Daily entries from the 17th century London diary
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Scarlet fever is a disease caused by an exotoxin released by Streptococcus pyogenes. 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. The rate of development of rheumatic fever in individuals with untreated streptococcal infection is estimated to be 3%. The rate of development is far lower in individuals who have received antibiotic treatment.
Streptococcus pyogenes (group A streptococcus) is responsible for scarlet fever. It can also cause simple angina, erysipelas, and serious toxin-mediated syndromes like necrotizing fasciitis and the so-called streptococcal toxic shock-like syndrome. The virulence of group A streptococcus seems to be increasing lately. The exanthem, or widespread rash, of scarlet fever is thought to be due to erythrogenic toxin production by specific streptococcal strains in a nonimmune patient. Besides erythrogenic toxins, the Group A streptococcus produces several other 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 the anti-streptolysin O titer, an assay for scarlet fever and erysipelas.
This disease was known before the twentieth century as scarlatina (from the Italian scarlattina). Since the middle of the twentieth century the disease has, for reasons which are not understood, become much milder in its effects, and the usage of the name scarlatina has now replaced the term "scarlet fever" in some areas.[1]
Many novels depicting life before the nineteenth century (see Scarlet fever in popular culture 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 or even due to the treatments tried. Prior to an understanding of how streptococcus was spread and modern medicine, 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.
Early symptoms indicating the onset of scarlet fever can include:[2][3]
Diagnosis of scarlet fever is clinical. The blood tests shows marked leukocytosis with neutrophilia and conservated or increased eosinophils, high erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and elevation of antistreptolysin O titer. Blood culture is rarely positive, but the streptococci can usually be demonstrated in throat culture. 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.
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.
In the 1950s, as a small child, I remember watching over our garden fence as the personal effects of a boy called John Holloway were burned in the garden after he had recovered from scarlet fever. It was impressed upon me that he was lucky to have survived. I regarded it as a solemn and serious occasion and watched as the pale and thin boy, wearing his school mac, poked at the burning pile with a stick. I knew he was sad.