مخملک اسکالت فیو فرنگان و

مخملک یک بیماری است عفونی و مسری که در دوره کودکی (بین ۳ تا ۷ سالگی) (سن کودکستانی) و در فصول سرما بیشتر دیده می‌شود.عامل این بیماری استرپتوکوک بتا همولیتیک A می‌باشد.[۱]


تصویر باکتری استرپتوکوک
باکتری استرپتوکوک در گلوی فرد تجمع و تکثیر می‌یابد و با ترشح نوعی سم یا اگزوتوکسین موجب پیدایش واکنش پوستی و بروز ضایعاتی روی پوست بدن می‌شود.

محتویات [نهفتن]
۱ روش سرایت
۲ علایم بیماری
۳ تشخیص و درمان
۴ منابع
روش سرایت [ویرایش]

انتقال بیمارِی بین کودکان دارای تماس نزدیک رخ می‌دهد .عامل بیماری بیشتر از طریق تنفس هوای آلوده و همچنین استفاده از وسایل مشترک آلوده مانند اسباب بازی و ظروف غذا انتقال می‌یابد. بیماری از یک روز قبل از بروز علایم بالینی تا پایان بیماری قابل انتقال است ولی هر قدر از شروع بیماری بگذرد خطر سرایت آن کاهش می‌یابد. در صورت عدم درمان در ۴ هفته اول بیماری قابل سرایت می‌باشد ولی با درمان مناسب، بیماری در عرض دو روز بهبود و سرایت آن متوقف می‌گردد. ابتلا به مخملک ایمنی نسبی ایجاد می‌کند.
علایم بیماری [ویرایش]

مخملک

آی‌سی‌دی-۱۰ A38
آی‌سی‌دی-۹ 034.1
دادگان بیماری‌ها 29032
مدلاین پلاس 000974
ای‌مدیسین derm/383 emerg/402, emerg/518
سمپ D012541
علایم مخملک معمولا با سوزش و درد گلو، تب ۳۸ درجه سانتیگراد یا بالاتر شروع می‌شود.
در ابتدای بیماری، روی زبان کودک بیمار پوشش سفید یا زرد کم رنگ پیدا می‌شود که مدتی بعد ممکن است به رنگ قرمز درآید. برجستگی‌ها و پرزهای زبان ممکن است بزرگتر از حالت طبیعی شوند که در این حالت زبان به شکل توت فرنگی در می‌آید و این علامت مهم در مخملک به "زبان توت فرنگی" موسوم است.[۲] لوزه‌های کودک نیز ممکن است باردار شده و قرمز و متورم به نظر برسد. صورت بیمار قرمز و برافروخته می‌شود در حالیکه اطراف دهان او بیرنگ و سفید است. سایر علائم عمومی در این بیماری لرز، درد، کاهش اشتها، متورم شدن غدد لنفاوی، بیقراری و ناخوشی، تهوع و استفراغ می‌باشد.
ضایعات پوستی معمولا روز دوم بیماری ظاهر می‌شود و حدود ۲ تا ۵ روز طول می‌کشد تا از بین برود. بثورات به شکل لکه‌های کوچک برجسته (راش) است که از ناحیه زیر بغل، گردن، پشت گوش و سینه شروع می‌شود و سپس سر تا سر بدن را فرا می‌گیرد. معمولا خارش دار است. گاهی این بثورات یا راش‌ها در ساعد، قسمت داخلی آرنج و کشاله ران به شکل خطوط در می‌آیند که به آن Pastia lines می‌گویند. در هفته دوم بیماری همراه با ناپدید شدن بثورات، پوست کودک بخصوص در ناحیه دست‌ها، پاها و کشاله ران شروع به پوسته ریزی می‌کند.( مرحله پوسته ریزی)[۳] ابتلا به مخملک در کودکان شیرخوار نادر است . در صورت عدم درمان عوارض کلیوی، گوشی، چرکی و قلبی محتمل است. اشکال خفیف مخملک گاهی باعث اشتباه در تشخیص می‌شود، البته در این حالت خطر سرایت آن زیادتر است زیرا بیمار درمان نمی‌شود. بثورات پوستی مخملک به خودی خود مسری و واگیردار نیستند اما استرپتوکوک موجود در حلق می‌تواند انتشار یابد و به فرد دیگری منتقل شود.
۲۴ ساعت بعد از دریافت اولین دوزآنتی بیوتیک بیماری دیگر مسری نیست.
اگر سایر اعضای خانواده دچار سوزش گلو شدند باید از نظر ابتلا به مخملک معاینه شوند حتی اگر ضایعات پوستی نداشته باشند.
تشخیص و درمان [ویرایش]



جوش خشک دانه ای در مخملک.
تشخیص بیماری مخملک کلینیکی است ولی از نظر آزمایشگاهی لکوسیتوز، افزایش ESR، افزایش تیتر آنتی استرپتولیزین A دیده می‌شود. همچنین می‌توان از حلق بیمار نمونه گیری شده و برای کشت فرستاده شود. برای نمونه گیری از سواپ (یک چوب مخصوص و نازک که سر آن مقداری پنبه قرار داده شده) استفاده می‌شود. در صورت درمان، بهبودی سریع خواهد بود، اگر چه راش‌ها ممکن است برای چندین روز باقی بماند. چندین هفته نیز ممکن است طول بکشد تا تورم لوزه‌ها و غدد لنفاوی به شکل عادی برگردد. درمان با آنتی بیوتیکها از جمله پنی سیلین می‌باشد. در موارد حساسیت به پنی سیلین می‌توان از اریترومایسین استفاده کرد.
اگر هر نوع عفونت استرپتوکوکی بدون درمان بماند، ممکن است موجب عوارض جدی مانند آبسه لوزه‌ها، تب روماتیسمی [۴] و مشکلات قلبی، کلیوی [۵]، پوستی [۶] شود که از عوارض دیررس مخملک بدون درمان است.[۷]
منابع [ویرایش]

↑ Group A Streptococcal Infections
↑ Bright red tongue with a "strawberry" appearance
↑ desquamation
↑ Rheumatic fever
↑ Glomerulonephritis
↑ Erythema nodosum
↑ Prevention of Perinatal Group B Streptococcal Disease

رده‌ها: بیماری‌های عفونیبیماری‌های واگیردارپزشکی کودکان

قس عربی

الحمى القرمزیة هو مرض یسببه ذیفان خارجی صادر عن العقدیة المقیحة [1]. ویستخدم مصطلح Scarlatina أحیانا بدلا من الحمى القرمزیة، على الرغم من أنه یستخدم عادة للإشارة إلى شکل أقل حدة من الحمى القرمزیة التی بدات فی الظهور منذ بدایة القرن العشرین. [1]
تتمیز الحمى القرمزیة بما یلى :
احتقان فی الحلق
الحمى
لسان أحمر یغلب علیه مظهر الفراولة
طفح ممیز، والذی:
احمر، خشن بعض الشئ ؛ یتحول للون الأبیض عند الضغط
یظهر بعد 12-48 ساعات من الحمى
یبدأ عادة على صدره، والآباط، وخلف الأذنین.
قطع الغیار وجهه (على الرغم من بعض شحوب حول الفم هو سمة).
هو أسوأ فی الجلد أضعاف س. هذه خطوط باستیا (حیث طفح یعمل معا فی الإبطین والأربیة) تظهر ویمکن أن یستمر بعد أن ینتهی الطفح.
قد تنتشر لتغطی اللهاة.
ویبدأ الطفح یتلاشى بعد ثلاثة إلى أربعة أیام بعد الظهور والتقشر (تقشیر) یبدأ. "وهذه المرحلة تبدأ مع قلیل من تقشیر الوجه. تقشیر حول الأصابع یحدث بعد حوالی اسبوع فی وقت لاحق. [3] کما یحدث التقشیر فی الإبطین ،و الفخذ، وبعض من أصابع الیدین والقدمین. [5]
تشخیص الحمى القرمزیة یجب أن یکون طبیا. حیث یظهر فحص الدم زیادة ملحوظة فی عدد الکریات البیضاء مع العدلات أو زیادة الحمضات، وارتفاع سرعة الترسب (اس ار) وبروتین جیم التفاعلی (سی آر بی)، وارتفاع antistreptolysin. ثقافة الدم إیجابیة، ولکن عادة ما یمکن العقدیات ان تظهر فی الحلق. مضاعفات الحمى القرمزیة تشمل مضاعفات التفسخ بسبب انتشار العقدیات فی الدم ومضاعفات توسطت فی مأمن بسبب استجابة مناعة شاذة. مضاعفات التفسخ، نادرة الیوم، وتشمل الأذن والتهاب الجیوب الأنفیة، التهاب العقدیات الرئوی، thoracis empyema والتهاب السحایا وکاملة الإنتان ،وهذا الذی یمکن ان یسمى الحمى القرمزیة الخبیثة.
المضاعفات المناعیة تشمل التهاب کبیبات الکلى الحاد، والحمى الروماتزمیة ، وحمامی عقدیة. scarlatinous الثانویة للمرض، أو الثانویة الخبیثة المکتسبة من الحمى القرمزیة، تشمل تجدید الحمى، والذبحة الصدریة متجددة ،تقرح الأذن، والأنف ،ومضاعفات فی الحلق والتهاب فی الکلى أو الحمى الروماتزمیة، وتظهر هذه فی حوالى الیوم الثامن عشر للحمى القرمزیة التی لم تعالج.


الحمى القرمزیة ومفروشة بالحصى، والطفح الجلدی الجاف.
محتویات [أخف]
1 أعراض المرض
2 العلاج
3 التاریخ
4 المراجع
[عدل]أعراض المرض

الطفح الجلدی هو العلامة الأکثر لفتا للالحمى القرمزیة. وعادة ما یبدأ یبحث مثل حروق شمس بالغة مع بثور صغیرة، وقد تسبب حکة. الطفح عادة ما یظهر أولا على العنق والوجه، وترک کثیر من الأحیان واضحة تتأثر منطقة حول الفم. وینتشر فی الصدر والظهر، ثم إلى بقیة أجزاء الجسم. فی ثنیات الجسم، وخصوصا حول تحت الإبطین والمرفقین، والطفح الجلدی یشکل شرائط حمراء (و على الجلد الغامق جدا، قد یبدو أکثر قتامة من الشرائط على بقیة الجلد). تتحول مناطق الطفح عادة ما تکون بیضاء (أو اشحب براون، وذوی البشرة الداکنة) عند الضغط على. عادة ما یتلاشى الطفح الجلدی فی الیوم السادس للعدوى، ولکن الجلد المصاب قد یبدأ فی التقشیر.
هناک جانبا أعراض أخرى التی تساعد على تأکید تشخیص الحمى القرمزیة، بما فی ذلک احمرار والتهاب الحلق، والحمى، وتورم الغدد فی الرقبة. یمکن أیضا أن تحدث الحمى القرمزیة مع حمى منخفضة. قد تکون اللوزتین ومؤخرة الحلق مغطاة بطبقة بیضاء، أو تبدو حمراء، منتفخة، وتتخللها بقع بیضاء أو صفراء من صدید. فی وقت مبکر من العدوى، قد یکون اللسان مغطى بطبقة بیضاء أو صفراء. ألف شخص مع الحمى القرمزیة أیضا قد یعانى من القشعریرة وآلام الجسم، والغثیان، والتقیؤ، وفقدان الشهیة.
عندما تحدثالحمى القرمزیة بسبب عدوى فی الحلق ،فانها عادة ما تتوقف فی غضون 3 إلى 5 أیام، والتهاب الحلق ینتهى بعد ذلک بقلیل. الطفح الجلدی للحمى القرمزیة عادة ما یختفی فی الیوم السادس بعد أن بدأت اعراض الالتهاب فی الحلق، ولکن الجلد التی کانت تغطیها الطفح قد تبدأ بالتقشر. هذا التقشیر قد تستمر مدة 10 أیام. وعادة ما تشفى العدوى من نفسها بعد 10 ایام من جرعات المضادات الحیویة، ولکن الامر قد یستغرق بضعة اسابیع لاللوزتین، وتورم الغدد فی العودة إلى وضعها الطبیعی.
فی حالات نادرة، قد تتطورالحمى القرمزیة من عدوى عقدیات جلدالى القوباء. فی هذه الحالات، یجوز للشخص أن لا تحصل على التهاب الحلق.
[عدل]العلاج

بخلاف حدوث الإسهال، والعلاج بالطبع من الحمى القرمزیة لا یختلف عن تلک التی فی أی من بکتیریا الحلق. فی حالة الحساسیة للبنسلین، یمکن استخدام کلیندامایسین أو الاریثرومیسین بنجاح. المرضى الذین لم یعد من الممکن المعدیة بعد أخذ المضادات الحیویة لمدة 24 ساعة. الأشخاص الذین تعرضوا لالحمى القرمزیة ینبغی أن یراقبوا عن کثب على مدى اسبوع کامل للأعراض، وخاصة الذین تتراوح أعمارهم بین 3 إلى الشباب البالغین. من المهم جدا أن یتم اختبار (الحلق) وإذا کان مصاب، یجب السعى إلى العلاج.
[عدل]التاریخ

الزوجان غلادیس هنری دیک وجورج فریدریک دیک طورا لقاحا فی 1920s الذی تفوق علیه فی وقت لاحق البنسلین فی 1940s.
[عدل]المراجع

^ فقط lysogenized العقدیات إنتاج السم مولد الکریات الحمر (ذیفان خارجی مولد للحمى) والذی یسبب طفح جلدی من الحمى القرمزیة
قالب:Exanthema قالب:Gram-positive bacterial diseases
تصنیفات: طب أطفالإصابات جلدیة بکتیریةالأمراض البکتیریةالطفولة Exanthems

قس ترکی استانبولی

Kızıl özellikle 3-7 yaş aralığında ki çocuklarda görülen bakteriyel bir enfeksiyon hastalığıdır. Adını genelde hastanın vücudunda, özellikle dil, yüz, koltuk altları ve kasık bölgesinde kırmızı lekeler oluşturmasından alır. Ancak bu lekelerin hiç oluşmadığı enfeksiyonlar da görülür. Yetişkin yaşlarda da hastalığa yakalanmak mümkündür.
[değiştir]Sebebi

Etkeni A grubu streptokoklardır (Streptococcus pyogenes). Toksin oluşturacak bakteriyofaja sahip olmaları halinde hastalık ortaya çıkar. Bunların farklı serotipleri olması nedeniyle insanlar birden fazla kere bu bulaşıcı hastalığa yakalanabilirler. Kızıl, damlacık enfeksiyonu ile ya da has­talıklı kişinin salgılarıyla doğrudan temas yoluyla bulaşır. Soyulan deri, hastanın vücut salgılarını taşımadığı sürece, zararsızdır.
[değiştir]Belirtiler

Ateş (38 °C ila 40 °C)
Halsizlik
Boğazda ağrı
Yutkunmada zorluk
Kızarıklıklar, normalden kırmızı yüz
Karın ağrısı
Bulantı ve kusma
Dilin çilek gibi kızarması ve dilin üstünde beyazlık olusması
Boyun tutulması
[değiştir]Tespit ve tedavisi

Bu hastalığın tespit ve tedavisinin bir doktor tarafından yapılması gerekir. Antibiyotiklerle tedavisi çoğunlukla mümkündür. Tedavi edilmemesi yüksek riskli sonuçlar doğurabilir ve başka hastalıklara sebebiyet verebilir.
Çevresinde kızıla yakalanmış hastalar bulunan kişilerin de bir doktora görünerek taşıyıcı olmadıklarını tespit etmeleri hastalığın yayılmasını önler.

Hastalık ile ilgili bu madde bir taslaktır. Madde içeriğini genişleterek Vikipedi'ye katkıda bulunabilirsiniz.
Kategoriler: Hastalık taslaklarıÇocuk hastalıkları

قس انگلیسی

Scarlet fever (also called scarlatina in older literature)[1] is an infectious disease which most commonly affects 4-8 year old children. Symptoms include sore throat, fever and a characteristic red rash. Scarlet fever is usually spread by inhalation. There is no vaccine, but the disease is effectively treated with antibiotics. Most of the clinical features are caused by erythrogenic toxin, a substance produced by the bacterium Streptococcus pyogenes (group A strep.) when infected by a certain bacteriophage.
Before the availability of antibiotics, scarlet fever was a major cause of death. It could also cause late complications such as glomerulonephritis and endocarditis leading to heart valve disease, all of which were protracted and often fatal afflictions at the time.
It is important to recognize that strains of Group A Strep which produce the erythrogenic toxin are not inherently more dangerous than other strains which do not but are more easily diagnosed as such because of the characteristic rash.
Contents [hide]
1 Epidemiology
2 Microbiology
3 Clinical
3.1 Rash
3.2 Other features
4 Diagnosis
5 Differential diagnosis
6 Course
7 Treatment
7.1 Antibiotic resistance
7.2 Vaccines
8 Complications
9 History
9.1 Dick Test and vaccine
10 In fiction
10.1 Opera
10.2 Literature
10.3 Film
11 Persons who suffered from scarlet fever
12 See also
13 References
14 Further reading
15 External links
[edit]Epidemiology

This disease is most common in 4–8 year olds with males and females being equally affected.[2] By the age of 10 years most children have acquired protective antibodies and scarlet fever at this age or older is rare.[3][dubious – discuss]
It is usually spread by the aerosol route (inhalation) but may also be spread by skin contact or by fomites. Although not normally considered a food borne illness an outbreak due to chicken meat has been reported in China.[4]
Asymptomatic carriage may occur in 15–20% of school-age children.
The incubation period is 1–4 days.
[edit]Microbiology

The disease itself is caused by secretion of pyrogenic exotoxins by the infecting Streptococcus.[5][6] Exotoxin A (speA) is probably the best studied of these toxins. It is carried by the bacteriophage T12 which integrates into the Streptococcal genome from where the toxin is transcribed. The phage itself integrates into a serine tRNA gene on the chromosome.[7]
The T12 virus itself has not been placed into a taxon by the International Committee on Taxonomy of Viruses. It has a double stranded DNA genome and on morphological grounds appears to be a member of the Siphoviridae.
The speA gene was cloned and sequenced in 1986.[8] It is 753 base pairs in length and encodes a 29.244 kiloDalton (kDa) protein. The protein contains a putative 30 amino acid signal peptide: removal of the signal sequence gives a predicted molecular weight of 25.787 (kDa) for the secreted protein. Both a promoter and a ribosome binding site (Shine-Dalgarno sequence) are present upstream of the gene. A transcriptional terminator is located 69 bases downstream from the translational termination codon. The carboxy terminal portion of the protein exhibits extensive homology with the carboxy terminus of Staphylococcus aureus enterotoxins B and C1.
Streptococcal phages other than T12 may also carry the speA gene.[9]
[edit]Clinical

Scarlet fever is characterized by:
Sore throat
Fever
Bright red tongue with a "strawberry" appearance
Forchheimer spots (fleeting small, red spots on the soft palate) may occur
Characteristic rash:
the rash is fine, red and rough-textured
blanches upon pressure
appears 12–72 hours after the fever
generally starts on the chest, armpits and behind the ears. It may also involve the groin.
the face often shows red cheeks and a characteristic pale area around the mouth (circumoral pallor)
is worse in the skin folds. These Pastia lines (where the rash runs together in the armpits and groin) appear and can persist after the rash is gone.
may spread to cover the uvula
begins to fade three to four days after onset and desquamation (peeling) begins. "This phase begins with flakes peeling from the face. Peeling from the palms and around the fingers occurs about a week later." Peeling also occurs in axilla, groin and tips of the fingers and toes.[1]
[edit]Rash
The rash is the most striking sign of scarlet fever. It usually begins looking like a bad sunburn with tiny bumps and may itch. The rash usually appears first on the neck and face, often leaving a clear unaffected area around the mouth. It then spreads to the chest and back and finally to the rest of the body. In the body creases, especially around the axillae (underarms) and elbows, the rash forms the classic red streaks known as Pastia lines. On very dark skin, the streaks may appear darker than the rest of the skin. Areas of rash usually turn white (or paler brown, with dark complected skin) when pressed on. By the sixth day of the infection, the rash usually fades, but the affected skin may begin to peel.
[edit]Other features
Usually there are other symptoms that help to confirm a diagnosis of scarlet fever, including a reddened sore throat, a fever at or above 101 °F (38.3 °C), and swollen glands in the neck. Scarlet fever can also occur with a low fever. The tonsils and back of the throat may be covered with a whitish coating, or appear red, swollen, and dotted with whitish or yellowish specks of pus. Early in the infection, the tongue may have a whitish or yellowish coating. Also, an infected person may have chills, body aches, nausea, vomiting, and loss of appetite.
In rare cases, scarlet fever may develop from a streptococcal skin infection like impetigo. In these cases, the person may not get a sore throat.
[edit]Diagnosis

Diagnosis of scarlet fever is clinical. The blood test shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) (both indications of inflammation), and elevation of antistreptolysin O titer. Blood culture is rarely positive but the streptococci can usually be demonstrated in throat culture.
[edit]Differential diagnosis

Cases need to be differentiated from Far East scarlet-like fever, an infectious disease first reported in the 1950s from Russia. Because its similar clinical presentation to scarlet fever it was initially thought to be caused by a Streptococcus. It is now known to be caused by a Gram negative bacillus - Yersinia pseudotuberculosis.
[edit]Course

When scarlet fever occurs because of a throat infection, the fever typically stops within 3 to 5 days, and the sore throat passes soon afterward. The scarlet fever rash usually fades on the sixth day after sore throat symptoms started, and begins to peel (as above). The infection itself is usually cured with a 10-day course of antibiotics, but it may take a few weeks for tonsils and swollen glands to return to normal.
[edit]Treatment

Other than the occurrence of the diarrhea, the treatment and course of scarlet fever are no different from those of any strep throat. In case of penicillin allergy, clindamycin or erythromycin can be used with success. Patients should no longer be infectious after taking antibiotics for 24 hours. People who have been exposed to scarlet fever should be watched carefully for a full week for symptoms, especially if aged 3 to young adult. It is very important to be tested (throat culture) and if positive, seek treatment.
[edit]Antibiotic resistance
A drug-resistant strain of scarlet fever, resistant to macrolide antibiotics such as erythromycin, but retaining drug-sensitivity to beta-lactam antibiotics such as penicillin, has emerged in Hong Kong in 2011, accounting for at least two deaths in that city - the first such in over a decade.[10] About 60% of circulating strains of the Group A Streptococcus that cause scarlet fever in Hong Kong are resistant to macrolide antibiotics, says Professor Kwok-yung Yuen, head of Hong Kong University's microbiology department. Previously, observed resistance rates had been 10-30%; the increase is likely the result of overuse of macrolide antibiotics in recent years.
[edit]Vaccines
No vaccines are currently available to protect against S. pyogenes infection, the vaccine developed by George and Gladys Dick in 1924 was discontinued due to poor efficacy and the introduction of antibiotics. Difficulties in vaccine development include the considerable strain variety of S. pyogenes present in the environment and the amount of time and number of people needed for appropriate trials for safety and efficacy of any potential vaccine.[11]
[edit]Complications

The complications of scarlet fever include septic complications due to spread of streptococcus in blood and immune-mediated complications due to an aberrant immune response. Septic complications—today rare—include ear and sinus infection, streptococcal pneumonia, empyema thoracis, meningitis and full-blown sepsis, upon which the condition may be called malignant scarlet fever.
Immune complications include acute glomerulonephritis, rheumatic fever and erythema nodosum. The secondary scarlatinous disease, or secondary malignant syndrome of scarlet fever, includes renewed fever, renewed angina, septic ear, nose, and throat complications and kidney infection or rheumatic fever and is seen around the eighteenth day of untreated scarlet fever.
An association between scarlet fever and hepatitis has been recognized for several decades.[12] The mechanism of causation is not known.
[edit]History

The first description of this disease is uncertain.[13] It is possible that Hippocrates in c. 400 BC described this in a case with a sore throat and skin ulcers, but the diagnosis is not entirely clear from the description. In the 10th/11th century, the physicians Rhazes, Ali Abbas and Avicenna described a measles-like illness that had a more vivid colour and was more dangerous. Again it is not certain that these descriptions refer to scarlet fever.
The disease appears to have been first described in the medical literature in the 1553 book De Tumoribus praeter Naturam by the Sicilian anatomist and physician Giovanni Filippo Ingrassia, where he referred to it as rossalia or rosania. It was redescribed by Johann Weyer during an epidemic in lower Germany between 1564 and 1565 who referred to it as scalatina anginosa. The first unequivocal description of scarlet fever was published by Jean Cottyar of Poieters in his book De febre purpura epidemiale et contagiosa libri duo published in 1578 in Paris. Daniel Sennert of Wittenberg described the classical 'scarlatinal desquamation' in 1572 and was also the first to describe the early arthritis, scarlatinal dropsy and ascites associated with the disease.
Bright in 1827 first recognised the involvement of the renal system in scarlet fever.
The association of streptococci and disease was first described in 1874 by Billroth in patients with wound infections. Billroth also coined the genus name Streptococcus. The organism was first cultured in 1883 by the German surgeon Friedrich Fehleisen who cultured it from perierysipelas lesions. It received its current name (Streptococcus pyogenes) in 1884 from Rosenbach.
The German physician Friedrich Loeffler was the first in 1884 to show the presence of streptococci in the throats of patients with scarlet fever. Because not all patients with pharyngeal streptococci developed scarlet fever, these findings remained controversial for some time. The association between streptocci and scarlet fever was confirmed by Dochez, George, and Dick in the early 1900s.
Scarlet fever serum from horses was used in the treatment of children beginning in 1900 and reduced mortality rates significantly.
In 1906 the Austrian pediatrician Clemens von Pirquet postulated that disease-causing immune complexes were responsible for the nephritis that followed scarlet fever.[14]
Bacteriophages were discovered in 1915 by Frederick Twort. His work was overlooked and phages were later rediscovered by Felix d'Herelle in 1917. The specific association of scarlet fever with the Group A streptococcus had to await the development of Lancefield's streptococcal grouping scheme in the 1920s. The Dicks showed that cell-free filtrates could induce the erythematous reaction characteristic of scarlet fever, proving that this reaction was due to a toxin. Karelitz and Stempien discovered that extracts from human serum globulin and placental globulin can be used as lightening agents for scarlet fever and this was used later as the basis for the Dick test. The association of scarlet fever and bacteriophages was described in 1926 by Cantucuzene and Boncieu.[15]
The discovery of penicillin and its subsequent widespread use has significantly reduced the mortality of this once feared disease.
The first toxin that causes this disease was cloned and sequenced in 1986 by Weeks and Ferretti.[8]
[edit]Dick Test and vaccine
The Dick Test was invented in 1924 and was used to identify those susceptible to scarlet fever.[16] A broth culture filtrate from an erythrogenic toxin producing group A streptococci was injected intracutaneously into susceptible persons. In those susceptible erythematous and oedematous skin reactions developed by 24 hours after injection. A second injection of antitoxin into the site neutralized the reactions. Non-reactors were considered to have sufficient antibodies to the toxin and thus were not susceptible to scarlet fever. The antitoxin was made by injecting horses with the broth filtrates and later collecting the serum from the horse.
Gladys Henry Dick and George Frederick Dick developed a vaccine in 1924 that was later eclipsed by penicillin in the 1940s. Broth filtrates were used as the basis for the patent the Dicks took out on their vaccine in 1924 in the United Kingdom and in 1925 in the United States.
Neither the vaccine or the Gladys Test are in use currently.
[edit]In fiction

Scarlet fever has been used as a plot device in a variety of fictional settings.
[edit]Opera
In Act II, Scene V of Rossini's opera, The Barber of Seville, Don Basilio is terrified and sent away to bed at a very crucial point in the plot under the false persuasion that he has contracted the dreaded "febbre scarlattina" (despite the fact that he is told he has turned yellow, rather than red).
[edit]Literature
In Mary Shelley's Frankenstein, Catherine Beaufort, Victor Frankenstein's mother, contracts scarlet fever from Elizabeth. The disease results in her death.
Beth, the third sister in Little Women, suffered from the effects of scarlet fever before dying.
Mary Ingalls from the Little House on the Prairie book and TV series lost her sight from the effects of scarlet fever. However, modern doctors believe this to be a misdiagnosis[17].
In the children's book The Velveteen Rabbit, a toy rabbit's owner contracts scarlet fever and all his toys, including the rabbit, are taken to be burned.
Also in another children's book written by Enid Blyton Five Are Together Again, Joan the Kirrin family cook contracts scarlet fever and is taken away in an ambulance just as The Famous Five have arrived at Kirrin Cottage to start their school holiday.
Scarlet fever was a major plot point in American Girl's Kit Kittredge short story Kit Uses Her Head, when Kit, along with her best friends Ruthie Smithens and Stirling Howard, were diagnosed with the disease.
[edit]Film
Gene Wilder's character in See No Evil, Hear No Evil went deaf due to scarlet fever.
In Osmosis Jones, the main antagonist, Thrax, is a Scarlet Fever virus intent on getting himself in the medical records by overheating Frank's body in record time.
In Love's Everlasting Courage, Ellen Davis dies of scarlet fever.
In the movie Anne of Green Gables: The Continuing Story, Gilbert Blythe (Anne's love interest) contracts scarlet fever from the hospital while studying medicine. During this time, Anne promises to marry him, which is said to be what helped him survive.
[edit]Persons who suffered from scarlet fever

Lope de Vega, the famous Spanish writer and poet died because of scarlet fever in 1635.
Caroline Matilda of Wales (1751-1775), titular queen of Denmark, died from the disease at the age of 23.
Johann Strauss I, composer of waltzes and other light classics, died in Vienna in 1849 from scarlet fever contracted from one of his illegitimate children.[18]
Myron Florin, the accordionist on The Lawrence Welk Show had scarlet fever as a child. His accordion playing saved his life, as the exertion strengthened his heart back to pre-fever performance.
Maria Franziska von Trapp, the second daughter of Captain Georg von Trapp, suffered from scarlet fever and infected her mother Agathe Whitehead, who died from the disease. Maria von Trapp then entered the family, giving rise to the story behind The Sound of Music.
Liu Tianhua (1895–1932), a Chinese musicologist died of scarlet fever in 1932 in Beijing.
August Lösch (1906–1945), German economist died of scarlet fever just after World War II ended
Hazel Hall (1888-1924), a poet based out of Portland. She created many beautiful bodies of work, including, "Curtains"
[edit]See also

List of cutaneous conditions
[edit]References

^ a b Edward J Zabawski Jr. "Scarlet Fever". MedScape Reference.
^ Czarkowski, M. P.; Kondej, B.; Staszewska, E. (2011). "Scarlet fever in Poland in 2009". Przegl Epidemiol 65 (2): 209–212. PMID 21913461.
^ Czarkowski, M. P.; Kondej, B. (2010). "Scarlet fever in Poland in 2008". Przegl Epidemiol 64 (2): 185–188. PMID 20731219.
^ Yang, S. G.; Dong, H. J.; Li, F. R.; Xie, S. Y.; Cao, H. C.; Xia, S. C.; Yu, Z.; Li, L. J. (2007). "Report and analysis of a scarlet fever outbreak among adults through food-borne transmission in China". J Infect 55 (5): 419–424. doi:10.1016/j.jinf.2007.07.011.
^ Zabriskie, J. B. (1964). "The role of temperate bacteriophage in the production of erythrogenic toxin by Group A Streptococci". J Exp Med 119 (5): 761–780. doi:10.1084/jem.119.5.761. PMC 2137738. PMID 14157029.
^ Krause, R. M. (2002). "A Half-century of Streptococcal Research: Then & Now". Indian J Med Res 115: 215–241. PMID 12440194.
^ McShan, W. M.; Ferretti, J. J. (1997). "Genetic diversity in temperate bacteriophages of Streptococcus pyogenes: identification of a second attachment site for phages carrying the erythrogenic toxin A gene". J Bacteriol 179 (20): 6509–6511. PMC 179571. PMID 9335304.
^ a b Weeks, C. R.; Ferretti, J. J. (1986). "Nucleotide sequence of the type A streptococcal exotoxin (erythrogenic toxin) gene from Streptococcus pyogenes bacteriophage T12". Infect Immun 52 (1): 144–150. PMID 262210.
^ Yu, C. E.; Ferretti, J. J. (1991). "Molecular characterization of new group A streptococcal bacteriophages containing the gene for streptococcal erythrogenic toxin A (speA)". Mol Gen Genet 231 (1): 161–168. doi:10.1007/BF00293833. PMID 1753942.
^ "Second HK child dies of mutated scarlet fever". Associated Press (online). 22 June 2011. Retrieved 23 June 2011.
^ "Initiative for Vaccine Research (IVR) - Group A Streptococcus". World Health Organization. Retrieved 15 June 2012.
^ Elishkewitz, K.; Shapiro, R.; Amir, J.; Nussinovitch, M. (2004). "Hepatitis in scarlet fever". Isr Med Assoc J 6 (9): 569–570. PMID 15373323.
^ Rolleston, J. D. (1928). "The History of Scarlet Fever". BMJ 2 (3542): 926–929. doi:10.1136/bmj.2.3542.926. PMC 2456687. PMID 20774279.
^ Huber, B. (2006). "100 years of allergy: Clemens von Pirquet - his idea of allergy and its immanent concept of disease". Wien. Klin. Wochenschr. 118 (19-20): 573–579. doi:10.1007/s00508-006-0701-3. PMID 17136331.
^ Cantacuzène, J.; Bonciu, O. (1926). "Modifications subies par des streptocoques d'origine non scarlatineuse au contact de produits scarlatineux filtrès". CR Acad Sci Paris 182: 1185–1187.
^ Dick, G. F.; Dick, G. H. (1924). "A skin test for susceptibility to scarlet fever". J Am Med Assoc 82 (4): 265–266. doi:10.1001/jama.1924.02650300011003.
^ Serena Gordon (4 Feb 2013). "Mistaken Infection 'On The Prairie'?". U.S. News and World Report.
^ "Johann Strauss I on Grove Music Online". Grove Music Online. Retrieved 5 October 2008.
[edit]Further reading

Wikimedia Commons has media related to: Scarlet fever
Rolleston JD (November 1928). "The history of scarlet fever". British Medical Journal 2 (3542): 926–9. doi:10.1136/bmj.2.3542.926. PMC 2456687. PMID 20774279.
[edit]External links

Scarlet Fever from PubMed Health
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Infectious skin disease: Viral cutaneous conditions, including viral exanthema (B00–B09, 050–059)
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Firmicutes (low-G+C) Infectious diseases · Bacterial diseases: G+ (primarily A00–A79, 001–041, 080–109)
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Categories: PediatricsBacterium-related cutaneous conditions