113 Puerperal Fever

Historically the terms puerperal fever and childbed fever referred to any acute fever occurring in puer­perae during the first few days after delivery. Less frequently, the terms were also applied to sympto­matically similar diseases that occurred during preg­nancy or even among the newborn.

Etiology and Epidemiology

A wide range of aerobic and anaerobic microorgan­isms have been associated with acute pelvic inflam­mation and with other postpartum inflammations that could be identified as puerperal fever. Group A streptococci (pyogenes) were probably the leading causal agent in most puerperal fever epidemics in earlier centuries. However, since the 1970s, group B streptococci (agalactiae) have become the most prev­alent causal agent.

Clinical Manifestations and Pathology

Among puerperae the clinical manifestations of puer­peral sepsis include acute fever, profuse Iochial flow, and an enlarged and tender uterus. Onset is gener­ally between 2 and 5 days after delivery. Normally there is inflammation of the endometrium and sur­rounding structures as well as of the lymphatic and vascular systems. One also finds pelvic cellulitis, septic pelvic thrombophlebitis, peritonitis, and pel­vic abscesses. Among neonates, infection usually be­comes apparent in the first 5 days after birth, but onset is sometimes delayed by several weeks. Symp­toms include lethargy, poor feeding, and abnormal temperature.

History and Geograpy

The Hippocratic corpus contains case histories of puerperal fever. Various epidemics were recorded in the sixteenth and seventeenth centuries. The dis­ease was first characterized and named in the eigh­teenth century when serious epidemics began to ap­pear with regularity in the large public maternity clinics of Europe. In the late eighteenth and early nineteenth centuries, various English and American obstetricians concluded that puerperal fever was sometimes contagious. Alexander Gordon and Oli­ver Wendell Holmes argued that physicians could transmit the disease from one patient to another, and they recommended various measures to reduce the frequency of such accidents. By the early nine­teenth century, the disease was responsible for a mortality rate of between 5 and 20 percent of mater­nity patients in most major European hospitals. Smaller hospitals had outbreaks in which, through a period of several months, 70 to 100 percent of mater­nity patients died from puerperal fever. The etiology of the disease was unclear, although seasonal pat­terns and its high incidence in the maternity clinics seemed to suggest that it was usually due to a local poison conveyed through the atmosphere. By the middle of the nineteenth century, the disease was receiving a great deal of attention in the medical literature, and cases were being reported from around the world.

In 1847, Ignaz Semmelweis became assistant in the Vienna maternity clinic. The incidence of puer­peral fever in the Vienna hospital was about 7 per­cent, which compared favorably with other hospitals around Europe. However, the Vienna clinic con­sisted of two divisions, one for obstetricians and the other for midwives; the first division consistently had a mortality rate three to five times greater than the second division. After several months of inten­sive investigation, Semmelweis concluded that the difference was due to decaying organic matter, usu­ally from autopsied corpses, which was conveyed to patients on the hands of the medical personnel in the first clinic.

By 1850 Semmelweis had become convinced that decaying organic matter was responsible for all cases of puerperal fever - even for the relatively few cases that occurred in the second clinic. Indeed, he provided an etiologic characterization of puerperal fever in which it became true by definition that all cases of the disease were due to contamination. Given Semmelweis’s definition it also followed trivi­ally that puerperal fever was not a unique disease but only a form of sepsis. Semmelweis had virtually no evidence for this strong position. His critics imme­diately cited cases in which women died from puer­peral fever without ever having been exposed to decaying organic matter. Semmelweis responded that in such cases the decaying matter must have been produced internally, perhaps by the decomposi­tion of blood or of placental fragments. Even the physicians who accepted his initial results rejected this bold and apparently unwarranted claim.

By the 1860s, Louis Pasteur’s work on fermenta­tion and putrefaction drew attention to the possible significance of microorganisms in some disease pro­cesses. Building on Pasteur’s work, and certainly aware of Semmelweis’s theories, Carl Mayrhofer ex­amined the vaginal discharges of more than 100 healthy and diseased patients in the Vienna mater­nity clinic. In 1865 he identified and described vari­ous microorganisms that seemed to be present only in discharges from women suffering from puerperal fever.

Using the best techniques that he had available, Mayrhofer isolated these organisms, cultured them in solutions of sugar, ammonia, and water, and then reproduced the disease by introducing the organisms into healthy test animals.

Mayrhofer’s work was unimpressive to his col­leagues in Vienna, but it received considerable atten­tion in Berlin.

Classical studies in the early decades of the twenti­eth century led to the serologic classification of strep­tococci and to the recognition that group A strains were the most prevalent agent in puerperal fever. Group B streptococci were first reported in puerperal sepsis in 1935 and recently have displaced the group A strains as the most prominent agents in puerperal sepsis in the United States and Great Britain. Infec­tions of group A streptococci are generally exogenous and affect puerperae, whereas infections of group B pathogens are usually endogenous and, although the mother may be affected, generally strike the fetus or neonate. The change in relative frequency of causal agents, therefore, has had important ramifications in clinical manifestations, prophylaxis, and therapy. The development and use of various antibacterial agents have obviously revolutionized the manage­ment of puerperal sepsis. Improved care for deliver­ing mothers has also had an important impact, and in recent years liberalization of abortion laws has re­duced the incidence of puerperal sepsis associated with illegal abortions. However, control of sepsis is now recognized to be more difficult and complex than might once have been believed, and it remains a par­ticularly difficult problem in Third World countries where medical care is not readily available.

K. Codell Carter

Bibliography

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Semmelweis₁ Ignaz. 1983. The etiology, concept and prophy­laxis Ofchildbed fever, trans. K. Codell Carter. Madi­son, Wis. (Originally published in German in 1861.)