メチシリン耐性黄色ブドウ球菌 methicillin resistant Staphylococcus aureus
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/11/08 23:12:49」(JST)
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MRSAの走査型電子顕微鏡写真
メチシリン耐性黄色ブドウ球菌（メチシリンたいせいおうしょくブドウきゅうきん、Methicillin-resistant Staphylococcus aureus、MRSA）とは、抗生物質メチシリンに対する薬剤耐性を獲得した黄色ブドウ球菌の意味であるが、実際は多くの抗生物質に耐性を示す多剤耐性菌である。なお、生物種としてはあくまで黄色ブドウ球菌であるので、生物学的な詳細は同記事を参照のこと。
目次
- 1 特徴
- 2 耐性機構
- 3 細菌叢調査
- 4 注釈
- 5 関連項目
- 6 外部リンク
特徴[編集]
MRSA は黄色ブドウ球菌が耐性化した病原菌であり、黄色ブドウ球菌と同様に常在菌のひとつと考えられ、健康な人の鼻腔、咽頭、皮膚などから検出されることがある。
そもそも薬剤耐性菌であるため薬剤の使用が多い病院で見られることが多く（耐性菌は抗生物質の乱用により出現すると言われている）、入院中の患者に発症する院内感染の起炎菌としてとらえられている。しかし病原性は黄色ブドウ球菌と同等で、健康な人にも皮膚・軟部組織感染症などを起こしうる。病院外での発症が最初に確認されたのは1960年代にさかのぼるが、近年では健康な人のごく一般的な感染症の起炎菌として見つかることもあり、本菌が病院から街中へと広がっていることが示唆されている。community-acquired MRSA (CA-MRSA) は、1999年に米国で死亡例がみられてからは、外来診療でも留意すべき菌種のひとつとなった。CA-MRSAは、院内感染でのMRSAとは異なり、ミノサイクリンやST合剤、クリンダマイシンが有効であることが多い。
MRSAによる膿瘍
本菌が免疫力が低下した患者に感染すると、通常では本菌が起こすことはないような日和見感染を起こすこともある。一旦発症するとほとんどの抗生物質が効かないため治療は困難である。特に、術後の創部感染、骨感染（骨髄炎）、感染性心内膜炎（IE）、臓器膿瘍は難治性化し、適切な治療を受けられないと後遺症ばかりか死の転帰をたどる事になる。
院内で感染者が判明した場合、感染者の治療も重要であるが、感染を広げないことも重要であり、標準予防策に基づく適切な感染管理が必要となる。MRSA の場合、接触感染予防策が適用である。
代表的な治療薬はバンコマイシン、テイコプラニン、アルベカシンである。2006年4月、リネゾリドが新薬として承認された。菌種（クローン）によっては、ミノサイクリンやレボフロキサシン、クリンダマイシン、ST合剤（スルファメトキサゾールおよびトリメトプリムの合剤）などが、有効か中等度有効であることがある。「抗菌薬使用のガイドライン」ではバンコマイシン、アルベカシンを第一選択薬とし、効果が得られなかった場合などにテイコプラニン、リネゾリドを使用するよう推奨されている｡また、国内では適応がとれていないが、欧米ではキヌプリスチン・ダルホプリスチン（商品名シナシッド）も有効であることが証明され、使用が認可されている。80%エタノールが消毒薬として有効である（エタノール消毒は芽胞を持たない細菌に有効）。
バンコマイシンは耐性菌の出現が少ない抗菌薬として MRSA の治療に汎用されていた。1996年のバンコマイシン低度耐性黄色ブドウ球菌（VISA）やバンコマイシンヘテロ耐性黄色ブドウ球菌（ヘテロVISA）の発見を始め、2005年現在、バンコマイシン耐性腸球菌（VRE）のバンコマイシン耐性遺伝子（vanA）を獲得したバンコマイシン耐性黄色ブドウ球菌（VRSA）の出現が報告されていることから、その使用には十分な注意が必要とされている。さらに、β-ラクタム系抗生物質との併用によってバンコマイシン耐性が発現する MRSA も出現している。これはbeta-lactam antibiotic induced vancomycin-resistant MRSA（BIVR）と呼ばれており、併用には注意が必要である。
耐性機構[編集]
ペニシリン系抗生物質をはじめとするβ-ラクタム系抗生物質は、細菌の細胞壁を構成するペプチドグリカンの合成を阻害することで作用する。これに対して、従来のペニシリン耐性ブドウ球菌はペニシリン分解酵素を産生することで薬剤耐性を獲得した。そこでこれらの細菌に対しても有効な、ペニシリン分解酵素によって分解されない薬剤が開発された。これがメチシリンであり、ペニシリン耐性菌の治療に効力を発揮した。
しかしながら MRSA は、従来のペニシリン耐性菌とは別の戦略を採ることでメチシリン耐性の獲得に成功した。MRSA は従来のブドウ球菌とは異なり、β-ラクタム剤が結合できないペプチドグリカン合成酵素（PBP2'）を作ることでβ-ラクタム剤の作用を回避する。この PBP2' というタンパク質はmecAという遺伝子にコードされているが、この遺伝子はDNAカセット染色体と呼ばれる部分に、他の薬剤耐性遺伝子とともに集まっており、ある菌から他の菌へ種を超えて伝達されることが解明された。
一般に薬剤耐性を獲得した細菌は、薬剤感受性の細菌に比べて増殖が遅い傾向があり[1]、MRSAもペニシリン感受性の黄色ブドウ球菌に比べると増殖が遅い[2]。
細菌叢調査[編集]
- 各細菌叢調査報告詳細に関しては、記載論文・抄録を参考にされたい。
- 伊藤重彦、吉永恵、大江宣春 他：救命センターにおけるMRSA感染（保菌）状況,日本臨床救急医学会雑誌第2巻1号,p.152,1999.
- 錦利佳、黒岩みゆき、小高香珠代 他：MRSA感染防止に対する看護婦の認識と行動の実態調査,医療第55巻増刊3,p.508,2001.
- 伊藤重彦、大江宣春、草場恵子 他：病院職員のMRSA鼻腔内保菌率調査とムピロシンによる除菌,日本環境感染学会 環境感染,第17巻3号,p.285-288,2002.
- 吉谷須磨子：MRSA感染患者に対する感染看護の評価,感染防止第14巻5号,p.27-29,2004.
- 馬笑雪、伊藤輝代、WalterPedreira 他：ウルグアイにおける市中獲得MRSAのoutbreak調査,日本細菌学会雑誌第59巻1号,p.214,2004.
- FujimuraShigeru、KatoSeiichi、HashimotoMotoya et al：Survey of methicillin-resistant Staphylococcus aureus from neonates and the environment in the NICU,Journal of Infection and Chemotherapy第10巻2号,p.131-132,2004.
- 久保真利子、名護博：老人ホームのMRSA保菌者状況,瀬戸内短期大学紀要第35号,p.31-37,2004.
- 上條篤、横尾英子、高橋吾郎 他：医療従事者の鼻前庭部MRSA保菌者における鼻疾患の有無についての検討,日本鼻科学会会誌第44巻2号,p.127-130,2005.
- 久保裕義、千葉直彦、横山宏 他：療養型病院における入院患者のMRSA保菌のリスクと医療従事者の意識についての調査,山梨医学第33巻,p.84-87,2005.
- 高橋尚人、崔信明、矢田ゆかり 他：新生児集中治療室におけるMRSA保菌に関する全国調査,日本小児科学会雑誌第109巻8号,p.1009-1014,2005.
- 小森由美子、二改俊章：市中におけるメチシリン耐性ブドウ球菌の鼻腔内保菌者に関する調査,日本環境感染学会 環境感染第20巻3号,p.164-170,2005.
- 平林円、川又攻、宮城伸浩 他：周産期病棟におけるMRSA感染,大阪市勤務医師会研究年報第32号,p.49-50,2005.
- 甘庶志帆乃、北元憲利、加藤陽二 他:一病院の患者および医療従事者におけるMRSA分子疫学調査,感染症学雑誌第79巻臨増,p.134,2005.
- 江藤由紀、田澤悠、花井美幸：MRSA伝播予防に関する意識と行動変容,東京医科大学病院看護研究集録第25回,p.84-89,2005.
- 柴田弘子、池野貴子、出口由美 他：看護学生の感染症の履歴認識およびMRSA保菌状況に関する調査,日本環境感染学会 環境感染第20巻Suppl,p.123,2005.
- 小笠原康雄、大野公一、播野俊江 他：MRSA保菌患者への対応に関する意識調査とその問題点 自施設と病診連携のある施設へのアンケート調査の結果,INFECTION CONTROL（メディカ出版）第14巻4号,p.382-386,2005.
- 渡辺朱理、佐藤法仁、苔口進、福井一博：歯科医療従事者および歯学部学生におけるメチシリン耐性ブドウ球菌の保菌状況調査,日本環境感染学会 環境感染第21巻Suppl, p.212,2006.
- 阿部哲士、市川日出勝、竹中信之 他：整形外科病棟における院内感染対策としてのMRSAサーベイランスの現状,日本骨・関節感染症研究会雑誌第19巻,p.22-25,2006.
- 渡辺朱理、佐藤法仁、苔口進、福井一博：感染防止と歯科医療受診行動III～歯科学生、歯科衛生士学生、非医療系大学生における歯科医院選択におけるMRSAに対する意識調査～．医学と生物学 150(9)，p.336-343，2006．
注釈[編集]
- ^ Andersson DI, Levin BR. (1999). “The biological cost of antibiotic resistance.”. Curr Opin Microbiol. 2 (5): 489-93.
- ^ Miriam Ender, Nadine McCallum, Rajan Adhikari, and Brigitte Berger-Bächi (2004). “Fitness Cost of SCCmec and Methicillin Resistance Levels in Staphylococcus aureus”. Antimicrobial Agents and Chemotherapy 48 (6): 2295-7.
関連項目[編集]
- ブドウ球菌
- 黄色ブドウ球菌
- 薬剤耐性菌
- 抗生物質
- 院内感染
- 院内感染対策チーム（感染制御チーム・感染対策チーム）（ICT）
- 院内感染対策委員会（感染制御委員会・感染対策委員会）（ICC）
外部リンク[編集]
- 2002年第18週号 メチシリン耐性黄色ブドウ球菌感染症 国立感染症研究所細菌第二部] - 国立感染症研究所 感染症情報センター
- メチシリン耐性黄色ブドウ球菌 (methicillin-resistant Staphylococcus aureus ;MRSA) 感染症の滅菌・消毒 - 横浜市衛生研究所 感染症・疫学情報課
| この項目「メチシリン耐性黄色ブドウ球菌」は、真正細菌（バクテリア）に関連した書きかけの項目です。加筆・訂正などをして下さる協力者を求めています。（Portal:生き物と自然／ウィキプロジェクト 生物） |
| この項目は、医学に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています（プロジェクト:医学／Portal:医学と医療）。 |
wiki en
"MRSA" redirects here. For other uses, see MRSA (disambiguation).
A colourised SEM of MRSA
Methicillin-resistant Staphylococcus aureus (MRSA) is a bacterium responsible for several difficult-to-treat infections in humans. It is also called oxacillin-resistant Staphylococcus aureus (ORSA). MRSA is any strain of Staphylococcus aureus that has developed, through the process of natural selection, resistance to beta-lactam antibiotics, which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins. Strains unable to resist these antibiotics are classified as methicillin-sensitive Staphylococcus aureus, or MSSA. The evolution of such resistance does not cause the organism to be more intrinsically virulent than strains of Staphylococcus aureus that have no antibiotic resistance, but resistance does make MRSA infection more difficult to treat with standard types of antibiotics and thus more dangerous.
MRSA is especially troublesome in hospitals, prisons and nursing homes, where patients with open wounds, invasive devices, and weakened immune systems are at greater risk of infection than the general public.
Contents
- 1 Signs and symptoms
- 2 Risk factors
- 2.1 Hospital patients
- 2.2 Prison inmates, military recruits, and the homeless
- 2.3 People in contact with live food-producing animals
- 2.4 Athletes
- 2.5 Children
- 3 Diagnosis
- 4 Genetics
- 4.1 SCCmec
- 4.2 mecA
- 4.3 Strains
- 5 Prevention
- 5.1 Screening programs
- 5.2 Surface sanitizing
- 5.3 Research on copper alloys
- 5.4 Hand washing
- 5.5 Use of surgical respirator
- 5.6 Proper disposal of hospital gowns
- 5.7 Isolation
- 5.8 Restricting antibiotic use
- 5.9 Public health considerations
- 5.10 Decolonization
- 5.11 Community settings
- 6 Treatment
- 7 History
- 7.1 US and UK
- 7.2 Worldwide
- 8 Research
- 8.1 Clinical
- 8.2 Pre-clinical
- 9 See also
- 10 Further reading
- 11 References
Signs and symptoms[edit]
S. aureus most commonly colonizes the anterior nares (the nostrils). The rest of the respiratory tract, open wounds, intravenous catheters, and the urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years. Patients with compromised immune systems are at a significantly greater risk of symptomatic secondary infection.
In most patients, MRSA can be detected by swabbing the nostrils and isolating the bacteria found inside. Combined with extra sanitary measures for those in contact with infected patients, screening patients admitted to hospitals has been found to be effective in minimizing the spread of MRSA in hospitals in the United States,[1] Denmark, Finland, and the Netherlands.[2]
MRSA may progress substantially within 24–48 hours of initial topical symptoms. After 72 hours, MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils; they may be accompanied by fever and, occasionally, rashes. Within a few days, the bumps become larger and more painful; they eventually open into deep, pus-filled boils.[3] About 75 percent of community-associated (CA-) MRSA infections are localized to skin and soft tissue and usually can be treated effectively.{ISDA MRSA guidelines http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/MRSA.pdf} But some CA-MRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional healthcare-associated (HA-) MRSA infections, and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome, and necrotizing ("flesh-eating") pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM, though PVL was recently found not to be a factor in a study by the National Institute of Allergy and Infectious Diseases (NIAID) at the National Institutes of Health. (NIH) It is not known why some healthy people develop CA-MRSA skin infections that are treatable while others infected with the same strain develop severe infections or die.[4]
People are very commonly colonized with CA-MRSA and are completely asymptomatic. The most common manifestations of CA-MRSA are simple skin infections, such as impetigo, boils, abscesses, folliculitis, and cellulitis. Rarer, but more serious manifestations can occur, such as necrotizing fasciitis and pyomyositis (most commonly found in the tropics), necrotizing pneumonia, infective endocarditis (which affects the valves of the heart), and bone and joint infections.[5] CA-MRSA often results in abscess formation that requires incision and drainage. Before the spread of MRSA into the community, abscesses were not considered contagious, because it was assumed that infection required violation of skin integrity and the introduction of staphylococci from normal skin colonization. However, newly emerging CA-MRSA is transmissible (similar, but with very important differences) from Hospital-Associated MRSA. CA-MRSA is less likely than other forms of MRSA to cause cellulitis.
Risk factors[edit]
Some of the populations at risk:
- People with weak immune systems (HIV/AIDS, lupus, or cancer sufferers; transplant recipients, severe asthmatics, etc.)
- Diabetics[6]
- Intravenous drug users [7]
- Users of quinolone antibiotics[8]
- Young children[citation needed]
- The elderly[citation needed]
- College students living in dormitories[7]
- People staying or working in a health care facility for an extended period of time[7]
- People who spend time in coastal waters where MRSA is present, such as some beaches in Florida and the west coast of the United States[9][10]
- People who spend time in confined spaces with other people, including occupants of homeless shelters and warming centers, prison inmates, military recruits in basic training,[11] and individuals who spend considerable time in changerooms or gyms.[citation needed]
- Veterinarians, livestock handlers, and pet owners[12]
Hospital patients[edit]
Many MRSA infections occur in hospitals and healthcare facilities. When infections occur in this manner it is known as healthcare acquired MRSA or HA-MRSA. These Rates of MRSA infection are also increased in hospitalized patients who are treated with quinolones. Healthcare provider-to-patient transfer is common, especially when healthcare providers move from patient to patient without performing necessary hand-washing techniques between patients.[8][13]
Prison inmates, military recruits, and the homeless[edit]
Prisons, military barracks, and homeless shelters can be crowded and confined, and poor hygiene practices may proliferate, thus putting inhabitants at increased risk of contracting MRSA.[12] Cases of MRSA in such populations were first reported in the United States, and then in Canada. The earliest reports were made by the Center for Disease Control (CDC) in US state prisons. Subsequently reports of a massive rise in skin and soft tissue infections were reported by the CDC in the Los Angeles County Jail system in 2001, and this has continued. Pan et al. reported on the changing epidemiology of MRSA skin infection in the San Francisco County Jail, noting MRSA accounted for more than 70% of S. aureus infection in the jail by 2002. Lowy and colleagues reported on frequent MRSA skin infections in New York State Prisons. Two reports on inmates in Maryland have demonstrated frequent colonization with MRSA.
In the news media hundreds of reports of MRSA outbreaks in prisons appeared between 2000 and 2008. For example, in February 2008, the Tulsa County Jail in the U.S. State of Oklahoma started treating an average of twelve Staphylococcus cases per month.[14] A report on skin and soft tissue infections in the Cook County Jail in Chicago in 2004–05 demonstrated that MRSA was the most common cause of these infections among cultured lesions and furthermore that few risk factors were more strongly associated with MRSA infections than infections caused by methicillin-susceptible S. aureus. In response to these and many other reports on MRSA infections among incarcerated and recently incarcerated persons, the Federal Bureau of Prisons has released guidelines for the management and control of the infections although few studies provide an evidence base for these guidelines.
People in contact with live food-producing animals[edit]
Cases of MRSA have increased in livestock animals. CC398 is a new variant of MRSA that has emerged in animals and is found in intensively reared production animals (primarily pigs, but also cattle and poultry), where it can be transmitted to humans. Though dangerous to humans, CC398 is often asymptomatic in food-producing animals.[15]
A 2011 study reported 47% of the meat and poultry sold in surveyed U.S. grocery stores was contaminated with S. aureus and, of those, 52%—or 24.4% of the total—were resistant to at least three classes of antibiotics. "Now we need to determine what this means in terms of risk to the consumer," said Dr. Keim, a co-author of the paper.[16] Some samples of commercially sold meat products in Japan were also found to harbor MRSA strains.[17]
Athletes[edit]
In the United States, there have been increasing numbers of reports of outbreaks of MRSA colonization and infection through skin contact in locker rooms and gyms, even among healthy populations.[citation needed] A study published in the New England Journal of Medicine linked MRSA to the abrasions caused by artificial turf.[18] Three studies by the Texas State Department of Health found that the infection rate among football players was 16 times the national average. In October 2006, a high school football player was temporarily paralyzed from MRSA-infected turf burns. His infection returned in January 2007 and required three surgeries to remove infected tissue, as well as three weeks of hospital stay.[19] In 2013, Lawrence Tynes, Carl Nicks, and Johnthan Banks, all of the Tampa Bay Buccaneers were diagnosed with MRSA. Tynes and Nicks are not believed to have contracted the infection from each other, but it is unknown if Banks contracted it from either individual.[20]
Children[edit]
MRSA is also becoming a problem in pediatric settings,[21] including hospital nurseries.[22] A 2007 study found that 4.6% of patients in U.S. health care facilities were infected or colonized with MRSA.[23] MRSA is becoming a major health concern in children because they are more likely to exhibit minor scrapes, cuts, bruises, and bug bites than adults. Children as well as adults are at higher risk of getting MRSA who come in contact with day care centers, playgrounds, locker rooms, camps, dormitories, classrooms and other school settings, and gyms and workout facilities. Parents should be especially cautious of children who participate in activities where there is shared sports equipment such as football helmets and uniforms.[24]
Diagnosis[edit]
Mueller Hinton agar showing MRSA resistant to oxacillin disk
Diagnostic microbiology laboratories and reference laboratories are key for identifying outbreaks of MRSA. New rapid techniques for the identification and characterization of MRSA have been developed.[25] This notwithstanding, the bacterium generally must be cultured via blood, urine, sputum, or other body fluid cultures, and cultured in the lab in sufficient quantities to perform these confirmatory tests first. Consequently, there is no quick and easy method to diagnose a MRSA infection. Therefore, initial treatment is often based upon 'strong suspicion' by the treating physician, since any delay in treating this type of infection can have fatal consequences. These techniques include quantitative PCR and are increasingly being employed in clinical laboratories for the rapid detection and identification of MRSA strains.[26][27]
Another common laboratory test is a rapid latex agglutination test that detects the PBP2a protein. PBP2a is a variant penicillin-binding protein that imparts the ability of S. aureus to be resistant to oxacillin.[28]
Genetics[edit]
Antimicrobial resistance is genetically based; resistance is mediated by the acquisition of extrachromosomal genetic elements containing resistance genes. Exemplary are plasmids, transposable genetic elements, and genomic islands, which are transferred between bacteria via horizontal gene transfer.[29] A defining characteristic of MRSA is its ability to thrive in the presence of penicillin-like antibiotics, which normally prevent bacterial growth by inhibiting synthesis of cell wall material. This is due to a resistance gene, mecA, which stops β-lactam antibiotics from inactivating the enzymes (transpeptidases) that are critical for cell wall synthesis.
SCCmec[edit]
Staphylococcal cassette chromosome mec (SCCmec) is a genomic island of unknown origin containing the antibiotic resistance gene mecA.[30][31] SCCmec contains additional genes beyond mecA, including the cytolysin gene psm-mec, which may suppress virulence in hospital-acquired MRSA strains.[32] SCCmec also contains ccrA and ccrB; both genes encode recombinases that mediate the site-specific integration and excision of the SCCmec element from the S. aureus chromosome.[30][31] Currently, six unique SCCmec types ranging in size from 21–67 kb have been identified;[30] they are designated types I-VI and are distinguished by variation in mec and ccr gene complexes.[29] Owing to the size of the SCCmec element and the constraints of horizontal gene transfer, a limited number of clones is thought to be responsible for the spread of MRSA infections.[30]
Different SCCmec genotypes confer different microbiological characteristics, such as different antimicrobial resistance rates.[33] Different genotypes are also associated with different types of infections. Types I-III SCCmec are large elements that typically contain additional resistance genes and are characteristically isolated from HA-MRSA strains.[31][33] Conversely, CA-MRSA is associated with types IV and V, which are smaller and lack resistance genes other than mecA.[31][33]
mecA[edit]
mecA is responsible for resistance to methicillin and other β-lactam antibiotics. After acquisition of mecA, the gene must be integrated and localized in the S. aureus chromosome.[30] mecA encodes penicillin-binding protein 2a (PBP2a), which differs from other penicillin-binding proteins as its active site does not bind methicillin or other β-lactam antibiotics.[30] As such, PBP2a can continue to catalyze the transpeptidation reaction required for peptidoglycan cross-linking, enabling cell wall synthesis in the presence of antibiotics. As a consequence of the inability of PBP2a to interact with β-lactam moieties, acquisition of mecA confers resistance to all β-lactam antibiotics in addition to methicillin.[30][34]
mecA is under the control of two regulatory genes, mecI and mecR1. MecI is usually bound to the mecA promoter and functions as a repressor.[29][31] In the presence of a β-lactam antibiotic, MecR1 initiates a signal transduction cascade that leads to transcriptional activation of mecA.[29][31] This is achieved by MecR1-mediated cleavage of MecI, which alleviates MecI repression.[29] mecA is further controlled by two co-repressors, BlaI and BlaR1. blaI and blaR1 are homologous to mecI and mecR1, respectively, and normally function as regulators of blaZ, which is responsible for penicillin resistance.[30][35] The DNA sequences bound by MecI and BlaI are identical;[30] therefore, BlaI can also bind the mecA operator to repress transcription of mecA.[35]
Strains[edit]
Diagram depicting antibiotic resistance through alteration of the antibiotic's target site, modeled after MRSA's resistance to penicillin. Beta-lactam antibiotics permanently inactivate PBP enzymes, which are essential for bacterial life, by permanently binding to their active sites. Some forms of MRSA, however, express a PBP that will not allow the antibiotic into their active site.
Acquisition of SCCmec in methicillin-sensitive staphylococcus aureus (MSSA) gives rise to a number of genetically different MRSA lineages. These genetic variations within different MRSA strains possibly explain the variability in virulence and associated MRSA infections.[36] The first MRSA strain, ST250 MRSA-1 originated from SCCmec and ST250-MSSA integration.[36] Historically, major MRSA clones: ST2470-MRSA-I, ST239-MRSA-III, ST5-MRSA-II, and ST5-MRSA-IV were responsible for causing hospital-acquired MRSA (HA-MRSA) infections.[36] ST239-MRSA-III, known as the Brazilian clone, was highly transmissible compared to others and distributed in Argentina, Czech Republic, and Portugal.[36]
In the UK, where MRSA is commonly called "Golden Staph", the most common strains of MRSA are EMRSA15 and EMRSA16.[37] EMRSA16 is the best described epidemiologically: it originated in Kettering, England, and the full genomic sequence of this strain has been published.[38] EMRSA16 has been found to be identical to the ST36:USA200 strain, which circulates in the United States, and to carry the SCCmec type II, enterotoxin A and toxic shock syndrome toxin 1 genes.[39] Under the new international typing system, this strain is now called MRSA252. EMRSA 15 is also found to be one of the common MRSA strains in Asia. Other common strains include ST5:USA100 and EMRSA 1.[40] These strains are genetic characteristics of HA-MRSA.[41]
It is not entirely certain why some strains are highly transmissible and persistent in healthcare facilities.[36] One explanation is the characteristic pattern of antibiotic susceptibility. Both the EMRSA15 and EMRSA16 strains are resistant to erythromycin and ciprofloxacin. It is known that Staphylococcus aureus can survive intracellularly,[42] for example in the nasal mucosa [43] and in the tonsil tissue.[44] Erythromycin and Ciprofloxacin are precisely the antibiotics that best penetrate intracellularly; it may be that these strains of S. aureus are therefore able to exploit an intracellular niche.
Community-acquired MRSA (CA-MRSA) strains emerged in late 1990 to 2000, infecting healthy people who had not been in contact with health care facilities.[41] A later study that analyzed data from more than 300 microbiology labs associated with hospitals all over the United States have found a seven-fold increase, jumping from 3.6% of all MRSA infections to 28.2%, in the proportion of community-associated strains of MRSA between 1999 and 2006.[45] Researchers suggest that CA-MRSA did not evolve from the HA-MRSA.[41] This is further proven by molecular typing of CA-MRSA strains[46] and genome comparison between CA-MRSA and HA-MRSA, which indicate that novel MRSA strains integrated SCCmec into MSSA separately on its own.[41] By mid 2000, CA-MRSA was introduced into the health care systems and distinguishing CA-MRSA from HA-MRSA became a difficult process.[41] Community-acquired MRSA (CA-MRSA) is more easily treated and more virulent than hospital-acquired MRSA (HA-MRSA).[41] The genetic mechanism for the enhanced virulence in CA-MRSA remains an active area of research. Especially the Panton-Valentine leukocidin (PVL) genes are of interest because they are a unique feature of CA-MRSA.[36]
In the United States, most cases of CA-MRSA are caused by a CC8 strain designated ST8:USA300, which carries SCCmec type IV, Panton-Valentine leukocidin, PSM-alpha and enterotoxins Q and K,[39] and ST1:USA400.[47] The ST8:USA300 strain results in skin infections, necrotizing fasciitis and toxic shock syndrome, whereas the ST1:USA400 strain results in necrotizing pneumonia and pulmonary sepsis.[36] Other community-acquired strains of MRSA are ST8:USA500 and ST59:USA1000. In many nations of the world, MRSA strains with different predominant genetic background types have come to predominate among CA-MRSA strains; USA300 easily tops the list in the U. S. and is becoming more common in Canada after its first appearance there in 2004. For example, in Australia ST93 strains are common, while in continental Europe ST80 strains (Tristan et al., Emerging Infectious Diseases, 2006), which carry SCCmec type IV, predominate.[48] In Taiwan, ST59 strains, some of which are resistant to many non-beta-lactam antibiotics, have arisen as common causes of skin and soft tissue infections in the community. In a remote region of Alaska, unlike most of the continental U. S., USA300 was found rarely in a study of MRSA strains from outbreaks in 1996 and 2000 as well as in surveillance from 2004–06 (David et al., Emerg Infect Dis 2008).
In June 2011, the discovery of a new strain of MRSA was announced by two separate teams of researchers in the UK. Its genetic makeup was reportedly more similar to strains found in animals, and testing kits designed to detect MRSA were unable to identify it.[49] This MRSA strain, Clonal Complex 398 (CC398), is responsible for Livestock-associated MRSA (LA-MRSA) infections.[40] Although it is known to be more persistent in colonizing pigs and calves, there have been cases of LA-MRSA carriers with pneumonia, endocarditis, and necrotising fasciitis.[50]
Prevention[edit]
Screening programs[edit]
Patient screening upon hospital admission, with nasal cultures, prevents the cohabitation of MRSA carriers with non-carriers, and exposure to infected surfaces. The test used (whether a rapid molecular method or traditional culture) is not as important as the implementation of active screening.[51] In the United States and Canada, the Centers for Disease Control and Prevention issued guidelines on October 19, 2006, citing the need for additional research, but declined to recommend such screening.[52][53]
In some UK hospitals screening for MRSA is performed in every patient[54] and all NHS surgical patients, except for minor surgeries, are previously checked for MRSA.[55] There is no community screening in the UK; however, screening of individuals is offered by some private companies.[56]
In a US cohort of 1300 healthy children, 2.4% carried MRSA in their nose.[57]
Surface sanitizing[edit]
NAV-CO2 sanitizing in Pennsylvania hospital exam room
Alcohol has been proven to be an effective surface sanitizer against MRSA. Quaternary ammonium can be used in conjunction with alcohol to extend the longevity of the sanitizing action.[citation needed] The prevention of nosocomial infections involves routine and terminal cleaning. Non-flammable Alcohol Vapor in Carbon Dioxide systems (NAV-CO2) do not corrode metals or plastics used in medical environments and do not contribute to antibacterial resistance.
In healthcare environments, MRSA can survive on surfaces and fabrics, including privacy curtains or garments worn by care providers. Complete surface sanitation is necessary to eliminate MRSA in areas where patients are recovering from invasive procedures. Testing patients for MRSA upon admission, isolating MRSA-positive patients, decolonization of MRSA-positive patients, and terminal cleaning of patients' rooms and all other clinical areas they occupy is the current best practice protocol for nosocomial MRSA.
Studies published from 2004-2007 reported hydrogen peroxide vapor could be used to decontaminate busy hospital rooms, despite taking significantly longer than traditional cleaning. One study noted rapid recontamination by MRSA following the hydrogen peroxide application.[58][59][60][61][62]
Also tested, in 2006, was a new type of surface cleaner, incorporating accelerated hydrogen peroxide, which was pronounced "a potential candidate" for use against the targeted microorganisms.[63]
Research on copper alloys[edit]
In 2008, after evaluating a wide body of research mandated specifically by the United States Environmental Protection Agency (EPA), registration approvals were granted by EPA in 2008 granting that copper alloys kill more than 99.9% of MRSA within two hours.
Subsequent research conducted at the University of Southampton (UK) compared the antimicrobial efficacies of copper and several non-copper proprietary coating products to kill MRSA.[64][65] At 20 °C, the drop-off in MRSA organisms on copper alloy C11000 is dramatic and almost complete (over 99.9% kill rate) within 75 minutes. However, neither a triclosan-based product nor two silver-containing based antimicrobial treatments (Ag-A and Ag-B) exhibited any meaningful efficacy against MRSA. Stainless steel S30400 did not exhibit any antimicrobial efficacy.
In 2004, the University of Southampton research team was the first to clearly demonstrate that copper inhibits MRSA.[66] On copper alloys — C19700 (99% copper), C24000 (80% copper), and C77000 (55% copper) — significant reductions in viability were achieved at room temperatures after 1.5 hours, 3.0 hours and 4.5 hours, respectively. Faster antimicrobial efficacies were associated with higher copper alloy content. Stainless steel did not exhibit any bactericidal benefits.
Hand washing[edit]
In September 2004,[67] after a successful pilot scheme to tackle MRSA, the UK National Health Service announced its Clean Your Hands campaign. Wards were required to ensure that alcohol-based hand rubs are placed near all beds so that staff can hand wash more regularly. It is thought that even if this cuts infection by no more than 1%, the plan will pay for itself many times over.[citation needed]
As with some other bacteria, MRSA is acquiring more resistance to some disinfectants and antiseptics. Although alcohol-based rubs remain somewhat effective, a more effective strategy is to wash hands with running water and an anti-microbial cleanser with persistent killing action, such as Chlorhexidine.[68] In another study chlorohexidine (Hibiclens), p-chloro-m-xylenol (Acute-Kare), hexachlorophene (Phisohex), and povidone-iodine (Betadine) were evaluated for their effectiveness. Of the four most commonly used antiseptics, povidone-iodine, when diluted 1:100, was the most rapidly bactericidal against both MRSA and methicillin-susceptible S. aureus.[69]
A June 2008 report, centered on a survey by the Association for Professionals in Infection Control and Epidemiology, concluded that poor hygiene habits remain the principal barrier to significant reductions in the spread of MRSA.
Use of surgical respirator[edit]
The US Food and Drug Administration (FDA) announced on 8 April 2011 that it had cleared a novel type of N95 Surgical Respirator, the SpectraShield 9500, that kills methicillin-resistant Staphylococcus aureus, Streptococcus pyogenes and Haemophilus influenzae. This mask is manufactured by Nexera Medical Ltd. of Richmond, British Columbia. The mask blocks at least 95% of small particles in a standardized test. The FDA clearance also included evaluation by the National Institute of Occupational Health and Safety.[70]
Proper disposal of hospital gowns[edit]
Used paper hospital gowns are associated with MRSA hospital infections, which could be avoided by proper disposal.[71]
Isolation[edit]
Excluding medical facilities, current US guidance does not require workers with MRSA infections to be routinely excluded from the general workplace.[72] Therefore, unless directed by a health care provider, exclusion from work should be reserved for those with wound drainage that cannot be covered and contained with a clean, dry bandage and for those who cannot maintain good hygiene practices.[72] Workers with active infections should be excluded from activities where skin-to-skin contact is likely to occur until their infections are healed. Health care workers should follow the Centers for Disease Control and Prevention's Guidelines for Infection Control in Health Care Personnel.[73]
To prevent the spread of staph or MRSA in the workplace, employers should ensure the availability of adequate facilities and supplies that encourage workers to practice good hygiene; that surface sanitizing in the workplace is followed; and that contaminated equipment are sanitized with Environmental Protection Agency (EPA)-registered disinfectants.[72]
Restricting antibiotic use[edit]
Glycopeptides, cephalosporins and in particular quinolones are associated with an increased risk of colonisation of MRSA. Reducing use of antibiotic classes that promote MRSA colonisation, especially fluoroquinolones, is recommended in current guidelines.[8][13]
Public health considerations[edit]
Mathematical models describe one way in which a loss of infection control can occur after measures for screening and isolation seem to be effective for years, as happened in the UK. In the "search and destroy" strategy that was employed by all UK hospitals until the mid-1990s, all patients with MRSA were immediately isolated, and all staff were screened for MRSA and were prevented from working until they had completed a course of eradication therapy that was proven to work. Loss of control occurs because colonised patients are discharged back into the community and then readmitted; when the number of colonised patients in the community reaches a certain threshold, the "search and destroy" strategy is overwhelmed.[74] One of the few countries not to have been overwhelmed by MRSA is the Netherlands: An important part of the success of the Dutch strategy may have been to attempt eradication of carriage upon discharge from hospital.[75]
The Centers for Disease Control and Prevention (CDC) estimated that about 1.7 million nosocomial infections occurred in the United States in 2002, with 99,000 associated deaths.[76] The estimated incidence is 4.5 nosocomial infections per 100 admissions, with direct costs (at 2004 prices) ranging from $10,500 (£5300, €8000 at 2006 rates) per case (for bloodstream, urinary tract, or respiratory infections in immunocompetent patients) to $111,000 (£57,000, €85,000) per case for antibiotic-resistant infections in the bloodstream in patients with transplants. With these numbers, conservative estimates of the total direct costs of nosocomial infections are above $17 billion. The reduction of such infections forms an important component of efforts to improve healthcare safety. (BMJ 2007)[citation needed] MRSA alone was associated with 8% of nosocomial infections reported to the CDC National Healthcare Safety Network from January 2006 to October 2007.[77]
This problem is not unique to one country; the British National Audit Office estimated that the incidence of nosocomial infections in Europe ranges from 4% to 10% of all hospital admissions. As of early 2005, the number of deaths in the United Kingdom attributed to MRSA has been estimated by various sources to lie in the area of 3,000 per year.[78] Staphylococcus bacteria account for almost half of all UK hospital infections. The issue of MRSA infections in hospitals has recently been a major political issue in the UK, playing a significant role in the debates over health policy in the United Kingdom general election held in 2005.
On January 6, 2008, half of 64 non-Chinese cases of MRSA infections in Hong Kong in 2007 were Filipino domestic helpers. Ho Pak-leung, professor of microbiology at the University of Hong Kong, traced the cause to high use of antibiotics. In 2007, there were 166 community cases in Hong Kong compared with 8,000 hospital-acquired MRSA cases (155 recorded cases—91 involved Chinese locals, 33 Filipinos, 5 each for Americans and Indians, and 2 each from Nepal, Australia, Denmark and England).[79]
Worldwide, an estimated 2 billion people carry some form of S. aureus; of these, up to 53 million (2.7% of carriers) are thought to carry MRSA.[80] In the United States, 95 million carry S. aureus in their noses; of these, 2.5 million (2.6% of carriers) carry MRSA.[81] A population review conducted in three U.S. communities showed the annual incidence of CA-MRSA during 2001–2002 to be 18–25.7/100,000; most CA-MRSA isolates were associated with clinically relevant infections, and 23% of patients required hospitalization.[82]
One possible contribution to the increased spread of MRSA infections comes from the use of antibiotics in intensive pig farming. A 2008 study in Canada found MRSA in 10% of tested pork chops and ground pork; a U.S. study in the same year found MRSA in the noses of 70% of the tested farm pigs and in 45% of the tested pig farm workers.[83] There have also been anecdotal reports of increased MRSA infection rates in rural communities with pig farms.[84]
Healthcare facilities with high bed occupancy rates, high levels of temporary nursing staff, or low cleanliness scores no longer have significantly higher MRSA rates. Simple tabular evidence helps provide a clear picture of these changes, showing, for instance, that hospitals with occupancy over 90% had, in 2006–2007, MRSA rates little above those in hospitals with occupancy below 85%, in contrast to the period 2001–2004. In one sense, the disappearance of these relationships is puzzling. Reporters now blame IV cannula and catheters for spreading MRSA in hospitals. (Hospital organisation and speciality mix, 2008)[citation needed]
Decolonization[edit]
Care should be taken when trying to drain boils, as disruption of surrounding tissue can lead to larger infections, or even infection of the blood stream (often with fatal consequences).[85] Any drainage should be disposed of very carefully. After the drainage of boils or other treatment for MRSA, patients can shower at home using chlorhexidine (Hibiclens) or hexachlorophene (Phisohex) antiseptic soap (available over-the-counter at many pharmacies) from head to toe. Alternatively, a dilute bleach bath can be taken at a concentration of 2.5 μL/mL dilution of bleach (about 1/2 cup bleach per 1/4-full bathtub of water).[86] Care should be taken to use a clean towel, and to ensure that nasal discharge doesn't infect the towel (see below).
All infectious lesions should be kept covered with a dressing.[85] Mupirocin (Bactroban) 2% ointment can be effective at reducing the size of lesions. A secondary covering of clothing is preferred.[87] As shown in an animal study with diabetic mice, the topical application of a mixture of sugar (70%) and 3% povidone-iodine paste is an effective agent for the treatment of diabetic ulcers with MRSA infection.[88]
The nose is a common refuge for MRSA, and a test swab can be taken of the nose to indicate whether MRSA is present.[89] If MRSA is detected via nasal culture, Mupirocin (Bactroban) 2% ointment can be applied inside each nostril twice daily for 7 days, using a cotton-tipped swab. However, care should be taken so that the swab doesn't penetrate into the sinus. Household members are recommended to follow the same decolonization protocol. After treatment, the nose should be swabbed again to ensure that the treatment was effective. If not, the process should be repeated.
Toilet seats are a common vector for infection, and wiping seats clean before and/or after use can help to prevent the spread of MRSA. Door handles, faucets, light switches (with care!), etc. can be disinfected regularly with disinfectant wipes.[87] Spray disinfectants can be used on upholstery. Carpets can be washed with disinfectant, and hardwood floors can be scrubbed with diluted tea tree oil (e.g. Melaleuca). Laundry soap containing tea tree oil may be effective at decontaminating clothing and bedding, especially if hot water and heavy soil cycles are used, however tea tree oil may cause a rash which MRSA can re-colonize. Alcohol-based sanitizers can be placed near bedsides, near sitting areas, in vehicles etc. to encourage their use.
Doctors may also prescribe antibiotics such as clindamycin, doxycycline or trimethoprim/sulfamethoxazole.
Community settings[edit]
The CDC offers suggestions for preventing the contraction and spread MRSA infection which are applicable to those in community settings, including incarcerated populations, childcare center employees, and athletes. To prevent MRSA infection, individuals should regularly wash hands using soap and water or an alcohol-based sanitizer, keep wounds clean and covered, avoid contact with other people's wounds, avoid sharing personal items such as razors or towels, shower after exercising at athletic facilities (including gyms, weight rooms, and school facilities), shower before using swimming pools or whirlpools, and maintain a clean environment.[90]
It may be difficult for people to maintain the necessary cleanliness if they do not have access to facilities such as public toilets with handwashing facilities. In the United Kingdom, the Workplace (Health, Safety and Welfare) Regulations 1992 requires businesses to provide toilets for their employees, along with washing facilities including soap or other suitable means of cleaning. Guidance on how many toilets to provide and what sort of washing facilities should be provided alongside them is given in the Workplace (Health, Safety and Welfare) Approved Code of Practice and Guidance L24, available from Health and Safety Executive Books. But there is no legal obligation on local authorities in the United Kingdom to provide public toilets, and although in 2008 the House of Commons Communities and Local Government Committee called for a duty on local authorities to develop a public toilet strategy [1] this was rejected by the Government [2].
Treatment[edit]
Both CA-MRSA and HA-MRSA are resistant to traditional anti-staphylococcal beta-lactam antibiotics, such as cephalexin. CA-MRSA has a greater spectrum of antimicrobial susceptibility, including to sulfa drugs (like co-trimoxazole/trimethoprim-sulfamethoxazole), tetracyclines (like doxycycline and minocycline) and clindamycin (for osteomyelitis), but the drug of choice for treating CA-MRSA is now believed to be vancomycin, according to a Henry Ford Hospital Study. HA-MRSA is resistant even to these antibiotics and often is susceptible only to vancomycin. Newer drugs, such as linezolid (belonging to the newer oxazolidinones class) and daptomycin, are effective against both CA-MRSA and HA-MRSA. Linezolid is now felt to be the best drug for treating patients with MRSA pneumonia.[91][dubious – discuss] Ceftaroline and ceftabiparole, new fifth generation cephalosporins, are the first beta-lactam antibiotics approved in the US to treat MRSA infections (skin and soft tissue only).[citation needed]
Vancomycin and teicoplanin are glycopeptide antibiotics used to treat MRSA infections.[92] Teicoplanin is a structural congener of vancomycin that has a similar activity spectrum but a longer half-life.[93] Because the oral absorption of vancomycin and teicoplanin is very low, these agents must be administered intravenously to control systemic infections.[94] Treatment of MRSA infection with vancomycin can be complicated, due to its inconvenient route of administration. Moreover, many clinicians believe that the efficacy of vancomycin against MRSA is inferior to that of anti-staphylococcal beta-lactam antibiotics against methicillin-susceptible Staphylococcus aureus (MSSA).[95][96]
Several newly discovered strains of MRSA show antibiotic resistance even to vancomycin and teicoplanin. These new evolutions of the MRSA bacterium have been dubbed Vancomycin intermediate-resistant Staphylococcus aureus (VISA).[97] [98] Linezolid, quinupristin/dalfopristin, daptomycin, ceftaroline, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.[99] Current guidelines recommend daptomycin for VISA bloodstream infections and endocarditis.[100]
There have been claims that bacteriophage can be used to cure MRSA.[101][102]
The psychedelic mushroom Psilocybe semilanceata has been shown to strongly inhibit the growth of Staphylococcus aureus.[103] The cannabinoids CBD and CBG powerfully inhibit MRSA,[104] in addition to the terpenoid pinene which occurs in cannabis.[105]
Initial studies at the University of East London have demonstrated that allicin (a compound found in garlic) exhibits a strong antimicrobial response to the bacteria, indicating that it may one day lead to more effective treatments.[106]
A report released in 2010 details the efficacy of the active ingredients of a new composite dressing (hydrogen peroxide, tobramycin, chlorhexidine digluconate, chlorhexidine gluconate, levofloxacin, and silver) against MRSA.[107]
A 1990 study tested MRSA isolates obtained from veterans and found they could be killed by several substances, including bacitracin, nitrofurantoin, hydrogen peroxide, novobiocin, netilmicin and vancomycin. The study went on to conclude that netilmicin might be useful as an alternative to intravenous vancomycin, and suggested that topical applications of hydrogen peroxide may be useful to reduce MRSA on skin and some mucous membranes.[108]
History[edit]
| The examples and perspective in this article may not represent a worldwide view of the subject. Please improve this article and discuss the issue on the talk page. (December 2010) |
US and UK[edit]
Incidence of MRSA in human blood samples in countries which took part in the study in 2008
In 1959 methicillin was licensed in England to treat penicillin-resistant S. aureus infections. Just as bacterial evolution had allowed microbes to develop resistance to penicillin, strains of S. aureus evolved to become resistant to methicillin. In 1961 the first known MRSA isolates were reported in a British study, and between 1961-1967 there were infrequent hospital outbreaks in Western Europe and Australia.[109] The first United States hospital outbreak of MRSA occurred at the Boston City Hospital in 1968. Between 1968-mid-1990s the percent of S. aureus infections that were caused by MRSA increased steadily, and MRSA became recognized as an endemic pathogen. In 1974 2% of hospital-acquired S. aureus infections could be attributed to MRSA.[110] The rate had increased to 22% by 1995, and by 1997 the percent of hospital S. aureus infections attributable to MRSA had reached 50%.
The first report of CA-MRSA occurred in 1981, and in 1982 there was a large outbreak of CA-MRSA among intravenous drug users in Detroit, Michigan.[109] Additional outbreaks of CA-MRSA were reported through the 1980s and 1990s, including outbreaks among Australian Aboriginal populations that had never been exposed to hospitals. In the mid-1990s there were scattered reports of CA-MRSA outbreaks among US children. While HA-MRSA rates stabilized between 1998–2008, CA-MRSA rates continued to rise. A report released by the University of Chicago Children's Hospital comparing two time periods (1993–1995 and 1995–1997) found a 25-fold increase in the rate of hospitalizations due to MRSA among children in the United States.[111] In 1999 the University of Chicago reported the first deaths from invasive MRSA among otherwise healthy children in the United States.[109] By 2004 MRSA accounted for 64% of hospital-acquired S. aureus infections in the United States.
The Office for National Statistics reported 1,629 MRSA-related deaths in England and Wales during 2005, indicating a MRSA-related mortality rate half the rate of that in the United States for 2005, even though the figures from the British source were explained to be high because of "improved levels of reporting, possibly brought about by the continued high public profile of the disease"[112] during the time of the 2005 United Kingdom General Election. MRSA is thought to have caused 1,652 deaths in 2006 in UK up from 51 in 1993.[113]
It has been argued that the observed increased mortality among MRSA-infected patients may be the result of the increased underlying morbidity of these patients. Several studies, however, including one by Blot and colleagues, that have adjusted for underlying disease still found MRSA bacteremia to have a higher attributable mortality than methicillin-susceptible S. aureus (MSSA) bacteremia.[114]
A population-based study of the incidence of MRSA infections in San Francisco during 2004–05 demonstrated that nearly 1 in 300 residents suffered from such an infection in the course of a year and that greater than 85% of these infections occurred outside of the healthcare setting.[115] A 2004 study showed that patients in the United States with S. aureus infection had, on average, three times the length of hospital stay (14.3 vs. 4.5 days), incurred three times the total cost ($48,824 vs $14,141), and experienced five times the risk of in-hospital death (11.2% vs 2.3%) than patients without this infection.[116] In a meta-analysis of 31 studies, Cosgrove et al.,[117] concluded that MRSA bacteremia is associated with increased mortality as compared with MSSA bacteremia (odds ratio = 1.93; 95% CI = 1.93±0.39).[118] In addition, Wyllie et al. report a death rate of 34% within 30 days among patients infected with MRSA, a rate similar to the death rate of 27% seen among MSSA-infected patients.[119]
According to the CDC, the most recent estimates of the incidence of healthcare-associated infections that are attributable to MRSA in the United States indicate a decline in such infection rates. Incidence of MRSA central line-associated blood stream infections as reported by hundreds of intensive care units decreased 50-70% from 2001-2007.[110] A separate system tracking all hospital MRSA bloodstream infections found an overall 34% decrease between 2005-2008.[110]
MRSA is sometimes sub-categorised as community-acquired MRSA (CA-MRSA) or healthcare-associated MRSA (HA-MRSA), although the distinction is complex. Some researchers have defined CA-MRSA by the characteristics of patients whom it infects, while others define it by the genetic characteristics of the bacteria themselves. By 2005, identified CA-MRSA risk factors included athletes, military recruits, incarcerated people, emergency room patients, urban children, HIV-positive individuals, men who have sex with men, and indigenous populations.[109]
Worldwide[edit]
The first reported cases of CA-MRSA began to appear in the mid-1990s in Australia, New Zealand, the United States, the United Kingdom, France, Finland, Canada and Samoa, and were notable because they involved people who had not been exposed to a healthcare setting.[5]
Because measurement and reporting varies, it is difficult to compare rates of MRSA in different countries. An international comparison of 2004 MRSA-attributable S. aureus rates in middle and high income countries released by the Center For Disease Dynamics, Economics, and Policy in showed that Iceland had the lowest rate of infection, and Romania had the highest at over 70%.[120]
Research[edit]
Clinical[edit]
It has been reported that maggot therapy to clean out necrotic tissue of MRSA infection has been successful. Studies in diabetic patients reported significantly shorter treatment times than those achieved with standard treatments.[121][122][123]
Many antibiotics against MRSA are in phase II and phase III clinical trials. e.g.:
- Phase III : ceftobiprole, Ceftaroline, Dalbavancin, Telavancin, Aurograb, torezolid, iclaprim etc.
- Phase II : nemonoxacin.[124]
Pre-clinical[edit]
An entirely different and promising approach is phage therapy (e.g., at the Eliava Institute in Georgia[125]), which in mice had a reported efficacy against up to 95% of tested Staphylococcus isolates.[126]
On May 18, 2006, a report in Nature identified a new antibiotic, called platensimycin, that had demonstrated successful use against MRSA.[127][128]
A 2010 study noted significant antimicrobial action of Ulmo 90 and manuka UMF 25+ honey against several microorganisms, including MRSA. The investigators noted the superior antimicrobial action of Ulmo 90 honey, and suggested it be investigated further.[129] A separate 2010 study examined the use of medical-grade honey against several antibiotic-resistant strains of bacteria, including MRSA. The study concluded that the antimicrobial action of the honey studied was due to the activity of hydrogen peroxide, methylglyoxal, and a novel compound named bee defensin-1.[130]
Ocean-dwelling living sponges produce compounds that may make MRSA more susceptible to antibiotics.[131]
Some semi-toxic fungi/mushrooms excrete broad spectrum antibiotics, not all of which have been fully identified.[132]
Cannabinoids (components of Cannabis sativa), including cannabidiol (CBD), cannabinol (CBN), cannabichromene (CBC), tetrahydrocannabinol (THC) and cannabigerol (CBG), show activity against a variety of MRSA strains.[133]
See also[edit]
- Carbapenem resistant enterobacteriaceae
- Necrotizing fasciitis
- Staphylococcus aureus
- Toxic shock syndrome
Further reading[edit]
There are several web-based resources available for further research and treatment options.
- The Center for Disease Control maintains MRSA pages that provide information surrounding the bacteria, including prevention, statistics, at risk groups, causes, educational resources, and environmental factors.
- The National Institute for Occupational Safety and Health maintains a webpage providing information on the bacteria, with respect to the workplace setting, and steps towards mitigating risk from MRSA infection.
- The National Institutes of Health maintains Medline Plus, a site for patients that provides information surrounding diseases, their causes, and treatments. Their MRSA pages provide research and information surrounding causes and treatment options.
- The Mayo Clinic maintains an online site, updated by Mayo Clinic staff, that covers the basic definition, symptoms, and patient education for MRSA.
- The online medical resource site, WebMD, maintains on MRSA that provide basic information about the bacteria, as well as some multimedia resources for patient education.
- MRSA MD is an online medical site devoted solely to MRSA education, treatment, and prevention. Maintained by Dr. Kirk Bortel, MRSA MD provides treatment information and prevention education.
References[edit]
- ^ Study at the Veterans Affairs hospital in Pittsburgh: "Science Daily". [dead link]
- ^ McCaughey B. "Unnecessary Deaths: The Human and Financial Costs of Hospital Infections" (PDF) (2nd. ed.). Archived from the original on July 11, 2007. Retrieved 2007-08-05.
- ^ "Symptoms". Mayo Clinic.
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- ^ Bayston R, Ashraf W, Smith T (2007). "Triclosan resistance in methicillin-resistant Staphylococcus aureus expressed as small colony variants: a novel mode of evasion of susceptibility to antiseptics". J. Antimicrob. Chemother. 59 (5): 848–53. doi:10.1093/jac/dkm031. PMID 17337510.
- ^ Wang J; Soisson, SM; Young, K; Shoop, W; Kodali, S; Galgoci, A; Painter, R; Parthasarathy, G et al. (May 2006). "Platensimycin is a selective FabF inhibitor with potent antibiotic properties". Nature 441 (7091): 358–361. doi:10.1038/nature04784. PMID 16710421.
|displayauthors=suggested (help) - ^ Sherlock O, Dolan A, Athman R, et al. (2010). "Comparison of the antimicrobial activity of Ulmo honey from Chile and Manuka honey against methicillin-resistant Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa". BMC Complement Altern Med 10: 47. doi:10.1186/1472-6882-10-47. PMC 2942791. PMID 20813024.
- ^ Kwakman PH, te Velde AA, de Boer L, Speijer D, Vandenbroucke-Grauls CM, Zaat SA (July 2010). "How honey kills bacteria". FASEB J. 24 (7): 2576–82. doi:10.1096/fj.09-150789. PMID 20228250.
- ^ Sponge's secret weapon restores antibiotics' power
- ^ Psilocybe semilanceata#Ecology and habitat
- ^ Appendino G, Gibbons S, Giana A, Pagani A, Grassi G, Stavri M, Smith E, Rahman M (2008). "Antibacterial Cannabinoids from Cannabis sativa: A Structure-Activity Study". J. Nat. Prod. 71 (8): 1427–30. doi:10.1021/np8002673. PMID 18681481.
UpToDate Contents
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- 1. 成人における侵襲性メチシリン耐性黄色ブドウ球菌感染症の治療 treatment of invasive methicillin resistant staphylococcus aureus infections in adults
- 2. 成人におけるメチシリン耐性黄色ブドウ球菌による皮膚および軟部組織感染症の治療 treatment of skin and soft tissue infections due to methicillin resistant staphylococcus aureus in adults
- 3. 成人におけるメチシリン耐性黄色ブドウ球菌感染症の疫学 epidemiology of methicillin resistant staphylococcus aureus infection in adults
- 4. 成人におけるメチシリン耐性黄色ブドウ球菌の予防および管理 prevention and control of methicillin resistant staphylococcus aureus in adults
- 5. 小児におけるメチシリン耐性黄色ブドウ球菌感染の疫学および臨床的な感染形式 epidemiology and clinical spectrum of methicillin resistant staphylococcus aureus infections in children
English Journal
- Risk factors for surgical site infections following spinal fusion procedures: a case-control study.
- Rao SB, Vasquez G, Harrop J, Maltenfort M, Stein N, Kaliyadan G, Klibert F, Epstein R, Sharan A, Vaccaro A, Flomenberg P.SourceDepartment of Medicine.
- Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.Clin Infect Dis.2011 Oct;53(7):686-92.
- Background.?Spinal fusion procedures are associated with a significant rate of surgical site infection (SSI) (1%-12%). The goal of this study was to identify modifiable risk factors for spinal fusion SSIs at a large tertiary care center. Methods.?A retrospective, case-control (1:3 ratio) analysi
- PMID 21890772
- Appropriate antibiotic dosage levels in the treatment of severe sepsis and septic shock.
- Taccone FS, Hites M, Beumier M, Scolletta S, Jacobs F.SourceDepartment of Intensive Care, Erasme Hospital, Universite Libre de Bruxelles (ULB), Route de Lennik, 808, 1070, Brussels, Belgium, ftaccone@ulb.ac.be.
- Current infectious disease reports.Curr Infect Dis Rep.2011 Oct;13(5):406-15.
- Antibiotic treatment of critically ill patients remains a significant challenge. Optimal antibacterial strategy should achieve therapeutic drug concentration in the blood as well as the infected site. Achieving therapeutic drug concentrations is particularly difficult when infections are caused by s
- PMID 21805081
Japanese Journal
- Carbapenem系抗菌薬の適正使用推進を目的とした医療薬学的アプローチに関する研究
- 室 高広
- 福岡大学薬学集報 11(0), 1-8, 2011-03
- NAID 110008138550
- 注目のTopics 感染・炎症 新生児感染症
- 高橋 尚人
- Fetal & neonatal medicine 3(2), 76-80, 2011-08
- NAID 40018949459
Related Links
- MRSA は黄色ブドウ球菌が耐性化した病原菌であり、黄色ブドウ球菌と同様に常在菌 のひとつと考えられ、健康な人の鼻腔、咽頭、皮膚など ... CA-MRSAは、院内感染での MRSAとは異なり、ミノサイクリンやST合剤、クリンダマイシンが有効であることが多い。 ...
Related Pictures
★リンクテーブル★
| 国試過去問 | 「110E061」「105C018」「109F017」「095D056」「101B060」「095B016」「100B068」「114E025」「103E012」「105E017」 |
| リンク元 | 「耐性菌」「バンコマイシン」「メチシリン耐性黄色ブドウ球菌」「抗MRSA薬」「テイコプラニン」 |
| 拡張検索 | 「MRSA腸炎」「高度バンコマイシン耐性MRSA」「市中獲得型MRSA」 |
| 関連記事 | 「MR」「MRS」 |
「110E061」
- 次の文を読み、61～63の問いに答えよ。
- 72歳の男性。発熱と全身の倦怠感を主訴に来院した。
- 現病歴：2か月前に37℃台の発熱があり、かかりつけ医から抗菌薬を処方された。7日後に解熱したが、倦怠感と食欲低下は持続していた。10日前から38℃台の発熱があり、再度かかりつけ医を受診した。抗菌薬と解熱薬とを処方されたが、発熱と倦怠感が持続するため受診した。
- 既往歴：高血圧症と糖尿病で内服治療中。
- 生活歴：一人暮らし。無職。喫煙は20本/日を50年間。飲酒はビール1,000～1,500mL/日を50年間。
- 家族歴：父親が胃癌で死亡。母親が大腸癌で死亡。
- 現症：意識は清明。身長 182cm、体重 90kg。体温 38.0℃。脈拍 108/分、整。血圧 138/80mmHg。呼吸数 20/分。SpO2 96%(room air)。皮膚は乾燥している。眼瞼結膜と眼球結膜とに異常を認めない。口腔内は乾燥が著明である。頸静脈の怒張を認めない。表在リンパ節を触知しない。心音と呼吸音とに異常を認めない。腹部は平坦、軟で、肝・脾を触知しない。腸蠕動音は正常。肋骨脊柱角に叩打痛を認めない。下腿に浮腫を認めない。神経学的所見に異常を認めない。
- 検査所見：尿所見：蛋白1＋、糖3＋、ケトン体1＋、潜血(－)、沈渣に白血球を認めない。血液所見：赤血球 440万、Hb 15.1g/dL、Ht 44%、白血球 14,500(桿状核好中球2%、分葉核好中球 88%、好酸球 0%、好塩基球 0%、単球 4%、リンパ球 6%)、血小板 32万、PT 87%(基準 80～120)。血液生化学所見：総蛋白 7.1g/dL、アルブミン 3.5g/dL、総ビリルビン 0.5mg/dL、直接ビリルビン 0.2mg/dL、AST 57IU/L、ALT 43IU/L、LD 355IU/L(基準 176～353)、ALP 349IU/L(基準 115～359)、γ-GTP 109IU/L(基準 8～50)、アミラーゼ 38IU/L(基準 37～160)、CK 76IU/L(基準 30～140)、尿素窒素 38mg/dL、クレアチニン 1.1mg/dL、尿酸 9.0mg/dL、血糖 284mg/dL、HbA1c 9.6%(基準 4.6～6.2)、総コレステロール 174mg/dL、トリグリセリド 179mg/dL、Na 135mEq/L、K 4.9mEq/L、Cl 105mEq/L。CRP 11mg/dL。心電図で洞性頻脈を認める。胸部エックス線写真で異常を認めない。
- その後の経過：精査のため入院とし、腹部超音波検査で肝膿瘍を認めた。超音波ガイド下膿瘍穿刺吸引検査を行い、採取した穿刺液を培養検査に提出し、抗菌薬の投与を開始した。培養検査ではGram陽性球菌が検出された。
- 原因菌として可能性が高いのはどれか。2つ選べ。
AC
※国試ナビ4※ ［110E060］←［国試_110］→［110E062］
「105C018」
- 病院内のある委員会の様子を示す。
- 委員長 :これから委員会を開催します。まず、 MRSAの分離状況について検査部から報告をお願いします。
- 検査部委員: 1月はMRSAの感染率、罹患率とも前月までと比較して大きく上回っていました。
- 委員長 :それは好ましくない状況ですね。手洗いの状況はどうですか。看護部から報告をお願いします。
- 看護部要員:先月は手洗い実施の程度を表す消毒用アルコールの消費量が少なかったようです。さっそく手洗いを各部署に徹底させたいと思います。
- 委員長 :よろしくお願いします。抗菌薬の使用状況はどうですか。薬剤部から報告をお癖いします。
- 薬剤部要員:先月はカルバぺネム系抗菌薬の長期使用件数が増加していました。
- 委員長 :それは好ましくない状況ですね。広域抗菌薬の使用は最小限にとどめ、抗菌薬を適正に使用するよう、各部署への通知をお願いします。
- この委員会の名称として考えられるのはどれか。
E
※国試ナビ4※ ［105C017］←［国試_105］→［105C019］
「109F017」
- 74歳の男性。脳梗塞で入院中である。1か月前、四肢麻痺にて緊急入院し、脳幹梗塞と診断された。入院中に肺炎を発症し、抗菌薬にて治療後に回復期リハビリテーション病棟に転棟した。転棟時、意識は清明。不全四肢麻痺のため車椅子への移乗と食事とに介助を要する。体温 36.4℃。血液所見：赤血球 421万、Hb 13.4g/dL、Ht 42%、白血球 6,400、血小板 21万。胸部エックス線写真に異常を認めない。転棟前に実施した喀痰培養でメチシリン耐性黄色ブドウ球菌(MRSA)陽性が判明した。リハビリテーションは訓練室で実施している。
- この患者への対応で誤っているのはどれか。
- a 院内で情報を共有する。
- b リハビリテーションは継続する。
- c バンコマイシン点滴静注を開始する。
- d 食事介助の際にマスクとガウンを着用する。
- e 使用したティッシュペーパーは感染性廃棄物とする。
C
※国試ナビ4※ ［109F016］←［国試_109］→［109F018］
「095D056」
- 67歳の男性。胃潰瘍の診断でヒスタミンH2受容体薬拮抗の投与中に胃癌の診断がなされ、幽門側胃切除術が施行された。術後5日目から頻回の水様性下痢が出現した。便の細菌培養検査からMRSAが検出されたので、感受性のある抗菌薬の投与を開始した。血液所見：赤血球550万、Hb 15.0 g/dl、Ht 52 ％、白血球13,600。血清生化学所見：総蛋白6.5 g/dl、尿素窒素38 mg/dl、クレアチニン1.3mg/dl、Na145mEq/l、K4.8mEq/l、CRP6.2mg/dl(基準0.3以下)。
- 更に行うべき処置はどれか。
C
※国試ナビ4※ ［095D055］←［国試_095］→［095D057］
「101B060」
- 咳、痰および発熱を訴えて入院した感染症患者を診察した医師が、医療スタッフにはN95マスクの着用を指示し、患者にサージカルマスクを着用させて陰圧個室に隔離するよう指示した。
- 原因病原体はどれか。
- a. 結核菌
- b. マラリア原虫
- c. ヒト免疫不全ウイルス HIV
- d. バンコマイシン耐性腸球菌 VRE
- e. メチシリン耐性黄色ブドウ球菌 MRSA
A
※国試ナビ4※ ［101B059］←［国試_101］→［101B061］
「095B016」
- 細菌性肺炎で正しいのはどれか。
D
※国試ナビ4※ ［095B015］←［国試_095］→［095B017］
「100B068」
- 肺感染症の原因微生物と治療薬の組合せで正しいのはどれか。
D
※国試ナビ4※ ［100B067］←［国試_100］→［100B069］
「114E025」
- 麻疹ウイルスと同様の感染経路別予防策を要するのはどれか。
- a A群レンサ球菌
- b ムンプスウイルス
- c 水痘帯状疱疹ウイルス
- d 多剤耐性緑膿菌(MDRP)
- e メチシリン耐性黄色ブドウ球菌(MRSA)
C
※国試ナビ4※ ［114E024］←［国試_114］→［114E026］
「103E012」
- 麻疹と同様の感染経路別予防策を行うのはどれか。2つ選べ。
- a. 結核菌
- b. A群レンサ球菌
- c. 水痘帯状疱疹ウイルス
- d. 多剤耐性緑膿菌 MDRP
- e. メチシリン耐性黄色ブドウ球菌 MRSA
AC
※国試ナビ4※ ［103E011］←［国試_103］→［103E013］
「105E017」
- a ①
- b ②
- c ③
- d ④
- e ⑤
E
※国試ナビ4※ ［105E016］←［国試_105］→［105E018］
「耐性菌」
医療系の雑誌より(日経カデット11月？)
表1抗菌薬投与後に出現する可能性か高い耐性菌
| 系統 | 前投与抗菌薬 | 抗菌薬投与後に高頻度に検出される細菌 | |
| 自然耐性菌 | 獲得耐性菌 | ||
| ペニシリン系 | アンピシリン | Klebsiella pneumoniae | 大腸菌、黄色ブドウ球菌(MSSA、MRSA) |
| ピベラシリン | 緑膿菌 | ||
| セフエム系(第1・2世代) | セフアゾリン、セフォチアム | 緑膿菌、腸球菌 | 黄色ブドウ球菌(MRSA)、大腸菌 |
| セフエム系(第3世代) | セフ卜リアキソン | 腸球菌 | 黄色ブドウ球菌(MRSA)、緑膿菌、大腸菌 |
| セフタジジム | |||
| セフエビム | |||
| カルバペネム系 | メロペネム | Stenotrophomonas maltophilia | 黄色ブドウ球菌(MRSA)、緑膿菌 |
| イミペネム | |||
| アミノグリコシド系 | アミカシン | 腸球菌、嫌気性菌 | 緑膿菌, Serratia marcescens |
| トブラマイシン | レンサ球菌、肺炎球菌 | ||
| マクロライド系 | クラリスロマイシン | 腸内細菌科 | 黄色ブドウ球菌、肺炎球菌、化膿性レンサ球菌 |
| アジスロマシン | |||
| テトラサイクリン系 | ミノサイクリン | Proteus mirabilis | 黄色ブドウ球菌(MRSA)、Brukholderia cepacia、Acinetobacter baumannii |
| Morganella morganii | |||
| Providencia rettgeri | |||
| キノロン系 | レポフロキサシン | レンサ球菌 | 黄色ブドウ球菌(MRSA、大腸菌、緑膿菌 |
表2主な耐性菌と治療薬
| 主な耐性菌 | 治療薬 |
| 緑膿菌 | アズトレオナム+ブラマイシン、シプロフロキサシン(感性株)、(コリスチン) |
| メチシリン耐性黄色ブドウ球菌(MRSA) | バンコマイシン、テイコプラ二ン、アルベカシン、リネゾリド、(ST合剤、リファンピシン) |
| ESBLs産生大腸菌 | ドリペネム、メロペネム、イミペネム、アミカシン、ST合剤 |
| グルコース非発酵性グラム陰性桿菌 | ミノサイクリン、ピベラシリン、アンピシリン+スルバクタム、クロラムフェニコール、ST合剤、(コリスチン) |
| バンコマイシン耐性腸球菌 | テイコプラ二ン(VanB型)、リネゾリド、キヌプリスチン/ダルホプリスチン |
| （）は多分保険適用かないか、日本では未発売 | |
「バンコマイシン」
- 英
- vancomycin, VCM
- 化
- 塩酸バンコマイシン vancomycin hydrochloride
- 商
- Vancocin, Luphocin、バンマイシン
- 関
- 抗菌薬一覧、テイコプラニン、メトロニダゾール
- first aid step1 2006 p.140,165,166,169,173,207
- グリコペプチド系抗生物質
特徴
- Streptomyces orientalisから分離
- 経腸管的に吸収されないため骨髄移植時の消化管内消毒に用いられる。
構造
作用機序
- 細胞壁合成阻害作用(block peptidoglycan synthesis)
- 細胞内で作られたmurein monomerの重合を妨げる？
薬理作用
抗菌スペクトル
- MRSAを含むほとんどのグラム陽性菌と一部の嫌気性菌に抗菌作用を示す
- 殺菌的に作用(bactericidal antibiotics)
動態
- 腸管からほとんど吸収されない→腸管殺菌のための経口投与、点滴静注による全身投与で用いられる
適応
- 感染性腸炎
- 骨髄移植時の消化管内殺菌
- [US?]MRSA(methicillin-resistant Staphylococcus aureus), penicillin-resistant Sreptococcus pneumoniae
適応菌種
- メチシリン耐性黄色ブドウ球菌、クロストリジウム・ディフィシル
注意
禁忌
副作用
- nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing(red man syndrome) (first aid step1 2006 p.169)
重大な副作用
- 添付文書
- 1)ショック：0.1%未満(血圧低下、不快感、口内異常感、喘鳴、眩暈、便意、耳鳴り、発汗等)
- 2)注射用塩酸バンコマイシン製剤：アナフィラキシー様症状、急性腎不全、間質性腎炎、汎血球減少、無顆粒球症、血小板減少、皮膚粘膜眼症候群(Stevens-Johnson症候群)、中毒性表皮壊死症(Lyell症候群)、剥脱性皮膚炎、第8脳神経障害、偽膜性大腸炎、肝機能障害、黄疸
その他
- 1)過敏症(発熱、発疹、潮紅、悪寒、蕁麻疹、そう痒)
- 2)血液(好酸球増多、白血球減少、血小板減少)
- 3)肝臓(AST・ALT・Al-P上昇)
- 4)消化器(下痢：48%、悪心：28%、嘔吐：34%、食欲不振) ←骨髄移植時の消化管内殺菌における発現頻度
- 5)腎臓(BUN・クレアチニンの上昇)
- 6)その他(口内炎、舌炎)
「メチシリン耐性黄色ブドウ球菌」
- 英
- methicillin-resistant Staphylococcus aureus methicillin resistant Staphylococcus aureus MRSA
- 関
- 黄色ブドウ球菌。VRSA、LRSA
耐性獲得機序
- 多種がもつβ-ラクタムに親和性の低いペニシリン結合蛋白を発現するようになったため
- 細胞壁合成酵素(penicillin-binding protein: PBP) PBP 2'の産生。このペニシリン結合タンパクはmecAにコードされている。
- βラクタム薬の投与により発現が誘導される、らしい。
抗菌薬
- QB.H-178
- バンコマイシン
- テイコプラニン：バンコマイシンと同様の作用機序
- リネゾリド
- アルベカシン：(アミノグリコシド系抗菌薬)
臨床関連
「抗MRSA薬」
- グリコペプチド系
- アミノグリコシド系
- オキサゾリジノン系
- 環状リポペプチド系
- セフェム系
- (セフトビプロール) 日本未発売
- グリシルサイクリン系
- (チゲサイクリン) 日本未発売
「テイコプラニン」
- 英
- teicoplanin, TEIC
- 商
- タゴシッド
- 関
- 抗菌薬、グリコペプチド系抗菌薬
「MRSA腸炎」
概念
- MRSAが原因の腸炎であり、院内感染症である。
- 多い患者背景：術前に第3世代セフェム系抗菌薬を使用した患者。第3世代セフェム系抗菌薬を使用した高齢者。 (SSUR.539)
治療
- 薬剤の中止 (SSUR.539) ← 第3世代セフェム系抗菌薬のこと？
- 補液による脱水の改善 (SSUR.539)
- バンコマイシンの投与 (SSUR.539)
鑑別診断
原因が分からない腸炎に対するバンコマイシンの安易な使用について
- IRE.698を参考にしつつ
- バンコマイシンは最後の切り札として温存すべきである。米国ではバンコマイシン使用は厳重に管理されている。日本の臨床ではどうであろうか。抗菌薬に投資開発のリソースをつぎ込んでいる企業はかつてより少なくなってきている。細菌の進化をなるべく遅くするために、抗菌薬をもっと丁寧に使わなければならない。
- かつては「MRSA腸炎」と疑診しただけでバンコマイシンを使用しており、経験的治療としては正しいかも知れないが、抗菌薬の適正利用とはほど遠い。
国試
(治療・管理)095D056