Metronidazole is widely used as a therapeutic agent for H. Metronidazole resistance is considered to be the main single factor responsible for treatment failure. The high frequency of use of metronidazole may select for resistance not only in H. Because of its well-known safety and efficacy in clinical practice, metronidazole is still the cornerstone for the management of anaerobic infections worldwide.
Supplement sponsorship. Google Scholar. Google Preview. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation.
Volume Article Contents Abstract. Therapeutic Use of Metronidazole for Anaerobic Infections. Metronidazole in Clinical Practice. Mechanisms of Action and Resistance to Metronidazole. Metronidazole and the Normal Microflora. Levels of Resistance to Metronidazole.
Figures and Tables. Oxford Academic. Charlotta Edlund. Carl Erik Nord. Reprints or correspondence: Prof. Carl Erik Nord, Div. Select Format Select format. Permissions Icon Permissions. Open in new tab Download slide. Google Scholar Crossref. Search ADS. Metronidazole versus anaerobes: in vitro data and initial clinical observations. Google Scholar PubMed. A comparison of vancomycin and metronidazole for the treatment of Clostridium difficile -associated diarrhea, stratified by disease severity.
Molecular basis of metronidazole resistance in pathogenic bacteria and protozoa. Chromosomal breakage in the B. Mutational analysis of metronidazole resistance in Helicobacter pylori. Nitroimidazole resistance genes nim B in anaerobic Gram-positive cocci previously Peptostreptococcus spp.
Inducible metronidazole resistance and nim genes in clinical Bacteroides fragilis group isolates. Transferable 5-nitroimidazole resistance in the Bacteroides fragilis group. Structural basis of 5-nitroimidazole antibiotic resistance: the crystal structure of NimA from Deinococcus radiodurans.
The role of Bacteroides conjugative transposons in the dissemination of antibiotic resistance genes. BmeRABC5 is a multidrug efflux system that can confer metronidazole resistance in Bacteroides fragilis. Efflux pump overexpression in multiple-antibiotic-resistant mutants of Bacteroides fragilis.
Mycobacterium bovis BCG rec A deletion mutant shows increased susceptibility to DNA-damaging agents but wild-type survival in a mouse infection model. Metronidazole resistance in Bacteroides spp.
Enhanced pathogenicity of susceptible strains of the Bacteroides fragilis group subjected to low doses of metronidazole. Association of antibiotic resistance and higher internalization activity in resistant Helicobacter pylori isolates. Effect of antimicrobial agents on the ecological balance of human microflora. Comparative effects of omeprazole, amoxycillin plus metronidazole versus omeprazole, clarithromycin plus metronidazole on the oral, gastric and intestinal microflora in Helicobacter pylori -infected patients.
Comparative pharmacokinetics of metronidazole and tinidazole and their tissue penetration. Evidence for extensive resistance gene transfer among Bacteroides spp. The role of conjugative transposons in spreading antibiotic resistance between bacteria that inhabit the gastrointestinal tract. Antimicrobial susceptibility of Bacteroides fragilis group isolates in Europe. National survey on the susceptibility of Bacteroides fragilis group: report and analysis of trends in the United States from to Multicenter survey of the changing in vitro antimicrobial susceptibilities of clinical isolates of Bacteroides fragilis group, Prevotella, Fusobacterium, Porphyromonas , and Peptostreptococcus species.
Susceptibility of the Bacteroides fragilis group in the United States in Decreased susceptibility to nitroimidazoles among Bacteroides species in Brazil. Third Belgian multicentre survey of antibiotic susceptibility of anaerobic bacteria. Antibiotic resistance among anaerobic Gram-negative bacilli: lessons from a French multicentric survey. Susceptibility of the Bacteroides fragilis group to newer quinolones and other standard anti-anaerobic agents.
Antibiotic susceptibility of blood culture isolates of anaerobic bacteria at a Norwegian university hospital. In-vitro antibiotic susceptibility and molecular analysis of anaerobic bacteria isolated in Cape Town, South Africa. Antimicrobial susceptibility of anaerobic bacteria in New Zealand: — Antimicrobial susceptibilities of Bacteroides fragilis and Bacteroides thetaiotaomicron strains isolated from clinical specimens and human intestinal microbiota.
Multicentre survey of the in-vitro activity of seven antimicrobial agents, including ertapenem, against recently isolated Gram-negative anaerobic bacteria in Greece. Metronidazole resistance among clinical isolates belonging to the Bacteroides fragilis group: time to be concerned? Anaerobes: antibiotic resistance, clinical significance, and the role of susceptibility testing.
Bacteroides fragilis resistant to metronidazole after long-term therapy. Bacteroides species highly resistant to metronidazole: an emerging clinical problem? Anaerobic sepsis due to multidrug-resistant Bacteroides fragilis: microbiological cure and clinical response with linezolid therapy.
Antimicrobial resistance and clinical outcome of Bacteroides bacteremia: findings of a multicenter prospective observational trial.
Susceptibility testing of Clostridium difficile against metronidazole and vancomycin by disk diffusion and Etest. Surveillance for resistance to metronidazole and vancomycin in genotypically distinct and UK epidemic Clostridium difficile isolates in a large teaching hospital. Review article: the treatment of refractory Helicobacter pylori infection.
Issue Section:. Download all slides. Comments 0. Add comment Close comment form modal. I agree to the terms and conditions. You must accept the terms and conditions.
The primary role of antimicrobials is to limit the local and systemic spread of infection. Surgical drainage is of primary importance. This includes debriding of necrotic tissue, draining the pus, improving circulation, alleviating obstruction and increasing tissue oxygenation.
Often the alternative diagnosis is suspected based on blood cultures obtained prior to the patient receiving broad-spectrum antibiotics in the emergency room. In the last 3 months we have seen patients with liver abscesses, endocarditis, and osteomyelitis initially felt to have community-acquired pneumonia whose blood cultures initiated prior to antibiotic therapy revealed a pathogen that caused a search for an alternative source of infection. The vast majority of patients only need 2 blood cultures from 2 sites 20 minutes apart before initiation of antibiotic therapy.
Patients in whom common skin contaminants may easily be interpreted as pathogens such as patients with prosthetic heart valves should have 3 sets of blood cultures to aid in the interpretation of cultures that are positive for skin contaminants such as coagulase negative staph. Diabetic patients who have infections related to foot ulcers or ischemic lesions require broad-spectrum antimicrobial therapy active against anaerobes, gram-positives, and gram-negatives.
However, diabetic patients who are not critically ill who are admitted with a clinical picture typical for cellulitis tend to be infected with the same pathogens as non-diabetic patients. We frequently encounter diabetic patients who present with a clinical picture of an uncomplicated cellulitis without ulcers or other lower-extremity lesions and are treated with broader-spectrum antimicrobial therapy than is needed for cellulitis.
Broader therapy is often more expensive, and it puts patients at risk for more adverse effects such as CDAD. The great majority of patients with cellulitis have infection with group A strep and other streptococci, and less often S. Cellulitis due to anaerobes and gram-negative organisms in the absence of foot ulcers or similar lesions is distinctly unusual.
The local findings may take 3 or 4 days to show improvement and there actually may be slight worsening despite 1 or 2 days of appropriate antibiotics. This is believed to be related to toxins produced by group A strep and other local tissue factors. Even if an antimicrobial is successful in eradicating strep, there are still toxins in the tissues that produce aggressive local findings. We often get consulted about patients with cellulitis who after 2 days of antimicrobial therapy may have some improvement in their fever curve and white blood cell count but have worsening of the local findings.
These patients almost never need a change in antimicrobial therapy, but need more time—and elevation. I was taught by one of my mentors of the importance of elevating an extremity when treating cellulitis. My clinical experience has borne out this wisdom. In addition, patients with lower-extremity edema or venous insufficiency or venous stasis who present with cellulitis must have edema and stasis aggressively treated for the cellulitis to respond to antimicrobial therapy.
Five years ago in Ohio, if a patient presented with pyelonephritis or a complicated UTI as a community-acquired infection, it was unusual for the causative pathogen to be quinolone resistant. Quinolones such as ciprofloxacin could be used as empiric therapy for serious gram-negative infections with a great deal of confidence that the causative agent would be sensitive.
In the last 5 years we have seen a steady, progressive increase in resistance to quinolones in both community acquired and nosocomial infections 7,8. Seriously ill patients with infections that are likely due to gram-negative rods should not be treated empirically with quinolone monotherapy in most settings.
Oral quinolones, due to their excellent oral bioavailability, continue to have in important role in treating gram-negative infections, but their use should be based on the results of a culture with antimicrobial susceptibility. Patients who are colonized with VRE in the stool will clear colonization over several weeks or months if there is no antimicrobial pressure to select for VRE. Infectious disease clinicians spend a lot of time trying to allay the fear of patients and families who become extremely nervous due to isolation procedures for VRE.
My usual approach is to tell the patients that the only reason they are in isolation is to prevent VRE from spreading to the very, very small group of patients who actually are susceptible to infection with VRE, such as liver transplant patients. I tell the family there is almost no chance that healthy family members will develop a VRE infection and that the VRE bacteria is normally found as a natural part of the human intestinal flora.
VRE is simply 1 strain that has particular resistance to antibiotics, making it difficult to treat when infection occurs, but it is not more pathogenic. Infection with VRE is relatively rare and with the possible exception of cystitis or bladder colonization there is an extremely low risk of any actual infection despite VRE colonization. Uncomplicated cystitis due to VRE can usually be treated with nitrofurantoin. In the last 5 years in the United States, there has been a steady increase in MRSA infections in patients without traditional risk factors 9, Historically, clinicians have been concerned about MRSA in nursing home patients, patients in other long-term care facilities, injection drug users, and hospitalized patients.
In the last 5 years there have been increasing numbers of patients with MRSA with none of these risk factors. Often these patients present with a serious life-threatening S. It is now appropriate to give vancomycin empirically for patients who have serious illnesses due to suspected S.
As ID practitioners, we do not want to encourage overuse of vancomycin, and clinicians should quickly switch to other agents if the patient proves not to be infected with MRSA. While vancomycin is a useful drug, it is considered inferior to the beta-lactams for many infections, such as bone or joint infections, and should only be used in patients with documented or suspected MRSA, or patients intolerant of beta-lactams.
Several new drugs provide alternatives to vancomycin for MRSA, including linezolid and daptomycin. Both of these agents are more expensive and have not proven in clinical trials to be superior with the possible exception of linezolid for MRSA pneumonia.
0コメント