As described in this issue, increased outbreaks of rheumatic fever were noted in the mid 1980s, while reports of "flesh eating strep" and a new "streptococcal toxic shock syndrome" became prominent in our literature during the late 1980s and 1990s. These recent changes in the virulence of this organism are best understood by reviewing the history of GABHS.
The modern history of GABHS begins with its bacteriologie identification in human infections.1,2 Pasteur was first to report isolation of this organism by growing it from the blood of a woman with puerperal fever in 1879. A few years later, the organism was isolated from the blood of a patient with scarlet fever by Loffler, and the organism was first named Streptococcus pyrogenes.1
Prior to the availability of bacteriologie diagnostic methods, the history of GABHS can only be traced by its clinical syndromes. Scarlet fever and necrotizing fasciitis have sufficiently distinct characteristics to allow an educated guess about their early history. And puerperal sepsis, being the first GABHS infection documented by culture, can be tracked during the 19th century.
THE HISTORY OF SCARLET FEVER
The clinical features of scarlet fever have been confused with diphtheria, measles, and other infectious exanthems until recent times. Because information that distinguishes these exanthems gradually accumulated over rime, the further one goes back, the greater is the uncertainty about whether an epidemic was scarlet fever.2,3 There is speculation that Hippocrates may have described scarlet fever in the 5th century BC and that scarlet fever may have caused the Plague of Athens of 430 to 426 BC that predated the end of Greece's Golden Age.3 In 1641, Daniel Sennert is given credit for first describing epidemics in sufficient detail to provide unequivocal evidence they were scarlet fever.
During the 18th century, scarlet fever was considered a mild illness in Europe and America, although some fatal epidemics did occur. Sydenham described "scarlet fevour" as a mild disease and recommended only simple conservative treatment for his upper-class London patients. Others who also cared for the upper class in London also described only mild cases. However, Morton, who worked with impoverished patients at that time, definitely saw more severe scarlet fever. The observation that crowded living conditions in London are associated with increased virulence of streptococcal infections can thus be traced back at least 300 years. Scarlet fever was first described in North America as a relatively benign outbreak that began in Massachusetts in 1735. It gradually spread down the Atlantic coast over the next 40 years, retaining its mild character.3
In the early part of the 19th century, streptococcal infections suddenly turned ugly. Bretonneau had studied scarlet fever for almost 25 years in Tours, France, without observing a death. But in 1824 he described an epidemic so severe that he compared it to plague.3 Lethal epidemics also occurred in Dublin, in 1831, and Augusta, Georgia, in 1832. Case fatality rates jumped to 15% in 1834 in Great Britain. And they were as high as 30% in Europe and the United States during the next 50 years.3 In 1843, an Irish physician wrote:
. . . the disease called scarlet fever assumed a very benign type in Dublin soon after the year 1804 (following an 1801-1804 epidemic of fatal scarlet fever), and continued to be seldom attended with danger until the year 1831, when we began to perceive a notable alteration in its character, and remarked that the usual undisguised and inflammatory nature of the attack was replaced by a concealed and insidious form of fever, attended with great debility. We now began occasionally to hear of cases which proved unexpectedly fatal, and of families in which several children were carried off; still it was not until the year 1 834 that the disease spread far and wide, assuming the forni of a destructive epidemic .... The contagion seemed to act as a more deadly poison on the individuals of some families than upon those of others, and, consequently, when one member of a family had died, there was always much reason to fear for I the others when attacked.3
One wonders if some of the deaths with multiple organ disease and a rapid downhill cause may have been similar to the current cases of streptococcal toxic shock. However, these historic epidemics differed in that disease was most severe for children. The Archbishop of Canterbury apparently lost five of his six daughters to scarlet fever in spring 1856, and another author describes a British family that, after losing four of five children, moved and had their home completely disinfected, but after they moved back, the remaining child also died of this disease.
Near the end of the 19th century, a gradual trend towards decreasing virulence for scarlet fever was noted in the United States and Europe. Case fatality rates in London changed from 16% in 1863 to 10.9% in 1883, 7.5% in 1887, 2.3% in 1890, and 0.9% in 1891. In 34 US states, mortality dropped from 10.2 per 100,000 population in 1900 to 4-6 in 1920, and 1.9 in 1926. Other countries varied in the timing of waning virulence. Russia experienced a case fatality rate of 22.3% from 1892 through 1915 and China lost between 50,000 and 200,000 to a 1921 epidemic.3 Corresponding to this loss of virulence was a drop in the incidence of acute rheumatic fever. Death rates for this complication in the United States dropped from almost 7 per 100,000 in 1910 to about 1.3 in 1940 and fewer than 0.5 between 1960 and 1977.4 Some correlation has been noted between changes in virulence and changes in types of streptococci during this century.
HISTORY OF NECROTTZING FASCIITIS
Necrotizing fasciitis made a dramatic appearance in the literature as part of the recent resurgence of GABHS.' The term flesh eating strep received lay recognition as a "new" problem. Actually, necrotizing fasciitis was making a return appearance. It, was rampant during the Civil War, and official records cite 2,642 cases, with a 46% mortality rate, during the War Between the States.5'8 Although GABHS is felt to have caused this epidemic, necrotizing fasciitis (alias necrotizing erysipelas, gangrenous erysipelas, streptococcal gangrene, or hospital gangrene) can be produced by other organisms such as Staphylococcus aureus. However, Pfauner demonstrated that GABHS could be isolated from necrotizing fasciitis by culture in 1918. Meleney reported 20 cases associated with GABHS from China in 1924, and others have reported similar cases between then and 1980.6-8
HISTORY OF PUERPERAL SEPSIS
Puerperal sepsis is unique in that its contiguousness and largely preventable nature were recognized before bactériologie techniques became available. During most of the 19th century, this infection made hospital delivery a disaster throughout the western world. Recurrent epidemics of puerperal fever made the risk of dying 5 or 10 times higher than it was for home deliveries. This was primarily a problem for affluent women who were more likely to have hospital births. The following events led to an understanding of the infectious nature and methods for prevention of puerperal fever.9-10 During a 1789 to 1792 outbreak in Aberdeen, Alexander Jordan "proved" an infectious cause by noting the contagious spread by birth attendants from case to case. This observation was also consistent with the sharply reduced rates for postpartum sepsis that White, Clark and Collins had achieved in England and Ireland at about this time through personal and environmental cleanliness. Then in 1843, the American physician-poet Oliver Wendell Holmes produced a paper, based on a review of literature, concluding that puerperal fever was an infection carried to mothers by physicians from other infected persons.
However, a Hungarian obstetrician, Ignaz Semmelweis, is generally given credit for first establishing the contagious nature and its control of puerperal fever. He noted that mortality rates were over 10% on wards where medical students were trained while always below 3% on wards staffed by midwives. Semmelweis also observed that medical students attended autopsies while midwives did not, that doctors and students came directly from autopsies to examine patients, and that women were infected in a pattern that followed the row of beds that had been examined that day. When one of Semmelweis1 surgical colleagues died after being cut by a scalpel used to autopsy a puerperal fever victim, this physician had autopsy findings similar to those of puerperal fever.
Based on these observations, Semmelweis believed puerperal fever was spread by "morbid matter," and he required students and physicians (under protest) to scrub and soak hands in chlorinated lime before and between patients. Over a few months, death rates dropped from 18% to 2.2%. However, it does not always pay to criticize peers and superiors. Semmelweis was ostracized, first by his service chief and then by the Medical Society of Vienna. He returned to Budapest where again his techniques lowered mortality rates. But after continued indifference from the profession, he was committed to an asylum and died in 1865 of a blood infection.10
Was the puerperal fever of the 18th and 19th centuries due to GABHS? This seems likely in view of the facts that this organism was first isolated from a patient with puerperal fever and that subsequent bacteriology studies revealed the great majority of puerperal fever deaths of this era were caused by this organism. In addition, as early as the 18th century, many of the patients with puerperal fever also had erysipelas, and erysipelas is generally ascribed to GABHS infections.9
COMMENTS ABOUT THIS ISSUE
Thanks to my former mentor, Elia Ayoub for serving as Guest Editor. He learned from Louis Wannamaker and others who studied GABHS disease when there was more of it and passed this knowledge to his students with grace and class. This issue is also the first with a "Resident Column". We hope to continue these whenever possible to add a viewpoint from those who will follow us.
1. Stouerman GH. The historical role of the dick test. JAMA. 1983;250:3OT7-3099.
2. McGraw RE. Encyclopedia of Medical History. McGiaw'Hill Book Company. 1985.
3. Kais AR, Morena DM. Severe streprococcal infections in historical perspective. Clin Infect Dis- 1 992; 14-298- 307.
4. Bisno AL. Group A streptococcal infections and acute rheumatic fever. N Engl J Med. 1991:325:783-791.
5. Bisno AL. Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Mei 1996;334:240-244.
6. Weinberger M. Haynes RE, Morse TS. Necrolizing fasciitis in a neonate. Am J Dis Child. 1972;123:591-594.
7. Beathard GA, Guckian JC. Necrociiing fasciitis due to group A U-hemolytic streptococci. Arch Intern Med. 1967; 120:63-67.
8. Wilson B. Nectotiiing fasciitis. AmJSurg. 1952 1 18:41 6-43 1.
9. Bynum WF, Porter R. Companion Encyclopedia of the History of Mediane, Vol. 2. Rutledge, London- 1993:1053-1061.
10. Lyons AS, Perrucelli RJ. Medicine: An Illusnuied Hijiorj. New York, NY; Henry N. Abrams. Inc. 1978:550-553.