K. Codell Carter - The Rise of Causal Concepts of Disease - Case Histories-Routledge (2017)
K. Codell Carter - The Rise of Causal Concepts of Disease - Case Histories-Routledge (2017)
Case Histories
The History of Medicine in Context
Department of History
The Open University
Reinventing Hippocrates
Edited by David Cantor
The Rise of Causal Concepts
of Disease
Case Histories
K. CODELL CARTER
First published 2003 by Ashgate Publishing
K. Codell Carter has asserted his moral right under the Copyright, Designs and
Patents Act, 1988, to be identified as the author of this work.
Notice:
Product or corporate names may be trademarks or registered trademarks,
and are used only for identification and explanation without intent to
infringe.
RB151.C37 2003
616.07’1—dc21
2002019418
or care much about the theories that inform their own professional
activities – they are too caught up treating patients. Imre Lakatos wrote
that ‘scientists tend to understand little more about science than fish
about hydro-dynamics’ (Lakatos, 1968, p. 148n.) which, if you think
about it, is not really an insult – after all, why should fish care about
hydrodynamics? Perhaps members of most professions know how to do
what they do (and even succeed in doing it well) without thinking much
about what they do or why. In any case, this seems true of most
physicians (which may be all for the best – what would happen to a fish
that became preoccupied with theories about how to swim?).
This book reflects my own modest efforts to figure out something
about the theories of disease that ground current medical practice.
History provides one kind of understanding; conceptual analysis
(philosophy) provides another. Ideally they are complementary. Adapting
a famous sentence from Immanuel Kant,1 Lakatos observed that
‘philosophy of science without history of science is empty; history of
science without philosophy of science is blind’ (Lakatos, 1971, p. 102)
– a comment that is no less true of the history and philosophy of
medicine. Having been trained as a philosopher, not as a historian, I’m
mainly interested in conceptual analysis, but, without historical context,
philosophical analysis can become sterile (if not quite empty). So, in
trying to figure out current theories of disease, my approach is to
embody analysis in an historical context. I like to think the result is the
sort of thing Lakatos himself advocated: ‘in writing a historical case
study, one should, I think, adopt the following procedure: (1) one gives
a rational reconstruction; (2) one tries to compare this rational
reconstruction with actual history and to criticize both one’s rational
reconstruction for lack of historicity and the actual history for lack of
rationality’ (Lakatos, 1968, p. 138).
Honestly speaking, I suspect that any philosopher who happens to
read this book will find the philosophy nearly empty, and I already
know that many historians regard my attempts at history as blind. So,
ironically, my work probably resembles (and in a way confirms what
I’ve always thought about) opera: combining drama and music ends up
serving neither interest well. Hopefully someday someone will come
along who will do it better. In the meantime, I can only say that I’ve had
great fun doing what I’ve done – I can’t think of anything I’d rather
have studied.
Parts of this book are based on earlier publications several of which
appeared in Medical History (Carter, 1977, 1980, 1982b, 1985a, 1985b)
and in The Bulletin of the History of Medicine (‘The Koch–Pasteur
Dispute on Establishing the Cause of Anthrax’ (1988) and ‘The Devel-
opment of Pasteur’s Concept of Disease Causation and the Emergence
PREFACE ix
Note
works that cite or are cited in those works, and so on. The collection of
all these works approximates a research programme. In logical terms,
over the domain of all published works, a research programme is ap-
proximately the equivalence class defined by any particular work under
the relation ‘cites or is cited by’. This criterion has obvious weaknesses;
however it provides a practical standard for the selection of materials,
and I have chosen the topics in this book with this criterion in mind.
The works here discussed are directly and indirectly linked by citations.
One final concept requires clarification. Lakatos defined ‘research
programme’ in terms of series of scientific theories, and most of this
book concerns ideas that are analytically connected to the concept of
theories. At the start, therefore, we must give some attention to how the
word ‘theory’ is to be understood. In ordinary life, ‘theory’ often refers
to any belief or opinion, but in science the term is used more narrowly.
Wim J. Van der Steen and Harmke Kamminga gave the following
succinct account (which is compatible with other recent discussions in
the philosophy of science):
A statement is a law if it satisfies the following criteria: (i) it is
general in the sense that it contains a universal quantifier, (ii) it is
general in the sense that it does not mention particular individuals,
times or places, (iii) it has empirical content, (iv) it is well-con-
firmed, and (v) it is well-entrenched (i.e. it belongs to a theory). …
Theories will be viewed as sets of interconnected laws.
(Van der Steen and Kammingen, 1991, pp. 445f.)
As this account makes clear, theories and laws are conceptually linked:
neither is possible without the other. When formalized, some of the
laws comprised by a theory typically function within the theory like
axioms in geometry or in other deductive systems. For example, here is
a set of assumptions (axioms) for the kinetic theory:
(1) A pure gas consists of a large number of identical molecules
separated by distances that are great compared with their size. (2)
The gas molecules are constantly moving in random directions
with a distribution of speeds. (3) The molecules exert no forces on
one another between collisions, so between collisions they move in
straight lines with constant velocities. (4) The collisions of mol-
ecules with the walls of the container are elastic; no energy is lost
during a collision.
(Oxtoby, 1990, p. 104).
These assumptions have the qualities identified by Van der Steen and
Kamminga (so they are laws in their sense), and from them, other laws
(for example, Boyle’s Law, Charles’ Law) can be derived mathematically
much as one derives theorems in geometry. As a second example, in
their classic book on the general theory of relativity, Charles W. Misner,
Kip S. Thorne, and John Archibald Wheeler observed that ‘of all theories
6 THE RISE OF CAUSAL CONCEPTS OF DISEASE
the 1860s and 1870s, there were many views on what disease-germs
were, for example, chemical poisons, ferments, degraded cells, fungi,
“bacteria” or a class of parasites’ (Worboys, 2000, p. 2). So what
Worboys is considering is different ‘views’ about germs and their possi-
ble relation to disease. I say for the most part Worboys seems to use the
term ‘theory’ in the loose sense because in his first chapter, he does once
refer to the narrow use of the word: ‘Yet, by the 1870s, the term [germs
of disease] was firmly linked to the modern concept of the “germ theory
of disease” [singular] – the etiological construction of disease in which
external agents entered the body to produce septic, infectious and other
diseases’ (p. 22). This reveals the first difference between my interests
and Worboys’: I use the term ‘theory’ exclusively in the narrow sense
explained in previous paragraphs and tersely exemplified in this quota-
tion from Worboys. Thus, it is no accident that, in my opinion, the first
explicit formulation of a bacterial theory (Klebs’) came in 1876 – the
same decade in which Worboys sees ‘germs of disease’ finally linked to
the modern concept of the germ theory. As I use the term ‘theory’, there
was no germ theory (at least no explicit germ theory) prior to that time
while obviously there were lots of opinions about germs. I am interested
in the laws (in Van der Steen and Kamminga’s sense) comprised by the
bacterial theory of disease (in the narrow sense of ‘theory’) – something
to which Worboys gives no attention.
A second difference between Worboys’ book and my own is this: my
main interest is not really even the bacterial theory of disease. Rather, it
is a broad movement – the etiological standpoint or research pro-
gramme – of which the bacterial theory is one part. For me, the bacterial
theory is only one example (albeit an important one) of the quest for
universal necessary causes that characterizes medicine since the middle
of the nineteenth century. Thus, while I have enormously enjoyed
Worboys’ fine book and have learned a lot from reading it, there is –
unfortunately for me – almost no intersection between his work and my
own.
The etiological research programme arose in the nineteenth century,
and, while boundaries are as much created as discovered, one can
distinguish three stages in this process. First, between about 1830 and
1860 a few researchers independently, nearly simultaneously, and ap-
parently for the first time in medical history, began to think of several
different organic disorders as having causes that were universal and
necessary. A new strategy arose – the adoption of etiological characteri-
zations – that provided a way of classifying individual illnesses so that,
in principle, every recognized disease could be ascribed to a universal
necessary cause. Basic methodological principles emerged forming what
Lakatos would call the heuristic of the programme, and researchers
8 THE RISE OF CAUSAL CONCEPTS OF DISEASE
Notes
1. The usual term is ‘specific cause’. However, as this term is currently used,
it is both vague and ambiguous. When possible I avoid the term altogether,
but when it appears, it should be understood to mean a natural, universal,
and necessary cause.
2. F. Kräupl Taylor uses the term ‘monogenic’ for diseases associated with
universal and necessary causes. In a philosophically sensitive and insightful
book that has received too little attention, he writes that while most
diseases recognized in medicine today are not monogenic ‘the final hope
and aim of medical science is the establishment of monogenic disease
entities’ (Taylor, 1979, p. 21). Alfred S. Evans has traced efforts to assimi-
late numerous new diseases to a model much like the one elaborated in this
book (Evans, 1993).
3. Lakatos writes that all of science can be seen as one huge research pro-
gramme within which special programmes focus on particular problems
(Lakatos, 1968, p. 132). In the same way the entire etiological standpoint
can be regarded as a single research programme or one can think of it as a
collection of separate programmes each dealing with a class of diseases
with similar causes. This is a useful ambiguity and there is no reason to
eliminate it arbitrarily.
4. I will have more to say about this in the chapter entitled ‘Some Final
Thoughts’ at the end of the book.
5. What could it mean to talk about ‘kinetic theories of gasses’? While differ-
ent accounts of the kinetic theory may employ different basic assumptions
or state equivalent assumptions differently, the consequences of every such
set must be isomorphic with the consequences of every other. In this sense,
there can be only one kinetic theory. No doubt, early on, there were
innumerable opinions about diseases and even about the nature of germs
and about their possible relations to diseases, but, in my mind, to use
‘theory’ in these contexts verges on false advertising. Worboys does cite
one 1878 work in which the word ‘theories’ (plural) was used in this way.
6. This point is related to Lakatos’s thesis that so-called crucial experiments
can never be seen as crucial until decades after they have been performed
(Lakatos, 1968, p. 158).
7. Back when they may have hoped there was still a chance of saving my
immortal soul, Adrian Wilson and Andrew Cunningham kindly presented
me with a copy of Butterfield’s The Whig Interpretation of History. But I
found Butterfield’s strawman arguments only about 40 per cent persuasive
so, while confessing, today, to be 60 per cent Whig is about like calling
oneself a witch in 1692 Salem, there is little point in denying what will,
soon enough, be apparent to the reader.
CHAPTER ONE
leading French internist, explained that one could investigate the causes
of pneumonia ‘by interrogating carefully a certain number of individu-
als struck by this affliction, and by directing one’s questions to the
causes that produced it’ (Chomel, 1842, pp. 165f). In his own study,
‘made with great care on seventy-nine pneumonia patients’, he found
the following: fourteen patients reported experiencing some form of
cooling, five had consumed too much wine, two had worked exces-
sively, one had experienced a lively emotion, and another had inhaled
carbon vapor. The 56 remaining patients were unable to explain how
they had become ill. Chomel also reported an earlier study of 125
patients in which the following causes had been established: contusions
of the throat, 2; cooling, 38; violent effort and fatigue, 12; depression,
4; excess of drink or upset regimen, 3; and in 66 cases no cause could be
identified.
Proceeding in this case-by-case way, physicians accumulated exten-
sive lists of possible causes for each disease. For example, in his account
of diabetes, Bardsley identified the following causes: frequent exposure
to sudden alterations of heat and cold, indulgence in copious draughts
of cold fluid when the system has been over-heated by labor or exercise,
intemperate use of spirituous liquors, poor living, sleeping out the
whole of the night in the open air in a state of intoxication, checking
perspiration suddenly, and mental anxiety and distress (Bardsley, 1845,
p. 609). Similar lists can be found for virtually any disease in most
German, English, or French medical texts from the period.
new relations that occur in the economy of the ill body’ (Lagasquie,
1849, p. 313). This made good sense until, under the influence of
pathological anatomy, some diseases were identified with specific le-
sions. Given such characterizations, the proximate cause and the disease
became one and the same: ‘The proximate cause is nothing else than the
actual disease itself – the actual condition of that part of the body, from
which the whole train of morbid phenomena essentially flows’ (Watson,
1858, p. 76). Writers acknowledged that this use of the term ‘cause’ was
confusing. ‘It is … a puzzling term, and tends to give to the study of
disease a scholastic and repulsive aspect’ (Watson, 1858, p. 76). Some
physicians dismissed all talk of proximate causes as redundant and
urged that the term be abandoned. ‘If we retain the term proximate
cause, it signifies … the pathological condition of the throat, the pleura,
or the joints; but we think the term may be advantageously banished
from medicine’ (Conolly, 1845, p. 677; Watson, 1858, p. 76).
In contrast to proximate causes, remote causes were factors normally
external to the patient that explained the onset of disease. This was the
most common sense in which the word was used, and all the causes
identified in the first section of this chapter were remote causes.
What was the relation between some particular remote cause, say
anxiety, and the disease it occasioned? Clearly, no one cause was neces-
sary for the onset of any specific disease since, as we have seen, different
cases of each disease were ascribed to different remote causes. Physi-
cians explicitly denied that the same cause was present in every case of
any disease: ‘No inference can fairly be drawn from the identity of the
effect, for certain diseased states are produced by a variety of remote
causes, this expression being used in the sense usually annexed to it by
medical men’ (Brown, 1845, p. 505). It is also clear that the remote
cause identified in a particular disease episode was not necessary even
for that episode because, if a given patient did not contract her disease
from one cause, she might contract the same disease from other causes.
Or, conceivably, several causes (no one of which was necessary) might
contribute equally to the onset of a particular episode. Thus no single
cause was regarded as necessary for any one of the diseases it could
cause.
However, particular remote causes seem not to have been thought of
as sufficient either. A typical factor, say anxiety, could be listed as a
possible cause for many diseases. For example, one widely used British
medical encyclopedia identified anxiety as a possible cause of dozens of
diseases including acne (1:48),1 catalepsy (1:379), diabetes (1:609),
ecthyma (1:739), fever (2:177), herpes (2:449), hydrocephalus (2:490),
impetigo (2:594), senile dementia (3:74), psoriasis (3:733), scrofula
(4:139), and tetanus (4:168). Thus anxiety was not expected always to
14 THE RISE OF CAUSAL CONCEPTS OF DISEASE
result in the same disease – one anxious person might become diabetic
but others might contract impetigo or tetanus. So remote causes were
not sufficient either. Christopher Hamlin, who has discussed accounts
of disease causation in this period, recognizes that ‘the presumption of a
single exciting cause as sufficient could not be sustained’ and seems to
infer that ‘all remote causes could plausibly be thought of as necessary
causes’ (Hamlin, 1992, p. 51). But clearly this doesn’t follow and (as we
have seen) it is inconsistent with what contemporary physicians them-
selves reported about how they used the words. Hamlin gives no further
evidence for this surprising claim.
However, while individual causes were not thought of as sufficient,
they could be part of a combination of factors that was sufficient. To
understand this, we must take account of another distinction important
in nineteenth-century etiology. Remote causes were classified as predis-
posing or exciting (or occasioning). Predisposing causes ‘render the
body liable to become the prey of something, which has a tendency to
excite the disease. The exciting cause of the disease might have no
effect, unless the body had been predisposed; and the predisposition
might not have had the effect, unless the exciting cause had occurred’
(Elliotson, 1844, p. 43). Typically, in an account of any disease, both
predisposing and exciting causes were listed. One discussion of tetanus
mentioned these predisposing causes: warm climate, humid situations,
bad or insufficient nutriment, close and ill-ventilated habitations, inat-
tention to cleanliness, and neglect of the bowels. The same discussion
listed these exciting causes: mechanical wounds, application of cold and
damp, the irritation of worms, terror, sympathy, mental anguish, the
suppression of perspiration, the accumulation of cherry-stones in the
intestines, suppression of lochia, and gastric inflammation (Symonds,
1845, p. 368). Contemporary writers observed that, over time, predis-
posing causes could become exciting, and what were usually exciting
causes could become predisposing (Elliotson, 1844, p. 45). Moreover
under suitable circumstances, either kind of cause alone could seem to
bring on a disease (Conolly, 1845, p. 678). One writer observed that
‘the same occasional cause can provoke the development of all the
diseases, and the same disease can be created by every kind of occa-
sional cause’ (Chomel, 1835, p. 425). If, as this suggests, a typical
remote cause is neither necessary nor sufficient, how can distinguishing
between predisposing and exciting causes help provide a complete suffi-
cient causal explanation?
Several discussions of disease causation included some version of this
hypothetical case:
Of several individuals exposed to the same exciting cause, scarcely
two will be affected alike. From exposure to cold, for instance, one
DISEASE IN NINETEENTH-CENTURY PRACTICAL MEDICINE 15
Farr’s idea was this: suppose a woman is exposed to some trauma, say
cold, and that an ensuing morbid process (that is, a disease) causes her
death. Then there was no distinction between the remote cause of the
disease and the remote cause of death.
Not only were particular causes of disease and of death similar and
sometimes the same, but causal explanations were also similar in kind
or form: for both disease and death, the object was to explain what
happened to one individual at one time. This called for identification of
a sufficient cause for a particular event. As we have seen, having found
causes of many individual disease episodes, physicians like Scanzoni
and Chomel tried to discern patterns. In the same way, Farr sought
patterns among the causes of individual deaths; for example, he thought
that the record of causes of death could help one decide which parts of
the country would be safe retreats from serious diseases like consump-
tion or whooping cough (Farr, 1839, p. 87).
The causes of death we identify, today, are still sufficient causes for
particular events. ‘The certificate wants to find out not why every
patient died but why this patient died’ (King, 1982, p. 213). And so,
although more precise and detailed, they are of the same general form
as the causes of death identified 150 years ago. Moreover, we still
accumulate information about causes of death by surveys like those that
Scanzoni and Chomel proposed for investigating the causes of childbed
fever and pneumonia. However, as will become clear in the course of
our investigation, the symmetry between causes of disease and causes of
death has been destroyed by a change in the kind of causes we now
identify for diseases (Carter, 1997).
We can now appreciate one important discontinuity between etiological
discussions in the 1840s and causes of death, on the one hand, and the
causes of disease that most interest us, today, on the other. Today, in
both ordinary everyday conversation and in technical medical discourse,
one speaks of ‘the cause of X’ where X is the name of some disease; for
example, ‘the cause of diabetes’ or ‘the cause of tuberculosis’. And the
causes that are typically identified in such contexts are among those
that nineteenth-century physicians would have called remote. However,
in literature from the early decades of that century, one looks in vain for
any talk of ‘the cause of disease X’. Among remote causes, one finds
only exciting and predisposing causes of individual cases such as those
we have listed and characterized. One reason for the apparent strange-
ness of James L. Bardsley’s discussion of the etiology of diabetes,
considered in the first section of this chapter (pp. 10–11), is that, in a
general discussion of the etiology of diabetes, such as he was purporting
to give, we now expect an account of the cause of diabetes (so far as it is
understood) not just a list of factors contributory to individuals becom-
18 THE RISE OF CAUSAL CONCEPTS OF DISEASE
ing diabetic. But in the early 1800s, there were no such accounts; there
simply was no concept of ‘the cause of disease X’. Why might this have
been?
One reason is this: given how diseases were then defined, it was
reasonable and virtually inevitable that different episodes of any disease
would be attributed to a variety of unrelated causes. In the early nine-
teenth century, individual diseases were almost always characterized in
terms of prominent signs and symptoms (or, under the influence of
pathological anatomy, of particular morbid alterations in the body). For
example, in a lecture delivered at the University of Paris in 1832 and
reprinted in the British journal, Lancet, Gabriel Andral defined ‘hydro-
phobia’ as ‘complete horror of fluids, reaching to such a degree, that
their deglutition becomes almost impossible’ (Andral, 1832–33, p. 806).
Thus, hydrophobia was defined in terms of one prominent symptom: an
extreme inability to swallow. However, if hydrophobia is a horror of
swallowing, then, as Andral cheerfully acknowledged, fully authentic
cases could be caused by blows to the throat or by psychological
problems as well as by the bites of rabid dogs.2 Given a symptomatic
definition like Andral’s (or even a definition in terms of a specific
lesion), it was logical and inevitable that hydrophobia, or any other
disease so defined, would have a range of different remote causes that
varied from case to case. So it is not simply that earlier physicians failed
to notice a commonality among individual cases that we have since
managed to discern. There was no commonality: within their system of
ideas, the phrase ‘the cause of disease X’ could have no meaning.
grounds that some genuine cases of phthisis did not involve tubers.
However, he wrote, ‘one cannot deny credit to the pathologists who
have provided this material basis for phthisis’. By providing a ‘material
basis’, the pathologists explained symptoms and made diagnosis more
objective and precise. For these reasons, and because it seemed so
enlightening, phthisis was ultimately recharacterized in terms of tubers;
non-tuberous cases, which had formerly been genuine instances of
phthisis, were reclassified in other categories.
Because the new characterization of phthisis seemed superior and
because, at the time, phthisis was such a prominent disease, this
approach was followed in characterizing other diseases. Physicians
dissected corpses, sought morbid remains, and, when possible, redefined
diseases in terms of what they found. The new characterizations were
greeted as important advances. ‘The great improvements which have
taken place of late years in pathology, by enabling practitioners to
connect symptoms with their organic causes more accurately, have nec-
essarily diverted attention from the artificial [symptomatic] combinations
of the old nosology’ (Forbes, 1845, p. 106). However, the influence of
pathological anatomy went further than just providing new ways of
defining diseases. Thomas Watson began a lecture on morbid anatomy
by noting that the topic
is not one of merely curious interest, but has a direct bearing upon
the proper treatment of diseases. It will teach us what we have to
guard against, what we must strive to avert, in different cases. In
speaking of particular diseases, I shall constantly refer to the facts
and reasonings which I am now about to lay before you.
(Watson, 1858, p. 68)
Thus, the examination of corpses became a major source of knowledge
about the proper and improper functioning of the body – about health
and disease. Physicians were inevitably influenced not only by the content
– the specific observations and explanations – but also by the form of
the explanations that pathologists provided.
Of what form were the causes that interested pathologists? The causes
pathologists identified (and that physicians took as a basis for their
‘facts and reasonings’ about diseases) were causes of death and causes
of the successive stages of morbid processes. As we have seen, it was
natural to associate causes of disease with causes of death. Indeed, it
could not have been otherwise: whenever possible, diseases were
defined as morbid processes, and unchecked morbid processes end in
death. Thus, in contemporary medical texts, the discussion of indi-
vidual diseases was often immediately preceded by a discussion of
causes of death (Watson, 1858, pp. 67–76). But, as we have seen, a
cause of death or the cause of a certain morbid alteration, like the cause
20 THE RISE OF CAUSAL CONCEPTS OF DISEASE
Even a casual reader of the medical literature from the early nineteenth
century must be struck with the extent to which medical theory and
practice were bound up with traditional morality.4 Etiological discus-
sions of most diseases included references to such factors as drunkenness
(1:79),5 intemperance (2:595), gluttony (1:89), luxury (1:219), indul-
gence (4:331), debauchery (2:209), dissipation (4:137), vicious habits
(2:559), solitary vice (4:139), excessive venereal indulgences (1:72),
lustful excesses (2:621), indolence (1:48), sloth (1:739), envy (2:631),
jealousy (2:631), and anger (1:116). Physicians observed that excess
was the foundation of most disease (Barlow, 1845a, p. 751). Indeed, in
the etiological discussions of one multi-volumed and multi-authored
medical encyclopedia, such terms as ‘excessive diet’, ‘gross and luxuri-
ous diet’, ‘gluttony’, ‘high feeding’, and ‘full and stimulating diet’ appear
four times as frequently as terms like ‘insufficient food’ or ‘want of
DISEASE IN NINETEENTH-CENTURY PRACTICAL MEDICINE 21
Notes
1. Through this sentence, such numbers as the preceding are volume and page
references to Dunglison (1845).
2. As this case illustrates, while early nineteenth-century physicians used
many of the same disease names we use today, such names applied to
dramatically different sets of cases, and they had altogether different mean-
ings than they now bear. Michel Foucault (Foucault, 1973) and others
(Schlich, 1994; Wilson, 2000) have made this point, but the lesson is
difficult to learn.
3. For an independent analysis of causes of disease in individual patients that
reaches similar conclusions see Wulff (1984). Michael Worboys has, ap-
propriately, emphasized that ‘germ theories of disease, explicitly or implicitly,
always included ideas about the interactions between germs and bodies …
the seed and soil analogy, or some variant, was routinely used to explain
both disease and its absence from the first uses of modern germ theories of
all types’ (Worboys, 2000, p. 281). John Harley Warner has discussed an
exactly parallel focus on individual cases in the therapy of the period
(Warner, 1986, pp. 58–80).
4. Charles E. Rosenberg has given attention to this issue but from a different
perspective (Rosenberg, 1989).
5. Through this sentence, numbers such as the preceding are volume and page
references to Dunglison (1845).
6. I occasionally use the phrase ‘chimbuki-medicine’ as a convenient label for
any medical system in which immorality, per se, is regarded as a cause of
disease in the sense that it is taken as part of a sufficient cause for particu-
lar episodes of illness. No disrespect is intended either to nineteenth-century
practitioners or to the chimbuki.
7. Lakatos pointed out that, in the absence of a research programme, there is
‘a mere patched up pattern of trial and error’ (Lakatos, 1968, p. 175) – so
something less than mature science. Arguably the first research programme
in medicine (that is, the first attempt to understand and control diseases by
the formulation of scientific theories) is the one we are investigating.
8. ‘Between the 1820s and the 1880s medical therapeutics in America was
fundamentally altered. Traditional medical practices, founded on assump-
tions about disease shared by doctor and patient and oriented toward
visibly altering the symptoms of sick individuals, began to be supplanted
by strategies grounded in experimental science that objectified disease
while minimizing differences among patients’ (Warner, 1986, p. 1; see also
Carter, 1982a).
CHAPTER TWO
Bassi concluded that, after the fungus penetrated the skin of dead
worms, it released germs that could infect new worms.
The contagion is communicated by food, by inoculation, and by
the mere contact of insects that have died of the terrible disease, of
any infected object, and even of air contaminated by the disease-
bearing germs. These are so abundant in a single calcified or
efflorescent insect, and so minute, that they spread with extreme
rapidity and in infinite numbers, cling fast even to the smoothest
and most polished objects, such as glass, metal, etc., and even rise
up into the air which they partially infect so long as they remain
suspended in it. (p. 8)
Bassi found that simply touching a healthy worm with a contaminated
pin would usually (but not always) bring on the disease (p. 9). Espe-
cially in high temperatures or in high humidity, the disease did not
always occur (pp. 31, 36). He also noted that other larvae were vulner-
able to muscardine and that, in forests, one occasionally found dead
worms covered with the same fungus; from these larvae he was able to
infect healthy silk worms (p. 9). Later Bassi demonstrated that blood
and tissue from diseased worms could also infect other worms. This
proved that the internal tissues contained elements of the contagious
fungus even before the appearance of the white excrescence.
Bassi’s understanding of the role of the fungus enabled him to explain
various facts about muscardine. The ease with which fungus germs
were carried through the air or became attached to animals explained
how the disease could spread to areas far from any known cases; the
vast numbers of germs released from each corpse explained how the
disease could suddenly destroy all the densely concentrated inhabitants
of a silkworm facility; the growth of the fungus explained the hardening
of the worm’s corpse (p. 14). Bassi’s discoveries also suggested practical
ways of controlling muscardine. He recommended strict cleanliness to
prevent the dissemination of germs. He found that, when exposed to
fresh air, muscardine germs gradually became inert, so he recommended
that breeding facilities be well ventilated. Bassi also identified chemical
washes that could disinfect eggs and even live silkworms after contami-
nation.
As Bassi recognized, his work hinted at the possible role of parasitic
organisms in other diseases. ‘My book … may perhaps resolve some of
the many anomalies which the doctrine of contagious disease in general
contains’ (p. 3).
The germs of the various animal and vegetable contagions travel
about, being transported hither and thither by so many bodies,
dead and alive, organic and inorganic, and on the wings of the
wind – especially the lightest germs and those that can live without
a liquid or an animal mucus to envelop and preserve them. …
UNIVERSAL NECESSARY CAUSES 31
recognizes that their entire tissue is filled with cryptogams’ (Zakon and
Benedek, 1944, p. 166).
Gruby’s reasoning in these passages is easy to characterize: in each
case he inferred causality simply from finding a cryptogam to be present
in (indeed to mostly constitute) the morbid materials of all of the
observed cases of each disease. For six different diseases, he inferred
causality after observing that disease products consisted mostly of the
fungi.
Notes
Etiological Characterizations
The only way of characterizing diseases so that each disease will have
a universal necessary cause is by defining them in terms of their
causes. For example, the tubercle bacillus is universally necessary for
tuberculosis only because ‘tuberculosis’ is defined as infestation by
this bacillus. One cannot be certain that no one (perhaps Fracastoro,
Paracelsus, Ugo Benzi of Siena, or Sinan ibn Thabit ibn Qurra) em-
ployed such characterizations before 1850 although, to date – loose
talk about disease specificity notwithstanding – no textual evidence
has been presented that anyone did. One reads that Fracastoro envi-
sioned defining diseases in terms of what he called ‘seeds’. But
unambiguous evidence has yet to be provided and, even if this had
been his intent, in the absence of any empirical means of distinguish-
ing among seeds (or, indeed, even of demonstrating their existence)
any such attempt would have been exactly as useless as defining
diseases in terms of assorted evil spirits; vacuous definitions explain
precisely nothing. However, this much is absolutely certain: Ignaz
Semmelweis was the first person to have adopted such definitions in
publications that are linked by citations directly into the etiological
research programme. The only way to dispute this fact would be to
exhibit citations in core works of the programme to writers before
Semmelweis who used this approach, and there simply are none.1
Semmelweis may or may not have been aware of the significance of
what he did; others may or may not have consciously followed his
example; it matters not. The facts are that Semmelweis employed this
strategy clearly and unequivocally, he did so without any identifiable
precedent (none of his teachers in Vienna ever proposed such charac-
terizations and neither did any of the horde of marginally significant
eighteenth-century English physicians who wrote on childbed fever),
and his work figured in the etiological research programme. For these
reasons we take his use of etiological characterizations to exemplify
this approach – an approach without which the systematic identifica-
tion of universal necessary causes is absolutely unthinkable.
Semmelweis’s story has been told and retold many times (although
usually by persons oblivious of the nature and significance of his contri-
bution).2 For our purposes only four claims require discussion:
In 1843, one year after Dubois’s essay appeared, the American physician
Oliver Wendell Holmes published an essay entitled ‘The Contagious-
ness of Puerperal Fever’. In 1855 the essay was reprinted with an
introductory note and an appendix containing additional references but
with no changes in the body of the text. The purpose of the essay was to
show that ‘the disease known as puerperal fever is so far contagious as
to be frequently carried from patient to patient by physicians and
nurses’ (Holmes, 1843, p. 131).4 Holmes’ conclusions and most of his
case histories were drawn from earlier British sources; he admitted,
both in the essay and again in the later introductory note, that his was a
majority view. ‘A few writers of authority can be found to profess a
disbelief in contagion – and they are very few compared with those who
think differently’ (p. 129). Indeed, one year before publication of
Holmes’s essay, Lancet reported a discussion of puerperal fever in the
London Medical Society in which ‘the chief apparent circumstance is
the diversity of opinion … as to the nature … the symptoms and the
treatment of the affection. … One fact only respecting the disease was
generally admitted, namely, its unquestionable contagiousness’ (Lancet,
1842–43). But, while Holmes had little new to say about childbed fever,
he felt that the existence of the minority, who questioned its contagious-
ness, justified his essay.
Holmes cited about twenty cases in which physicians examined or
treated patients with puerperal fever or in which they performed autop-
sies on women who died from puerperal fever and in which their other
patients subsequently contracted the disease. He warned obstetricians
against taking ‘any active part in the post-mortem examinations of
cases of puerperal fever’ and that ‘on the occurrence of a single case of
puerperal fever in his practice, the physician is bound to consider the
next female he attends in labor … as in danger of being infected by him’
(p. 168). Holmes considered cases suggesting that puerperal fever could
be produced ‘by an infection originating in the matter or effluvia of
erysipelas’. But he found the relation of puerperal fever to other dis-
eases ‘remote and rarely obvious’. Thus, while he mentioned reports
that ‘puerperal fever has appeared to originate from a continued prox-
imity to patients suffering with typhus’, these cases were so rare that
they ‘hardly attract our notice in the midst of the gloomy facts by which
they are surrounded’ (p. 165). Holmes never suggested that patients
with other diseases or corpses of persons who died from other diseases
constituted a risk to maternity patients. Indeed, he observed that
the number of cases of serious consequences ensuing from the
dissection of the bodies of those who had perished of puerperal
fever is so vastly disproportioned to the relatively small number of
autopsies made in this complaint as compared with typhus or
42 THE RISE OF CAUSAL CONCEPTS OF DISEASE
When Oliver Wendell Holmes’ essay was published, Eduard Lumpe was
an assistant physician in the first section of Vienna’s charity obstetrical
clinic. In 1845, two years after publication of Holmes’ essay, Lumpe
wrote a carefully documented and thorough survey of contemporary
views of puerperal fever (Lumpe, 1845). It is a good sample of Viennese
thinking about the disease.
Lumpe gave sympathetic attention to the view, dominant among
pathologists, that what was called puerperal fever was actually a group
of symptomatically similar but anatomically distinct disorders; for this
reason, he acknowledged, many preferred the term ‘puerperal diseases’
rather than ‘puerperal fever’ (Lumpe, 1845, p. 342).5 Lumpe also men-
tioned that, while inconsistent with the meaning of ‘puerperal’, women
sometimes contracted these disorders even before delivery. He accepted
the common view that puerperal diseases usually began in the uterus.
This could be the point of attack even if autopsy disclosed only minor
changes in the uterus itself. Lumpe recognized that the morbid remains
in puerperal fever resembled those found when decaying organic matter
was accidentally introduced into the blood of a healthy patient or of a
surgeon or pathologist (pp. 350f.).
Lumpe gave considerable attention to the causes of puerperal fever.
He felt that maternity patients may be vulnerable because ‘lochial secre-
tions, the purpose of which is to remove waste matter, can be retained
or absorbed and thereby induce decay of the blood’ (p. 345). The
ETIOLOGICAL CHARACTERIZATIONS 43
could account for some cases of disease, Braun denied that it could have
the significance that Semmelweis (supposedly) attributed to it. In an
1858 letter to Semmelweis, D. Everkin of the Paderborn maternity
clinic wrote: ‘I could not imagine that this circumstance is the universal
cause, but I was led [by your communication] to avoid undertaking any
procedures on maternity patients after examining corpses.’ He then
warned Semmelweis that nowhere outside medicine is one so frequently
tempted by the post hoc ergo proper hoc fallacy (Semmelweis, 1861b,
p. 228). In the same year, Paul-Antoine Dubois wrote that while ‘one
could not dispense with precautionary measures to guard against conta-
gion, the contagious element is neither as effective nor as pervasive as
Semmelweis has claimed, … even before delivery other factors predis-
pose women to the disease’ (Semmelweis, 1861a, p. 458). Through the
early months of 1858, the French Academy of Medicine hosted a series
of 26 lectures on puerperal fever by prominent French obstetricians
(l’Académie, 1858). Semmelweis was mentioned in six of the lectures,
but there was little discussion of his work. Some speakers associated his
views with those of the British (l’Académie, 1858, p. 228). Some
acknowledged that chlorine washings may be useful. Only one speaker,
M. Danyau, considered Semmelweis’s claim to have identified a univer-
sal cause; Danyau rejected this claim but urged physicians to do
everything possible to avoid infecting patients (l’Académie, 1858, p.
228). In 1859 Hermann Lebert, Professor at Breslau, wrote: ‘It is ques-
tionable whether those who have died of this disease can have been
directly inoculated by poison from corpses. Semmelweis has elevated
this possibility into an entire system. In any case this would be only one
of many possibilities of conveyance’ (Semmelweis, 1861b, p. 221).
Thus, through the 1850s, several physicians acknowledged that chlo-
rine washings could be useful; some mistakenly associated Semmelweis’s
concept of childbed fever with that of the British; some mistakenly
assumed that Semmelweis was concerned only with cadaveric poison-
ing. However, Semmelweis’s view that the disease always had one
common cause was invariably either ignored or rejected. In this respect,
there was greater agreement between Semmelweis’s opponents and those
he regarded as supporters than there was between Semmelweis and his
supposed supporters. Those who realized that Semmelweis was making
this strong claim, rejected it. The few who thought they agreed with
Semmelweis did so only because they ignored what was unique and
original in his position. There is no textual evidence that, as late as
1862, anyone in Europe had accepted Semmelweis’s claim.
In 1858 Semmelweis published a short essay entitled ‘The Etiology of
Childbed Fever’; two years later he published a second essay entitled:
‘The Difference in Opinion between Myself and the English Physicians
48 THE RISE OF CAUSAL CONCEPTS OF DISEASE
per cent to 0.3 per cent] – a much lower figure than the [1 per cent] rate
in the early days of the Vienna Lying-in Hospital [that was the basis for
Semmelweis’s estimate of the rate of self-infection]’ (Loudon, 2000,
p. 98). Presumably, Loudon thinks Semmelweis would find this fact
awkward because the discrepancy suggests deaths due neither to self-
infection (which, according to Loudon’s figures, could only account for
a 0.2 per cent mortality) nor to contamination from external sources
(which, according to Semmelweis, could only account for deaths above
1 per cent). So how would Semmelweis explain the other deaths? Very
easily. Most likely Semmelweis would have admitted that his estimate of
the rate of self-infection was too high (his figure, after all, was arrived
at only empirically and even in the early days of the hospital some
decaying organic matter would have been conveyed – for example, from
patients with superficial infections or medullary carcinomas that gener-
ated decaying organic matter in his time as well (Semmelweis, 1861b,
pp. 93f.). But he could also have simply denied that the excess deaths
(any above 0.2 per cent but below his 1 per cent standard) were really
childbed fever.10 For example, suppose, from our present point of view,
a woman contracted a fever from fomites bearing strep organisms and
that no decaying matter was involved. Such a woman simply did not
have childbed fever in Semmelweis’s sense – nothing awkward about
that at all.
Loudon also finds it ‘extraordinary’ that Semmelweis denied that
‘puerperal fever was ever contagious, or that it ever occurred in the
form of epidemics’ (Loudon, 2000, p. 98). But clearly it all depends on
what one means by ‘contagious’ and ‘epidemic’: Semmelweis never
denied that the disease could spread from patient to patient (which, he
agreed with the British, happened only rarely) or that it could be spread
by way of other healthy persons such as medical personnel (which, he
agreed with the British, was the means by which it was usually con-
veyed). Semmelweis also never denied that the disease occurred more
frequently sometimes than others – that observation, after all, was the
main basis for his argument. However, given his definitions, the only
way the disease could spread at all or occur more frequently sometimes
than others was through conveyance of decaying organic matter. If
illness arose under other circumstances, once again, Semmelweis would
simply deny that the cases were really childbed fever. But how could he
deny that such other cases (which everyone knew to be childbed fever)
really were childbed fever? In exactly the same way that, once Robert
Koch had defined tuberculosis as infestation by the tubercle bacillus, he
could deny that all other cases (which everyone knew to be tuberculo-
sis) really were tuberculosis (namely, symptomatically and pathologically
indistinguishable cases ‘due to leprosy bacilli, brucella bacteria, histo-
ETIOLOGICAL CHARACTERIZATIONS 53
theory was better than anything else around. Now, to be sure, the subtle
shift in meaning that differentiated Semmelweis from the British would
not have mattered much to the hundreds of thousands (possibly mil-
lions) of young women sacrificed in the maternity clinics, and it may
not matter much today to physicians busy trying to keep their patients
healthy. But if one claims to understand Semmelweis’s theory (and
especially if one undertakes to explain how it is wrong or unoriginal),
one must, at the very least, be clear about this rather subtle but pro-
foundly important distinction. Because, for the last 150 years, all those
who have failed to grasp it end up either rejecting Semmelweis’s theory
for reasons that are totally irrelevant or saying that his theory wasn’t all
that original after all. Somehow, Loudon manages to do both.13
Semmelweis probably had little interest in the purely methodological
significance of his definitions; he was interested only in saving lives. But
methodologically they were singularly brilliant. The definitions effec-
tively created a new disease, albeit one called by the same name and
encompassing most (but not all) instances of what had previously been
called childbed fever. The definitions excluded from consideration all
cases that failed to have the one common cause, and that cause became,
thereby, universal and necessary. By what could be seen as nothing more
than a verbal trick – which Lumpe astutely, correctly, and precisely
characterized as an egg of Columbus (Lumpe, 1850, pp. 392f) –
Semmelweis made it possible, at least in principle, to identify reliable
strategies against the disease and to give coherent explanations of dis-
ease phenomena. Semmelweis provided not merely new facts about the
fever or practical advice for avoiding it; he offered a coherent and
empirically verifiable explanatory theory. In this respect, his account
was vastly superior to anything else that had been written on the
disease. As Semmelweis’s great contemporary Charles Darwin observed,
in reference to his own (similarly flawed yet powerful) theory of evolu-
tion, it would be impossible for an altogether false theory to explain so
much (Darwin, 1876, p. 239).
seems to have been generally associated with him (Roser, 1860). ‘Before
the time of Semmelweiss [sic], the idea of the identity of puerperal fever
with pyemia was very far from the minds of the obstetricians, puerperal
fever being regarded as something essentially inherent in the relations
presented by the puerperal woman’ (Hoag, 1887, p. 832). Perhaps
because clinical cases of puerperal fever and surgical fever were readily
available in nearly every hospital, discussions of these two diseases, and
especially of childbed fever, became prominent in the literature on
wound infections. Thus, given the historical situation and the knowl-
edge available at the time, studies of puerperal fever were central to the
development of the bacterial theory.
In 1865, Mayrhofer’s views were mentioned in connection with a
paper on epidemic puerperal fever which was presented by a doctor
Kaufmann in the annual meeting of the German Natural Scientists and
Physicians (Kaufmann, 1866). After mentioning Semmelweis, Kaufmann
rejected the possibility of septic infectious matter, and endorsed, in-
stead, a miasmatic explanation of childbed fever. However, according
to the published report:
Veit (Bonn), [Franz Ludwig Wilhelm] Winckel (Rostock), Pernice
(Greifswald), and [Eduard] Martin (Berlin) were inclined to the
infectious theory. … Martin mentioned Mayrhofer’s theory of
vibrions, and Mankiewitz (Mühlhausen) referred to the injuries to
genitals, particularly in operations with forceps.
(Kaufman, 1866, p. 424)
Thus all who are reported as having responded to Kaufmann’s lecture
favored the infection theory, and Mayrhofer was explicitly mentioned.
This report appeared in the same issue of the periodical that contained
Veit’s article (cited above) in which Mayrhofer was associated with
Semmelweis.
In 1866, F.L. Winckel published an important text on obstetrics. His
detailed historical account of various theories of childbed fever included
a summary of Semmelweis’s position (Winckel, 1866, p. 264). Winckel
mentioned that Lange of Munich had been among the first to adopt
Semmelweis’s views. He also discussed and agreed with Veit’s conclu-
sion that prevention of fever depended less on ventilation than on
absolute cleanliness – a view Winckel had already supported in the
discussion of Kaufmann’s paper one year earlier (Kaufmann, 1866,
p. 424). Near the end of his account, Winckel gave detailed and positive
attention to Mayrhofer’s work and to other publications based on it
(Winckel, 1866, pp. 274f.).
Also in 1866 Leon Coze and Victor-Timothee Feltz mentioned
Mayrhofer in an historical survey that initiated one of their series of
highly influential studies of wound infections (Coze and Feltz, 1866,
ETIOLOGICAL CHARACTERIZATIONS 57
There is no reason to think Henle saw any relation between his call for a
rational system of medicine built on universal necessary causes and
Semmelweis’s definition of ‘childbed fever’ in terms of decaying organic
matter. For all we know, Henle, like most of his contemporaries, regarded
Semmelweis as an aberration. Moreover, Semmelweis almost certainly
never thought of his theory in terms of Henle’s aspirations for rational
medicine. Yet the two are inseparably linked: only by way of etiological
characterizations can the range of human illnesses be systematized into
diseases with universal necessary causes, and only in the creation of such
a system can the potential strength of Semmelweis’s innovation be real-
ized. However, Semmelweis showed no interest in generalizing from his
60 THE RISE OF CAUSAL CONCEPTS OF DISEASE
Notes
Microorganisms as Causes
In this chapter we will review some of Louis Pasteur’s early attempts
to prove that germs cause certain organic processes. Today, it seems
obvious that microorganisms cause various natural phenomena such
as fermentation, decomposition, and disease, but in the early nine-
teenth century this was not clear. There were inherent obstacles to
accepting germs as causes, and overcoming some of these obstacles
required more than simply making the right empirical observations.
Causes are not discovered in the same way that one might discover
shells on a beach.
As described by Imre Lakatos, a ‘research programme consists of
methodological rules: some tell us what paths of research to avoid
(negative heuristic), and others what paths to pursue (positive heuris-
tic)’ (Lakatos, 1968, p. 132). Such rules are often left implicit. However,
if stated, they may resemble very general claims about the world –
claims that exceed any possible empirical confirmation.1 Lakatos says
that such principles are made ‘“irrefutable” by the methodological
decision of its protagonists’ (Lakatos, 1968, p. 133). However, strictly
speaking, being rules and not empirical claims, they are neither true nor
false and they are not subject to proof or refutation. Like any rules, they
can be shown to be useful in achieving certain objectives (for example,
in explaining and controlling nature) and, once seen as useful, they may
become standard conventions (one might say made irrefutable) by the
consensus of the researchers who adopt them.
Three such heuristic rules emerged in early work leading to the
etiological research programme. We will refer to these rules as the
Distinguishability, Dissemination, and Bacterial Hypotheses.2 These hy-
potheses cannot be confirmed empirically yet they were required before
microorganisms could be accepted as causes of the natural processes
with which they are now universally associated. In this chapter we will
encounter the first two of these, the Distinguishability and Dissemina-
tion Hypotheses; the third, the Bacterial Hypothesis, will appear at the
end of the next chapter. In this chapter we will also examine several of
Pasteur’s early arguments to see how he attempted to prove that germs
are causes.
MICROORGANISMS AS CAUSES 63
human infections, his work was based on the same ideas and methods
that had guided him in his earlier studies (Pasteur, 1873a, p. 415). In
this chapter we will consider only Pasteur’s early publications on the
theory of germs – those appearing before 1870.
(Pasteur, 1861b, p. 142) and that these ferments could not be trans-
formed into one another (Pasteur, 1862). Given that he could not
always distinguish ferments other than by their fermentation processes,
this conviction could not be confirmed universally without begging the
question. However, it could be illustrated in some cases (since some
organisms could be distinguished morphologically) and thereby made
plausible, and it was an absolutely essential presupposition if one wished,
as Pasteur did, to explain different fermentation processes strictly in
terms of the ferments themselves. If, as some researchers then believed,
all ferments were ultimately the same and transformable into one an-
other (that is if they were not truly distinct), then different fermentation
processes could not be explained simply in terms of the organisms
themselves – such explanations would require an appeal to whatever
other factors accounted for their different effects in different circum-
stances. Thus, insofar as the ferments themselves were to be the basis
for explaining fermentation, it was essential to assume that different
fermentation processes were due to distinct ferments. Of course the
same assumption would be equally essential if one attempted, as Pas-
teur and others later did, to explain different kinds of spoilage or
different diseases in terms of organisms. Here and throughout his ca-
reer, therefore, Pasteur required a crucial assumption that could not be
conclusively demonstrated – an assumption that would constitute part
of what Lakatos would call the negative heuristic of his research pro-
gramme. Pasteur had to assume that different organic processes, whether
fermentation, spoilage, or disease, are caused by distinct organisms. As
we will see later (p. 105) this assumption need not be understood as a
claim about the world although it is natural to think of it in this way. As
Imre Lakatos explained regarding other basic scientific hypotheses, this
assumption may be best regarded as a rule that guides research: always
suppose that different organic processes are due to distinct organisms.
We will refer to this as the Distinguishability Hypothesis4 and I will
have more to say about it later on.
Notes
3. Geison observed that this paper is ‘astonishing in its audacity and scope’
and that it introduced nearly all ‘the basic convictions and techniques that
would thereafter guide [Pasteur’s] study of fermentation in general’ (Geison,
1995, p. 90).
4. Geison wrote that, among the basic convictions introduced in Pasteur’s
first (1857a) paper on lactic fermentation was ‘his notion of specificity,
according to which each fermentation could be traced to a specific mi-
crobe’ (Geison, 1995, p. 90).
5. This situation was made even more complex by the fact, recently un-
earthed by Geison, that Pasteur actually believed in a kind of spontaneous
generation and conducted numerous (unsuccessful) experiments to verify
it. However, Pasteur was not quite inconsistent; his view seems to have
been that spontaneous generation could not come about using the ordinary
techniques available in chemical or biological laboratories (Geison, 1995,
pp. 136–42). This aspect of Pasteur’s work does not concern us in the
present context.
6. I will have more to say about Latour under ‘Some Final Thoughts’ at the
end of this book.
7. Pasteur first reported this discovery in remarks before a special meeting of
the Comice agricole d’Alais in 1867 (Pasteur, 1867b). Pebrine is now
attributed to a protozoan, Nosema bombycis, and flacherie to a virus that
predisposes the silkworm to infection by the bacterium, Bacillus bombycis,
that Pasteur had observed (Lechevalier and Solotorovsky, 1975, p. 40).
CHAPTER FIVE
anthrax nor even the bearers of the contagium (Brauell, 1858, p. 463).
Given that Brauell relied on visual inspection to determine whether
blood samples contained rod-shaped bodies, he may simply have over-
looked isolated organisms. Since he did not distinguish anthrax bacilli
from ordinary decomposition organisms, it is also possible that some of
his test animals died from other diseases. In any case while Brauell
believed the rod-shaped bodies conclusively indicated that a diseased
animal was about to die, he was not persuaded that they caused
anthrax.
ing one fact I believe to be new. The examination of six animals suffer-
ing or dead of anthrax has six times revealed in their blood the same
microscopic beings. These corpuscles evidently develop during the life
of the infected animal, and their relation to the disease that leads to
death cannot be in doubt’ (Davaine, 1863a, p. 223).
Whether he realized it or not, Davaine’s reasoning followed a familiar
pattern. It was like Pasteur’s arguments that various organisms cause
fermentation and wine spoilage, it was like Gruby’s arguments that vari-
ous fungi cause human mycoses, and it was like Bassi’s argument that
Beauvaria bassiana causes muscardine: having observed a particular or-
ganism regularly present in some process (fermentation, putrefaction,
disease), each inferred that the organism caused the process. Each author
inferred causality from observational evidence of necessity. Partly in re-
sponse to his critics (whom he identified as pathologists), Davaine soon
provided other evidence of causality. However, in the preceding argu-
ment, which was his first attempt to prove a causal connection, and in
others that came later, the evidence that Davaine seems to have found
most compelling was evidence of necessity. Like Bassi, Gruby, Semmelweis,
and Pasteur, Davaine began by thinking in terms of necessary causes.
Given Davaine’s interest in Pasteur’s work, it is possible that this prefer-
ence reflects Pasteur’s influence.
In his second paper Davaine confirmed his earlier findings and re-
ported new experiments in which he inoculated rabbits with fresh blood
containing anthrax bacteria. He reported the organisms were present in
the rabbits’ blood before the onset of morbid changes and that very
small quantities of infected blood could kill healthy rabbits. Davaine
also found that anthrax blood, after being rapidly dried, could be
heated to 100 degrees without losing its contagious powers. On the
other hand, putrefied blood from which the organisms had disappeared
was incapable of conveying anthrax. Davaine concluded that there was
no reason to seek some further ‘contagious element, mysterious and
unknown’, that presumably developed and destroyed when and only
when the bacterium was also present. The bacterium ‘is visible and
palpable; an organized being, endowed with life, that develops and
propagates as a living being. By its presence and rapid multiplication in
the blood, it brings about, in the constitution of this liquid, without
doubt after the manner of a ferment, those modifications from which
the infected animal quickly dies’ (Davaine, 1863b, p. 387).
cause was some other entity – an otherwise unknown virus – that was
regularly associated with bacteridia.
Brauell reported that blood from anthracoid animals sometimes con-
tained no trace of rod-shaped bodies, and he also confirmed that
inoculations with such blood could sometimes induce anthrax. He men-
tioned other researchers, including even Davaine himself, who had
acknowledged similar results. Thus, he concluded, far from proving
causality, the research Huppert cited actually contained evidence against
it (Brauell, 1866, p. 294). Brauell wrote that he would be pleased if
Pasteur’s theory of fermentation could be applied to the contagious
diseases and if the rod-shaped bodies could be shown to cause anthrax
by blood fermentation. However, he regarded this as unlikely: he doubted
that all fermentation was due to living organisms, but even if it were, he
observed, it would still be doubtful that anthrax was a kind of fermen-
tation. Brauell wrote that, even if Pasteur’s work had been available
when he had conducted his own study of anthrax, his conclusions
would have been precisely the same.
concluded that the cause of the disease had to be a living organism that
could multiply within the victim.
Even after all of Davaine’s work, both French and German critics
remained unpersuaded. In their minds, he had not excluded the possibil-
ity that anthrax could arise spontaneously or through some combination
of factors not involving bacteridia (that is he had not proven causal
necessity), and he had not proven that bacteridia, when isolated from
every other ingredient of anthrax blood, would themselves bring on the
disease (that is, he had not proven causal sufficiency). A German writer
observed that Davaine had been unable to perform ‘the one experiment
that would have overcome all objections to his opinion on the signifi-
cance of bacteridia: namely, freeing the blood from bacteridia by filtration
through clay and inoculating the filtrate’ (Steudener, 1872, p. 304).
Explained in this way, the deficiency in Davaine’s argument appears to
have been purely technical – he seems only to have needed a more
reliable way of isolating bacteridia from the other ingredients in anthrax
blood. Indeed, Davaine and other researchers devoted considerable
effort to progressively more rigorous methods of separating bacteridia
from every contaminant that could have been causally relevant. How-
ever, no such effort could be completely successful until there was
agreement as to exactly which potential contaminants could be causally
relevant. In the absence of such agreement, no matter what steps were
taken to insure the purity of a given culture, skeptics could always
maintain there could still be some unknown substance that had not
been excluded and that could be the true cause of anthrax.
The only way of silencing this objection would have been by appeal-
ing to some hypothesis such as this: every disease is caused by bacteria.
We will call this the Bacterial Hypothesis, and we will defer until the
next chapter the objection that it is obviously false. No one questioned
that bacteridia were the only bacteria involved in anthrax. Thus if
Davaine’s critics had accepted something like the Bacterial Hypothesis,
they would clearly have accepted the bacteridium as the cause, rather
than continue holding out for some possible unknown entity. This is
like saying (1) if Davaine’s critics had accepted what Pasteur called the
Dissemination Hypothesis – the assumption that bacterial cultures never
arise spontaneously but only from antecedent bacteria – they would not
have taken seriously the idea that anthrax could occur spontaneously,
or (2) if Leplat and Jaillard had accepted the Distinguishability Hypoth-
88 THE RISE OF CAUSAL CONCEPTS OF DISEASE
Note
the very breadth of his interests gave Klebs a perspective from which to
approach philosophical issues. He gave more extensive and more ex-
plicit attention to causal criteria than any of his contemporaries, and he
stated explicitly some of the basic assumptions underlying the bacterial
theory of disease to which he was contributing. These are the two
aspects of his work that will be of interest to us, but before we examine
Klebs’ views, we must briefly review some developments in bacteriology
that provided the context of Klebs’ own investigations.
Since the late eighteenth century, pathologists had discussed the morbid
alterations typical of infected wounds. In infected tissues one found soft
gray spots the size of pin heads. In advanced cases the spots became
larger and more numerous, they merged, and their centers degenerated
into a substance resembling pus. These spots seemed to be new sites to
which infection was spreading, and they were called metastases. In
1866 Eduard Rindfleisch, a German pathologist, found that metastases
did not contain pus corpuscles, but rather microorganisms (Rindfleisch,
1867–69, pp. 183, 204). In harmony with existing terminology, he
identified the organisms as vibrions. Rindfleisch reported that metastases
originally contained vibrions densely packed between strands of muscle
tissue; later the organisms spread into surrounding tissues and the
muscle fibers decomposed. Another common morbid product of wound
infections was a gray film that gradually spread over wound surfaces.
Similar structures developed in the throats and lungs of diphtheria
patients. As early as 1868 researchers reported finding clusters of small
spherical organisms in these gray films. These organisms were called
micrococci. However, finding living organisms in infected wounds did
not prove they caused the morbid processes, and the exact role of the
organisms remained a matter of dispute.
By the beginning of the 1870s, many different observations of micro-
organisms had been reported, but the reports were of uneven quality
and, in the absence of photographs, they were supported at best by
freehand drawings of the organisms in question. Under these conditions
there was confusion about who had seen what and this uncertainty was
compounded by the lack of a consistent nomenclature. Many writers
followed Christian Gottfried Ehrenberg’s 1824 taxonomic system, but
as new organisms were discovered, this scheme became progressively
less adequate and researchers simply made up names of their own (like
Davaine’s ‘bacteridium’). Often there was considerable variation in ter-
minology even within the works of a single author.
A BACTERIAL THEORY OF DISEASE 93
several papers Klebs cited Obermeier’s work and seems to have taken it
for granted that Obermeier had proven causation (Klebs, 1878a, p. 51).
Thus, relapsing fever became the first disease widely believed to be
caused by a spirochete.
not arguing that some particular organism causes some disease (an argu-
ment that would require E1 or E2); instead, he is addressing the
fundamental and more general issue of establishing a context within
which any causal demonstration can be given. He is asking: what are the
basic conditions on which any such demonstration depends? Rephrasing
the question in terms of his analogy with the exact sciences, Klebs is
asking: what conditions must be met in order successfully to ask nature
(by applying E1 or E2) whether a particular schizomycete causes a certain
disease? Read in this way, the Grundversuche are ideal or simplifying
conditions basic to any investigation of disease causation.
Klebs writes:
In respect to the pathological influence of the schizomycetes, as
such fundamental tests [Grundversuche], I give heed to the follow-
ing: first, the proof that they never occur in the body fluids or in
some part of the secretions of a healthy organism; second, that they
do not develop spontaneously in liquids appropriate to their nour-
ishment … third, the fact that with the mechanical separation or
the natural death of the schizomycetes, the potency of the liquids
that contained them ceases; and fourth, the fact that local or gen-
eral infections of the [different] individual forms of pathogenic
schizomycetes, which have now been at least partially character-
ized, bring forth changes that are precisely characterized, uniformly
similar, and adequately distinguishable from [those associated with]
the operation of schizomycetes of other forms.
(Klebs, 1875–76, pp. 376f.)
As an idealized basis for a theory of disease, the Grundversuche tell
us schizomycetes have these properties: first, they are absent from the
body fluids and secretions of healthy animals; second, they never arise
spontaneously, not even in fluids that satisfy their nutritional needs;
third, once removed (artificially or otherwise) from some liquid, the
liquid alone has no pathogenic effect; and fourth, distinct schizomycetes
cause different pathological processes. In this passage, Klebs speaks of
the third and fourth Grundversuche as ‘facts’ and of the first as ‘a
proof’. However, the second resembles what we have called the Dis-
semination Hypothesis (p. 66 above), and as Pasteur realized, this
hypothesis can be neither proved nor disproved. While such principles
can be illustrated and made plausible, strictly speaking they cannot be
proven and they are not facts in the ordinary sense of the word. It seems
most plausible to refer to all four as hypotheses, and this is consistent
with Klebs’ idea that the Grundversuche are simplifying conditions
under which one can ‘put questions to nature’.
Four hypotheses emerge from the Grundversuche that are of particu-
lar interest. In stating these, we use the more common term ‘bacterium’
in place of Klebs’ term ‘schizomycete’.
102 THE RISE OF CAUSAL CONCEPTS OF DISEASE
Notes
1. Klebs’ papers appeared in volumes 16, 32, 33, 34, and 38 of Archiv für
pathologische Anatomie, Physiologie, und klinische Medizine (Virchows
Archiv).
2. For example, in an 1861 discussion of puerperal fever, Virchow insisted
that ‘just as a man who is overheated will contract facial erysipelas if he
exposes his face to a draft, so too the puerpera, overheated by the process
of delivery, can become ill if her uterus is chilled’ (Monatsschrif für
Geburtskunde … , 1861, p. 380).
3. The term ‘schizomycete’ was coined by the Swiss microscopist Carl Naegeli,
as a generic term including both bacteria and fungi. Ferdinand Cohn
objected to the term as implying a false connection between bacteria and
fungi (Cohn, 1872, p. 191; 1875, p. 201), but Klebs seems to have liked
the term and used it regularly.
4. For an enlightening discussion of the nature and possibility of theories and
laws in the biological sciences see Van der Steen and Kamminga (1991).
5. The roots of this compound plural noun are Grund (ground, basis or
foundation) and Versuch (test, trial or attempt); literally, the word means
something like ‘basic tests’. However, the combination itself is uncommon,
perhaps unique to this context, and Klebs does not explain what he means.
6. For another example, in discussing phenylketonuria (PKU), F. Kräupl Taylor
writes: ‘From such ambiguity, there is only a small step to apparent self-
contradiction. The parents of PKU patients, being heterozygous for the
pathological gene, can have PKU (the clinical sign) after a meal rich in
phenylalanine, though they do not have PKU (the [disease] or the morbus).
Similarly, a PKU patient, when on a diet poor in phenylalanine from his
earliest days, still has PKU (the morbus) without PKU (the illness or the
clinical sign) (Taylor, 1979, p. 84).
7. For example, as early as 1855 Semmelweis’s bitterest enemy, Carl Braun,
speculated about the possible causal role of Henle’s ‘botanical parasites’ in
childbed fever – he even mentioned Beauvaria bassiana (then called Botrytis
bassiana) in muscardine as a possible analogy. Braun classified ‘botanical
parasites’ among 30 kinds of possible remote causes of the disease (Braun,
1855, pp. 477–85).
8. In the same way, glass is either a solid or it is a viscus liquid – there is
nothing in between, and there can be no possibility of gradually moving
from one definition to the other. See p. 53 above.
CHAPTER SEVEN
attention – and ascribed the commonest form of beer spoilage ‘to the
presence of a microscopic filiform organism’:
This fact is so true, the relation of cause and effect is so evident,
that it is absolutely impossible to produce an alteration of beer
when it does not contain the germs of this inferior organism. On
the other hand, I can demonstrate that no beer, whether from
England, France, or Germany, can be conserved beyond a certain
time; beer always becomes altered because it contains the germs of
the organized ferments of which I speak. The correlation between
the disease and the presence of the organism is certain and indis-
putable.
(Pasteur, 1873b, p. 5)
Members of the Academy objected to Pasteur’s claim that fermentation
could only occur because of a living ferment. Pasteur responded sarcas-
tically that only physicians could take seriously the possibility of
putrefaction without a putrefying agent, he demanded proof that such a
phenomenon had ever been observed, and he immediately associated
spoilage without organic agents with spontaneous generation (Pasteur,
1874b, pp. 6–7; 1874a). He responded to critics by reviewing his argu-
ments for the Dissemination Hypothesis; however, this response was
not quite to the point. One could maintain, as his critics apparently did,
that spoilage could result from a suitable combination of inert factors
without regarding those factors as sufficient to generate living organ-
isms. For some time Pasteur and his critics argued at cross purposes:
Pasteur recounting his contributions to science and denouncing sponta-
neous generation; his opponents insisting that putrefaction could occur
without living organisms (Pasteur, 1922–39, vol. 6, pp. 90–99, 20–26,
26–8, 28–37, 37–58 and vol. 5, pp. 344f.). The debate ceased in 1879
when other members of the Academy finally pointed out that most
physicians had given up spontaneous generation even before Pasteur’s
experiments, and that he could not answer his critics by this evasion
(Pasteur, 1879b, pp. 235–7). In these discussions Pasteur effectively
assumed that the cause of spoilage must be universal; his opponents did
not share this assumption.
In 1874 and 1875, Pasteur gave more lectures on putrefaction, and he
began reporting studies on ammoniacal urine. He continued making
assertions exactly in line with his earlier research and he continued to
encounter opposition. Pasteur’s opponents rejected his claim that an
organism was ‘the sine qua non of ammoniacal urine’ (Pasteur, 1875b,
p. 78) and insisted the disorder could occur without a living ferment.
Perhaps because of these discussions, in the second chapter of his
1876 book on the spoilage of beer, Pasteur gave increased attention to
establishing causality. Pasteur insisted that ‘all the alterations to which
wort and beer are subject have as their exclusive cause the development
PROVING DISEASE CAUSATION 113
when one of the two exists the other follows. This is the case here; if the
ferments are present in the intestinal canal, there is flacherie, and if
there is flacherie there are ferments in the intestinal canal’ (Pasteur,
1878b, p. 692). These remarks show clearly that Pasteur sought to
establish necessity and sufficiency, that he understood the difference,
and that he recognized his inoculation test as a means of demonstrating
the latter. Pasteur’s concept of causality and his account of how to
prove necessity and sufficiency are more explicit here than in any of his
earlier publications on flacherie.
animals that died of natural anthrax (Koch, 1876, p. 1), but of those
examinations, he reported only that he found bacilli in the spleen of one
anthrax horse – the only horse he had examined (Koch, 1876, p. 13).
Koch cited earlier researchers who identified bacilli in natural cases, but
he also mentioned that other researchers had been unable to find them.
As Koch explained in the introduction to his paper, his study grew out
of Davaine’s research that was widely accepted as presenting the strong-
est evidence that anthrax was caused by bacteria. However, Koch did
not have access to Davaine’s papers (Koch, 1878a, p. 51); he knew
Davaine’s work only from abstracts in which Davaine’s arguments were
described as supporting the necessity of the anthrax organism (Steudener,
1872). In harmony with the abstracts, Koch noted that Davaine ‘as-
serted that the rods were bacteria and that [anthrax] could occur only
when these rods from anthrax blood were present’ (Koch, 1876, p. 1).
One objection to Davaine’s view was that anthrax sometimes seemed to
have been caused by inoculations with bacteridia-free blood. Koch
answered this objection by arguing that the bacilli were often difficult
to find and could easily be overlooked.
However, explaining away apparent counter evidence did not consti-
tute a proof that the bacilli caused anthrax and, in spite of what Koch
himself later claimed, his paper contained remarkably little direct evi-
dence of causation. Moreover, the evidence it did contain was not
persuasive to contemporaries. Koch’s argument for causation appears
toward the end of his paper. He observed that anthrax and septicemia
bacilli were distinct because the latter never caused anthrax (Koch,
1876, p. 11) – an argument that presupposes the Distinguishability
Hypothesis. He mentioned he had been unable to cause anthrax by
injecting hay infusion bacilli or a species of bacillus resembling the
anthrax bacillus that developed accidentally in one of his cultures. On
the other hand, he reported that animals inoculated with spore masses
‘derived from entirely pure cultures of Bacillus anthracis … invariably
died of anthrax’ (Koch, 1876, p. 11). However, at this point Koch’s
inoculation cultures were grown in liquid media, as Davaine’s had been,
and his only evidence that the cultures were pure was that microscopic
examination revealed no contamination. For more than a decade, Davaine
had tried, unsuccessfully, to persuade critics with arguments at least as
strong as these. Yet Koch insisted his argument was conclusive:
‘Anthrax substances, whether they are fresh, decayed, or dried, can only
cause anthrax if they contain Bacillus anthracis or its viable spores.
This fact removes all doubt that Bacillus anthracis is the actual cause
and contagium of anthrax’ (Koch, 1876, p. 13). In an 1881 paper, Koch
claimed he had established causality by this argument. In that later
paper, after reviewing the earlier argument and without any additional
PROVING DISEASE CAUSATION 117
also claimed to have used this method to study a disease called chicken
cholera (Pasteur, 1879c, p. 495), and he discussed the applicability of
the method to puerperal fever (Pasteur, 1879d, pp. 498f). On two
occasions during these months, Pasteur observed: ‘everything is hidden,
obscure, and open to discussion when one ignores the cause of some
phenomena, but everything is clear when one possesses it’ (Pasteur,
1922–39, vol. 6, pp. 110, 114).
In contrast to Pasteur, after his initial paper, Koch seems not to have
continued studying anthrax. Apart from incidental references, between
1876 and 1880 Koch discussed anthrax in only one paper – his long
1878 work on wound infections (Koch, 1878a, pp. 46–48).7 The only
new result Koch announced was his use of methyl violet as a stain.
Having observed that anthrax was not recidivous, in 1880 Pasteur
began looking for a vaccine (Pasteur, 1880c). This observation, together
with similar results for other diseases, suggested what Pasteur called
‘the general law of the non-recidiviousness of virulent diseases’ (Pasteur,
1881a, p. 339). Early in 1881, Pasteur reported he could attenuate the
virulence of the bacilli of chicken cholera; this led to his important
discovery that one could also attenuate anthrax bacilli (Pasteur, 1881b).8
Pasteur began using a vaccine in tests on thousands of livestock in
various European countries. His results, along with other findings, were
announced in a series of papers. Like many of Pasteur’s earlier studies,
his anthrax inoculations promised profound economic benefits and
were widely publicized.
In 1881, Koch published a detailed criticism of Pasteur’s work (Koch,
1881b) – this was only Koch’s second major paper on anthrax. Accord-
ing to Koch, Pasteur’s work had contributed nothing to the etiology of
the disease. ‘Only a few of Pasteur’s beliefs about anthrax are new, and
they are false’ (Koc, 1881b, 65).9 He accused Pasteur of confusing
anthrax bacilli with unrelated contaminants (p. 62) and wrote that
Pasteur had probably never observed anthrax uncomplicated by other
diseases (p. 60). Koch rejected some of Pasteur’s experiments as worth-
less and naive (p. 70) and ridiculed his work with chickens and
earthworms. Koch also reviewed his own argument for causality and
asserted that ‘no more conclusive proof can be given that anthrax
bacilli are the true and only cause of anthrax’ (p. 64). In respect to the
demand to isolate bacilli from every contaminant – the condition that
most observers then expected in any proof of causality – Koch wrote:
‘this is impossible … no one can take seriously such an undertaking’.
Koch acknowledged that, even in the face of his experiments, ‘one
could still object that … some other substance associated with the
bacteria, rather than the bacilli themselves, causes the disease’. But, he
continued, ‘for all practical purposes, this objection is meaningless’
120 THE RISE OF CAUSAL CONCEPTS OF DISEASE
(p. 64). However, critics did not find the objection meaningless. In
reviewing Koch’s paper, a Professor Zuber observed: ‘how opinions can
differ! We think, and much of the world with us, that this objection has
a capital importance and we reproach precisely those authors who …
subject complex liquids to complicated procedures and thereby reach
dubious results’. Zuber praised those who tried to isolate the bacillus by
subcultures (Zuber, 1882, pp. 104f).
In September 1881 Koch and Pasteur met in an international medical
congress in London. Pasteur had not yet seen Koch’s recent scathing
criticism and veiled insults, and their relations were cordial (Geison,
1974, p. 397). Pasteur praised some of Koch’s new techniques. In a
plenary session, Pasteur summarized the results of his inoculation pro-
gramme (Pasteur, 1881c).
In March 1882, in the midst of his debate with Pasteur, Koch an-
nounced discovery of the tuberculosis bacillus (Koch, 1882a) – the
announcement created an immediate sensation throughout Europe. Af-
ter reporting he had identified a specific organism in hundreds of natural
and artificial cases of tuberculosis, Koch turned to the question of
causality. He began by explaining that in order to prove causality,
it is necessary to isolate the bacilli from the body, to grow them in
pure culture until they are freed from every disease product of the
animal organism, and, by introducing isolated bacilli into animals,
to reproduce the same morbid condition known to follow from
inoculation with spontaneously developed tuberculosis materials’.
(Koch, 1882a, p. 87)
Koch’s paper was organized around attempts to meet these conditions.
His proof of causality by isolation and inoculation is remarkable for
two reasons. First, it is his earliest use of the causal criteria later known
as Koch’s Postulates. Second, by claiming that this strategy was essen-
tial for proving causality – a strategy he had rejected as impossible just
a few months earlier – Koch was effectively admitting the inadequacy of
his own attempt to prove causality for anthrax. Moreover, his claim
implies that Pasteur’s demonstration, although conceivably inexact or
even unoriginal, at least followed the general procedure that Koch now
described as essential for proving causality. Of course, Koch never
explicitly admitted either that endorsing the new strategy undercut his
earlier claims or that Pasteur’s work had been more relevant to proving
causality than his own, yet both conclusions follow from claims he
made in the tuberculosis paper and in several papers that followed.
Koch’s adoption of isolation and inoculation probably resulted from a
combination of factors: his dispute with Pasteur; discussions with his
PROVING DISEASE CAUSATION 121
friend, Edwin Klebs, during the 1878 meetings of the German Natural
Scientists and Physicians; and his introduction of solid culture media
that enabled him to isolate bacteria much more reliably than had been
possible using only liquid media.10
Pasteur answered Koch’s criticisms in a lecture at a medical congress
in Geneva in the fall of 1882 (Pasteur, 1882). Pasteur pointed out that
critics had rejected Koch’s initial work on anthrax as inconclusive. He
explained that he himself had followed the only method for proving
causation that satisfied existing standards, and he mentioned Paul Bert
who had rejected Koch’s argument but had been persuaded by his own.
He also answered some of Koch’s specific objections. Given the tone of
Koch’s attack, Pasteur’s response was remarkably restrained. Yet Koch,
who attended Pasteur’s lecture, took offense and registered a formal
protest (Schwalbe, 1912, vol. 1, pp. 207f.; Ellenberger, 1970, p. 269).
Koch responded quickly with a long and polemical attack on Pasteur’s
inoculation programme (Koch, 1882b). Koch insinuated that Pasteur was
falsifying results (Koch, 1882b, pp. 106, 111), and he misrepresented
Pasteur’s work. Near the beginning of his paper he explained how his
methods differed from Pasteur’s. Koch claimed he first became oriented
by undertaking a thorough investigation of all the diseased tissues of the
body to determine the distribution of the organism.11 Koch then claimed
to use isolation and inoculation, which he described as ‘the only method
that meets current scientific standards’ (Koch, 1882b, p. 98). As usual, he
did not mention that Pasteur had preceded him in using this strategy or
that his initial papers on anthrax, in which he still claimed to have proved
causality, were defective for not using it.
This time Pasteur responded to Koch in an emotional open letter
(Pasteur, 1883). Pasteur expressed surprise at the virulence of Koch’s
attack. He reviewed his contributions to medicine and to science gener-
ally and mentioned that several prominent researchers, including both
Davaine and Joseph Lister, had based their studies on his own early
work. Pasteur summarized earlier research on anthrax, reiterated his
claim to have been the first to have identified spores (while admitting
Koch had first seen anthrax spores), and reviewed his argument for
causality. He again cited researchers who had rejected Koch’s causal
argument but had been persuaded by his own.
One year later, in 1884, Koch published another long criticism of
Pasteur’s attempt to attenuate anthrax bacilli (Koch, 1884a). In 1887 he
again criticized Pasteur’s inoculation program (Koch, 1887). However,
by this time, Pasteur’s programme had achieved significant success and
had been dramatically corroborated by his work on rabies; he re-
sponded to Koch’s criticism with a brief note (Pasteur, 1887). These
were the last publications by either Koch or Pasteur on anthrax.
122 THE RISE OF CAUSAL CONCEPTS OF DISEASE
One can appraise the controversy between Koch and Pasteur in dif-
ferent ways. On a personal level, Koch comes off poorly: his arguments
were sarcastic, polemical, unfair, and often included personal attacks.
While Koch regularly minimized the significance of Pasteur’s work and
misrepresented his opinions, Pasteur’s appraisals of Koch were fair and
consistent with opinions expressed by others.
In respect to their arguments for causality, Pasteur’s work obviously
came closer than Koch’s to satisfying existing expectations. Since most
contemporary researchers expected evidence of sufficiency, Koch’s argu-
ments were not seen as compelling, in spite of his technical achievements.
He seems to have tried to obscure the perceived inadequacy of his argu-
ment by ad hominem attacks on Pasteur. From what we have seen, there
is a certain irony in using the phrase ‘Koch’s Postulates’ to refer to the
causal strategy that Koch ultimately adopted and that continues with us
today. If one takes the strategy to focus on isolation and inoculation, both
Klebs and Pasteur used it before Koch and both applied it to a wider range
of diseases than Koch ever did. Moreover, Koch’s early work was deemed
inconclusive precisely because he was slow to adopt this approach.
In any case, by the mid-1880s, in France and in Germany, a consen-
sus had emerged as to how one must go about proving that specific
bacteria cause particular diseases. From this time on, everyone accepted
isolation and inoculation as crucial to proofs of causality.
went mad and died, but the patient seemed to have been cured of
hydrophobia. Some writers noticed that rabies is spontaneous only in
animals that do not perspire; to them, vigorous perspiration seemed to
offer hope. Others wrote that in animals that do not perspire, saliva
must carry off large quantities of effete matter; they advocated vigorous
salivation. One physician recommended that patients be poisoned by
curare – the South American arrow poison – and then be revived by
artificial respiration. For a time it was believed that lead, mercury, and
turpentine would cure rabies, but that victims were sometimes poisoned
in the process. One case was reported in which massive doses of croton
oil and prussic acid had apparently converted hydrophobia into a fatal
case of typhoid fever. Some physicians recommended that patients be
kept in a constant state of nausea or given small but continuous
enemata. One physician tried soaking a rennet in water, saturating it
with savanilla and forcing it down the patient’s throat; after being
placed in the sun and sleeping for 48 hours the patient awoke com-
pletely recovered.
For several reasons nineteenth-century research on rabies was par-
ticularly frustrating. First, it is difficult to convey rabies reliably among
test animals. Even deep bites by rabid animals produce new cases of
rabies only infrequently. Second, when the disease is conveyed, there
may be an incubation period of several weeks or even months (Pasteur,
1881d, p. 574). Finally, while many physicians were fairly confident
that rabies was caused by a microorganism, the best efforts of the
leading experts failed to identify it. For several years Pasteur searched
for rabies microbes – ‘On two occasions he suspected he had seen them
– in 1881 in the form of encapsulated bacteria and in 1883 as fine
particles in the brain tissue of rabid animals’ (Hughes, 1977, p. 32).
From a modern point of view, the failures were due, in part, to the fact
that the causal agent is a virus and, therefore, too small to be detected
given the equipment and methods then in use. However, Pasteur was
not deterred by his inability to identify a causal organism.
Pasteur tried injecting saliva from rabid dogs directly into the brains
of live rabbits. He found that brain fluids taken from these rabbits were
maximally virulent. Inoculating these fluids into healthy dogs usually
produced rabies within days. Although he could not identify a causal
organism, Pasteur may have wondered if the virulence of the supposed
organism could be reduced in the same manner he had attenuated the
bacteria of anthrax and chicken cholera. Developing results that had
been announced by other researchers, Pasteur confirmed that the viru-
lence of the rabies virus for animals of one species could be affected (in
some cases increased, in others decreased) by passage through series of
animals of a different species. Early on, Pasteur also concluded that the
PROVING DISEASE CAUSATION 125
elusive virus was most likely to be found in brain tissue rather than in
blood or saliva. These insights led to experiments involving spinal cords
from rabbits that had been dried in sterile air. He found that the longer
the spinal cords were allowed to dry, the longer the incubation period
for inoculations using matter taken from those cords. Pasteur inferred
that the causal agents contained in the dried cords had become less
virulent (Pasteur, 1884, pp. 593f.). Beginning with injections of tissues
that had dried for two weeks and were nearly inert, he injected dogs
with matter that was progressively more virulent. He hypothesized that
at some stage test animals would be immune. This, he believed, could
be shown if injecting full-strength brain tissue into immunized dogs had
no ill effects (Pasteur, 1885, p. 603).14
While still engaged in this research and before he had conclusive
evidence his methods would work, Pasteur was urged to try his proce-
dure on a human being. On 4 July 1885, a nine-year-old Alsatian boy,
Joseph Meister, had been badly bitten by a rabid dog, and the boy had
been brought to Pasteur.15 Pasteur knew that only a small percentage of
similarly bitten humans would contract rabies. He also acknowledged
that his experiments were incomplete and that he had never tried inocu-
lations on test animals after they had already been bitten (Pasteur,
1885, p. 606). Yet Pasteur took a chance that could be described as
irresponsible: on 6 July he began inoculating Meister with tissues from
the dried spinal cords of diseased rabbits. On 16 July 1885, having
given Meister 13 shots in 10 days, Pasteur used fluids containing fresh
and fully virulent rabies material. When this produced no evidence of
the disease, Pasteur pronounced the boy cured. Given that inoculations
did not always produce rabies and that the disease had an uncertain
incubation period, the announcement was premature. However, Joseph
Meister remained healthy, and Pasteur’s work was proclaimed around
the world as a brilliant success.
Within months thousands of exposed persons began flocking to Pas-
teur’s laboratory from all over the world. Between 1886 and 1934,
34,111 persons who had been bitten by confirmed rabid animals were
treated at the Pasteur Institute. Of these thousands, only three persons
died; among untreated victims, the average mortality was 16 per cent
(Malkin, 1986, p. 45). Thus, even though the cause of rabies had not
been identified (and even though it turned out, ultimately, not to be
bacterial), since the inoculations clearly emerged from what Pasteur
called the theory of germs, the success of the inoculations was taken as
further support for that theory.
126 THE RISE OF CAUSAL CONCEPTS OF DISEASE
Notes
Koch used explicit causal criteria in fewer than ten of his more than 100
published papers, and, with the exception of one 1890 lecture, all of
130 THE RISE OF CAUSAL CONCEPTS OF DISEASE
these papers appeared between 1878 and 1884. There are important
differences in the causal criteria that Koch stated: later versions in-
cluded conditions absent from the earlier ones, and some of the conditions
were given in several non-equivalent versions. We will examine Koch’s
discussions of causation in his first anthrax paper, in two 1878 papers
on wound infections, and in several papers published between 1882 and
1884. However, his later accounts are most interesting, and discussion
of individual criteria will be postponed until we have reviewed all the
publications.
We have already considered Koch’s 1876 anthrax paper; in this con-
text, a few additional comments are necessary. In this first paper, Koch
neither discussed nor even mentioned causal criteria; he gave little explicit
attention to proving that anthrax bacilli cause anthrax, and the few
arguments he put forward focused on necessity. By the time Koch wrote
this paper, he knew that the mere presence of anthrax bacilli in a suscep-
tible host was not sufficient to insure onset of anthrax: ingesting bacilli
did not usually provoke the disease (Koch, 1876, p. 11), some inocula-
tion procedures were unreliable (Koch, 1876, p. 2), and among exposed
susceptible animals, vulnerability varied (Koch, 1882b, pp. 101f.). Koch
never claimed the bacilli were sufficient to cause anthrax. After some
early failures, he developed a reliable inoculation procedure; thus, this
procedure (as opposed to the organisms alone) was sufficient for the
disease. However, in describing the procedure, he wrote only that it
provided a useful test for the viability of his cultures (Koch, 1876, p. 2).
Nowhere did he suggest that the inoculations constituted direct or con-
clusive evidence that bacilli caused anthrax. Instead, here is his only
argument for causation: ‘anthrax substances, whether they are fresh,
decayed, or dried, can only cause anthrax if they contain Bacillus anthracis
or its viable spores. This fact removes all doubt that Bacillus anthracis is
the actual cause and contagium of anthrax’ (Koch, 1876, p. 13). Thus, as
he himself presented his argument, he seems to have been most influenced
by his unsuccessful inoculations with substances lacking bacilli and spores.
Of course, such experiments provided evidence of necessity.
In 1878, Koch published two papers on wound infections. The first
was a summary lecture; the second was a long account of his research.
Koch began the summary by observing that the regular identification of
microorganisms in infected wounds did not prove that these diseases
come about only when organisms enter the body and proliferate
there, in other words, that the diseases are parasitic. This is be-
cause in many cases of unquestionably infectious diseases, either
no organisms are found or too few are found to explain the symp-
toms or the fatal termination of the disease.
(Koch, 1878b, p. 58)
THE ETIOLOGICAL STANDPOINT 131
isolate the suspected disease agent in pure culture and to confirm it was
alive. Even after all of this,
it remains to prove the isolated parasite is really the cause of the
disease. To accomplish this, one must show that animals inoculated
with pure culture contract the original disease. The inoculation
must succeed not only sometimes, but in every attempt as is achieved
in such infectious diseases as anthrax.
(Koch, 1882c, pp. 446f.)
In substantial sections of both 1882 papers, Koch reported attempts to
inoculate materials from pure cultures. The effort devoted to this part
of the argument, together with his own explicit assertions, show clearly
that he regarded this as the decisive step in proving causation. After
reporting his inoculation experiments, he concluded, ‘All these facts,
taken together, show that the bacilli in tuberculous substances are not
merely coincidental with tuberculosis, but cause it. These bacilli are the
real tuberculosis virus’ (Koch, 1882a, p. 93). Koch reclassified, as one
disease, all the symptomatically and pathologically distinct cases in
which the organism could be identified and excluded all other cases as
not true tuberculosis (Koch, 1882a, pp. 93f.) thereby, in effect, giving a
new definition to ‘tuberculosis’ (Taylor, 1979, pp. 18f.).
In 1882 Koch also published a paper criticizing Pasteur’s attempts to
immunize animals against anthrax (Koch, 1882b). In this paper, he
described what he called his own method of studying infectious disease,
and he contrasted this method with what was supposedly Pasteur’s
method. Koch claimed to begin by examining ‘all the body parts that
are altered by the disease. In this way, one can establish the presence of
the parasites, their distribution in the diseased organs, and their relation
to body tissues’ (Koch, 1882b, p. 98). However, this study provides
only ‘a complete orientation’ to the disease – it still remains to prove
causation. For this purpose, the organisms ‘must be cultured in pure
form. Then, after they have been freed from all the parts of the diseased
body with which they were originally associated, they must be inocu-
lated back into animals of the same species as those in which the disease
was originally observed’ (Koch, 1882b, p. 98). Koch mentioned tuber-
culosis as a disease for which these criteria had been fully satisfied.
Thus, in this 1882 anthrax paper, Koch endorsed the same steps for
proving causality as in the tuberculosis papers appearing in the same
year. As we have seen, these were not the steps he himself followed in
his original work on anthrax; in fact, Pasteur’s study of anthrax came
closer to following these steps than did Koch’s.
Koch’s monumental 1884 paper on the etiology of tuberculosis con-
tains his most complete discussion of causation. He wrote:
136 THE RISE OF CAUSAL CONCEPTS OF DISEASE
Through the 1880s, Koch and his fellow workers discovered the
causal agents for a range of bacterial diseases. They also published
important papers on applying bacteriology to public health, they an-
nounced techniques for measuring the bacterial content of air, soil, and
drinking water, they tested new methods for disinfection, and they
developed a procedure for steam disinfection. Later, Koch discussed the
methods that produced these results:
These new methods proved so helpful and useful in dealing with
various problems that one could regard them as the keys for the
further investigation of microorganisms, at least insofar as they
relate to medicine. Once I had developed them and gained some
experience in their use, I utilized them in the study of the patho-
genic microorganisms. In a rapid sequence, my colleagues and I
were successful in discovering the cause, and thereby the etiology,
of a number of infectious diseases. These included the wound
138 THE RISE OF CAUSAL CONCEPTS OF DISEASE
both harbor the causal agent and manifest symptoms of a certain inten-
sity or otherwise require medical intervention. Thus, for practical reasons,
we often decide against making causes definitionally sufficient for their
diseases.
Exactly what evidence is furnished by Rt1, Rt4 and Rt5? One can
think of Rt1 as providing observational evidence of sufficiency; alterna-
tively, Koch suggested that one could also regard this criterion as
providing motivation (what he called an orientation (Koch, 1882b, p.
98)) for investigating causality rather than as part of the actual proof.
What about Rt4 and Rt5 – the isolation and inoculation test? In a
tuberculosis paper, Koch insisted that ‘inoculation must succeed not
only sometimes, but in every attempt as is attained in such infectious
diseases as anthrax’ (Koch, 1882c, pp. 446f.). Even if this is achieved, it
does not mean the organism is sufficient for the onset of symptoms. As
we have seen, Koch knew that the mere presence of anthrax bacilli was
not sufficient for anthrax: ingesting them did not usually provoke symp-
toms (Koch, 1876, p. 11), even some inoculation procedures were
unreliable (Koch, 1876, p. 2), and vulnerability varied among suscepti-
ble animals (Koch, 1882b, p. 101). Koch never claimed bacilli alone
were sufficient for anthrax, and current definitions of ‘anthrax’ allow
organisms to occur in test animals in the absence of the disease. Thus,
even the invariable success of inoculations does not – and, given most
definitions, can not – demonstrate that the organism alone is strictly
sufficient: universal success shows only that the organism can be used in
an inoculation procedure that is sufficient. This claim is obviously
weaker than the claim that the factor itself is sufficient. Because criteria
like Rt4 and Rt5 support only this weaker claim, they have been called
weak sufficiency criteria (Carter, 1985b, pp. 358f.). As here defined, a
weak sufficiency condition requires that there is some means by which
the organism can be introduced into a host in such a way that the host
will invariably become diseased.
Are weak sufficiency criteria essential to proving causation? As we
have seen, both Koch and Pasteur started out arguing for causation
using only evidence of necessity. However, after criticism by contempo-
rary physicians who expected causal arguments to establish sufficiency,
both adopted weak sufficiency criteria. Indeed, both insisted that isola-
tion and inoculation was the only way of proving causation. Yet within
months of making this claim, Koch admitted he was unable to find an
animal vulnerable to experimental cholera; he also acknowledged that
no susceptible animals had been found for leprosy or for abdominal
typhus. He concluded: ‘we must therefore be content that we have
established the constant occurrence of a specific species of bacteria in
some disease, and that these bacteria do not occur in other diseases. …
140 THE RISE OF CAUSAL CONCEPTS OF DISEASE
from which the bacterial theory had emerged – to the etiological stand-
point. Even in the face of substantial obstacles, no one seems to have
questioned that all pathological processes could be so organized that
each disease would have a specific cause. By the 1890s the quest for
such causes drove virtually all medical research.
How do Koch’s Postulates relate to identifying causes for non-bacterial
diseases? While there is little textual evidence that Koch envisioned using
the Postulates beyond bacterial diseases, he would likely have been open
to the possibility. He consistently resisted the idea that all diseases were
bacterial, and his concept of an etiological standpoint surely encom-
passed more than bacterial diseases. But, whatever Koch himself may
have thought, in fact, one can easily interpret Rt1 through Rt5 as a
heuristic for finding causes generally rather than merely as causal criteria
within the bacterial theory. Indeed given that the whole point of the
etiological research programme – Koch’s etiological standpoint – is un-
derstanding and controlling diseases by means of causes, it would be
surprising if the Postulates could not be generalized in this way.
By reorganizing the order slightly, by supplementing the Postulates
with other considerations we have found to be necessary, and by ab-
stracting from bacteria (the particular causes in terms of which Rt1
through Rt5 were originally stated), we can recast the Postulates as a
series of steps that constitute a general strategy for finding causes:
Note
function like the ovary in provoking and arresting attacks but whose
location varies from patient to patient; (4) the manifestation of a defi-
nite series of stages in hysteric attacks; and (5) paraplegic or hemiplegic
paralysis (Charcot, 1892–95, vol. 3, pp. 115f.). Charcot first presented
this scheme in 1883 (Charcot, 1883, p. 39) and the first German trans-
lation (Freud’s) appeared in 1886. Charcot’s work was known and
followed in Austria and Germany. In 1882, Moriz Rosenthal, who
maintained personal contact with Charcot, characterized hysteria in
terms of Charcot’s stigmata, and distinguished three major classes of
hysterics depending on which symptoms were most pronounced
(Rosenthal, 1879). Eduard Heinrich Henoch’s text on childhood dis-
eases, which went through 11 editions beginning in 1881, contained a
discussion of hysteria based on Charcot. Henoch, like Rosenthal, distin-
guished classes of hysterics depending on which symptoms were most
apparent: psychotic hallucinations; convulsions; motor disturbances in-
cluding paralysis; and sensory disturbances including hemianesthesia
(Henoch, 1881). Henoch’s system was adopted by both Herz and Cohn
in works cited above. Strümpell’s account of hysteria in his text on
diseases of the nervous system was heavily dependent on Charcot. In
the second edition of his text, published in 1885, Strümpell cited Char-
cot ten times in a 22-page account (Strümpell, 1885, vol. 2, pp. 450–71).
He discussed and adopted Charcot’s five stigmata and the stages that
Charcot identified as characteristic of hysteric attacks. Strümpell’s dis-
cussion reflects a thorough grasp of Charcot’s main ideas; the text was
among the most widely used in the field, and would certainly have been
well known in Vienna.
Standard characterizations of hysteria were symptomatic: ‘hysteria,
like neurasthenia, is only a symptom or a complex of symptoms’ (Herz,
1885, col. 1305); ‘we seek the constituent elements of hysteria, the
hysterical symptoms’ (Tuczek, 1886, p. 511); and ‘hysteria designates a
series of the most variable symptom-complexes’ (Cohn, 1883, p. 51). In
each of these passages, hysteria was identified with certain combina-
tions of symptoms. This seemed particularly appropriate (indeed
necessary) given that no organic lesions could be conclusively demon-
strated in autopsies of hysterics – what could hysteria be besides
symptoms? Charcot’s stigmata were obviously of this nature. Weiss,
Henoch, Herz, Cohn, and Oppenheim (Oppenheim, 1890, p. 554) all
adopted symptomatic characterizations. Ludwig Seeligmuller argued
that chorea should be regarded as a form of hysteria since choreatics
invariably display hysterical symptoms (Seeligmuller, 1881, p. 584);
later F. Tuczek argued that hysteria could only be defined symptomatically
(Tuczek, 1886, p. 511). Given that other nervous disorders were also
characterized symptomatically and that, in some cases, it was difficult
AN IDEATIONAL THEORY OF DISEASE 151
Freud on hysteria
mind’ (Freud, 1925, pp. 19f.). Apparently Freud began studying hyste-
ria when he was unable to obtain adequate laboratory facilities for the
neurological research that had been his first interest (Freud, 1886, pp.
8f.). James Strachey estimates that this momentous shift occurred in
early December 1885 (Strachey, 1955–74, vol. 1, p. 4).
After Freud returned to Vienna, he presented a paper on male hyste-
ria before the Viennese Society of Physicians. This paper has not survived.
The contents of his presentation and the events of the meeting are
known only from reports published in Viennese and German medical
journals and through a preliminary report that Freud presented to the
Viennese Medical Faculty (Freud, 1886). In this preliminary report,
Freud discussed ‘what was completely novel’ in the studies of Charcot:
he claimed that, prior to Charcot, hysteria had not been well defined,
and that no definitive symptomatology had been assigned to it (Freud,
1886, pp. 10f.). Freud objected to the ‘widespread prejudices’ that
hysteria was attributable to genital irritation, and he credited Charcot
with having refuted this prejudice by demonstrating the unsuspected
frequency of male hysterics. He further attributed to Charcot the dis-
covery of special somatic signs by which hysteria could be conclusively
diagnosed. ‘Thus,’ Freud concluded, by Charcot’s efforts, ‘hysteria was
lifted out of the chaos of the neuroses, was differentiated from other
conditions with a similar appearance, and was provided with a symp-
tomatology which makes it impossible any longer to doubt the rule of
law and order’ (Freud, 1886, p. 12). These claims were certainly not
impressive to Freud’s audience: Charcot’s attempts to systematize the
symptomatology of hysteria were neither unique nor unknown. The
‘widespread prejudices’ to which Freud objected had, in fact, been
abandoned years earlier, and Briquet’s estimation of the frequency of
male hysteria, which formed the basis of Charcot’s opinions, had been
accepted by the Viennese and Germans for years (Carter, 1980, p.
265n.). Freud, who first became seriously interested in hysteria while in
Paris, may simply not have been familiar with existing literature on the
disease. In any case, Freud’s misconceptions, together with his un-
restrained admiration for Charcot, no doubt contributed to the
disappointing reception his paper received (Freud, 1925, p. 15).
Between 1886 and 1893 Freud published little about hysteria. Apart
from an unsigned article in one medical encyclopedia, which Freud
almost certainly wrote (Freud, 1888), there are only items of minor
interest. Assuming that the article is Freud’s, it shows that as late as
1888 Freud had not departed significantly from the position taken in
his report: hysteria is still described as an orderly disease accurately
characterized by Charcot’s stigmata; there is no indication that Freud
had become interested in an etiological account of hysteria; the causes
AN IDEATIONAL THEORY OF DISEASE 155
of the disease are still the familiar predisposing and exciting factors
(Freud, 1888, pp. 50f.). Perhaps the most significant difference between
Freud’s preliminary report and the 1888 article is that the article reveals
a greater familiarity with the literature on hysteria.
Freud’s publications in 1893 – the year following the publications by
Möbius and Strümpell considered above – depart, for the first time,
from Charcot’s symptomatic characterization of hysteria. Freud’s trans-
lation of Charcot’s lectures, which was published in that year, contains
a series of footnotes clearly indicating the new direction of his thought.5
In one note, he objects that Charcot’s etiology did not separate the
disposition to neuroses from the disposition to organic nervous disor-
ders (Charcot, 1892–95, 1:237n.6). Given a purely symptomatic concept
of the neuroses there would be no reason to expect etiology to make
this separation. Indeed such a distinction would be impossible if, as
most people assumed, symptomatically-defined functional disorders could
be caused by the same factors that, on other occasions, caused related
organic diseases. After adopting symptomatic definitions of hysteria,
various writers explicitly denied that hysteria could be causally distin-
guished from other organic or functional disorders. One would expect
etiology to reflect this distinction only if one assumed that distinguish-
able diseases must have distinguishable causes – that is, only if one
assumed the Distinguishability Hypothesis which we encountered in the
bacterial theory. In fact, in an 1892 publication, Möbius rejected as
nonsense the idea that different diseases could have the same cause
(Möbius, 1892, p. 290). But this would be nonsense only to those who
viewed diseases from the etiological standpoint. At the time he was
translating Charcot’s lectures, Freud knew Möbius’s publication and, in
a footnote, recommended it to Charcot’s readers (1:149n). In the same
publication, Möbius observed (as Strümpell had before him) that rede-
fining the nervous diseases in causal terms would entail reclassifying
them. Several of Freud’s footnotes express objections to Charcot’s scheme
for classifying the nervous disorders, the so-called famille neuropathique.
In one note Freud explained that his objections to Charcot’s scheme
were at least partially the result of his work on the etiology of tabes
(1:8n). In another note, he observed that his own theory of ‘hysterical
counterwill’, connected together various hysterical symptoms and thereby
cast light on the mechanism of the hysterical condition (1:137n). At
about the same time, in a preliminary draft for a subsequent joint
publication, Freud and Josef Breuer objected that Charcot had only
described hysteria, and that ‘this description throws no light at all on
any connection there may be between the different phases, on the
significance of attacks in the general picture of hysteria, or on the way
in which attacks are modified in individual patients’ (Freud, 1893,
156 THE RISE OF CAUSAL CONCEPTS OF DISEASE
p. 151). Strümpell and Möbius had pointed out that the etiological
definitions of the bacterial theory had shed light on just these factors in
the infectious diseases.
Thus, Freud’s writings from 1893 and 1894 show he was moving
away from Charcot’s symptomatic treatment of hysteria and toward an
etiological approach. It has been universally recognized that Freud be-
gan criticizing Charcot in 1893, but the significance of the criticism has
been generally overlooked. Ernst Jones wrote: ‘What Freud maintained
as the result of his observations was that, whenever a thorough investi-
gation of the patient could be carried out, sexual etiological factors
would be found which were different in [hysteria and the anxiety neu-
roses]; this was his justification for separating them’ (Jones, 1953, vol.
1, p. 256). Jones mentions Möbius only as one ‘from whom … Freud
could have derived but very little’ (Jones, 1953, vol. 1, p. 370). There is
no indication that Jones sees any novelty or special importance in this
new strategy, and Freud’s other commentators generally overlook the
change altogether.7 Yet these steps, which Möbius and Strümpell had
advocated, fundamentally severed Freud’s work from the ideas of most
of his other predecessors; he thereby adopted an orientation, never to
be abandoned, that brought his work on psychopathology into har-
mony with the prevailing orientation of medical research in his time.
These facts can be ignored only at the cost of failing to understand the
true nature of Freud’s contribution.
We must now consider Freud’s work in the few years following 1893.
It is unnecessary to follow the evolution of Freud’s thought or to sum-
marize his ultimate views. Our goal is only to trace Freud’s quest for
etiological characterizations of the nervous disorders, especially hyste-
ria, and his use of those characterizations to provide explanations that
were exactly analogous to the explanations that were, at the same time,
being derived from the etiological definitions of the infectious diseases.
To accomplish this it will be necessary only to review certain prominent
themes in Freud’s writings through 1896, the year in which Freud
published both ‘Heredity and the Etiology of the Neuroses’ and ‘The
Etiology of Hysteria’.
In ‘Heredity and the Etiology of the Neuroses’ Freud asks: ‘Is it
possible to establish a constant etiological relation between a particular
cause and a particular neurotic effect, in such a way that each of the
major neuroses can be attributed to a specific etiology?’ (Freud, 1896a,
p. 149). His answer is that each neurosis ‘has as its immediate cause one
particular disturbance of the economics of the nervous system’ and, in
particular, disturbances of ‘the subject’s sexual life, whether they lie in a
disorder of his contemporary sexual life or in important events in his
past life’. After considering the specific causes of some of the other
AN IDEATIONAL THEORY OF DISEASE 157
given by one famous French researcher, Pierre Janet. Both forms are
defined etiologically (Freud, 1894, pp. 46f.). Similarly, in a long paper
on anxiety neuroses, Freud distinguished six forms of neuroses in women,
four in men, and two found in both sexes; all 12 forms were defined
etiologically (Freud, 1895). It is clear that Freud used his etiological
account of the nervous disorders to generate a nosology more coherent,
rational, and precise than had been possible before.
By 1896, the sexual etiology of hysteria had become definitional.
Freud repeatedly exploited the tactic of redefining diseases in terms of
causes. In ‘Heredity and the Etiology of the Neuroses’, he set forth a
‘nosographic innovation’ resulting from his researches into the etiology
of the major neuroses (Freud, 1896a, p. 146). His innovation was a
fourfold scheme in which each specific neurosis was attributed to a
particular abnormality in the subject’s sexual behavior. ‘What gives its
distinctive character to my line of approach,’ he wrote, ‘is that I elevate
these sexual influences to the rank of specific causes, that I recognize
their action in every case of neurosis, and finally that I trace a regular
parallelism, a proof of a special etiological relation between the nature
of the sexual influence and the pathological species of the neurosis’
(Freud, 1896a, p. 149). In the next few pages, Freud discussed neuras-
thenia, other anxiety neuroses, hysteria, and obsessional neuroses; each
of these was differentiated from the others by the specific etiology of the
symptoms.
However, as Freud saw, the etiological definitions and nosological
innovations were not an end in themselves. In an early draft of their
book on hysteria, Freud and Breuer objected that Charcot’s account
explained virtually nothing about the disease (Freud, 1893, p. 151).
By contrast, in his own writings, Freud used the etiological account of
the nervous disorders to explain an impressive variety of phenomena
including certain hysterical symptoms (Strachey, 1955–74, vol. 3, p.
348), the incidence of hysteria (p. 153) and the hysterogenic zones (p.
163), the response of hysterics to hypnosis (p. 59), certain similarities
among the neuroses (p. 99), patterns of incidence of anxiety neuroses
among married couples (p. 101), neurasthenia occurring in some cases
of sexual abuse (p. 113), the suppression of those events that cause
specific cases of hysteria (p. 154), the predominance of hysteria among
women and of obsessional neurosis among men (p. 169), the apparent
familial neurotic disposition and various pathological symptoms (p.
209), habits (p. 169), and phobias (pp. 130f.), the course of develop-
ment of obsessional neuroses (p. 146), the success and failure of
various therapeutic measures (p. 195), the rare occurrence of hysteria
in the lower social orders (p. 211) and much much more. Moreover,
Freud considered observed facts that could not be explained as possi-
AN IDEATIONAL THEORY OF DISEASE 159
Why have Freud’s commentators ignored the parallels between his early
work and simultaneous research on the bacterial diseases? In part, this
may reflect a simple lack of historical perspective. We have become so
accustomed to etiological characterizations and classifications that Freud’s
etiological approach may appear to require no special consideration. In
his time, however, the situation was different: this approach was still
relatively new, even in accounting for the infectious diseases. Until 1884
no one seems to have envisioned characterizing the nervous disorders
etiologically, and until the end of the 1880s no one actually tried to do
so. Freud was certainly the first to use this approach to provide coher-
ent explanations for the nervous diseases.
In recent years, Freud’s work has been eulogized as revolutionary – as
the introduction of a new paradigm in science (Mujeeb-ur-Rahman,
1977). Freud’s admirers (beginning with Freud himself) have compared
him with Darwin and Copernicus.9 Viewed in relation to any of his
recognized sources, his work does seem revolutionary and without
precedent. Charcot – like most other late nineteenth-century physicians
who dealt with nervous disorders – started with symptoms and ended
up with total chaos in the discussion of causes. As a result there were no
coherent explanations of anything. By starting with causes, Freud was
able to explain the symptoms as well as many other facets of the
nervous diseases – and, ultimately, everything from jokes and dreams to
spelling errors. In the context of his recognized sources, this was indeed
a revolution. However, if we inquire into the nature of this revolution,
and if we view Freud against the background of nineteenth-century
medicine, from which his thinking emerged, his work takes on the
appearance of an ingenious application of a strategy that was already
being employed with enormous success in other areas – a strategy Freud
applied with considerable ingenuity but did not create. From this point
of view, therefore, we must be more cautious about describing Freud as
a paradigm initiator or scientific revolutionary. These facts, too, may
relate to his commentators’ inability to see what must be among the
crucial factors that guided his work and helped to secure its acceptance.
It now appears that the model of comprehension exemplified by the
bacterial theory underlies our way of thinking about other classes of
diseases that have nothing to do with bacteria. The current pervasive-
ness of this way of thinking is illustrated by the fact that none of Freud’s
commentators sees any change at all when Freud completely reversed
himself and adopted it. Thus, while taking account of the relation
AN IDEATIONAL THEORY OF DISEASE 161
between Freud’s work and the etiological standpoint may challenge his
role as a paradigm initiator, by so much the more does it confirm, in
that role, those who first adopted the basic principles of the etiological
standpoint.
Notes
1. Hannah S. Decker (Decker, 1977), Ernest Jones (Jones, 1953) and Ola
Andersson (Andersson, 1962) also ignore the bacterial theory in their
discussions of the origins of Freud’s doctrines.
2. Through this paragraph, references such as this one are volume and pages
references to Charcot (1892–95).
3. Under heredity Charcot included such factors as a father abandoning his
family (2:6), alcoholic aunts (2:227), and a suicidal father (2:319) in
addition to hysteric, epileptic, or nervous relatives. Even Freud objected
when Charcot called an arthritic tendency in relatives a hereditary neuro-
pathic disposition (1:237).
4. This definition presupposes what we could call an Ideational Hypothesis.
It implicitly identifies a domain of causes for a new theory of disease, and
in this respect it is parallel to the Bacterial Hypothesis discussed in earlier
chapters.
5. For an enlightening study of ‘Freud’s rebellion’ from Charcot’s point of
view, see Gelfand (1989).
6. Through this paragraph, references such as this one are volume and page
references to Charcot (1892–95).
7. Ola Andersson writes ‘In the late 1880s and 1890s P. J. Möbius and A. v.
Strümpell had published papers on the traumatic neuroses and on hysteria
in which they espoused views very similar to those of Charcot [!]’
(Andersson, 1962, p. 115).
8. Through this paragraph, page numbers in parentheses are references to
volume 3 of Strachey (1955–74).
9. For a review and references see, Nigel D. Walker, ‘A New Copernicus?’
and especially David Shakow and David Rapaport, ‘Darwin and Freud: a
Comparison of Receptions’; both reprinted in Mujeeb-ur-Rahman (1977,
pp. 35–42 and 43–63).
CHAPTER TEN
Protozoal and
Viral Theories of Disease
A research programme ‘consists of methodological rules: some tell us
what paths of research to avoid … , and others what paths to pursue’
(Lakatos, 1968, p. 132). The result of following such rules is a sequence
of theories, ‘T1, T2, T3 … where each subsequent theory results from
adding auxiliary clauses to … the previous theory in order to accommo-
date some anomaly’ (Lakatos, 1968, p. 118). By technical innovations
and dedicated research, nineteenth-century scientists successfully ex-
plained an impressive array of bacterial diseases; each success could be
regarded as yielding a new member in a Lakatosian sequence of bacte-
rial theories of disease. A set of basic assumptions such as Klebs’
Grundversuche was common to all such theories.
However, as medical research continued, various obviously conta-
gious diseases became prominent precisely because, while superficially
similar to known bacterial diseases, their causal agents eluded every
attempt at identification. In 1894, William Henry Welch observed:
We have a large number of infectious diseases which have thus far
resisted all efforts to discover their specific infectious agents. Here
belong yellow fever, typhus fever, dengue, mumps, rabies, Oriental
pest, whooping cough, smallpox and other exanthematous fevers,
syphilis, and some other infectious diseases in human beings. It will
be noted that many of these are the most typically contagious
diseases, which it might have been supposed would be the first to
unlock their secrets.
(Hughes, 1977, p. 25)
One way of explaining these failures is to say that the diseases in
question were caused by such entities as protozoa, viruses, or rickettsia
that were different from the bacteria studied by classical bacteriologists.
However, this explanation suggests that discovering new causes is like
finding previously overlooked shells on a beach – it obscures the theo-
retical innovations required in recognizing new kinds of specific causes.
A theory of disease must specify a domain of entities over which the
theory is to be applied and it must include causal criteria that indicate,
in part, how the word ‘cause’ is to be used within the theory. Given
such a theory and some new illness, there may simply be nothing within
the domain of the theory that satisfies the criteria with respect to that
PROTOZOAL AND VIRAL THEORIES OF DISEASE 163
self was skeptical about Laveran’s conclusions. He did not believe the
elements were parasites, partly because malaria was not contagious; he
recommended a commission be established to appraise the validity of
future communications. One month later, Colin presented another pa-
per on Laveran’s behalf, and this time Colin was even more skeptical.
He suggested that what Laveran took to be parasites were actually only
leukocytes that had ingested pigment (Colin, 1880b).
In October 1881, Laveran himself presented a paper before the Acad-
emy of Sciences. Laveran reported that
the blood of malaria patients contains parasitic elements which
present themselves under the following aspects: (1) cylindrical ele-
ments, tapered at their extremes, almost always curved into a
crescent. … (2) transparent spherical elements containing movable
grains of pigment … on whose boundaries one can often observe
very fine filaments, [the spherical elements] are animated, in every
sense, with a very rapid movement. … (3) spherical or irregularly
shaped transparent elements that contain pigment [but with prop-
erties] that enable one to distinguish them clearly from pigmented
leukocytes. (4) spherical transparent pigmented elements smaller
than those mentioned above.
(Laveran, 1881, pp. 627f.)
According to Laveran ‘the spherical bodies containing mobile grains of
pigment and armed with actively mobile peripheral filaments are un-
doubtedly alive’ (Laveran, 1881, p. 629). By the time he presented this
paper, Laveran had examined the blood of 192 victims of different
forms of malaria and had identified the parasites in blood samples from
148 of them. Most of the patients in whose blood the elements could
not be found had been treated with quinine, and, as Laveran confirmed,
quinine killed the parasites. He noted that parasitic elements were only
found in the blood of malaria patients and that the parasites were most
likely to be present just before the onset of fever. Laveran believed that,
between attacks, the parasites were concealed in such organs as the
spleen and liver. He concluded that ‘attacks of malaria are caused by
the introduction, into the blood, of parasitic elements that present
themselves under the aspects described above; sulfate of quinine leads
to the termination of malarial attacks because it kills these parasites’
(Laveran, 1881, p. 630).
Laveran’s conclusions were challenged both by those who still ques-
tioned the role of living parasites in any disease and by those who
believed malaria was caused by a bacterium. However, M. Richard, a
physician who was one of Laveran’s friends and who was also stationed
in a hospital in Algeria, confirmed Laveran’s findings, and suggested
that the presence of the parasites could be taken as a diagnostic crite-
rion for malaria. This, in effect, meant recharacterizing the disease in
PROTOZOAL AND VIRAL THEORIES OF DISEASE 165
region free from malaria, (2) the patient who supplies the blood must
have no other infectious diseases, (3) the subjects to be inoculated must
volunteer and must not be required, by the experiment, to sacrifice an
opportunity for gainful employment, and (4) the subjects’ temperature
curves must have been recorded since long before the inoculation to
insure that they were free from fever (Gerhardt, 1884, pp. 373f.).
Gerhardt was able to induce artificial malaria in two volunteers who
met these conditions and, subsequently, to control both cases by admin-
istering quinine. Gerhardt did not mention Laveran’s work, and he did
not report any microscopic examinations of the subjects’ blood before
or after the inoculations.
By 1885, Marchiafava and Celli had been converted to the idea that
malaria was parasitic. They cited Laveran, Richard, and Gerhardt and
reported further microscopic studies of malarial blood (Marchiafava
and Celli, 1885a). They described an attempt to transmit malaria by
injecting a volunteer with blood freshly drawn from a malarial patient;
the injection produced typical fever symptoms. Marchiafava and Celli
identified the characteristic organisms in the blood of the volunteer, and
controlled the disease by administering quinine. ‘All of these condi-
tions,’ they concluded, ‘make probable our hypothesis that these forms
are living agents’ (Marchiafava and Celli, 1885a, p. 353). Marchiafava
and Celli also reported attempts to cultivate the parasites in various
media. The attempts failed, but they reported finding an organism in
mud from swamps that, when cultured, appeared ‘morphologically simi-
lar to the initial forms’ of the supposed malarial parasite, and, they
reported, ‘the multiplication of these bodies was especially obvious in
slide cultures of malarial blood’ (Marchiafava and Celli, 1885a, p.
354). According to Bloomfield, this comment reveals ‘that Marchiafava
and Celli were still unclear about the significance of their findings’; he
concludes that they ‘did little more than confirm Laveran’s findings’
(Bloomfield, 1958, pp. 350f.). However, their paper had this heuristic
significance: for the first time, it brought together observational reports
of the parasite and Gerhardt’s reports of successful inoculation experi-
ments on human volunteers.
By the end of the nineteenth century, it was becoming progressively
more clear that Laveran’s protozoan played a role in malaria. Moreo-
ver, the study of malaria had been supplemented by research on other
diseases that also appeared to be caused by protozoa. In 1890, Koch
summarized the situation as follows:
In many areas … indeed precisely where one would least have
expected it, bacteriological investigation has been of no avail. This
has been the case in the study of several infectious diseases which,
because of their pronounced infectiousness, appeared to be easy
PROTOZOAL AND VIRAL THEORIES OF DISEASE 167
the small quantity of diluted sap that was sufficient to infect healthy
plants, his serial inoculations persuaded him that ‘the contagium, al-
though liquid, replicates itself in the living plant’ (Beijerinck, 1898, p.
5). Beijerinck used the term ‘contagium vivum fluidum’ to refer to this
unusual replicating yet liquid disease agent whose existence seemed to
be implied by his experiments.
Beijerinck made the remarkable observation that injections of infec-
tive sap did not affect mature leaves, but only new growing buds and
shoots in which cell division was in progress. He astutely inferred that
the contagium vivum fluidum, being ‘unable to grow independently, is
drawn into the growth of the dividing cells and multiplies powerfully
therein but without losing its own individuality’ (Beijerinck, 1898, p.
9). Of course, contemporary scientists who were studying viral diseases
in animals found no counterpart to these discoveries, and Beijerinck’s
observation and the inference he drew from it were inadequately appre-
ciated. In a sequel to this paper, Beijerinck pointed out that the
impossibility of culturing the contagious substance in artificial media
suggested it was a liquid that could not multiply outside living proto-
plasm. However, he admitted that this concept was not easy to
comprehend:
The reproduction or growth of a dissolved body is not unthinkable
but it is difficult to imagine. It is not easy to accept a process of
division in the molecules which would lead to their multiplication,
and the idea of self-sustaining molecules, which is thereby presup-
posed, seems unclear to me, if not contrary to nature. It is to some
extent an explanation to consider that, in order to reproduce itself,
the contagium must be incorporated into the living protoplasm of
the cell into whose multiplication it is, so to speak, passively in-
cluded. … However, there is no denying that even if the incorporation
of a virus into the living protoplasm is confirmed as factual, it
cannot be regarded as a clearly comprehensible process.
(Beijerinck, 1899, p. 31)
Lise Wilkinson suggested that Beijerinck’s early interest in chemistry
may have ‘enabled him in later life to consider chemical molecules and
even their possible role in biological systems in a more realistic way
than could most of his fellow biologists and pathologists’ (Wilkinson,
1976, p. 117).
By the time Beijerinck published his first work on tobacco mosaic
disease, Friedrich Johannes Loeffler and Paul Frosch had begun pub-
lishing studies of foot-and-mouth disease (Loeffler and Frosch, 1898).
Beijerinck knew of their work, and believed that Loeffler and Frosch
were dealing with causal factors related to those he was studying, but
he wrote that he could not support their conclusions ‘in respect to the
corpuscular nature of the virus’ (Beijerinck, 1898, p. 7n). While Beijerinck
PROTOZOAL AND VIRAL THEORIES OF DISEASE 171
facts about the new disease may lead one to prefer some theories over
others.
Recognizing new kinds of causes also requires one to adopt new
causal criteria.3 In 1937, Thomas M. Rivers wrote:
The idea that an infectious agent must be cultivated in a pure state
on lifeless media before it can be accepted as the proved cause of a
disease has … hindered the investigations of certain maladies, inas-
much as it denies the existence of obligate parasites, the most
striking phenomenon of some infections, particularly those caused
by viruses
(Rivers, 1937, p. 5).
In the same paper, Rivers also discussed possible causal criteria for
viruses. About 20 years later, R.J. Huebner, proposed another set of
causal criteria for viruses (Huebner, 1957). Both Rivers and Huebner
took account of developments that came after Koch – for example, they
included criteria that involved immunological reactions to pathogens.
However, the only respect in which their criteria differed from those
suitable for use in the study of bacteria was that neither Rivers nor
Huebner had a counterpart to Koch’s Rt4; they did not require that a
purported causal agent be cultivated in inert media outside diseased
animals. Instead, the corresponding weak sufficiency criterion stipu-
lated only that inoculations of fluids drawn from a diseased animal
(and possibly filtered) were followed by the same disease in test
animals.
ideas than for miasms, attempts to include ideas and viruses within the
research programme threatened to become what Lakatos called degen-
erating problem shifts (Lakatos, 1968, p. 118).
At this point, researchers could simply have abandoned these two
attempts to expand the programme. By 1898, childbed fever, diphthe-
ria, anthrax, cholera, tuberculosis, and several other bacterial diseases
had been assimilated to the etiological standpoint. However, for other
diseases, rather than hypothesizing the existence of viruses or ideas
(each undetectable except through the very pathologicality it was in-
tended to explain), one could have fallen back on traditional causal
thinking: foot-and-mouth disease, tobacco mosaic disease, hysteria, anxi-
ety neuroses, and the other disorders in both groups, could have been
regarded as having no necessary causes and as being due to the tradi-
tional factors to which conventional wisdom had long ascribed them.
One could simply have acknowledged that inoculations from diseased
sources or sexual attacks before puberty (respectively) were among the
many ways in which diseases of these two kinds could be caused. This
approach would not have undercut the success of the bacterial theory
and would have been compatible with all the observed facts. Moreover,
in contrast to hypothesizing unknown viruses or pathogenic ideas, this
would not have been question begging. However, this approach meant
abandoning the quest for specific causes – the very core of the research
programme. And, as Lakatos explained, in situations of this kind, the
negative heuristic of the programme shields the core from refutation:
In Newton’s program the negative heuristic bids us to divert the
modus tollens [of apparent counter-examples] from Newton’s three
laws of dynamics and his law of gravitation. This ‘core’ is ‘irrefuta-
ble’ by the methodological decision of its proponents: anomalies
must lead to changes only in the ‘protective’ belt of auxiliary,
‘observational’ hypotheses and initial conditions.
(Lakatos, 1968, p. 133)
At the core of our research programme was the assumption that every
disease could be characterized in terms of a universal necessary cause,
and this assumption simply could not be given up. Instead, researchers
began looking for non-circular ways of establishing the existence and
identity of the new purported causes.
Distinguishing viruses was a formidable task. At least by 1902, scien-
tists had concluded that viruses were too small ever to be revealed by
light microscopes, and some realized that, being obligate parasites, they
could never be cultured in an inert medium (Joest, 1902, p. 378). This
meant that, in principle, it would be impossible ever to gain knowledge
about viruses through the means that had proven most enlightening in
the study of bacteria. Moreover, since most viral diseases were species
PROTOZOAL AND VIRAL THEORIES OF DISEASE 177
Notes
A Nutritional
Deficiency Theory of Disease
By the beginning of the twentieth century, many diseases had been
explained as infestations of microscopic parasites or of filterable vi-
ruses. However, other important diseases defied such explanations. One
such disease was beriberi which, in some populations, was responsible
for more deaths than all known parasitic diseases combined (Carter,
1977, p. 1191). Identifying the cause of beriberi required a new theory
of disease: a deficiency theory.
In conventional wisdom, the bacterial theory of disease is seen only
as a positive obstacle to development of a deficiency theory: Aaron J.
Ihde and Stanley L. Becker claim that ‘the germ concept proved a major
barrier to the recognition and study of deficiency diseases’ (Ihde and
Becker, 1971, p. 16). C. P. Stewart writes, ‘one factor which undoubt-
edly held up the development of the concept of deficiency diseases was
the discovery of bacteria in the 19th century and the consequent preoc-
cupation of scientists and doctors with positive infecting agents in
disease’ (Stewart, 1953, p. 408). Numerous writers assert that the defi-
ciency concept was difficult to accept because the bacterial theory
suggested that only a positive agent could cause something. In his
history of nutrition, Emer Verner McCollum notes that ‘improved mi-
croscopes and the staining and other technics applicable to the study of
the problems of pathology so monopolized the attention of investiga-
tors that they had little incentive to consider any aspect of malnutrition
as a cause of disease’ (McCollum, 1957, pp. 225f). In Toward the
Conquest of Beriberi, Robert R. Williams treats the bacterial theory
only as the source of one false explanation for the etiology of beriberi
(Williams, 1961, pp. 13–15, 18f., 35). Such claims, so frequently re-
peated, pass for common sense – never mind that they are usually
unsupported by any evidence whatsoever. Do these authors really mean
to assert that, if there had been no bacterial theory, the deficiency
concept would have been more readily accepted? What evidence could
there possibly be for a contrafactual claim of this kind? Who can say
what might have been?2
However, all these claims are based on a serious misconstruction of
the historical context. That the study of bacteria did not monopolize
late nineteenth-century etiology is obvious from the variety of causes
180 THE RISE OF CAUSAL CONCEPTS OF DISEASE
In the early nineteenth century, scurvy and rickets were generally be-
lieved to be diet-related. In 1830, Lancet published a series of clinical
lectures by John Elliotson, Professor of Medicine in University College,
London. In discussing scurvy, Elliotson noted that ‘the cause … is
always, I believe, a want of fresh animal and fresh vegetable food’
(Elliotson, 1830–31, p. 651). Seven years later, in a similar lecture,
Marshall Hall observed
scorbutus is generally induced by a deficiency of fresh vegetable
food. It is also occasionally referred to other errors in diet, to the
respiration of a crowded or otherwise impure atmosphere, to ex-
cessive fatigue, anxiety, etc. … The prevention and cure of scorbutus
consists in the administration of fresh and vegetable food, but,
above all, of citric acid
(Hall, 1837–38, p. 851).
Both men refer to works by Gilbert Blane (1753) and James Lind
(1785) that were, by that time, recognized sources on scurvy. Neither
Elliotson nor Hall suggested that his views were new or atypical; in-
deed, both acknowledged that lemon juice had been the standard cure
for scurvy for more than 200 years.
In 1840, George Budd summarized clinical knowledge of scurvy in an
article in Alexander Tweedie’s A System of Practical Medicine (Budd,
1840). Budd discussed various fruits and vegetables generally known to
cure scurvy. Knowing of François Magendie’s experiments demonstrat-
ing the inadequacy of certain macronutrients, Budd speculated that ‘the
182 THE RISE OF CAUSAL CONCEPTS OF DISEASE
been substantially responsible for the rise of beriberi, did not become
common in Asia until then. By the last quarter of the nineteenth century
the disease was widespread and growing at an alarming rate.
It is difficult to gauge accurately the growth of beriberi; we must be
content with a few hints. First, in the Japanese Army in 1876 there were
3,868 cases of beriberi from among 35,300 men (11 per cent), in 1877
there were 2,687 cases among 19,600 men (14 per cent), and in 1878
there were 13,629 cases among 36,100 men (38 per cent) (Scheube,
1894, p. 14). This percentage remained roughly constant through 1884
and then declined because of dietary reforms, but during the war between
Japan and Russia (l904–05) there were nearly 100,000 cases of beriberi
(Takaki, 1906, p. 1521). Second, in 31 district hospitals in the Malay
peninsula, Chinese patients admitted for beriberi increased from 1,206 in
1881 to 3,175 in 1891, and to 6,767 in 1901. In that period, beriberi
accounted for more than 100,000 deaths among Chinese laborers in the
Malay States – over half the total death rate for that population (Braddon,
1907, pp. 1–4, 513–21). Third, in 1883 August Hirsch reported that
within the preceding 20 years, beriberi had appeared in many areas for
the first time, and that it was epidemic in coastal areas of Japan and of
other Asian countries (Hirsch, 1885, pp. 573–8). Ten years later, B.
Scheube reported that the disease had recently appeared for the first time
in Siam and in the Philippines, that it was spreading in Africa and in
South America, and that it was now endemic throughout Japan (Scheube,
1894, pp. 10–16). In 1907, Patrick Manson gave the disease an even
more extensive distribution (for example, he stated that it was then
common in southern China where, according to Hirsch and Scheube, it
had been rare), and in most areas incidence of the disease seemed to have
increased (Manson and Daniels, 1907, pp. 615–43). Finally, one can
appreciate the remarkable rise of the disease by surveying the medical
literature of the period. Scheube’s nearly complete bibliography includes
two publications on beriberi between 1800 and 1809; in subsequent
decades the publications numbered 8, 10, 11, 30, 64, 80, and between
1880 and 1889, 181 (Scheube, 1894, pp. 207–18). Leonard Braddon’s
incomplete bibliography lists nearly 200 articles and books between 1890
and 1899 (Braddon, 1907); another incomplete bibliography lists 250
publications between 1900 and 1910 (Schaumann, 1910, pp. 699–709).
A complete bibliography for this decade alone would approach 500
items. Writers in the late 1870s still regarded beriberi as an exotic and
unfamiliar topic; about 30 years later, an editorial in Lancet observed
that ‘there is probably no disease concerning which so much discussion as
to its etiology has taken place as beriberi’ (Lancet, 1911, p. 842).
We can, somewhat arbitrarily, take 1880 as the beginning of serious
western interest in beriberi. By that time there was a strong and broadly
186 THE RISE OF CAUSAL CONCEPTS OF DISEASE
based opinion that the disease was diet-related. It was obvious to every-
one that the disease was prominent only where rice was the staple diet.
Between 1850 and 1890, several observers attributed beriberi to an
‘insufficient diet or a diet not corresponding to the metabolisms and
bloodmaking, or to the needs of the body’ (Hirsch, 1885, p. 589). Of
those who ascribed it to insufficient diet, some seem to have believed
the problem was simply quantitative – those who got beriberi had too
little to eat; however, others believed the problem was qualitative –
sufferers had too little of certain essential foods.
Among the most important early observers to espouse a dietary ex-
planation was Kamehiro Takaki. Takaki was the first to collect systematic
evidence on a large scale that supported the deficiency concept. He first
heard of beriberi from his father who was a guard at the Japanese
Imperial Palace. Many of the guards suffered from beriberi; ‘they attrib-
uted the cause to food and called a provision box the “beriberi box”’
(Takaki, 1906, p. 1370). Takaki became a naval doctor, spent five years
studying medicine in London, and was appointed director of the Tokyo
Naval Hospital. By 1882 Takaki’s own observations led him to at-
tribute beriberi to a poor diet. His view was that ‘wide departure of
nitrogen and carbon from the standard proportion (one to fifteen)
essential to the maintenance of health, resulting from a great deficiency
of nitrogenous substances and a great excess of carbohydrates in food,
is the cause of kakke (beriberi)’ (Takaki, 1885, p. 29). Takaki persuaded
the skeptical Japanese admiralty to initiate massive dietary reforms –
crews ate more meat (especially fresh meat), more vegetables and, at
some meals, barley instead of rice. The effects were dramatic: in 1882
there were over 400 cases of beriberi for each 1,000 men, within five
years the disease had been eliminated. Takaki’s work was reported in
major European medical periodicals, he was honored at home and
abroad, and his evidence was ultimately important in understanding
beriberi.
However, Takaki’s ideas about the disease were inconsistent with a
large, if unsystematic, body of epidemiological facts widely known
before his studies even began. In 1835, John G. Malcolmson observed
that ‘the comparative cheapness of all kinds of grain in the Circars, and
the easy circumstances of many of the native soldiers who suffered, are
fatal to any supposition of the disease depending on deficient and
unhealthy diet’ (Hirsch, 1885, p. 592). By 1880 it was common knowl-
edge that those who contracted beriberi often ate more and a better
range of foods than those who did not (Hirsch, 1885, p. 592). More-
over, populations that seemed especially vulnerable often lived amid a
larger population that remained healthy, and the only apparent dietary
difference between the groups was that the larger and immune popula-
A NUTRITIONAL DEFICIENCY THEORY OF DISEASE 187
In Java, prison inmates were usually fed whichever form of rice was
commonly consumed by the local population. As it happened, in 27
prisons inmates ate unpolished rice, while in 74 others the rice was
decorticated to some extent. This provided an ideal opportunity for
determining whether beriberi was correlated with the consumption of
decorticated rice. Eijkman’s colleague, A. G. Voderman, who was then a
Civil Medical Inspector, conducted surveys of the prisons in Java. The
preliminary results were astonishing: of nearly 300,000 prisoners, only
one in 10,000 of those who ate unpolished rice had beriberi while one
in 39 of those who ate polished rice had the disease (Eijkman, 1897b).
These results exhibited a striking correlation between the incidence of
beriberi and the consumption of particular kinds of rice.
Within a few years, studies of other populations confirmed these
results. Braddon noted that in the Malay States, Chinese, who ate
190 THE RISE OF CAUSAL CONCEPTS OF DISEASE
polished rice, were seriously afflicted whereas Tamils, who ate unpolished
rice, and native Malays, who ate rice that was not mechanically milled,
were almost free from the disease (Braddon, 1907, pp. 150–198). Both
Voderman’s and Braddon’s evidence was demographic and not subject
to controls. Eijkman’s studies on fowl could yield only analogical argu-
ments that many found unconvincing. ‘The favorite view of most
physicians who knew of [Eijkman’s] work at all, was to dismiss the
matter with the assertion that polyneuritis in fowls had no relation to
human beriberi’ (Williams, 1961, p. 14). However, toward the end of
the decade, William Fletcher (Fletcher, 1907), and Henry Fraser and
Thomas Stanton (Fraser and Stanton, 1909) published important stud-
ies on small but carefully controlled populations. These studies probably
did more than anything else to persuade physicians that consumption of
decorticated rice was connected with beriberi.
By 1910, the evidence was clear enough for a meeting of the Far
Eastern Association of Tropical Medicine to adopt a motion stating that
‘in the opinion of this association sufficient evidence has now been
produced in support of the view that beriberi is associated with the
continuous consumption of white (polished) rice as the staple article of
diet’ (BMJ, 1910, p. 1000). In a 1911 meeting of the Society of Tropical
Medicine and Hygiene, the consensus of opinion favored a dietary
theory for beriberi, and Patrick Manson, admitting that his ideas about
beriberi ‘belong to a past age’, was almost alone in expressing reserva-
tions about such a theory (Manson, 1911–12, p. 85).
diseases, the success of the bacterial theory was the most vivid source
both of motivation for their work and of the standards for comprehen-
sion that their etiological investigations were required to satisfy.
Notes
1. In this earlier paper (‘The Germ Theory, Beriberi, and the Deficiency Theory
of Disease’), which forms the basis for this chapter, I took a position that I
now regard as incorrect. It was not ‘the germ theory [per se] that revived
interest in scurvy and … motivated researchers to seek a theoretical under-
standing of scurvy’ (Carter, 1977, p. 136), but rather what I am here
calling the etiological research programme of which the germ theory [more
precisely the bacterial theory] of disease was a part. So while I still think
that my earlier argument is essentially correct, the conclusion as stated in
the earlier paper requires modification.
2. Kenneth J. Carpenter has recently written books on scurvy and beriberi
(1986, 2000). Carpenter is much more reserved in his judgments about the
relation of bacteriology and the deficiency concept than those quoted
above so they constitute the foil for my argument. Carpenter provides
more details about research on both scurvy and beriberi, but, from the
point of view of this book, what he says neither adds to nor (with one
minor exception to be discussed below) challenges the position I advocated
in my 1977 paper or that I now present. Therefore, his interesting and
engaging work has not occasioned any substantial change in my argument.
Some Final Thoughts
In these case studies, my goals have been twofold: to present modern
medicine as a Lakatosian research programme focusing on the quest for
universal necessary causes, and to identify some of the heuristic princi-
ples required in that undertaking. The cases we have examined are by
no means exhaustive. Alfred S. Evans has shown that Koch’s Postulates
can be expanded to encompass diseases of several different kinds – for
example, those caused by ‘slow viruses’ and occupational and immuno-
logical diseases (Evans, 1993). Given the broad interpretation of the
Postulates proposed in Chapter 8, Evans’s account is obviously compat-
ible with my objectives. In the last two decades, other writers have
discussed still other diseases in ways that also fit well with the point of
view here presented (Ghesquier, 1999; Harden, 1987 and 1992; Kunitz,
1988; Schlich, 1994). The process by which causes were finally identi-
fied for chromosomal disorders provides a further example (Carter,
2002).
This way of thinking reveals mistakes in current beliefs about the rise
of modern medicine. Thinking that nineteenth-century medicine means
the germ theory, historians have almost totally ignored the broader
movement of which it was a part. As a result, most writers entirely
overlook the role of the research programme in the origins of Freudian
psychology. A related flaw is evident in accounts of the deficiency
theory: historians see only competition with the germ theory and are
oblivious of the movement that nurtured them both and endowed each
with its own objectives and research orientation. By failing to grasp the
nature of the programme, historians also misconstrue the work of those
who contributed to it. For example, Semmelweis is seen only as having
introduced chlorine washings – in spite of his own clear and repeated
claims that his opinions mattered most and distinguished him from
other early advocates of disinfection and in spite of subsequent obstetri-
cians who praised his theory of childbed fever because of its explanatory
power. Finally, as another example, there has been almost universal
neglect of early nineteenth-century studies of parasitic diseases, yet
these were arguably more important in the rise of medicine than was
pathological anatomy (which, partly through the unfortunate influence
of Foucault, has attracted far more attention than its significance war-
rants). In my view, Rennucci, Bassi, and Gruby, Semmelweis, Davaine,
Klebs, Pasteur and Koch, the early Freud, Loeffler and Frosch, Eijkman
and Funk (each of whose work was, demonstrably, focused almost
exclusively on the quest for universal necessary causes) and virtually
SOME FINAL THOUGHTS 197
by which his theories won out (which, by the way, reduces Pasteur
himself to little more than a fool). Suppose, as Latour seems to fancy,
power relations alone explain why any one theory surpasses its rivals
(p. 153). So what? Even if this were true, at some point scientific
theories deserve attention as examples of the best thinking the species
has yet achieved (‘There’s no point in listening to Bach’s music any
more; now we understand the system of patronage that gave him influ-
ence at court.’). So what can be the point (other than to sustain a fad
nearly on a par with leisure suits) of writing books arguing that one can
dispense with arguments? Moreover, Latour, like everyone else, sees
only bacteriology – not the quest for universal necessary causes. French
bacteriology, a local phenomenon after all, is less in need of explanation
than is the research programme of which it was one part. Perhaps
Latour should be arguing that the origin and growth of the entire
international programme can be reduced to social forces. That would
be a more interesting thesis and it has a certain plausibility – the
broader an intellectual change, the less likely it can be explained in
strictly rational terms. Moreover, that thesis might at least force one to
transcend Gallic chauvinism.
We make up words and give them meanings, and they can be used
however we like. But this does not imply that meanings should be
changed capriciously. Current scientific usage embodies what is argu-
ably the best thinking that our species has achieved through several
thousand years of intellectual groping, and it should be adjusted cau-
tiously only when there are compelling reasons for doing so. On the
other hand, as we have seen, language must be open to change if science
is to progress at all.
It isn’t a fact about the world that some cases of illness come pack-
aged together with universal necessary causes; rather, it’s a fact about
how we have learned to characterize diseases. When possible, we define
diseases so they have necessary causes because there is great utility in
doing so. But there may be diseases for which this is impossible either in
principle or simply in fact.
On the one hand, it is impossible, in principle, to explain why one
unstable atom decays at a certain time while identical atoms around it
do not. As currently understood, there are no sufficient causes for such
events; they simply happen. This is a metaphysical issue not an episte-
mological one; it stems from the way the world is, not from the weakness
of our intellects. By a loose analogy, there could conceivably be indi-
vidual cases of illness (perhaps those that start on the chromosomal
level) whose beginnings have no sufficient causes; they may simply
happen. It would obviously be impossible to group such cases in such a
way that a new disease could be so characterized that all its instances
would share a necessary cause. If this is how the world turns out to be,
202 THE RISE OF CAUSAL CONCEPTS OF DISEASE
the very most one could hope for would be risk factors (and even these
may ultimately prove impossible). Of course, even if there were such
illnesses, we would probably never come to know it and, in the absence
of such knowledge, we could continue seeking non-existent causes for
as long as the species shall live.
Alternatively, there could be cases of illness that do share sufficient
causes but causes whose identification requires more intellectual, finan-
cial and/or temporal assets than the human species will ever have at its
disposal. In short, there could be causes that we simply are not smart
enough to identify.
As a species, we have spent more time and money on cancer research
than on any other single problem in our history. Yet, while we have
learned a lot, we may be no closer to identifying sufficient causes in
terms of which classes of cancers can be characterized than we were
100 years ago.3 And this could be because there simply are no such
causes or it could be because, so far (and maybe forever), we are not
smart enough to find them. Perhaps at this point (and maybe forever),
the best we can do is find risk factors. So how should we respond? By
wringing our hands and insisting that no one speaks until we find
causae verae sine qua non? Of course not. We do our best to understand
and to control the world in whatever ways we can, and this may require
changes in how we talk.
We all know that risk factors are different from the causes Koch
identified. So what? At some point we may confront diseases for
which causes of his kind can never be found. But language evolves to
accommodate and to foster new ways of thinking. What form of
speech should we adopt? We cannot prescribe for the future, but here
are two obvious candidates: either we could exploit the similarity
(family resemblance) between traditional causes and theory-poor sta-
tistical correlations and simply broaden our concept of causation to
include some risk factors; or we could continue to talk about risk
factors as different from traditional causes. At this point, the choice
seems arbitrary. Scientific medicine is unlikely to collapse, whichever
course we adopt. But, however we end up speaking, this much is
absolutely certain: just as dead languages have no names for whatever
new concept of causation may emerge, dead philosophers (Aristotle,
Hume, Mill, Popper, and so on) are in no position to advise epidemi-
ologists about how to talk.
Half a century from now, historians may document when and how
we resolved these issues (assuming they finally get around to looking at
theories again), and philosophers, with their gray in gray, may clarify
why the resolution took the form it did. But how we talk about causes
will certainly be no more binding on scientists in 2060 than James L.
SOME FINAL THOUGHTS 203
Notes
1. Which, of course, doesn’t deter the bold from trying. First try: ‘Cause is
here used as the essential antecedent [i.e. the cause] or sole prerequisite
determinant [i.e. the cause] by which the disease is brought about [i.e.
caused]’ (Stehbens, 1992, pp. 99f.). In short: a cause is the cause by which
the disease is caused. Second try: ‘Cause is something that occasions [i.e.
causes], produces [i.e. causes], or effects [i.e. causes] a disease’ (Stehbens,
1992, p. 102). In short: a cause is something that causes, causes, or causes
a disease.
2. And that, by the way, seems to me to have been – at least at the beginning –
the real point of contention between Peter Duesberg and his opponents in
the AIDS establishment. While the arguments were generally stated in
terms of the necessity and sufficiency conditions of Koch’s Postulates, the
real issue was usually whether a retrovirus like HIV could possibly explain
AIDS.
3. To be sure, we may be a whole lot closer, but, until such causes are found,
there is no telling – not knowing where the goal lies, we can’t be sure
whether we are getting closer to it or not.
Bibliography
l’Académie Impériale de Médecine (1858), De la fièvre puerpérale,
Paris: Baillière et fils.
Ackerknecht, Erwin H. (1946), ‘Natural Diseases and Rational Treat-
ment in Primitive Medicine’, Bulletin of the History of Medicine,
19:467–497.
Adelon, Nicholas Philibert (ed.) (1832–46), Dictionnaire de médecine,
2nd edn, 30 vols, Paris: Bechet.
Anderson, William (1876), ‘On Kakke, or the Beri-beri of Japan’, Saint
Thomas Hospital Reports, 7:5–30.
Andersson, Ola (1962), Studies in the Prehistory of Psychoanalysis,
Stockholm: Svenska Bokförlaget.
Andral, Gabriel (1832–33), ‘Hydrophobia’, Lancet, 1:806–808.
Audouin, Jean Victor (1836a), ‘Recherches anatomiques et physiologiques
sur la maladie contagieuse qui attaque les vers à soie, et qu’on désigne
sous le nom de muscardine’, Annales des Sciences Naturelle: Zoologie,
2nd series, 8:229–245.
——— (1836b), ‘Nouvelles expériences sur la nature de la maladie
contagieuse qui attaque les vers à soie, et qu’on désigne sous le nom
de muscardine’, Annales des Sciences Naturelle: Zoologie, 2nd series,
8:257–269.
Balsamo-Crivelli, Joseph (1839), ‘Ueber den Ursprung und die
Entwicklung der Botrytis bassiana und eine andere schmorotzende
Art von Schimmel’, Linnaea, 16:118–123.
Bamberger, Heinrich von (1883), ‘Hysterie’, Allgemeine wiener
medizinische Zeitung, 28:529f.
Bar, Paul (1883), Des méthodes antiseptiques en obstétrique, Paris:
Alexandre Coccoz.
Bardsley, James L. (1845), ‘Diabetes’, in Dunglison (1845), vol. 1, pp.
606–625.
Barlow, Edward (1845a), ‘Education (Physical)’, in Dunglison (1845),
vol. 1, pp. 750–765.
——— (1845b), ‘Plethora’, in Dunglison (1845), vol. 3, pp. 553–574.
Barnes, David S. (2000), ‘Historical Perspectives on the Etiology of
Tuberculosis’, Microbes and Infection, 2:431–440.
Bassi, Agostino (1835), Del mal del segno, calcinaccio o moscardino,
trans. P.J. Yarrow, ed. G.C. Ainsworth, (1958), Ithaca, NY: Phy-
topathological Classics, Number 10.
Beaude, Jean Pierre (1849), ‘Anthrax’, in J.-P. Beaude (ed.), Dictionnaire
BIBLIOGRAPHY 205
et al. (eds), Dictionnaire de médecine, 2nd edn, Paris: Bechet, vol. 26,
pp. 336–359.
Dudley, Sheldon F. (1953), ‘The Lind Tradition in the Royal Naval
Medical Service’, in C.P. Stewart and Douglas Guthrie (eds), Lind’s
Treatise on Scurvy, Edinburgh: Edinburgh University Press, pp. 369–
385.
Duméril et al. (1838), ‘Rapport sur divers travaux entrepris au sujet de
la maladie des vers à soie, connue volgairement sous le nom de
muscardine’, Comptes rendus de l’Académie des sciences, 6:66–102.
Dunglison, Robley (ed.) (1845), Cyclopaedia of Practical Medicine,
American Edition, 4 vols, Philadelphia: Lea and Blanchard.
Durham, Herbert E. (1904), ‘Notes on Beriberi in the Malay Peninsula
and on Christmas Island (Indian Ocean)’, Journal of Hygiene, Cam-
bridge, 4:112–155.
Eade, Peter (1880), ‘Civil Practice’, Lancet, 1:992f.
Eijkman, Christiaan (1897a), ‘Eine beriberi-ähnliche Krankheit der Huh-
ner’, Archiv für pathologische Anatomie, Physiologie, und klinische
Medizine (Virchows Archiv), 148:523–532.
——— (1897b), ‘Ein Versuch zur Bekampfung der Beriberi’, Archiv für
pathologische Anatomie, Physiologie, und klinische Medizine
(Virchows Archiv), 149:187–194.
——— (1906), ‘Ueber Ernährungspolyneuritis’, Archiv für Hygiene,
58:150–177.
Ellenberger, Henri F. (1970), The Discovery of the Unconscious, New
York: Basic Books.
Elliotson, John (1830–31), ‘Clinical Lectures: Scurvy’, Lancet, 1:650–
655.
——— (1844), Principles and Practice of Medicine, 2nd edn, Philadelpia:
Carey and Hart.
Evans, Alfred S. (1976), ‘Causation and Disease: The Henle-Koch Pos-
tulates Revisited’, Yale Journal of Biology and Medicine, 49:175–195.
——— (1989), ‘Does HIV Cause AIDS? an Historical Perspective’, Jour-
nal of Acquired Immune Deficiency Syndromes, 2:107–113.
——— (1993), Causation and Disease: A Chronological Journey, New
York: Plenum Medical Book Company.
Evans-Pritchard, E.E. (1976), Witchcraft, Oracles, and Magic Among
the Azende, abridged edn, Oxford: Oxford University Press.
Farr, William (1839), ‘Letter to the Registrar-General’, in First Annual
Report of the Registrar-General of Births, Deaths, and Marriages in
England, London: W. Clowes and Sons.
——— (1840), ‘Letter to the Registrar-General’, in Second Annual Re-
port of the Registrar-General of Births, Deaths, and Marriages in
England, London: W. Clowes and Sons.
BIBLIOGRAPHY 211
Hughes, Sally Smith (1977), The Virus: a History of the Concept, New
York: Science History Publications.
Huppert (1865), [Review of Anthrax Literature], Schmidts Jahrbucher
der in- und ausländische Medizin, 132:37–43.
Ihde, Aaron J. and Stanley L. Becker (1971), ‘Conflict of Concepts in
Early Vitamin Studies’, Journal of the History of Biology, 4:1–33.
Iwanovski, Dimitri Iosifovitch (1892), ‘Ueber die Mosiakkrankheit der
Tabakspflanze’, Bulletin Académie Impériale de Science St. Petersburg,
3:67–70.
——— (1902), ‘Die Mosiak- und die Pockenkrankheit der Tabakspflanze’,
Zeitschrift für Pflanzenkrankheiten, 7:202f.
——— (1903), ‘Ueber die Mosaikkrankheit der Tabakspflanze’,
Zeitschrift für Pflanzenkrankheiten, 13:1–41.
J.F.S. (1836), ‘Discovery of an Insect in Itch’, Lancet 1:59–62.
Jaggard, W.W. (1884), ‘The Pathology, Etiology, Prophylaxis, and Treat-
ment of Puerperal Fever, from the Vienna Standpoint’, Medical News,
44:442–445.
Jeannel, Maurice (1880), L’infection purulente ou pyohémie, Paris: J.-B.
Baillière et fils.
Joest, Ernst (1902), ‘Unbekannte Infektionsstoffe’, Centralblatt für
Bakteriologie Parasitenkunde und Infektionskrankheiten, Abt. I,
31:361–384, 410–422.
Jones, Ernest (1953), The Life and Works of Sigmund Freud, 3 vols,
New York: Basic Books.
Kamminga, Harmke (1993), ‘Taking Antecedent Conditions Seriously:
A Lesson in Heuristics from Biology’, in Steven French and Harmke
Kamminga (eds), Correspondence, Invariance and Heuristics: Essays
in Honor of Heinz Post, Dordrecht: Kluwer.
Kaufmann (1866), ‘Ueber die Ursachen des epidemischen Puerperalfiebers
in Gebäranstalten’, Monatsschrift für Geburtskunde und
Frauenkrankheiten, 26:422–424.
King, Lester S. (1982), Medical Thinking: A Historical Preface, Princeton,
NJ: Princeton University Press.
Klebs, Edwin (1865), ‘Zur Pathologie der epidemischen Meningitis’,
Archiv für pathologische Anatomie, Physiologie, und klinische
Medizine (Virchows Archiv), 34:327–379.
——— (1871), ‘Die Ursache der infectiösen Wundkrankheiten’,
Correspondenz-blatt für Schweizer Aerzte, 1:241–246.
——— (1872), Beiträge zur pathologischen Anatomie der Schusswunden,
Leipzig: V.C.W. Vogel.
——— (1873), ‘Beiträge Zur Kenntniss der Micrococcen’, Archiv für
experimentelle Pathologie und Pharmakologie, 1:31–64.
BIBLIOGRAPHY 215
Malkin, Harold (1986), ‘Louis Pasteur and “le rage” – 100 Years Ago’,
Perspectives in Biology and Medicine, 30:40–46.
Manninger, Vilmos (1904), Der Entwickelungsgang der Antiseptik und
Aseptik, Breslau: J.U. Kerns.
Manson, Patrick (1901–02), ‘The Etiology of Beriberi’, Transactions of
the Epidemological Society, 21:1–17.
——— (1911–12), ‘[Discussion following] The Etiology of Beriberi [by
Alex Holst]’, Transactions of the Society for Tropical Medicine and
Hygiene, 5:81–90.
——— and C.W. Daniels (1907), ‘Beriberi’, in T.C. Allbutt and H.D.
Rolleston, A System of Medicine, 9 vols, London: Macmillan, vol. 2,
part 2, pp. 615–643.
Marchiafava, Ettore and Angelo Celli (1883), ‘Die Veränderung der
rothen Blutscheiben bei Malaria-Kranken’, Fortschritte der Medizin,
1:573–575.
——— and ——— (1885a), ‘Untersuchungen über die Malariainfection’,
Fortschritte der Medizin, 3:339–354.
——— and ——— (1885b), ‘Weitere Untersuchungen über die
Malariainfection’, Fortschritte der Medizin, 3:787–806.
Marjolin (1833), ‘Anthrax’, in Adelon (1832–46), vol. 3, pp. 193–200.
Mayer, Adolf (1886), ‘Ueber die Mosaikkrankheit des Tabaks’,
Landwirtschaftlichen Versuchs-Stationen, 32:451–467.
McCollum, Elmer Verner (1957), A History of Nutrition, Boston:
Houghton Mifflin.
McFadyean, John (1908), ‘The Ultravisible Viruses’, Journal of Com-
parative Pathology and Therapeutics, 21:58–68, 168–175, 232–242.
Medical Research Committee (1919), Report on the Present State of
Knowledge Concerning Accessory Food Factors (Vitamines), Special
Report No. 38, London: HMSO.
Medical Research Council (1932), Vitamins: a Survey of Present Knowl-
edge, London: HMSO.
Mendel, Emanuel (1884), ‘Ueber Hysterie beim mannlichen Geschlecht’,
Deutsche Medizinische Wochenschrift, 10: 241–244.
Misner, Charles W., Kip S. Thorne and John Archibald Wheeler (1973),
Gravitation, San Francisco: W.H. Freeman and Company.
Möbius, P.J. (1888), ‘Ueber den Begriff der Hysterie’, Centralblatt für
Nervenheilkunde und gerichtliche Psychiatrie, 11:66–71.
——— (1892), ‘Ueber die Eintheilung der Krankheiten’, Centralblatt
für Nervenheilkunde und Psychiatrie, 15:289–301.
Mollaret, H.H. (1983), ‘Contribution à la connaissance des relations
entre Koch et Pasteur’, NTM-Schriftenreihe für Geschichte der
Naturwissenschaften, Technik, und Medizin, 20:57–65.
Monatsschrift für Geburtskunde und Frauenkrankheiten, (1861),
BIBLIOGRAPHY 219
Breuer, Josef, 152–3, 155, 157, 83–4, 87, 96, 98, 103, 110, 113–15,
158–9 117, 130, 134–5, 138–41, 145; of
Brock, Thomas D., 115, 133 childbed fever 10, 40–43, 45–51,
Brown, Joseph, 13 109, 126, 143, 175; of death 16–17,
Bruce-Chwatt, Leonard J., 165 19–20, 31; of diabetes 10, 11,
Budd, George, 181–4 13–14, 17; of individual events 12,
Butler, Samuel, 1 17, 19–20, 22, 23, 146; of pneu-
butyric acid and ferment, 64, 78, 93 monia 11; predisposing, 12, 14–15,
Bynum, William F., 197 17, 20, 40, 43, 47, 155; proximate,
12–13, 16, 106–8; remote, 12–17,
Cagniard-Latour, Charles, 63 20, 25, 40, 90, 106–8; specific, 9,
Campbell, William C., 37 108, 143–4, 156, 158, 171, 176; see
cancer research, 4, 202 also causes, natural, universal, and
Carnap, Rudolf, 200 necessary
Carpenter, Kenneth J., 194–5 Celli, A., 165–6, 178
Carter, K. Codell, 22, 23, 44, 55, 61, characterizations of diseases, 7–8,
98, 100, 128, 139, 151, 154, 159, 18–20, 36–7, 38–61, 80–81, 103,
179, 182, 183, 184, 195, 196, 197 106–8, 109–10, 129, 138–9, 145,
Castiglioni, Arturo, 22, 147 151–2, 155–6, 158, 160, 164–5,
causal arguments, 31, 33–4, 36, 193, 200
73–4, 81–3, 87–8, 110, 122, 126, Charcot, Jean Martin, 149–61
138–9, 163–4, 172, 190, 198; Charles’ Law, 5
Davaine’s, 79, 82, 83–5; Klebs’, childbed or puerperal fever, 38–61,
95–8, 101, 163; Koch’s, 115–17, 93, 109, 119, 176, 196
119–22, 130–31, 134–5, 141; etiology of 10, 40–43, 45–51, 74,
Pasteur’s, 64, 70–73, 111–15, 109, 126, 143, 175; Semmelweis on,
117–18, 119–22 44–54; opinions about, in the
causal criteria, 8, 70, 73–4, 102–3, 1840s, 39–44
110–11, 122, 140, 162–3, 167, 174, chicken cholera, 119, 124
177, 178, 181; Klebs on, 92, 96–9, chickens: anthrax in, 118, 119, 140;
100; Koch’s use of 111, 131–2, 142, polyneuritis in, 188–90, 192
144; see also Koch’s Postulates Chimbuki, 21; medicine 22, 23, 39,
causal explanations, 30, 53, 54, 57, 197
60, 65, 105, 107, 119, 142, 144, chlorine washings, 44–7, 53
152, 196, 199, 200; in Davaine cholera, 55, 176, 198; discovery of
85–6; in Freud 158–60; in Koch bacillus, 127, 138, 139
132, 137, 198; in Semmelweis Cholera morbus, 31
48–51, 57 Chomel, A.F., 10–11, 14, 17, 20
causal webs, 4 chorea, 149, 150
causes, 88, 198, 203; exciting, 12, circularity of arguments for theories,
14–15, 17, 20, 40, 43, 108, 151, 126
155; in nineteenth-century medicine citations in scientific literature, 4–5,
10–23, 28, 104, 106–8, 151, 167–8, 38
176, 180; moral transgressions as, cofactors in disease, 140
20–22; natural, universal, and Cohn, Ferdinand Julius, 93–4, 109,
necessary, 1–4, 7, 24–37, 38, 51, 133
53–4, 59–60, 103, 106–8, 110, 112, Cohn, Martin, 148–50
118, 129, 142–3, 176, 180, 193–4, Cohnheim, Julius, 104, 133
196–9, 201 (see also causes, spe- Colin, Léon, 163–4
cific); necessary or sufficient 11–15, Collard, Patrick, 132
20–22, 23, 24–5, 48, 66, 70–73, 81, Columbus, egg of, 45, 54
INDEX 231
rabies or hydrophobia, 18, 31, 36, schizomycetes, 97, 99, 101, 109
121–6, 143, 162 Schlich, Thomas, 22, 23, 180, 196
Ralfe, Charles Henry, 182–3 Schmidt, Joseph Hermann, 46
Rapaport, David, 161 Schneider, Joseph W., 2
rational medicine, Henle’s program Schönlein, Johann Lucas, 18–19, 25,
for, 24–5, 59, 140 32, 91
Ravitsch, J., 55 Schrödinger, Erwin, 53
Rayer, Pierre-François-Olive, 76–7 Schüller, Max, 99
Recklinghausen, Friedrich Daniel Schwann, Theodor, 63
von, 93 Schweninger, Franz, 57
relapsing fever, 55, 94–5, 108 science, 1, 2–6, 9, 22, 23, 24–5, 31,
relativity, theory of, 5–6 68–9, 99–100, 104, 108, 109, 121,
Remak, Frederick, 91 200–201; see also research pro-
remote causes, 12–17, 20, 25, 40, 90, grammes
106–8 scientific: laws, 5–6, 25, 68–9, 74,
Renucci, Simon-François, 25–7, 36, 102, 109; see also heuristic of
196 research programme, hypotheses;
research programme, etiological see method, 68–9; progress, 3, 99,
etiological standpoint or research 200–201; see also Whiggish inter-
programme pretation of history; theories, 2–3,
research programmes, 2–5, 7–8, 62, 5–7, 54, 69, 88, 100, 102, 105–6,
104, 106, 142, 162; see also science 109, 162, 197–9; see also theories
resorption, of decaying organic of disease; medicine, 104, 147, 196,
matter, 48, 57 200–202; see also etiological
Richard, M., 164–6 standpoint or research programme,
Richmond, Phyllis A., 141 rational medicine
Richter, Hermann Eberhard, 57 scrofula, 106, 132–3; see also
ricidivousness of disease, 119 tuberculosis
rickets, 181, 192 scurvy, 181–4, 192–5
rickettsial diseases, 162, 178 Seeligmuller, Ludwig, 150
Ricord, Philippe, 25, 37 Semmelweis, Iganz, 38–9, 44–61,
Rindfleisch, Eduard, 92 72–3, 79, 90, 96, 107, 109, 138,
risk factors, 4, 140, 201–2 143, 145, 196; influence of, in
Rivers, Thomas M., 174, 199 etiological research programme, 39,
Rokitansky, Karl, 46 54–60
Rokitansky, Karl Jr., 58 septicemia, 116, 118
Rosenberg, Charles, 23 Sharkow, David, 161
Rosenthal, Moriz, 150 silkworms, diseases of, 25, 28–32,
Roser, W., 56–7 60, 66, 71–4, 75, 76, 79, 109, 111,
Röthlin, Otto Mario, 90 114–15, 117, 126–7, 143
Roux, Pierre Paul Emile, 165, 172–3, Simpson, James Young, 53
175 smallpox, 143, 162, 172
Rupert, J., 187 solid culture, media introduced, 121,
Russell, Bertrand, 200 132
Solotorovsky, Morris, 75, 134, 141
Salomonsen, Carl Julius, 133 Sontag, Susan, 133
scabies, 25–7, 37, 60, 143 Späth, Joseph, 55, 57
Scanzoni, Wilhelm Friedrich, 10, 17, specific causes, 9, 108, 143–4, 156–8,
20, 46, 59 171, 176; see also causes, natural,
Schaumann, H., 185 universal, and necessary
Scheube, B., 185, 187 Spencer, M.H., 188
236 INDEX
Watson, Thomas, 13, 19, 106–8 wine, spoilage of, 60, 70–71, 72,
weak sufficiency criteria, 139–41, 111, 113
181 Winkler, A., 187–8
Wegscheider, Max, 57 Wittgenstein, Ludwig, 8
Weiss, J., 148–50 Wöhler, Friedrich, 63
Welch, William Henry, 162–3 Worboys’ Michael, 6–7, 9, 23
Wertheimer, M., 59 wound infections, 55–6, 58, 60, 90,
Westphal, Carl, 94 92, 95–6, 108, 119, 130–32, 137–8,
Wheeler, John Archibald, 5–6 141–2
Whiggish interpretation of history, 8, Wright, Hamilton, 187
9; see also scientific progress Wulff, Henrik R., 23
Wieger, Friedrich, 58
Wilkinson, Lise, 169–70 yeast 63–4, 113; see also fermentation
Williams, Robert R., 179, 190 Yerushalmy, J., 199
Wilson, Adrian, 9, 23
Winckel, Franz Ludwig Wilhelm, 56, Zakon, S.J., 33–4, 37, 60
59 Zenker, Friedrich Alberti, 34–6