| 黄色ブドウ球菌 |
|
電子顕微鏡写真
|
| 分類 |
| ドメイン |
: |
真正細菌 Bacteria |
| 門 |
: |
フィルミクテス門
Firmicutes |
| 綱 |
: |
バシラス綱
Bacilli |
| 目 |
: |
バシラス目
Bacillales |
| 科 |
: |
ブドウ球菌科
Staphylococcaceae |
| 属 |
: |
ブドウ球菌属
Staphylococcus |
| 種 |
: |
黄色ブドウ球菌
Staphylococcus aureus |
|
| 学名 |
Staphylococcus aureus
Rosenbach 1884 |
黄色ブドウ球菌（おうしょくブドウきゅうきん、Staphylococcus aureus）とは、ヒトや動物の皮膚、消化管（腸）常在菌（腸内細菌）であるブドウ球菌の一つ。
ヒトの膿瘍等の様々な表皮感染症や食中毒、また肺炎、髄膜炎、敗血症等致死的となるような感染症の起因菌でもある。学名はStaphylococcus aureus（スタフィロコッカス・アウレウス）。属名StaphylococcusのStaphylo-は「ブドウの房状の」、coccusは「球菌」の意であり、種小名aureusは「黄金色の」を意味する（金の元素記号や、オーロラなどと同じ語源）。
目次
- 1 性状
- 2 医学的特徴
- 3 病原因子
- 4 疫学
- 5 臨床像
- 5.1 感染症
- 5.1.1 皮膚感染症
- 5.1.2 肺炎、肺化膿症
- 5.1.3 その他の病巣感染症
- 5.2 毒素性疾患
- 5.2.1 食中毒
- 5.2.2 毒素性ショック症候群
- 5.2.3 新生児TSS様発疹症
- 5.2.4 ブドウ球菌性熱傷様皮膚症候群
- 6 治療
- 7 関連項目
- 8 外部リンク
性状
ブドウ球菌は、通性嫌気性のグラム陽性球菌である。顕微鏡で観察すると、ブドウの房のように複数の細菌が集団を形成している。他の細菌と比較して高濃度 (10%) の食塩存在下でも増殖が可能であり、またカタラーゼ活性、ブドウ糖発酵性を持つなどの生化学的特徴を利用して分離・同定される。
他のブドウ球菌と黄色ブドウ球菌の違いは、コアグラーゼと呼ばれるウサギ血漿を凝集させる酵素を産生するかどうかで決まり、ヒトの体表に生息してコアグラーゼを産生するものが黄色ブドウ球菌である。また典型的な一部の黄色ブドウ球菌は黄色の色素を産生するため、培地上で培養したとき黄色いコロニー（細菌の集落）を形成する。当初はこの性質によって判別されており、これが「黄色」と呼ばれる由来であったが、現在は色素産生の有無ではなく、コアグラーゼ産生能で判別される。
医学的特徴
黄色ブドウ球菌は人体の皮膚表面、毛孔に存在する。特に鼻腔内に存在する常在細菌であり、約30%〜100%のヒトが保有していると言われる(諸説あり)。ヒトの皮膚に常在するブドウ球菌の中では毒性が高く、他のブドウ球菌では健常者に対して病気を起こさない（ただし日和見感染を起こすことはある）のに対し、黄色ブドウ球菌は健常者に対しても病気を起こしうる。ただし黄色ブドウ球菌も、健常者では通常の生育場所である皮膚表面や鼻腔などでの増殖自体が発病につながることは少なく、創傷部などから体内に侵入した場合に発病することが多い。感染力は強い部類に属するが、菌が少なければ通常その毒性は弱い。
病原因子
黄色ブドウ球菌の病原性に関わる因子には以下のものが知られている。
- 細胞に局在する病原因子
- プロテインA - 細胞壁に存在するタンパク質で、黄色ブドウ球菌のほとんどが有する特徴的な成分の一つ。抗体（免疫グロブリン）のFc領域に結合する性質を持ち、これによって抗体の持つ生物活性を抑制することで、菌が免疫系によって排除されることを防ぐ働きを持つ。
- フィブロネクチン結合因子 - 細胞壁に存在するタンパク質で、フィブロネクチンと結合して体内に定着する働きを持つ（定着因子）
- タイコ酸 - 細胞壁に存在する分子で宿主細胞との結合を高める（定着因子）
- 外毒素（細胞外に放出される毒素）
- エンテロトキシン群 - 食中毒の原因となる黄色ブドウ球菌が産生する。下痢や腹痛などの直接の原因になる他、嘔吐中枢にも作用して嘔吐の原因にもなる。スーパー抗原としての活性を持つ。
- TSST-1（毒素性ショック症候群毒素-1） - 毒素性ショック症候群（後述）の原因となる毒素。強いスーパー抗原活性を持ち、発熱や悪心、ショック症状を引き起こす。免疫系をかく乱する役割を果たす。高吸収性の月経用、鼻腔用タンポンの使用によって、本毒素の産生が著しく増大することが知られている。
- 表皮剥脱毒素 - スーパー抗原の一種。
- 溶血素（ヘモリジン）- 赤血球を破壊する溶血活性を持つ毒素群であり、特にα毒素が重要な病原因子。免疫細胞を破壊することで菌の排除を防ぐ働きを持つ。また組織破壊によって病巣部から周辺組織に侵入する際にも働く。
- ロイコシジン - 白血球を殺す毒素であり、免疫細胞の破壊によって菌の排除を防ぐ。
- 酵素（病原性に関わる酵素群）
- コアグラーゼ、クランピング因子 - 血漿を凝固させ、フィブリン形成を起こす。これによって菌の増殖の場となる凝集塊を作り出し、白血球や血漿中の抗体による排除を防ぐ働きがあると考えられている。
- スタフィロキナーゼ - 析出したフィブリンを溶解させる働きを持つ。菌が凝集塊の中で増殖した後、その凝集塊を分解して周囲に感染を広げる際に働くと考えられている。
- プロテアーゼ、DNase、リパーゼ - タンパク質、核酸、脂質を分解し、周辺組織を分解して感染の拡大に関わる。
疫学
毎年、アメリカ合衆国では50万人が黄色ブドウ球菌感染症で医療機関を受診する。抗生物質の安易な処方が原因で、黄色ブドウ球菌は、特に多くの一般に利用される抗生物質に耐性（抵抗性）を持つ変種を生み出してきた。特に問題となるのは、そのような耐性菌に対し開発された薬剤に対する耐性菌が出現する事である。 単一の薬剤に対し耐性を獲得した菌は、耐性を有する薬剤名を冠しペニシリン耐性菌、メチシリン耐性菌はMRSA、バンコマイシン耐性菌はVRSAと呼ばれる。また複数の薬剤に対し耐性を獲得した菌は多剤耐性菌と呼ばれる。なお、メチシリンに対する感受性のある菌はMSSAと呼ばれる。
- 薬剤に対する耐性に関しては、薬剤耐性を参照。
臨床像
黄色ブドウ球菌による疾患は、感染病原性と毒素病原性とに大別される。前者はブドウ球菌が体内で感染・増殖することによる疾患であり、各種の化膿性疾患や肺炎、急性心内膜炎、菌血症が含まれる。後者は感染や増殖そのものよりも、ブドウ球菌が産生する毒素による症状であり、食中毒、毒素性ショック症候群(Toxic shock syndrome, TSS)、熱傷様皮膚症候群がこれにあたる。
感染症
黄色ブドウ球菌による感染は、表皮およびその直下の組織に限局した部位に見られることが多い。毛孔や創傷部から感染が起きると、伝染性膿痂疹（とびひ、インペティーゴ）、癤（せつ、フルンケル）、癰（よう、カルブンケル）、蜂巣炎など、表皮限局性の化膿性疾患の原因になる。また、カテーテルや心臓弁など、医療行為に用いる異物に付着して、そこで骨髄炎、関節炎などの深部限局性感染を起こすことがある。これらの疾患で生じる膿瘍内で細菌は増殖するが、さらに細菌の増殖が進むと、スタフィロキナーゼや各種プロテアーゼなどの働きによって病巣周辺の組織を破壊しながら周囲に浸潤し、ときに血流に入って、菌血症や敗血症、急性心内膜炎、肺炎などを引き起こすことがある。
皮膚感染症
黄色ブドウ球菌による感染症としては頻度が高く、正常な免疫を持つヒトにもしばしば発症する。
皮膚感染症のうち最も表面に近い部分に起こるのが伝染性膿痂疹（Impetigo、「とびひ」）である。皮膚表面にべったりとした黄色の膿痂（かさぶた）を伴ったびらんが現れる。びらんは痛痒いため、特に小児ではこのびらんを掻破してしまう。びらんを掻破した爪で他の健常皮膚面を掻破することにより、その健常皮膚面に新たなびらんを形成する。こうして病巣が播種していくのが「伝染性」膿痂疹の特徴である。
毛孔から感染し、毛嚢およびその周囲の真皮・皮下組織の一部に炎症を起こすのが癤（せつ、Furuncle）である。癤が複数の毛孔におよび、癒合したものは癰（よう、Carbuncle）と呼ばれる。特に顔面にできた癤や癰は面疔と呼ばれ、放置すると髄膜炎を起こす危険があるため、確実な治療が必要とされる。
表皮内部に感染を起こすのが蜂窩織炎（蜂巣炎）である。通常の細胞構造を細菌及び炎症細胞が破壊し、｢蜂の巣｣状の病理組織を形成することがこの名の由来である。蜂窩織炎の局所は発赤・腫脹し、熱感と疼痛を伴う。境界はやや不明瞭であることが多い（A群β溶血性連鎖球菌で起こる丹毒では境界明瞭である）。
膿痂疹は局所を消毒し、掻破しないように心がけるだけでも治ることがある。他の皮膚感染症には抗菌薬の投与が必要である。ペニシリン系のクロキサシリン (MCIPC)、スルバクタム/アンピシリン合剤 (SBT/ABPC)、第1世代セフェムのセファゾリン (CEZ) などが通常用いられる。正常な免疫を持つ患者ではMRSAによる皮膚感染の頻度は低く、治療の最初から抗MRSA薬を用いることはしない。
肺炎、肺化膿症
高齢者や人工呼吸器管理中の患者などには、黄色ブドウ球菌による肺炎、肺化膿症が起こりうる。これらの患者の多くでは過去に抗菌薬を投与されており、MRSAの頻度が高いことに注意が必要である。喀痰および胸水のグラム染色が迅速診断に有用であり、適切な抗菌薬の選択が必要である。
その他の病巣感染症
人工弁、人工関節、中心静脈カテーテルなど体内に異物が存在する患者では、血流中に侵入した黄色ブドウ球菌がこれら異物に定着して感染症を起こすことがある。また、異物がなくても、骨髄炎や関節炎などの特殊な病巣感染症を起こす場合がある。黄色ブドウ球菌によるこれらの病巣感染症では、しばしば抗菌薬投与のみでは不足であり、病巣に対する外科的処置が必要となる（人工弁の入れ替え、カテーテル抜去、関節腔の切開排膿など）。
毒素性疾患
食中毒
黄色ブドウ球菌による食中毒は、食品中で増殖してそこで黄色ブドウ球菌エンテロトキシン毒素を産生するために起きるものである。この毒素は耐熱性で、食品を加熱することによってブドウ球菌そのものが死滅しても、毒素は耐熱性のためそのまま残る。それを食べた場合に激しい嘔吐を伴う食中毒を引き起こす。このような食中毒を毒素型食中毒と呼ぶ。一方、サルモネラや病原大腸菌などの場合は生きた細菌が腸内に感染することによって起きる感染型食中毒を引き起こす。すなわちブドウ球菌による食中毒は感染症ではなく、むしろ毒キノコを食べるケースに近い。
黄色ブドウ球菌による食中毒は潜伏期が短く、汚染された食品を食べたあと2〜3時間(エンテロトキシン濃度が高ければ数十分程度)で発症し、その後すみやかに終息する。しかし、症状が激しい場合には、ショック症状に陥る場合もあるため、健康に異常を感じた場合は医療機関に受診するのが望まれる。主に悪心と嘔吐が現れ、場合によっては腹痛や下痢を伴うこともある。黄色ブドウ球菌による食中毒は、症状が嘔吐に集中するのが特徴でもある。黄色ブドウ球菌自体が体内に入る感染症ではないため、抗菌薬の投与は不要であり、輸液により水分・糖・電解質を補充して症状の改善を待つ。
毒素性ショック症候群
毒素性ショック症候群 (Toxic shock syndrome, TSS) は、黄色ブドウ球菌の産生するTSST-1 (Toxic shock syndrome toxin 1) という毒素による症候群。TSST-1がスーパー抗原として働き、発疹、下痢・嘔吐、血圧低下（ショック）、播種性血管内凝固、多臓器不全などを来たす致命的な疾患である。
昇圧剤、輸血、蛋白分解酵素阻害薬などの対症療法のほか、毒素の除去および急性腎不全に対する治療のために血漿交換や持続的血液濾過透析などの血液浄化法を行う。
新生児TSS様発疹症
新生児TSS様発疹症（Neonatal TSS-like Exanthematous Disease, NTED（エヌテッド、と読まれることが多い））は、生後数日以内の新生児に発症する毒素性疾患で、原因菌はほとんどMRSAである。TSST-1 like toxinという毒素がスーパー抗原となって発症する。発疹、軽度の発熱、ときに哺乳不良が症状であり、血液所見では血小板減少と軽度の炎症反応を伴う。
ときに血小板輸血が必要となることもあるが、TSSとは異なり、おおむね予後良好な疾患である。治療法として特異的なものはないが、多くの場合抗MRSA薬が投与される。
ブドウ球菌性熱傷様皮膚症候群
ブドウ球菌性熱傷様皮膚症候群（Staphylococcal Scalded Skin Syndrome, SSSS（フォーエス、と読まれることが多い））は、乳幼児に特有の毒素性疾患である。黄色ブドウ球菌が産生するExfoliative (Epidermolytic) toxin-A,Bがその原因であり、毒素が表皮に沈着してスーパー抗原として働くことで、表皮の細胞間結合が破壊される。
症状は全身の皮膚のびらん、水疱形成で、著しい痛みを伴う。一見正常に見える皮膚面でも、物理的刺激により水疱を形成する(ニコルスキー現象)。そのため、水疱・びらんは間擦部、つまりひじの内側やわきの下、首の周りなどにできやすい。多くの場合、口周囲には膿痂疹ができており、膿痂からは黄色ブドウ球菌が検出される。治療に特異的なものはないが、膿痂疹を伴っていることが多いためセファゾリンなどの抗菌薬を使うことが多い。MRSAが検出されることも少なくないが、抗MRSA薬は通常用いない。また、不機嫌で経口摂取を取れなくなることがしばしばあり、輸液が必要となることが多い。SSSSそのものは、数日で自然軽快する疾患である。
治療
いわゆる抗生物質（抗細菌薬）の投与による化学療法を行う。ただしさまざまな薬剤に対する耐性を獲得したものも多い。ほとんどの黄色ブドウ球菌はもともとペニシリン感受性であったが、現在分離されるもののほとんどはペニシリン耐性である。セフェム系やストレプトマイシンなどの薬剤にも耐性のものが多い。メチシリンやバンコマイシンが、これらの耐性菌に有効であったが、現在はMRSA、VRSAなども報告されている。これらの事情から、用いる薬剤については分離された菌に対する薬剤感受性試験を行って有効なものを用いるべきであるとされる。
関連項目
|
ウィキメディア・コモンズには、黄色ブドウ球菌に関連するカテゴリがあります。 |
外部リンク
- 黄色ブドウ球菌食中毒 和歌山県
- 黄色ブドウ球菌食による中毒 北海道立衛生研究所
|
気道感染 |
|
| 上気道 |
|
風邪
|
ライノウイルス - アデノウイルス - パラインフルエンザウイルス - RSウイルス - コロナウイルス - エコーウイルス - エンテロウイルス
|
|
|
喉頭炎
|
急性喉頭蓋炎 - クループ
|
|
|
咽頭炎
|
|
|
| 下気道 |
急性細気管支炎
|
|
| 肺炎 |
|
原因
|
|
定型肺炎
|
|
グラム陽性
|
肺炎球菌 - 黄色ブドウ球菌
|
|
|
グラム陰性
|
肺炎桿菌 - インフルエンザ菌 - モラクセラ - 大腸菌 - 緑膿菌
|
|
|
|
非定型肺炎
|
|
ウイルス性
|
RSウイルス - インフルエンザ肺炎 - 重症急性呼吸器症候群
|
|
|
肺真菌症
|
ニューモシスチス肺炎 - クリプトコッカス症 - アスペルギルス症
|
|
|
レジオネラ菌 - マイコプラズマ - クラミジア肺炎 - オウム病
|
|
|
|
抗酸菌症
|
結核 - 非結核性抗酸菌症
|
|
|
|
機序
|
市中肺炎 - 院内肺炎 - 誤嚥性肺炎
|
|
|
病態
|
|
肺胞性肺炎
|
大葉性肺炎 - 気管支肺炎
|
|
|
化膿性肺炎
|
|
|
|
| 胸壁 |
膿胸
|
|
| Staphylococcus aureus |
|
| Scanning electron micrograph of S. aureus; false color added. |
| Scientific classification |
| Domain: |
Bacteria |
| Kingdom: |
Eubacteria |
| Phylum: |
Firmicutes |
| Class: |
Bacilli |
| Order: |
Bacillales |
| Family: |
Staphylococcaceae |
| Genus: |
Staphylococcus |
| Species: |
S. aureus |
| Binomial name |
Staphylococcus aureus
Rosenbach 1884 |
Staphylococcus aureus is a gram positive coccus bacterium that is a member of the Firmicutes, and is frequently found in the human respiratory tract and on the skin. It is positive for catalase and nitrate reduction. Although S. aureus is not always pathogenic, it is a common cause of skin infections (e.g. boils), respiratory disease (e.g. sinusitis), and food poisoning. Disease-associated strains often promote infections by producing potent protein toxins, and expressing cell-surface proteins that bind and inactivate antibodies. The emergence of antibiotic-resistant forms of pathogenic S. aureus (e.g. MRSA) is a worldwide problem in clinical medicine.
Staphylococcus was first identified in 1880 in Aberdeen, United Kingdom, by the surgeon Sir Alexander Ogston in pus from a surgical abscess in a knee joint.[1] This name was later appended to Staphylococcus aureus by Rosenbach who was credited by the official system of nomenclature at the time. It is estimated that 20% of the human population are long-term carriers of S. aureus[2] which can be found as part of the normal skin flora and in anterior nares of the nasal passages.[2][3] S. aureus is the most common species of staphylococcus to cause Staph infections and is a successful pathogen due to a combination of nasal carriage and bacterial immuno-evasive strategies.[2][3] S. aureus can cause a range of illnesses, from minor skin infections, such as pimples, impetigo, boils (furuncles), cellulitis folliculitis, carbuncles, scalded skin syndrome, and abscesses, to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock syndrome (TSS), bacteremia, and sepsis. Its incidence ranges from skin, soft tissue, respiratory, bone, joint, endovascular to wound infections. It is still one of the five most common causes of nosocomial infections and is often the cause of postsurgical wound infections. Each year, some 500,000 patients in American hospitals contract a staphylococcal infection.[4]
| Staphylococcus aureus |
| Classification and external resources |
| ICD-9 |
041.11 |
Contents
- 1 Microbiology
- 2 Role in disease
- 2.1 Atopic dermatitis
- 2.2 Animal infections
- 3 Virulence factors
- 3.1 Enzymes
- 3.2 Toxins
- 3.3 Other immunoevasive strategies
- 4 Classical diagnosis
- 4.1 Rapid diagnosis and typing
- 5 Treatment and antibiotic resistance
- 5.1 Mechanisms of antibiotic resistance
- 6 Carriage of Staphylococcus aureus
- 7 Infection control
- 8 See also
- 9 References
- 10 External links
Microbiology
Further information: Coagulase-positive staphylococcal infection
Gram stain of
S. Saprophyticus" cells which typically occur in clusters. The cell wall readily absorbs the crystal violet stain.
Yellow colonies of
S. aureus on a blood agar plate, note regions of clearing around colonies caused by lysis of red cells in the agar (beta hemolysis).
S. aureus (/ /, Greek σταφυλόκοκκος, "grape-cluster berry", Latin aureus, "golden") is a facultative anaerobic Gram-positive coccal bacterium, also known as "golden staph" and Oro staphira. In medical literature the bacteria is often referred to as S. aureus or Staph aureus. Staphylococcus should not be confused with the similarly named and medically relevant genus Streptococcus. S. aureus appears as grape-like clusters when viewed through a microscope, and has large, round, golden-yellow colonies, often with hemolysis, when grown on blood agar plates.[5] S. aureus reproduces asexually by binary fission. The two daughter cells do not fully separate and remain attached to one another. This is why the cells are observed in clusters.[6]
S. aureus is catalase-positive (meaning it can produce the enzyme catalase). Catalase converts hydrogen peroxide (H
2O
2) to water and oxygen. Catalase-activity tests are sometimes used to distinguish staphylococci from enterococci and streptococci. Previously, S. aureus was differentiated from other staphylococci by the coagulase test. However it is now known that not all S. aureus are coagulase-positive[5][7] and that incorrect species identification can impact effective treatment and control measures.[8]
Role in disease
SEM of methicillin-resistant
Staphylococcus aureus.
S. aureus is responsible for many infections but it may also occur as a commensal. The presence of S. aureus does not always indicate infection. S. aureus can survive from hours to weeks, or even months, on dry environmental surfaces, depending on strain.[9]
S. aureus can infect tissues when the skin or mucosal barriers have been breached. This can lead to many different types of infections including furuncles and carbuncles (a collection of furuncles).
S. aureus infections can spread through contact with pus from an infected wound, skin-to-skin contact with an infected person by producing hyaluronidase that destroys tissues, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person. Deeply penetrating S. aureus infections can be severe. Prosthetic joints put a person at particular risk of septic arthritis, and staphylococcal endocarditis (infection of the heart valves) and pneumonia. Strains of S. aureus can host phages, such as Φ-PVL (produces Panton-Valentine leukocidin), that increase virulence.
Atopic dermatitis
S. aureus is extremely prevalent in persons with atopic dermatitis. It is mostly found in fertile, active places, including the armpits, hair, and scalp. Large pimples that appear in those areas may exacerbate the infection if lacerated. This can lead to staphylococcal scalded skin syndrome (SSSS). A severe form of this, Ritter's disease, can be observed in neonates.[10]
The presence of S. aureus in persons with atopic dermatitis is not an indication to treat with oral antibiotics, as evidence has not shown this to give benefit to the patient.[11] The relationship between S. aureus and atopic dermatitis is unclear.[11] Evidence shows that attempting to control S. aureus with oral antibiotics is not efficacious.[11]
Animal infections
S. aureus can survive on dogs,[12] cats,[13] and horses,[14] and can cause bumblefoot in chickens.[15] Some believe health-care workers' dogs should be considered a significant source of antibiotic-resistant S. aureus, especially in times of outbreak.[12] S. aureus is one of the causal agents of mastitis in dairy cows. Its large polysaccharide capsule protects the organism from recognition by the cow's immune defenses.[16]
Virulence factors
Enzymes
Staphylococcus aureus produces various enzymes such as coagulase (bound and free coagulases) which clots plasma and coats the bacterial cell to probably prevent phagocytosis. Hyaluronidase (also known as spreading factor) breaks down hyaluronic acid and helps in spreading of Staphylococcus aureus. S.aureus also produces DNAse (deoxyribonuclease) which breaks down the DNA, lipase to digest lipids, staphylokinase to dissolve fibrin and aid in spread, and beta-lactamase for drug resistance.[17]
Toxins
Depending on the strain, S. aureus is capable of secreting several exotoxins, which can be categorized into three groups. Many of these toxins are associated with specific diseases.[18]
- Superantigens
- (PTSAgs) have superantigen activities that induce toxic shock syndrome (TSS). This group includes the toxin TSST-1, enterotoxin type B, which causes TSS associated with tampon use. This is characterized by fever, erythematous rash, hypotension, shock, multiple organ failure, and skin desquamation. Lack of antibody to TSST-1 plays a part in the pathogenesis of toxic shock syndrome. Other strains of S. aureus can produce an enterotoxin that is the causative agent of S. aureus gastroenteritis. This gastroenteritis is self-limiting, characterized by vomiting and diarrhea one to six hours after ingestion of the toxin with recovery in eight to 24 hours. Symptoms include nausea, vomiting, diarrhea, and major abdominal pain.[19][20]
- Exfoliative toxins
- EF toxins are implicated in the disease staphylococcal scalded-skin syndrome (SSSS), which occurs most commonly in infants and young children. It also may occur as epidemics in hospital nurseries. The protease activity of the exfoliative toxins causes peeling of the skin observed with SSSS.[20]
- Other toxins
- Staphylococcal toxins that act on cell membranes include alpha toxin, beta toxin, delta toxin, and several bicomponent toxins. The bicomponent toxin Panton-Valentine leukocidin (PVL) is associated with severe necrotizing pneumonia in children.[21][22] The genes encoding the components of PVL are encoded on a bacteriophage found in community-associated methicillin-resistant S. aureus (MRSA) strains.
Other immunoevasive strategies
- Protein A
Protein A is anchored to staphylococcal peptidoglycan pentaglycine bridges (chains of five glycine residues) by the transpeptidase sortase A.[23] Protein A, an IgG-binding protein, binds to the Fc region of an antibody. In fact, studies involving mutation of genes coding for protein A resulted in a lowered virulence of S. aureus as measured by survival in blood, which has led to speculation that protein A-contributed virulence requires binding of antibody Fc regions.[24]
Protein A in various recombinant forms has been used for decades to bind and purify a wide range of antibodies by immunoaffinity chromatography. Transpeptidases, such as the sortases responsible for anchoring factors like Protein A to the staphylococcal peptidoglycan, are being studied in hopes of developing new antibiotics to target MRSA infections.[25]
Staphylococcus aureus on Tryptic Soy Agar. The strain is producing a yellow pigment staphyloxanthin.
- Staphylococcal Pigments
Some strains of S. aureus are capable of producing staphyloxanthin — a golden coloured carotenoid pigment. This pigment acts as a virulence factor, primarily by being a bacterial antioxidant which helps the microbe evade the reactive oxygen species which the host immune system uses to kill pathogens.[26][27]
Mutant strains of S. aureus modified to lack staphyloxanthin are less likely to survive incubation with an oxidizing chemical, such as hydrogen peroxide than pigmented strains. Mutant colonies are quickly killed when exposed to human neutrophils, while many of the pigmented colonies survive.[26] In mice, the pigmented strains cause lingering abscesses when inoculated into wounds, whereas wounds infected with the unpigmented strains quickly heal.
These tests suggest the Staphylococcus strains use staphyloxanthin as a defence against the normal human immune system. Drugs designed to inhibit the production of staphyloxanthin may weaken the bacterium and renew its susceptibility to antibiotics.[27] In fact, because of similarities in the pathways for biosynthesis of staphyloxanthin and human cholesterol, a drug developed in the context of cholesterol-lowering therapy was shown to block S. aureus pigmentation and disease progression in a mouse infection model.[28]
Classical diagnosis
Typical Gram-positive cocci, in clusters, from a sputum sample, Gram stain
Depending upon the type of infection present, an appropriate specimen is obtained accordingly and sent to the laboratory for definitive identification by using biochemical or enzyme-based tests. A Gram stain is first performed to guide the way, which should show typical Gram-positive bacteria, cocci, in clusters. Second, the isolate is cultured on mannitol salt agar, which is a selective medium with 7–9% NaCl that allows S. aureus to grow, producing yellow-colored colonies as a result of mannitol fermentation and subsequent drop in the medium's pH.
Furthermore, for differentiation on the species level, catalase (positive for all Staphylococcus species), coagulase (fibrin clot formation, positive for S. aureus), DNAse (zone of clearance on DNase agar), lipase (a yellow color and rancid odor smell), and phosphatase (a pink color) tests are all done. For staphylococcal food poisoning, phage typing can be performed to determine whether the staphylococci recovered from the food were the source of infection.
Rapid diagnosis and typing
Diagnostic microbiology laboratories and reference laboratories are key for identifying outbreaks and new strains of S. aureus. Recent genetic advances have enabled reliable and rapid techniques for the identification and characterization of clinical isolates of S. aureus in real time. These tools support infection control strategies to limit bacterial spread and ensure the appropriate use of antibiotics. Quantitative PCR is being increasingly employed in clinical laboratories as a technique to identifying outbreaks.[29][30]
Treatment and antibiotic resistance
The treatment of choice for S. aureus infection is penicillin; in most countries, however, penicillin resistance is extremely common, and first-line therapy is most commonly a penicillinase-resistant β-lactam antibiotic (for example, oxacillin or flucloxacillin). Combination therapy with gentamicin may be used to treat serious infections, such as endocarditis,[31][32] but its use is controversial because of the high risk of damage to the kidneys.[33] The duration of treatment depends on the site of infection and on severity.
Antibiotic resistance in S. aureus was uncommon when penicillin was first introduced in 1943. Indeed, the original petri dish on which Alexander Fleming of Imperial College London observed the antibacterial activity of the Penicillium fungus was growing a culture of S. aureus. By 1950, 40% of hospital S. aureus isolates were penicillin-resistant; and, by 1960, this had risen to 80%.[34]
Methicillin-resistant S. aureus, abbreviated MRSA and often pronounced // or / /, is one of a number of greatly feared strains of S. aureus which have become resistant to most β-lactam antibiotics. MRSA strains are most often found associated with institutions such as hospitals, but are becoming increasingly prevalent in community-acquired infections. A recent study by the Translational Genomics Research Institute showed that nearly half (47%) of the meat and poultry in U.S. grocery stores were contaminated with S. aureus, with more than half (52%) of those bacteria resistant to antibiotics.[35]
- The article Methicillin-resistant Staphylococcus aureus contains related information on this topic
Researchers from Italy have identified a bacteriophage active against S. aureus, including methicillin-resistant strains (MRSA), in mice and possibly humans.[36]
Mechanisms of antibiotic resistance
Bacterial cells of
Staphylococcus aureus, which is one of the causal agents of mastitis in dairy cows. Its large capsule protects the organism from attack by the cow's immunological defenses.
Staphylococcal resistance to penicillin is mediated by penicillinase (a form of β-lactamase) production: an enzyme that cleaves the β-lactam ring of the penicillin molecule, rendering the antibiotic ineffective. Penicillinase-resistant β-lactam antibiotics, such as methicillin, nafcillin, oxacillin, cloxacillin, dicloxacillin, and flucloxacillin, are able to resist degradation by staphylococcal penicillinase.
Resistance to methicillin is mediated via the mec operon, part of the staphylococcal cassette chromosome mec (SCCmec). Resistance is conferred by the mecA gene, which codes for an altered penicillin-binding protein (PBP2a or PBP2') that has a lower affinity for binding β-lactams (penicillins, cephalosporins, and carbapenems). This allows for resistance to all β-lactam antibiotics, and obviates their clinical use during MRSA infections. As such, the glycopeptide vancomycin is often deployed against MRSA.
Aminoglycoside antibiotics, such as kanamycin, gentamicin, streptomycin, etc., were once effective against staphylococcal infections until strains evolved mechanisms to inhibit the aminoglycosides' action, which occurs via protonated amine and/or hydroxyl interactions with the ribosomal RNA of the bacterial 30S ribosomal subunit.[37] There are three main mechanisms of aminoglycoside resistance mechanisms which are currently and widely accepted: aminoglycoside modifying enzymes, ribosomal mutations, and active efflux of the drug out of the bacteria.
Aminoglycoside-modifying enzymes inactivate the aminoglycoside by covalently attaching either a phosphate, nucleotide, or acetyl moiety to either the amine or the alcohol key functional group (or both groups) of the antibiotic. This changes the charge or sterically hinders the antibiotic, decreasing its ribosomal binding affinity. In S. aureus, the best-characterized aminoglycoside-modifying enzyme is aminoglycoside adenylyltransferase 4' IA (ANT(4')IA). This enzyme has been solved by x-ray crystallography.[38] The enzyme is able to attach an adenyl moiety to the 4' hydroxyl group of many aminoglycosides, including kamamycin and gentamicin.
Glycopeptide resistance is mediated by acquisition of the vanA gene. The vanA gene originates from the enterococci and codes for an enzyme that produces an alternative peptidoglycan to which vancomycin will not bind.
Today, S. aureus has become resistant to many commonly used antibiotics. In the UK, only 2% of all S. aureus isolates are sensitive to penicillin, with a similar picture in the rest of the world. The β-lactamase-resistant penicillins (methicillin, oxacillin, cloxacillin, and flucloxacillin) were developed to treat penicillin-resistant S. aureus, and are still used as first-line treatment. Methicillin was the first antibiotic in this class to be used (it was introduced in 1959), but, only two years later, the first case of MRSA was reported in England.[39]
Despite this, MRSA generally remained an uncommon finding, even in hospital settings, until the 1990s, when there was an explosion in MRSA prevalence in hospitals, where it is now endemic.[40]
MRSA infections in both the hospital and community setting are commonly treated with non-β-lactam antibiotics, such as clindamycin (a lincosamine) and co-trimoxazole (also commonly known as trimethoprim/sulfamethoxazole). Resistance to these antibiotics has also led to the use of new, broad-spectrum anti-Gram-positive antibiotics, such as linezolid, because of its availability as an oral drug. First-line treatment for serious invasive infections due to MRSA is currently glycopeptide antibiotics (vancomycin and teicoplanin). There are number of problems with these antibiotics, such as the need for intravenous administration (there is no oral preparation available), toxicity, and the need to monitor drug levels regularly by blood tests. There are also concerns glycopeptide antibiotics do not penetrate very well into infected tissues (this is a particular concern with infections of the brain and meninges and in endocarditis). Glycopeptides must not be used to treat methicillin-sensitive S. aureus (MSSA), as outcomes are inferior.[41]
Because of the high level of resistance to penicillins and because of the potential for MRSA to develop resistance to vancomycin, the U.S. Centers for Disease Control and Prevention has published guidelines for the appropriate use of vancomycin. In situations where the incidence of MRSA infections is known to be high, the attending physician may choose to use a glycopeptide antibiotic until the identity of the infecting organism is known. After the infection is confirmed to be due to a methicillin-susceptible strain of S. aureus, treatment can be changed to flucloxacillin or even penicillin, as appropriate.
Vancomycin-resistant S. aureus (VRSA) is a strain of S. aureus that has become resistant to the glycopeptides. The first case of vancomycin-intermediate S. aureus (VISA) was reported in Japan in 1996;[42] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[43] Three cases of VRSA infection had been reported in the United States as of 2005.[44]
Carriage of Staphylococcus aureus
The carriage of Staphylococcus aureus is an important source of nosocomial infection and community-acquired methicillin-resistant S. aureus (MRSA). Although S. aureus can be present on the skin of the host, a large proportion of its carriage is through the anterior nares of the nasal passages.[2] The ability of the nasal passages to harbour S. aureus results from a combination of a weakened or defective host immunity and the bacteria's ability to evade host innate immunity.[45]
Infection control
Spread of S. aureus (including MRSA) generally is through human-to-human contact, although recently some veterinarians have discovered the infection can be spread through pets,[46] with environmental contamination thought to play a relatively unimportant part. Emphasis on basic hand washing techniques are, therefore, effective in preventing its transmission. The use of disposable aprons and gloves by staff reduces skin-to-skin contact and, therefore, further reduces the risk of transmission. Please refer to the main article on infection control for further details.
Recently, there have been myriad reported cases of S. aureus in hospitals across America. Transmission of the pathogen is facilitated in medical settings where healthcare worker hygiene is insufficient. S. aureus is an incredibly hardy bacterium, as was shown in a study where it survived on polyester for just under three months;[47] polyester is the main material used in hospital privacy curtains.
The bacteria are transported on the hands of healthcare workers, who may pick them up from a seemingly healthy patient carrying a benign or commensal strain of S. aureus, and then pass it on to the next patient being treated. Introduction of the bacteria into the bloodstream can lead to various complications, including, but not limited to, endocarditis, meningitis, and, if it is widespread, sepsis.
Ethanol has proven to be an effective topical sanitizer against MRSA. Quaternary ammonium can be used in conjunction with ethanol to increase the duration of the sanitizing action. The prevention of nosocomial infections involves routine and terminal cleaning. Nonflammable alcohol vapor in CO
2 NAV-CO2 systems have an advantage, as they do not attack metals or plastics used in medical environments, and do not contribute to antibacterial resistance.
An important and previously unrecognized means of community-associated MRSA colonization and transmission is during sexual contact.[48]
Staff or patients who are found to carry resistant strains of S. aureus may be required to undergo "eradication therapy", which may include antiseptic washes and shampoos (such as chlorhexidine) and application of topical antibiotic ointments (such as mupirocin or neomycin) to the anterior nares of the nose.
S. aureus is killed in 1 minute at 78 °C and 10 minutes at 64 °C.[49]
The nonprotein amino acid L-homoarginine is a growth inhibitor of S. aureus as well as Candida albicans. It is assumed to be an antimetabolite of arginine.
Biological control might be a new possible way to control Staphylococcus aureus in body surfaces. Colonization of body surfaces (especially in the nose) by Staphylococcus epidermidis(inhibitory strain JK16) impairs the establishment of S. aureus.
A 2011 study[50] points to this new possible way to control S. aureus. This study was performed from observations of the nasal microbial flora of a diverse group of people. It was discovered that there are two different strains of S. epidermidis, one that inhibits biofilm formation by S. aureus, S. epidermidis strain JK16 (inhibitory type), and one that does not (non-inhibitory type) S. epidermidis strain JK11. In this study they observed that there were some patients that were not affected by Staphylococcus aureus; this was because these patients had S. aureus together with S. epidermis (inhibitory type), in their nasal microbial flora. This is due to an amensalistic relationship between these microorganisms, the inhibitory strain of S. epidermidis and Staphylococcus aureus.
These findings open the way to a biological control therapy to help in the treatment of S. aureus infections which are becoming a growing threat due to the rise of resistance to conventional antibiotic treatments.
See also
- Facultative anaerobic organism
- Gram-positive bacteria
- List of cutaneous conditions
- MRSA
- Staphylococcal infection
- Vancomycin-resistant Staphylococcus aureus
References
- ^ Ogston A (1984). ""On Abscesses". Classics in Infectious Diseases". Rev Infect Dis 6 (1): 122–28. doi:10.1093/clinids/6.1.122. PMID 6369479.
- ^ a b c d Kluytmans J, van Belkum A, Verbrugh H (July 1997). "Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated risks". Clin. Microbiol. Rev. 10 (3): 505–20. PMC 172932. PMID 9227864.
- ^ a b Cole, A. M.; Tahk, S.; Oren, A.; Yoshioka, D.; Kim, Y. H.; Park, A.; Ganz, T (November 2001). "Determinants of Staphylococcus aureus nasal carriage". Clin Diagn Lab Immunol 8 (6): 1064–9. doi:10.1128/CDLI.8.6.1064-1069.2001. PMC 96227. PMID 11687441.
- ^ Bowersox, John (27 May 1999). "Experimental Staph Vaccine Broadly Protective in Animal Studies". NIH. Archived from the original on 5 May 2007. Retrieved 28 July 2007.
- ^ a b Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9.
- ^ "Staphylococcus aureus: Reproduction". palexander13.webs.com.
- ^ PreTest, Surgery, 12th ed., p.88
- ^ Matthews KR, Roberson J, Gillespie BE, Luther DA, Oliver SP (1997). "Identification and Differentiation of Coagulase-Negative Staphylococcus aureus by Polymerase Chain Reaction". Journal of Food Protection 60 (6): 686–8.
- ^ Cimolai N (July 2008). "MRSA and the environment: implications for comprehensive control measures". Eur. J. Clin. Microbiol. Infect. Dis. 27 (7): 481–93. doi:10.1007/s10096-008-0471-0. PMID 18273652.
- ^ Curran JP, Al-Salihi FL (1980). "Neonatal staphylococcal scalded skin syndrome: massive outbreak due to an unusual phage type". Pediatrics 66 (2): 285–90. PMID 6447271.
- ^ a b c American Academy of Dermatology (February 2013), "Five Things Physicians and Patients Should Question", Choosing Wisely: an initiative of the ABIM Foundation (American Academy of Dermatology), retrieved 5 December 2013 , which cites
- Birnie, A. J.; Bath-Hextall, F. J.; Ravenscroft, J. C.; Williams, H. C. (2008). Interventions to reduce Staphylococcus aureus in the management of atopic eczema. In Birnie, Andrew J. "Cochrane Database of Systematic Reviews". The Cochrane database of systematic reviews (3): CD003871. doi:10.1002/14651858.CD003871.pub2. PMID 18646096.
- ^ a b Boost MV, O'Donoghue MM, James A (2008). "Prevalence of Staphylococcus aureus carriage among dogs and their owners". Epidemiol. Infect. 136 (7): 953–964. doi:10.1017/S0950268807009326. PMC 2870875.
- ^ Hanselman BA, Kruth SA, Rousseau J, Weese JS (2009). "Coagulase positive staphylococcal colonization of humans and their household pets". Can. Vet. 50 (9): 954–958. PMC 2726022.
- ^ Burton S, Reid-Smith R, McClure JT, Weese JS (2008). "Staphylococcus aureus colonization in healthy horses in Atlantic Canada". Can. Vet. J. 49 (8): 797–799. PMC 2465786. PMID 18978975.
- ^ "Staphylococcosis, Staphylococcal Arthritis, Bumble Foot", The Poultry Site, http://www.thepoultrysite.com/diseaseinfo/143/staphylococcosis-staphylococcal-arthritis-bumble-foot, Retrieved 2013-10-22
- ^ Cenci-Goga BT, Karama M, Rossitto PV, Morgante RA, Cullor JS (September 2003). "Enterotoxin production by Staphylococcus aureus isolated from mastitic cows". Journal of food protection 66 (9): 1693–6. PMID 14503727.
- ^ Medical Laboratory Manual For Tropical Countries vol two
- ^ Dinges et al. (January 2000) "Exotoxins of Staphylococcus aureus", Clin Microbiol Rev.; 13(1): 16–34.
- ^ Jarraud et al. (October 4, 2000) "egc, A Highly Prevalent Operon of Enterotoxin Gene, Forms a Putative Nursery of Superantigens in Staphylococcus aureus", J. of Immunology, Bethesda MD
- ^ a b Becker et al. (April 2003) "Prevalence of Genes Encoding Pyrogenic Toxin Superantigens and Exfoliative Toxins among Strains of Staphylococcus aureus Isolated from Blood and Nasal Specimens", J Clin Microbiol.; 41(4): 1434–1439.
- ^ Lina et al. (June 9, 1999) "Involvement of Panton-Valentine Leukocidin—Producing Staphylococcus aureus in Primary Skin Infections and Pneumonia", Clinical Infectious Diseases Volume 29, Issue 5 Pp. 1128-1132
- ^ Gillet et al. (March 2, 2002) "Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients", The Lancet Vol. 359 pp. 753–59
- ^ Schneewind O, Fowler A, Faull KF (April 1995). "Structure of the cell wall anchor of surface proteins in Staphylococcus aureus". Science 268 (5207): 103–6. doi:10.1126/science.7701329. PMID 7701329.
- ^ Patel AH, Nowlan P, Weavers ED, Foster T (December 1987). "Virulence of protein A-deficient and alpha-toxin-deficient mutants of Staphylococcus aureus isolated by allele replacement". Infect. Immun. 55 (12): 3103–10. PMC 260034. PMID 3679545.
- ^ Zhu J, Lu C, Standland M et al. (February 2008). "Single mutation on the surface of Staphylococcus aureus Sortase A can disrupt its dimerization". Biochemistry 47 (6): 1667–74. doi:10.1021/bi7014597. PMID 18193895.
- ^ a b Clauditz A, Resch A, Wieland KP, Peschel A, Götz F (August 2006). "Staphyloxanthin plays a role in the fitness of Staphylococcus aureus and its ability to cope with oxidative stress". Infection and immunity 74 (8): 4950–3. doi:10.1128/IAI.00204-06. PMC 1539600. PMID 16861688.
- ^ a b Liu GY, Essex A, Buchanan JT, Datta V, Hoffman HM, Bastian JF, Fierer J, Nizet V (2005). "Staphylococcus aureus golden pigment impairs neutrophil killing and promotes virulence through its antioxidant activity". J Exp Med 202 (2): 209–15. doi:10.1084/jem.20050846. PMC 2213009. PMID 16009720.
- ^ Liu CI, Liu GY, Song Y, Yin F, Hensler ME, Jeng WY, Nizet V, Wang AH, Oldfield E (2008). "A cholesterol biosynthesis inhibitor blocks Staphylococcus aureus virulence". Science 319 (5868): 391–94. doi:10.1126/science.1153018. PMC 2747771. PMID 18276850.
- ^ Francois P and Schrenzel J (2008). "Rapid Diagnosis and Typing of Staphylococcus aureus". Staphylococcus: Molecular Genetics. Caister Academic Press. ISBN 978-1-904455-29-5.
- ^ Mackay IM, ed. (2007). Real-Time PCR in Microbiology: From Diagnosis to Characterization. Caister Academic Press. ISBN 978-1-904455-18-9.
- ^ Korzeniowski O, Sande MA (1982). "Combination antimicrobial therapy for Staphylococcus aureus endocarditis in patients addicted to parenteral drugs and in nonaddicts: a prospective study". Ann Intern Med 97 (4): 496–503. doi:10.7326/0003-4819-97-4-496. PMID 6751182.
- ^ Bayer AS, Bolger AF, Taubert KA et al. (1998). "Diagnosis and management of infective endocarditis and its complications". Circulation 98 (25): 2936–48. doi:10.1161/01.CIR.98.25.2936. PMID 9860802.
- ^ Cosgrove SE, Vigliani GA, Campion M et al. (2009). "Initial low‐dose gentamicin for Staphylococcus aureus bacteremia and endocarditis is nephrotoxic". Clin Infect Dis 48 (6): 713–721. doi:10.1086/597031. PMID 19207079.
- ^ Chambers HF (2001). "The changing epidemiology of Staphylococcus aureus?". Emerg Infect Dis 7 (2): 178–82. doi:10.3201/eid0702.010204. PMC 2631711. PMID 11294701.
- ^ "US Meat and Poultry Is Widely Contaminated With Drug-Resistant Staph Bacteria". ScienceDaily. 15 April 2011.
- ^ "Phage Therapy May Control Staph Infections In Humans Including MRSA". Sciencedaily. 22 August 2007. Retrieved 18 September 2009.
- ^ Carter AP, Clemons WM, Brodersen DE, Morgan-Warren RJ, Wimberly BT, Ramakrishnan V (September 2000). "Functional insights from the structure of the 30S ribosomal subunit and its interactions with antibiotics". Nature 407 (6802): 340–8. doi:10.1038/35030019. PMID 11014183.
- ^ Sakon J, Liao HH, Kanikula AM, Benning MM, Rayment I, Holden HM (November 1993). "Molecular structure of kanamycin nucleotidyltransferase determined to 3.0-A resolution". Biochemistry 32 (45): 11977–84. doi:10.1021/bi00096a006. PMID 8218273.
- ^ Jevons MP (1961). "Celbenin-resistant staphylococci". BMJ 1 (5219): 124–5. doi:10.1136/bmj.1.5219.124-a.
- ^ Johnson AP, Aucken HM, Cavendish S, Ganner M, Wale MC, Warner M, Livermore DM, Cookson BD (2001). "Dominance of EMRSA-15 and -16 among MRSA causing nosocomial bacteraemia in the UK: analysis of isolates from the European Antimicrobial Resistance Surveillance System (EARSS)". J Antimicrob Chemother 48 (1): 143–4. doi:10.1093/jac/48.1.143. PMID 11418528.
- ^ [verification needed]Blot SI, Vandewoude KH, Hoste EA, Colardyn FA (2002). "Outcome and attributable mortality in critically Ill patients with bacteremia involving methicillin-susceptible and methicillin-resistant Staphylococcus aureus". Arch Intern Med 162 (19): 22293–5. doi:10.1001/archinte.162.19.2229. PMID 12390067.
- ^ Hiramatsu K, Hanaki H, Ino T, Yabuta K, Oguri T, Tenover FC (1997). "Methicillin-resistant Staphylococcus aureus clinical strain with reduced vancomycin susceptibility". J Antimicrob Chemother 40 (1): 135–6. doi:10.1093/jac/40.1.135. PMID 9249217.
- ^ Chang S, Sievert DM, Hageman JC, Boulton ML, Tenover FC, Downes FP, Shah S, Rudrik JT, Pupp GR, Brown WJ, Cardo D, Fridkin SK (2003). "Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene". N Engl J Med 348 (14): 1342–7. doi:10.1056/NEJMoa025025. PMID 12672861.
- ^ Menichetti F (2005). "Current and emerging serious Gram-positive infections". Clin Microbiol Infect 11 (Suppl 3): 22–8. doi:10.1111/j.1469-0691.2005.01138.x. PMID 15811021.
- ^ Quinn, G. A.; Cole, A. M (September 2007). "Suppression of innate immunity by a nasal carriage strain of Staphylococcus aureus increases its colonization on nasal epithelium". Immunology 122 (1): 80–9. doi:10.1111/j.1365-2567.2007.02615.x. PMC 2265977. PMID 17472720.
- ^ Sing A, Tuschak C, Hoermansdorfer S (March 2008). "Methicillin-Resistant Staphylococcus aureus in a Family and Its Pet Cat". N Engl J Med 358 (11): 1200–1. doi:10.1056/NEJMc0706805. PMID 18337614.
- ^ Neely AN, Maley MP (February 2000). "Survival of enterococci and staphylococci on hospital fabrics and plastic". J. Clin. Microbiol. 38 (2): 724–6. PMC 86187. PMID 10655374.
- ^ Cook H, Furuya E, Larson E, Vasquez G, Lowy F (2007). "Heterosexual transmission of community-associated methicillin-resistant Staphylococcus aureus". Clin Infect Dis 44 (3): 410–3. doi:10.1086/510681. PMID 17205449.
- ^ Shafiei Y, Razavilar V, Javadi A (2011). "Thermal Death Time of Staphylococcus Aureus (PTCC=29213) and Staphylococcus Epidermidis (PTCC=1435) in Distilled Water" (PDF). Australian Journal of Basic and Applied Sciences 5 (11): 1551–4.
- ^ Iwase, Tadayuki; Uehara, Yoshio; Shinji, Hitomi; Tajima, Akiko; Seo, Hiromi; Takada, Koji; Agata, Toshihiko; Mizunoe, Yoshimitsu (20 May 2010). "Staphylococcus epidermidis Esp inhibits Staphylococcus aureus biofilm formation and nasal colonization". Nature 465 (7296): 346–9. doi:10.1038/nature09074. PMID 20485435.
External links
- StopMRSANow.org — Discusses how to prevent the spread of MRSA
- TheMRSA.com — Understand what the MRSA infection is all about.
- Firmicutes (low-G+C) Infectious diseases
- Bacterial diseases: G+
- primarily A00–A79, 001–041, 080–109
|
|
| Bacilli |
Lactobacillales
(Cat-) |
| Streptococcus |
| α |
| optochin susceptible: |
|
|
| optochin resistant: |
- S. viridans: S. mitis
- S. mutans
- S. oralis
- S. sanguinis
- S. sobrinus
- milleri group
|
|
|
| β |
| A: |
- bacitracin susceptible: S. pyogenes
- Erysipelas
- Rheumatic fever
- Streptococcal pharyngitis
|
|
| B: |
- bacitracin resistant, CAMP test+: S. agalactiae
|
|
| ungrouped: |
- Streptococcus iniae
- Cutaneous Streptococcus iniae infection
|
|
|
| γ |
- D
- BEA+: Streptococcus bovis
|
|
|
| Enterococcus |
- BEA+: Enterococcus faecalis
- Enterococcus faecium
|
|
|
Bacillales
(Cat+) |
| Staphylococcus |
| Cg+: |
- S. aureus
- Staphylococcal scalded skin syndrome
- Toxic shock syndrome
- MRSA
|
|
| Cg-: |
- novobiocin susceptible
- novobiocin resistant
|
|
|
| Bacillus |
- Bacillus anthracis
- Bacillus cereus
|
|
| Listeria |
|
|
|
|
| Clostridia |
| Clostridium (spore-forming) |
| motile: |
- Clostridium difficile
- Clostridium botulinum
- Clostridium tetani
|
|
| nonmotile: |
- Clostridium perfringens
- Clostridial necrotizing enteritis
|
|
|
| Peptostreptococcus (non-spore forming) |
- Peptostreptococcus magnus
|
|
|
| Mollicutes |
| Mycoplasmataceae |
- Ureaplasma urealyticum
- Mycoplasma genitalium
- Mycoplasma pneumoniae
|
|
| Anaeroplasmatales |
- Erysipelothrix rhusiopathiae
|
|
|
|
|
|
gr+f/gr+a (t)/gr-p (c)/gr-o
|
drug (J1p, w, n, m, vacc)
|
|
|
|
