in the cell and reaches the site live? is not able to the activity?? T of the target because of structural changes Worm? The changes in the mol? Cle? The inhibited. Ent? Rocoques as naturally r? Sistent with c? Phalosporines, because the enzymes responsible f? A synth? To the cell wall (peptidoglycan polymer production? Re are taken into account), appeal?’re Prot? Ines linking p? Nicilline have a low affinity?? Tf? R and they are therefore not inhibited? E. Most Mrs St? Streptococcus pneumoniae are tr? S ANF? Lliga f? R? both p? nicillines and c? phalosporines k? Can the DNA of other bacterial? Ries, the enzyme modified? E ver Sun? This affinity? lower? Tf? For your pet develops the p? Nicilline and r with in.? Er and r? Tants? inhibition by p? nicillines. Worm? Peptidoglycan synthetic enzyme? Tis? Chang e? again, but now has a structure diff? annuity. Mutants of Streptococcus pyogenes that are r? Tants? p? nicilline can? be handselected worm s and p? nicilline-Express? Chang? prot? ines in the laboratory handselected? K?, But they don ‘? Taient not? T? observed? patients who m? Glicherweise not bind? Because of the anti-phagocytic cell wall? Ren M-prot? Ine. OF t? Deterioration of track m? Metabolism: Ben E. g. certain bacterial? ries r? tants sulfa? Confirm that no para-aminobenzoic? That? Acid (PABA), a leading pr? Cursor f? A synth? Is of folate? Nucl-Acid? Ic and? Acids of bacterial? Ries INHIB? E by sulfonamides. ugerzellen place, such as S?, they turn to help pr? form? folic s? acid. efflux rapid efflux pump is a m? mechanism of f? R extruding toxic substances and antibiotics? Outside the cell, because it is an essential part of the? Be x? Nobiotiques. Ce m? Mechanism is important in the m? Medicine, the fa? We can help it? r? bacterial resistance? Saharan Africa to antibiotics. system? my efflux function? About an d? Pendence? Energy? Tick? Ngigen m? Pumping mechanism (active transport), you requested? unerw toxic substances from the pumps? efflux sp? cific. Some system? Efflux my m? Cines sp? Cific, w? While other meters? Glicherweise take several m? Cines, thereby? multi? bacterial resistance? Saharan Africa (MDR). There are three m? Nisms known r? Resistance to fluoroquinolones. Some types of pumps? efflux can k? Intracellular Act? For r? Reduce the concentration of re-quinolone. In bacterial? Ries? No Gram? Ative producing g? Ties r? Resistance plasmid, the prot? Ines can bind? DNA gyrase, beautiful they protected? g? are against the effects of quinolones. Schlie? Mutations Ckgang Lich k? Then in the most important sites of DNA gyrase and topoisom? Shaves IV, his affinity?? T quinolone R?, Efficacy? d? growing drugs. pumps? bacterial efflux? riennes are eiwei? container carriers in the cytoplasmic membrane of all types of cells localized? are. They are active transporter means they fill bin a source? Chemical energy boarding? its function erf?. Some of them are prime? Carriers use the active R ad? Adenosine triphosphate hydrolysis as the source of? Energy, w? While other school? R active transporter (uniporter, symporter or antiporters) o? transport is a process? d? ? Electrochemical diff? Reference potential by pumping hydrogen? Do or sodium ions? Produced? the Outdoors of the cell are coupled? s. bacterial efflux transporters? riennes are f? Big E Nf superfamilies, the amin? S? s? acid frequency and the source of? energy used? e function to export their substrates: The superfamily of m? the most important mediators (MFS) superfamily of ATP-binding cassette (ABC), Multi Family small r? strength class? es (SMR), the r? Kn-resistance? llchen cell division superfamily (RND) and the Multi Family of prot? ines antimicrobial extrusion (MATE). Of these, only the superfamily of ABC transporters are first? Re, the rest is secondary? Re Carriers using proton or sodium gradient as a source? Energy. W? Although MFS is dominant in bacterial? Ries? Gram-positive, RND family unique? Gram-n? Negative. In the case of Pseudomonas aeruginosa r? Tants? the iMIP? No? me, the lack of D2 porin sp? cific conf? re a r? resistance, as iMIP? No? I can not p? No? penetrate into the cell. This m? Mechanism is? Also observed? with a low r? resistance to fluoroquinolones and aminoglycosides. Erh? Efflux Hte? This is a feed pump n? Incom-patible of? Energy is a practice? Table r? Resistance to t? And tetracycline is coded? E by a wide? Ventail g? Ties, as tet (A ) which is distributed? ent in? robact? ries. Although antibiotics are clinically important feature of substrates of system? My efflux, it is likely that most efflux pumps other nat? Have natural physiological functions. Examples of our work are to r: the bacterial? Series E. coli system? me AcrAB efflux, an r? the physiological bile Shit? Acids and fatty acids? Their Toxicity?? T is less. The MFS family Ptr pump in Streptomyces pristinaespiralis seems Autoimmune? Pump T f? R of this organization when he turns on the production of pristinamycin I and II AcrAB TolC system? Me in E. coli is suspected? onn? have an r? in the transport component of calcium channels in the bacterial? series E. coli c? do. The system? Me MtrCDE plays a role? The protector in the r? Resistance? the f? Calendar of lipids in rectal isolates of Neisseria gonorrhoeae. The system? Me AcrAB efflux of Erwinia amylovora is f? A major virulence of this organism, plant (h? Te), colonization and r? Resistance against plant toxins. the capacity? S? the system? my efflux, a large number of connections e, the other as its nat? Know-natural substrates is probably because the recognition of the substrate on the properties? t? s physico-chemical as hydrophobic?? T aromatize? T and ionizable character? Re down? E on the properties? T? S of chemicals? Finite, as in classical enzyme-substrate or ligand-r? Receiver recognition. Because most antibiotics have recognized me? “Amphiphilic vehicles? Len -? both hydrophilic and hydrophobic character? re, they are easily accessible from the pumps? efflux of many. Impact on the r? Antimicrobial resistance, the effects of m? Nisms efflux Gro r? Resistance to antibiotics? is, it is g? n? ally of c? t? of? ckzuf Lead Off:? l? tion g? n? tick encoding the pumps? efflux can on chromosomes and / or plasmids, thus contributing? both intrinsic nat? that (? natural cod?) and acquired a r? resistance or as a? l? tial element m? mechanism of g? ties r? resistance efflux pump can survive? a hostile environment? (Eg, in the pr? Presence of antibiotics), the f? r the s? selection of mutants? over-express these g? ties erm? cr?? the possibility?. Her? S? Tion g? N? Tick as transposons or plasmids transpoable is? Also benefit f? A micro-organisms, such as f? R allows easy sharing of g? Born between varieties can? Remoteness?’re Efflux. Antibiotics may act as inducers and r? Troller of the expression of some pumps? efflux. Expression of pumps? efflux of a number of esp? this Particular of bacterial re? ries can produce a wide spectrum of r? resistance when f the common substrates of several pumps? efflux, which can pump? efflux r? resistance against a broad spectrum of antibiotics? give?. The? Pid? Epidemiology mol? Dicular of g? Ties r? Resistance among bacterial? Ries kr? Resistance? Can be brought intrinsic? That or acquired. r? intrinsic resistance? that is NAT? Natural occurring character? teristic of the biology of the organism, for example r? resistance? vancomycin, in Escherichia coli. The r? Acquired resistance occurs when the bacterial? Series is sensitive? r? resistance to antibiotics by mutation of which can be brought or made cr?? s the acquisition of new DNA. The mutation is one? V? Ment spontan? which is independent? pending waiting to know if the antibiotics are produced? below. A bacterial GT tr? Series such a big advantage because changing it will quickly susceptible cells by antibiotics? Clever by a subpopulation r? Sistent. ? R? Resistance was transmissible? T? recognized in 1959 when the g? ties r? resistance in Shigella? Posted by e-coli plasmids. Plasmids are r? Apply it round her m? Me? Form St? Bridge DNA, smaller than the g? Nome bact? Nothing, encode their own? Transmission by the r? Cation in a strain or varieties can diff? Annuities. They transport? K transmitted? Can multiple g? Ties r? Resistance, which is on a section of DNA in the circumferential position? Petitive? Case of a plasmid? another or k? In the g? Nome of a transposon (or? Jump of g? Ties “). Since the spectrum of bacterial? Ries, plasmids can spread is often limited? E are transposons in the dissemination of g? Ties r? resistance? About these limitations. The g? mecA in MRSA can not have? t? acquired by transposition.? plasmid evolution can be brought complex, but the techniques mol? lar modern, improved tablet? hension? Add ndnis ( as is the case with plasmids containing gonorrhoeae FiltreteTM g? do and are all over the world Neisseria) found?. The bact? riophages (viruses that infect bacterial? ries) can? also transf? rer r? tance, and it h? en Seen? quently in staphylococci. When bact? ries die, they lib? rer DNA, which can? be taken by bact? ries comp? tents, a process known as name change. This process is no longer considers f? r? as important? DR? tect? the environment and is probably the itin f? rary most important? G? ties spread pneumoniae R r? resistance? p? nicilline Streptococcus,? through the cr? ation of p? nicilline mosaic? as prot? ine binding. Orig? length g? ties r? resistance Origins? length g? ties r? resistance antibiotics are not known as? the? era o? antibiotics are the biochemical and mol? lar to r? resistance have? t? introduced? m? does not yet? t? d? covered . bact? ries collect? are 1914-1950 (the Murray collection) have? t? sp? ter is complete? ment? constantly sensitive to antibiotics. They have, however, contain a number of conjugative plasmids No measure St? Ms. Murray? t? r? sistent sulfonamides, although these have? t? introduced in the mid-Sch? es 1930? m? do? t?, r? resistance? silent in FR? report? hen in 1940 streptococci and gonococci. The Ins? site of streptomycin in the treatment of tuberculosis by d? rapid development thwarted? r? resistance through mutation of g? ing targets. mutation is now recognized as the h? m? mechanism of Mycobacterium tuberculosis to r? strength, and nature mol? cular changes of r? resistance? most m? cines against tuberculosis is now known. beneficial mutations occur in bacterial? ries, mobilis? s for k can? by s? insertion sequences and transposons on plasmids, then the diff? annuities varieties can bact? riennes? transmitted. In view of the eye evolution and spread of the r? resistance Antibiotic g? ties, it is important to the speed of bacterial multiplication? Saharan Africa and? exchange Standing bact? ries in animals, humans Tzen? sch?, and h? your farm? worldwide. It ago, supports f? r id? that e d? determinants of the r? resistance to antibiotics is not observed similarities?’re currently am? bact you? nothing, which saw the r? resistance plasmid. DNA? s studies? quen? age lactamases and aminoglycoside inactivating enzymes derived show that, in d? pit of? in? studies on the prot? ines, the two families, there are diff? significant differences in order. Since the? evolution? d? must re lais? to be lower? Interior? 50 years, it is not m? like? t? fact, a mod? in which the the? evolution by mutation alone? from g? common ancestral ties have k? nnte? to be? riv? es. m you? have to draw a capital E and insurance pool vielf g? nic probably valid? j? in the environment of bacterial ? ries. Many bacterial? ries and fungi that produce antibiotics poss? tooth? determinants of the r? assistance that? similar? those found?’re in bact? ries clinics. Exchange g? ties K? nnten pr? that appear in the ground or, more likely, in the intestines of humans or animals. One ad? covered only commercial DNA containing antibiotics Pr?’s disparate production and g? ties r? resistance to Antimicrobial s? sequences k? can use the r? action cha? not by polymer? shaves identification? s g? ties to either exists? j? in nature or k? can quickly r? results in mutation. rapid change? t Find? e? using (a) TEM-lactamase, r? sult? Verl? ngerung profile of the substrate c? phalosporines the third? me g? No-operation (first are indicated? s in 1963? Ath? ties, a year after? s the Ins? Channel ampicillin) and (b) of the lactamase IMI-1 (signal? by an h? pital of California before iMIP? No? me f? r use approved? e to? United States). The pressure of s? selection is cumbersome and inappropriate?? em use of antibiotics, especially in the field m? dical practice is probably responsible, m? me if Agricultural and v? t? rinary gt r? r? resistance of pathogenic? ing humans. Antibiotics, food or water, whether for Wachstumsf? promotion or, more importantly,? en The mass production of the treatment or pr? tion (or both treatment and prophylaxis) in farm animals factory is clearly an effect not quantified? are the levels of r? resistance. Bacteria a wonderful choice the system? biochemical and my g? n? ticks have weight? hrleistung the d? development and spread of the r? resistance to antibiotics. M? mechanism of r? resistance to important antibiotics first?-lactam r? resistance? lactam go? s? a family of antibiotics by one?-lactam. p? nicillines, c? phalosporines, clavams is (or are oxapenams), c? phamycines and members of this family CARBAP? n? my. L ‘int? grit?? t?-lactam ring is n? necessary f? r, T? activity?, which entered? does inactivation of a number of transpeptidase that catalyze the final valid insurance r? shares r ? particles of synth? peptidoglycan is Best.? lactams impartial? cons? - in clinical isolates is mainly due? hydrolysis of antibiotics by? v? ments?-lactamase. mutational? Following? change PBP (prot? ines linking p? nicillines) or cell? perm? abilit? re? t can also lead??-lactam r? resistance.?-lactamases are a group h? t? rog? no enzymes. Several classifications for their hydrolytic spectrum, the sensibility?? About inhibitors, location g? n? tick (plasmid or chromosomal), g? do or prot? ine amin? s? s? frequency acids have? t? About? es. The functional classification?-lactamases of Bush, Jacoby and frapp? Medeiros (1995) d? ends four groups according to their substrate and inhibitor profiles. c? phalosporinases are a group that is not also Clavulanic? acid INHIB?; Group 2 p? nicillinases, c? phalosporinases and? broad spectrum?-lactamases, which are g? n? ally INHIB? e by active site directed? e?-lactamase inhibitors; Group 3 Metallo-? - lactamases, the p? nicillines, c? phalosporines and CARBAP? n? my hydrolyze and poorly INHIB? e by almost total? len?-lactam containing mol? vehicles?, Group 4 p? nicillinases who did not ? t? Clavulanic? acid INHIB?. subgroups, m? my price? finished by hydrolysis carb? nicilline and cloxacillin (oxacillin) in group 2 p? nicillinases. zun The classification? CHST Ambler (1980 ) and on the basis of amin? s? s? frequency of acid introduced? mol leads to four classes? lar s? sign? A to D. Classes A, C and collect the? evolution FOR r diff groups ? enzyme ent s? navy and Class B zinc-d? pending wait (EDTA-inhibited “) enzymes. Fig:?-Lactamases Gebr? markers r? B-lactam resistance uchliche in Biology mol? cular the g? encoding gene bla f? Dr. TEM-1? - Lactamases? DMPA markers in biology mol? dicular (ACB and plasmids are pUC). using TEM-1 encounters a plasmid g? n? RALIS? e?-lactamases, c? phalosporines? spectrum? strait, c? famandole and c? fop? Razon, and all attacks against Gram-n? ative p? nicillines bact? series is t? mocilline exception. aminothiazole chephalosporins, c? phamycines, monobactams and CARBAP? n? are my r? persistent, your mom? particip?. It Go? rt Group 2B Bush-Jacoby-Medeiros and soft? dicular Class A. The TEM-1 enzyme? T? isolated? for the initial registration time signal? ? from a bacterial? series E. coli in 1965 and is now the h? to?-lactamase? Enterobacteriaceae found?. R? Resistance in more than 50% of clinical isolates of E. DMPA coli? stretched by most TEM-initial registration of the spectrum?-lactamases (ESBLs) is? riv? TEM-1, TEM-2 and SHV-1 mutations produce 1 -? 4-amino? substitutions s? frequency acids. aminoglycosides r? second resistance to aminoglycosides (streptomycin, kanamycin, tobramycin, amikacin ,…) are composed? s which are li? s by pr? aminocyclitol presence of a ring, in which the amino sugars? s in structure. bact? ricide your activity?? t irr is the connection? reversible on the ribosome, although their interaction with other cellular structures s? and Stoffwechselvorg? INVESTIGATION? long as you exp? award? ft. They have an antimicrobial? wide. They are active against them? And robies? Optional bact robie? Ries? No Gram? Ative and bacterial? Ries? Are Gram-positive staphylococci. Aminoglycosides inactive against the ana? Robies and rikettsia. spectinomycin, an amino sugar aminocyclitol? is? naked?, by extension, in the aminoglycoside family. It stands? Also by their bacterial tivities? Riostatique? t and its mode of action. Spectinomycin acts on the synthesis? is the prot? ines w? at the mRNA-ribosome interaction and not as aminoglycosides f? lead? bersetzungsfehler do. Three meters? Nisms r? Resistance have? T? recognized, no? Mlich ribosome Worm? change, decrease? perm? ables? perm? abilit? and inactivation of m? cines? through? change aminoglycosides enzymes. The last m? Mechanism of more clinical importance, because the g? Ing f? r k aminoglycoside-modifying enzymes? can be spread by plasmids or transposons. CHANGE ribosome high r? resistance? streptomycin and spectinomycin k? may only? type? from chromosomal mutations in the g? ing f? r prot? ribosomal ines: RPSL R? Result (or street), SDB (or Rama or sud2) FSDP (eps or SPC or SPCA). mutations in STRC (or STRB) produce r? resistance? Low streptomycin. perm? abilit? Decrease? t? Missing or Worm? change in transport aminoglycosides, the absence of membrane potential can k? changes? in LPS (lipopolysacchaccarides) Phil? ph? phenotype in r? strength think? e? all aminoglycosides lead f?. inactivation of aminoglycosides These enzymes are divided? s three major e classes, depending on the type class? are? chang?: AAC (ac? tyltransf? shave), ANT (Nucleotidyltransferases or ad? nyltransf? shave), APH (phosphotransf? shave). This classification? T? widely? tudi? Shaw et al. (1993). H? en? quently aminoglycoside markers r? strength of biology mol? dicular ant (3”)-Ia (synonyms: aada, AAD (3”) (9)) conf? re a r? resistance? streptomycin and spectinomycin used?. The g? Has not? T? found? in the context of several transposons (TN7, Tn21, …) and is UBIQUITE? r in bact? ries Gram-n? negatively. APH (3 ‘)-II (synonyms: APHA-2, nptII) conf? Re a r? Resistance? Km (kanamycin), Neo (n? Omycine), PRM (paromomycin), RSM (ribostamycin), but (Butirosin), GMB (GentamycinB). This g? Is only rarely found? in clinical isolates. APH (3 ‘)-II is associated? ? transposon Tn5 and observed? among bacterial? ries Gram-n? negatively and Pseudomonas sp. However, the H? impact in the environmental isolates seems kanR? very low (al Recorbet et al. 1992; Leff et al. 1993; Smalla et al., 1993). APH (3 ‘)-III (synonyms: nptII) conf? Re a r? Resistance? Km (kanamycin), Neo (n? Omycine), PRM (paromomycin), RSM (ribostamycin) Lvdm (lividomycin), but (Butirosin), GMB (GentamycinB). AMK (amikacin) and ISP (is? Pamicine) are? Also chang? in v. vitro?, but according to the standards of the Beg date? ch? ance? r? NCCLS resistance is only? low levels by many St? expressed? mmen. APH (3 ‘)-III is g? N? Ally r? Party between bact? Ries Gram-positive, but also? T? observed? e Campylobacter spp. NPTII is not h? en? quently biology mol? lar, but may in certain vectors of Agrobacterium f? r transformation v? g? rate (Bevan, 1984) 3. t? tetracycline t? tetracycline r? resistance (t? tetracycline, doxycycline, minocycline, oxtetracycline? be found?) are antibiotics which inhibit bacterial growth? Saharan Africa by the district? t synth? is the prot? ines. They? Taient h? en? quently f? r last forty? res ann? es, th agent? peutic rmedizin used in? human and v? t? veterinarian?, but also as Wachstumsf? supporters in the? lifting. The? Emergence of the r? Bacterial resistance? Saharan Africa? these antibiotics has NKT now use r? product? . Three diff? M ent? Nisms sp? Cific r? Resistance? the t? tetracycline have? t? identification? s: efflux of the t? tetracycline, ribosomal protection and modification of the t? tetracycline. efflux t? tetracycline is achieved by a prot? ine export of major facilitator superfamily (MFS). The protein? Ine? the export? t? found? for? be a functional system? me antiport? lectroneutre which catalyzes the? cation exchange m? metallic complex t? tetracycline divalent f? r a proton. In bacterial? Ries? No Gram? Ative of the prot? Ine contains export? 12 TMS (transmembrane fragments), w? lt in any Gram-bacterial? ries positive, it displays 14 TMS. ribosome protection m? di? e by an L? prot? ines soluble, which shares with homolgy GTPases involved? synth? is the prot? ines, N? Mlich EF-Tu and EF-G. The third? Me m? Mechanism involves a prot? Cytoplasmic ine that chemically modified the t? Tetracycline. This r? Action occurs only in pr? Presence of oxygen? And NADPH do not work in the nat?-H? You natural (Bacteroides). The first two m? Nisms are the most r? Generally distributed and most of their g? Ties are normally? About? d? envelope? s transmissible plasmids and / or transposons. Both m? Nisms have? T? observed? s in both a? robies and ana? robies? No Gram? Negative or Gram positive bacterial? Ries show their r? Partition between bact? Ries K? Kingdom. Up? what we have now? approximately sixty-one of g? ties r? strength of the t? tetracycline have? t? s? QuEnc? s and zweiunddrei? ig g classes? ties among non-producers and producers (Streptomyces) have? t? identification? s. Each new class is distinguished by its Unf? capacity?, identification? hybridize with one of the g? ties Tet known under strict conditions. A new nomenclature f? r f d? determinants of the r? resistance? r the future with the SB Levy group about? the name of the h? en? quently used? s r? resistance? the t? tetracycline markers in biology mol? dicular Several of? Determinants r? resistance? the t? tetracycline are currently used? s in rep? re mol biology? lar. Most gesto? This feature? Situ?