Scarlet fever

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Scarlet fever is an exotoxin-mediated disease that occurs most often in association with a sore throat and rarely with impetigo or other streptococcal infections. It is characterized by sore throat, fever, a ‘strawberry’ tongue, and a fine sandpaper rash over the upper body that may spread to cover almost the entire body. Scarlet fever is not rheumatic fever, but may progress into that condition as the infection develops (rheumatic fever is an autoimmune disease that can occur after infection with Group A strep).

Scarlet fever is an infectious disease which most commonly affects 4-8 year old children. Symptoms include sore throat, fever and a characteristic red rash. It is usually spread by inhalation. There is no vaccine, but the disease is effectively treated with antibiotics.

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.

Scarlet fever is caused by erythrogenic toxin, a substance produced by the bacterium Streptococcus pyogenes (group A strep.) when infected by a certain bacteriophage.

The term scarlatina may be used interchangeably with scarlet fever, though it is most often used to indicate the less acute form of scarlet fever seen since the beginning of the twentieth century.^[1]

Scarlet fever usually develops in children, just like colds or the flu are common in children. This disease is most common in 3-15 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]

Diagnosis of scarlet fever is clinical. The blood tests shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high ESR and CRP , and elevation of antistreptolysin O titer. Blood culture is rarely positive, but the streptococci can usually be demonstrated in throat culture.

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. Antibiotic treatment is usually given. It has however never been shown to reduce the chance that rheumatic fever develops.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

This disease was also once known as Scarlatina (from the Italian scarlattina). Many novels depicting life before the 19th century (see Scarlet fever in literature below) describe scarlet fever as an acute disease being followed by many months spent in convalescence. The convalescence was probably due to complications with rheumatic fever. Prior to an understanding of how streptococcus was spread, it was also not uncommon to destroy or burn the personal effects of a person afflicted with scarlet fever to prevent transmission to other people.

The first description of this disease is uncertain.^[1] 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.

The Dick Test was invented in 1924 and was used to identify those susceptible to scarlet fever.^[2] 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 nor the Dick Test are in use currently.

Scarlet fever has been used as a plot device in a variety of fictional settings.

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).

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.

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.

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.

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.

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.^[3]

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.^[4]

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.

Lope de Vega, the famous Spanish writer and poet died because of scarlet fever in 1635.

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.^[5]

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,刘天华（1895-1932, a Chinese musicologist died of scarlet fever in 1932 in Beijing.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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.^[1]

Asymptomatic carriage may occur in 15–20% of school-age children.

The incubation period is 1–4 days.

This illness can be caught from contact with the sick person because this germ is carried in the mouth and nasal fluids. The disease can be spread through contact with droplets shed when an infected person coughs or sneezes. If you touch your mouth, nose, or eyes after touching something that has these fluids on them, you may become ill. Also, if you drink from the same glass or eat from the same plate as the sick person, you could also become ill. The best way to keep from getting sick is to wash your hands often and avoid sharing eating utensils. It is especially important for anyone with a sore throat to wash his or her hands often and not share eating or drinking utensils.

The disease itself is caused by secretion of pyrogenic exotoxins by the infecting Streptococcus.^[2][3] 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.^[4]

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.^[5] 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.^[6]

CDC Scarlet fever

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Streptococcus pyogenes (group A strep) is responsible for scarlet fever. It can also cause simple angina, erysipelas and serious toxin-mediated syndromes like necrotizing fasciitis and the so-called streptococal toxic shock-like syndrome. The virulence of group A strep seems to be increasing lately. The exanthem of scarlatina is thought to be due to erythrogenic toxin production by specific streptococcal strains in a nonimmune patient. Along with erythrogenic toxins, the Group A strep produces several toxins and enzymes. Two of the most important are the streptolysins O and S. Streptolysin O, an hemolytic, thermolabile and immunogenic toxin, is the base of an assay for scarlatina and erysipelas – the anti-streptolysin O titer.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Scarlet fever must be differentiated from other diseases that cause skin rash, fever, fatigue, abdominal pain and punctate red macules on the hard and soft palate and uvula, including chickenpox, herpes zoster, erythema multiforme, among others.

Different rash-like conditions can be confused with scarlet fever and are thus included in its differential diagnosis. The various conditions that should be differentiated from scarlet fever include:^{[1][2][3][4][5][6][7]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Scarlet fever usually develops in children, just like colds or the flu are common in children. This disease is most common in 3-15 year olds with males and females being equally affected.^[1] By the age of 10 years most children have acquired protective antibodies and scarlet fever at this age or older is rare.^[2]

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Although complications may arise if not treated, scarlet fever goes away after a course of antibiotics.

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 otitis, sinusitis, streptococcal pneumonia, empyema thoracis, meningitis and full-blown septicaemia ( malignant scarlet fever).

Immune complications include acute glomerulonephritis, rheumatic fever and erythema nodosum. The secondary scarlatinous disease (or secondary malignant syndrome of scarlet fever) included renewed fever, renewed angina, septic ORL complications and nephritis or rheumatic fever and is seen around the 18th day of untreated scarlet fever.

Illness usually begins with a fever and sore throat. There also may be chills, vomiting, and abdominal pain. The tongue may have a whitish coating and appear swollen. It may also have a “strawberry”-like (red and bumpy) appearance. The throat and tonsils may be very red and sore, and swallowing may be painful.

One or two days after the illness begins, the characteristic red rash appears (although the rash can appear before illness to as many as 7 days later). Certain strep bacteria produce a toxin (poison) which causes some people to break out in the rash—the “scarlet” of scarlet fever. The rash may first appear on the neck and chest, then spread over the body. Typically, the rash begins as small, flat red blotches which gradually become fine bumps and feel like sandpaper.

Although the cheeks might have a flushed appearance, there may be a pale area around the mouth. Underarm, elbow and groin skin creases may become brighter red than the rest of the rash. These are called Pastia’s lines. The scarlet fever rash generally fades in about 7 days. As the rash fades, the skin may peel around the finger tips, toes, and groin area. This peeling can last up to several weeks.

Scarlet fever is treatable with antibiotics. Since either viruses or other bacteria can also cause sore throats, it’s important to ask the doctor about a strep test (a simple swab of the throat) if your child complains of having a sore throat. If the test is positive, meaning your child is infected with group A strep bacteria, your child’s doctor will prescribe antibiotics to avoid possible, although rare, complications.

CDC Scarlet fever

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