80:
289:
17:
147:
243:
to the beta-lactam ring which is a structural characteristic for beta-lactams and hydrolyze the ring. This renders the antibiotic inactive. The spread of the penicillinase resistance was much faster compared to the chromosomal-mediated resistance mechanisms. The plasmids containing TEM-1 could be passed from bacterium to bacterium via conjugation
196:
component of the bacterial cell wall. PBPs cross-link the amino acid strands of peptidoglycan during synthesis. Normally, beta-lactams bind the PBPs and thereby inhibit the cross-linking of peptidoglycan. When this occurs, the cell wall of the bacterium is compromised and often results in cell death. When
242:
is mediated by the plasmid borne TEM-1 type beta-lactamase which falls under the third general mechanism for beta-lactam resistance. There have been over 200 beta-lactamases described and some of them are antibiotic specific. TEM-1 is a penicillinase specific for penicillins. This enzyme will bind
381:
class of antibiotics. These antibiotics bind to the 16s rRNA of the 30S subunit of the bacterial ribosome, thereby inhibiting mRNA translation and protein synthesis. Resistance appears to be acquired through porin-related mechanisms, much like the cephalosporin resistance mechanism. This mechanism
275:
gene, which encodes for the DNA gyrase, have been seen extensively. DNA gyrase is an enzyme that binds to DNA and introduces negative supercoiling. This helps unwind the DNA for replication. If there is a mutation in the DNA gyrase, then the quinolone will not be able to bind to it resulting in
195:
gene encodes an alternative penicillin-binding protein, PBP-2. This mechanism falls under the second general mechanism for beta-lactam resistance. PBPs, also known as transpeptidases, are targets for beta-lactams. These enzymes (PBPs) are involved in peptidoglycan synthesis which is a major
341:
Tetracyclines are a class of antibiotics that inhibit protein synthesis by binding to the 30s ribosomal subunit of bacterial cells, keeping transcription of the bacterial genome from occurring. Tetracyclines are bacteriostatic, which means that the growth of the bacterium will be slowed.
48:
became available, but by the 1970s resistant strains predominated. Resistance to penicillin has developed through two mechanisms: chromosomally mediated resistance (CMRNG) and penicillinase-mediated resistance (PPNG). CMRNG involves step wise mutation of penA, which codes for the
251:
Quinolones are a class of synthetic antibiotics that inhibit DNA replication, recombination, and repair by interacting with the bacterial DNA gyrase and/or topoisomerase IV. Second generation quinolones like ciprofloxacin and ofloxacin have been widely used to treat
211:(multiple transferable resistance) gene encodes for an efflux pump. Efflux pumps mediate resistance to a variety of compounds including antibiotics, detergents, and dyes. This mechanism falls under the first general resistance mechanism to beta-lactams.
263:
gene and provides resistance to fluoroquinolones. The NorM efflux pump is a member of the MATE (multidrug and toxic compound extrusion) family and functions by a Na+ antiporter. It is also known that a point mutation upstream of the
346:
because the treatment regimen requires many doses, which may affect compliance and contribute to resistance. Tetracycline is still used as treatment for this infection in developing countries because the cost for the drug is low
226:
contains porins which are holes within the cell wall in which some molecules are able to diffuse into or out of the cell membrane. This mechanism falls under the first general mechanism for beta-lactam resistance. The
551:
Centers for
Disease Control Prevention (CDC). (Aug 10, 2012). "Update to CDC's Sexually Transmitted Diseases Treatment Guidelines, 2010: Oral Cephalosporins No Longer a Recommended Treatment for Gonococcal Infections".
382:
would result in the access of the antibiotic to the bacterial cell being inhibited. There is a possibility of future enzymes (made by the bacterium) that will be able to denature and inactivate the aminoglycosides.
219:. MtrD is among the Resistance Nodulation Division (RND) efflux pump superfamily. These pumps are proton antiporters where the antibiotic is pumped out of the cell while a proton is pumped into the cell.
358:(efflux pump formation) mutations mediate chromosomal resistance. These adaptations will also affect the ability of the antibiotic to get into, or stay in the bacterial cell. High level resistance of
79:
271:
High-level resistance to quinolones has been seen through target modification acting on the DNA gyrase and topoisomerase IV. Multiple amino acid substation mutations in the
98:
have been used to treat gonorrhoea since 2007, but resistant strains have emerged. As of 2010, the recommended treatment is a single 250 mg intramuscular injection of
725:
Wilson, Brenda A., Abigail A. Salyers, Dixie D. Whitt, and
Malcolm A. Winkler. Bacterial Pathogenesis: A Molecular Approach. 3rd ed. Washington DC: ASM Press, 2011. Print.
332:
gene that encodes for the bacterial porin. This form of resistance has only been observed with ceftriaxone which is administered through an intramuscular injection.
786:
605:"Extensively drug-resistant (XDR) Neisseria gonorrhoeae causing possible gonorrhoea treatment failure with ceftriaxone plus azithromycin in Austria, April 2022"
176:
developing high resistance to penicillin through two main mechanisms: chromosomally mediated resistance (CMRNG) and penicillinase-mediated resistance (PPNG).
318:
an alteration of more than four amino acids in the C-terminal end of the PBP-2, which would result in the antibiotic being unable to bind to its target
936:
972:
941:
280:
gene which encodes for the topoisomerase IV. Topoisomerase IV acts similarly to DNA gyrase and is involved in unwinding DNA for replication.
259:
Low-level quinolone resistance has been linked to changes in cell permeability and efflux pumps. The NorM efflux pump is encoded by the
235:
and when this gene undergoes mutations, there is a decrease in permeability of the cell wall to hydrophilic antibiotics like penicillin.
779:
668:
Murray, Patrick R., Ken S. Rosenthal, and
Michael A. Pfaller. Medical Microbiology. 6th ed. Philadelphia: Mosby/Elsevier, 2009. Print
256:
infections. Resistance to these antibiotics has developed over the years with chromosomal resistance being the primary mechanism.
90:
were a useful next-line treatment until resistance was achieved through efflux pumps and mutations to the gyrA gene, which encodes
905:
772:
711:
Drlica, Zhao (1997) DNA gyrase, topoisomerase IV, and the 4-quinolones. Microbiology and
Molecular Biology Reviews 61:377–392
742:
Mosaic Allele in a
Successful International Clone Causes Treatment Failure. Antimicrobial Agents and Chemotherapy 1273–1280
158:
in the 1940s. There are three general mechanisms that may allow bacteria to become resistant to beta-lactam antibiotics:
931:
62:
50:
179:
Chromosomally mediated resistance occurred through step-wise changes over many years. Chromosomal mutations in the
307:. The cephalosporins are part of a larger beta-lactam family of antibiotics. The newly discovered H041 strain of
204:, the new PBP-2 that is synthesized is no longer recognized by the beta-lactams rendering the bacterium resistant.
915:
884:
851:
846:
73:
38:
76:, and as a result, the existence of any strain resistant to a given drug could spread easily across strains.
734:
Unemo, Golparian, Nicholas, Ohnishi, Gallay, Sednaoui (2011) High-Level
Cefixime- and Ceftriaxone-Resistant
311:, originally isolated from a commercial sex worker in Japan, was shown to be resistant to this antibiotic.
858:
841:
399:
392:
54:
29:
288:
83:
Cases of
Neisseria Gonorrhoeae with decreased susceptibility or resistance to antibiotics (2017-2018).
946:
87:
910:
967:
642:
512:
Deguchi T, Nakane K, Yasuda M, Maeda S (September 2010). "Emergence and spread of drug resistant
292:
Basic structures of penicillins(1) and cephalosporins(2) with beta-lactam ring highlighted in red
276:
the activity of DNA gyrase not being inhibited. Multiple mutations have also been noted in the
699:
Van
Bambeke, Balzi, Tulkens (2000) Antibiotic Efflux Pumps. Biochemical Pharmacology 60:457–470
889:
755:
mosaic alleles and prediction of reduced susceptibility to expanded-spectrum cephalosorins in
634:
561:
533:
436:
868:
624:
620:
616:
525:
494:
428:
146:
863:
579:
419:
Ligon BL (2005). "Albert Ludwig
Sigesmund Neisser: discoverer of the cause of gonorrhea".
131:
58:
820:
629:
604:
378:
95:
65:
57:
that removes penicillin from the cell; and penB, which encodes the bacterial cell wall
961:
825:
810:
796:
646:
119:
16:
682:
Rouquette-Loughlin, Dunham, Kuhn, Balthazar, Shafer (2003) The NorM Efflux Pump of
135:
127:
114:
can be resistant to antibiotics that are normally used to treat it. These include:
103:
690:
Recognizes
Antimicrobial Cationic Compounds. Journal of Bacteriology 185:1101–1106
296:
123:
107:
99:
529:
486:
432:
815:
91:
45:
759:. Acta Pathologica, Microbiologica et Immunologica Scandinavica 116:1001–1008
155:
34:
638:
565:
537:
440:
268:
gene will causes overexpression of NorM, and mediate elevated resistance.
751:
Unemo (2008) Real-time PCR and subsequent pyrosequencing for screeing of
314:
The possible mechanisms of resistance to this antibiotic are as follows:
303:
are third generation cephalosporins and are often used as treatments for
300:
115:
764:
362:
to tetracyclines was first reported in 1986 with the discovering of the
498:
325:, resulting in the overexpression of genes that code for efflux pumps
287:
162:
inability to access/target penicillin-binding protein (PBP) enzyme
145:
78:
15:
41:
to many antibiotics. The bacteria was first identified in 1879.
768:
33:, the bacterium that causes the sexually transmitted infection
580:"Biggest Threats - Antibiotic/Antimicrobial Resistance - CDC"
342:
Tetracyclines are not often recommended for the treatment of
168:
hydrolysis/inactivation of the antibiotic by beta-lactamases.
366:
determinant. The mechanism of resistance is still unknown.
165:
inhibition of binding to PBP via modification of the enzyme
215:
encodes for the protein MtrD which is the efflux pump for
154:
Beta-lactams like penicillin were widely used to treat
678:
676:
674:
924:
898:
877:
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803:
480:
478:
476:
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191:genes are the major mechanisms for CMRNG. The
468:
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450:
780:
8:
24:showing characteristic diplococci morphology
554:MMWR. Morbidity and Mortality Weekly Report
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773:
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150:Old advertisement for penicillin treatment
937:Antibiotics in poultry farming in America
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719:
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621:10.2807/1560-7917.ES.2022.27.24.2200455
411:
350:As with the penicillin resistance, the
942:Subtherapeutic antibiotic use in swine
44:In the 1940s effective treatment with
321:mutations in the promoter regions of
238:Penicillinase-mediated resistance in
172:Overuse of penicillin contributed to
61:. PPNG involves the acquisition of a
7:
14:
377:has also shown resistance to the
102:, sometimes in combination with
603:Pleininge, Sonja (April 2022).
126:(an injectable cephalosporin),
53:(PBP-2); mtr, which encodes an
906:Antimicrobial pharmacodynamics
110:. However, certain strains of
1:
973:Antibiotic-resistant bacteria
493:. World Health Organization.
487:"Antimicrobial resistance in
231:gene encodes the porins for
932:Antibiotic use in livestock
989:
530:10.1016/j.juro.2010.04.078
433:10.1053/j.spid.2005.07.001
51:penicillin-binding protein
916:Production of antibiotics
885:Antimicrobial stewardship
305:N. gonorrhoeae infections
847:Antimicrobial resistance
421:Semin Pediatr Infect Dis
74:horizontal gene transfer
72:has a high affinity for
524:(3): 851–8, quiz 1235.
859:Antibiotic prophylaxis
842:Antibiotic sensitivity
485:Tapsall, John (2001).
354:(porin formation) and
293:
151:
84:
25:
757:Neisseria gonorrhoeae
736:Neisseria gonorrhoeae
688:Neissera meningitidis
684:Neisseria gonorrhoeae
514:Neisseria gonorrhoeae
489:Neisseria gonorrhoeae
400:Antibiotic resistance
393:Neisseria gonorrhoeae
291:
174:Neisseria gonorrhoeae
149:
82:
39:antibiotic resistance
30:Neisseria gonorrhoeae
22:Neisseria gonorrhoeae
19:
947:Pesticide resistance
911:List of antibiotics
94:. Third-generation
294:
152:
85:
26:
955:
954:
890:Antibiotic misuse
738:in France: Novel
609:Euro Surveillance
328:mutations in the
222:The cell wall of
980:
869:Directed therapy
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88:Fluoroquinolones
37:, has developed
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797:antimicrobials
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379:aminoglycoside
375:N. gonorrhoeae
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360:N. gonorrhoeae
344:N. gonorrhoeae
338:
335:
334:
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326:
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309:N. gonorrhoeae
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284:Cephalosporins
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254:N. gonorrhoeae
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240:N. gonorrhoeae
233:N. gonorrhoeae
224:N. gonorrhoeae
217:N. gonorrhoeae
198:N. gonorrhoeae
170:
169:
166:
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112:N. gonorrhoeae
96:cephalosporins
70:N. gonorrhoeae
66:beta-lactamase
20:Gram stain of
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2:
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560:(31): 590–4.
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427:(4): 336–41.
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63:plasmid-borne
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899:Pharmacology
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587:. Retrieved
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136:tetracycline
128:azithromycin
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104:azithromycin
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925:Agriculture
584:www.cdc.gov
499:10665/66963
297:Ceftriaxone
142:Penicillins
124:ceftriaxone
108:doxycycline
100:ceftriaxone
55:efflux pump
962:Categories
816:Antifungal
589:2016-05-05
407:References
247:Quinolones
92:DNA gyrase
46:penicillin
968:Gonorrhea
852:multidrug
821:Antiviral
647:249747652
156:gonorrhea
118:(an oral
35:gonorrhea
835:Concepts
639:35713023
566:22874837
538:20643433
441:16210113
386:See also
301:cefixime
200:encodes
116:cefixime
795:Use of
630:9205165
518:J. Urol
645:
637:
627:
615:(24).
564:
536:
439:
187:, and
134:, and
59:porins
804:Types
643:S2CID
753:penA
740:penA
686:and
635:PMID
562:PMID
534:PMID
437:PMID
364:tetM
352:penB
330:penB
299:and
278:parC
273:gyrA
266:norM
261:norM
229:penB
207:The
202:penA
193:penA
189:penB
181:penA
625:PMC
617:doi
526:doi
522:184
516:".
495:hdl
429:doi
356:mtr
323:mtr
213:mtr
209:mtr
185:mtr
122:),
106:or
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