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Puerperal fever in britain : failed models of disease causation
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Wells, Jessica
University of South Florida
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Childbed fever
History of medicine
History of science
Intellectual history
Dissertations, Academic -- History -- Masters -- USF   ( lcsh )
non-fiction   ( marcgt )


ABSTRACT: In eighteenth- and nineteenth-century Britain, a bacterial infection which we now know to be caused primarily by a streptococcus, was killing women in childbirth at an alarming rate. The disease, called puerperal, or childbed, fever, was being transmitted primarily from doctor to patient by a doctor's unwashed hands and filthy, contaminated clothing and linens. Despite this evident and, in retrospect, obvious vector, the doctors of this period never discovered how to prevent their patients from dying a gruesome and painful death. Many physicians wrote extensive accounts of the illness but often ended their works in despair, unable to find the cause. Much of the historical literature blames this befuddlement on personality traits of the physicians, arguing that egos and professional hostilities prevented the kind of cooperation that could have led to progress. This study attempts to show that this failure was not a product of personalities but of the modern physicians' assumptions and logic. The assumptions were the still-powerful, but often unnoticed, dictates about the human body handed down from ancient Greek medicine. The logical errors were a product of pre-scientific notions of definition, explanation, and evidence. The author argues that it was not a lack of data that thwarted the physicians, but a series of these intellectual roadblocks that prevented them from understanding and extended the terror of puerperal fever for another two centuries.
Thesis (MA)--University of South Florida, 2010.
Includes bibliographical references.
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by Jessica Wells.
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Puerperal fever in britain :
b failed models of disease causation
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by Jessica Wells.
[Tampa, Fla] :
University of South Florida,
Title from PDF of title page.
Document formatted into pages; contains X pages.
Thesis (MA)--University of South Florida, 2010.
Includes bibliographical references.
Text (Electronic thesis) in PDF format.
Mode of access: World Wide Web.
System requirements: World Wide Web browser and PDF reader.
3 520
ABSTRACT: In eighteenth- and nineteenth-century Britain, a bacterial infection which we now know to be caused primarily by a streptococcus, was killing women in childbirth at an alarming rate. The disease, called puerperal, or childbed, fever, was being transmitted primarily from doctor to patient by a doctor's unwashed hands and filthy, contaminated clothing and linens. Despite this evident and, in retrospect, obvious vector, the doctors of this period never discovered how to prevent their patients from dying a gruesome and painful death. Many physicians wrote extensive accounts of the illness but often ended their works in despair, unable to find the cause. Much of the historical literature blames this befuddlement on personality traits of the physicians, arguing that egos and professional hostilities prevented the kind of cooperation that could have led to progress. This study attempts to show that this failure was not a product of personalities but of the modern physicians' assumptions and logic. The assumptions were the still-powerful, but often unnoticed, dictates about the human body handed down from ancient Greek medicine. The logical errors were a product of pre-scientific notions of definition, explanation, and evidence. The author argues that it was not a lack of data that thwarted the physicians, but a series of these intellectual roadblocks that prevented them from understanding and extended the terror of puerperal fever for another two centuries.
Advisor: Golfo Alexopoulos, Ph.D.
Childbed fever
History of medicine
History of science
Intellectual history
Dissertations, Academic
x History
t USF Electronic Theses and Dissertations.
4 856


Puerperal Fever in Britain: Failed Models of Disease Causation by Jessica Wells A thesis submitted in partial fulfillment of the requirements for the degree of Master of Arts Department of History College of Arts and Sciences University of South Florida Major Professor: Golfo Alexopoulos, Ph.D. Giovanna Benadusi, Ph.D. David Johnson, Ph.D. Date of Approval: October 28 2010 Key words: childbed fever, Semmelweis, history of medicine history of science, intellectual history Copy rig ht 2010, Jessica Wells


i Table of Contents Abstract ii Introduction 1 Historiograph y 5 Etiology S ym ptomology, Statistics 1 4 Earl y Accounts 2 0 Humoural Theory : Hippocrates and Galen 2 4 Miasma Theory : The Persistent Dead End 2 7 Medical E ducation : The Resilience of a Dogma 3 1 Mechanism : A New Metaphor 3 3 In flammation Theory : The Bleeding Continues 40 Pathology : New Techniques with Old Results 43 Contagionism and the Environment : Definitions and Confusion 4 7 Success: Treatments Break Free From Galen 59 Conclusion 6 2 References Cited 6 5


ii Abstract In eighteenth and nineteenth century Britain, a bacterial infection which we now know to be caused primarily by a streptococcus, was killing women in childbirth at an alarming rate. The disease, called puerperal, or childbed, fever, was being transmitted primarily from doctor to patient by a doctor’s unwashed hands and filthy, contaminated clothing and linens. Despite this evident and, in retrospect, obvious vector, the doctors of this period never discovered how to prevent their patients from dy ing a gruesome and painful death. Man y ph ys icians wrote extensive accounts of the illness but often ended their works in despair, unable to find the cause. Much of the historical literat ure blames this befuddlement on personality traits of the ph ys icians, arguing that egos and professional hostilities prevented the kind of cooperation that could have led to progress. This study attempts to show that this failure was not a product of pe rsonalities but of the modern ph ys icians’ assumptions and logic. The assumptions were the still powerful, but often unnoticed, dictates about the human body handed down from ancient Greek medicine. The logical errors were a product of pre scientific notion s of definition, explanation, and evidence. The author argues that it was not a lack of data that thwarted the phy sicians, but a series of these intellectual roadblocks that prevented them from understanding and extended the terror of puerperal fever for a nother two centuries.


1 Introduction Puerperal fever was the leading cause of maternal death prior to the twentieth century It was a disease that, in the late eighteenth and earl y nineteenth centuries defied m odern medical understanding. The vario us theories of disease causation that made up the classical medical curriculum struggle d unsuccessfully to explain a host of frustrating inconsistencies surrounding the disease Puerperal fever was unpredictable in location, timing, and severity It struck women of all classes and constitutions. I t was frightening in tragic isolated cases, but in epidemic form it was a blind biological terror causing the deaths of countless mothers and babies in ly ing in hospitals and homes all over the world. The story o f puerperal fever in the eighteenth and nineteenth centuries is one of failed logic. This is not a my stery of missing data: data that, had it been discovered, would have prevented or cured puerperal fever. In fact, the doctors had more than enough data, wh ich they freely shared, to recognize that puerperal fever passed from doctor to patient and that basic sanitary procedures would have prevented the disease. The question at hand is wh y, in the face of clear, repeated associations of phy sician contact and p uerperal fever the medical establishment failed to incorporate this data into their model of disease causation The answer is that a combination of ancient assumptions and pre scientific logical deficiencies prevented them from making the conceptual break through that would have prevented the disease.


2 Also known as childbed fever, puerperal fever is a post partum infection that strikes ly ing in women during or within a few days after childbirth. It can also be contracted during a miscarriage or abortion. P rior to the advent of antibiotic treatments in the mid twentieth century, puerperal fever was a deadl y complication of a significant percentage of births. In Great Britain it account ed for approximately half of all deaths related to childbirth. 1 It killed more women than cancer and ranked second only to tuberculosis in deaths of women of childbearing age. 2 The emerging obstetric profession’s attempts to apply theories of classical medicine, using concepts from Hippocrates and Galen, proved unsuccessful in e ither prevention or cure of the disease. There were scattered attempts to isolate causal factors: an earl y ex ample of the scientific method making its way into medicine. These attempts to construct correlations that might have led to a new understanding of causation were handicapped by ambiguity in the meanings of key concepts and hidden assumptions about how the biological world worked. The inability to break free of long standing assumptions led the medical community in circles and fostered intense debate over every aspect of this confusing disease. Because of this, progress was sporadic at best, even after the development of germ theory in the last half of the nineteenth century. 1 Robert Thomas, The Mode rn Practice of Physic (London: Longman, Rees, Orme, Brown, and Green, 1828), 932. Charles Delucena Meigs, Obstetrics: The Science and the Art (Philadelphia: Blanchard and Lea, 1852), states on page 614, “…it is well known that child bed fever destroys more wo men than all the other diseases and accidents of parturition put together. No physician can long practice the art of Midw ifery without discovering that a constant and wise vigilance is necessary to obviate the causes of such attack, and cure the patient who has been unhappily seized with it. There is scarcely any form of dangerous disorder that is more insidious in its approach, or more rapid in its development when once its terrific train is set in mo tion; a development so rapid that the loss of a few h ours, at the commencement, renders all after interposition fruitless and unavailing. Not a few of the victims are known to perish within tw elve hours, and som e even within six hours after the first manifestation of the symptoms.” 2 Irvine Loudon, Death in Childbirth: An International Study of Maternal Care and Maternal Mortality, 1800 1950 (Oxford : Oxford University Press, 1992), 163.


3 Compounding these difficulties puerperal fever was an especially perplexi ng disease. Compared to other contagious diseases, which doctors enjo yed modest success in explaining and treating during this period, puerperal fever remained a puzzle. Further, the developing focus on pathology in medicine which might be expected to her ald new insights, only compounded confusion about puerperal fever. Most historical analy ses have attributed these failures to personal shortcomings of the phy sicians involved, their turf battles, antagonistic personal relations, and a stubborn resistance t o the few visionary heroes that could have led the way had the medical profession only been willing to listen. This is, at best, a simplistic and largely misleading interpretation of the issues of intellectual history at work during this period. The his to ry of puerperal fever is not a story of heroes and villains, of people who ma d e glorious breakthroughs onl y t o be shunned by ego blinded colleagues. I t is rather an account of ph ys icians and midwives, dedicated but perplexed, daily confronting a predictabl y t errible disease against which they had little hope of triumph. Nor is it a story of a flash of insight, or a momentous discovery, that w on the day The brave people who tried to understand this scourge were intellectually disarmed. They were fighting an intractable foe with outdated conceptual tools, medical teachings that had varied little over the previous millennia. Instead of pett y and transient issues, this period was marked by dramatic disputes involving both substantial advances and persistent er rors, most involving the hidden assumptions of a classical medical education a nd the worldview it promulgated. These assumptions were bolstered by the practice employ ed by many phy sicians of responding to any possible progress by crafting ad hoc addendum s to their theories to show that


4 contrary to first appearances, this latest discovery could be made to fit nicely into their established views Finally pervasive confusion and ambiguities involving the definitions of key concepts related to the disease fragmented the modest advances that were achieved. This fragmentation, presented when advances in understanding transmission sanitation, and even germ theory should have heralded major progress, is the sad story of the largel y unsuccessful fight against p uerperal fever.


5 Historiography Failure is the unfortunate icon of the history of puerperal fever: failure in communication, failure in data collections, and failure of treatments. But, in retrospect, there were also substantial failures of logic. Mov ing from the ancients with their animated and spirit ridden view of the world into the mechanistic, observable, verifiable anal ys es of the scientific revolution, we can see that the fundamental impediment to the triumph over this disease has consistently b een an intellectual one. We find that all parties involved had roughly the same data. The task which commands the attention of historians has been to comprehend the inability of phy sicians to produce breakthroughs, either in prevention or treatment, that s aved lives. A majority of medical histories can be classified into two opposing camps. The progressive, Whig interpretations depict the “march of progress” in medicine by glorify ing certain medical advances and the “heroes” associated with discovering them These histories focus on the “Great Men” of medicine, doctors and researchers who took advantage of the steps laid before them by their equally heroic predecessors to climb the ladder of success and add their own contributions to medicine for the betterm ent of mankind. They chronicle the greatest inventions and innovations of medicine as a single trajectory of medical discovery on an inevitable march forward. 3 3 Amanda Carson Banks, Birth Chairs, Midwives, and Medicine (Jackson, MS: University Press of Mississippi, 1999), xvi ; Mar y Lindemann, Medicine and Society in Early Modern Europe (Cambridge, UK : Cambridge University Press, 1999), 1 2 ; Irvine Loudon, “Medical Practitioners 1750 1850 and the Period of Medical Reform in Britain,” in Medicine in Society: Historical Essays ed. A ndrew Wear


6 Revisionist histories claim that, rather than an intellectual march of progress, medicine has b een marked by the tragic inability of doctors to do any thing to alleviate human suffering, offering onl y t reatments that more often added to a patient’s pain. Revisionist histories claiming to debunk the Whig assumption of progress first became popular aft er the 1963 publication in French of Michel Foucault’s The Birth of the Clinic the first genuine critique of the role of medicine in society 4 Foucault broke with the traditional way of viewing the history of medicine by describing the origin of the clini c as a spontaneous creation distinct from the medical knowledge that preceded it. I nstead, he described the medical knowledge of the clinic as being a re presentation of knowledge and power within that particular societ y at that particular time. I llness be came an identifier that lumped individuals into a category that needed to be monitored and treated in a way that reinforced norms of societal behavior and existing medical knowledge. However revisionist histories of medicine are often guilty of similar p ersonalization. I nstead of searching the past for individuals that create links between concepts, forming a sequential timeline of discovery revisionists often search for their own “heroes” who made amazing discoveries but were ignored b y t he medical esta blishment. I n this way revisionist histories often use their “Great Men” to explain medicine’s often halting, unsure progress in much the same fashion as the traditional school celebrates its exciting achievements. Because of this, both versions of the st ory oversimplify the problems and the play ers, creating stories with bold characters but little nuance. (Cambridge, UK : Cambridge University Press, 1992), 220 ; Richard W. Wertz and Dorothy C. Wertz, Lying In: A History of Childbirth in America (New Haven: Yale University Press, 1989), xvii xviii. 4 Michel Foucault, The Birth of the Clinic: An Arc haeology of Medical Perception (London: Routledge, 1973).


7 Histories of puerperal fever offer a good example of this same personalization. The majority of these focus on selected heroes such as Ignaz Semmelweis Alexander Gordon, and Oliver Wendell Holmes, crediting these men with the discovery of the contagiousness of the disease while demonizing known anti contagionists such as Charles Meigs. A good example of this type of history is David Wootton’s Bad Medici ne: Doctors Doing Harm Since Hippocrates which sets itself apart in its introduction as being diametricall y opposed to the Whig interpretation of progress in medicine. Instead, Wootton states, “what we need…is a history not of progress, but of delay…” and he seeks to do just that, dividing his chapters into specific events wherein a medical non hero is ignored or derided for, in retrospect, a revolutionary discovery 5 In his chapter discussing puerperal fever, Wootton pay s homage to the familiar heroes and in doing so, overstates their innovation while quietly explaining away their logical failings. The best secondary source on puerperal fever is Irvine L oudon’s book The Tragedy of Childbed Fever 6 Although it is not without flaws, it is by far the most co mprehensive and useful treatment of the disease While this book is the least biased source on puerperal fever, it does not present a coherent analy sis but is instead a report of relevant information describing the history of puerperal fever from the eight eenth to the twenty first centuries. While L oudon offers several minor arguments, they are often tangential to the main goal of his book which is to compile information about a relativel y obscure and forgotten disease. The book is full of primary source m aterial and was obviously 5 David Wootton, Bad Medicine: Doctors Doing Harm since Hippocrates (Oxford : Oxford University Press, 2006), 21. 6 Irvine Loudon, The Tragedy of Childbed Fever ( Oxford: Oxford University Press, 1995 ).


8 carefully researched. But the crowning jewels of this book are its statistics. L oudon has compiled a massive amount of statistical evidence with which to support his assertions and they are conveniently catalogued in tables found throughout the book. He uses this data to present several excellent anal ys es, including his allegation that the adoption of Listerian antisepsis did little to affect the overall statistics of maternal death due to puerperal fever in Great Britain until aft er World War II. His background as a medical doctor allows him to explain the biological effects of puerperal fever, its causes, and nomenclature in a clear and concise manner. Besides The Tragedy of Childbed Fever he has also written Death in Childbirth : An International Study of Maternal Care and Maternal Mortality, 1800 1950 and edited Childbed Fever: A Documentary History both concentrating on puerperal fever, as well as several other books on medical history in the m odern period. 7 However, Loudon i s not a historian; he is a general practitioner who turned to writing medical history after retirement. And not all of his assertions are borne out by evidence. He is, at times, guilty of the same personalization found in the Whig medical histories. For ex ample, Loudon’s “prematurity ” argument centers on the fact that the discoveries of Alexander Gordon of Aberdeen, mainly that puerperal fever could not have been caused b y a m iasma and that it was related to ery sipelas, predated germ theory He states, “In science, an idea may be rejected ‘if its implications cannot be connected b y a series of simple logical steps to canonical, or generall y accepted, knowledge.’ Unfortunatel y fo r Gordon, almost a century had passed before the bacterial basis of 7 Loudon, Death in Childbirth ; Irvine Louden Childbed Fever: A Documentary History (London : Garland Publishing, 1995)


9 puerperal fev er was beginning to be accepted.” 8 However, science has many examples when discoveries have been utilized without the scientific principles behind them being fully understood: electricity selective breeding, etc. L oudon fails to admit that Gordon not only disregards his own most important achievements, discussing the prevention of puerperal fever in onl y 3 00 words, but instead spends the majority of space in his thesis arguing for the inflammatory nature of puerperal fever and bloodletting as the only appr opriate treatment. Christine Hallett has written a comprehensive overview of the eighteenth century treatises on puerperal fever, and on the development and importance of i nflammation and putrid theorie s 9 Rather than offering a Whig or revisionist argum ent, Halle t t presents an excellent documentary analy sis of eighteenth and earl y nineteenth century primary sources, describing each work as an example of two opposing theories of puerperal fever causation: inflammation theory and putrid theory Hallett is currentl y t he director of the UK Centre for the History of Nursin g and Midwifery She holds Ph.D. s in Nursing and in History and has written many articles on the history of nursing in the First World War and in industrial settings 10 Other excellent source s on puerperal fever are the works of Gail Pat Parsons. She has written a number of articles that truly discuss the differences between contagionist 8 Loudon, The Tragedy of Childbed Fever 32 33. 9 Christine Hallett, “The Attempt to Understand Puerperal Fever in the Eighteenth an d Early Nineteenth Centuries: The Influence of Inflammation Theory,” Medical History 49 no. 1 (2005). Inflammation theory wa s a disease causation model which focused on the buildup of pressure which led to stagnation of the blood while putrid theory charac terized a chain reaction of putrescence wherein putrid material taken into the body would then cause healthy tissues to putrefy also. Both of these vie wp oints will be more fully explained later in this thesis 10 Christine Hallett, “The Personal Writings o f First World War Nurses: A Study of the Interplay of Authorial Intention and Scholarly Interpretation,” Nursing Inquiry 14 no. 4 (2007): 320 329 ; Christine Hallett, M. Abendstern, and L. Wade, “Industry and Autonomy in Early Occupational Health Nursing: The Welfare Officers of the Lancashire Cotton Mills, 1950 1970,” Nursing History Review 14 (2006): 89 109.


10 and anticontagionist doctors. 11 Parsons explains how the disease causation model a doctor chose determined the ty pe of prevention program that he would advocate and contextualizes his arguments for and against describing puerperal fever as a contagious disease. 12 Current historians who fail to comprehend these divisions within the medical community are liable to make false claims concerning the intent of their primary sources. Parsons’ work is an example of well done revisionist history in that she seeks to describe the medical practitioners as they truly were rather than taking a progressive or regressive stance While she is critical of some secondary source work on puerperal fever, these are primarily revisionist histories that have claimed that the first half of the nineteenth century was characterized by anticontagionism and feminist histories that have sugge sted that male phy sicians deliberatel y allowed their female patients to die, either due to some “enmity ” toward women or because “they were simply too ‘bus y’ to wash their hands or change their clothing.” 13 Other secondary source material, both Whig and re visionist, unfortunately tends to idolize or stigmatize various individual doctors, developing theories of why isolated breakthroughs in preventing puerperal fever never influenced the practices of the greater medical establishment. Common heroes are Charl es White of Manchester, Alexander 11 Gail Pat Parsons, “The British Medical Profession and Contagion Theory: Puerperal Fever as a Case Study,” Medical History 22 (1978): 138 150 ; Gail Pat Parsons, “Puerperal Fever, Anticontagionists, and Miasmatic Infection, 1840 1860: Tow ard a New History of Puerperal Fever in Antebellum America,” Journal of the History of Medicine 52 (1997). Just as inflammation and putrid theories characterized the e ighteenth century debates on causation, contagionist and anticontagionist camps characterized the nineteenth century. The contagionists believed that puerperal fever was caused by a specific contamination which could spread puerperal fever to others. Antic ontagionists believed that a non specific contamination led to an unhealthy state of disease being spread, though not specifically puerperal fever. A thorough description of these opposing theories will be provided later in this thesis How ever, it is impo rtant to note that these theories were often contingent on the disease being discussed and that doctors could vacillate betw een the two theories depending on the evidence at hand. 12 Parsons, “Puerperal Fever, Anticontagionists, and Miasmatic Infection.” 13 Parsons, “The British Medical Profession and Contagion Theory,” 138, 147n43, 148n49.


11 Gordon of Aberdeen, Oliver Wendell Holmes of Boston, and the Hungarian physician Ignaz Semmelweis. 14 Many of the current claims that are made about the ingenuity of these doctors, b y s econdary source authors such as Kay Cod ell Carter, David Wootton, Hal Hellman, and Sherwin B. Nuland, are overstated while the insights of physicians such as Sir Thomas Watson and Robert Storrs of Doncaster are practically ignored in the secondary literature. 15 Watson described puerperal fever as earl y as 1842 as “instances of direct inoculation” — Recollect, that the hand of the accoucheur is brought, almost of necessity into frequent contact with the uterine fluids of the newly made mother. Recollect,…, with what tenacit y t he smell, which is t hus contracted, clings to the fingers, in spite even of repeated washings; and, whilst this odour remains, there must remain also the matter that produces it. Recollect how minute a quantity of an animal poison may be sufficient to corrupt the whole mass o f blood,…Recollect the raw and abraded state of the parts concerned in parturition; the interior of the uterus forming a large wound, and presenting,…, an exact analogy to the surface 14 Charles White, A Treatise on Pregnant and Lying in Women (London: E. and C. Dilly, 1773) ; Alexander Gordon, A Treatise on the Epidemic Puerperal Fever of Aberdeen ( London : G. G. and J. Robinson, 1795) ; Oliver Wendell Holmes, “The Contagiousness of Puerperal Fever,” New England Quarterly Journal of Medicine and Surgery 1 (1843): 503 530 ; Ignaz Semmelweis, The Etiology, Concept, and Prophylaxis of Childbed Fever tra ns. K Codell Carter (Londo n : University of W isconsin Press, 1983). Charles White of Manchester was perhaps the first English author on the subject to suppose that the retention of the lochia led to putrefaction which entered the bloodstream and caused puer peral fever. Alexander Gordon w as among the first to show that he could trace w hich patient would contract puerperal fever by knowing which birth attendant delivered her. Oliver Wendell Holmes wrote an impassioned address citing many examples of apparent c ontagion of puerperal fever. Ignaz Semmelweis showed that hand washing in chlorinated lime solution significantly lowered the rates of infection in the Allegemeines Krankenhaus lying in hospital in Vienna. 15 K. Codell Carter, “Semmelweis and His Predecess ors,” Medical History 25 (1981): 57 72 ; K. Codell Carter, The Rise of Causal Concepts of Disease: Case Histories (A ldersot, UK : Ashgate Publishing Co., 2003) ; K. Codell Carter, Childbed Fever: A Scientific Biography of Ignaz Semmelweis (New Brunswick, NJ : Transaction Publishers, 1995) ; David Wootton, Bad Medicine ; Hal Hellman, Great Feuds in Medicine: Ten of the Liveliest Disputes Ever (New York: John Wiley & Sons, Inc., 2001) ; Sherwin B. Nuland, The Doctor’s Plague: Germs, Childbed Fever, and the Stra nge Story of Ignc Semmelweis (New York: W.W. Norton & Company, Inc., 2003). Ignaz Semmelweis, in particular, has received an enormous am ount of attention for his analysis in 1847 that contact with decaying animal organic ma tter in post mo rtem dissections caused puerperal fever after it was introduced into the birth canal by the hands of attending medical students. While the hand w ashing program that he subsequently implemented saved countless women from death, the limitations of Semmelweis’ analysis, with its many mistaken assumptions and his unwillingness to modify his theory to fit incompatible data, has been blissfully glossed over by those who have promoted his contemporary veneration. While Semmelweis is, undoubtedly, a hero for pledging his life to sa ving the lives of these women, had he been less obstinate in his technically incorrect beliefs, he might have saved far more lives.


12 of a stump after amputation;…, that the hand which is relied upon for su ccor in the painful and perilous hour of childbirth,…, may literally become the innocent cause of her destruction; innocent no longer, however, if after warning and knowledge of the risk, suitable means are not used to avert a catastrophe so shocking. 16 Storrs gave a lecture discussing how contact with p uerperal fever victims and post mortem dissections evinced disease and death in medical practitioners, family members, husbands, and the recently delivered children of the deceased. 17 In doing so, his work o pened the possibility that a far broader range of people were at risk for the disease and, consequently, undermined the assumption that puerperal fever was exclusively a women’s disease. The works of these doctors, despite their contemporary prominence, do not enjoy the status accorded to others in the secondary literature. Instead of a discussion of the medical establishment’s worldview and how individual breakthroughs were positioned in their greater intellectual context, the historiograph y on puerperal fever tends to focus on sensationalized accounts of troubled personalities and interpersonal disputes between doctors. This study offers an alternative interpretation of the primary sources, one that focuses on the deficiencies of the reasoning and the me thodologies of the pre scientific era and on the role of ancient medical 16 Sir Thomas Watson, Lectures on the Principles and Practice of Physic: Delivered at King’s College London (London: J ohn W. Parker, 1843), 423 430. Watson goes on to say, “Whenever puerperal fever is rife, or w hen a practitioner has attended any one instance of it, he should use most diligent ablution; he should even wash his hands with some disinfecting fluid, a weak solution of chlorine for instance: he should avoid going in the same dress to any other of his midwifery patients: in short, he should take all those precautions which, when the danger is understood, common sense will suggest, against his clothes or his body becom ing a vehicle of contagion and death between one patient and another. … In these days of ready invention, a glove, I think, might be devised, which should be impervious to fluids, and yet so thin and pliant as not to interfere materially with the delicate sense of touch required in these manipulations. One such glove, if such shall ever be fabricated and adopted, might well be sacrificed to the safety of the mo ther in every labour.” His suggestion of hand w ashing in a chlorinated disinfecting solution was m ade at least four years before Semmelw eis, yet he is rarely given credit for it. It was not until 1890 that sterilized medical gloves were first used in surgery. 17 Robert Storrs, Esq., “On the Contagious Effects of Puerperal Fever on the Male Subject; or on Persons Not Child Bearing,” Provincial Medical and Surgical Journal 9 no.19 (1845): 289 293.


13 assumptions that were still current in the eighteenth and nineteenth centuries. Even those historians, such as Wootton and Carter, who address the problem of a reliance on ancient med icine, still do not adequately anal yz e issues of reasoning and language. This study attempts to fill that void. Thomas Kuhn is not known for work related to puerperal fever, but his influence on the subject of theory formation and its relationship to the i ntellectual environment is extremely important. Starting with the publication of The Structure of Scientific Revolutions in 1962, Kuhn became a very influential thinker in science, including both “hard” and social sciences, as well as the philosophy of sci ence and logic. 18 His concept of the paradigm shift, describing the abrupt replacement of long held assumptions and theories with new “paradigms” became a dominant area of study and debate over the past fifty ye ars. His basic argument is that scientific pro gress is not smooth and linear but is instead characterized by long periods of steady accumulative scientific work under an accepted set of assumptions. Eventually this accepted “paradigm” becomes unable to accommodate the discovery of incompatible data, f orcing an abrupt overthrow of the old intellectual framework, and the relativel y r apid adoption of a new intellectual framework under which to work. He emphasized that each paradigm is both a guide to assist in gathering new information and a limiting fac tor, circumscribing those who work within it to understand data onl y a s the paradigm allows. This appeared to man y t o be a form of relativism, a charge that Kuhn discussed and rejected. Although bey ond the scope of this paper, the transition from the humou ral framework to germ theory marks just the sort of dy namic tha t Kuhn anal yzed and would be a fruitful topic for future historical w ork. 18 Thomas Kuhn, The Structure of Scientific Revolutions (Chicago, The University of Chicago Press, 1962).


14 Etiology, Symptomology, Statistics To better understand puerperal fever’s role in the history of medicine, it is im portant to understand what is now known about this disease : what causes it, how it progresses through the body and how it can be treated. With the benefit of hindsight, historians today can use this knowledge to understand the paraly zing confusion about t his disease that lasted well into the twentieth century Puerperal fever is a serious bacterial infection that can develop into puerperal sepsis as the infection spreads into a woman’s blood stream. Depending on the pathogenic organism at fault and on how far the infection has progresse d before treatment, puerperal fever can be fatal. Unfortunately, a great variet y of organisms can cause puerperal fever and the virulence of the strains varies from year to year. This creates difficulties in interpreting the statistics of maternal deaths attributed to puerperal fever. Nevertheless, this data, when properl y r ecorded, reveals cy clical pattern s of maternal morbidity due to epidemic puerperal fever. 19 The majority of the organisms responsible for causing puerpera l fever, and all of those responsible for causing epidemic puerperal fever, are not normall y fo und in the 19 Irvine Loudon, The Tragedy of Childbed Fever 155. T his cyclical pattern shows that, periodically, the active strains of the organisms which cause puerperal fever became especially virulent. These more tenacious strains were more likely to be spread to puerperal patients and, when infected, these patients w ere mo re likely to die. Carefully kept statistics in lying in hospitals throughout Europe show that, for certain years, epidemics of puerperal fever claimed an unusually high number of women’s lives. How ever, after a time, the bacterial strains w ould retur n to a normal, low ly ing level of virulence and the epidemics would stop. Puerperal fever cases w ould continue but more sporadically and more often resulting in recovery. This pattern often led doctors to suppose that treatments they had used to combat the epidem ic had eventually proved successful, when in actuality, the statistics were cyclical irrespective of treatment.


15 vaginal tract of l yi ng in women. They are introduced from an outside source. Directly after birth, the womb is particularl y vulnerable to infection. A number of factors coalesce to create an environment wherein the woman’s reproductive tract is temporarily unprotected against pathogens. First, the normal acidity of the vaginal secretions is rendered neutral during the birth process. Second, the cervix i s widened and shortened, allowing accessibility to the uterus. Third, the endometrium, the inner lining of the uterus, which constitutes a natural, antibacterial barrier, is stripped away Fourth, placental separation creates a particularl y abraded surface Fifth, blood vessels of the uterus are exposed creating an environment ripe for septicemia. 20 A number of pathogenic organisms can cause puerperal fever: Groups A, B, C, D, and G Streptococci, Staphy lococci coliform bacteria, anaerobic bacteria, Chlam ydia, my copla sm a and very rarely Clostridium welchii. Some have argued that fecal contamination can cause E. coli infections and that even normal vaginal flora can become infective in this opportune environment. 21 However, the attention of medical histori ans has alway s been on the Group A beta hemoly tic Streptococcus, abbreviated GAS, which is thought to have been the primary cause of puerperal fever epidemics throughout history There are man y di fferent strains of GAS, but all hemoly tic streptococci are aerobic bacteria, that is, they grow in the presence of oxy gen. Their eas y communicability comes from the fact that they can live for a surprisingl y l ong time in the 20 Ibid., 7 ; Gail Pat Parsons, “Puerperal Fever, Anticontagionists, and Miasmatic Infection, ” 425. 21 Parsons, “Puerperal Fever, Anticont agionists, and Miasmatic Infection,” 8, 11 ; Edw ard Shorter, Women’s Bodies: A Social History of Women’s Encounter with Health, Ill Health, and Medicine (New Brunswick, NJ: Transaction Publishers, 1991), 127 128.


16 open air without losing their virulence. 22 While less deadl y s trains of GAS are common caus es of skin infections, the more dangerous strains, such as Streptococcus py ogenes, attack the throat. The problem with this strain of bacteria, particularly for birth attendants, is that Streptococcus p yo genes is regularly found in the human nasophary nx (t he upper area of the throat which lies behind the nose). It may be communicated to the vaginal tract b y t he hands of the attendants, an y f amily members present, particularly children, or even b y t he mother herself. 23 In addition to being a major cause of ep idemic puerperal fever, Streptococci are also responsible for impetigo, scarlet fever, “inflammatory or malignant sore throat” and er ys ipelas an infection of the skin which was often seen in tandem with epidemics of puerperal fever. 24 The sy mptomology of puerperal fever is surprisingl y predictable if the infection arises from GAS organisms. Within the first to the third post partum day an increasing tenderness begins in the lower abdomen as the infection begins to invade the tissues of the uterus. The inf ective organisms begin to multiply in this oxy genated blood rich environment. From here, they may move into the peritoneal cavity of the abdomen causing peritonitis evinced by severe pain, nausea, diarrhea, and fever. Shallow, quick breaths are a response to the pain of a full breath as the diaphragm presses against the stomach. As the infection slowly necrotizes the tissues, gasses are given off that distend and harden the bell y. In advanced stages, extremely virulent strains will move into the 22 Shorter, Women’s Bodies 117. 23 Parsons “Puerperal Fever, Anticontagionists, and Miasmatic Infection,” 425. 24 D. B. Stew art and J. G. Williams, “Bleeding and Purging: A Cure for Puerperal Fever?” Journal of Hospital Infection 34 (1996): 85. Referring to a paper read to the Medico Chirurgical Society of Edinburgh on November 12, 1845 by Dr. Peddie, reprinted in the Provincial Medical and Surgical Journal, edited by Robert J. N. Streeten (London: John Churchill, 1846), Dr. Gairdner notes on page 234, “It was also rem arked, that almost every ind ividual who had visited at Mrs. K.’s during her illness, complained soon afterwards of one kind or another, particularly with slight feverishness and sore throat; and it w as at this time that Dr. Peddie himself became affected in the same way.”


17 blood strea m causing an overall septicemia. The ominous chills associated with the onset of epidemic puerperal fever are a direct result of this blood poisoning. 25 The rapid decline of infected patients, as described in eighteenth and nineteenth century treatises o n puerperal fever, was predictable and heartbreaking. “The patient is immediately seized with the strongest apprehension of her danger, and labors under vast anxiety her countenance shewing (sic) indubitable marks of the great suffering both of body and m ind.” 26 “The whole features, indicate anxiety if not terror, and great debility …The secretion of milk stops, and the patient inquires very seldom about the child.” 27 “…there is vast prostration of strength with anxiety depression of spirits, a disinclinati on to suckle, carelessness about her child, and watchfulness… an indifference to all external objects, denotes certain and speed y death.” 28 According to Alexander Gordon, a telltale final symptom of puerperal fever was a sudden cessation of pain. Often misr ead as a sign of recovery b y relieved famil y m embers, Gordon explains that this was in actuality a sign that the tissues have necrotized and was the announcement of approaching death. 29 When fatal, most puerperal fever victims succumbed during the first w eek following delivery 30 It was a horribly painful way to die and women in childbed, as 25 Parsons, “Puerperal Fever, Anticontagionists, and Miasmatic Infection,” 438. 26 Thomas Denman, Essays on the Puerperal Fever, and on Puerperal Convulsions (London: J. Walter, 1768), 10. 27 John Burns, The Principles of Midwifer y (London: Longman, Orme, Brown, Gree n, & Longmans, 1837), 599, 600. 28 Thomas, The Modern Practice of Physic 934, 936. 29 Alexander Gordon, A Treatise on the Epidemic Puerperal Fever of Aberdeen 12 13. Th is strange symptom was also mentioned by Thomas in The Modern Practice of Physic 925, 929, 936 and C. H. F. Routh, “On the Causes of the Endemic Puerperal Fever of Vienna,” Medico Chirurgical Transactions 32 (1849), reprinted in The Edinburgh Medical and Surgical Journal 75 (1851), states on page 249, “ The pain generally disappeared an hou r before death; the face gradually assuming a more sallowish, yellow, and cadaveric expression.” 30 Meigs, Obstetrics: The Science and the Art, states, “The progress of puerperal fever is sometimes so very rapid, particularly in warm climates and hot season s, as to destroy the patient in forty eight hours. Even in cases seemingly the most favourable, w e should look on the event as doubtful, as the complaint is apt to be


18 well as their birth attendants, were extremel y f earful of this disease and sought every possible way to avoid it. 31 Unfortunatel y, the risk of developing a fatal infect ion was inescapable for the majority of women. Edward Shorter has stated in his book, Wo men’s Bodies that during the era of traditional midwifery four percent of women were likel y t o contract a serious post partum infection. He argues that if the average woma n in this historical period were to survive to age fort y five, she would likely give birth six times. Using these average estimates, Shorter calculates the lifetime risk of these women to be twenty five percent. This means that a woman in this environm ent had a one in four chance of contracting a potentially lethal case of puerperal fever at some point during her reproductive years. 32 However, puerperal fever statistics are difficult to evaluate. Records were not carefully kept in home deliveries and pr ivate practice; even in hospitals the numbers are often suspect. Differences of opinion amongst doctors of this period on what constituted puerperal fever have led some to believe the number of cases has been underestimated. Many puerperal fever deaths wer e also likely to have been misdiagnosed as enteritis or pneumonia. 33 Some have even accused hospitals of intentionally mislabeling the cause of death to hide the high incidence of epidemic mortality 34 accompanied with delusive remissions; and indication arise in its progress which are by n o m eans equal to the danger.” 935 6. 31 Denman, Essays on the Puerperal Fever, and on Puerperal Convulsions, states on page 20, “A disease in which the dangerous symptoms come on with such impetuosity, and where the event is very often fatal, could not fai l to alarm every man solicitous for the welfare of his patient. His anxiety would be increased by the want of a distinct history of the disease; and experience w ould convince him that the method of cure, generally directed, w as not to be depended upon.” 32 Shorter, Women’s Bodies 108. 33 Ibid., 106. 34 Loudon, The Tragedy of Childbed Fever 191.


19 The best statistics that can be offered, taking into a ccount these limitations indicate that in the eighteenth and nineteenth centuries, approximately six to nine cases of sporadic puerperal fever were found in one thousand deliveries. Less than half of these cases terminated fatall y. During puerperal fever epidemics, the number of cases sky rocketed and the mortality rate grew toward eight y percent. 35 It is estimated that between a quarter and a half a million women died from puerperal fever in the eighteenth and nineteenth centuries in England and Wales alone 36 Helpless in the face of this staggering mortality rate, at least one British physician told his students, Of those attacked b y t his disease, treat them in an y manner you will, at least three out of four will die. Upon examining the bodies, the uterus the viscera, and every other part of the abdomen are found to be inflamed. There is a quantity of purulent matter in the cavity of the abdomen, and the intestines are all glued together. We tried various methods, (bleeding, refrigerants, stimulants, mithridate,) but every thing failed. 37 35 David Wootton, 211 ; Christine Hallett, “The Attempt to Understand Puerperal Fever ,” 1 ; Loudon, The Tragedy of Childbed Fever 190. 36 Loudon, The Tragedy of Child bed Fever 6. 37 Robert Gooch, An Account of Some of the Most Important Diseases Peculiar to Women (London: John Murray, 1831), 9. Burns, The Principles of Midwifer y, also states on pages 602 603, “With regard to the best mode of treatment, there has been a great difference of opinion, which partly depends, on giving the name of puerperal fever, to different disorders. I am sorry that I find it much easier to say, what remedies have failed, than what have done good.”


20 Early Accounts Historical interest in puerperal fever has centered primarily on the eighteenth and nineteenth centuries. However, the disease can be found in ancient Greek and Hindu medical texts dating back a s far as 1500 BC. These texts refer to a potentially fatal fever in women who had just given birth and some, including one b y t he Greek phy sician Soranus, provide advice to birth attendants on proper h ygi ene, leading some to suggest that these early writer s may have recognized the role that birth attendants play ed in spreading infection. 38 The well known story of Dromeades in Athens in the fifth century B.C. could have easily been written two thousand y ears later. It described how Dromeades’ wife, after bi rthing a daughter, came down with chills and a high fever on the second day after delivery Her s ym ptoms included abdominal pain, irregular breathing, and thick, muddy urine. On the sixth day her body wracked with spasms and delirious, she died. The descr iption of her illness and the care with which the author recorded each sy mptom has led historians to confidently conclude that, not only was this puerperal fever, but that these sy mptoms were recognized as being a frequent complication of labor and deliver y in the ancient world. 39 38 Caroline M. De Costa, “The Contagiousn ess of Childbed Fever: A Short History of Puerperal Sepsis and its Treatment,” The Medical Journal of Australia 177 no. 11/12 (2002): 668. 39 Shorter, Women’s Bodies, 103.


21 An Alsatian proverb states that “heaven stay s open nine day s for the woman in childbed.” 40 According to Edward Shorter, this refers to the realization that puerperal fever s ym ptoms may not surface for a few day s after delivery and the hope that, if the mother did not show signs of infection b y t his time, she had likely escaped the disease. Shorter also describes a Sty rian belief that “if one woman dies in childbed, so must two others also die soon afterward.” 41 He argues that this sa yi ng alludes to the communicability of the disease. Despite the ease with which we find references to post partum infections throughout the ancient and medieval periods, it was not until the seventeenth century that the scope of the disease became clear. And it was no t until 1716 that the term “puerperal fever” was coined in Edward Strother’s Criticon F ebrium 42 Until this time, the disease was termed “the weed” or “milk fever.” It was assumed that a mother’s milk originated in the blood and that the fever accompanied the milk when it left the blood and entered the woman’s breasts. 43 Indeed, throughout the e arl y m odern period, popular and medical characterizations of “milk fever” described it as a normal part of the birth process which resolved itself within a few day s. 44 Still, it was also recognized that this “normal” fever could turn deadl y and take the life of the mother. Apparentl y, a baseline infection rate of 40 Ibid., 104. 41 Ibid. 42 Loudon, The Tragedy of Childbed Fever, 15. Edw ard Strother, C riticon Febrium: Or, A Critical Essay on Fevers; with the Diagnosticks and Methods of Cure, in all the different species of them (London: Charles Rivington, 1718), 169, 194, 203, 212. 43 Ibid. 18 9 ; Shorter, Women’s Bodies, 105. How ever, Denman, Essays o n the Puerperal Fever, and on Puerperal Convulsions, states on pages 15 16, “This fever is easily distinguished from the febrile disturbance, occasioned by the milk, if it comes on at the time the milk is expected, by the symptoms before mentioned, and by the flaccidity of the breasts; yet the consent between these and the uterus is so intimate, and the transition of the humours from one to the other so instantaneous, that an excuse may be readily accepted for those who have mixed diseases, in some respects similar, yet essentially different.” 44 Shorter, Women’s Bodies, 105.


22 the less virulent bacteria that cause puerperal fever was ubiquitous in the population. Occasion all y, more virulent strains produced fatal effects as the local uterine infection spread to produce peritonitis and septicemia. Despite these sporadic descriptions of post partum fevers, very few tracts on fevers in puerperal women were published in Brita in before 1760. 45 However, an epidemic of puerperal fever at the British Lying in Hospital in that y ear generated a flurry of interest in the medical community 46 Throughout the late eighteenth and early nineteenth centuries, many medical practitioners began publishing descriptions of puerperal fever cases they had attended, h ypothesizing on the cause of the disease and recommending various methods of treatment. By 1860, an “extensive sy nthesis of knowledge” had been offered for the consideration of the medic al community on what had, by then, become a fearful scourge to medical practitioners and their parturient patients. 47 Unfortunatel y, this abundance of new data was forced into the same old categories. L ittle had changed in models of disease causation from c lassical to m odern 45 Hallett, “The Attempt to U nderstand Puerperal Fever,” 2. Before the creation of lying in hospitals in the seventeenth century, women gave birth at home. The low incidence of maternal death in the e arly m odern period can be traced to the fact that the majority of puerperal infections would be caused by infective organisms within the mother’s normal environment. It has been argued that women have a higher resistance to pathogens found in their own homes to which they are routinely exposed. Therefore, the mortality rate of hom e births attributed to puerperal fever was almost always low er than found in the hospital environment. Som e historians argue that the rise in puerperal fever deaths c an be directly correlated to the transition from traditional midwifery to obstetrics dominated by male doctors. The statistics are not available to prove this assertion, but it is highly unlikely that general practitioners were more or less likely to sprea d puerperal fever than midwives in a home delivery setting. It w as in the hospitals, that epidemic puerperal fever ranged out of control and inflated the mortality statistics. 46 Ibid. The first epidemic of puerperal fever w as recorded in 1646 at the Htel Dieu, a maternity hospital in Paris John Leake, Practical Observations on the Child Bed Fever: Also on the Nature and Treatment of Uterine Haemorrages, Convulsions, and such other Acute Diseases As are most fatal to Women during the State of Pregnancy (Lo ndon: R. Baldw in, 1775), states on page 234, that tw enty fo ur wo men died in the London epidemic betw een the 12 th of June and the end of December. London lying in hospitals had apparently never seen such mortality, but epidemics such as these soon began to recur frequently in Britain and on the Continent. 47 Ibid., 3.


23 times. Many of the same basic tenets of a ncient medicine were still held to be true, though they were often disguised in m odern metaphor. In the pre scientific world, the assumption was that there was an absolute truth to be found, one t hat no data would ever contradict. People were taught, often from ancient texts, that understanding these received final words about a subject was the key to operating in that realm. This attitude toward knowledge had powerful consequences. If it appeared that some discovery was incompatible with a “true” theory either the data had to be wrong or the phy sicians were somehow misunderstanding the implications of how the theory would manifest itself in actual cases.


24 Humoural Theory : Hippocrates and Ga len The humoural theory put forth by the Hippocratic school in ancient Greece, was based on four cardinal humours that were thought to exist in every individual at vary ing levels, dependent upon the person’s disposition. These humours included blood, ph legm, choler or yellow bile, and melanchol y or black bile. A delicate balance of these four humours existed within each individual body as a whole and within each body part. The levels of these humours established mental and physical health as well as dete rmining the individual’s personality Any imbalance of these humours would cause suffering in the form of ph ys ical disease or mental anguish. Hippocratic writings spent a great deal of time describing how diet and lifesty le contribute to healthy or unhealt hy habits and dispositions. Treatment of these conditions involved making changes that would bring the humours back to their natural balance. 48 The Roman phy sician Galen of Pergamon went one step further. His description of anatom y was based on the dissec tion of monkey s, as human dissections were still taboo, but he was able to expand upon the humoural theory and advocate more elaborate treatments of disease. He correlated the four humours to the four elements: blood with warm, moist air; phlegm with cold, moist water; yellow bile with warm, dry fire; and black bile with cold, dry earth. He then used treatments that corresponded with these properties to influence the humours within the body appl yi ng medicines with the 48 Joan Lane, A Social History of Medicine: Health, Healing, and Disease in England, 1750 1950 (London : Routledge, 2001), 2.


25 opposite warm/cold, moist/dry comb ination of whatever humour was overly dominant. 49 This primitive notion harkens back to the pre Socratic thinkers, especially Anaximenes, in the century before Hippocrates and their attempts to explain all nature by reducing it to a few primary substances a nd then account for the motion of these substances as a product of the constant pull of opposites. 50 Galen staunchl y defended and promoted the treatment of venesection, or bloodletting, for disease. Venesection involved making an incision in a vein and allo wing the venereal blood to flow out of the body This treatment was based on the belief that black bile was “not a pure liquid, but one that darkens other liquids, producing states of suffering.” 51 The venereal blood, lacking ox ygen, is much darker than art erial blood. Galen also compiled lists of medicinal preparations which contained a variety of ingredients “from which the body would select what the disease required.” 52 Unfortunatel y, the cornerstone of Hippocrates’ humoural theory was a reliance on data that was, in principle, unobservable. It y ielded explanations with no test implications. As humo u rs were characterized in most versions of the theory, including the mechanistic variation, one could not correlate humo u rs with sy mptoms because humo u rs were q uasi phy sical. Since one could not observe the phenomena in question, such as levels of humoural imbalance, it was impossible to single out causal agents. If, for example, a phy sician postulated that puerperal fever was produced b y cold weather – an assert ion that could be easily tested – then an investigation could be conducted to 49 Ibid. 50 Geoffrey Stephen Kirk, John Earle Raven, and Malcolm Schofi eld, The Presocratic Philosophers: A Critical History with a Selection of Texts (Cambridge, UK : Cambridge University Press, 1983). 51 Michael Worton and Nana Wilson Tagoe, National Healths: Gender, Sexuality, and Health in a Cross Cultural Context (London : UCL Press; Cavendish Publishers, 2004), 10. 52 Lane, A Social History of Medicine 2.


26 ascertain whether the incidence of the disease was less in warm weather. If, on the other hand, one said that an excess of a given humor caused disease X when it was impossible t o measure said humor, one was forced to assume that this humor was present in those that had the disease, i.e. that it was a necessary condition for the disease to occur. At this point, the humor is no longer a cause of the disease but one of its defining characteristics. Lacking an y m eans, even theoretical, to remove the humor to see if the disease could still thrive, the humor becomes an unquestioned characteristic of the disease and not a cause. It has covertl y become part of the disease’s definition. T here is nothing that could be examined or measured that would count for or against that explanation. Another aspect of a humour’s unobservability was that, in many of its formulations, a humour was characterized as internally generated b y ill defined proce sses, independent of external influences. Insofar as it was thought that puerperal fever could be internally generated, an y new data was undermined b y t he fact that phy sicians believed that external factors could not be the “true” cause of the disease as l ong as a significant portion of the disease might have been spontaneousl y gen erated within the patient. This undermined the creation of effective prevention programs since it was assumed b y ph ys icians that no preventative treatment, no matter how well it m ay have worked in an y one instance, was likel y t o stop another incidence of the same disease. 53 53 Ignaz Semmelweis, The Etiology, Concept, and Prophylaxis of Childbed Fever. This w as an obvious flaw in the work of Ignaz Semmelweis as he used the category of “spontan eous auto infection” to explain any residual cases that occurred after he had implemented his hand w ashing technique in the Allgemeines Krankenhaus. Semmelweis was also unable to account for the large number of cases that occurred in home deliveries in Bri tain with no possible connection to post mo rtem dissections. Because Semmelweis had specifically argued that an introduction of “animal organic matter” from these dissections w as the ultimate cause of puerperal fever, he was forced to resort to “spontaneou s auto infection” to explain away the contradictions in his theory.


27 Miasma Theory : The Persistent Dead End Another subtle yet powerful element undermining a physician’s ability to make sense of infectious disease was the curious theory of miasmas. Miasma theory like humoural theory was another popular view of disease causation that had its roots in a ncient Greece. Less a formal theory than an ongoing accumulation of conjectures, this view held that foul smelling air or s ome noxious quality of the atmosphere was responsible for causing disease. Revived during the m iddle a ges, it was thought to be capable of causing almost any infectious disease and was used to explain all epidemics. 54 This theory was based on the observat ion that rotting items smelled bad. Ergo, smelly items must be rotting. It was also understood that coming into contact with rotting substances, eating rotting meat or coming into close contact with animal and human wastes for example, caused people to bec ome violently ill. These observations gave rise to the theory that the decomposition of organic matter gave off foul smelling air that could, in turn, cause disease. Throughout the e arl y m odern period, regional governments circulated letters decry ing prac tices, such as the keeping of pigs and silkworms within certain residential areas and of the overflow of ill managed cesspits because the stench would spread disease. 55 The odiferous particles entering the air were referred to, in the m odern period, 54 Lindemann, Medicine and Society in Early Modern Europe 179 184. 55 Carlo M. Cipolla, Miasmas and Disease: Public Health and the Environment in the Pre Industrial Age (Essex, UK: Yale University Press, 1992), 10.


28 as “pu trid effluvium.” 56 Overcrowding in urban areas, hospitals, jails, etc. were recognized as producing infectious diseases. These environmentall y produced diseases were explained using the miasmatic theory and fevers, in particular, that were spread b y miasma were seen as routinely infectious. 57 In fact, the term “epidemic” at this time did not necessaril y imply a large number of cases. Epidemics were diseases that were caused by “atmospheric, cosmic, or terrestrial influences” and could just as easily have bee n an epidemic involving onl y one patient. 58 It was the environment that created the conditions under which an epidemic could take place. This disease model helped to explain why diseases were often local occurrences and wh y m any epidemics were seasonal. The “epidemic constitution” helped to explain why all people within a given area, and under the same atmospheric influence, did not get sick. Onl y t hose with certain predispositional factors would have their humours altered b y t he atmospheric influence. 59 The notion, used b y m any phy sicians, that there was such a thing as a “ pre disposition” to contracting puerperal fever, or any other disease, proved to be a 56 Hallett, “The Attempt to Understand Puerperal Fever,” 3, 11 12. 57 Ibid., 13. 58 Ignaz Semmelweis, The Etiology, Concept, and Prophylaxis of Childbed Fever 86 ; Carter, “Semmelweis and His Predecessors,” 65. Samuel Kneeland, “On the Contagiousness of Puerperal Fever,” The American Journal of Medical Science 11 (1846), states on page 49, “Another point which has much confused this question is the vague signification of the word ‘epidemic,’ which by many is understood as im plyin g some mysterious quality of a disease, in virtue of which it attacks a great number of individuals… — Again, a disease is said to be ‘epidemic,’ when its propagation is attributed to a morbific principle contained in the air. Strictly speaking, the term ‘ep idem ic’ implies a number of patients that such an affection is judged to be epidemic ; and it is also by the epidemic quality attributed to the affection that the number of patients is explained — here, then, is a circle of confusion, in which the cause becom es the effect, and the effect the cause, according to the will or caprice of the observer.” 59 Thomas, The Modern Practice of Physic, states on pages 932 933, “Some have been accustomed to look on [puerperal fever] as only a simple modification of the known species of fever, taking its origin from the leaven of the prevailing epidemic constitution, whether inflammatory or putrid, modified by the habit of body, the mode of living, the age and temperament of the patient, the preceding causes, the season of the year, and temperature of the air, &c.”


29 powerful impediment to understanding the causal framework of disease. Ty pically a doctor would have a clear notion of several causal factors that produced the disease but no way of explain ing why its e ffect was not universal. Thus they created the notion that some patients had a pre disposition for the disease and that they and onl y t hey would contract the illness when exposed to the other causative agents. The logic of this is clearly defective. If one asserts that a given ailment is caused by X Y and Z in onl y t hose patients “ pre di sposed” to getting the disease, they are at best, say ing that there i s another cause for the disease. Even more troublesome: If one has no independent way of determining which potential patients have such a pre disposition, the n the pre disposition becomes part of the definition of the disease. Patients with puerperal fever, a priori have the disposition, those without puerperal fever, do not. This renders the concept of the “ pre disposition” logically incapable of explaining the ailment, or of assisting in the discovery and anal ys is of its true cause. It creates a dead end for those who use the concept, covertly characterizing the disease as inherentl y m ys terious and unsolvable. Miasmatic theory has often been incorrectly regarded as leading ph ys icians toward a theory of droplet infection wherein disease could be transmitt ed through the air. But in the writings describing miasmas as the cause of disease, there were no references to particles transferring diseases through the atmosphere; miasmas were instead characterized as: “poisonous vapors,” “foul air,” and “morbid influ ences,” often attributed to astrological influence, “mineral exha lations,” “fermenting vegetable fluids,”


30 etc. 60 Li ke humours, miasmas were not a useful method of explanation because a miasma was not observable. Although it was sometimes spoken of as margin ally tangible, much like a foul smelling air, it was more commonl y described in more abstract terms of noxious influences. As such, the miasma often took on the character of a supernatural entity powerful yet hidden and yielding no possible methods by whi ch to isolate, and thereb y t est, its effects. This spirit like “influence” represented a dead end for an y i nquiry into disease. If it could not be isolated and identified then it could be invoked as the cause of an yt hing and no data could be relevant to th e claim. 60 G. Motherby, A New Medical Dictionary; or, General Repository of Physic ( London: J. Johnson, 1775), 257.


31 Medical Education: The Resilience of a Dogma The tenets of this a ncient, “ c lassical” worldview were fundamental to eighteenth century medical education. Such an education included extensive study of Hippocrates and Galen who, despite their ancient origin s were still regarded as the foundation of eighteenth century medicine. Discussing the Oxford curriculum, M. D. W arren quotes Dr. Campbell Hone as writing, …the licenses for the practice of medicine and surgery were issued b y t he Universit y without an y a dequate inquiries as to the qualifications of applicatio n, and the requirements for the degree of Bachelor of Medicine were meagre indeed. The candidate must have taken his M.A., have spent three years in medicine and attended lectures of th e Regius Professor on Hip pocrates and Galen twice a week.. .The D.M. degree could not be taken till four years after the B.M. degree, and during those four years the candidate had to attend the lectures of the Regius Professor and also to give three or four lectures himself on Galen. 61 University education, even one specializing in medicine, was primaril y grounded in classical learning, particularly in Latin and Greek. Hippocrates furnished the primary metaphor of humoural based health; Galen promoted bloodl etting as a primary treatment to reestablish humoural balance. Neither seriously considered the idea of contagion, instead arguing that environmental factors bred disease which prey ed upon individuals with certain predisposing factors. 62 Their combined doct rines were so pervasive that they formed a powerful intellectual roadblock to medical advances in the eighteenth century 61 Warren, M. D. “Medical Education During the Eighteenth Century.” Post Graduate Medical Journal 27 (1951): 306. 62 Lindemann, Medicine and Society in Early Modern Europe 9 17.


32 This encouraged ad hoc interpretations of the humoural theory An ad hoc hy pothesis is a fallacious technique whereby an established idea is saved in the face of fundamentall y i ncompatible data, data that would normally mark the overthrow of the theory In its purest case, it takes the form of a new hy pothesis, added to an established theory after an apparently conflicting piece of dat a is discovered. The new ad hoc hy pothesis claims that the established theory is now compatible with this new data. Until the data was discovered it was not previously thought to be a consequent of the theory Perhaps it was even thought to be a falsify i ng instance of that theory but in order to save the theory the ad hoc hy pothesis extends the theory to include the otherwise negative discovery The effect is to “save” but seriously weaken it. If the theory can accommodate discoveries that had been thoug ht to falsify it, little of the original theory ’s explanatory power will remain. For contemporary scientists, it is an error of logic, but to phy sicians of the period, working before the details of scientific logic had been developed, it was a way to subsu me newly discovered data within the a ncient humoural theory a theory they were not y et inclined to fundamentally challenge. The ad hoc adjustment was often presented as an advance and was couched in the language of newl y developed metaphors, utilizing the “vocabulary of machine culture,” to describe how Hippocratic and Galenic principles could still be considered true and their attendant treatments valid. 63 M odern medical treatises on puerperal fever reveal how man y models of disease causation continued to be influenced b y t he classical, Hippocratic and Galenic worldview, while being expressed in the emerging m odern, technical language of mechanism 63 Erin O’Connor, Raw Material (Durham : Duke University Press, 2000), 10.


33 Mechanism : A New Metaphor While miasmas were openly blamed for causing disease well into the nineteenth century the humoural theory maintained its hold on medical discourse in a more obscure fashion. Scientific advancement in biology in the e arl y m odern period had begun to chip away at the foundation of the humoural theory For example, William Harvey ’s des cription of the circulation of the blood in 1628 directly refuted Galen’s justification for bloodletting as, in a closed circulatory s ys tem, there was in fact no difference between venous and arterial blood. The ancient s were sure that blood was fundamenta l to human life, but its source, pathway and exact function eluded them. The humo u ral theory by the time it was espoused b y Galen, maintained that there were two kinds of blood, arterial and venous, each following a separate path. Arterial blood was cont inually produced b y t he heart, flowed through the bod y and was consumed b y t he organs. Venous blood followed a similar path: only its source, the liver, was different. The lungs were though t to cool the blood. This theory was so entrenched, and portions of it so old, that it had achi e ved iconic status and was, for many an unchallengeable maxim. William Harvey a man who did the most to undermine this sy stem noted, We are too much in the habit, neglecting things, of worshipping specious names. The word b lood, signify ing a substance, which we have before our ey es, and can tou c h, has nothing of grandiloquence about it; but before such titles as spirits, and


34 calidum inaatum or innate heat, we stand agape. But the mask removed, as the error disappears, so doe s the idle admiration. 64 Harvey ’s arguments and conclusions, derived from meticulous dissections and observations, were carefully presented in 1628 in a small volume titled De Motu Cordis ( On the Motion of the Heart and Blood). After evaluating several cha racterizations of the bloodstream popular a t the time, some of which Harve y t raced back to Galen himself, Harvey revealed his empirical and experimental data to show that such theories were unworkable. For example, based on his measurements of the heart ra te and the amount of blood it pushed out with each stroke, if estimated at one ounce, the heart, were it the source of all arterial blood, would need to produce 166 pounds of blood per hour. 65 His solution was that the bloodstream was a sin gle, circulating, closed loop sy stem. There could be no good blood or bad blood because all blood flowed through the same sy stem. This was a demonstrable conclusion, drawn on publicall y av ailable observations. It was all, in the spirit of the new m echanism, entirel y ph ys ic al. Given the near sacred status of the sy stem it overthrew Harvey ’s conclusions faced only modest opposition and were widely adopted. Harvey ’s insights came at an auspicious time, for the next century erupted with new knowledge about fluids and their be havior. Fascination with hy draulics was about to begin. Within twenty ye ars of Harvey ’s publication Evangelista To rricelli invented the barometer enabling precise measurement of atmospheric pressures. In 1661, Christi a an 64 William Harvey, “On Generation,” in The Works of William Harvey, M.D.: Physician to the King, Professor of An atomy and Surgery to the College of Physicians trans. Robert Willis (London: C. and J. Adlard, 1847), 511. 65 William Harvey, “An Anatomical Disquisition on the Motion of the Heart and Blood in Animals,” in The Wo rks of William Harvey, M.D.: Physician to the King, Professor of Anatomy and Surgery to the College of Physicians trans. Robert Willis (London: C. and J. Adlard, 1847), 9 86.


35 Huy gens measured the elasticity of gases in 1676 Denis Papin developed the air pump and by 1728 Stephen Hales had devised the m eans to measure blood pressure. Finall y, in 1728, Daniel Bernoulli publishes his opus, Hydrodynamics 66 The se pioneers were discovering and developing the princip les which describe the behavior of fluids under pre ssure, in the open air, and traveling through tubes. The topic captured the imagination of inventors and ph ys icians alike and h ydraulics became t he new metaphor for understanding liquids, even in the human body With it, Hippocrates and Galen’s grip on the working s of the human body had been weakened, but not completely broken The father of the new “mechanism” was Rene Descartes. Descartes was a powerful mathematician – he invented analy tic geometry – and a philosopher who, more than an y other, presented an elaborate and carefully reasoned attempt to explain and justify a mechanical understanding of the universe, including the human body He argued that events in the phy sical world are exclusively a produ ct of matter in motion. As such, they are observable and, to the limits of our understanding, predictable. In Meditations on First Philosophy Descartes goes to considerable length to establish that the changeable, corporeal world is distinct from, and ope rates under a different set of principles than, the eternal, non corporeal world comprised of God, minds and souls. 67 To understand the ph ys ical world, he argues, we have a powerful tool, mathematics, which is itself eternal but can be applied to the tempor ar y i tems of the ph ys ical realm. 66 Bryan Bunch and Alexander Hellemans, The History of Science and Technology (New York: Houghton Mifflin Co., 2004), 187, 191 2,199, 215, 229. 67 Ren Descartes, Meditations on First Philosophy: With Selections from the Objections and Replies trans. John Cottingham (Cambridge, UK : Cambridge University Press, 1996).


36 His descriptions which isolated the human bod y f rom the soul supplied the foundation which made a scientific, experimental medicine possible Animals were purely phy sical, as was the human body Spiritual entities were n on phy sical. Only a human possessed both: a spiritual, eternal, non phy sical soul, and a phy sical, temporary body This hard “dualism,” the separation of things, including human beings, into distinct phy sical and non phy sical categories, had an important consequence for medicine. Descartes went so far as to argue that the human body was an automata albeit one with a soul. 68 But there was nothing about the bod y i tself that was not matter in motion. All of it was corporeal therefore all of it was observable. Humans had souls but they were separate and distinct and not an appropriate topic for medicine. The thinkers of the eighteenth century did not have a full y formed notion of experimental logic. Nor did they have the sophistication in hy pothesis creation a nd testing that we now call science. But, after Descartes, they did have a solid structure for understanding the human body without resorting to unobservable, spirit like entities in their explanations. While we find the primary literature full of physicia ns using the new mechanistic concepts the notion of non observable entities hung on tenaciously Knowing that the humoural theory had practical disadvantages, the medical establishment sought to rework the theory so that it would be compatible with recent scientific discoveries. The first attempt to create a m odern metaphor of disease causation came from this philosophical theory of mechanism. I n the early eighteenth century Hermann Boerhaave, began to incorporate Descartes’ mechanism into his description s of 68 Ren Descartes, “The Treatise on Man,” in The World and O ther Writings trans. Stephen Gaukroger (Cambridg e, UK : Cambridge University Press, 1998).


37 disease, particularl y fevers. 69 The scientific revolution and earl y i ndustrial revolution spurred an understanding of the bod y as a machine whose internal parts worked together in a mechanical sy stem of healthy operation. If parts of the machine wore o ut or broke, or if corrosive substances entered the s ys tem, disease would follow. Boe r haave’s work proved highl y influential Later writers on puerperal fever, and on fevers in general, were particularly influenced by the mechanistic metaphor of the circ ulatory sy stem as a fluid hy draulic device. By describing the circulatory sy stem in such a way humoural descriptions of imbalance could be understood as mechanistic descriptions of pressure. Any blockage in the h ydraulic valves would cause backups and dan gerous stagnation in the sy stem. Pressure would build to an unhealthy degree. Blood would pool and stagnate causing the liquids to putrefy 70 Thus, a return of this crucial sy stem to normal functioning would ensure that the body would heal itself, as long as the treatment was delivered before too much damage to the sy stem had occurred. Galen’s justification for the use of venesection may have lost its theoretical underpinnings, but phy sicians were still able to maintain, ad hoc the use of venesection as a popular treatment b y pointing out that it was a perfect way to relieve the pressure of inflammation and allow for the return of proper blood flow. 71 The 69 Hallett, “The Attempt to Understand Puerperal Fever,” 4 5. 70 Ibid., 4. 71 Thomas, The Modern Practice of Physic, states on pages 926 and 930, “By an early attention to the disease on its first approach, we may often subdue it, and prevent the inflammation from proceeding to any great height. Our immediate and speedy care ought, therefore, to be directed tow ards diminishing the quantity of the circulating fluids, and w eakening the action of the heart and arteries; and this is to be done by drawing blood from the system, regulating the quantity which we take away by the violence of the symptoms, the state of the pulse, and the age and habit of the patient…Such a decision will soon be justified by a greater freedom in the action of the arterial system, by an abatement of the languor, and by a dim inution of the pain and tenderness.”


38 mechanistic metaphor allowed the medical establishment to maintain their time honored traditions and ad miration of ancient icons while appearing modern and scientific. A number of conditions were posited as causing these blockages. According to her examination of eighteenth century documents on puerperal fever, Christine Hallett chronicles that stagnation of the blood, or of other important bodily fluids, was recognized as being caused by: … pressure, contortion, or erosion, acrid substances either taken as food, or applied externally severe cold, and contusions…any thing acrid which entered the blood vesse ls themselves and caused them to contract…an yt hing which caused the blood to ‘concrete or cohere’, such as ‘too great motion; a consumption of the thinner parts of the blood by sweat s, urine, spitting, or a diarrhoe a.’ 72 She also argues that it would have been eas y fo r this wide explanation of the man y causes of blockage, resulting in dangerous inflammation, to have led doctors to the realization that the natural course of pregnancy and delivery was likely to create the conditions under which blockages occ urred. 73 There was, therefore, argument in the eighteenth century over whether puerperal fever was, in fact, a disease of the bod y, or a natural consequence of childbirth that should be left alone to resolve itself. Perhaps due to the staggering figures of maternal mortality attributed to puerperal fever in the l yi ng in hospitals throughout Europe, the majority of the medical establishment decided to advocate for intervention. The central problem came down to what kind of intervention would be applied and t his was 72 Ibid. 73 Ibid., 7 8. Denman, Essays on the Puerperal Fever, and on Puerperal Convulsions, states on page 16, “Some constitutions are naturally subject to diseases proceeding from a redundancy of the quantity, or an exaltation of the quality of the bile; and that the secretion of that humor is much disturbed during gestation, we need no other p roof than the obstinate costiveness, or almost perpetual vomiting of bilious matter, with which many are afflicted at that time.”


39 dependent on whether a doctor supported a view of puerperal fever being fundamentally an inflammatory or a putrid disease.


40 Inflammation Theory : The Bleeding Continues If puerperal fever was primarily an inflammatory disease, then the mechani stic metaphor of circulatory distress would explain its disease process. Puerperal fever would be classified as a disease of the circulatory s ys tem, either of the blood’s composition or of its action within the vessels, and early “copious” bleeding would be prescribed as its cure. Inflammation theory, a bod y o f ideas centered on this pooling and resultant stagnation of blood, was essential to the eighteenth century understanding of puerperal fever and appeared in works by such preeminent authors as William Cullen, John L eake, Alexander Gordon, Thomas Denman, William Campbell, and John Clarke. 74 Treatments used under inflammation theory were based on the idea of “remote counter excitement.” With its theoretical foundation in humoural theory treatments such as bleeding and blistering ( also known as vesication, this treatment involved raising blisters on the patient’s skin) were thought to treat internal inflammation that doctor’s could not reach b y “ determining the inflammation to the external parts, and ther eb y lessening it on the in ternal ones,…” 75 “…the manifest utility of blistering near the part affected in inflammatory diseases leads us to think, that blistering, b y deriving to the 74 William Cullen, First Lines of the Practice of Physic (Edinburgh: Bell & Bradfute, 1796) ; John Leake, Practical Observation s on the Child Bed Fever ; Gordon, Epidemic Puerperal Fever of Aberdeen ; Thom as Denman, Essay on the Puerperal Fever (London: J. Cooper and J. Walter, 1773) ; Thomas Denman, Essays on the Puerperal Fever, and on Puerperal Convulsions ; William Campbell, A Treatise on the Epidemic Puerperal Fever: as it prevailed in Edinburgh in 1821 22 (Edinburgh: Bell & Bradfute, 1822) ; John Clarke, An Essay on the Epidemic Disease of Lying in Women, of the Years 1787 and 1788 (London: J. Johnson, 1788). 75 Thomas, The Mod ern Practice of Physic, 931


41 skin, and producing an effusion there, relaxes the spasm of the deeper sea ted vessels.” 76 Thus, b listering agents were used as counter irritants that somehow pulled the blood away from the areas of congestion thereb y relieving pressure in much the same way as did bleeding b y v enesection or the use of leeches As a theory which h ad the power to illuminate the development and progression of puerperal fever but also to validate a treatment that had ancient theoretical support, albeit one that required the employ ment of inaccurate assumptions, inflammation theory was held b y t he majo rit y of the medical establishment as puerperal fever’s most valuable explanatory theory both in practical and academic circles. 77 However, as a direct descendant of humoural theory this mechanistic classification would invite doctors to conceive of puerper al fever as a disease that was expected to behave in ways predicted b y that theory This fact elucidates the troubling underestimation of puerperal fever throughout the eighteenth century Putrid theory was the competing theory of disease causation in ei ghteenth century treatises on puerperal fever. It described diseases such as puerperal fever as being caused by an introduction or absorption of putrefy ing matter that would in turn create putrefaction in the tissues with which it came into contact. Putrid theory in the eighteenth century was formed as a practical application of miasmatic theory in diseases which involved bodily sy stems other than the respiratory sy stem. As miasmatic theory was initially fashioned to deal with illnesses that were thought to be taken in through 76 Encyclopaedia Britannica 11 (Edinburgh: A. Bell and C. Macfarquhar, 1797), 131 ; Robley Dunglison, A Dictionary of Medical Science (Philadelphia: Lea Brothers & Co., 1895), states on pages 148 149, “…a blister plaster…when ap plied to the skin, irritates it and occasions serous secretion, raising the epidermis and inducing vesicles, as canthar ides, mustard, ammonia, etc.” 77 Hallett, “The Attempt to Understand Puerperal Fever,” 4.


42 respiration, putrid theory explained how that process occurred within the body but also extended the theory to describe how the “putrid effluvium,” or other acrid substances which entered the bod y t hrough other means, would set off a c hain reaction of putrefaction. Putrid theory would lead to some scientific insights in the nineteenth century namely in I gnaz Semmelweis’ animal organic matter thesis, but in the eighteenth century it was little understood as any thing more than a mechan istic version of miasmatic theory albeit with a more extensive application. 78 As in the argument over whether inflammation was normal or not, doctors also speculated whether putrefaction arose as a disease process or was simply the body ’s attempt to get ri d of these poisonous substances. 79 While doctors advocated for a more inflammatory or a more putrid understanding of puerperal fever, most sat somewhere in the middle as it was still unclear as to whether the putrefy ing bodily tissues were a result of some kind of infection with acrid matter or if it was caused b y t he suppression or obstruction of fluids. 80 Eighteenth century treatises on puerperal fever were fixated on the question of which came first, the inflammation or the putrefaction. 78 Ignaz Semmelweis, The Etiology, Concept, and P rophylaxis of Childbed Fever 79 Hallett, “The Attempt to Understand Puerperal Fever,” 13 15. 80 Ibid., 11 13.


43 Pathology : New Techniques, Old Results The nineteenth century brought further confusion for doctors dealing with puerpe ral fever with the ideological shift in academics t oward the dominance of pathology 81 In an attempt to make the medical classroom more scientific, medical schools began using postmortem dissection to teach their students the ph ys iological changes that took place within the diseased bod y. The dissecting room became the new arena where students of medicine would learn about the disease processes that the mechanistic theory had uncovered. However, for doctors writing about puerperal fever, postmortem dissection became yet another avenue of divergence and disagreement. Those who postulated that the disease was fundamentally inflammatory began looking f or the beginnings of inflammation in the bodies of the mothers they dissected. 82 As the anal ys is of morbid structural changes was now the holy grail of nineteenth century science based medicine, the findings of these autopsies fueled further debate as to th e “seat” of the disease or where and how it originated in the body 83 Because puerperal fever is a bacteriological infection which ultimately leads to significant destruction of tissues, the ty pe of organism and the amount of damage done to the internal o rgans before the patient’s death would produce differing degrees of 81 Meigs, Obstetrics: The Science and the Art, refers to both the “library of this discreditable w arfare of opinions” on page 615 and the “scandalou s confusion in Medicine as to child bed fever” on page 617. 82 Hallett, “The Attempt to Understand Puerperal Fever,” 10 11. 83 Loudon, The Tragedy of Childbed Fever 15 20 ; Parsons, “British Medical Profession and Contagion Theory,” 139.


44 damage. 84 Nineteenth century treatises on puerperal fever almost alway s published the findings of autopsies and many doctors argued over whether the disease was inflammatory or putrid and w hether it really began in the uterus as had been previously supposed or if it originated in the omentum, perineum, or even the intestines. The debate yi elded few areas of consensus among the man y w riters tackling the subject and led some to return to the v iew held in the earl y ei ghteenth century that puerperal fever was not a unique disease at all. I t was instead declared that puerperal fevers were a group of man y distinct illnesses that happened to occur during the puerperal period. 85 Pathological finding s that were used to argue for the seat of puerperal fever originating in one organ or another fueled a return to growing lists of possible exp lanations and classifications of puerperal fever. 86 In 1846, Samuel Kneeland wrote, …indeed since morbid anatomy h as of late y ears so absorbed the attention of phy sicians, constant attempts have been made to localize the disease in question. Having been supposed from the time of Hippocrates to that of Boerhaave, to be dependent on an inflammation of the uterus, it was afterwards localized in the peritoneum by Johnston, in England, Walter, in Prussia, and Bichat, in France; and the name of peritonitis was given to it. Then as inflammation of the uterus was found combined with that of the peritoneum, the name was changed to metro peritonitis; metritis was the next appellation; then uterine phlebitis, pus having been found in the veins of the uterus; as this was sometimes found only in the ly mphatics, it was hence called l ym phangitis; others, especiall y t he Germans (with B or at their head,) discarded all these as false, and substituted putrescence or softening of the uterus; this again did not satisfy the French pathologists, who, 84 Thomas, The Mo dern Practice of Physic, states on page 934, “Under different circumstances, the disease assumes different appearances, and accordingly different distinctions have been laid down by writers betw een its various forms; but such distinctions are of no use in practice, and may, perhaps, be productive of embarrassment to the practitioner. We may conclude, I think, that the only essential difference in the cases that ought to be considered puerperal fever, consists in their degree of violence, and their being epi demic, or simply sporadic; for it seems to be admitted that whenever the disease exists epidemically, it is mo re urgent in all its symptoms.” 85 Meigs, Obstetrics: The Science and the Art, states on page 618, “the disorder here to be treated of is observed only in pregnant and lying in w om en; yet it is not one, but many…It is inflammation of the womb alone; too it is inflammation of the veins of the womb; or it is inflammation of the peritoneum; or it is metro phlebitis, or metro peritonitis; or else a combi nation of metro peritonitis with phlebitis. These are the several forms of the disease.” 86 Hallett, “The Attempt to Understand Puerperal Fever,” 10.


45 having met with pus in the cellular tissue, in the viscera, and the articulations, without le sion of the uterus or peritoneum, came to the conclusion that it was a purulent fever, which is the prevailing opinion in the present French school. Thus, by attempting to localize and simplify, this system has only rendered still more confused and difficu lt this important subject. Each observer has described faithfully his epidemic; each has been so far in the right: but all have been wrong in maintaining that the type of disease observed by them was the true t ype of puerperal fever, to the exclusion of al l others. 87 (italics added for emphasis) In this way pathology acted as a hindrance to developing prevention practice for there was very little prevention that could occur if the disease was so ill defined that it was not certain if it was a single diseas e at all. For if it was not it might be prevented in many different way s, again according to the specifics of each case. Describing the contradictory findings of autopsies in puerperal fever cases, Gail Pat Parson stated, “The Practitioner of 1830 had gain ed one advantage over earlier colleagues — science had legitimized his confusion about puerperal fever.” 88 This confusion can be further understood b y r emembering that the very definition of puerperal fever was based on an ancient understanding of disease as that affecting a certain population and was classifiable b y a recognizable collection of symptoms. I n this case, puerperal fever was defined as a fever that to ok place during the puerperium – th e period between childbirth and the return of the uterus to i ts normal size. The fairl y r egular sy mptoms of a bacterial infection which turned septic in the population of women having given birth are what caused puerperal fever to be classified as a separate disease from other illnesses that might be caused b y t he s ame bacteria. Diseases are classified today by their causative pathogen because in our current bacteriological paradigm, treatment for disease is geared toward killing or inhibiting the 87 Samuel Kneeland, “On the Contagiousness of Puerperal Fever,” 45 46. 88 Parsons, “British Medical Professi on and Contagion Theory,” 139.


46 growth of that particular pathogen in the affected body. Before it wa s understood that germs play ed a vital role in disease, the disease causation models of the m odern period continued to classify disease by population and s ymptomology because the available treatment was of ancient origin where the classification of symptom s and the predispositional factors of the population infected were what determined the correct treatment course. Those doctors stud yi ng puerperal fever in the eighteenth and earl y nineteenth centuries c ould not have known about bacteria. And as puerperal fever can be caused b y many different microorganisms, it can have very different disease courses with varying lengths of illness, s ym ptoms, and outcomes. Some cases are more deadl y t han others. So puerperal fever was confusing because it was a collection o f many different infections, but with the same ultimate cause: an introduction of bacteria into the birth canal of the mother. Therefore, prevention would have included making it more difficult for these bacteria to be thus introduced. Unfortunatel y, p rior to the development of the germ t heory the pathological findings of the dissecting room acted more as a distraction than an arena of discovery and little achievement was made in overall prevention. 89 89 Meigs, Obstetrics: The Science and the Art states on page 615, “Diseases that are clearly understood, and methods that are proved to be salutary and successful, unite all voices in the proposition as to their nature and u se; but, in our disorder, the utmost latitude seems to have been given to the imagination, so that a complete distraction of the professional mind appears, in the command of this one to regard it as a fever — of that one, as an inflammation — of another, as s ynocha or typhus; to bleed — no t to dare to bleed — to salivate — to rely on opium — on ipecacuanha, on turpentine — on purgative drugs, on saline draughts; and so of every possibly suggestion of treatment, until the Student, confused and baffled at last in his sea rch after some sure foundation to rest upon, gives up the search for truth in despair, and resolves to wait until the conflict arises, and then to do as best he may.”


47 Contagion and the Environment : Definitions and Con fusion In the nineteenth century the argument over disease causation shifted from inflammation theory vs. putrid theory to one of contagion vs. anticontagion. Actually this debate was split many way s though most historians of puerperal fever have igno red the subtle shifts in terminology which make this issue so perplexing to the careful reader of these primary sources. Most histories on puerperal fever have been concerned with what kept the contagionist camp from convincing the medical profession of th e contagiousness of puerperal fever They rarel y discuss the anticontagionists, other than to quote their more extreme assertions so as to support their contemporary marginalization. 90 The real debate, as it took place in the nineteenth century writings on puerperal fever, was not simply among contagionists and anticontagionists Intent on more clearl y describing the various groups of contagionist and anticontagionist doctors, with each group further separated into enviro nmental and iatrogenic factions, Gai l Pat Parsons describes the oft overlooked, yet fundamental differences between these viewpoints in her article on puerperal fever in antebellum 90 Wertz and Wertz, Lying In: A History of Childbirth in America, 122. For example, Charle s Delucena Meigs, who is often vilified in the secondary literature because of his staunch anticontagionist philosophy is repeatedly quoted in revisionist literature as saying, “Doctors are gentlemen and gentlemen’s hands are clean.” This statement has bee n characterized as an extremely arrogant way of dismissing the need for hand wa shing and other cleanliness procedures. How ever, if one read s Meigs’ works or those written by physicians who kne w hi m well, he was a staunch believer in cleanliness to the poin t that his contemporaries rem arked on his fastidiousness, “at all times ready to enter either the sick chamber or the draw ing room,” as quoted in Parsons. His words, taken in appropriate context then, read closer to, “Doctors are gentlemen and gentlemen’s hands [should always be] clean.”


48 America. 91 She presents a categorization of the doctors’ theories as to the spread of puerperal fever b y describ ing four different positions: iatrogenic contagionists, environmental contagionists, iatrogenic anticontagionists, and environmental anticontagionists. Basically diseases are caused iatrogenically when they are initiated b y a h ealth care worker or b y s om e medical treatment. All nosocomial infections, or infections acquired in a hospital, are iatrogenically produced. Surgical wound infections are a recurrent example. Therefore, iatrogenic contagionists and iatrogenic anticontagionists believed that the med ical practitioner was likely to blame for spreading the disease to his or her patients. Environmental contagionists and anticontagionists did not believe that the doctor or midwife spread puerperal fever, but that the environment, be it the home, hospital, or town, was to blame. Ultimately both of these viewpoints were directly related to miasmatic theory in that the putrid effluvium which acted as the instigating agent was what caused the disease, irrespective of whether the mother had been contaminated w ith the effluvium by the medical staff or b y t he environment itself. The distinction between contagionists and anticontagionists in the nineteenth century according to Parsons, centers on the definition of “contagion.” Today the definitions of contagio n and infection, or contagious and infectious, are much the same. But in the early nineteenth century Parsons argues, these medical terms were separate and distinct. She quotes William Dewees, professor of midwifery at the University of Pennsy lvania, as w riting in 1826, “By contagion is understood effluvia (miasmata) arising directl y or indirectly from the human bod y under particular diseases, and capable 91 Parsons, “Puerperal Fever, Anticontagionists, and Miasmatic Infection.”


49 of exciting the same disease in other persons to whom it may be applied.” 92 For a definition of infect ion, she turns to Noah Webster in his History of Epidemic and Pestilential Diseases published in 1799, which reports that the term was used to indicate “that quality of a disease which may or may not excite it in a sound body within a suitable distance, o r b y c ontact; and which depends on heat, fouled air [and] an apt disposition in the receiving bod y.” 93 Therefore, the main criteria for diseases being contagious were that they regularl y replicated themselves within the environment and conferred upon thei r vict ims the exact disease as that which created the transmi tting agent, the putrid effluvia The disease most exemplify ing this theory was smallpox. An infection, by contrast, was a general state of unhealthy air which could render a subpopulation with c ertain predisposing factors susceptible to a variet y o f illnesses. As medical theory evolved, the definitions of contagion and infection merged to become s ynonymous under germ theory. Readers of primary source documents who do not understand the evolution of these theories of disease causation often mistakenly argue that the use of these terms in the pre bacteriological era indicates an earl y understanding of the role of germs in producing disease. 94 For example, contemporary medical historians of puerperal fever often fail to realize that doctors they consider “h eroes,” such as Ignaz Semmelweis would have considered themselves to have been anticontagionists alongside so called “villains” such as Charles Delucena Meigs. Semmelweis would have fallen into the 92 Ibid., 431 ; William P. Dew ees, A Treatise on the Diseases of Females (Philadelphia: Blanchard and Lea, 1854), 384n. 93 Parsons, “Puerperal Feve r, Anticontagionists, and Miasmatic Infection,” 433. Noah Webster, A Brief History of Epidemic and Pestilential Diseases Vol 2 (Hartford: Hudson & Goodw in, 1799), 141. 94 Vivian Nutton, “The Reception of Fracastoro’s Theory of Contagion: The Seed That Fel l Among Thorns?” Osiris 6 (1990): 196 234.


50 iatrogenic an ticontagionist camp while Meigs was a staunch environmental anticontagionist who resentfully condemned the bran ding of medical professionals, by those who argued for an iatrogenic source as “murderers.” Gail Pat Parsons is quick to point ou t that the observations of the environm ental anticontagionists supported their beliefs in an environmental cause of the disease. 95 These doctors described cases that were sporadic with no obvious tie to a physician’s other patients. And while many phy sician s may have come across a succession of patients that became infected after he delivered them, a fact frequently cited b y t hose arguing for an iatrogenic link in transmission, the overall landscape of puerperal fever cases were so random that an environment al cause seemed the only explanation that could account for all scenarios. 96 Environmental anticontagionists were not simply ignoring the facts or attempting to save their own reputations. Their position was simply a testament to the widespread assumption of the plausibility of a miasma. They were a significant collection of highl y educated, well respected doctors who, far from refusing to cooperate, were in fact using well established miasmatic principles in their attempts to prevent puerperal fever. State of the art hospitals in the nineteenth century were built in a locale, perhaps on a hill facing the wind, which would be less likely to imprison miasmas. Proper ventilation and 95 Parsons, “Puerperal Fever, Anticontagionists, and Miasmatic Infection,” 440. 96 Semmelweis, The Etiology, Concept, and Prophylaxis of Childbed Fever, states on page 118, “This explains why the conflict over whet her childbed fever is or is not contagious could never be conclusively resolved. Those w ho believe in contagion cite cases in which childbed fever had undeniably spread from an ill patient to a healthy one. Their opponents cite cases in which the disease d id not spread as it w ould have done if it had been contagious. Childbed fever is not a contagious disease, but it can be conveyed from diseased to healthy patients by decaying animal organic matter…” Kneeland, “On the Contagiousness of Puerperal Fever,” st ates on page 49, “For those who consider as epidemic disease those propagated by a mo rbific atmospheric principle, it w ill always be easy to make objections to the contagionist, unless the proofs are so convincing as to silence all opposition; which is rar ely the case.”


51 treatment of bedding would ensure that puerperal fever victims’ putrid effluvi um did not contact healthy patients. Evacuation from the vicinity might be ordered as a last resort in an epidemic while the hospital was scrubbed and whitewashed in an attempt to rid the environment of the infectious miasmas. These last precautions often lowered the frequency of puerperal fever for a time, a fact that reinforced the belief that the environment was to blame. 97 Other important observations about puerperal fever were used to argue against its contagiousness. In fact, the link made b y doctors such as Alexander Gordon between er ys ipelas and puerperal fever, which is lauded b y many contemporary historians as an earl y clue to the contagiousness of puerperal fever, actuall y l ed doctors to conclude that puerperal fever was a miasmatic infection rath er than a contagion U nder the definition of the term as described b y P arsons a contagious disease could onl y have been caused b y another i ncidence of that same disease. Therefore, t hose doctors who claimed that cases of puerperal fever followed cases of er ys ipelas were forced to conclude that puerperal fever was not a contagious disease but a b yproduct of an infected environment that was causing both diseases. 98 Loudon’s The Tragedy of Childbed Fever casuall y mentions Parsons and her contention that thes e terms were separate and distinct. But L oudo n takes the position that she has overstated the degree to which these doctors employ ed such distinctions. He states, “C ertainl y both words were used, but careful distinctions between infections a nd 97 Ibid., 429. 98 Ibid.


52 contagions w ere, I believe, rarel y i mportant.” 99 However, based on a careful reading of the primary sources, his dismissal seems premature. It is true that, no matter how hard one tries, the primary sources do not fit neatly into the four category sy stem that Parsons proposes. However, she introduces a distinction in terms that is by no means “rarel y i mportant.” The ambiguities and frequent outright confusions over these important key terms contained in the primary sources often escapes notice. Without such careful di stinctions in the analy sis of terminology the various positions attributed to the ph y sician’s attempts to understand puerperal fever can become hopelessly muddied. For example, there are those, such as Alexander Gordon and Oliver Wendell Holmes, who writ e of puerperal fever using the terms “contagion” and “infection” as almost sy nony mous, much as we do today Gordon states, “That the cause of this disease was a specific contagion, or infection, I have unquestionable proof.” 100 One may deduce that Gordon is simply unsure of the specific nature of the disease being spread, particularl y s ince he argues that puerperal fever and ery sipelas were concomitant epidemics, a fact that would place the disease in Par sons’ category of infectious and therefore not contagio us. However, he then proclaim s “I n short, I had evident proofs of its infectious nature, and that the infection was as readil y communicated as that of the smallpox or measles…” 101 According to Parsons, smallpox was the contagious disease par excellenc e a standard against which all doctor’s judged the contagious quality of other disease s Gordon’s use of the metaphor of smallpox to argue for the infectious 99 Loudon, The Tragedy of Childbed Fever 79 80. 100 Gordon, A Treatise on the Epidemic Puerperal Fever of Aberdeen 62. 101 Ibid., 63.


53 nature of the disease seems to contradict her argument. However, in a following statement he states th at, “ … every person who had been with a patient in the P uerperal Fe ver became charged with an atmosphere of infection, which was communicated to every pregnant woman who happened to come within its sphere.” 102 This phrase “atmosphere of infection,” is com monly found in the arguments of those who do f it clearl y into the iatrogenic anticontagionist category and so we are again left wondering as to his meaning of the term “infection” He further states, These facts fully prove, that the cause of the puerper al fever, of which I treat, was a special contagion or infection, altogether unconnected with a noxious constitution of the atmosphere…That the infection, which produces the puerperal fever is not a specific contagion, but of the same nature with s ynoch us or ty phus, has been asserted b y a late writer on the P uerperal F ever. This author say s, “that the disorder is not one, sui generis confined to in ly ing women, but merely an unusual form of a very common disease, and is in reality no other than the common infectious fever, complicated with a more or less extensive inflammation of the peritoneum.” … The cause of both is undoubtedly infection, but the two infections are of a very different nature. For the circumstance, which excites the infection of the puerperal fever, seems to prevent ty phus. 103 Again, this statement seems to place him firmly in the anticontagionist camp. Yet he continues to use the terms “ contagion ” and “ infection ” in such way s that cause confusion if the terms are to have differe nt meanings He states, “I have had an opportunity of attending a great number of cases of puerperal fever, arising from various causes besides contagion; for I have seen it produced b y cold, b y f ear, b y e rrors in diet, by too earl y fatigue, and premature endeavours to appear well, b y t he application of putrid matter to the uterus, &c.” 104 And so the reader is left ultimately wondering if 102 Ibid., 64. 103 Ibid., 67 68. 104 Ibid., 118 119.


54 Gordon espouses a view of contagion and infection being fundamentall y di fferent, if he is simply unsure as to which term i s best appropriate in describing this disease, or if he considers the disease to be caused b y a multitude of factors ultimatel y en compassing both terms, whether distinctl y defined or not. Meigs, admittedl y a much clearer case is a fierce supporter of en vironmental causation who argues against contagion and who rarel y us es the term “infection” in his writings on puerperal fever, states that, As to the contagiousness of small pox, I cannot deny it, since I cannot deny the contagiousness of any inoculable m alady But the contagious nature of puerperal fever, though asserted b y so many of the b rethren,…, I cannot for a moment admit. Its epidemic power is for me a sufficient explanation of all the asserted examples of its communication by direct contagion… I f a disease be contagious, it must be so by virtue of a material, or essence produced in and evolved from the person of an individual ;… 105 (italics added for emphasis) And so he agrees that small pox is the standard under which contagion can be understood, howe ver he does so because he can readily observe the “inoculable” matter which is transmitted that causes the contagion to be passed from one person to another. He not only argues that puerperal fever has no contagious essence that he can readily imagine, but he concludes that the very definition of the disease prohibits one of thinking of contagion. He states, A woman who is to be attacked with puerpe ral fever is a woman in health,… though she may have a proneness to fall ill with what y ou call child bed fev er. If you fire a bullet through her womb, or tear it, or contuse it with a pair of forceps or a sharp crochet, and she die of the inflammation resulting from the accident, she will die of puerperal fever…if, from whatsoever cause, the blood vessel sy stem of the uterus becomes the seat of a local inflammation, that inflammation will determine in her the onset of child bed fever… 106 105 Meigs, Woman; Her Diseases and Remed ies: A Series of Letters to His Class (Philadelphia: Lea and Blanchard, 1851), 604. 106 Ibid., 603.


55 And so, if one agreed that puerperal fever was a type of peritoneal or uterine inflammation, then a discussion of puerperal feve r being contagious was not only inappropriate, but irrelevant. Puerperal fever, for Meigs, was defined b y t hat inflammation, no matter what conditions helped to produce it. Inflammation as a bodily process, could not be contagious. In an opposite vein, Semmelweis argued for the non contagious character of the disease because there was inoculable material that caused puerperal fever. Semmelweis states, Chil d bed fever is not a contagious disease A contagious disease is one that produces the contagion by which the disease is spread. This contagion brings about only the same disease in other individuals. Smallpox is a contagious disease because smallpox generates the contagion that causes smallpox in others. Smallpox causes only smallpox and no other diseas e…Childbed fever is different. This fever can be caused in healthy patients through other diseases… However, childbed fever cannot be transmitted to a healthy maternity patient unless decaying animal organic matter is conveyed …For example, suppose a patient is seriously ill with a form of childbed fever in which no decay ing matter is produced. Then the disease cannot be transmitted to healthy patients. On the other hand, if the patient with childbed fever has septic endometritis or discharging metastases, th en her disease can be convey ed to healthy patients. 107 (italics added for emphasis) Here, Semmelweis is arguing that puerperal fever is not contagious because the term “contagion” for him means the same that it does for Parsons: that a contagious disease cr eates effluvium that can onl y cause that particular disease in others. Because puerperal fever, in Semmelweis’ opinion, is caused by an y d ecay ing animal organic matter, such as that introduced into the vagina on the hands of a doctor after he assisted in a postmortem dissection, that matter constitutes an inoculable poison. And because man y 107 Ignaz Semmelweis, The Etiology, Concept, and Prophylaxis of Childbed Fever 117.


56 diseases or injuries result in decay ing matter, a number of diseases can cause puerperal fever. This leads the reader to further question sources that describe the link between puerperal fever and erysipelas because Semmelweis argues that, Childbed fever bears the same relation to erysipelas and its sequelae that it does to every other disease that generates decay ing matter…I n recognizing onl y er ys ipelas and its sequela e, bey ond puerperal fever itself, as sources of childbed fever, English ph ys icians draw their boundaries much too narrowl y…Thus childbed fever is the same disease that occurs among surgeons and anatomists, and following surgical operations, it is the same disease whether decay ing matter is brought into the circulation sy stem of males or of females. 108 Therefore, Semmelweis cites cases of inoculation with the decay ing matter of er ys ipelatous abscesses as causing puerperal fever. He does so while arguing that puerperal fever is not contagious However, Storrs cites examples of ery sipelas leading to cases of puerperal fever and vice versa as evidence that puerperal fever is contagious a fact that further discredits Parson’s view that links between cases of er ys ipelas and puerperal fever necessarily argue for its infectiousness. And so it goes for the vast majority of primary sources on puerperal fever. Some sources set out a clear distinction between the terms “contagion” and “infection.” Some do not and see m to use these terms interchangeably Some argue that the causes of the disease are unknown and that a discussion of contagiousness is premature. And some deal with the apparent contradiction in data by separating cases of the disease into different forms of puerperal fever: some contagious, some infectious, and some produced b y direct inoculation. 108 Ibid.


57 Therefore, while Parsons’ categories are not as useful as one might hope for sifting through the apparent contradictions between and within the treatises on pue rperal fever, Loudon’s assertion that the distinction between terms was “rarel y i mportant” is a gross underestimation of the ambiguit y with which these terms were used. On the contrary such differences in definitions are seldom trivial. The definitions o f the central terms in any advanced explanation are alway s theory laden, in that they make implicit claims about the natural world. Such theoretical definitions contain within them the assumptions of the theory How one define s the key feat ures of a given disease impacts basic assumptions about that disease and diseases in general. No two physicians could accuratel y communicate, much less successfully craft an explanation of a disease, if their definitions of the key features of that disease contained signi ficant discrepancies. If one ph ys ician defined a miasma as an unobservable noxious spirit while another claimed that it was composed of fine, wind blown particles, clearl y t heir “agreement” that the disease was caused by a miasma does not mean they endorse the same theory Worse, we find these ph ysicians, sometimes very good ph ys icians, being rather cavalier about consistently using the same meanings for key terms in their own writings. This inconsistency appears both in labeling the causative agents of the disease and in the sy mptoms that they believed indicated the presence of the disease. Either way such internal inconsistencies cripple d an y attempt at forming a coherent explanation of the disease. In part, this inconsistency has been a product of the ir refusal to drop bleeding as a treatment. Small ad hoc adjustments to a theory may have seem ed trivial or go ne unnoticed for a long time, but hundreds of these small adjustments over decades or


58 centuries create d a theory that look ed nothing like its predece ssor. In this way a theory can become so convoluted, so unable to sustain itself, that it becomes unworkable Finally the unfortunately common practice of citing long strings of agents they believe d produced puerperal fever, most of which we re ill defin ed fatally complicate d an y hope of clear theory formation.


59 Success: Treatment s Break Free from Galen Even after the acceptance of germ theory in the lying in hospitals of Europe in the second half of the nineteen th century little progress was refl ected in the statistics of maternal deaths in Great Britain Despite the fact that L isterian antiseptic procedures were finally made mandatory in British hospitals, ninety five percent of deliveries still took place at home attended by a general practition er or midwife 109 While the prevention of puerperal fever was finally vindicated as hospital cross infection dropped close to zero, the overall death rate from puerperal fever actually rose in Great Britain. I t was not until after World War II that British m aternit y hospitals became the site of the majority of middle class deliveries. Helen Roberts points out that since Great Britain began keeping records of maternal deaths in 1835, these statistics remained at a constant high until 1935. 110 It was in the mid 1930s that sulphonomide drugs were first used to treat puerperal fever. Suddenl y, the outcomes of home birth infections improved considerably to meet those established around the turn of the century in the closely monitored environment of the ly ing in hosp itals. Only after the introduction of this dramaticall y s uccessful 109 Loudon, The Tragedy of Childbed Fever 159 60. Despite antisepti c procedures being introduced into the hospitals on the Continent as early as 1868, neither British nor American lying in hospitals standardized Listerian procedures until the 1880s. These procedures included sulphurous or carbolic acid sprays used to disi nfect the clothing of all birth attendants and solutions of carbolic acid or chloride of lime to w ash the hands and to sterilize any metal instruments. Some hospitals w ent so far as to inject carbolic acid directly into the vagina of their patients and/or to cover the vulva in a carbolized oil or a mixture of salicylic acid in wheat flour. Whenever possible, the rooms were left vacant and fumigated in between patients and the bedding was burned when patients exhibited the symptoms of puerperal fever so as t o lessen the chance of an epidemic spreading. 110 Helen Roberts, Women, Health, and Reproduction (London : Routledge & Kegan Paul, 1981).


60 treatment did the maternal death rate in Great Britain decline to meet that of other countries on the continent whose culture of maternal delivery was centered in the hospital. L isterian an tiseptic procedures had proven an effective prevention against nosocomial infection, but in Great Britain, a program of prevention was not an effective treatment because the culture relied almost exclusively on home birth facilitated b y general practitione rs who had many objections to the use of Listerian practices. These objections ranged from the expense and the difficulty of controlling the environment in the patient’s home to older, tradition al beliefs in spontaneous infection and the inherent differenc es between cases of puerperal fever. 111 Until a more successful treatment was discovered, no change in models of disease causation would change the behavior of the majority of British phy sicians. While the main treatment for puerperal fever bloodletting, r emained fundamentally humoural in origin, all models for explaining and understanding the disease would be made to justify that treatment. Even after the introduction of germ theory was shown, in British ly ing in hospitals and elsewhere in Europe, to signi ficantl y change the outcome of these puerperal infections, prevention and treatment for the majority of British mothers continued to be influenced b y old ideology For puerperal fever, the treatment alway s dictated the philosophy Today puerperal fever i s almost unheard of. The widespread availability of antenatal care, chemotherap y, antibiotics, and blood transfusions has made puerperal fever, and man y other complications of childbirth, a thing of the past in most 111 Loudon, The Tragedy of Childbed Fever, 164 5.


61 industrialized nations. 112 However, it has not been completely eradicated. In the United Kingdom, between the years 2003 and 2005, the number of maternal deaths directly attributed to genital tract sepsis was 18 in 100,000 deliveries. 113 T his number includes abortion with sepsis which is the leadin g cause of current infections in Britain. Another significant risk factor for infection is Caesarean section. Most women giving birth in hospitals or in midwifery birthing centers today receive regular screening for bacterial infection and the majority of hospitals give routine antibiotics for streptococcus. Most of these same women have no idea that these precautions are to guard against puerperal fever. A program of prevention has been the first line of defense against puerperal infection and strong anti biotics are given when infection is even remotely suspected. However, agencies that work to promote better outcomes of pregnancy and birth, for both mother and child, stress that medical staff must be trained to recognize the signs of puerperal and genital tract sepsis as many cases turn fatal because of misdiagnosis or an underestimation of just how serious these infections can be. 112 Roberts, Women, Health, and Reproduction 21. 113 Confidential Enquiry into Maternal Death, “Saving Mothers’ Lives: Reviewing Maternal Deaths to Make Motherhood Safer – 2003 2005” (Executive Summary and Key Recommendations prepared for the Confidential Enquiry into Maternal and Child Health, London, December, 2007).


62 Con clusion The central puzzle of puerperal fever in Britain in the eighteenth and nineteenth centuries is thus one of re asoning and assumptions. Neither an absence of data, perso nal shortcomings, nor a lack of dedication account for the inability of two centuries of British doctors to find a way to prevent this killer. It was their commitment to outdated, ancient Greek ass umptions about the human body and their pre scientific use of terminology and reasoning that blocked the way With so many women’s lives at stake it is dismay ing to see the number of m odern practitioners and thinkers who resorted to subtle shifts in defin itions, or appeals to near my stical forces, or ad hoc explanations of their findings rather than change their clinical techniques. The temptation is great to join the many commentators who have castigated these phy sicians, attacking their motives, institut ional politics, or personal foibles. To do this is both unfair and historically shortsighted. The m odern struggle against puerperal fever is an account of an intellectual quest wherein major concepts of the past began to crumble under the weight of new d ata and, faced with the impotence of their customary cures and preventions, people were challenged to look at the world in a fundamentally new way. To use Thomas Kuhn’s language, the eighteenth century explanation of disease was ripe for a paradigm shift. The battle against puerperal fever illustrates the difficulties involved in an especially complex example of one such shift.


63 The effort to understand nature is not just the accumulation of data nor the inventing of new explanations. I n order for data and explanations to be cogent, they must fit into the intellectual fabric of the time. And the medical fabric of m odern Britain was dominated by a ncient concepts. To a contemporary scientist, this longevit y alone would make such ideas suspect. For these ph ys ic ians, unaccustomed to our frantic pace of monumental upheavals (true paradigm shifts such as natural selection, relativity and quantum mechanics) the length of a medical doctrine’s reign was an endorsement of its strength and veracit y. Whatever the need for a new paradigm, of course, phy sicians at the time could not see their place in history Kuhn notes that most of what scientists do consists of gathering data and forming h ypotheses that support the established paradigm. This was the role of the m odern phy sician. The hope was alway s that they were engaged in an exhausting but ultimately fruitful quest for a cure. The anticipation was that a new discovery, a new technique, would perfect the device of bleeding or prevent miasmas, and puerperal fever would be conquered. In retrospect, we see that this hope was futile. The preponderance of unobservable, at times almost ghostly, agents that were invoked as causes, the ambiguities in the definitions of key concepts, and the temptation to “fit” any novel data into the old theories, ad hoc had created a complex of notions that lacked internal coherence and ultimately, could explain nothing. The classical explanations of Hippocrates and Galen were revered, and those ad hoc adjustments, the sometime subtle but o ften flagrant “repositioning” of one’s explanations, ensured recent discoveries would alway s conform to classical explanations.


64 It is easy to forget that the scientific method is a relative newcomer on the stage of human knowledge. While a full paradigm s hift, germ theory was a century away from wide adoption, the central concepts that would break the hold of Hippocrates’ and Galen’s ideas were beginning to emerge, and several m odern ph ys icians gladly grasped these tools. Mechanism, fluid dy namics, and an atomy were all building blocks of the new intellectual world and each would have a fundamental role in the new knowledge of medicine. While the story of puerperal fever is essentiall y over, the battle against similar infectious diseases continues. Our c urrent antibiotics are becoming progressively less effective and strains of streptococcus could undergo dramatic mutations at any time. Our challenge remains similar to that of these m odern phy sicians. Flu pandemics, infectious prions, and ever evolving ba cteria are sure to demand greater feats of understanding if they are to be controlled. Despite decades of concentrated study we confront innumerable medical dead ends and some diseases that remain as deadly as ever. The history of the brave ph ys icians who fought puerperal fever holds a lesson for our medical future. There is no signal that tells scientists that a new paradigm is needed. It will never be eas y or obvious. But without the willingness to abandon established wisdom, scientific knowledge flounder s and progress can be terribly prolonged.


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