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Two cases of scarlet fever are described, both following super-infection of chickenpox. Enterotoxin B and C producing staphylococci were the only pathogens identified. The role of staphylococcal and streptococcal toxins in the pathogenesis of scarlet fever and toxic shock syndrome is discussed.
There are controversies about the problem of the source of "lanhousha" (scarlet fever) in the field of modern medical history, whether it is an epidemic appeared from the ancient time in our country or imported from other countries. Now, almost all researches were carried out around the classic medical books, especially "Medical Records of Ye Tianshi", and hardly dealing it in a historical context at that time. Through contrastive analysis between the records in medical books and historical facts, it is concluded that Ye Tianshi's records of scarlet fever have nothing to do with Ye Tianshi himself, and is by author of allonym. It perhaps was exogenous cold diseases spread when a severe epidemic diseases happened at Southern Jiangsu in the 11th year of Yongzheng reign. Even though there was some scarlet fever, it was not the first spread of scarlet fever in fact. Actually, in late Kangxi reign, scarlet fever was regarded as an epidemic disease seldom seen at Southern Jiangsu.
In 1987 there was an unexplained increase in severe streptococcal diseases in Norway and other western countries. In Norway this increase was not accompanied by a corresponding increase in acute rheumatic fever. This study investigated the occurrence of scarlet fever and acute rheumatic fever in a rural district (approximately 15,000 inhabitants) of western Norway during the years 1862-1884. Four epidemics of severe scarlet fever occurred during this period. The local doctor treated 1,155 patients (96% children), of whom 154 (13.3%) died. Acute glomerulonephritis with subsequent kidney failure seems to have been a major cause of death. During the same period 76 patients (96% adults) were treated for acute rheumatic fever. These cases were not related to the severe epidemics of scarlet fever. It is probable that different, co-circulating strains of streptococci caused the infections, which were followed by glomerulonephritis and rheumatic fever. It is possible that rheumatic fever was caused by the strain that induced the more benign "Angina tonsillaris".
From 48 out of 143 scarlet fever patients in the age range of 3-15 years, Staphylococcus aureus strains were isolated in the course of hospitalization or convalescence (isolation rate 33.6%). Staphylococcal enterotoxin (SE) was produced by 19 (39.6%) of these isolates. The most frequent SE types detected were A (47.4%) and C (36.8%); type B was produced by 2 strains, type E by 1, while type D, or a combination of SE types, was not detected at all (by means of immunodiffusion in a micromodification). So far no significant correlation has been found between the clinical course of scarlet fever or accompanying complaints and presence of SE-positive S. aureus strains. The significance of these findings is discussed.
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Annual deaths from scarlet fever in Liverpool, UK during 1848-1900 have been used as a model system for studying the historical dynamics of the epidemics. Mathematical models are developed which include the growth of the population and the death rate from scarlet fever. Time-series analysis of the results shows that there were two distinct phases to the disease (i) 1848-1880: regular epidemics (wavelength = 3.7 years) consistent with the system being driven by an oscillation in the transmission coefficient (deltabeta) at its resonant frequency, probably associated with dry conditions in winter (ii) 1880-1900: an undriven SEIR system with a falling endemic level and decaying epidemics. This period was associated with improved nutritive levels. There is also evidence from time-series analysis that raised wheat prices in pregnancy caused increased susceptibility in the subsequent children. The pattern of epidemics and the demographic characteristics of the population can be replicated in the modelling which provides insights into the detailed epidemiology of scarlet fever in this community in the 19th century.
In 1997, two years after the last epidemic peak of scarlet fever, the speed of decrease of the number of registered cases has been slower than after earlier epidemics. However, the seasonal distribution of cases does not forecast an increase of incidence of scarlet fever in the near future. The age, sex, urban/rural distribution of scarlet fever remain stable. The highest incidence rates are noted in 7-8-year old children. Scarlet fever cases are hospitalized in 1%.
A case of surgical scarlet fever is described in a 57-year-old woman. Identification of beta-haemolytic streptococci and treatment with penicillin is essential to prevent spread of surgical scarlatina.
We report a 3-year-old boy with varicella complicated by cellulitis and scarlet fever. He developed a typical rash of scarlet fever following the onset of varicella. Streptococcus pyogenes was isolated from the ulcers due to varicella. The present case suggests that scarlet fever may rarely develop following varicella and should be considered in children with complicated varicella.
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There was a marked rise in scarlet fever mortality in England and Wales in the mid-nineteenth century and spectral analysis of the registration details, 1847-80, shows that the interepidemic interval was 5-6 years, but after 1880 the endemic level fell and the fatal epidemics disappeared. The dynamics of the scarlet fever epidemics can be represented by a linearized mathematical model and because the system is lightly damped, it could be driven by an oscillation in susceptibility. Epidemics were significantly correlated with dry conditions in spring/summer (P < 0.001), suggesting that these produced a low amplitude oscillation in susceptibility which drove the system. Epidemics also correlated (P < 0.001) with an oscillation in wheat prices but at a lag of 3 years, suggesting that malnutrition during pregnancy caused increased susceptibility in the subsequent children which interacted synergistically with seasonal dry conditions. Scarlet fever mortality was sharply reduced after 1880 in parallel with falling wheat prices suggesting that the remarkable period of high scarlet fever mortality (1840-80) was dependent on poor nutritive levels during that time.