MRSA Action UK | Cdiff
Self-Archiving Policy · Dispatch Dates · Terms and Conditions In recent years , infections with Clostridium difficile have become more as to the optimal management and prevention of this problem, particularly in the Risks factors .. Online ISSN ; Print ISSN ; Copyright © clinical practice guideline on Clostridium difficile infection; idsa; shea; guideline;. Intestinal infection known as C. diff can spread through spores and cause Without strict precautions, spores are inadvertently transmitted to.
Widespread overuse and misuse of antibiotics is illustrated by the data of the US medical system. Antibiotic agents that are active against anaerobic bacteria present the greatest risk because they alter the intestinal microecology [ 15 ]. Clindamycin, cephalosporins in particular third generation cephalosporins such as cefotaxime and ceftriaxone and broad spectrum penicillins are notorious for provoking CDAD.
According to Aronsson et al.
Clostridium difficile-related complications are uncommon with linezolid [ 18 ] and the same is true for aminoglycosides, metronidazole, rifampicin and vancomycin. An important risk factor is the duration of antimicrobial therapy. In a large prospective study, Wistrom et al. Apart from the duration of treatment with antibiotics, further risk factors include advanced age, gastrointestinal surgery, long duration of stay in health care settings, serious underlying disease and use of proton pump inhibitors [ 20 ].
CDAD is rare in patients who have not been exposed to antibiotics [ 21 ]. Their true incidence presumably is masked because antibiotics and chemotherapeutic agents are often used concomitantly, especially in neutropenic patients [ 22 ].
Chemotherapeutic agents such as adriamycin, cyclophosphamide, methotrexate and 5-fluorouracil have the capacity to precipitate CDAD, as demonstrated by Cudmore et al.
According to Svenungsson et al. Fulminant CDAD has also been described in lung transplant recipients exposed to high dose immunosuppression and repeated courses of antimicrobials because of frequent pulmonary infections [ 6 ].
Several reports pointed to the risk of CDAD associated with the use of tacrolimus [ 25 ]. Most cases of Clostridium difficile diarrhoea make a full recovery.
However, elderly patients with other underlying conditions may have a more severe course. Occasionally, infection in these circumstances may be life threatening. For mild or moderate symptoms of Clostridium difficile infection, it is best to stop taking the antibiotics that may have caused the infection, if this is possible. This will allow the natural 'good' bacteria to regrow in your gut. In many cases where the symptoms are mild or moderate, this is often enough to ease the symptoms and clear the infection.
If you have symptoms that are more severe, such as severe diarrhoea or colitis swelling and irritation of the lining of the bowelyou may need to take an antibiotic that can kill Clostridium difficile bacteria.
Clostridium Difficile : OSH Answers
This will usually be either metronidazole or vancomycin, which should ease the symptoms within two to three days. Possible side effects of these antibiotics are stomach ache, nausea and vomiting. Some patients treated for a Clostridium difficile infection will have a repeat of their symptoms. In rare and serious cases of Clostridium difficile infection, surgery may be needed to repair damage to the intestines bowelespecially if there are tears in the lining of the small intestine.
What should I do to prevent the spread of Clostridium difficile to others? If you are infected you can spread the disease to others.
However, only people that are hospitalized or on antibiotics are likely to become ill. In order to reduce the chance of spreading the infection to others: If you have had diarrhoea it is sensible to put down the toilet seat cover down, if there is one, in order to prevent aerosol contamination of the environment. How can hospitals and care homes prevent the spread of Clostridium difficile? Clostridium difficile bacteria can spread easily, particularly in healthcare environments, such as a hospital or care home.
All isolates were sensitive to metronidazole and vancomycin.
Unfortunately, the same cannot be said for other antibiotics. Recently, the complete genome of C. These mobile genetic elements are often involved in the transfer of antimicrobial resistance and virulence factors. Bourgault et al[ 83 ] found that for the B1 epidemic strain the quinolones, macrolides and other commonly used antibiotics have succumbed to the antibiotic resistance mechanisms of C.
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All historical NAP1 isolates were resistant to quinolones, suggesting that the epidemic may be more associated with the increased use of fluoroquinolones, as opposed to the recent development of quinolone resistance by the epidemic strain.
The oft-quoted reasons for metronidazole assuming the status of preferred agent for treating CDI has been the potential for development of vancomycin-resistant enterococci VRE and the higher cost of oral vancomycin.
In contrast to this notion, a small study looking specifically at the issue of developing VRE found no patients developed VRE while being treated with oral vancomycin[ 85 ]. Further, retail costs are much higher. Most hospitals avoid the extraordinary cost of vancomycin capsules by using the generic intravenous formulation and compounding it in water as a liquid vancomycin solution.
Despite issues related to fostering VRE and cost, prior comparative studies of metronidazole and vancomycin have not revealed a statistically significant difference between the two antibiotics[ 8889 ].
However, the number of patients was small and neither study was stratified by severity of disease. Despite similar response rates, there are significant pharmacologic concerns related to metronidazole, which tilt the balance in favor of vancomycin.
Fecal metronidazole levels have been noted to increase with colonic inflammation, probably from transudation into the lumen, but these levels decrease as inflammation subsides and are undetectable upon recovery[ 3791 ].
This was not due to resistance, as those strains tested, were all sensitive to metronidazole. Interestingly, in this study there was no difference in outcomes between those who were continued on metronidazole despite clinical failure compared to those who were changed to vancomycin. Musher et al[ 92 ] suggested that patients with severe disease could have decreased blood flow to the colon, which would result in less transudation of metronidazole into the lumen and either a slower response or clinical failure[ 93 ].
Despite this potential for low metronidazole levels, in vitro the drug has been shown to be very rapidly bactericidal at 8-times the minimum inhibitory concentration MICa level which is usually reached in the colon. This rapid bactericidal effect can be compared to vancomycin, which has been shown to be only inhibitory of bacterial growth[ 40 ].
As opposed to the poor pharmacokinetics of metronidazole, vancomycin has near perfect characteristics for a drug used to treat an infection limited to the lumen of the colon.
Al-Nassir et al[ 94 ] have shown that vancomycin is much more effective than metronidazole in removing C. By day 5 of treatment, patients treated with vancomycin were 3. In this study, 10 of 34 patients were switched from metronidazole to oral vancomycin between days 2 and 10 due to suboptimal clinical response, of whom 8 of the 10 had less than a one log decrease in C. Once they were switched to oral vancomycin, 7 of these 8 patients had undetectable C.
Freeman et al[ 9596 ] confirmed the favorable characteristics of oral vancomycin in a human gut model composed of three vessels operating in a weir cascade system in an oxygen free nitrogen atmosphere. They found that cytotoxin titers were unaffected by metronidazole, while vancomycin resulted in a marked decrease in toxin and the C. Another issue which may decrease the effectiveness of metronidazole is inactivation by Enterococcus faecalis, which has been shown to allow protection of organisms which would normally be killed by metronidazole[ 97 ].
There also appears to be a higher failure rate with metronidazole when the physician is forced to continue the offending antibiotics, which is often the case. In one series, all patients who could have the offending antibiotic discontinued had resolution of diarrhea by 14 d when treated with metronidazole[ 98 ].Nurse Training & Infection Control: C. difficile
Because rifampin has been shown to have markedly superior in vitro activity in comparison with other antimicrobials against C. Lagrotteria et al[ ] conducted a prospective, randomized, single-blind study of metronidazole alone vs metronidazole plus rifampin[ ]. One of the most important recent advances in the treatment of CDI has been the development of scoring systems, which allow the physician to determine which patients are at highest risk for severe CDI.
The development of scoring systems was started by Pepin et al[ 78 ] who developed local recommendations, because of the overwhelming epidemic in Quebec caused by the new epidemic B1 strain.
In January ofthey developed local recommendations for the use of oral vancomycin: Zar et al[ ] conducted the first randomized, double-blind, placebo controlled trial comparing metronidazole and vancomycin in the treatment of CDI that stratified patients at study entry based upon severity of disease.
The authors developed a scoring system giving 1 point each for the presence of age greater than 60 years, temperature greater than They also gave 2 points for endoscopic evidence of pseudomembranous colitis or treatment in an intensive care unit setting. Mild disease was defined as 0 or 1 points and severe CDI was defined as greater than or equal to 2 points. The authors concluded that metronidazole and vancomycin are equally effective for the treatment of mild CDI; however, vancomycin is superior for treating patients with severe CDI.
Critiques of the Zar et al[ ] article were that one of the criteria for failure was persistent toxin positivity at day 6 and 10 of therapy.