Studies in History

and Philosophy of
Biological and
Biomedical Sciences
Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042
www.elsevier.com/locate/shpsc

Was there a Bacteriological Revolution

in late nineteenth-century medicine?
Michael Worboys
Centre for the History of Science, Technology and Medicine and Wellcome Unit for the History of Medicine,
University of Manchester, Manchester M13 9PL, UK

Received 20 January 2006; received in revised form 7 July 2006

Abstract

That there was a Bacteriological Revolution in medicine in the late nineteenth-century, associ-
ated with the development of germ theories of disease, is widely assumed by historians; however, the
notion has not been dened, discussed or defended. In this article a characterisation is oered in
terms of four linked rapid and radical changes: (i) a series of discoveries of the specic causal agents
of infectious diseases and the introduction of Kochs Postulates; (ii) a reductionist and contagionist
turn in medical knowledge and practice; (iii) greater authority for experimental laboratory methods
in medicine; (iv) the introduction and success of immunological products. These features are then
tested against developments in four important but previously neglected diseases: syphilis, leprosy,
gonorrhoea and rabies. From these case-studies I conclude that the case for a Bacteriological Rev-
olution in late nineteenth-century medicine in Britain remains unproven. I suggest that historians
have read into the 1880s changes that occurred over a much longer period, and that while there were
signicant shifts in ideas and practices over the decade, the balance of continuities and changes was
quite uneven across medicine. My argument is only for Britain; in other countries the rate and extent
of change may have been dierent.
2006 Elsevier Ltd. All rights reserved.

Keywords: Bacteriology; Historiography; Medicine; Nineteenth century; Revolution

E-mail address: michael.worboys@man.ac.uk

1369-8486/$ - see front matter 2006 Elsevier Ltd. All rights reserved.
doi:10.1016/j.shpsc.2006.12.003
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 21

1. Introduction

Revolutions are out of fashion in history.1 In recent decades historians have increas-
ingly abandoned the notion, so while terms like the Scientic Revolution and Industrial
Revolution continue to be used in popular histories and as a shorthand, they no longer
have much currency in academic discourses.2 In comparison to the history of science,
which once upon time had many revolutionsthe Copernican, Chemical and Darwinian
immediately come to mindmedical history has been relatively devoid of them.3 The main
candidate has been the Bacteriological Revolution, in which historians have claimed that
the germ theory of disease and its associated practices transformed every aspect of med-
icine.4 In The greatest benet to mankind, Roy Porter refers to one of medicines few true
revolutionsbacteriology.5 In my book Spreading germs I argued against there having
been a Bacteriological Revolution, specically with regard to Britain and with the hope
the question would be re-examined in other countries.6 My conclusion has been generally
accepted, perhaps unsurprisingly as it goes with the ow of historiographical fashion,
though some, for example David Barnes, have argued that I underestimated the epistemo-
logical impact of Kochs postulates which forever changed the nature of medical knowl-
edge.7 This and similar responses have led me to reect again on my argument and to
discuss the historiography of medical bacteriology in the last quarter of the nineteenth
century more systematically. In this article I set out further reections, based on my
own new work on germs and other recently published studies. In order to make it clear
where all this is heading, I should say straightaway that my answer to the question in
my title remains the samethere was no Bacteriological Revolution in late nineteenth-cen-
tury medicine in Britain.8
A useful starting point would be a denition of the Bacteriological Revolution, but this
proves to be a most elusive notion. Despite its currency, I have been unable to nd an
explicit characterisation in the literature, nor is the term used in the any of the texts that
are routinely cited to support it: for example, Bullochs History of bacteriology, Stevenson
on critiques of bacteriology, Brocks writing on Koch, or Duboss biography of Pasteur.9
Nor is it mentioned in the recent writings of Bill Bynum, Gerry Geison, Nancy Tomes and
John Harley Warner.10 To be fair, Brock refers to Koch as a one of the true scientic rev-
olutionaries and many French historians write of a Pasteurian Revolution, but a Bacte-
riological Revolution is usually taken to mean something much widernot just the
establishment of bacteriology as a scientic discipline and medical specialism with its
own knowledge claims, methods and institutions, but rapid and radical changes across
medicine.11

1
Burke (2005), pp. 14171; but see Porter & Teich (1986).
2
Shapin (1996); Golinski (1992); Bowler (1988); Mokyr (1987).
3
Porter (1997), passim. Cf. Singer & Underwood (1962), pp. 351, 701, 752753.
4
Rosenberg (1987), p. 141.
5
Porter (1997), p. 428.
6
Worboys (2000), p. 278.
7
Barnes (2003), p. 115.
8
The situation in other countries may have been dierent. See Gradmann (2005); Salomon-Bayet (1986).
9
Bulloch (1938); Stevenson (1955); Brock (1988); Dubos (1960).
10
Bynum (1993); Geison (1995); Tomes (1998); Tomes & Warner (1997).
11
Brock (1988), p. viii.
22 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

As far as I can tell, the term Bacteriological Revolution rst came into use in the 1970s,
seemingly in the wake of Thomas Kuhns work when it became common for any and every
branch of science to have its revolution or revolutions.12 Bacteriology was said to have
wrought a paradigm shift in medicine, symbolised by radically new ideas and practices; for
example, in public health where attempts to combat elusive aerial miasmas were replaced
by measures targeted at demonstrable disease-germs spread directly by interpersonal con-
tact or indirectly by water; and in surgery where best practice was reversed, from leaving
healing wounds open to ensure that healing processes were well supplied with oxygen, to
covering them with elaborate antiseptic dressings. In the 1970s, there was in fact a claim
for nothing less than a scientic revolution in late Victorian medicine, where progress in
bacteriology was linked with changes in physiology, surgery, therapeutics and professional
developments.13 Another common phrase was George Rosens notion of Era or Golden
Age of Bacteriology, though to me this implies less a rapid turning point than an extended
period of innovation and inuence around the new subject.14 Latterly in the 1990s, histo-
rians tended to absorb the coming of bacteriology into discussions of a laboratory revo-
lution in medicine, an alleged radical shift of the locus of medical education, research and
authority from the clinic to the laboratory.15
There was some writing on a Revolution in late nineteenth-century medicine amongst
historians of medicine before the 1970s, though they tended to stress continuities. Garrison
absorbed bacteriology in long-run changes in pathology, aetiology and practice, suggest-
ing a continuous accumulation of knowledge.16 This was also the view of Richard Shry-
ock, who, arguing against what he termed the episodical interpretation of history,
portrayed bacteriology as emerging from developments in pathology, and from work on
contagia and surgical methods. However, he did write that the eects of bacteriology were
far-reaching, acknowledging a veritable revolution in the knowledge of disease causa-
tion after 1870.17 Erwin Ackerknecht was also equivocal, balancing the breath-taking
advances in the 1870s and 1880sthe most important [medical] development of the event-
ful nineteenth century and perhaps of all time when the whole of medicine was trans-
formed, with the observation that medical opinion was slowly to change.18 He
comments on how disease classications changed little, it being amazing how many dis-
ease units, originally isolated on purely clinical and pathological anatomical grounds, were
now identied and conrmed by bacteriological discovery.19 Oswei Temkins widely
quoted views on how bacteriological discoveries were decisive in altering the very meaning
of disease, advancing the ontological conception of disease so familiar to us today, might
be read as pointing to an epistemological revolution.20 However, he qualied this in his
observation that the simple monocausal aetiological models and ontological assumptions
of the 1880s rapidly broke down in the 1890s and 1900s with the rise of immunological
knowledge and ecological perspectives. Pelling has characterised the Bacteriological

12
Kuhn (1962).
13
Youngson (1979).
14
Rosen (1958).
15
Cunningham & Williams (1992); Jewson (1978); Gradmann & Sclich (1999).
16
Garrison (1917), pp. 606 .
17
Shryock (1936), pp. 246, 273.
18
Ackerknecht (1968), pp. 175185.
19
Ibid., p. 184.
20
Temkin (1977), pp. 436438.
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 23

Revolution as chain reaction of nding in the 1870s and 1880s, set o by Kochs methods
and Postulates.21 However, this claim comes at the end of a discussion of long-term shifts
in ideas of contagion, germs and disease specicity, and is not elaborated upon. In his
essay Transforming the plague, Andrew Cunningham makes the case for a complete dis-
continuity between old Plague and new bacteriologic plague around 1894, but he accepts
that for many years the new identity of the disease was only held by bacteriologists, and
acceptance across medicine only came in the 1930s.22 Most recently, Andrew Mendelsohn
has made a similar argument, though in dierent terms, arguing for two bacteriological
revolutions.23 First, the familiar revolution precipitated by the invention of bacteriology
and pioneered by Pasteur and Koch in the 1870s and 1880s, followed by a revolution
in bacteriology in the 1890s and 1900s. In the latter transformation, echoing Temkin,
he suggests that the relatively simple models and methods introduced earlier were compli-
cated by new ndings about bacterial variability, asymptomatic infection and the carrier
state, immunological processes, and so on. Mendelsohn is more concerned with the revo-
lution in bacteriology and says little on why events in the 1870s and 1880s qualify to be a
revolutionan assumption made somewhat problematic given his delineation of dierent
bacteriologies, with dierent chronologies, in France and Germany.
It seems that the term Bacteriological Revolution is, like many historical revolutions,
widely used but poorly articulated. If those who use the term have not bothered to dene
their great moment, I will have to do if for them. Firstly, what kind of revolution was it?
Historians use the term revolution in one of two ways: either for a moment of very rapid
change, or a period with radical discontinuities. Needless to say, the term is least contested
for revolutions that seem to qualify on both counts, for example the Russian Revolution is
mostly seen to have been rapid and radical.24 I will assume that Bacteriological Revolution
was rapidconcentrated in the 1880s and that it was radicalit transformed every aspect
of medicine.25 Its equivalent of the seizure of the Winter Palace in 1917 might be said to
be Robert Kochs announcement of the Tubercle bacillus on 22 March 1882. This discov-
ery has been said to have introduced a fundamentally new understanding of infectious dis-
eases and to have successfully demonstrated the value of novel methods for investigating
the causes and processes of disease in the laboratory.26 What was critical was not just the
discovery of the essential causal micro-organism of tuberculosis, though this was dramatic
as the disease switched from being hereditary to communicable, but the new meanings of
disease and the new ways of knowing its causes, processes and consequences. The latter
have been canonised as Kochs Postulates, though his colleague Loeer rst set them
out and it arguable whether Koch himself ever held to them.27 The so-called Postulates
are that: (i) a specic micro-organism must be shown to be constantly present in diseased
tissue; (ii) the specic organism must be grown and isolated in pure culture; (iii) the pure
culture must produce the disease when inoculated into a healthy animal.28 The alleged

21
Pelling (1992), p. 329.
22
Cunningham (1992), pp. 238240. I am grateful to Christoph Gradmann for this specic point.
23
Mendelsohn (1996), pp. 912.
24
Porter & Teich (1986).
25
Rosenberg (1987), p. 141.
26
Brock (1988), pp. 117139.
27
Gradmann (2005).
28
Ibid., pp. 179182; Carter (1985).
24 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

radical shift was that diseases could be and were dened aetiologically, and that the goal of
medical science became that of identifying single necessary causes.29 The case for a Bacte-
riological Revolution could be elaborated further by showing how the new ideas and
methods produced more eective practices, principally through reductionism and narrow-
ing the focus of medical interventions. This was exemplied in Listers focus on the entry
of aerial germs to control wound infection, which though developed in the 1860s, was
given new meanings by Kochs work on wound infection in the late 1870s.30 The case
might be concluded by highlighting two further innovations that quickly became available:
laboratory methods of diagnosis where medical investigators did not need even to meet the
patient, and new ways of preventing and treating diseases with vaccines and antisera, her-
alded by the introduction in 1885 of a treatment for rabies and followed by diphtheria
antitoxin in the early 1890s.31
In summary, the notion of there having been a Bacteriological Revolution seems to rest
on four linked changes that were both rapid and radical, and which were concentrated in
the 1880s:

1. A series of discoveries of the specic causal agents of infectious diseases and the intro-
duction of Kochs Postulates.
2. A reductionist and contagionist turn in medical knowledge and practice.
3. Greater authority for experimental laboratory methods in medicine.
4. The introduction and success of immunological products.

The Bacteriological Revolution is normally presented as an international phenomenon,

occurring across medical science in an era when knowledge was circulating more rapidly
through the proliferation and international circulation of publications and the movement
of doctors and patients.32 Historiographically, it is much easier to sustain the phenomenon
of a revolution if one can pick and choose developments across countries and disciplines.
However, recent work has shown the persistence and importance of sites of practice and
specically of national cultures in medicine, so if the task is to determine the extent and
pace of change in medical ideas and practice, then the best level for doing this is the
national, though with sensitivity to regional dierences.33 This is because there were
national standards of education, national publications and above all institutions. Also, I
showed in Spreading germs that British doctors and scientists were not isolated from devel-
opments in Continental Europe and North Americathere was dense, two-way trac in
people, ideas and practices. By focussing on Britain, it could be argued that I am loading
the dice against nding a Bacteriological Revolution, as this was the country where few
discoveries were made, where there was relatively little experimental research, and where
clinicians had the strongest hold on medical knowledge. However, as I have argued pre-
viously, Britain was not a bacteriological backwater.34 It had spawned Listerian antisepsis

29
Carter (2003). Carter sees the shift towards universal necessary causes occurring over a period from the work
of Ignaz Semmelweiss to the early years of the twentieth century.
30
Worboys (2000), pp. 139147.
31
Dubos (1960), pp. 117123.
32
Weisz (2005).
33
Warner (1986).
34
Worboys (2000).
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 25

and by the 1880s there was a cadre of bacteriological workers and followers, who were
part of international networks, and themselves contributed to new developments. They
were also close to, if not integrated into medicine and surgery, which they were able to
inform, if not always to shape to their model of modern practice.
To explore the claims for there having been a Bacteriological Revolution in British
medicine, I will consider each of the four characteristics set out above in turn. In doing
this I draw upon new work on syphilis, leprosy, gonorrhoea and rabies. These are diseases
about which there are few published medical histories, yet each was as medically and
socially important as tuberculosis and cholera, the usual focus of histories of germs in
the 1880s. All four were being studied by international networks and all were prime can-
didates for germ aetiologies and pathologies. Moreover, syphilis was the subject of intense
public attention due to the Contagious Diseases Acts, which were repealed in the 1880s,
while in the same decade leprosy was the subject of growing concern as a threat to the
new imperialism in Asia and Africa, and threatened to be imported back into Europe.35
Gonorrhoea was the most prevalent of the venereal diseases and in the 1880s was the sub-
ject of growing attention because of claims of its eects on womens fertility and health,
and the recognition that it was the largest cause of blindness in infants.36 Pasteurs rabies
vaccine was, to adapt the words of Bert Hansen, the worlds rst medical breakthrough,
attracting press attention and direct public interest as evident in the monies raised to found
Pasteur Institutes.37 If the medical understanding and management of these diseases was
not transformed by the new bacteriology, then the case for a Bacteriological Revolution
must continue to be unproven. In the next four sections I discuss each disease with respect
to one feature of my typology for a Bacteriological Revolution: germ discoveries with
regard to syphilis, contagionism with regard to leprosy, the authority of the laboratory
over the clinic with regard to gonorrhoea, and immunological products with regard to
rabies.

2. A series of discoveries of the specic causal agents of infectious diseases and the
introduction of Kochs Postulates: syphilis

A time line of bacterial discoveries is common in history of medicine textbooks and

encyclopaedias and, as usually presented, oers evidence for a clustering of signicant dis-
coveries in the early 1880s.38 The following list of the dates of the discovery of specic
bacterial pathogens is typical:

1873 Relapsing fever

1876 Anthrax
1878 Staphylococcal wound infection
1879 Gonorrhoea; Leprosy
1880 Typhoid fever
1881 Pneumonia; Streptococcal wound infection

35
There is, of course, a large literature on venereal diseases in the context of the history of prostitution, and of
imperialism in the context of imperialism. Walkowitz (1980); Gussow (1989); Buckingham (2002).
36
Worboys (2004), pp. 3149.
37
Hansen (1998).
38
Dubos (1960), p. 103.
26 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

1882 Tuberculosis; Glanders

1883 Cholera
1884 Diphtheria; Tetanus; Pneumonia
1885 E coli
1887 Bacterial meningitis; Malta fever
1888 Salmonella

However, there is an equally impressive list of diseases where germs were expected to be
found, but proved elusive and remained unidentied at the end of the 1880s, or the 1890s
for that matter. This listwhich included Measles, Scarlet fever, Smallpox, Syphilis,
Typhus fever, Whooping cough and Yellow fevercontained many of the most conta-
gious and specic of diseases, and hence those for which germs were most anticipated.39
Indeed, it is often forgotten that bacterial germs were rst associated with some unlikely
diseases; for example, with supposedly air-borne zymotic diseases like cholera, where any
disease-agent seemed most likely to be a volatile chemical, while with tuberculosis, the
main pathological indicatorstubercles in the lunghad been understood to develop
spontaneously due to hereditary inuences. That said, one of the main arguments in
Spreading germs was that lists of discoveries of disease-agents are misguided. Historians
of science, technology and medicine are increasingly uncomfortable with notion of discov-
ery because it implies nave realisma moment of revelation to an individualrather than
the construction of knowledge and practices that have meaning and currency in a commu-
nity.40 Second, observing a disease-germ was one thing; determining how it spread and
how it interacted with the body in disease processes, and in health, was something else.
No disease aetiology was settled in a moment; rather there were always negotiations over
various causal factors and complex pathological processes, with dierent settlements
reached at dierent times by dierent professional groups. For example, the British med-
ical profession was underwhelmed by the Tubercle bacillus, with hardly any group quickly
remaking tuberculosis a contagious condition caused by the bacillus alone.41 The most
common reaction was to dene the role of the bacillus in terms of the seed and soil met-
aphor, marrying existing assumptions the importance of constitutions with the new knowl-
edge of the bacillus as an exciting agent. As one doctor put it: physico-chemical changes
must precede botanical aggression.42 With the other high prole discovery of the early
1880s, that of the Cholera bacillus, there were protracted negotiations. This was true in
Germany, despite Kochs inuential position and state backing of his view.43 In Britain
there was a range of responses from outright rejection of the bacillus, by leading state bac-
teriologists and most Anglo-Indian doctors, through to the view that it played some role in
causation along with many other factors, held by most public health doctors, and to
enthusiasm for the idea that it was the essential cause, held by British followers of Robert

39
Hughes (1977). Most of these diseases were eventually found to be caused by viruses, which until the
development of in vivo culturing techniques and new techniques in microscopy in the twentieth-century remained
elusive agents, and were dened by their laboratory properties (ultramicroscopicallterable). or their eects as
disease agents.
40
Golinski (1998), pp. 1346.
41
Worboys (2000), pp. 193233.
42
Midland Medical Society: Ordinary Meeting (1885), p. 897.
43
Coleman (1987).
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 27

Koch.44 Through these and other examples, I argued in Spreading germs that simple bac-
teriological models of aetiology and pathology were never adopted in the 1880s only to be
revised into more complex models later, rather that such matters were always understood
by doctors and medical scientists to be complicated. While not denying the importance of
military metaphors with regard to infection at this time, it is too simple to suggest that
notions of invasion dominated in the 1880s and were complemented by notions of
defence when immunology emerged in the 1890s. I still contend that the metaphor of seed
and soil had the widest currency and inuence in medical understandings of infection from
the 1860s to the 1900s. I must emphasise that I do not doubt that the bacteriological model
of infection became very inuential across medicine; this is evident in the number and
range of diseases given bacterial aetiologiesfor example, cancer, scurvy, madness.45
Rather, I wish to suggest that what dened the period of Bacteriomania in the 1880s
and after was not the rapid and decisive adoption of new ideas and practices, but the
uncertainties and possibilities of the new aetiological and pathological models. It was
the ongoing ambiguities that were most productive in leading doctors and scientists to
think about, investigate and manage disease in new ways. One window on this is to look
at the failures of bacteriologywhat was the view of enthusiasts, neutrals and sceptics to
the missing discoveries I highlighted earlier?
Amongst the most widely anticipated bacterial discoveries was the germ of syphilis, a
disease that was indisputably contagious, and the one about which the state, doctors
and the public would most have welcomed greater knowledge.46 The syphilis germ eluded
the best minds and technicians of the new science of germs for a generation. It did not yield
to microscopy in the 1870s, or to microscopy plus culture methods and inoculation exper-
iments of the 1880s and 1890s. Consensus on a germ came in 1905 when the Trepanoma
pallida was rapidly accepted as the specic cause. Yet, this was not a period of stagnation
and silence on syphilis: between 1882 and 1905 it was estimated that some 125 causal
agents of syphilis were announced, mostly by German medical scientists.47 These discov-
eries were reported in the British medical press and followed up by British experts.48 Yet,
throughout this period the absence of a syphilis germ caused relatively little concern
amongst clinicians and for that matter, bacteriologists. Why?
First, as I have already mentioned, disease aetiologies and pathologies were not chan-
ged in discovery moments; certainly not in a new science with novel methods and ideas.
With the newly made bacterial diseases, doctors and scientists tended to work with the cur-
rent best t germ. Thus, for much of the 1880s it was assumed that the syphilis germ had
been found in the shape of the so-called Lustgarten bacillus.49 Conrmation, if it came,
was expected to derive from better microscopy and when a culture medium or animal
model for inoculations was found. In the meantime, this organism had a very similar sta-
tus in Britain to Kochs cholera bacillus; it was associated with the disease, but its exact
rolecause, concomitant, carrier, or contingentremained to be settled. Other organ-
isms, or rather their discoverers, had their day: the diphtheria-like Van Neissen bacillus,

44
Harrison (1994), pp. 99116; Worboys (2000), pp. 247254.
45
Carpenter (2000), pp. 3135.
46
Walkowitz (1980).
47
Lassar (1905), p. 440.
48
Marshall (19051906), p. 481.
49
Erichsen (1888), p. 1114; Treves (1895), p. 37.
28 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

the mixed infection theory of Tarnowsky and the protozoan parasites of Doehle and
Scheiller.50 Germ discoveries were not experienced by contemporaries as moments of
revelation, rather as ongoing negotiations over the exact role of certain disease agents
in aetiology and, I would emphasise, pathogenesis and morbid pathology.
The second reason for the lack of concern for the missing germ was the view that know-
ing its identity would be unlikely to alter accepted ideas and practice. It was not the case,
as for example some studies of the Contagious Diseases Acts suggest, that before the iden-
tication of the Trepanoma pallida knowledge of the disease was limited and uncertain;
nothing could be further from the truth.51 Syphilis was amongst the most studied and best
understood conditions, for which doctors had detailed knowledge of its signs and symp-
toms, its morbid pathology, its patho-physiology and its aetiology.52 As mentioned previ-
ously, at this time doctors did not characterise diseases aetiologically, hence, nding
specic, necessary causes was something that was only just beginning to become impor-
tant. Indeed, the aetiology of syphilis was not an issue; doctors and the public knew it
was spread by a virus that was transmitted through sexual intercourse, and knew many
ways to prevent infection. There was continuing discussion amongst doctors about the
routes of hereditary infection, but the fact that children born to uninfected mothers could
show signs of the disease and its specic stigmata (serrated teeth, keratitis, eye disease).
indicated that transmission of the germs or poisons of the disease was complex.53 The
diagnosis and prognosis of the disease beyond its initial venereal stage was not straightfor-
ward, yet this was something in which doctors could show their clinical acumen and
insights. In the 1880s there was clearly room for improvement in the accepted mercury-
based therapeutics, yet as an atypical virus-cum-constitutional aiction, doctors assumed
that treatment would always be largely ameliorative.54 In Britain, despite the introduction
of the Contagious Diseases Acts at a time of growing support for the scientic investiga-
tion of disease, the Chief Medical Ocer commissioned no experimental investigation into
the disease in the period 1865 to 1890. This contrasted with the many and elaborate inqui-
ries into cattle plague, cholera, smallpox, typhoid fever and other zymotic diseases. Why
was there so little interest in research on syphilis? It was certainly not Victorian prudery, as
the Contagious Diseases Act had made the disease a very public issue and doctors were not
reticent about publishing clinical and other studies in the medical press. My view is that
there was little research, because syphilis was amongst the best understood diseases and
because microscopical and experimental studies promised to add little to current
knowledge.
The third reason why nding a specic germ was not a high priority was that the under-
standing of syphilis was not static in the period 18751905; it did change, not least due to
the inuence of the wider development of germ theories and bacteriology. Over the period,
the aetiology and pathology was remade by doctors through a series of analogies with, in
turn, smallpox, cancer, tuberculosis, leprosy and diphtheria as each came to be seen as
contagious or infective in new ways. Doctors often distinguished contagious diseases
spread by direct contact from infections spread indirectly via air, water or carried on

50
Keetley (1884), p. 122; Eve & Lingard (1886), pp. 680681.
51
Lindenmann (2001, 2002); van den Belt (2002).
52
Cooper (1884); Hutchinson (1887).
53
Hutchinson (1886), pp. 239240.
54
Gowers (1889), p. 345; Erichsen (1888), p. 1132.
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 29

clothes and objects. Around 1870, syphilis was linked with smallpox, scarlet fever and
measles, with each seen as being highly contagious and produced by a chemical poison
or virus that aected the blood to produce local and systemic eects.55 However, at this
time syphilis was not considered to be a true zymotic disease, as these were understood
to be well dened, associated with fever and of short duration. Syphilis was experienced
as the most protean and complex of all ailments, commonly mimicking the signs and
symptoms of other conditions, and with infection perhaps lasting a lifetime. Its virus or
poison was primarily seen not as the disease itself, but as a catalyst that precipitated
changes in physiology and anatomy, which became self-perpetuating, permanent and
inheritable as the suerers very cellular constitution was altered.56 In the early 1870s,
these properties made syphilis an ideal candidate to be caused by Lionel Beales bioplasm
germsdegraded protoplasmic elements of diseased human cells that could spread and
initiate lesions.57 In this sense, syphilitic bioplasm behaved like cancer cells, having the
property of metastatic spread to many organs within the body as well as transmitted
between bodies.
From the late-1870s, when zymotic diseases became candidates for germ status, syphilis
was put forward as having the new key features of such diseases: there was an incubation
period (where a germ was developing), the absence of a dose-eect (due to the germs abil-
ity to multiply), the syndrome showing growth and decade of the disease (revealing the life
history of the germ), and in some cases immunity to further infection. The zymotic anal-
ogy broke down on the last two pointsrecovery from syphilis was uncertain and there
was no immunity after infection. However, no one at this time was certain what germs
were and how they acted, and that as protean things they might have many and variable
properties.58 Early converts to living-germ theories of disease expected that the syphilis
agent would be easy to identify. The fact that it was only spread by contact suggested it
was liquid or particulate, unlike the poisons of smallpox and other zymotic diseases where
aerial transmission pointed to an elusive volatile agent. There were obvious places to seek
the poison in the many types of syphilitic lesions throughout the body. In 1876, Jonathan
Hutchinson, Britains leading venereologist and a germ enthusiast, told the Pathological
Society of London that he had anticipated the early identication but that With regret
I admit that I have never seen with my outward eye the cryptogamic germ-poison of syph-
ilis; but to my minds eye it is as certainly as if I had.59 Hutchinson continued to champion
a germ aetiology for syphilis for the next thirty years on analogical grounds.60
The arrival of the Tubercle bacillus in the early 1880s oered a new analogue for syph-
ilis. Tuberculosis, which as I noted earlier was remade as a contingently contagious bac-
terial disease, was also chronic, variable and constitutional. It was this construction of
TB and the technical methods that came with it which produced the Lustgarten bacillus.

55
de Meric (1876), p. 391.
56
Greeneld (1876). Greeneld argued that the syphilitic poison modies the tissue elements themselves, hence,
it becomes truly a blood disease, modifying probably the blood-cells, and through them the nutritive uids. From
this period we have a tendency to the production throughout the system of growths . . . either as minute growths,
inltrations, or larger tumours (ibid., pp. 432433).
57
Beale (1872).
58
This theory dominated the special session on syphilis at the Pathological Society of London in February 1876;
Discussion on the pathology of syphilis (1876), pp. 341466.
59
Hutchinson (1876), p. 446; Report on syphilis (1876).
60
Hutchinson (1887), p. viii; (1909).
30 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

However, it was the related disease of leprosythe Tubercle and leprosy bacilli had sim-
ilar forms and were assumed to have similar propertiesthat had the most durable asso-
ciation.61 Medically, leprosy had a similar pathology to syphilis with skin lesions, tissue
degeneration and systemic eects on the nervous system, while socially its suerers were
stigmatised.62 In both cases, the disease might be quiescent for long periods, so that cures
were never certain, leading to suerers being constructed as types of person: the leper and
syphilitic. There was speculation both ways, for example, that congenital syphilis, where
doctors supposed the virus was carried by the sperm or ovum, suggested how leprosy
might be transmitted between generations.
At the end of the 1880s, doctors and researchers became increasingly interested in the
disease-producing mechanisms of bacteria, principally around the idea that most produced
physiological changes and lesions by secreting chemical poisons or toxins, as in diphtheria.
Investigators stressed that this was not a return to earlier ideas of a chemical virus, but was
part of the new study of ptomaines or bacterial poisons. For example, there was a toxine
theory of syphilis, which suggested that the germ operated covertly, hiding deep in some
tissue or other secreting toxic poisons into the blood.63 Britain had a strong group of
researchers working on this aspect of bacteriology, which followed from longstanding ana-
lytical studies of the poisons of putrefaction, the strength of physiology in Britain, espe-
cially under Foster at Cambridge, and because this was an area of research that
required only limited use of vivisection. The most prominent gure in Britain was Sidney
Martin who boldly and originally suggested in 1892 that there ought to be a fth Loeer
Koch postulate: the identication of the chemical toxin of each disease.64
Doctors and scientists ideas about the aetiology and pathology of syphilis continued
to develop in the 1890s and early 1900s along bacteriological lines, encouraged and inu-
enced by the ever more variable bacterial models of disease causation. They did so despite
there being no great discovery, no epistemological switch to seeing syphilis as an entity, no
signicant alterations in prevention and treatment, no laboratory tests and no immune
products. In other words, none of the features that have come to dene the Bacteriological
Revolution were present, yet new understandings ourished.

3. A reductionist and contagionist turn in medical knowledge and practice: leprosy65

I discussed changes in surgery and public health in Britain extensively in Spreading

germs, so with this topic I will turn to the larger canvas of imperial health to look at
changes in the understanding and control of leprosy after the announcement of another
rst-wave germ discoveryHansens Leprosy bacillus. This was trailed by Hansen in
1874 and formally announced in 1880 by Albert Neisser, who after his success with the
gonococcus went germ hunting in search of further prizes. His claim to priority over Han-
sen prompted a controversy that rumbled on.66 My concern here is not with the credit for
discovery, but with the changing aetiological meanings of the bacillus and whether there

61
Cooper (1895), p. 51.
62
Gowers (1889), p. 346.
63
Ward (1892, 1896).
64
Worboys (2000), p. 180.
65
Robertson (2003), Worboys (Forthcoming).
66
Fite & Wade (1955).
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 31

was a narrowing of control measures, with a shift towards contagionism and a focus on
people and their interactions.
My argument on the narrowing thesis in Spreading germs was: rst, that reductionism
and a move away from board-based, environmentally-focussed public health work pre-
dated bacteriology and, secondly, that changes in understanding and policy were variable
and are best considered disease by disease, not least because public health was becoming a
specialised and mature activity. The leprosy bacillus was amongst the most rapidly and
widely accepted germs, but rather than necessarily leading to an acceptance that the dis-
ease was contagious and in turn to a narrowing of interventions to controlling contagion
by halting person-to-person contact, control policies in fact moved the other way. Support
for non-contagion grew after 1880, and governments and charities were encouraged to
close leper asylums. By the early 1890s, one of Britains leading bacteriologists advised
that the best means of control was to address the problems of bad hygiene, poverty, insuf-
cient feeding; leprosy was after all harmless to healthy men, living under sound condi-
tions.67 How this came about is a complex story involving the interaction of British,
European and imperial governments, many dierent groups of doctors and various lay
organisations.
The dominant medical view of leprosy in the 1870s was that it was an incurable consti-
tutionaland hence an inheritedaiction. The most authoritative published work
advanced the view that leprosy was a non-contagious, systemic condition that aected
the blood, rather than being a local disease of the skin and nerves.68 Although it was more
common in the tropics, doctors accepted that leprosy could appear at any latitude, in any
race, and that the disease was the same across the world. It is important to remember that
multiple factor aetiologies were the norm at this time and that single cause explanations
appeared to be simplistic and in no way congruent with clinical experience or epidemiolog-
ical evidence. In the mid-1870s, the views of Robert Liveing on the origins of leprosy were
typical:
Firstly, that its primary [exciting] cause is not known. Secondly, that of subordinate
causes, diet and hereditary tendency are by far the most important, and that climate,
soil and race are not without inuence on the development and progress of the dis-
ease. Lastly, that leprosy, if not contagious, is capable of propagation by the imbi-
bition of the excreta of lepers.69
The question of the degree of contagiousness was not only important for policies on the
segregation of lepers, it became a marker of medical expertise. Leprosy experts and the
medical profession as a whole contrasted their experience and up-to-date knowledge with
lay opinion, which continued to hold that leprosy was highly contagious. They maintained
that this led to misguided public actions, such as placing lepers in colonies and stigmatising
them, which was contrasted with the more scientic and humane advice of doctors.
The dierences between lay and medical opinion were certainly an issue in 1862 when
the Colonial Secretary, in response to a request from the Governor of Barbados on how
best to control the disease, asked the Royal College of Physicians for advice. The College
formed an expert Leprosy Committee which reported that most doctors were strongly of

67
Kanthack (1893), p. 468.
68
Liveing (1873), passim.
69
Ibid., p. 100.
32 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

the opinion that the disease was not contagious or communicable to healthy persons by
proximity or contact with the diseased.70 In subsequent years, the ocial view against
contagion and segregation was challenged repeatedly, but there were consistent rebuttals
from the Royal College and the Colonial Oce.
The announcement of the leprosy bacillus in 1874 and then again in 1879 made little
impact on this controversy.71 Epidemiological data and clinical experience was, of course,
valued far above novel knowledge claims emerging from laboratories. All the more so with
leprosy because of the diculties of working with the bacillusit was hard to stain and
see, no culture medium was found and no susceptible animal was found for experimental
studies.72 The morphological similarities between the Leprosy and Tubercle bacilli, and
between the two disease syndromes where heredity was very important, led many doctors
to view leprosy through the lens of the changing aetiological and pathological assumptions
of tuberculosis.
There continued to be minority medical support for leprosy being contagious, a view
whose prole grew in the late 1880s when it was taken up by missionaries and those
who had apocalyptic visions of immigration leading to racial contamination and decline.73
In 1887 the Leprosy Committee of the Royal College of Physicians was asked to give a
fresh verdict on contagion and whether leprosy was an Imperial Danger. Once again it
concluded against contagion, stating that the discovery of the Hansen bacillus did not
point to the disease being contagious, no more than the discovery of the tubercle bacillus
established the contagiousness of phthisis.74 The Committee argued that the disease was
only rarely contagious and in exceptional circumstances, hence there was no justication
for compulsory segregation of suerers. None the less, the Committee added that some
state provision for lepers might be provided, not for isolation, but as refuges where kind-
ness, care and enjoyment could be given.75
These recommendations coincided with the death of Father Damien in Molokai, an
event that gained international attention and which supporters of contagion seized upon,
highlighting the tragedy of someone catching a fatal disease from those he had devoted his
life to caring for. In London there was a campaign to mark the death, which amongst
other things gave funding for a full and complete inquiry into the question of leprosy
in India.76 India had became the focus of metropolitan anxiety, in part because that
was where leper missions had concentrated their work, in part because of polarised opin-
ion within the Indian Medical Service over contagion, and in part because the record of
the Government of India on leprosy was being used by Indian critics as part of its overall
attack on the sanitary record of the Raj.77 However, the majority of Anglo-Indian medical
opinion was unimpressed by the alarmist claims that leprosy was an imperial danger and
relished the opportunity to confound popular opinion once again.

70
Report on leprosy (1867).
71
On the etiology of leprosy (1875), pp. 459489; Milroy (1876, 1877, 1880).
72
Thin (1883), pp. 11781180; Manson (1884), p. 342.
73
Wright (1885); Mackenzie (1889), pp. 925941.
74
Lancet, 130 (1887), p. 26.
75
The Times (11 November 1887), p. 3.
76
Abraham (1890), p. 6.
77
Kakar (1996); Pandya (1998).
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 33

The Father Damien Fund Leprosy Investigation Committee was despatched in Novem-
ber 1890, they toured India and Burma until May 1891 and then went to Simla for ve
months to undertake bacteriological laboratory work. The rst phase of data collection
produced a huge amount of epidemiological evidence and gave the Committee the chance
to hear every shade of opinion on the aetiology and pathology of the disease. The bacte-
riological researches went less well and produced no useful results. The Committees
Report was issued in June 1893 and, largely on epidemiological grounds, stood out against
contagion.78 On the question of the bacillus and contagion, they based their view not on
their own researches, but on Flugges observation in 1886 that the diusion of leprosy by
contagion is exceeding rare, and evidently can only take place under special and predispos-
ing favourable conditions.79 From this they went on,
that the more weight is [rightly] attached to special favourable conditions : : : the
further contagion disappears into the background. Indeed, for all practical pur-
posesand these are what the legislator or sanitary reformers has to considerit
vanishes altogether.80

The aetiology favoured by the Committee was that the leprosy bacillus was widely distrib-
uted through the environment in endemic areas, hence the great majority of infections oc-
curred not from person-to-person, but from environment-to-person, or they developed de
novo. In making these conclusions, they were adamant that that they were not looking
back to zymotic theory and old style anticontagionism, but were advocating advanced
bacteriological ideas on variable modes of infection and the complex actions of disease-
germs in and out of the body.
Their overall conclusion was that the best means of controlling leprosy was the
advancement of civilisation; after all, this is what had produced its decline in Europe.
The Committees one surprise nding was, contrary to popular belief, that the incidence
of leprosy was actually declining in India, a fact they explained as due to the introduction
of the sanitary improvements under the Raj. Shoes were also vital to this view. It was
widely surmised in India that the epidemiology of the disease was best explained by the
number of people who went barefoot. The supposition was that the Leprosy germs, having
fallen o with the skin of suerers or carried in their excreta, were in the dirt and dust of
streets and homes, waiting to enter the body through tiny cuts in the feet. This also
explained the social class and racial incidence of the disease, and its limited
communicability.
These conclusions on its essential non-contagiousness were contested. First, a number
of colonial governments were passing legislation to increase the extent and strictness of the
segregation of lepers, responding to the fears of local elites about the poor, vagrants and
coloured races as sources of infection.81 In retrospect, it is clear that these new measures,
which were mostly permissive and underfunded, were also gestures towards problems that
colonies were facing for the rst time: urbanisation, immigration and environmental deg-
radation. Second, international medical opinion had moved decisively towards supporting
contagion and linking this to the need to provide for the isolation of suerers. This

78
Indian Leprosy Commission (1893).
79
Report of the Leprosy Commission in India, 189091 (1893), p. 1026.
80
Ibid.
81
Deacon (2001), pp. 190206.
34 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

position was endorsed at the meeting of the rst International Leprosy Congress in Berlin
in 1897, though interestingly there was no ocial British delegate.82 The following year the
RCPs Leprosy Committee met for the last time. They accepted the verdict of the Berlin
meeting, though qualied it with provisos over the need for adaptation of control methods
to local circumstances. Few colonial governments committed resources to isolation and
segregation, or risked their strict enforcement; hence in most colonies person-centred mea-
sures were small scale, voluntary and relied mainly on missionaries, whose approach was
anything but reductive. And why bother when the advance of civilisation and the wearing
of shoes was solving the problem?

4. Greater authority for experimental laboratory methods in medicine: gonorrhoea83

If laboratory methods failed to meet the newly dened aetiological standards of the new
science of bacteriology with syphilis and leprosy before 1890, it is perhaps unsurprising
that its methods were little used for diagnosis. The potential of the laboratory was slow
to be realised, not least because those with the skills to undertake the tests were few in
number and the costs were high in terms of time and money. Doctors today can take a
sample, send it to the laboratory and expect a result quite speedily. In the 1880s, doctors
were untrained in taking samples and the technologies of protection and preservation were
undeveloped. Testing laboratories did not exist, hence the work had to be undertaken by
the doctors themselves, or they had to pay for individual, bespoke procedures. All of the
early bacteriological textbooks were do-it-yourself manuals, with advice on what instru-
ments and reagents to buy and where they could be bought. Diagnostic laboratories
and services only began to be established in the 1890s. There is also the larger point that
the great triumph of hospital medicine before 1850 had been to link pathological anatomy
with clinical symptoms; hence, most diseases at this time were classied and recognised by
their clinical symptomsso the value of other types of knowledge in diagnosis, especially
of causes that might no longer be active, was not obvious.
Where laboratory tests were used in diagnosis, it was to reinforce clinical judgements, as
two Irish doctors explained in 1890 with respect to gonorrhoea:
A given diagnosis can be regarded as entirely free from suspicion only when the
purely clinical tests and the bacterial tests are quite coincident and quite absolute.
An undue weight and value should not be attached to bacteriological investigations,
because after all said and done, it is essential that a rm clinical substratum should
underlie the whole.84

Gonorrhoea is an interesting case as it was arguably the rst disease for which Kochs four
postulates for the establishment of a bacterial aetiology were conrmed. This claim was
made in 1887 by William Japp Sinclair, a Manchester gynaecologist and obstetrician.85
According to Sinclair, a year after Neissers announcement of the gonococcus in 1879,
Bokai cultured the organisms and produced the disease by inoculating the urethras of
six medical students. In 1883, Bockhart reported the rst formal demonstration of the

82
Lancet, 150 (1897), p. 1127.
83
Worboys (2004), pp. 4159.
84
Blake & Shuldham (1890b), p. 4.
85
Sinclair (1888). The articles were published as a book in the following year.
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 35

newly announced postulates, based on the inoculation of pure cultures into a man suer-
ing from dementia. However, the patient died within ten days, so Bockhart was unable to
re-establish pure cultures with pus taken at post mortem. However, for Sinclair, the den-
itive modern view of gonorrhoea was set out in 1885 by Ernst Bumm, the German gynae-
cologist and obstetrician. Bumm oered sophisticated methods of staining to dierentiate
the true gonococcus from other organisms, and reliable methods of pure cultivation on
blood serum.86
An alternative story of the rst decade of the gonococcuswhich highlighted observa-
tional uncertainties, experiments with ambiguous results and a growing mismatch between
laboratory and clinicwas told by George Bantock to the Section of Obstetric Medicine
and Gynaecology at the Annual Meeting of the British Medical Association in July 1891.87
Bantock was a practising gynaecologist who held views that were typical of some surgeons
continuing scepticism towards bacterial accounts of disease. He maintained that the most
signicant feature of Bumms work was the identication of ve distinct types of cocci,
including a possible pseudo-gonococcus. Indeed, it was to distinguish these types that
Bumm had developed very complex staining methods, involving the use of Grams stain.
Sinclair had regarded all this as a triumph of bacterial technique with potential for accu-
rate diagnosis; Bantock concluded that these methods were now so delicate and compli-
cated that surgeons must fall back on rigid clinical observation.88 Bantock also noted
that Sanger had found that the gonococcus was not present in every case of the disease,
raising important questions about the reliability of bacteriological diagnoses and the
meaning of negative results. Also, after the cases mentioned above, there were no further
reports of human experiments and no animal model was found. Thus, the case for the role
of gonococcus in gonorrhoea did not rest on the routine demonstration of Kochs postu-
lates, but upon constant association and the way the properties of the gonococcus could be
linked to the clinical presentation of the disease. By the late 1880s, Bumm himself was
speculating on what he called compound infections, suggesting that gonococci often acted
in tandem with other organisms, for example, providing the conditions for septic germs to
enter tissues.89 The expectation of germ theorists that there would be a single, simple germ
for every disease and that germicidal agents would be found to destroy every germ, was
slow to materialise. Instead, the bacteriologists of the 1880s showed germs to be ever more
complex, with there being many strains of individual pathogens and the same strain show-
ing variable virulence. There remained also the constant question of the relationship
between the seed of the disease and the human soil; one obvious question was that in
a world full of germs, where infection was likely to be almost universal, why was not every-
one ill all of the time? Germ theories of disease logically implied germ theories of health.
Sinclair, an enthusiast for bacteriology, conceded in 1890 that perhaps the days of lab-
oratory investigation were over for gonorrhoea; certainly there was no need in the con-
sulting room to call in the aid of bacteriology as exemplary laboratory researches had
conrmed the eectiveness and eciency of established clinical methods.90 Jonathan

86
Bumm (1885).
87
Bantock (1891).
88
Bantock (1991), p. 750.
89
Drysdale (1882), pp. 391392.
90
Sinclair (1890), p. 1244.
36 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

Hutchinson warned against microscopy in gonorrhoea due to the number of similar

organisms to the gonococcus and the questionable value of negative results.91 Medical
understanding of gonorrhoea changed over the 1880s, not least as doctors recognised that
it could aect women as well as men. However, those who were arguing that gonorrhoea
was an entity, caused by a specic micrococcus that could aect any mucous membrane,
struggled against the view that the disease required the combination of a poison, impure
sex and male uro-genital organs.92 The persistence of diagnosis by clinical signs and symp-
toms was a key factor in the continuing failure to recognise the prevalence and possible
severity of the disease in women.

5. The introduction and success of immunological products: rabies

Any claims to revolutionary developments in immunological products in the 1880s is

necessarily about the work of Louis Pasteur, who from the late 1870s had worked on vac-
cines against fowl cholera, anthrax, swine erysipelas and, most famously, rabies.93 The lat-
ter brought Pasteur further fame in 1885 when he introduced treatment for the victims of
rabid dogs. This innovation raised expectations of the potential of bacteriology and lab-
oratory medicine to prevent and cure a number of human and animal diseases. So, what
was the reaction in Britain to this dening moment?
The rst point to make is that by calling his immunological substance vaccines, Pas-
teur deliberately associated his work with the Jennerian practice of using an infection of
cowpox to protect against smallpox. This move had the advantage of associating Pasteurs
novel, laboratory produced agents with materials and procedures that were natural, long-
established and successful. This tactic was used by John Tyndall when he wrote on Kochs
announcement of the Tubercle bacillus in April 1882 and held out the prospect of a vac-
cine against tuberculosis and the eradication of the disease.94 However, in Britain it also
alerted the well organised and vocal antivaccinationist groups, who quickly pointed out
that Pasteurs new vaccine worked, not by producing a related, natural and mild disease,
but by trying to give a sub-clinical infection with the altered germs of a killer disease.95
The reception of Pasteurs medical breakthrough in the United States was mediated
through the experience of four New Jersey boys who were sent across to Paris to be treated
in December 1885.96 In Britain, its was mediated through the story of a group of ve chil-
dren and three adults from Bradford who were taken to Paris by the towns medical ocer
of health, Thomas Whiteside Hime.97 Hime was a bacteriologically-minded practitioner
who upon his return travelled the length of the country lecturing on and extolling the vir-
tues of Pasteurian methods. However, locally Hime had to contend with three competing
treatment regimes that all claimed to be as good as if not better than Pasteurs. First, one
of Britains leading experts on rabies and hydrophobiaThomas M. Dolanwas based in
the nearby town of Halifax. Echoing the view of many surgeons, he maintained that local

91
Hutchinson (1895), p. 433.
92
Worboys (2004).
93
Dubos (1960), pp. 109126.
94
Worboys (2000), p. 211.
95
Durbach (2005).
96
Hansen (1998).
97
Pemberton & Worboys (Forthcoming).
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 37

Table 1
Percentage of rabid dog bite victims from England and Wales seeking the Pasteur treatment
Year Hydrophobia deaths Rabid dog bites Patients to Pasteur %-age to Pasteur
1885 60 600
1886 26 260 91 35
1887 29 290 64 22
1888 14 140 21 15

treatments were best and advised the cauterisation of wounds with a hot iron or acid.98 He
promoted his views within medicine through his editorship of the Provincial Medical Jour-
nal, locally through letters to the press to local chemists, some of which were published in
Almanacs, and nationally through two books on the subject.99 He pointed out that rabies
and hydrophobia were very rare conditions and that Pasteur had helped foster a hysterical
reaction which was leading to over-diagnosis, over-reporting and public panics. Second,
Hime was also aware that many dog bite victims chose self-help measures from folk rem-
edies, such as the hair of the dog that bit you, through to nationally marketed brands like
the Ormskirk Cure.100 Thirdly, antivivisectionists constructed the Buisson or vapour bath
treatment as the direct equivalent of the Pasteur treatment. It also had a French pedigree,
though it had been developed in the 1830s when a French physician, thinking that he was
developing hydrophobic symptoms after a dog bite, chose to end his life by asphyxiation in
a vapour bath set at 42 C.101 He survived and subsequently oered the same regime to
other dog bite victimshe presumed that the heat led to the rabies poison being sweated
out of the body. Indeed, in Bradford in March 1886, the antivivisectionists captured a
ninth victim who was sent to the Preissnitz baths in London for several days of closely reg-
ulated baths and constitutional treatments. Doctors and the public knew that only 10% of
those bitten by an allegedly rabid dog went on to develop hydrophobia, hence, all four
treatment regimes in Bradford seemed to oer equally favourable success rates. Pasteurs
treatment in a foreign location was dicult to access and provide reassurance about, espe-
cially when the antivivisectionists ensured that every death of a Pasteur patient was widely
publicised in poster titles like Pasteurs Hecatomb.
For much of 1886 and 1887 it became customary for rabid dog victims in Bradford and
surrounding towns to be sent to Pasteur, but this pattern did not survive Hime departing
in 1888. Indeed, nationally the percentage of rabid dog victims going to Pasteur seems to
have declined over time. Table 1 has been created with the assumption that the number of
actual rabid dog victims was ten times the number of hydrophobia deaths reported, which
gives an estimate of the number of possible Pasteur patients. When this is compared with
the numbers actually going, it shows that 35% of estimated victims went in 1886, 22% in
1887 and only 15% in 1888. Apart from deaths, these gures are, of course, hypothetical;
nonetheless what is signicant is the trendaway from a peak in 1886 of 1 in 3 rabid dog
bite victims taking the Pasteur treatment to just over 1 in 7 in 1888.
In 1886, the British government set up an expert committee of leading laboratory sci-
entists to report on the value of Pasteurs treatment and to recommend policies to control

98
Dolan (1890).
99
Dolan (1878, 1890).
100
Hunter (1986).
101
Pirkis (1896).
38 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042

rabies in Britain.102 The committees report strongly endorsed the treatment, but recom-
mended against the establishment of a Pasteur Institute in London, maintaining that any-
one bitten could readily travel to Paris for treatment. The main policy recommendation
was that rabies should be tackled as a contagious animal disease and that an attempt
should be made to stamp it out through veterinary police measures, such as rounding
up strays, enforcing muzzling and requiring dogs to be led. The question of a Pasteur Insti-
tute for London was raised again in 1889, but there was little support for such a vaccine
establishment. First, rabies was already being controlled by other means and second, such
a move would have produced erce opposition from antivivisectionists. Pasteurs work on
rabies had changed the public prole of vivisection in contradictory ways. Supporters of
vivisection at last had a specic, life-saving medical innovation that was directly derived
from animal experimentation, plus the promise of further similar benets to humankind.
However, opponents now had a new focus for their cause, for Pasteur was not just using
single animals in demonstrations or for research, but vivisecting and killing rabbits, dogs
and other mammals on an industrial scale. There were accusations that In the name of
Pasteur there has been a holocaust of dogs and graphic descriptions of Pasteurian sites.103

6. Conclusion

As I said at the outset, I remain unpersuaded of the case for there having been a Bac-
teriological Revolution in late nineteenth-century medicine. With none of the four impor-
tant diseases discussed here was there a clear-cut discovery moment, with rapid closure on
a new mode of transmission and pathogenesis. Nor was there any major change in preven-
tive or curative practice, and no rapid shift towards reductionist and/or contagionist
approaches that focussed on people and their interactions. In no case did experimental
laboratory work become decisive either in prevention, diagnosis or treatment, plus in
the one case where immunological products were availablerabies and hydrophobia
they were not used in Britain. In the examples I have discussed we do not see laboratory
knowledge challenging that of the clinic, or displacing it, rather we see clinical understand-
ing gaining enhanced authority from the laboratory. In other words, none of the features
of the classic bacteriological revolution as I dened it were present. It seems to me that
historians have read into the 1880s changes that occurred over a much longer period,
and that while there were signicant shifts in ideas and practices over the decade, the bal-
ance of continuities and changes was quite uneven across medicine. What I have argued
again here is that germ theories of disease and bacteriology were associated with changes
in ideas and practice in many and varied ways. New aetiological and pathological models
were widely discussed and used, especially as changes with one disease opened up new pos-
sibilities for analogical and analytical reasoning with others. Changes in disease prevention
and treatment, where they occurred, were contingent on many factors and there was no
general reductionist trajectory. New comparisons and contrasts were developed as diseases
were reconceptualised through the growing numbers and types of aetiological and patho-
logical lenses, and managed through a growing repertoire of techniques and technologies.
In short, it was the richer uncertainties and possibilities that dened the transformation of

102
Local Government Board (1887).
103
Zoophilist (18831884), p. 262.
 M. Worboys / Stud. Hist. Phil. Biol. & Biomed. Sci. 38 (2007) 2042 39

medical knowledge and practice in the half-century between 1870 and 1910, not new, rap-
idly accumulating certainties in a single decade.

Acknowledgements

This article was rst presented as the A and B Lecture at the University of Madison
Wisconsin. I would like to thank Professor Ronald Numbers for inviting me to give the
Lecture. I would also like to thank the Wellcome Trust for their support of this work
and my colleagues Christoph Gradmann, John Pickstone and Carsten Timmermann for
comments on drafts of this article.

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