In May 1939, a review of the American yearbook of dermatology and syphilology observed:
While this statement rightly reflects on improvements in Britain,
its perception of ringworm in the United States was wrong. Across the Atlantic,
it was not a problem amongst immigrants and African Americans; rather it had
been framed as a public health menace in the affluent classes, especially
amongst those who frequented swimming pools, and college students and, of
course, athletes. While its prevalence had seemingly shifted up the social scale
and from children to adults, its principal site of infection had moved too, from
head to toe, with ‘athlete’s foot’ being one of the most
common and most talked about diseases in America in the 1930s.
Manufacturers of popular remedies gave ringworm of the foot the name
‘athlete’s foot’ and this was adopted by the public, but
in medicine the infection was known as tinea pedis. It was seen as new disease,
or in modern parlance an emerging infection, having been first described by
Arthur Whitfield, a dermatologist at King’s College Hospital, London in
1908.3 Nonetheless, it
was in the United States that tinea pedis became an epidemic, seemingly spread
by modern lifestyles and hygiene practices, and encouraged by modern socks and
shoes, which made infection liable to chronicity by keeping the feet moist and
warm. It is perhaps surprising, given the unhygienic conditions of previous
centuries and the ubiquity of ringworm of the scalp, that the feet of Europeans
and Americans had been seemingly free of ringworm infection until the
mid-twentieth century. Nonetheless, there was a clear understanding in the
inter-war years that tinea pedis was new disease and one linked to modernity.
One consequence of the growth of medical attention to tinea pedis was the
stimulus it gave to the specialism of medical mycology, with investment in
diagnostic services, research on the conditions in which mycoses spread and
their treatment. In turn, this led to the creation of a cadre of medical
mycologists, who identified more fungal infections in specific social groups and
the general population.
We begin this chapter with a discussion of the development of medical mycology,
especially in the United States, which led the world in the creation of centres
of expertise, training and research. We then discuss the movement of medical and
public concern about ringworm from children’s heads to athlete’s
toes. In the 1940s, the condition was also recognised as a problem amongst
soldiers and miners, and was seen in terms of greater exposure to new pathogenic
species of fungi and the increased vulnerability of the human soil in tropical
and specific work conditions. While orthodox medicine approached tinea pedis as
something that was difficult to treat and needed to be prevented, proprietary
medicine companies peddled remedies that filled the therapeutic vacuum with
numerous ‘certain cures’. We follow the controversies around
popular and medical treatments, and the emergence in the late 1950s of medically
approved, clinically trialled antifungal drugs, modelled on the antibiotics
developed for bacterial infections. The most important of these was
griseofulvin, which promised to be effective and safe with topical and oral
administration. This was followed in the 1970s with a range of azole drugs.
These antifungals accelerated the disappearance of athlete’s foot as a
medical, if not public term, thereby divorcing ringworm from its locus of
infection or site of contagion, making it a type of dermatophytosis, literally,
skin fungal infection.
Medical mycology: ‘An Orphan Science’4
Glenn S. Bulmer has recently characterised the manner in which work on human
fungal diseases developed in the inter-war period as the result of the
movement and coalescence of specialists: ‘botany types came forth
and usually joined Departments of Microbiology &/or Immunology –
two subjects that most had never taken in school’.5 He may have had in mind
the founders of the first specialist medical mycology laboratory in the
United States, which opened in 1926 at the Columbia-Presbyterian Medical
Center (C-PMC). One leading light was the botanist was Bernard O. Dodge, who
then worked at the New York Botanical Gardens.6 He was known for his work on genetics
and for introducing T. H. Morgan to Neurospora, an organism
that became a widely used experimental model in genetics.7 Dodge was interested in fungal
diseases in humans and animals, and between 1928 and 1939 he was a
consultant in mycology at the C-PMC, while at the same time lecturing on
dermatology at the College of Physicians and Surgeons. The other founder as
a clinician, the dermatologist J. Gardner Hopkins, who worked at the
C-PMC’s Vanderbilt Clinic; previously he had worked on a cure for
the plague with Hans Zinsser in Serbia during the First World War.8 Indeed, his research
spanned infectious diseases, especially syphilis and moniliasis. In the
1920s and 1930s it was mainly ‘botany types’, with the
ability to identify types of fungi, who dominated the new field, which was
principally concerned with diagnosis, requiring microscopy and culturing
skills, combined with taxonomy. In 1926, Hopkins hired Rhoda W. Benham
– a botanist by training – to undertake mycological
diagnoses, and went on to develop a research laboratory from this base.9 His initiative was aided
by a grant of $50,000 from the Rockefeller Foundation in 1929, which
eventually enabled Columbia to develop the first specialist training in
human fungal diseases in 1935.
Hopkins’s laboratory became an influential research centre, producing
key figures such as Chester W. Emmons (1900–1985), the first medical
mycologist employed by the National Institutes of Health (NIH) in
Bethesda.10 Emmons
took his PhD with Robert A. Harper in the Botany Department at Columbia on
the subject of mildew, before working with Dodge and publishing two articles
on dermatophytes in Archives of Dermatology and Syphilis.
Neither author was medically qualified. Emmons stated later that when he
sought a reference to move to Hopkins’s laboratory, Harper had
asked, ‘Why do you want to study those abortive and uninteresting
medical fungi?’11 Indeed, Emmons referred to medical mycology as
‘an orphan science’ as it was never taught by mycologists,
whose main interest, outside of taxonomy, reproduction and other purely
biological matters, was in plant pathology. In his first medical
publications, Emmons proposed redefining the genera of the main fungal
causes of skin infection: Microsporum,
Trichophyton and Epidermophyton. His
approach was to use their morphologies, rather than their pathological
effects, pioneering what became the preferred method of standardising
diagnoses and avoiding the variability and inconsistency of clinical
criteria.12 Emmons
then worked with Arturo Carrión in Puerto Rica on
chromoblastomycosis, publishing in the Puerto Rico Journal of Public
Health and Tropical Medicine. In the event, the move to fungal
diseases turned out well, as his appointment at NIH was as principal
mycologist. He stayed for 30 years, becoming recognised as one of
‘founding fathers’ of medical mycology in the United
States.
The first monograph in the field was Harry Jacobson’s Fungous
Diseases: A Clinico-Mycology Text published in 1932. The author
was a dermatologist in Los Angeles and he presented ten chapters on
‘dermomycoses, moniliasis, maduromycoses, sporotrichoses,
blastomycoses, actinomycoses, coccidioides, toruloses and
aspergilloses’.13 A review in Archives of
Dermatology concluded that the book was
‘useful’ and, perhaps surprisingly, observed that
‘the mycologic aspects of the subject are better handled than the
clinical aspects’. The second monograph was published from Harvard,
where there had been instruction since 1924, and it was this course that was
written up in 1935 by Carroll W. Dodge, a botanist who was no relation of
Bernard O. Dodge.14 The
book was compiled at the suggestion of Roland Thaxter, who was medically
trained, but had switched to botany, eventually becoming professor of
cryptogamic botany at Harvard. Carroll Dodge’s Medical
Mycology: Fungous Diseases of Man and Other Animals was the
first use of ‘medical mycology’ in a book title. Here, and
in later works, the primary focus was on fungi and their identification,
with little on the pathology of the infections they caused. Before
publication, Dodge had moved to become professor of botany at Washington
University and continued to research fungal diseases in Central America,
before moving to Lichenology after 1950.
Writing the New England Journal of Medicine in August 1936,
Jacob H. Swartz, of the Department of Cryptogamic Botany at Harvard
University, maintained that,
Mycology is no longer a mysterious subject known only to a few. It
has been proved to be a part of medicine just as bacteriology,
physiology and so forth. Some knowledge of mycology is necessary for
a better understanding of disease.15
He was contributing to a discussion on fungi and internal medicine, where the
focus was not on skin diseases, but on systemic infections and allergy, with
an emphasis on the importance of predisposition – the human soil
– as a factor with infection. Many contributors stressed the role of
the laboratory in confirming clinical diagnoses; though Swartz worried that
since the ‘mystery’ of fungi had been largely solved,
clinicians were no longer turning to the laboratory and were relying solely
on clinical signs. The ‘orphan science’ had been adopted by
doctors, but it was not being nurtured. Swartz closed the discussion
demanding the creation of a mycological department in every medical school
and hospital, stating that ‘Mycology at present is in chaos’
and calling for the field to be ‘simplified and made useful to all
branches of medicine’.16 Arthur Greenwood, a dermatologist at
Massachusetts General Hospital, suggested the way forward was to create more
people trained to work between clinicians and mycologists.17 One factor fuelling
the demand for more medical mycologists, reflected in the discussion
prompted by Swartz, was recognition of geographically localised foci of
fungal disease, which we examine in Chapter 4. Meanwhile, athlete’s foot or tinea pedis was
emerging as a dominate concern for dermatologists and nascent medical
mycologists.
Athlete’s foot
Infection in areas other than the scalp came to the fore in the First World
War, when ringworm of the groin (‘dhobi itch’) was found to
be prevalent amongst American and British troops in France.18 Some doctors thought
that damp and crowded conditions of the Western Front increased
susceptibility and were ideal for contagion; others believed a new fungus
had been brought to Europe and the Americas by troops returning from the
tropics.19 The
bacteriological facilities available to the military medical services meant
that specific pathogens were identified, using the methods developed by
Sabouraud in the 1900s. Most cases were of Trichophyton
interdigitalis, but there were increasing reports of
Trichophyton rubrum, though at this time there was
little interest in the epidemiology of types of infection.20 Rather, discussion
focused on the observation that, paradoxically, tinea pedis was a disease of
hygiene. In the British military, the highest rates of infection were found
amongst officers, who through bathing regularly opened themselves to
infection through contact and softening of the skin. Also, tightly laced,
anklehigh army boots, worn in hot, damp environments, for long periods
without changes of socks, were understood to provide ideal conditions for
tinea pedis to flourish.21
In the United States too, ringworm of the feet was
‘discovered’ as a malady of soldiers in the First World War.
Two West Coast American doctors, Oliver Ormsby and James Mitchell, put
ringworm of the feet on the medical map in the United States in 1916, in an
article on infection of the hands and feet.22 The alleged first use of the term
‘athlete’s foot’ was in December 1928, in an article
in the Literary Digest, prompted by reports from Dr Charles
F. Pabst, of Greenpoint Hospital Brooklyn.23 Pabst claimed that the condition was already
well-known in the United States, with an estimated ten million sufferers,
three quarters of whom were unaware of the infection. The article stated
that the problem was of recent origin, but that ‘at least half the
adult population suffer from this malady at some time’. However, the
term athlete’s foot took hold, not as a disease of the masses, but
one of the America’s affluent classes, who could now afford to enjoy
leisure activities and modern hygiene facilities. Pabst, perhaps revealing
his limited social circle and awareness, claimed that ‘almost
everyone who uses a swimming-pool, golf club, athletic club, or any place
where there is a common dressing room, has the infection on his
feet’.24
Further medical recognition came in May 1929, when three doctors, working at
the University of California student health service, published data that
showed tinea pedis was endemic amongst students.25 They wrote that many students
arrived at college with the infection: 53% of males and 15% of females, and
the incidence rose to 85% in those final year students who took gymnasium
classes. In a follow up study, the doctors showed at the end of their first
year, the incidence amongst freshmen had risen from 53% to 78%, but was only
2% higher in female students.26 The sex differences suggested to
contemporaries four factors in the emergence of tinea pedis: the new male
enthusiasm for using gymnasia, swimming baths and other sports facilities;
the poor facilities for changing and showering at these locations; male
indifference to personal hygiene; and the types of socks and shoes worn for
sport and after, where the lighter, open shoes of women militated against
infection taking hold. Athlete’s foot was also possibly a
consequence of public sanitary facilities, where the sexes, social classes,
races and different ages mingled, and where anyone might be a
‘carrier’.
Awareness of the problem grew quickly. The link between tinea pedis and
athletes was evident in 1931 when the Los Angeles Times
termed it the ‘gymnasium malady’.27 In the same year, W. L. Gould, a
physician from Albany, New York State, reported to the United States Public
Health Service that possibly 50% of all adults suffered from tinea pedis and
that its incidence was particularly high in the states bordering the Gulf of
Mexico and in California, due to heat and humidity.28 At the 1932 Olympic Games in Los
Angeles, special antiseptic footbaths were provided to prevent
infection.29 By the
mid-1930s there was recognition that it was not just students and athletes
who were vulnerable. J. H. Swartz wrote of ‘the addiction of our
generation to the frequenting of gymnasiums (sic), baths
and locker rooms … and the tendency to exercise violently and
perspiring in unsterilizable socks and body clothing’. He went on to
wonder if the Romans were similarly affected?30 Dermatologists also saw tinea pedis
as threat to the family, through cross-infection in the home, where baths
and showers were becoming more common.31 However, Ayu Majima has shown that ringworm
amongst the poor – even tinea pedis – was never described
with the neologism of athlete’s foot and sufferers remained
stigmatised.32
Doctors prescribed a variety of remedies for tinea pedis, but because of
mixed results, their advice was mainly that prevention was better than cure.
Thus, anyone visiting a swimming baths and showering in public facilities
was told to disinfect their feet where possible, to avoid walking on floors
in bare feet, to dry their feet and toes after bathing, never to share
towels or clothing, and to wash socks at high temperatures. The main
remedies were topical antifungal creams. The standbys were
Whitfield’s ointment (the active ingredients were 5% salicylic acid
and 3% benzoic acid in petroleum jelly) and Castellani’s
carbol-fuchsin paint. However, the variable presentation of the condition
and its tendency to chronicity encouraged innovations, both in combinations
of remedies and new chemicals.33 There were many complaints of
overtreatment.34
Proprietary medical companies, which already had a significance market with
topical antiseptic remedies, seized on the new epidemic, producing new
products and rebranding older ones as having antifungal as well as
antibacterial properties.35 The most prominently advertised remedy in
newspapers and magazines was a derivative of a veterinary liniment –
‘Absorbine Jr.’, marketed by W. F. Young, Inc.36 The company claimed to
have coined the term athlete’s foot and in the late 1930s, the
advertisements for Absorbine Jr. echoed public posters against venereal
disease and referred to earlier fears, from the time of Typhoid Mary, to
unrecognised carriers (see ).
‘ABSORBINE JR.’ Athlete’s foot
advertisement, Life, 3(7)16 August 1937, 81.
The advertisement is ©2013 DSE Healthcare Solutions,
used under Creative Commons Attribution – Non-commercial
licence: http://creativecommons.org/licenses/by/3.0/. (more...)
Older products for ‘skin disorders of the feet’, such as Dr
Scholl’s ‘Solvex’, were rebranded to target the new
consumers, thus, its advertisement claimed it was effective against
‘gym or athlete’s foot’, ‘foot itch’
and ‘golfer’s itch’.37 While doctors promoted the
possibilities of prevention and commercial drug companies sold
‘sure-cure remedies’, there was also a sense that the high
prevalence of tinea pedis meant that it was an inevitable consequence of
wearing socks and shoes; or, as it was later put, ‘a penalty of
civilization’.38
In Britain there was less medical and public awareness of tinea pedis and the
term athlete’s foot was not widely adopted until the late 1930s.
Medical writings concentrated on diagnosis and treatment in individual
patients rather than any social group. However, doctors noted that it was a
disease with ‘something of the nature of a social qualification,
being commonly met among the upper and middle classes’ and, being
mostly spread through bathing; it was, then ‘paradoxically …
a penalty of cleanliness’.39 This changed in the 1940s, when Britain found
its equivalent of American athletes – coal miners. Tinea pedis was
identified as the commonest cause of miner’s dermatitis, a new
condition resulting, again paradoxically, from the provision of pithead
baths for communal bathing at the end of underground shifts. The Sankey
Commission, which had reported on the future of the coal industry in 1919
had recommended measures to improve the health and welfare facilities for
miners and the largest proportion of its expenditure (35%) went on pithead
baths.40 Baths were
introduced only slowly and the prevalence of tinea pedis only gained a
national profile during the Second World War, when absenteeism due to
illness and injuries was a threat to production in a pivotal industry.
Soldiers and miners
Concern about the incidence of tinea pedis amongst military personnel had
been expressed between the wars. A study for the United States Navy
published as early as 1924, showed 13% of all ranks were affected, but
levels were as high as 91% amongst officers recruited from college. The same
scenario was reported in the late 1930s in the Royal Navy, with the
condition being prevalent amongst all ranks in tropical stations.
Surgeon-Commander J. C. Souter expressed the opinion that tinea pedis was a
submerged problem, where itching and discomfort was tolerated by men,
‘yet every sufferer is a potential casualty’ should the
condition worsen, as it might on active duty when changes of clothing were
difficult, or in the tropics.41
During the Second World War, skin diseases were a major cause of invalidism
due to poor skin hygiene in combat locations, communal washing facilities
and exposure to new pathogens.42 In tropical theatres there were reports that
skin conditions were responsible for three quarters of sick bay attendances
in the Pacific.43 One
response at home was that in 1943, the Walter Reed Army Medical Centre in
Washington established a mycology laboratory headed by Norman Conant who had
started his career in Botany at Harvard, training with Raymond Sabouraud in
Paris before taking a post in the Department of Microbiology at Duke
University, specialising in mycology. He had worked on allergies and tinea,
but gained international recognition in 1944 with the publication of a
Manual of Clinical Mycology, co-authored with D. S.
Martin, D. T. Smith, R. D. Baker and J. L. Callaway, all from Duke’s
Medical faculty. There were also problems at home amongst soldiers being
exposed to geographically specific fungi at training bases in Western and
Midwestern states, which we discuss in the Chapter 4.
However, the highest profile incident with tinea pedis during the war
concerned a treatment on the home front. A mixture of phenol and camphor was
very popular, but there were reports of overtreatment and high levels of
exposure, leading to deaths.44 The remedy was championed by Paul de Kruif in an
article, entitled ‘A Working Cure for Athlete’s
Foot’ in The Reader’s Digest in May
1942.45 De Kruif is
best known today for his book Microbes Hunters and for
assisting Sinclair Lewis in the writing of Arrowsmith, but
in the 1920s and 1930s he was a significant figure in American
medicine.46 He had
worked for the Rockefeller Institute and become as publicist for medical
science, serving as secretary to the President’s Commission for
Infantile Paralysis in 1934. However, by the 1940s he had become a
controversial personality, mainly through publicising various medical
innovations, of which his athlete’s foot cure was seen as another
questionable example.47
Indeed, such was de Kruif’s reputation that the FDA issued a public
warning against the use of phenol camphor mixture later in 1942.48
Amongst British forces in South East Asia, the prevalence of all forms of
ringworm was so serious that the Royal Army Medical Corps set up a research
unit there on soldier’s dermatitis. Surveys by unit staff revealed
that amongst soldiers in Malaya and Hong Kong, 79.5% had tinea pedis and
33.5% had tinea corporis, tinea cruris or all three.49 However, ringworm received most
attention in Britain, not because of its military toll, but due to its
incidence in workers at home, along with the investment in fungus research
prompted by the discovery of the antibiotic properties of penicillin and
emerging problem of systemic mycoses. In Britain, the Medical Research
Council (MRC) appointed a Medical Mycology Committee in 1943.50 One goal was to
rationalise taxonomies and tinea pedis was a particular problem. At the time
the following terms were used by doctors across the Empire:
‘athlete’s foot’; ‘Hong Kong’,
‘Shanghai’ and ‘Singapore foot’;
‘gym’, ‘golfers’ and
‘swimmers’ itch; ‘toe-rot’;
‘ringworm of the feet’; ‘Cantlie’s foot
tetter’, ‘eczematoid ringworm of the extremities’;
‘dermatomycosis’; ‘epidermomycosis’; and
‘epidermophytosis’.51 Perhaps this variety was further evidence of
the novelty of the infection, or even the diversity of specific pathogens
producing different types of lesion, but most likely it reflected the
multiplicity of practitioners, locations and presentations.
The Committee’s work during the war focused on coal miners. The first
detailed study was made in 1943 by R. B. Knowles in the coalfields of the
north Midlands and South Yorkshire. He confirmed the widely held view that
the introduction of pithead baths in the 1920s and 1930s had created the
problem.52 After
the nationalisation of the industry in 1946 and the creation of the National
Coal Board (NCB), surveys and reporting on the welfare of miners
increased.53 One
study of miners in Warwickshire in 1946 found that 52% of the men had
‘intradigital disease’, 15% had ‘foot lesions other
than fungus infection’, and only 33% had ‘healthy
feet’.54 It
was against this background that in November 1951, a Committee on Industrial
Epidermophytosis (CIE) was established within the MRC’s Industrial
Health Research Board (IHRB). The Committee’s membership indicates
how tinea pedis had become a multi-specialist problem. The CIE was chaired
by John T. Ingram, a dermatologist from Leeds, who had considerable
experience in the army and was joined by two other dermatologists, George H.
Percival (Edinburgh) and H. Renwick Vickers (Sheffield).55 Geoffrey C. Ainsworth provided
mycological expertise, D. D. Reid from the London School of Hygiene and
Tropical Medicine dealt with medical statistics, while R. E. Lane from the
University of Manchester provided wider occupational health expertise.56 Another member was
Archibald L. Cochrane, who was then at the MRC’s Pneumoconiosis
Research Unit in Penarth, and later became a champion of randomised clinical
trials, where his legacy has been institutionalised in the network of
Cochrane collaborations.57 Also on the Committee were T. E. Howell, the
Principal Medical Inspector of Mines at the Ministry of Fuel and Power, and
J. M. Rogan, Principal Medical Officer at NCB.58
The initial brief was quite wide, but Ingram argued that the CIE should
‘deal in the first place especially with epidermophytosis of the
feet in coal miners and to leave all side issues … until
later’.59
Rogan stressed the NCB’s economic objectives of reducing absenteeism
and other costs, wanting the CIE to focus on practical measures, such as
prevention and methods for mass treatment.60 However, Ingram had other ideas and fostered
work across specialisms in epidemiology, the natural history of the disease,
clinical and mycological diagnosis, research on fungal growth, the chemistry
of the skin and the histopathology of the condition.61
Finding out the nature and scale of the problem in miners was the priority.
Epidemiological studies were commissioned from J. G. Holmes, a dermatologist
in Cardiff, and Jimmy Gentles, a mycologist who, during his term of
appointment, moved to the University of Glasgow. Early results came from a
pilot that Rogan arranged for Holmes to conduct at a colliery in Allerton
Bywater, near Leeds.62
There were issues with compliance and Holmes complained that miners showed a
‘lack of footconsciousness, thoughtlessness and in a few cases,
selfishness’.63 A larger study of 2,101 men working in mines
across the country was published in 1956.64 Clinical examinations found that 1,900 men
(90%) had some abnormality of the skin of the foot, yet in only 438 cases
(21%) was there laboratory-confirmed fungal infection. However, rates
varied, from 50% in one East Midlands pit to 3.5% in the Yorkshire coalfield
overall. The problems of reconciling clinical and laboratory diagnoses were
shown by the fact that 75 patients ‘showed so-called
“diagnostic” lesions without any evidence of fungus being
found’, while 4% of those with ‘clinically normal
feet’ tested positive in the laboratory.65
The Medical Mycology Committee’s post-war survey on the incidence of
mycoses in Britain, published in 1948, confirmed a view widely held within
the medical profession, that the incidence of tinea capitis, the new term
for ringworm of the scalp, in children had risen during the war. The rise
was attributed to the suspension of X-ray treatment, the relaxation in
school hygiene, and to the evacuation of children, with a consequent decline
in hygiene and greater exposure to cats, dogs and cattle.66 An increase in tinea pedis in adults
was explained by continuing improvements in hygiene, the exposure of men to
infection in military settings, and the circulation of ringworm species
around the world with troop movements.67 A particular concern was the importation of
T. rubrum to Europe from the Far East, as it was one of
the most difficult ringworm species to treat. However, the reported
incidence of tinea pedis in Britain was nowhere near that in the United
States. In 1950, Jacqueline Walker reported on a survey of 1,010 army
recruits, 857 of whom were free of infection and of the 123 suspected cases,
only 39 (4%) were confirmed in the laboratory.68 One reason for the low incidence was
the relative paucity of sports and college facilities, and there were
certainly fewer homes with bathrooms where infection could spread within
families. The place where the spread of tinea pedis was most common was in
elite public schools, which had the best sports facilities.69
One problem in surveys was the discrepancy between clinical and laboratory
diagnoses. Doctors accepted that microscopy and culturing were more reliable
than clinical methods; however, there were few laboratories available to
provide the tests and a reluctance amongst dermatologists to use them.70 For some, the
reliability of laboratory results was a moot point. They depended on many
factors: from the quality of the skin sample taken, through to the
competence of staff in particular laboratories. Accuracy mattered more in
epidemiological studies than it did in clinical practice. False positives in
a low incidence population would skew the result significantly, whereas
dermatologists and general practitioners were prescribing broad spectrum,
topical fungicides for all presentations of ‘inter-digital
dermatitis’ without laboratory confirmation. Better-targeted
treatment would have prevented what one doctor later termed ‘a
chemical assault’ on the feet of the nation in the post-war
era.71
The uncertainties over diagnosis, especially when fungi were found without
clinical disease in ‘symptomless carriers’, reopened the
question: were the fungi causing tinea pedis external contagious agents
caught from other people, or were they saprophytic parasites of the skin
that only caused disease in certain conditions?72 While patterns of infection in
particular groups and the identification of infective fungi on floors in
baths and showers pointed to the overriding importance of contagion, some
doctors argued that infection was more complicated. The seed and soil
analogy was used to suggest both that prior physico-chemical changes had to
make the skin open to infection, as in pre-pubescent children, or that a
‘factor X’ was involved.73 Such views were important because doctors were
only too aware of the limitations of topical remedies and, hence, were keen
to promote specific and general preventative measures.
Chemical abuse of the nation’s feet
In the late 1940s, the American market was flooded with topical
treatments for athlete’s foot. Writing in JAMA
in 1946, G. B. Underwood and colleagues wrote on the
‘unbelievable chemical abuse’ of the feet of
Americans.74 In
their practice they reported:
Feet are seen daily, painted all the colors of the rainbow or
daubed so thick with salves that removal with a tongue blade is
necessary to view the underlying dermatitis. The shoes smell of
solution of formaldehyde and are caked on the inside with
fungicidal powders. The patients, when questioned about the
number of remedies used, shrug their shoulders and exclaim
‘I couldn’t begin to recall. I’ve used
everything. You are the sixth or seventh doctor I have seen.
I’ve had this stuff between my toes for years. Just when
I think it is well, it’s back again. Each time it comes
back I try something else. I’ve spent a small fortune
for remedies, and look at my poor feet.’ These patients
are sure of the cause of their dermatitis. It is the
‘athlete’s foot’ or the
‘fungus.’75
They reproduced examples of the ways that companies selling topical
remedies portrayed athlete’s foot as dire threats to individual
and public health. Potions were said to ‘Kill Athlete’s
Foot Germs on Contact’, to cure ‘Factory Feet’
and warned ‘YOU PROBABLY HAVE ATHLETE’S FOOT or will get
it’. Brands had names like ‘Soretone’,
‘Korium’, ‘Octofen’ and
‘Desitin’. Some remedies were cure-alls, such as
‘3XB ’, which also
helped with ‘minor wounds, blisters resulting from ivy
poisoning, or similar conditions, corns, calluses, tired feet, chafing,
prickly heat or similar skin conditions’. Underwood and his
colleagues reported analyses of 106 popular remedies, finding the most
common ingredients were phenol, ethyl aminobenzoate and, most
worryingly, mercurial compounds. The Mennem Company’s leading
brand ‘Quinsana’, whose advertising regularly featured
the threat of catching athlete’s foot on the beach, contained
Hydroxy-Quinolene, Magnesium stearate and boric acid. Underwood and his
colleagues ended with a plea to dermatologists to ‘take steps to
prevent the commercial commandeering of scientific reports and
formulas’, and called for the regulation of popular skin
treatments.
Whether the rash of new products was due to a real increase in the
incidence of fungal skin infections is unclear, but the post-war
increase in tinea capitis in American schools suggests that there was
more ringworm in communities.76 Infected children were treated with
X-rays, as well as topical remedies and there were calls for public
health agencies to take up the matter.77 Laboratory reports showed that the main
cause was no longer Microsporon canis caught from pet
and farm animals, but Microsporon audouini, the main
European ringworm species.78 State and county authorities started
campaigns, which were claimed to be effective. The reported incidence of
tinea capitis fell in the 1950s, even though X-rays, the former
treatment of choice, was dropped because of concern about the long term
health effects of exposure to radiation.79
The most notorious example of the enthusiasm for developing and trialling
treatments for athlete’s foot were the investigations on
prisoners undertaken by Arthur Kligman in Pennsylvania and discussed in
Arthur M. Hornblum’s book Acres of Skin.80 Kligman worked in
the Department of Dermatology at the University of Pennsylvania Medical
School, then headed by David Pillsbury. Prior to his work with
prisoners, Kligman had made experimental studies of children in mental
defective homes to test the effects of X-rays used to treat tinea
capitis.81 He
wrote in 1952 that,
The work was carried out at a state institution for congenital
mental defectives … The experimental circumstances were
ideal in that a large number of individuals living under
confined circumstances could be inoculated at will and the
course of the disease minutely studied from its very onset.
Biopsy material was freely available. By contrast,
Sabouraud’s researches were largely limited to the
clinical opportunities presented by ringworm patients appearing
at the Paris clinic.82
This work was part of wider studies of treatments for ringworm,
especially the new topical creams versus depilation, either mechanically
or by X-rays.83
In 1957, Kligman published an article with John Strauss that opened with
the following statement.
So much has been written about the subject of athlete’s
foot that one can hardly add still another paper to an already
mountainous pile without some justification. We thought we could
gain some fresh appreciation of this disease by studying it
experimentally in a prison population. With this group it was
possible to do a number of things which would otherwise have
been rather difficult. Rigid control over the subjects, adult
males in the age range of 20–50 years, offered many
experimental advantages.84
Kligman’s research at the prison, which ran from 1951 to 1974,
grew from initial studies of athlete’s foot treatments, to
medications for a wide range of other skin conditions and cosmetics. He
worked closely with pharmaceutical companies and prisoners were paid to
be human guinea pigs. Kligman became infamous because of the ethical
status of his trials, however, in American dermatology he remained a
hero, with his death marked by an article with the by-line
‘Albert the Magnificent’ and no mention of the
criticisms of his work.85 Controversy was fed by the fact that Kligman
was unapologetic; he considered retrospective judgements of the ethics
of his work unfair and that he defended it, arguing that medicine had
benefited and ‘no prisoner suffered long-term harm, as far as he
knew’.86 Nonetheless, the furore caused by criticisms
of his work in the 1970s, including the development of the anti-wrinkle
cream Retin- A, prompted stricter Federal regulations on medical
experiments with prisoners and human subjects more widely.87
In both the United States and Britain, the reported prevalence of tinea
capitis waxed and waned in the 1960s. One clear trend in the United
States was the growing importance of infection with T.
tonsurans, seemingly imported from Central America and the
Caribbean, with M. audouinii seemingly in decline
across the northern hemisphere.88 Some dermatologists speculated that the
fall in incidence in the late 1960s was due to the fashion for long hair
in both men and women, and for ‘Afros’ amongst
African-Americans, both being protective against hair root
infection.89
Griseofulvin: ‘Epoch making’ antifungal
treatment
From the early 1940s, state and pharmaceutical company laboratories
sought novel approaches to fungal infections following the model of
antibiotics with bacteria; that is, chemicals that could be injected or
taken orally, that would act as ‘magic bullets’,
affecting the pathogenic microorganism and not the host’s cells.
There had been hopes in the early 1940s that penicillin, or similar
fungally derived products, would be antagonist to pathogenic fungi, but
these were unfulfilled. Nonetheless, the treatment of fungal infections
did benefit from the increase in the scale and intensity of biomedical
and pharmaceutical research.90 Nystatin, which we discuss in Chapter 3, introduced in the
early 1950s, was the only success in the search for antifungal
antibiotics for a decade; but it was ineffective against ringworm and
could not be taken orally. Researchers turned to other approaches. One
was to build upon the observation that vulnerability to tinea capitis
seemed to end at puberty, which pointed to changes to the chemistry of
hair follicles and the identification of heavy fatty acids that seemed
to have antifungal properties. The most important was undecylenic acid
and its salts.91
The effectiveness of this fatty acid was similar to compounds already in
use, but it had the advantage, allegedly, of being less irritant because
it was ‘natural’. In Britain, the following proprietary
preparations that were widely used from the late 1940s, all contained
zinc undecylenate: ‘Tineax’ from Burroughs Wellcome and
Co.; ‘Mycota’ from Boots and ‘Desenex’
from Wallace and Tierman. The salts of two other fatty acids, proprionic
and caprylic, were also used in the same way. The market leader in
Britain was ‘Mycil’, produced by British Drug Houses
(BDH). Its active substance was
p-chlorophenyl-a-glycerol ether,
marketed as ‘chlorphenesin’ and discovered in 1947 by
Frank Hartley, then Research Director at BDH, in 1947.92 In the United
States, ‘Desenex’ ointment and foot powder, produced by
Wallace and Tiernan, led the way, and were used in the Korean War and
later enjoyed endorsement from celebrities from the National Football
League, such as Johnny Unitas.
An editorial in the Lancet in July 1946 had wryly
observed that most doctors ‘take a personal interest in tinea
pedis, for – like piles, toothache, and sore throats –
if we manage to escape it ourselves, it will not be long before some
member of our family is clamouring for attention’.93 The editorial
bemoaned the fact that, despite the flood of new remedies, most
treatments had limited effectiveness, particularly in the longer term.
Over a decade later, reviewing treatments for general practitioners in
May 1958, Grant Peterkin, head of the Skin Department at the Edinburgh
Royal Infirmary, reflected that old favourites, such as
Whitfield’s ointment and Lassar’s paste, were still
second to none.94
He noted the recent impact of nystatin on the treatment of
Candida infections, both in topical applications
and when taken orally for intestinal infection, and regretted that there
had been no similar advance with tinea pedis. However, he was hopeful:
‘Yet it seems possible that in the future fungus infections of
the skin may be eradicated by some antibiotic given parenterally
[orally].’95 By the end of the year his hope had been
fulfilled with the announcement of the oral antifungal drug –
griseofulvin.96
Griseofulvin had been first isolated from the fungus Penicillium
griseofulvum by Harold Raistrick at the London School of
Hygiene and Tropical Medicine (LSHTM) in 1939.97 Raistrick was Britain’s
leading figure in the biochemistry of fungi, having worked on industrial
fermentation for the government in the First World War and then for
Imperial Chemical Industries (ICI), before his appointment to the LSHTM
in 1929. He had worked on penicillin in the early 1930s, following up
Alexander Fleming’s early publications, and his laboratory had
continued to use Penicillium spp. as experimental
models.98
Surprisingly perhaps, griseofulvin was not screened for antibiotic
properties in the early 1940s and its antifungal potential was only
recognised at the end of the decade, and then in an agricultural rather
than medical context.
Researchers at the Butterwick Research Laboratories of ICI found that it
produced ‘curling’ in the hyphae of certain fungal
species, inhibiting cell wall formation and cell division.99 Further work
showed it to be an effective, broad spectrum fungicide, though it had no
great advantage over existing and cheaper commercial compounds.
Mycologists remained interested in the compound, as did researchers at
Glaxo’s Sefton Park and ICI’s Alderley Park
Laboratories. Parallel, but separate, investigations showed that
griseofulvin had a low toxicity when high doses were given to
experimental animals. It also proved to be valuable as a laboratory
agent for inhibiting the growth of hyphae-forming fungi, even at quite
low concentrations.100 However, its potential as an oral antifungal
seemed limited because it was largely insoluble in water and, hence,
could not be made available for absorption through the gut.101
Griseofulvin’s promise as a fungicide in agriculture led Glaxo
researchers to test its toxicity to humans to determine safe exposures
for farm workers.102 These trials showed few, if any, toxic
effects. However, commercial development was not fast-tracked because
griseofulvin was expensive to produce. In the mid-1950s, Glaxo
researchers learnt that two other groups were interested in
griseofulvin: Gentles through his work for the NCB, and workers at ICI
who were exploring veterinary and human uses. Both Glaxo and ICI had
taken out provisional patents on different aspects of the production and
use of griseofulvin, and in an unusual move, signed a joint agreement in
the spring of 1957 on their respective rights in all areas, from patents
through to licensing. Glaxo continued to work with Gentles on animal
studies, which led to a publication in Nature in August
1958.103
However, work at ICI showed that griseofulvin could affect mammalian
cell division and this prompted further collaboration between
researchers in both companies.104 In comparing data, it seemed that the
different results were due to the particle size and that the coarser
Glaxo compound was safer. Three dermatologists approached Glaxo for
samples to test in patients with ringworm: Gustav Riehl in Vienna,
Harvey Blank in Miami and David Williams at King’s College
London. The first results from these clinics were presented in late
1958.105
David Williams and colleagues published a report of nine patients with
T. rubrum infection who had been successfully
treated with orally administered griseofulvin, supplied by Glaxo.106 There was great
excitement about the work. Williams concluded his article with the claim
that griseofulvin ‘represents a fundamentally new therapeutic
approach’.107 One Cambridge dermatologist, hearing of the
development, had written to the MRC claiming that the work was
‘epoch making’.108 The London trial had followed on from a
report in August 1958, by Gentles, of successful oral treatment of
ringworm in experimentally infected guinea pigs.109 Gentles had rushed to publish
and was similarly excited; though he went for understatement, ending
with the remark that this work ‘may be of some important for
future progress in this hitherto unrewarding field of
investigation’.110
Gentles and Williams spoke on griseofulvin at the annual meeting of the
British Dermatological Society in July 1959.111 Gentles reviewed the clinical
literature and the growing consensus that it was effective for two
reasons: first, through its deposition in keratin (the structural
protein of hair and nails), and second in being fungistatic, that is,
inhibiting the growth of the fungus. This meant that it was likely to be
effective in deep-rooted infections of the hair follicles and in
toenails. David Williams began his talk by reflecting on the reputation
of dermatology within the medical profession and how this might have to
change.
Once upon a time – and thus all good stories begin
– there was an old retired general practitioner who said
that he could treat all skin diseases although he could diagnose
none. Those were the slap happy days when local treatment was a
magnificent pseudo-science – not even now do we have
much understanding of how local applications work – and
internal treatment was a desperate matter of letting justice
seem to be done, not too critically … . But in the last
fifteen years there have been remarkable advances in the
chemical and antibiotic field. Treatment is becoming so specific
that there is much to be said for a proper diagnosis before
starting it. Penicillin has made syphilis so rare that it is
easy to forget its existence. Anti-tuberculous drugs have ruined
for us a fascinating, a lovely group of dermatological
conditions. And now griseofulvin.112
Williams stated that in his clinic the ‘experience so far has
been so gratifying that it is difficult to be restrained about what
seems to be happening’. He gave the drug a ringing endorsement,
stating ‘griseofulvin is a remarkable drug with minimal toxic
effects and that it has come to stay, we have no doubt’.113 Questions
remained about dosage, resistance, re-infection and toxicity, yet in a
call-to-arms, he concluded, ‘As Montgomery must have said, the
break-through has been achieved and our forces can now pour through the
gap to consolidate our gains.’114
Harvey Blank, who worked at the University of Miami School of Medicine,
had also been prompted by Gentles’s article to obtain
griseofulvin from Glaxo.115 He first tried it on ‘a desperate
and unique case’ of T. rubrum infection, with
some success, before a more organised trial on 31 patients with various
forms of ringworm. The results were ‘uniformly
favorable’, though he cautioned that toxicity still needed to be
tested with prolonged use, and that it was too early to say anything
about the likelihood of relapses. Nonetheless, the drug was cleared for
use in the United States in July 1959, less than a year after
Gentles’s paper had been published.116 Blank organised a symposium on
griseofulvin in Miami in October 1959, funded by McNeil Laboratories, a
subsidiary of Johnson and Johnson, at which 37 papers were given by
speakers from 11 countries, including Gentles and Williams. The rapid
spread and trialling of the drug indicates the intense medical interest,
across so many countries, that there was in finding oral antifungal
drugs. Introducing the proceedings in Archives of
Dermatology in May 1960, Blank reflected that the
development of griseofulvin ‘appears to be assuming the
proportions of an historical nature’.117 A key factor in the
enthusiastic response in the United States was to explore the potential
of the drug to treat persistent infection, such as fungal nail infection
– onychomycosis.118
The St John’s Hospital Dermatological Society organised a British
meeting on griseofulvin in May 1960, attended by 189 doctors and
scientists, with 24 papers published in a special issue of the
Society’s Transactions.119 It was already clear that the
drug was being widely used in general practice, as well as in
dermatological clinics, and this despite the fact that it was
expensive.120
The introduction to the volume drew parallels between the ten-year lag
in recognising the therapeutic potential of penicillin, with the 20
years taken from Raistrick’s isolation of griseofulvin to its
first clinical use.121 The meeting heard a report of the first
controlled clinical trial, led by Brian Russell at St John’s
Hospital, which was about to be published in the
Lancet.122 The trial showed griseofulvin was
‘a striking effective remedy’ and that ‘In
retrospect, it is questionable whether a double-blind trial was
necessary.’ There were 64 patients in the study: just one person
of the 31 receiving the drug showed no clinical improvement, whereas 30
out 34 patients given the placebo were ‘unimproved’.
However, the study showed that the drug was no cure-all. There was
considerable variation in the responses of individuals and even the toes
of the same person! In addition, when laboratory rather than clinical
assessments of cures were used, things were less positive still. Thus,
after many weeks and months of treatment, over half of patients
continued to harbour the fungus in the skin between their toes, and 26
of 32 patients had some abnormality in their nails. The redeeming
feature was that no side-effects were reported; hence, the very
long-term treatments that seemed to be necessary were felt to be
safe.
Summing up at the St John’s Symposium, Brian Russell stated that
griseofulvin should be the treatment of choice for all forms of tinea
capitis, except that due to M. canis, and,
disappointingly, tinea pedis due to T. rubrum.123 The drug was
also recommended for other types of ringworm and favus, but was said to
be only moderately effective against animal ringworm species.
Interestingly, its value was ‘doubtful or occasional’
against the species that had been the main cause tinea pedis in earlier
decades: T. interdigitale, T.
mentagophytes and E. floccosum. Russell
emphasised again that griseofulvin was fungistatic and not fungicidal,
hence, ‘clinical clearance is not synonymous with cure’,
while ‘mycological clearance’, if it could be achieved
at all, took much longer. He also pointed to issues with re-infection,
carriers, immunological effects, and its impact on the ecology of the
body, responding to some reports that griseofulvin opened the body to
Candida infections.
Griseofulvin became available as a prescription drug in Britain in April
1959; marketed as ‘Grisovin’ by Glaxo and
‘Fulcin’ by ICI.124 There was no expectation within Glaxo
that griseofulvin would be another penicillin in terms of sales and
profit. Hector Walker, the head of research and development, observed,
‘Dermatologists – at least some of them – seem a
little bit disturbed that a specific treatment is now available that
represents a not unsizeable part of their total practice, and there are
reactionary dermatologists just as there are physicians when new
treatments appear.’125 The expectation was that topical
treatments for ringworm would continue to be preferred, with
griseofulvin used for persistent infection and onychomycosis. Soon, even
these qualified hopes were being moderated. An editorial in
Lancet mocked the recent meetings on the drug.
Massed choirs met at international symposia in Miami last October
and in London under the wing of the St. John’s Hospital
Dermatological Society on May 13 and 14 to add their paeans of
praise. They sang, for doctors, in surprisingly close harmony.
The main theme has been the remarkable success of griseofulvin,
with pitch according to skill and experience. More recent
variations have wandered a little into the more pensive, minor
keys as certain problems and failures have become evident.126
Two years later, there was another sceptical editorial, this time
responding to an epidemiological study of tinea pedis by Mary English
that showed that only a small proportion of lesions of the toe-webs were
fungal in origin and that there very few healthy carriers.127
Griseofulvin has not lived up to expectations, and often does not
eliminate fungus from the feet. In acute cases, topical
fungicides often do more harm than good … For chronic
cases, Whitfield’s ointment is still the most usual
remedy, and some difficult cases are kept symptom free by
wearing sandals.128
However, Glaxo had been working on the drug with its
American licensees and in 1962 developed fine particle form –
GRISOVIN FP – for clinical trials. This was better absorbed
through the gut, giving more even blood levels of the drug, even at half
of the previously recommended dose. Nonetheless, results were still
mixed and worries about toxicity remained.
129Despite the problems, in the 1960s griseofulvin became a standard
treatment for susceptible forms of ringworm and joined nystatin in the
new armoury of antifungal antibiotics.130 Research on this class of
drugs burgeoned in the decade, as mycological researchers in
universities, government laboratories and pharmaceutical companies
joined the search for natural and synthesised compounds with similar
properties.131
In the wake of the thalidomide scandal and the introduction of stricter
safety regulations, much of the further work on griseofulvin was on its
toxicity.132
However, while many side effects were identified, they were all either
relatively minor (headaches, gastrointestinal, photosensitivity, liver
function, allergic reaction), or cleared up after treatment ended.
Griseofulvin was given prophylactically to American troops in Vietnam,
though this did not stop ringworm being a major cause of
disability.133
Only reduced exposure, in shorter combat rotations, affected the overall
incidence of ringworm and relapses were blamed on poor compliance in
prolonged treatment.134
Griseofulvin, as a treatment for most forms of ringworm, united
athlete’s foot with other sites of infection, such that tinea
pedis became distanced from hygiene and fitness. This shift exemplified
a trend in medicine from the late nineteenth century of moving
definitions of infections based on symptoms to specific causes. Ringworm
was not unified by a specific cause, because there were many fungal
pathogens, but rather by a treatment – griseofulvin. The drug
was a major contributor to athlete’s foot and other forms of
ringworm, becoming defined as types of
‘dermatophytosis’, a term which grew in popularity from
the 1960s. It was in fact a quite general, hybrid causal-symptomatic
definition, literally, skin infection with fungi.
Azoles: ‘A major advance in medical mycology’135
The success of griseofulvin, more than the earlier nystatin for
candidiasis, changed the prospects of antifungal therapy and further new
drugs were anticipated.136 In the event, a widely adopted, oral
antifungal alternative to griseofulvin for dermatophytosis did not
emerge for nearly 20 years, until in 1977 the Belgian company Janssen
announced ketoconazole.137 Branded as ‘Nizoral’, it
was one of the group of synthetic compounds called
‘imidazoles’, or more generally
‘azoles’, that the company had been screening since the
late 1960s. The first two widely used drugs from this work were
announced in 1969: clotrimazole from Bayer and miconazole, also from
Bayer, which were targeted at Candida infection and
deep seated systemic mycoses. Ketoconazole was different. It was
promoted as a broad spectrum antifungal that could be used to treat
dermatophytosis as well as candidiasis, histoplasmosis and
cryptococcosis.138
Following the precedent of griseofulvin, Janssen sponsored a meeting to
review progress and spread the word. The first international symposium
on ketoconazole was held in Medellin in Columbia in November 1979,
linked to the Ninth Ibero-Latin American Dermatology Congress.139 The participants
concluded that they were at ‘the threshold of an important new
advance’ and that ketoconazole was the orally administered drug
that was effective for a range of conditions, from acute systemic
mycosis through to the growing problem of onychomycosis, that clinicians
had been looking for.140 The drug had been developed by researchers at
Janssen Laboratories from the modification of miconazole, which they
made less toxic and more suitable for oral administration.141 The new drug was
effective against many of the regionally specific fungal infections
discussed in the next
chapter and with immunocompromised patients. The concluding
address was given by William Dismukes, who worked at the University of
Alabama School of Medicine in Birmingham and was a founding member of
the newly formed, NIH funded, Mycoses Study Group. He hoped that
ketoconazole would be ‘the first “total”
antifungal agent with a broad spectrum of activity’ and that
very promising results in vitro and early clinical
trials now needed to followed by longer term studies.142
The question with ringworm was this, was ketoconazole more effective than
griseofulvin? Two reports by clinicians were presented at Medellin, one
from Oregon in the United States and other Mexico. The group from Oregon
reflected that,
During more than 20 years of clinical experience with
griseofulvin, the subject of failure of therapy has received
scant notice. Only rarely do patients fail to respond to this
drug because of either resistance of the organism or inadequate
tissue levels of griseofulvin. Much more commonly,
dermatophytoses respond to the drug but then either fail to
clear or recur soon after discontinuance of therapy.143
The conclusion of the Oregon study was that ketoconazole
was effective in cases that did not respond to griseofulvin, but whether
it should be the first choice was left open. The second report was
similarly positive. Ketoconazole was approved for clinical use and
became available in 1982. The results of comparative trials with
griseofulvin were published in 1985, which found they were equally
effective for hair, skin and nail infection.
144 On balance, griseofulvin
remained the first choice therapy because of concerns about liver
toxicity of ketoconazole, which was recommended for patients who were
griseofulvin-intolerant.
145 In the 1990s, two new, broad spectrum
remedies that could be used topically and given orally became available
for ringworm: itraconazole, another triazole developed by Janssen and
marketed as Sporanox; and terbinafine developed by Novartis and marketed
as Lamisil. Thus, the options available to doctors for treatment at all
sites, and with all types of infection increased. However, there was
some evidence of the development of drug resistance and tinea pedis
increasingly presented along with the more difficult to treat,
onychomycosis. Many of the azole compounds, when patent protection
lapsed, became available for topical use in over-the-counter creams,
competing with every other post-war antifungal back to nystatin. The
development of azole drugs consolidated the remaking of
athlete’s foot as another type of dermatophytosis.
In this chapter, we have charted the rise and fall of athlete’s
foot as a disease of fitness and hygiene. It is not clear if the
reported rise in incidence in the 1920s was due to the greater
awareness, or presence of new pathogens in Western populations, or new
conditions for ringworm fungi to spread and flourish. At the time, the
majority of doctors maintained the latter and, specifically, that
ringworm of the feet was a ‘penalty of civilisation’. In
all contexts, medical and public concern was linked to new lifestyles,
new clothing, new military conditions or new working environments, the
latter especially so in Britain, where coal miners rather than athletes
put the condition on the map. While medical advice initially stressed
prevention over treatment, proprietary medicine manufacturers turned the
full weight of product development and promotion on the condition,
typically selling their wares as products of medical progress.
Athlete’s foot was also at the forefront of the antibiotic
revolution with fungal infections, through the development of
griseofulvin, coincidentally a compound derived from a species of the
Penicillia. The arrival of griseofulvin and then in
the 1970s of the azoles, accelerated the redesignation of
athlete’s foot and other ringworm infections as dermatophytoses.
They were no longer framed as ‘diseases of modernity’,
but as fungal infections that were conquerable, if not yet fully
conquered, by medical progress.