History and Geography

The early history of scarlet fever prevalence is obscure. It is possible that outbreaks were observed by Near Eastern practitioners of the Arabian school, but the first undoubted account of a disease with a fiery rash as a characteristic was provided by Giovanni Filippo Ingrassia of Palermo in 1553. The disease was apparently present in Germany and Italy in the early seventeenth century, and we know of a severe outbreak in Poland in 1625. At that time, the disease was variously known as rossalia, purpurea epidemica maligna, and febris miliaria rubra. It is clear from observations by Daniel Sennert in 1619, Michael Düring in 1625, and Johann Schultes in 1665 that the scarlatinal manifestations of desquamation, nephritis, and dropsy were well known before the disease received its modern name. Although in 1683 Sydenham wrote of the disease as having a mild character, he nevertheless established its autonomy, and distinguished it from other acute exanthema, notably measles, by naming it. By the end of the seventeenth century, the identity of scarlet fever was well recognized, although much epidemiological confusion remained, and still remains, over the respective roles of scarlet fever, streptococcal sore throat, and diphtheria (cynanche maligna) in seventeenth-century and eighteenth-century epidemics.

During the eighteenth century, scarlet fever was present in epidemic form throughout Europe and the United States. It appeared in Copenhagen in 1677, in Scotland in 1684, in the United States in 1735, and in Sweden in 1744. In general, however, the evidence suggests that the disease made irregular epidemic appearances, and that its mortality varied considerably. During the early eighteenth century, it seems to have been of fairly mild character, but

Dutch and Swedish evidence suggests that by mid-century a very virulent strain was also present.

The character of scarlet fever as a relatively new disease may be reflected in the age incidences reported during this period. Sydenham noted that it attacked whole families, though more especially the infants, whereas Nils R6sen von Rosenstein observed in 1744 the simultaneous occurrence of sore throat without rash in children in infected households. This pattern was observed in adults by Maxmilian Stoll in 1786. In the last years of the century, scarlet fever was extensive and virulent in Europe, with severe outbreaks in Denmark and Finland in 1776-8, and in central Germany in 1795-1805. By 1814 it was again very mild, but continued its global spread, appearing in South America in 1892, in Greenland in 1847, and in Australia and New Zealand in 1848.

During the 1820s and 1830s, however, a more virulent form reappeared, and consequently, the disease was the leading cause of death among infectious childhood maladies until 1875. During the 1880s, the disease continued to be widely prevalent but began to decline as a cause of death, and by the 1890s its character was again relatively mild, although not as mild as it has become today. This decline in severity was first apparent in Britain and western Europe, although a malignant form was still present in Poland, Russia, and Romania during the 1930s. Observations by Edward Wilberforce Goodall made in the Metropolitan Asylums' Board's Eastern Hospital, London, showed that as fatality dwindled, so did the more serious clinical forms.

Streptococci were first isolated from the blood of scarlet fever patients by Edward Klein in 1887, but he failed to reproduce the disease in animals. In 1911 Kari Landsteiner produced a similar disease in monkeys by inoculating them with faucial exudate from scarlet fever patients, but until about 1922 the streptococci were generally considered to be secondary invaders.

It was ultimately observation of human beings that proved scarlet fever to be a result of streptococcal infection. Seminal work by George Dick and Gladys Dick in the early 1920s proved scarlet fever to be primarily a local infection of the throat caused by type A hemolytic streptococci. In 1923 the Dicks successfully inoculated volunteers, and in 1924 developed the Dick test: the intradermal injection of a diluted filtrate of a broth culture of a scarlatinal strain of streptococcus which, by the resultant appearance or not of a local erythemateous reactiori, determines the susceptibility of the subject to scarlet fever. In other words, a negative Dick test is an indication of antitoxic immunity.

Anne Hardy

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