The Dutch Cholera Epidemic of 1832
as Seen through 19th Century Medical Publications

Antoinette van der Kuyl

Eburon
Utrecht 2021

ISBN 978-94-6301-378-9 (paperback)
ISBN 978-94-6301-388-8 (ebook)

Eburon Academic Publishers, Utrecht, The Netherlands

www.eburon.nl

Cover image: Nicolaas Johannes Roosenboom (1805-1880), Several people near fishing boats on the beach at Scheveningen. (Museum am Herrenberg, Bad Bentheim, Germany)

Cover design: Textcetera, The Hague

© 2021 A. van der Kuyl. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing from the proprietor.

Contents

Chapter 1

Why Write about Cholera?

Chapter 2

Cholera, the Bacterium and the Disease: an Introduction

Chapter 3

The Netherlands from the 18th Century up until the 1832 Cholera Outbreak

Chapter 4

Cholera in the British and Dutch Asian Colonies 1817-1832

Chapter 5

Preparing for the Asiatic Cholera Pandemic: the Professionals

Chapter 6

Preparing for the Asiatic Cholera Pandemic: the Public

Chapter 7

The 1832 Asiatic Cholera Epidemic in the Netherlands

Chapter 8

Cholera Hospitals in the Netherlands

Chapter 9

The Treatment of Asiatic Cholera Patients

Chapter 10

The Essence of the 1832 Asiatic Cholera

Chapter 11

Clinical Symptoms: Description and Diagnosis of Asiatic Cholera

Chapter 12

Asiatic Cholera: A Contagious Disease?

Chapter 13

“He Attempts—but ….in vain..”: What Can we Conclude?

Short Biographies of Dutch Doctors active during the 1832 Cholera Outbreak

Acknowledgments

Bibliography

Notes

Chapter 1

Why Write about Cholera?

The second Asiatic cholera pandemic, which formally lasted from 1829-1849, shocked the West, as it was generally believed that the era of deadly epidemic diseases was long over in Europe. At first, it was assumed that the disease would be limited to Asia, as it had been during the first cholera pandemic (1817-1823). But when the cholera morbus reached Russia in 1830, European countries started to prepare themselves for the inevitable, a disease with, apparently, a high rate of fatalities, known to the English-speaking world as either Asiatic, spasmodic, epidemic, Indian, malignant, or blue cholera. The cholera disaster of the 1830s came as a severe blow to a continent that was trying to emerge from the revolutionary era of the late 18th century that ended in the Napoleonic wars. Governments were fighting poverty, disease, perceived debauchery, and political instability, by attempting to return to the values of the past. In hindsight, it can be said that the cholera debacle, ultimately, became the beginning of a new era, where advances in science, medicine, public health, and human rights laid the foundations for modern western civilisation.

In the Netherlands, the first cholera outbreak appears to have started in the summer of 1832, in the little fishing port of Scheveningen. But questions such as, whether the disease came from ports in Britain, whether it started through illegal fishing practices which avoided state control, or, indeed, who were the first patients, remained in doubt. Whether the first patients were two sailors, Leendert Knoester and Cornelis Harteveld, suffering with diarrhoea in late June 1832, or 60 year-old Arie Mooiman1, who died, unmistakably, of Asiatic cholera in early July 1832, sparked a fierce discussion at the time which those involved did not succeed in getting a definitive answer.

This second cholera pandemic did not, however, go unrecorded. It was preceded, and succeeded, by an explosion of professional, and not so professional, publications. There was an abundance of historical eyewitness reports on the pestilence in all major European languages. These, in turn, led to a large number of modern studies on the subject. According to Christopher Hamlin, a North American historian who specialises in the history of science and medicine, studies on cholera can be divided into three categories: 19th century accounts, cholera histories, and modern cholera science.2 There are numerous examples of contemporary English-language volumes on local outbreaks in European countries. These include François Delaporte’s work on the 1832 cholera outbreak in Paris and Richard Ross’s publication on the cholera epidemic in Prussia in 1831. There were also smaller studies in scientific journals, such as Sean Burrell and Geoffrey Gill on the 1832 cholera in Liverpool, Catherine Kudlick on the 1832 Parisian cholera, Margaret Barnet on the 1832 outbreak in York, and many others.3

A wealth of written reports on the cholera outbreak of 1832 appeared in the Netherlands at the time. These publications contained everything from early preparations, to epidemiological data, and patient case descriptions, as well as the various treatments that were tried. In addition, a debate raged on the contagiousness of the disease, a highly controversial issue at that time. This book is an investigation of the original Dutch medical publications on that Asiatic cholera pandemic, describing the different aspects from a historical perspective with an emphasis on the medical insights and their development. It is, primarily, meant to fill a gap in the scientific literature regarding the first cholera pandemic in the Netherlands by describing, for an international audience, the Dutch responses to the novel infectious threat. According to Hamlin’s scheme, the research for this book should be classified as a cholera history, based on 19th century accounts supplemented with modern science. As Hamlin further points out, cholera studies, from the 1960s onwards, first evolved from describing the cultural and social history of cholera to descriptions of the cholera pandemics, and, after 1985, reverted back to descriptions of local outbreaks similar to that which had been popular in previous times. This study is consistent with the evolutionary timeline by returning to a detailed description of a local outbreak, namely the first Dutch cholera pandemic of 1832.

But why choose cholera as the subject of study? What is its significance? The recurring cholera pandemics during the whole of the 19th century helped shape both medicine and politics, awaken social awareness, and reform public health. These are the topic of further publications, such as Christopher Hamlin’s own comprehensive biography of cholera, Peter Baldwin’s study on how historical contagious diseases influenced public health policies in Britain, France, Germany, and Sweden, Rosenberg’s ‘The cholera years’ on how the cholera pandemics influenced society in the USA, and Kotar & Gessler’s more general cholera history.

In addition, I chose cholera because, as Eddy Houwaart, who has described the effect of cholera epidemics on the emergence of sanitary reforms in the Netherlands has stated that, in the first place: ‘No other disease evoked so many emotions as the cholera’; and secondly, ‘because cholera has been, until the end of the 19th century, the subject of fierce scientific and political controversies over the cause of the disease and its control, respectively.’ Furthermore, over the years, Houwaart wrote in 1991: ‘the number of cholera deaths became a measure of the effectiveness of health policy and of the validity of any scientific theory of communicable diseases.’4 And the former statement still holds true almost three decades later, as in 2017, forty-seven countries were listed as ‘affected by cholera’, with nine countries experiencing large outbreaks.5 So, roughly estimated, two centuries after the first global cholera alarm, the infection remains, according to the Global Task Force on Cholera Control: ‘a highly sensitive, highly specific indicator for extreme poverty and harsh living conditions’, as ‘the presence of cholera indicates that a population does not have access to even basic water or basic sanitation’. The Task Force, which aims to reduce, considerably, cholera’s morbidity and mortality by 2030 stresses the importance of indicating cholera control once again as the ‘pathway to improved equity’, because ‘the continued existence of cholera outbreaks is a violation of human rights and dignity’.6 Very little has changed over time in this respect, despite being aware of cholera’s causes and despite being able to take effective measures.

In addition to the authors of the original publications, I am indebted to earlier studies on the cholera epidemics in the Netherlands, which were published in Dutch, such as Martinus van Andel’s 1938/1939 papers on the cholera in Gorinchem, Pieter ‘t Hart’s description of cholera epidemics in Utrecht, and Har Meijer’s 2005 PhD thesis on the cholera outbreaks in Leiden. Eddy Houwaart wrote an insightful and elaborate study on the reformation of the 19th century public health system in the Netherlands as a consequence of the cholera pandemics, which was a great help when describing the medical situation in the Netherlands at that time.

Epidemiologists, and others, define an epidemic as an infectious disease that affects many persons at the same time and spreads in a region or community where the disease is normally not prevalent. A ‘pandemic’ is an epidemic disease that has travelled the world, affecting people on most, or all, continents. An increase of cases of a disease that is already locally present, a so-called endemic disease, is commonly termed an ‘outbreak’, although the World Health Organization also uses ‘outbreak’ – at least one case with evidence of local transmission – for epidemic diseases. At first glance, however, these terms appear to simply describe various levels of disease spread, namely local (‘outbreak’), regional or national (‘epidemic’), or worldwide (‘pandemic’). Since it seems illogical to write about, for instance, the cholera pandemic in Amsterdam, I will here use the terms outbreak and epidemic to indicate the first cases (outbreak) and subsequent increase in the prevalence of cholera in a town, city, province, or country (epidemic), and use the term pandemic only when referring to the global situation. Indeed, 19th century authors likewise used ‘epidemic’ to describe the cholera dispersal and prevalence at the local level.

Chapter 2

Cholera, the Bacterium and the Disease: an Introduction

The root cause of the severe gastroenteritis known to us as cholera is Vibrio cholerae 1854 Pacini7, a curved, rod-like bacterium that prefers salty water as its habitat. Because of its comma-like shape, the bacterium has sometimes alternatively been referred to as Vibrio comma, after the comma bacillus observed by Robert Koch in 1883. The Vibrio cholerae bacterium possesses, at one end, a single powerful flagellum, a tail-like structure, enabling it to move at a surprising speed. However, environmental Vibrio cholerae are commonly not pathogenic for humans. They do not encode a toxin called cholera toxin, which is essential for inducing the massive outflow of water and electrolytes from the intestinal epithelium, a characteristic of severe cholera.8 The capacity to encode toxins, however, is often carried by a bacteriophage, a virus that infects bacteria and, after doing so, commonly adds its genes to the bacterial genome. So, toxigenic Vibrio cholerae are infected by a toxin encoding virus, in this case the CTX (Cholera ToXin) phage.

During the devastating cholera pandemic of 1854, an Italian anatomist from Florence with a passion for microscopy, Filippo Pacini (1812-1883), took an interest in the disease. He analysed stools, vomit, blood, as well as stomach and intestinal samples from cholera victims, using an advanced microscope manufactured in the workshop of Giovanni Battista Amici of the University of Bologna.9 Pacini was the first to see millions of trapped objects in mucosal filaments (‘miriadi di vibrioni’). When he broke up the filaments, the objects easily spread into the surrounding fluid. These so-called ‘vibrions’ were repeatedly observed by Pacini in the intestinal samples and faeces of those who succumbed to cholera, and so he postulated that they were the likely cause of the disease.10 However, as he did not try to culture the vibrions in a laboratory setting, he could not confirm a causal relationship between these apparent ‘living, parasitic contagions’ and the diarrhoeal disease, a flaw in his research he dutifully acknowledged.11 Filippo Pacini published his research on cholera in Italian in multiple papers during 1854-1880. His memoirs, which include his original observations, are kept at the Central National Library in Florence. However, Pacini’s research received hardly any notice and was soon forgotten, while at approximately the same time a similar concept of a living contagion was being proposed, albeit without laboratory evidence, by the now famous British doctor, John Snow.12 In his second edition of, ‘On the Mode of Transmission of Cholera’, published in 1855, Snow suggested that cholera is transmitted from person to person, not in the form of effluvia, invisible emanations such as vapours arising from patients which can get inhaled by bystanders, but as a ‘morbid matter or poison’ that ‘enters the alimentary canal’ and has the ‘property of reproducing its own kind’. As such it ‘must necessarily have some sort of structure, most likely that of a cell’.13 Snow was also the first to show that cholera is transmitted via water contaminated with sufferers’ excretions.14

Eventually, however, Pacini did receive recognition for his discovery of the cholera bacterium. In 1965, the Judicial Commission of the International Committee on Bacteriological Nomenclature decided that the correct name for the microbe was to be Vibrio cholerae 1854 Pacini and not Vibrio Müller 1773. The first description of Vibrio-like microbes, apparently, had been attributed to the Danish zoologist Otto Friedrich Müller (1730-1784).15

It was not until the fifth cholera pandemic was tormenting the world during 1883-1894 that genuine scientific interest was brought to bear in discovering the cause of cholera. The German scientist, and later Nobel prize winner, Dr Robert Koch (1843-1910), discoverer of numerous pathogenic bacterial species, was sent to Alexandria in 1883 by the State Secretary of the Interior for the German Imperial Health Service, Karl Heinrich von Boetticher.16 In 1884, Koch was working on, and would soon, in 1890, finalise, the famous Koch’s postulates, the four criteria which need to be fulfilled for a causal relationship to be established between a pathogen and a disease.17 Robert Koch also led the Deutschen Cholera-Commission, the German Cholera Commission, which was to investigate the extant outbreak in Egypt.18 Comprising of, besides Koch, medical doctors Georg Gaffky, Bernhard Fischer, and chemist Hermann Treskow, the commission rediscovered the comma bacillus in microscopic preparations of the intestinal mucosa of cholera victims and in the watery stools of advanced cholera patients. They were, most likely, completely unaware of the earlier work of Pacini.19 At the same time, a French team, consisting of two co-workers of the notable Dr Louis Pasteur, namely Drs Emile Roux and Louis Thuillier (who died of cholera during the investigations), medical Professor Dr Isidore Strauß, and veterinary Professor Dr Edmond Nocard, detected, independently, the curved bacillus, again exclusively in cholera patient samples. The French drew a similar conclusion about this bacillus being, in all probability, associated with the disease.20 In 1884, Koch, who had relocated to India as the cholera epidemic in Egypt had subsided, reported that he had been able to grow the microbe in pure culture, one of the requirements he himself had devised. Nonetheless, the comma bacillus could not be reliably linked to disease due to the lack of an animal model for cholera. One of the postulates formulated by Koch, namely, ‘to reproduce the disease in healthy organisms’, could, thus, not be fulfilled. Attempts to infect mice, dogs, monkeys, and chickens with the cholera germ had proved fruitless as no signs of disease were seen. These negative results were a major obstacle to the acceptance of the comma bacillus as the causative agent of cholera. It was not just Koch’s critics who believed this, but also Koch himself who stated that he: ‘wasn’t sure whether [the presence of the bacillus in patients] was cause or consequence.’21 Likewise, French scientists had also been unable to find an animal species suitable as a model for cholera. They had also tried to infect rodents such as mice and guinea pigs, birds, such as chickens, pigeons, turkeys and quails, and also rabbits, pigs and again a monkey.22 Disappointed, they concluded that the microbe observed in abundance in the majority of cases could not be attributed at present to a specific action in the disease process.23 After their return, they pointed out to the Société de Biologie in Paris that they, indeed, could not associate the ‘abundant microbes’ to the disease, but that they had seen some remarkable ‘small bodies’ in patients’ blood samples. Koch, however, dismissed these objects as blood platelets.24

Nevertheless, Koch and his team finally returned to Berlin, and were welcomed as heroes, although the medical profession remained divided on the importance of Koch’s findings for the aetiology of cholera.25 In July 1884, a congress to discuss the cholera problem, the Erste Konferenz zur Erörterung der Cholerafrage, was held in Berlin with Robert Koch as the principal speaker.26 However, a notable absentee was the leading cholera expert at that time, hygienist Dr Max Joseph von Pettenkofer (1818-1901), founder of the Hygienische Institut in Munich in 1879. He was a major opponent of Koch’s bacterial origin theory about cholera. Instead, von Pettenkofer, after having studied the 1854 epidemic in Munich, described cholera as a complex multi-faceted disease, with influences from both time and place in collaboration with an individual disposition, combining contagious and miasmic (‘bad air’) concepts of the disease.27 This Boden (soil) theory stated that cholera germs were changed into a miasma by a specific type of soil. People would then inhale that bad air and become ill. The quality of the soil was important. For the transformation to occur, it needed to be low, wet, and permeable, not high, dry, and stony. The theory, therefore, explained why some regions were not affected by cholera.28 Furthermore, the famous pathologist and public health advocate, Dr Rudolf Virchow (1821-1902), speaking at the First Conference in 1884, more or less agreed with the aetiology of von Pettenkofer’s Boden theory for cholera. He had also fought the germ theory of Louis Pasteur, as Virchow attributed all diseases to the degradation of the state of cells.29 Of course, this is true, but the cause of cellular pathology could be the invasion by an external organism, a possibility Virchow first rejected.30 However, by the end of the conference, Virchow had to admit that he was now much more convinced that the bacillus was the organism which caused the disease in cholera cases.31 Von Pettenkofer’s theories meanwhile had disastrous results. As he had claimed that the groundwater level was equally important in the generation of the miasma, he thus did not advocate water filtration. This led to a devastating epidemic of cholera in Hamburg in 1892 where 1.3% of the population died of the disease.32 By contrast, in the neighbouring city of Altona, where water filtered through sand had been made available, there were only a few cholera deaths registered. The Prussian Government then summoned Koch to Hamburg, where he introduced disinfection and quarantine of patients. In an attempt to save his theory that cholera was not caused by a solitary contagion, 74-year-old von Pettenkofer agreed to swallow a culture of the comma bacillus which would fulfil the third Koch postulate. This postulate implied that a similar disease should be induced in a healthy organism after infection with the microbe. Fortunately for him, he only developed some diarrhoea after drinking the poisonous concoction, although the comma bacterium could be found in his stools. Thus, the action did not meet the third postulate, but nevertheless, von Pettenkofer’s fate was sealed.33 Koch’s ideas had already been incorporated in a new set of laws for epidemic control in the German Empire.

During his cholera studies, Dr Koch speculated that the comma bacillus generated some kind of toxin. In his view, cholera symptoms resembled intoxication.34 In fact the idea that the cause of cholera was a type of poison had also been postulated during the 1831 Berlin epidemic.35 In addition, Dr Horn had stated that during autopsies of cholera deaths: ‘little or no inflammation is seen. The most important and specific nature of this disease, that should be attributed to an organic poison, is that the blood has been changed into a tar-like, greasy substance like that which is found after intoxication with prussic acid (hydrogen cyanide), arsenic, or carbon monoxide, and which is never seen in epidemic-miasmic diseases.’ These speculations turned out to be correct, for in 1959 the toxin produced by Vibrio cholerae was isolated by the Indian scientist Dr Sambhu Nath De working at the Medical College of Calcutta (now Kolkata).36 After culturing Vibrio cholerae bacteria, Dr De discarded the bacterial cells and filtered the remaining liquid. Subsequently, he introduced this liquid containing the presumed toxin into loops artificially created in the small intestine of rabbits. After 24 hours, the inoculated intestinal loops were filled with rice water-like fluid and the villi (small structures shaped like fingers in the small intestine) had, in some places, completely disappeared, both of which are hallmarks of cholera. Dr De, thus, showed that Vibrio cholerae bacteria do indeed produce a toxic substance that is essential for inducing the peculiar choleric changes in the intestinal lining. In addition, the rabbit model, used by Dr De at the same time, delivered the missing evidence for Robert Koch’s third postulate, requiring the induction of the symptoms of the particular disease in a healthy organism.

While the ancient Greeks had already used the word ‘cholera’ to describe a severely unsettled stomach, it was not until the beginning of the 19th century that cholera, caused by toxin-expressing Vibrio cholerae bacteria, became a familiar disease in the West. In 1817, the first epidemic of ‘Asiatic cholera’ was recognised in India after an outbreak in the vicinity of Calcutta. It subsequently spread to that city and then throughout the country. Most likely, cholera had already been present in India before 1817, as Dr John Snow mentioned in his 1855 publication:

The existence of Asiatic Cholera cannot be distinctly traced back further than the year 1769, …… (when it) was prevalent at Madras and that it carried off many thousands of persons in the peninsula of India from that time to 1790’. From 1790 till 1814, ‘we have very little account of the disease’, ‘although, of course, it might exist in many parts of Asia without coming under the notice of Europeans’. In June 1814, the cholera appeared with great severity in the 1st battalion of the 9th Native Infantry regiment, on its march from Jaulnah to Trichinopoly; while another battalion, which accompanied it, did not suffer, although it had been exposed to exactly the same circumstances, with one exception. In 1817, the cholera prevailed with unusual virulence at several places in the Delta of the Ganges.37

From 1820 onwards, cholera became a pandemic after travelling to South-East Asia, Central Asia, the Middle East, Eastern Africa, and along the Mediterranean coast. After a second cholera outbreak in 1829, again in India, the disease journeyed north into Russia (August 1830) and then onward to Hungary (June 1831), Poland (February 1831), Finland (August 1831), and Prussia (August 1831). Cholera reached the British Isles in October 1831 and then migrated with Irish immigrants to Canada (1832), and subsequently to the United States of America. In 1832, it was introduced into other European countries such as the Netherlands, possibly via England. Here the disease was named Cholera Asiatica, or occasionally Cholera Morbus -cholera disease-, or simply Cholera, especially in the newspapers.38 Sometimes, the name Cholera morbus was used to indicate the endemic, sporadic disease that resembled its Asian counterpart, Cholera Epidemica, in symptoms but not in severity.39 The French and English mostly referred to the disease as plain cholera morbus, without capitals.40 From the Netherlands, the disease threatened the western borders of what is now Germany.41 The second cholera pandemic, meanwhile, also extended to the Norwegian city of Drammen and some heavily populated areas around the Drammen fjord, arriving there in autumn 1832.42 However, relatively few people were affected in Norway, resulting in only 80 deaths.

Of course, the opinion had already been voiced that ‘plagues could come from afar’. Describing the diseases prevalent in the Netherlands around 1824, Dr Henricus Thijssen, a former student of Dr Gerardus Vrolik (1775-1859), stated that many pestilences such as plague and leprosy had been imported from the East. He attributed most illnesses to the wet climate, the marshy land, the bad dietary habits, and the moral and physical weakening of the Dutch population. However, he also raised concerns about the importing of much-appreciated ‘invigorating spices’ used for cooking. In his opinion, the ‘early and extensive trade’ had opened a Pandora’s box from which diseases flowed into Europe.43

The two early cholera pandemics were not the last to trouble the world. A total of seven pandemics, ranging from 1817-1823, 1826-1837, 1846-1862, 1864-1875, 1883-1894, 1899-1923, and from 1961 to the present day, the seventh is still ongoing, are recognised today. The closely-related seventh pandemic strains left the Bay of Bengal in three waves since their putative origin in the 1950s. Named El Tor, they belong to a different bacterial biotype than the strains which caused earlier epidemics.44 These early strains are referred to as the classical biotype. Both classical and El Tor biotypes are variants of the O1 serogroup of Vibrio cholerae. This was confirmed by the analysis of old bacterial genomes preserved in an intestinal sample collected by Dr John Neill from a patient who died in the 1849 cholera outbreak in Philadelphia.45

Comparing the 1849 Vibrio cholerae genome with modern isolates, evolutionary biologists Alison Devault and her co-workers from the Anthropology Department of Canada’s McMaster University in Ontario calculated that the common ancestor of all pathogenic cholera strains probably arose only 430 to 440 years ago, when assuming a constant rate of evolution. However, others, who had been analysing much larger data sets showed that the evolutionary trajectory of cholera bacteria has not been that straightforward.46 The Canadians accepted the new evidence and that the real origin of cholera likely lies much further back in time, well before all historically described pandemics.47 Vibrio cholerae comprises a very diverse species with around 200 recognised serotypes. The marine bacterium normally inhabits the brackish water of river deltas, and is especially prevalent in the Ganges delta in India. It can be found there either as free-living bacteria or in association with organisms such as algae, plankton, oysters, crustaceans, and fish. Most serotypes of this bacterium cannot colonise the human gut, but a transition was probably made by members of the O1 serogroup at some time in the past.48 As river deltas are commonly densely populated, it is likely that a substantial number of people eating either fish or shellfish from these waters, or drinking water contaminated with inflowing seawater, ingested these bacteria so often as to enable the species to adapt to the human body.

Although Vibrio strains may differ in virulence and an awareness now exists of the options to avoid or treat the infection, cholera is still a major killer in our time with an estimated 1.4 to 4.3 million cases each year, resulting in 28,000 to 142,000 deaths worldwide.49

Today, cholera is diagnosed by culturing Vibrio cholerae on selective growth media from suspect stool samples. Suspicions of the disease are aroused in particular when individuals present with acute watery diarrhoea. Dark-field microscopy may help in identifying the microbe. In addition, solid surface Rapid Diagnostic Tests, often in the form of dipsticks, which rely on modern biochemical techniques to recognise parts of the bacterium, are available.50 However, diagnosing cholera from symptoms alone, as was required in the past, is difficult. Especially mild cases, which comprise up to 80% of those infected, may resemble other diarrhoeal maladies.51 What is unique to cholera, however, is the abundant rice water-like diarrhoea smelling of fish, a watery stool with flecks of whitish materials originating from mucus and discarded intestinal epithelial cells. Other symptoms such as vomiting and abdominal cramps may be more general. In some cases, extensive and rapid loss of fluids and electrolytes leads to severe dehydration, which can be fatal within a few hours. This swift and remarkable decrease in blood volume due to diarrhoea and vomiting is also quite characteristic of cholera. Symptoms of significantly dehydrated patients include lethargy, sunken eyes, dry mouth, cold clammy skin, decreased skin turgor, and wrinkled hands and feet. Due to the loss of electrolytes such as potassium, calcium, and magnesium, and the decreased flow of the now concentrated blood, muscle weakness and cramping occur. Renal failure can be a complication too due to the reduced urine output. In infected children, low blood glucose levels (hypoglycaemia) can lead to coma. Fever is only infrequently seen in cholera, probably because the microbe does not usually enter the bloodstream.

However, cholera is relatively easy to cure. In the majority of cases oral rehydration salts dissolved in water are usually sufficient. More severe cases require intravenous fluid administration, which necessitates clinical care. Antibiotics are seldom needed and are only given in advanced cases that involve hospitalisation, but adequate rehydration is still essential for the drug treatment to have any effect.52 To prevent cholera, two vaccines with a somewhat limited efficiency are available. Better results are achieved by improving sanitation and providing access to good-quality drinking water.53

Without 21st century knowledge of the cause, diagnosis, and suitable therapy for cholera, which took decades to gain, the Dutch political and medical establishment in 1832 faced huge challenges as the novel disease named cholera threatened Europe. Anxiety and misinterpretations arose from ignorance and unfamiliarity, but at the same time the foundations were laid for a rational approach to understanding why and how pathogens attack humankind.

Chapter 3

The Netherlands from the 18th Century up until the 1832 Cholera Outbreak

In the 17th century, the Dutch Republic was an important nation. Despite hostilities and warfare, which reached their peak in the ‘disaster year’ 1672 54, the country had grown rich in trade. The United East India Company (VOC, Vereenigde Oostindische Compagnie, established in 1602) sailed the world and traded goods in Africa and Asia. The city of Amsterdam was an important trade centre and home to the largest seaport of Europe. Arts and sciences flourished, with renowned citizens such as scientists, Christiaan Huygens (1629-1695) the mathematician, physicist, and astronomer, and Antoni van Leeuwenhoek (1632-1723) founder of the field of microscopy. But also the philosopher and theologian, Baruch Spinoza (1632-1677) and painters Frans Hals (ca. 1583-1666) and Johannes Vermeer (1632-1675).

The 18th century, by contrast, was marked by a decline in trade and collapse of the economic system.55 The Amsterdam seaport lost its prime position in Europe. This was because it became difficult to access as ships had to enter it through a detour around the ‘Southern Sea’, or Zuiderzee in Dutch, a large shallow bay of the North Sea56 which suffered from silting. The political system added to its problems as it was ruled by favouritism and corruption, with Protestants occupying all official and administrative functions. For those with different religious beliefs such as the Roman Catholics and the Mennonites, positions such as burgemeester (‘mayor’) or schout (‘sheriff’) were simply unattainable. The distance between the ruling class, the rich merchant families, and the citizens grew, and this widening gap between the upper and lower classes was characterised by turmoil and riots.

At the end of the century, the fourth Anglo-Dutch war (1780-1784) exacerbated the friction between the Patriots who advocated a republic and the Orangists, who were in favour of the aristocracy. The Patriots were mainly affluent citizens whose political aspirations included increased freedom and equality, and a greater say in governance. They were highly influenced by the ideas of the Enlightenment, concepts such as liberty, reason, and tolerance.57 Patriots also strongly supported the separation of church and state. The Orangists were both aristocrats, who supported the nobility, and the lower echelons of society yearning for royalty. The Orangists were, therefore, in favour of the Stadtholder Willem V, who was a Prince of Orange, hence their name. By 1794 the French invaded the Republic to help the Patriots and, facilitated by the cold winter weather freezing the waters of the Dutch rivers, established the Bataafse Republiek (the ‘Batavian Republic’) on 20 January, 1795. Stadtholder Willem V escaped to England.58 In the same year the revolutionary regime, calling themselves the Provisional Representatives of the People of Holland, passed the Human Rights Act, which stated that all men were born equal and had the same legal rights, in line with the French motto liberté, egalité, fraternité. Jews, however, were only included in the enactment in 1796, after the establishment of an Advisory Committee and a few fierce debates. They had been forgotten initially by the regime.

The early years of the Batavian Republic saw ample interaction with the French. The French invaders had been warmly welcomed by the population as ‘liberators’, and the newly-established French Republic was seen as an excellent example of a modern state. In reality French politics were rather unstable. In 1804, Napoleon Bonaparte crowned himself emperor of the country, thus ending the republican system. Then in 1806, dissatisfied with the weak government of the Batavian Republic, he appointed his brother Louis Napoleon as king, ruling the Kingdom of the Netherlands. However, clashing with his brother, he abdicated in 1810 and for the next three years the Netherlands was once again part of the French empire. After Napoleon Bonaparte was defeated in the Battle of Leipzig in 1813, Prince Willem of Orange, son of the last Stadtholder, returned to the low countries and was installed as sovereign monarch. Then after Napoleon’s defeat at Waterloo, the Congress of Vienna combined the Netherlands (the ‘Northern Netherlands’) and Belgium (the ‘Southern Netherlands’) into the United Kingdom of the Netherlands, with both Amsterdam and Brussels as its capitals and Prince Willem Frederik of Orange-Nassau (1772-1843) as its king, Willem I.59 Although the process of redesigning Europe in 1813-1815 was called the ‘Restoration’, there was little to restore in the Netherlands in terms of an ancient régime, as before the French occupation, the country had been a republic. Admittedly, there were times when a Stadtholder acted as chief magistrate, but the Stadtholder, although a nobleman, did not have the powers of a monarch. Certainly, in the first decades of the 19th century, the country was in a process of redesigning and reinventing itself, although it maintained the reforms introduced by the French, such as the Civil Registry, the compulsory military service, and the decimal system.

Willem I was a king with a vision and a powerful desire to transform the Netherlands into a modern, rational, and united state with a strong centralised government. This was in contrast to the former Republic of the United Netherlands, where the provinces were more or less autonomous. This Republic had been more of a loose grouping of the seven Dutch provinces, although it was dominated by the administrations of the provinces of North and South Holland. Indeed, even as late as the 1830s, much land elsewhere in the north and east of the country remained remote, frequently marshy, uncultivated and thinly populated, with hardly any sufficiently wide rivers and other streams for transport. Travellers were forced to make slow journeys there on wheels over poor roads.

In order to boost the weak economy and decrease unemployment rates, Willem I founded many trade organisations thus he became known by the nickname, the Merchant King. In an effort to stimulate an easier access to the port of Amsterdam, he ordered the digging of new waterways, specifically the Noord-Hollands kanaal, an almost 50 mile (80 km) channel connecting Amsterdam to the North Sea.60 Most transport in the Netherlands, both of goods and passengers, was still then by water. People would travel comfortably, though not very fast, by trekschuit, which were boats pulled by horses or men that operated on regular schedules throughout the country. Ferries, freighters, and other ships were available for sailing the major waterways and crossing the Zuiderzee. Paved roads, however, remained uncommon with only approximately 300 miles of them in 1815.61 In addition, travelling by stagecoach had a reputation of being both uncomfortable and slow, and so waterways still remained the preferred mode of travel by 1830. It meant increased anxiety in 1832 because it was feared that cholera would arrive by ship. Incoming vessels from Asia were quarantined in Dutch ports, while guards were placed on inland waterways, all to little avail.

Willem I also founded new universities adding to the three long-established institutions in Leiden, Utrecht, and Groningen. Those who wished to take a university degree could choose between the three Artes liberales, the liberal arts of theology, law, and medicine. Up until the time of the Batavian Republic, medicine in the Netherlands, just as in most other European countries, was practised by two distinct groups. These were the medical doctors in possession of a university degree, who analysed the diseased mainly from a philosophical point of view, and those who did not, such as the chirurgijns (‘barber surgeons’), craftsmen who were members of guilds and who took a more practical approach. Midwives, chemists, pharmacists, and other drug sellers also belonged to the latter category. Barber surgeons did not only cut hair, shave beards, and extract teeth, but also performed minor, and sometimes major surgery. This was looked down upon by the more educated doctors. Their medical interventions were described as heelkunde (‘surgery’), as opposed to geneeskunde (‘medicine’) practised by those with a university education, who had the exclusive right to prescribe medicinal drugs.

However, during the French rule and the installation of the Batavian Republic between 1795 and 1804, many political and social reforms were carried out, one of which granted the right to free choice of occupation. This liberty heralded the end of professional organisations such as the guilds and the Collegia Medica, organisations of medical doctors.62 A restructuring of the medical system was warranted, and the new administration had ambitious plans.63 The constitution of 1798 contained laws forcing the new-born Republic to take care of its citizens’ health. It was acknowledged that the wealth of a country depended as much on a healthy population as it did on natural resources and other assets.64 For the first time in history, public health concepts were introduced in order to minimise the ‘formation of miasmas’ in the environment, combat unhealthy living conditions, and halt quackery by supervising, strictly, those who were practising medicine, surgery, pharmacology, and obstetrics. To this end, a six volume publication by the German-born medical doctor Johann Peter Frank served as an important guideline. Dr Frank was a pioneer of social medicine and public health, who advocated the establishment of a medical police force, consisting of medically trained police officers, to guard the quality of the soil, air, and water, as well as the quality of medical services, care for the poor, and design and construction of houses, hospitals, prisons, and cemeteries.65 Apart from setting up such a medical police system, the Batavian reformers advocated a complete reorganisation of the national health system through, for instance, the founding of a national health council, centralised supervision of hospitals and “madhouses”, a housing law, a law on the practice of medicine, and a national system of identical recording of births, marriages, and deaths to enable proper statistics to be collected.66 Unfortunately, the time was not yet ripe for such a firm governmental influence on healthcare, and the period available to execute the laws was limited, for in 1804 the political situation changed again. What was achieved, however, was the association of all legal medical professionals into an organisation that acted either on a local level through the local medical supervisory committee (Plaatselijke Commissie van Geneeskundig Toevoorzicht), or a departmental level—covering a larger area—in the Departmental Committee for Medical Research and Supervision (Departementale Commissie van Geneeskundig Onderzoek en Toevoorzicht). This legislation, developed in 1806, was finally laid down in law in 1818.67 The members of these committees had to be ‘skilled men from every profession of medicine’, and their chairmen and members had to swear an oath of allegiance to the above-mentioned law.68 Importantly, articles 41-50 regulated the actions to be taken by the committees in case of an outbreak of ‘epidemic and contagious diseases’, making such outbreaks notifiable and subject to investigation.69 The committees were also responsible for the examination of all medical professionals, regardless of whether or not they had been trained at a university. The British physician, Harry William Carter of the University of Oxford, who went on a trip in 1819 to inspect hospitals in mainland Europe, described the Dutch situation as follows:

‘In 1801 it was decreed by the executive, that there should be a college of officers of health in every department of the province of Holland. That of Amsterdam was formed of eight members, viz. two physicians, two surgeons, two accoucheurs (obstetricians), and two apothecaries, assisted by a professor of chemistry and pharmacy, a professor of osteology and physiology, and four lecturers, on the theory of surgery, on pathology, natural history, &c. The college was charged to examine all surgeons, accoucheurs, apothecaries, and midwives, and to do its utmost to prevent the science of medicine from falling into the hands of the ignorant’.70

However, the division between those who practised academic medicine, and those who practised it without a university education, remained and became even stricter. Medical doctors now included the doctores medicinae, chirurgicae, and obstreticiae, and an exam in the latter two disciplines could only be taken after passing the more general medical degree. Barber-surgeons, now simply called heelmeesters or surgeons, and midwives constituted the non-academic medical professionals. Similarly to the old ways of the guild system, they were generally trained hands-on by those already working in the profession. Pharmacy could also be studied at the universities. A pharmacopoeia to guide pharmacists, the Pharmacopoea Batavia, was published in 1805 and was mandatory in every university.71 Another development, the smallpox vaccination, was a practical medical intervention introduced by the French in 1808 and made compulsory by King Louis Napoleon for infants from a poor background. It was then continued when the United Kingdom of the Netherlands was established after 1815.72 From the 1820s onwards, vaccination certificates were required for children attending primary school. It was Dr Carter again who, on an inspection tour of 1818-1819, remarked that in Amsterdam he had encountered: ‘an institution for vaccination gratis, and since it has been established, the mortality which was formerly occasioned by smallpox, has been greatly diminished. It seems likely that the latter disease will be lost upon the continent, where, when reasoning fails to convince, the strong arm of power compels obedience.’73 However, because legislation was imposed by provincial and local protocols, vaccination was easily evaded until 1872, with the passing of a national Contagious Diseases Act.

These modern developments in the organisation of the healthcare system, however, only concerned the Northern Netherlands. Although in 1815 the country of Belgium was added to the Dutch Kingdom, by 1830 the two states were separated again. During the 1832 cholera outbreak, Belgium was unofficially no longer part of the Netherlands. The earlier decision to unite the northern and southern (e.g. Belgium, but also the province of Limburg) parts of the ‘Netherlands’ had, from the start, struggled to be a success, as these two countries had very different historical, economic, and cultural backgrounds. In 1815, the north and the south differed substantially in population density, economic systems, wealth, and religion. The Northern Netherlands was traditionally heavily dependent on trade and was primarily Protestant, whereas Belgium embraced industrialisation and was less prosperous, more populous, and mainly Roman Catholic. The way for Belgium’s independence was paved by the Belgian rebellion in 1830, which was proclaimed on 4 October, but only formally recognised by the Dutch as late as 1839. Leopold, the younger brother of Duke Ernst I of Saxe-Coburg and Gotha, became the first King of Belgium in June 1831. Immediately, Dutch troops invaded the country, but to no avail.

Perhaps more significantly for public health was the long Dutch history of seafaring during which it had been establishing trading posts, occupying territories—and coming into contact with infectious diseases—since the late 16th century. The Congress of Vienna in 1815 had partly restored the Dutch colonies to the new Kingdom, whether or not those countries appreciated the reinstated authority. Now, on the island of Java in the East Indies, an upheaval that ended in 1830, caused 15,000 deaths among the Dutch military and half a million deaths among the indigenous population.74 Then from April until December 1821, a cholera epidemic had blighted the same island, resulting in 110,000 deaths in just a few months.75 The outbreak, which reached the island of Borneo in December 1821, China in 1822, and the Moluccan islands in April 1823, was the first time the Dutch made acquaintance with this particular disease.

When the second cholera pandemic was approaching Europe, around 1830, the political situation in the Kingdom of the Netherlands was quieter, but the country was still far from prosperous.76 In 1815, at the birth of the new kingdom, King Willem I faced a crushing sovereign debt burden, an empty treasury, a difficult economic climate, as well as poverty and a perceived moral decay among the people. A large part of the population had been experiencing hard times ever since the start of the disastrous Fourth Anglo-Dutch War in 1780.77 It has been estimated that between 1814 and 1854, approximately 25% of the population was dependent on some kind of charity to survive.78 Especially in the cities, poverty rates were high as not only the poor journeyed there in order to seek employment, but also because any food scarcity hit cities harder than rural areas. And by around 1830, the western provinces of the Netherlands were already greatly urbanised, with around 55% of the population living in cities.79 The absolute number of city dwellers, however, had declined since the seventeenth century, likely owing to the economic malaise. Vacant or demolished houses, often turned into garbage dumps, were a common sight in many neighbourhoods.

Dr Carter noted in 1818 that in both the Foundling Hospital in Antwerp in Belgium and the Foundling and Orphan Hospital in Amsterdam, the number of children living there had drastically increased within a few years. He speculated about the reasons why and remarked that: ‘marriage is less frequent than it used to be, while illicit connexion is more common. Or perhaps even many married persons may, through poverty, be compelled to abandon their offspring.’80

Dr Diederik Arntzenius from Amsterdam, who would play a key role in the fight against cholera, sketched the living conditions in the small fishing port of Scheveningen on the North Sea coast near The Hague, where the Asiatic cholera epidemic apparently started in the summer of 1832:

The village is very small, no more than 16,000 square meters, yet it harbours around 4,600 inhabitants divided over 513 houses, which equals to about nine people per house. However, numbers vary, as the bigger houses in the Kerkstraat have no more than six inhabitants, while the very small dwellings in the Weststraat are inhabited by twelve to fourteen people. And the huts of the poor, consisting of a single room with a small loft, are home to up to sixteen persons [............] Beds are shared there by four to six sleepers, if you can call it a bed at all, and the living space in these huts is so limited that it happened to me several times that upon visiting a sick person, I had to ask the people in attendance to leave the hut so as to be able to approach the patient. […...] No, if an epidemic is enabled by tight living conditions, it is no surprise that this one started in Scheveningen’.81