Mechanisms Of Tetracycline Resistance

Resistance to tetracycline can be caused by mutations to host efflux pumps, their 16S rRNA sequences, or the altering permeability of the cell. This usually provides low-level stepwise resistance, which until recently has rarely been clinically important. The more common method is the acquisition of new genes conferring tetracycline resistance. It is believed that this second method occurred in the last hundred years, as illustrated by a study of Enterobacteriaceae collected between 1917 and 1954 where only 2% was resistant to tetracycline.1-1,2-1

Numerous studies have characterized acquired resistance genes. Presently, two genes are considered related and given the same gene designation if they share > 80% of amino acid sequences in common with each other. Two genes are considered different and given different designations if they share < 79% amino acid sequence identity.[3] This comparison can now be performed using GenBank sequence information. The number of tet genes has reached the end of the Roman alphabet and to accommodate new tet genes numbers are being assigned.[3] Levy et al.[3] have agreed to be the contact persons to confirm proposed new numbers for a new tetracycline resistance gene to prevent two distinct tet genes from being assigned the same numbers, or two related genes being assigned different numbers. There have been 33 different tetracycline-resistant tet genes characterized and three oxytetracy-cline-resistant (otr) genes characterized (Table 1).[4] This includes the otr(C) gene, which was recently sequenced in the laboratory and is another efflux protein. Nineteen of the tet genes and two of the otr genes code for efflux pumps, 11 tet genes and one otr gene, [otr(A)], code for ribosomal protection proteins, and three genes code for enzymatic alterations of the tetracycline molecules [tet(X), tet(36) and tet(37)]. (Table 1).[4] The tet(U) sequence is known but seems to be unrelated to other types of resistance genes (Table 1).[1]

In general, clinically important Tcr pathogens rarely owe their resistance to mutations.[1] Some exceptions have been described including Tcr cutaneous propioni-bacteria with mutations in the 16S rRNA.[1] Previously, little work has been performed specifically on the detection of tetracycline mutations, although more work is now being done.

Table 1 Mechanism of resistance for characterized tet and otr genes

Efflux (21) Ribosomal protection (11) Enzymatic (3) Unknowna tet(A), tet(B), tet(C), tet (D), tet(E) tet(M), tet(O), tet(S), tet(W), tet(32), tet(X) tet(U)

tet(G), tet(H), tet(J), tet(V), tet(Y), tet(Q), tet(T), tet (36) tet(37)

tet(Z), tet(30), tet(31), tet(33) tet(A), tetB(P),b tet tet(34)

tet(35)

tetA(P)

tcr3

atet (U) has been sequenced but does not appear to be related to either efflux or ribosomal protection proteins. btetB(P) is not found alone and the tetA(P) and tetB(P) genes are counted as one operon.

Getting Started With Dumbbells

Getting Started With Dumbbells

The use of dumbbells gives you a much more comprehensive strengthening effect because the workout engages your stabilizer muscles, in addition to the muscle you may be pin-pointing. Without all of the belts and artificial stabilizers of a machine, you also engage your core muscles, which are your body's natural stabilizers.

Get My Free Ebook


Post a comment