Fungal Disease in Britain and the United States, 1850–2000: Mycoses and Modernity by Aya Homei and Michael Worboys

Whether in the worlds of medical practice and healthcare or in historical scholarship, fungi have not been fashionable. Despite the ubiquity of fungal infections in Western civilization, what we now consider to be an entire biological kingdom has been systematically neglected in histories of medicine and biomedical science (before Robert Whittaker proposed a separate kingdom for fungi in 1969 they were formally classified as plants). In Fungal Disease, Aya Homei and Michael Worboys set out to redress this imbalance and move the focus away from higher-profile disease-causing agents – bacteria, viruses, prions – which have dominated our understanding of the historical relationship between animal hosts and agents of pathological occupation. Underpinning their enterprise is a reanimation of the “seed-and-soil” metaphor employed by Jean and Rene Dubos in their 1952 history of pulmonary tuberculosis (The White Plague: Tuberculosis, Man and Society, London, Victor Gollancz, 1952; cited in the footnotes, curiously absent from the bibliography). In this case, their ‘seeds’ are fungal pathogens in whatever form they took while soil covers, it seems, nearly everything else, including “the human body, social relations and structures, and the medical, material, and technological environment” (4). Through a series of five Anglo-American case studies from the mid-nineteenth century to the turn of the twenty-first, the book interrogates links between fungi themselves, their manifestation as human infections, and their bio-social consequences. Chapters one and two focus on ringworm and so-called athlete’s foot (both caused by an overlapping pantheon of species, including Trichophyton, Epidermophyton, and Microsporum); chapter three examines the thrush-causing genus Candida; chapter four focuses on a series of “endemic mycoses and allergies,” while chapter five takes as its object the recent manifestation of invasive aspergillosis.

The unappealing qualities of the most popularly recognised fungal infections have undoubtedly contributed to the neglect of that whole class of micro-organisms by historians, even as the discipline of the history of medicine has burgeoned in the past 30 years. This is perhaps unsurprising, since the generally most familiar mycoses are ringworm and athlete’s foot, the former the scourge of Victorian classrooms, the latter of the modernist lifestyles of the interwar and immediate post-Second World War years. Field sports, swimming pools, and socks and shoes made of new materials which kept feet moist, inflicted new physical indignities on generations of school children and college students. But mycoses have since then broadened their fields of activity in humans through developments in modern medicine, and it was the enthusiasm for the subject manifested by the Director of the British National Aspergillosis Centre at Manchester, that opened the eyes of the city’s medical historians to the potential of the subject. The result is this oddly engaging little book, which takes the reader on an intriguing journey from the grimy occupants of Victorian classrooms to the most up-to-date medical facilities of the late twentieth century. If the first two chapters disarm the reader by their uncovering of forgotten social history, the last three intrigue and appal in their deft depiction of the havoc wrought by the forces of later twentieth-century social, economic and scientific progress.

Aya Homei and Michael Worboys, Fungal Disease in Britain and the United States, 1850–2000: Mycoses and Modernity (Basingstoke: Palgrave Macmillan, 2013), pp. xiii, 225, $23.00, paperback, ISBN: 9781137392633. - Volume 59 Issue 3

Aya Homei and Michael Worboys. Fungal disease in Britain and the United States 1850–2000: mycoses and modernity. (November 2013) Palgrave Macmillan. Available as a free download from: http://www.palgraveconnect.com/pc/doifinder/10.1057/9781137377029.0001

To examine mortality from ischaemic heart disease and cerebrovascular disease in England and Wales by country of birth of the deceased. Standardised mortality ratios were computed by country of birth groups for ischaemic heart disease and cerebrovascular disease for 1979-83 and 1970-2 by using the five year age-sex specific rates for England and Wales for 1979-83 as standard. England and Wales 1970-2 and 1979-83. In 1979-83 mortality from ischaemic heart disease was highest in men and women born in the Indian subcontinent (standardised mortality ratio 136 and 146 respectively). Young Indian men suffered the greatest excess (313 at ages 20-29). Other groups with raised mortality included Irish, Scottish, and Polish born immigrants. Those born in the Caribbean, the old Commonwealth, west Europe, and the United States had low death rates. In England and Wales mortality from ischaemic heart disease declined by 5% in men and 1% in women between 1970-2 and 1979-83, with greatest percentage declines in immigrants born in the United States, South Africa, the old Commonwealth, the Caribbean, and France. immigrant groups with raised mortality in the earlier period showed little improvement, and mortality from ischaemic heart disease increased among Indians (6% in men and 13% in women). In 1979-83 mortality from cerebrovascular disease was highest in Caribbeans (standardised mortality ratios 176 in men and 210 in women), followed by Africans, Indians, and Irish. Rates were low in west Europeans. Mortality from stroke declined by 28% overall in this period, a rate of decline shared by most groups. Men from the Indian subcontinent showed a decline of only 3%. In the 1980s mortality from ischaemic heart disease and cerebrovascular disease differed significantly between ethnic groups in England and Wales. In general, ethnic groups that experienced lower mortality from ischaemic heart disease in the 1970s showed the greatest improvement over the following decade.

Mortality from Parkinson's disease in England and Wales was re-examined using published government statistics. The 300% increase in the crude mortality rate between 1921 and 1989 was largely attributable to the increase in the elderly population who suffer a higher prevalence of the disease. The dramatic fall in 1940 and rise in 1984 were artefacts caused by changes in certification. Age-specific mortality fell after 1940 in all groups below 70 years and in both sexes, but increased in those over 75 years. Analysis by birth cohort showed a progressive decline in mortality at younger ages with successive cohorts but stable mortality in the elderly. Younger patients were probably misclassified cases of "late-onset" Parkinsonism following encephalitis lethargica who can be differentiated from older cases of idiopathic Parkinson's disease. Mortality decreased in all age groups in the 1970s but then increased in the early 1980s. This is comparable to trends in the United States and Scandinavia and suggests that the beneficial effects of levodopa delay death for several years.

THE appearance of a new plant disease in England is rightly treated as a serious matter, and the unexpected appearance of the rust fungus, Puccinia Antirrhini, on the cultivated snapdragon in several districts in the south of England this summer, will be viewed with alarm by many growers. Although the antirrhinum is a European plant, hitherto no rust fungus has been recorded on it in that Continent, the British Isles included, but curiously enough the disease has become a menace in the United States, where the snapdragon was introduced from Europe a long time ago. The same rust also occurs in Canada and Bermuda, but has not as yet been recorded elsewhere. The source of the outbreaks in England this year are unknown, but the hot weather has probably favoured their development. The disease is easily recognised by the dark brown or snuffcoloured pustules on the leaves and stems and all affected plants (and healthy ones in proximity to them) should be immediately burnt if the pest is to be prevented from obtaining a permanent foothold. In the event of an outbreak of rust having occurred, no antirrhinums should be allowed to carry over the winter, or there will be a danger of a recurrence of the trouble in the following summer. The disease is not thought to be seed-borne.

Fungal Disease in Britain and the United States 1850–2000

In this book, we discuss the changing medical and public profile of fungal infections in the period 1850–2000. We consider four sets of diseases: ringworm and athlete’s foot (dermatophytosis); thrush or candidiasis (infection with Candida albicans); endemic, geographically specific infections in North America (coccidioidomycosis, blastomycosis and histoplasmosis) and mycotoxins; and aspergillosis (infection with Aspergillus fumigatus). We discuss each disease in relation to developing medical knowledge and practices, and to social changes associated with ‘modernity’. Thus, mass schooling provided ideal conditions for the spread of ringworm of the scalp in children, and the rise of college sports and improvement of personal hygiene led to the spread of athlete’s foot. Antibiotics seemed to open the body to more serious Candida infections, as did new methods to treat cancers and the development of transplantation. Regional fungal infections in North America came to the fore due to the economic development of certain regions, where population movement brought in non-immune groups who were vulnerable to endemic mycoses. Fungal toxins or mycotoxins were discovered as by-products of modern food storage and distribution technologies. Lastly, the rapid development and deployment of new medical technologies, such as intensive care and immunosuppression in the last quarter of the twentieth century, increased the incidence of aspergillosis and other systemic mycoses.

We have presented 73 patients (48 adults and 25 children) with microbiologically documented M. bovis infections identified over the 12-year period from 1980 through 1991. Epidemiologic investigation of these patients revealed that the majority (80%) were of Hispanic origin. The non-Hispanic patients either had traveled extensively outside the United States, were born in the United States during its endemic period or in other countries with endemic bovine tuberculosis, or were exposed to a close relative with a positive PPD and known exposure to M. bovis. For Hispanic patients, the presence of reactivation disease in adults and primary disease in children indicate that this mycobacterium remains endemic in Mexican beef and dairy herds, a position supported by United States monitoring of Mexican cattle transferred across the border. Our review of the historical and contemporary efforts to eradicate this animal and human pathogen from the livestock industry in the United States and abroad shows that the implementation of similar methods could be effective in Mexico. The detailed presentations of selected patients and summaries of the clinical manifestations in the remainder of our 73 patients reveal striking similarities to historical accounts and to more contemporary studies of reactivated disease in England. Although M. bovis infections are still expressed predominantly in extrapulmonary sites (cervical and mesenteric nodes, the peritoneum, and the GU tract), as many as 50% of adult patients will present only with pulmonary disease. Underlying immunosuppressive disorders were particularly prominent in adults with extrapulmonary disease. For example, HIV positive patients accounted for 12 of 48 adults and 1 adolescent patient in our series. Overall, M. bovis infections accounted for almost 3% of all tuberculous disease reported in San Diego County during the study period. The intrinsic resistance of M. bovis to PZA could threaten the response of patients with bovine tuberculosis to the short-course chemotherapeutic regimens now recommended by the CDC and the American Thoracic Society. We strongly recommend continued surveillance for this forgotten pathogen because the importation of Mexican cattle, the migration of Hispanic immigrants from border areas to the United States interior, and the persistence of extrapulmonary disease in immunocompetent and HIV-infected United States citizens assure its persistence in this country.

Reviewed by: Spores, Plagues, and History: The Story of Anthrax Michael B. A. Oldstone Chris Holmes . Spores, Plagues, and History: The Story of Anthrax. Dallas: Durban House, 2003. 227 pp. Ill. $15.95 (paperbound, 1-930754-45-0). Spores, Plagues, and History contains a mix of topics: the medical identification and treatment of anthrax, the history of the recent anthrax bioterror attack in the United States, the history of presumed anthrax use as a weapon of terror, and the influence of anthrax through history. These subjects are coupled with a discussion of past biowarfare programs, primarily of Japan, the United States, and Russia. The book is an enjoyable and overall informative read, although some [End Page 381] parts are superficially presented, lacking detail, while others, especially the history sections, provide more questions than answers. The clear strength of the volume is Chris Holmes's discussion of the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID), the Army Dugway testing program, and the account of the anthrax bioterror attack in the United States in 2001. The reader is transported into the events occurring in Florida, post offices, the U.S. Senate, and NBC/CBS news networks. Holmes emphasizes that this investigation is still not complete four years later, and he relates the costs of surveillance and investigating hoaxes. Chapters on biowarfare experiments done by the Japanese in Manchuria and China in the 1930s and 1940s are chilling, as is the author's discussion of the agreements regarding the fate of Japan's biological weapons between Japan and the United States, and Japan and Russia, after World War II—and the effect of these bargains on the Cold War. Unfortunately, there are a number of weaknesses that lessen the value of this book. For one, there are overt errors. For example, the statement "Anthrax was diagnosed by Polymerase Chain Reaction (PCR) testing, a technique which produces large amounts of bacteria from a single cell" (p. 13) is incorrect: PCR amplifies the DNA of a sample, and does not enhance organisms' growth. Second, there are also a number of omissions. For example, although there is detail as to the clinical diagnosis of anthrax and the treatment of the disease, there is minimal information as to why anthrax is virulent: mention is made of "protective antigens," "lethal factor," and "edema factor"—but what they are, and how they work, is given short shrift. This is unfortunate, given the enormous knowledge on the structure and function of these toxins that has accumulated over the last several years. Similarly, there is no information on either how the antibiotics work against anthrax, or how the vaccine works. Other omissions that lessened the value of the book to this reader were the lack of discussion on host susceptibility, or why certain people got sick and others did not, and what separates sickness from death. Later in the book (p. 133), Table 2 lists the advantages of various biological weapons in terms of influencing a population of 500,000 to become predictably ill or to die. Its source is listed as only WHO: there is no bulletin, volume, page, or year listed, in either the text or the references, to allow the interested reader to further explore this issue. Similarly, the outbreak of anthrax in Sverdlovsk, Russia, in the 1970s is presented in a way that the reader is unable to satisfactorily evaluate because the total number of those exposed is not given—just the numbers of those who died, entered hospital, or were ill. Lastly, although it is interesting for discussion, there is little evidence to support the author's claim that anthrax was probably one (the fifth and sixth) of the ten plagues visited on the pharaoh of Egypt through God's messenger, Moses; or that anthrax killed Alexander the Great; or that it caused the Plague of Athens; or that it was involved in the Great Plague of the thirteenth century. However, the discussion of woolsorter's disease in England and of Pasteur's anthrax vaccine study in Pouilly-le-Fort, and the association of anthrax as a bioterror weapon with the Iraqis in the Gulf War and the period leading up to the...

A study on cardiovascular mortality in Japan and in the United States for the years 1950, 1955 and 19, 60 was previously reported. Present work is a descriptive study of vital records on cardiovascular disease in England & Wales for the years 1951, 1955 and 1961. This study is carried out by calculating the age-sex-adjusted death rates for four selected cardiovascular diseases, such as vascular lesions of the central nervous system, chronic rheumatic heart di sease, arteriosclerotic and degenerative heart disease and other diseases of heart to compare with Japan and the United States. Higher death rate for chronic rheumatic heart disease than Japan and the United States is observed in England & Wales. Death rate for other diseases of heart increases during the ten years of study. Age-specific death rates in the younger age group for all forms studied are lower than Japan and the United States. Cardiovascular mortality of England & Wales bears a close parallel to that of the United States in other general respects.

Worldwide incidences of neonatal early- and late-onset invasive group B streptococcal disease (iGBS), estimated at 0.4 and 0.3 cases per 1000 live births, mask considerable heterogeneity even between countries with similar resources.1 Within-country differences in infant iGBS related to ethnicity are also evident. In the United States, the national picture indicates up to twofold higher iGBS rates in Black compared with White infants against a backdrop of declining early-onset but not late-onset disease.2 Black women in the United States are more likely to be identified as colonized with Streptococcus agalactiae during pregnancy and to have iGBS infection.3 In England, maternal iGBS rates were similarly higher in non-White groups, with some evidence of higher GBS colonization rates in Black women from a study in London.4,5 Here we report rates of infant iGBS by ethnicity using national data for England over a 5-year period.Laboratory-confirmed iGBS cases with specimen dates between January 1, 2016, and December 31, 2020, were extracted from the United Kingdom Health Security Agency (UKHSA) national microbiology surveillance system.6 Infant iGBS was defined as isolation of Streptococcus agalactiae from a normally sterile site at 0 to 6 days of life for early-onset iGBS and 7 to 90 days for late-onset disease. Parent-reported infant ethnicity was obtained by linking iGBS cases to National Health Service [NHS] Digital Hospital Episode Statistics hospital admission records. Hospital records from the NHS in England use ethnic categories defined by the United Kingdom Office for National Statistics. Annual live births data from the Office for National Statistics by ethnic group were used to calculate iGBS rates and rate ratios. All data were collected within statutory approvals granted to UKHSA for infectious disease surveillance and control.There were 2512 infant iGBS cases in England during 2016 to 2020, of which 1639 (65.3%) were early-onset and 873 (34.8%) late-onset (0.52 and 0.28 cases per 1000 live births). Linkage was successful for 92.3% (2318) of cases, of which 92.7% (2149) had ethnicity data. Compared with White infants (0.43 per 1000 live births), Black infants had 48% higher (0.63) and Asian infants 40% higher (0.60) rates of early-onset iGBS (Table 1), the latter driven by 87%, 38% and 55% higher rates in infants of Bangladeshi (0.81), Pakistani (0.59), and other Asian (0.67) descent. In contrast, Indian infants had a similar early-onset rate (0.47) to White infants. Black infants had 57% higher rates of late-onset iGBS (0.37) than White infants (0.24), accounted for by 74% higher rates among Black African infants (0.41), who represented 70% of live births among all infants of Black ethnicity.This population-wide data analysis reveals marked differences in iGBS rates among Black and minority ethnic infants in England, excepting infants of Indian heritage. Differences in iGBS rates may reflect differential maternal GBS carriage, including for late-onset iGBS,7 with a hospital study in England reporting higher prevalence of GBS colonization in mothers from Black and some Asian ethnic groups, but lower prevalence in mothers from the Indian subcontinent (mainly from India).4 National data show higher rates of maternal iGBS in Black and minority ethnic groups, albeit without differentiating Indian mothers,5 whereas international data show higher early- and late-onset iGBS rates in Africa than in Europe, North America, and Australia, but lower or similar rates in Asia (again, without differentiating between countries).1Our findings echo differentials by ethnicity in maternal colonization and neonatal iGBS incidence in the United States.2,3 The factors to which these differences might be attributed may not be the same in both countries, given that race and ethnicity are social constructs. Studies in the United Kingdom and United States have shown that differences in pregnancy outcomes by ethnicity cannot simply be explained by socioeconomic inequalities.8–10 In the United Kingdom, intrapartum antibiotic prophylaxis is offered to mothers who present with specific risk factors for infection in the neonate, such as preterm labor or a previous infant with iGBS.11,12A strength of our study is that it uses whole population data because the NHS provides 98% of hospital care in England. However, whereas all NHS laboratories feed data automatically to the UKHSA national microbiology surveillance system, reporting of GBS is not mandatory. Observational data such as these do not allow elucidation of causality, such as whether higher preterm birth rates in minority ethnic groups (for reasons other than GBS carriage or infection) lead to increased iGBS risk in neonates or whether maternal GBS leads to higher preterm birth rates and subsequent neonatal iGBS. Future linkage of NHS maternal and infant data could support a more in-depth investigation of pregnancy duration, mode of delivery, and other factors that might account for some of the observed differences by ethnicity.Understanding the factors underpinning differences in rates of early-onset iGBS within south Asian groups in England may lead to new opportunities for prevention such as prioritized antenatal screening. Strategies to prevent neonatal iGBS must be tailored from high-quality quantitative and qualitative data to reach all women and protect all infants, irrespective of racial or ethnic background.

Despite impressive declines in cardiovascular disease (CVD) over the last half-century, stroke and coronary heart disease (CHD) still constitute the greatest disease burden in the developed world. Moreover, there is accumulating evidence that developing countries will be faced with stroke and CHD epidemics in the relatively near future.1 Much of our understanding of the etiology of CVD has been gained from prospective cohort studies such as the British Regional Heart Study (BRHS), and in this issue of Stroke , Morris and colleagues2 supplement a previous report from this study of geographical patterns of CHD incidence3 by extending the length of follow-up and examining geographical variations in stroke. The BRHS is an ideal study for investigating the geographical inequalities in CVD. Indeed, the study was established with this aim in mind, specifically to test the hypothesis that water quality was a determinant of CVD risk, which proved not to be the case.4 However, despite the fact that the study generated >250 articles, mostly on the causes and consequences of CVD, it was not until 2001 (>20 years after the initiation of the study) that the “definitive paper about the causes of regional variation in coronary heart disease appeared.”5 This most recent contribution is therefore welcome. The authors found that among men the risks of both CHD and stroke were greater in the rest of Britain compared with the south of England and that this …

Epidemiology and public health significance of "Norovirus" in Switzerland