Antimicrobial Resistance in Anaerobes

Rasmussen, Beth A.; Bush, Karen; Tally, F. B.

doi:10.1093/clinids/24.supplement_1.s110

Cited by 160 publications

(87 citation statements)

References 118 publications

(219 reference statements)

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“…It is well known that staphylococcal organisms and some gramnegative bacilli can produce ß-lactamase. [25][26][27][28] In the present study, ß-lactamase was detected in aerobic and strictly anaerobic gram-negative bacilli, while none of the Staphylococcus isolated produced this enzyme. The incidence of ß-lactamase-producing anaerobic gram-negative bacilli has been reported in several studies.…”

Section: Discussionmentioning

confidence: 71%

Past administration of β-lactam antibiotics and increase in the emergence of β-lactamase–producing bacteria in patients with orofacial odontogenic infections

Kuriyama¹,

Nakagawa²,

Karasawa³

et al. 2000

Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, an

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Section: Discussionmentioning

confidence: 71%

Past administration of β-lactam antibiotics and increase in the emergence of β-lactamase–producing bacteria in patients with orofacial odontogenic infections

Kuriyama¹,

Nakagawa²,

Karasawa³

et al. 2000

Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, an

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“…An obvious problem and important health issue associated with repeated exposure to the same antibiotic is resistance of those microbes targeted by the drug, which can result in an alteration of flora and possible persistence of BV-associated pathogens. Resistance to metronidazole, despite its use for over 3 decades, is rare (14,27). Recent studies have shown an emergence of clindamycin-resistant genital organisms among clinically relevant bacteria, including group B streptococci (17,20).…”

mentioning

confidence: 99%

Microbiologic Response to Treatment of Bacterial Vaginosis with Topical Clindamycin or Metronidazole

et al. 2005

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To compare the frequencies, concentrations, and antimicrobial susceptibilities of vaginal microbes isolated from women with bacterial vaginosis (BV) before and after therapy, 119 nonpregnant women aged 18 to 45 with clinical and Gram stain evidence of BV were randomized to receive intravaginal clindamycin or metronidazole. Vaginal swabs were collected at baseline and 7 to 12 days, 35 to 45 days, and 70 to 90 days following therapy for quantitative vaginal culture. For the 99 women completing all four visits, statistical analyses were performed comparing differences in vaginal microflora between the two treatment arms and between visits in the same treatment group. Antimicrobial susceptibility testing using the agar dilution method was performed for anaerobic gram-negative rods. Although both therapies resulted in decreased colonization by Gardnerella vaginalis and Mycoplasma hominis, only metronidazole treatment resulted in a significant decrease in the frequency and concentration of Prevotella bivia and black-pigmented Prevotella species. Of the 865 anaerobic gram-negative rods evaluated for susceptibility, only 3 (0.3%) were resistant to metronidazole, whereas clindamycin resistance increased significantly for P. bivia and black-pigmented anaerobic gram-negative rods persisting following clindamycin therapy. Clindamycin-resistant subpopulations of P. bivia and black-pigmented Prevotella species emerged 7 to 12 days after therapy even among women colonized initially by clindamycin-susceptible strains. These resistant subpopulations persisted at high frequencies (42 to 50%) 70 to 90 days following therapy. The two topical agents for treatment of BV have differing microbiologic effects on the vaginal microflora. The emergence of clindamycin-resistant anaerobic gram-negative rods following therapy is of concern.

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“…This was based in part on observations that nominally Mtz r clinical isolates differ in the levels of Mtz that they tolerate (resistance level, or MIC), and also fit with precedents of multiple mechanisms of drug resistance in other bacterial species (9,33,37). In principle, resistance might also result from (i) diminished Mtz uptake or its active export (26,40), (ii) more efficient DNA damage repair (6,43), or (iii) enhanced scavenging of oxygen radicals that are produced according to certain models of Mtz activation (23,41).…”

mentioning

confidence: 99%

Sequential Inactivation of rdxA (HP0954) and frxA (HP0642) Nitroreductase Genes Causes Moderate and High-Level Metronidazole Resistance in Helicobacter pylori

et al. 2000

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Helicobacter pylori is a human-pathogenic bacterial species that is subdivided geographically, with different genotypes predominating in different parts of the world. Here we test and extend an earlier conclusion that metronidazole (Mtz) resistance is due to mutation in rdxA (HP0954), which encodes a nitroreductase that converts Mtz from prodrug to bactericidal agent. We found that (i) rdxA genes PCR amplified from 50 representative Mtz r strains from previously unstudied populations in Asia, South Africa, Europe, and the Americas could, in each case, transform Mtz s H. pylori to Mtz r ; (ii) Mtz r mutant derivatives of a cultured Mtz s strain resulted from mutation in rdxA; and (iii) transformation of Mtz s strains with rdxA-null alleles usually resulted in moderate level Mtz resistance (16 g/ml). However, resistance to higher Mtz levels was common among clinical isolates, a result that implicates at least one additional gene. Expression in Escherichia coli of frxA (HP0642; flavin oxidoreductase), an rdxA paralog, made this normally resistant species Mtz s , and frxA inactivation enhanced Mtz resistance in rdxA-deficient cells but had little effect on the Mtz susceptibility of rdxA ؉ cells. Strains carrying frxA-null and rdxA-null alleles could mutate to even higher resistance, a result implicating one or more additional genes in residual Mtz susceptibility and hyperresistance. We conclude that most Mtz resistance in H. pylori depends on rdxA inactivation, that mutations in frxA can enhance resistance, and that genes that confer Mtz resistance without rdxA inactivation are rare or nonexistent in H. pylori populations.Helicobacter pylori is a gram-negative microaerophilic bacterium that chronically infects human gastric epithelial cell surfaces and the overlying gastric mucin, a niche that few if any other microbes can occupy. It is carried by more than half of all people worldwide and is an important human pathogen: a major cause of peptic ulcer disease, and a contributor to other illnesses, ranging from childhood malnutrition to gastric cancer, and to increased susceptibility to other food-and waterborne pathogens (7,8,32,38,47). There is great intrinsic and public health interest in fully elucidating H. pylori's metabolic pathways and how H. pylori maintains its redox balance during microaerobic growth. Such knowledge should help us to understand the extraordinary chronicity of H. pylori infection and factors that determine whether a given infection will be benign or virulent, elucidate mechanisms of drug susceptibility and resistance, and identify potential targets for new effective antimicrobial agents.Here we focus on mechanisms of susceptibility and resistance of H. pylori to metronidazole (Mtz), a synthetic nitroimidazole that is a key component of popular and affordable anti-H. pylori therapies worldwide and that is also widely used against various anaerobic and parasitic infections (13,36,45). Resistance to Mtz is common among H. pylori strains, with frequencies among clinical isolates ranging from 10 ...

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Antimicrobial Resistance in Anaerobes

Cited by 160 publications

References 118 publications

Past administration of β-lactam antibiotics and increase in the emergence of β-lactamase–producing bacteria in patients with orofacial odontogenic infections

Past administration of β-lactam antibiotics and increase in the emergence of β-lactamase–producing bacteria in patients with orofacial odontogenic infections

Microbiologic Response to Treatment of Bacterial Vaginosis with Topical Clindamycin or Metronidazole

Sequential Inactivation of rdxA (HP0954) and frxA (HP0642) Nitroreductase Genes Causes Moderate and High-Level Metronidazole Resistance in Helicobacter pylori

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