Otto S. Knottnerus

Malaria Around the North Sea: A Survey

© Springer-Verlag 2002


Published in: Gerold Wefer, Wolfgang H. Berger, Karl-Ernst Behre, Eynstein Jansen (ed.), Climatic Development and History of the North Atlantic Realm: Hanse Conference Report. Berlin Heidelberg: Springer-Verlag, 2002, pp. 339-353


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Abstract: Malaria may have been introduced into the North Sea Basin in late Antiquity. It has been endemic at least since the 7th century, but its high-days were the Little Ice Age. After 1750 the disease retreated until it disappeared in the 1950s. The hotbeds of malaria were largely restricted to brackish coastal zones, where the mosquito Anopheles atroparvus could thrive. In these zones death-rates were 25-50 pct higher than in inland areas. This was not caused by tropical malaria, but by the prolonged debilitating effect of tertian and quartan fevers. High summer temperatures as well as storm surges were usually followed by an outbreak of malaria.

The impacts of ecological changes are discussed, as well as the effects of widespread malaria on popular health and local culture. In spite of the high death-rates, popular concern with malaria fevers diminished during the 17th and 18th centuries. This was due to a medical fallacy according to which the chronic effects of malaria were diagnosed as 'land-scurvy'. The eradication of malaria in North-Western Europe had more to do with agricultural changes, hydrological measures and rising standards of living than with medical progress.

The rise and fall of malaria took place largely independent of long-term climatic change. Apparently, mean summer temperatures were only partially affected by general tendencies. Detailed analysis on a ten-year level might show more pronounced climatic effects.



Local environment, epidemiology and climate

Malaria as the 'great debilitator'

Introduction and expansion (500-1500)

High-days (1500-1750)

Repercussions on coastal society

Retreat (1750-1950)






Local environment, epidemiology and climate

During many centuries Northwest Europe's coastal populations have been better off than their inland neighbours. The marshland environment with its diversity of fish, shellfish, fowl and wild plants has been exploited since the 5th millennium BC by the sedentary Ertebølle and Swifterbant peoples. Subsequently, Neolithic, Bronze and Iron Age settlers learned to use the fertile salt marshes and riparian thickets for pasturage and agriculture. Extensive cattle-holding, as well as the cultivation of grains, broad beans, oil-seeds and vegetables provided the coastal population with a nutritious diet which fostered physical strength and body size. Hence, disorders caused by malnutrition or vitamin deficiencies, such as scurvy or rickets, must have been relatively scarce.

Medieval and early modern sources suggest that disease patterns in the coastal marshes were rather different from the inland districts (Dobson 1997; Haeser 1875-82; Hirsch 1883-86, vol 1). Inland, we find many indications of ergotism and chorea, goitre, brucellosis, typhus, tuberculosis, relapsing fevers and respiratory infections, particularly after crop failures. In coastal areas, on the other hand, hunger crises hardly occurred, at least since the mid-16th century, when coastal wealth warranted regular grain supplies from the Baltic. Soaking terrains, damp atmospheres and chilling winds, however, reinforced many diseases. Hence, arthritic complaints (gout), asthma and hay fever were common. During hot summers intestinal infections could spread easily through canals and ditches, through which drinking water reservoirs were contaminated. Low-lying fields harboured fascioliasis, leptospirosis, tetanus and probably anthrax. Intestinal worms were common. Abundant clothing and insufficient hygiene may have reinforced cutaneous infections, including endemic syphilis and lepra. Regular commercial contacts made coastal areas more vulnerable to pandemics, such as influenza, smallpox, sweating disease and bubonic pest, as well as to sexually transmitted diseases. Additionally many cases of alleged scurvy have been reported, but this may be attributed to other causes, as we will see below. Although death rates were dropping on the whole, malnutrition and poverty related diseases, such as endemic syphilis, typhus and cholera, became more common after 1750, due to increasing social tensions.

The most important disease of the coastal marshes, however, must have been malaria. Though nowadays associated with the (sub)tropics, indigenous malaria has been present in Northwest Europe from the Early Middle Ages until the 1950s (Bruce-Chwatt & De Zulueta 1980; Winkle 1997:707-81; Bruce-Chwatts in Wernsdorfer & McGregor 1988:1-59; Schimitschek & Werner 1985:13-70; Jantsch 1948; Maisch 1938). As its occurrence is largely dependent on mean summer temperatures above 15°C, we might expect it to be fairly susceptible to long term climatic change.

The impact of climatic change on coastal epidemiology has not been determined yet. We are inclined to think that the medieval climatic optimum fostered the spread of malaria as well as intestinal infections. Moreover, rising sea levels associated with higher temperatures must have boosted humidity and salt water infiltration, thereby creating a more favourable habitat for both types of diseases. On the other hand, the drop in temperatures during the 14th century and more pronounced in 16th and 17th centuries should have intensified the effects of diseases associated with coldness and humidity, whereas malaria and intestinal infections should have been in retreat.

However, the rise and fall of malaria took place largely independent of global climatic fluctuations. This raises questions about the effectiveness of global models for explaining regional climatic change.

Malaria as the 'great debilitator'

The coastal marshes of Northwest Europe have been invaded by malaria at least since the first millennium AD. Few places with a temperate climate have been more afflicted by the disease than the embanked flood plains, fens and river estuaries surrounding the North Sea basin.

For many centuries, the main vector Anopheles atroparvus has occupied the coastal areas in considerable numbers, as it was unchecked by competing mosquito species which could not stand the regular influx of seawater. Its larvae were able to grow up in stagnant pools and ditches with a salinity of 500 to 2,500 mg/l. In experiments some individuals are known to have endured a mixture containing almost a third seawater. In inland areas, on the other hand, the malaria mosquito was pushed aside by A. messae, which prefers bovine blood, as well as by other species which rarely feed on humans. Only in marshland areas where cattle was scarce, A. messae could become an important vector on its own. A. messae is able to transfer malaria at extremely low temperatures, down to 6°C (though by then it takes at least 44 days for the mosquito to become infectious). This may explain why cases of malaria have been reported from Scotland and Norway, where competing mosquito species were virtually absent. In contrast, A. atroparvus is largely restricted to the 15°C July-isotherm. In the Southern Baltic A. atroparvus and messae are both made responsible for malaria outbreaks, but current literature on the subject is obsolete. Another common species, A. maculipennis s.s. (A. maculipennis typicus), which prefers hilly areas, is only considered to be a risk in Southeast Europe. Finally, during prehistoric and medieval times A. plumbeus, which breeds in hollow trees, may have been a vector too (Jetten & Takken 1994; Jaenson & al. 1986; Bayliss 1985; Swellengrebel and De Buck 1938; Wesenberg-Lund 1920-21).

Malaria is caused by a parasite that incubates in the human liver, from where the victim's blood is being infected. Female mosquitoes feeding on humans convey the disease, as the ingested gametocytes develop into sporozoites, which are injected into the next host again. The patient is struck by intermittent fever attacks, which are regulated by the parasite's reproductive cycle. As soon as the attack starts, the victim is suffering from a shivering cold, which led to the popular expression that he or she has caught a 'cold'. Hence, intermittent fever and 'cold fever' were synonymous. The attack proceeds with high temperatures, lots of sweating and a deep sleep. Before the rise of modern medicine, the disease was known to become latent after several weeks or months, although the attacks often returned during the next spring or autumn, or even after a pause of several years.

In temperate zones 'benign' tertian fevers caused by Plasmodium vivax were most common. But particularly in areas where malaria was rampant also quartan fevers induced by P. malariae occurred. The formers were identified by a two-day reproductive cycle, the latter by a three-day cycle. As a consequence, they were often referred to as two-day or three-day fever. These shifting terminologies are to blame for much confusion regarding the interpretation of historical sources. In addition, quotidian regular fever attacks could be observed, which used to be considered as a separate disease. Not before the second half of the nineteenth century was it recognised that quotidian fevers resulted from multiple infections in the patient's body.

P. vivax spreads far more easily than P. malariae. The latter is a rather ineffective agent, as it produces fewer gametocytes that might infect mosquitoes. Only when vector incidence is high and mean summer temperatures are above 16.5°C it can become epidemic. Even then, P. malariae is a rather slow agent: its spread depends on 35 to 45 days of favourable weather, followed by an incubation period of another 20 to 40 days or more (Jetten & Takken 1994:45-47). The spread of P. vivax takes less time and lower temperatures. Nevertheless, quartan infections could be very persistent as they were able to remain dormant for decades. While tertian fevers mainly attacked children and adolescents, adults are known to have suffered from quartan fevers for many years. As soon as mosquitoes were abundant during a warm summer, the disease might spread again. On the other hand, the conditions favouring an outbreak of quartan fever would allow simultaneous outbreaks of tertian fever as well.

Apparently, tropical or 'malignant tertian malaria' with its oscillating fever attacks rarely occurred in Northwest Europe. It had to be imported from overseas areas, as its agent (P. falciparum) was poorly adapted to the available local mosquito species and was not able to survive in the patient for more than a year. To spread effectively mean temperatures had to be at least 18 or 19°C for several months (Jetten & Takken 1994:45-47; Wernsdorfer & McGregor 1988:711, 927). Nevertheless, subsequent hot summers may have been sufficient to cause incidental outbreaks. Apparently a series of epidemic fevers, which struck the southern North Sea coast in the years 1826 and 1827 was partly caused by tropical malaria (Martini 1938). In the city of Groningen 10 percent of the urban population died, while the surrounding countryside showed a death rate of 5 percent. Diseases were able to spread very rapidly, because most of the canals and ditches had been salted up during a severe storm surge in February 1825. The impacts of the outbreak, which was mixed up with local strains of tertian malaria and typhoid, were to be felt in the entire coastal area from Flanders to Denmark, as well as in the Baltic and in Britain (Ramaker 1998; Bruce-Chwatt & De Zulueta 1980:83; Andersen 1980; Haeser 1875-92, vol 3:639-47). Even then, the tropical component of the outbreak must have been brought in from Southern Europe, since local mosquitoes were not susceptible to African or Asian malaria strains (Jetten & Takken 1994:47). Similar outbreaks have been observed in 1581/82, 1638 and 1859 (Knottnerus 1999:28; Bruce-Chwatt 1976:169; Fraatz 1929).

Compared to tropical malaria, the effects of tertian or quartan fevers seemed to be insignificant. Hardly ever did people perish as the direct consequence of an uncomplicated intermittent fever. Often people felt that the recurrent fever attacks were, though inconvenient, rather harmless. In the case of young children and pregnant women, who were most severely afflicted, the virulent manifestations of the disease were recklessly put down to other causes. In 1889 the medical doctor Wilhelm Olbers Focke from Bremen conducted an inquiry into the former occurrence of malaria in Northern Germany. From his own experience he recalled almost laconically: "Most marshland dwellers used to pass two fever periods during their life: First as children between the age of 2 and 10, later as adolescents from 15 to 24. Each fever period lasted one to two years" (1889:9). Therefore, it seems that local people merely put up with the disease, whereas they blamed the high death rates on other maladies.

On this point, contemporaries must have been wrong: intermittent fevers were only a transitory phase during the course of the malaria infection. Much more dangerous were the chronic consequences, such as headaches, painful limbs, anaemia, hydrops, damage on spleen, liver and kidneys (in case of quartan malaria), and general exhaustion or cachexia. Chronic anaemia is known to cause many other disorders, from miscarriages to osteoporosis and porotic hyperostosis. Moreover, in the long run relatively mild quartan infections could do much damage as tertian ones, because they were rather long-lived.

Malaria acted, as Mary Dobson states, "as a great debilitator. It was a disease which the people of the marshes permanently had to live with until they succumbed to its frequent attacks or died of secondary causes". Dobson was able to prove from demographic records that 16th and 17th century death rate in the Kent, Essex and Sussex marshes more than doubled the inland figures. The least healthy districts were those in which A. atroparvus was prevalent (Dobson 1980:376; 1997:287-367).

It was not only due to unfavourable ecological conditions that former marshland dwellers led an ailing life. Though the mosquito can be blamed for passing malaria from one individual to the next, humans sustain the disease. As soon as substantial parts of the human population are infected, the chance that mosquitoes transmit the disease increases greatly. On the other hand, malaria will gradually disappear as soon as the infection is contained to a few cases. In areas where a particular strain of malaria is endemic, almost everybody is infected. The local population will develop a certain immunity, which, however, can only been acquired through a brutal selection process which kills many children under five years old. Moreover, the immunity acquired is specific only for a distinctive strain. Any one who has endured a tertian infection, can always catch another quartan or tropical infection. Foreign immigrants, seasonal workers and travellers who lack immunity will be heavily affected too. Whenever tropical malaria is endemic, the selection process can be so effective, that immunity is genetically passed down to the next generation.

Our literature suggests that until the 19th century the North Sea coastal marshes were one of the so-called 'stable malaria regions', where the disease was hyperendemic. Nowadays this is a phenomenon restricted to tropical and subtropical regions. Therefore, several medical historians were doubtful if the mild strains of malaria of northern latitudes could ever have caused such strong demographic effects, as has been observed in tropical regions where P. falciparum is present. They may have been mislead, however, either by contemporary records which ignored the risk while immunity was still widespread, or by successive medical reports which failed to appreciate the impact of the disease because it was in decline by then (cf. Swellengrebel and De Buck 1938). Already the 19th century many virulent malaria outbreaks were considered as incidents, which were to be contained by medical progress. Rather, one should consider the possibility that malaria only became epidemic (instead of endemic) after the chain of infection had been broken and the coming generations were without immunity. We had better heed the judgement of malaria-expert Peter Mühlens, who stated in 1936 that the epidemiology of the German coastal marshes originally "had a certain resemblance with the malaria of many tropical and subtropical beaches and flood plains" (cited in Knottnerus 1999:30).

Though they are normally associated with tropical malaria (De Zulueta in Bynum & Fantini 1994:9-10), it may be possible that some genetically based patterns of immunity, well known to the Mediterranean, were extant in Northwest Europe too. Several findings indicate that severe types of anaemia, such as thalassemia and dehydrogenase(G6PD)-deficiency or favism, which are specific for stable malaria regions, might have been present in our area (Knottnerus 1999:30). The latter harms individual male children, when they eat raw or insufficiently heated broad beans (Vicia faba), or when they inhaled the corresponding pollen. As noted before, broad beans have been one of the most important foodstuffs in the coastal marshes since the Bronze Age. Moreover, their toxicity may have offered some protection against malaria to other individuals. A certain ambiguity towards beans, which can be found in popular folklore, may have been caused by these phenomena. Precisely because only specific individuals were affected by the deficiency disease, beans were ascribed with magical functions (Green and Danubio 1997; Burke 1996:2260-66; Katz, in Harris and Ross 1987:133-59). Another indication that selection processes were at work might be that blood group A, which enhances the susceptability to malaria, is less frequent in certain coastal areas (Vonderach 1999; Bayliss 1985:193).

Three types of evidence can establish that it was primarily malaria that caused the raging fevers and enhanced death rates of the coastal marshes. Firstly, the manifest symptoms of the disease, such as intermittent fevers, anaemia and splenomegaly, which has been described as 'ague cake', 'side-stitch' or 'tightening of the heart'. Secondly, the geography of the disease, which shows that enhanced death rates were largely restricted to the brackish coastal zones in which A. atroparvus mosquitoes were indigenous. Thirdly, the seasonal pattern of disease, since it escalated in dry and warm summers when salt water infiltration intensified and when mosquitoes as well as plasmodiae could multiply more rapidly because of the high temperatures at hand. At 16°C P. vivax requires up to 30 days of development within the mosquito, followed by a two weeks incubation period within the human body, to complete its reproduction cycle. With mean temperatures of 23-24°C the first period is reduced to 10-12 days or less. Only with temperatures above 32°C P. vivax does not survive (Jetten & Takken 1994:45-47).

Once malaria had exhausted the patient, other diseases often made an end to his or her life. Epidemics of (para)typhoid, dysentery, viral hepatitis A and leptospirosis raging during hot summers, as well as common cold virus, influenza, pneumonia and typhus during wintertime, completed the destructive work which malaria had started. Measles and smallpox killed many children too. Intestinal diseases were fostered by the unfavourable drinking-water conditions in the coastal marshes, whereas leptospirosis could easily be caught during hard labour in the soggy fields. The effects of the frequent bubonic plague epidemics that have harassed Holland until 1667 and Northern Germany up to 1714 must have been aggravated by malaria outbreaks. Several of these so-called plagues might be explained by malaria altogether. In 1617 the English ambassador Sir Dudley Carleton wrote about the Dutch Republic that "the pest is general ... and in some places hot". Obviously, he did not refer to the plague, but to common diseases such as malaria fevers and diarrhoea (cited in Knottnerus 1999:31).

Indeed, contemporary aetiologies were hardly fit to discriminate between the pestiferous 'hot fevers' observed and the seemingly 'cold fevers' of malaria. Intermittent, remittent, bilious, catarrhic and putrid fevers were easily combined into a general notion of miasmic disease. Moreover, Galenian medical doctrine tended to classify tertian malaria as a bilious fever, thereby reckoning it among the intestinal diseases. Quartan fevers, on the other hand, were categorised as a chronic disease caused by obstipation of the spleen, due to unhealthy food and lack of exercise (Swellengrebel and Honig 1925-28).

Introduction and expansion (500-1500)

The history of malaria is intrinsically connected with the occupational history of the area concerned. Just as clearing the African jungle preceded the spreading of tropical malaria, so the occupation of the coastal marshes in the later Bronze and early Iron Age paved the way for the spreading of temperate malaria strains. In both cases a mosquito species occupied a recently created niche in the human habitat. A. atroparvus was only able to survive in the unfavourable coastal environment because of the hibernation chances it found in byres, pig-sties and human living quarters. Artificial ponds, natural pools and stagnant river branches provided the necessary sites for breeding.

Probably malaria was already present in Europe during the Neolithic, but it was hardly ever effectively transmitted. Not before the 5th century BC did the existing malaria strains become hyperendemic in the most heavily populated parts of the central Mediterranean. The recent advance of the mosquito species A. labranchiae and A. sacharovi may have intensified this. As a consequence, men, mosquitoes and plasmodia were able to familiarise at large, so that little by little A. atroparvus became a significant vector as well. In addition, tropical malaria entered the scene, taking a high death toll on the indigenous population (Burke 1996; Bruce-Chwatt & De Zulueta 1980).

To what extent A. atroparvus populations were susceptible to different strains of malaria remains unknown. It seems, however, that the advance of tropical malaria into the western Mediterranean was delayed for some time. Maybe through Spain and southwestern France, where competing mosquito species must have been absent, the P. vivax infection spread northward. Here it gradually accommodated to colder climatic conditions by improving its ability to hibernate in the human liver as a hypnozoite (Wernsdorfer & McGregor 1988:947).

It is an open question when malaria became endemic in the North Sea basin. It is very plausible, however, that the decimation of the coastal population during the 4th and 5th centuries was not only caused by rising sea-levels, large-scale migration and political turmoil, but also by epidemiological factors (Knottnerus 1999:32). As a rule, populations that are newly exposed to malaria suffer great losses. Although skeletal remains showing porotic hyperostosis or osteoporosis, resulting from childhood anaemia’s, have not been reported yet, future archaeological findings might provide us with a more precise date for the genesis of malaria endemicity (Burke 1996:2262; Stuart-Macadam 1992).

Once a new strain of malaria had arrived, it could also accommodate to inland mosquito species. At the same time, other strains may have spread northward through the river valleys, swamps and flood plains of Central Europe, where summer temperatures were high enough to sustain the disease. Though the mosquito might be a poor vector, quartan infections could hold out for many years. In either case A. messae, which had been a minor vector in the Mediterranean for long, must be held responsible for its further expansion.

By the 8th century, Britain's coastal plains had a bad reputation altogether. Literary sources such the Vitae of Saint Cuthbert and Saint Guthlac claim that the "fens and marshes were haunted by the evil seed of Cain" (Newton 1993:143). The distinguished medievalist Hilda Ellis-Davidson actually assumes that "the monster Grendel in the poem Beowulf symbolised the dangerous climate of the fens, bringing plague to the king's hall" (1964:18). During the last years of Cuthbert's life (he died 687) the Lincolnshire marshes were depopulated by an unidentified epidemic. The abbess Hilda of Whitby died in 680 after six years of fever. An 8th-century translator identified her disease as 'lenctenadl' (spring ailment); therefore we might be sure that spring relapses from tertian fever were known by then. Hence, the year 673 must be seen as a minimum date for the arrival of P. vivax in the North Sea basin (MacArthur 1951).

Anglo-Saxon medical prescription books largely confirm that malaria was a main cause of disease. Bald's Leachbook (9th century) is very specific about the symptoms of malaria. Here the distinction is made between tertian fever, quartan fever and the frequent relapses in spring mentioned before. But even more attention is being paid to the chronic consequences of malaria, such as splenomegaly, side-stitches and severe anaemia, described as 'the halfdead disease'. Other medical books report about the cold fevers ('þa colan feforas') and the shiverings ('þe riþaþ'), which accompanied the attack. Apparently, possession by evil spirits or 'dweorgs' (little people) was to be blamed for it (Cameron 1993). Subsequent Anglo-Norman sources describe the 'febris frigidas' or 'freide fevre'. The modern word 'ague' came into use in the 13th century. According to the malariologist Bruce-Chwatt, it has been derived from the French 'fièvre aigue' or Latin 'febris acuta', referring originally "to any acute febrile disease, and especially to a fever accompanied by a shaking or shivering fit" (1976:168).

On the Continent sources begin to flow rather late. Nevertheless, the 9th-century Old High German expression 'ritto, rito' (Middle Dutch 'ridde, rijde', Old Norse 'riða, riðusótt') closely parallels the Anglo-Saxon terminology, whereas it seems to indicate that the shivering patient is being ridden by a demon. Interestingly enough, a late medieval saint's legend from Scandinavia identifies tertian fevers as possession by a demonic snake ('vindormr'). Individual cases of possible malaria have been noted more than once. The founder of the archdiocese of Bremen, Saint Willehad, died of a severe fever in 789, while he was visiting the coastal marshes. According to the chronicler Saxo Grammaticus king Sven Estridsøn of Denmark passed away in Southern Jutland, probably autumn 1076, when his heart felt tightened during a pestiferous fever attack. An early report about a possible malaria epidemic dates from 988, when diseases were rampant in the Southern Netherlands during a warm summer after widespread inundations. The Weser and Elbe riverbanks are said to have been hit by a severe 'pestilence' after a storm surge in 1020 (Meineke & Schier 1995; Knottnerus 1999:32; Buisman 1995-98).

Though the coastal inhabitants had created a niche in the wetlands protecting them against human predators, their defence against natural enemies was largely insufficient. From the 11th century onward they even became more vulnerable, as they began to throw up embankments against the sea, thereby creating a brackish habitat that generated additional risks. Storm surges were to become more destructive, whereas the fields were imbued with slugs, mice, leather-jackets (Tipula paludosa), fluke-eggs, mosses and horsetail (Equisetum arvense). Furthermore the canals and ditches, being isolated from the sea, supplied new breeding-places to all kinds of insects, including malaria mosquitoes.

The inhabitants of the coastal marshes must have acquired a certain degree of immunity against malaria by then. Apparently, the Frisian warriors who - according to the sagas - captured Rome at about 1085 were able to endure the raging fevers that had wrecked earlier attempts. On the other hand, the crusaders and pilgrims coming back from Rome and Jerusalem must have brought many novel infections with them (Knottnerus 1999:32; Maisch 1938:53-54; Martens & Hall 2000). A genuine epidemic of quartan fever is reported by the chronicle of the abbey of Gembloux, south of Brussels, during the hot summer of 1136 or 1137. The city of Cologne was struck by a quartan epidemic in 1192 (Lersch 1896:84, 91; Keil 1993). A Danish cleric, who suffered from a quartan fever, is said to have caught it while studying in Paris about 1175. Indeed, it seems that P. malariae had become endemic along the moist and relatively warm riverbanks of Rhine, Danube and Rhone, from where it spread northward. A hundred years later the presence of quartan fevers or 'shivering disease' is attested as far north as Linköping in Sweden. Only Iceland kept free from malaria (Meineke & Schier 1995; Møller-Christensen 1959).

Reports about malaria abound in the Later Middle Ages. In 15th-century East Anglia the coastal parishes suffered high losses during warm summers. The famous chronicle of the abbey of Wittewierum (near Groningen) recounts an outbreak of various fevers during the warm summer of 1237, when the abbey's founder died of a quartan fever. The infirmaries had been overcrowded and all over Friesland hardly enough people had been left to nurse the sufferers (Gottfried 1978:129-36; Fraatz 1929:37-39). At the grave of the Frisian abbot Siardus of Mariengaarde (d. 1230) many sufferers of tertian fever were said to have been healed. According to a recent survey article, malaria may have had stronger restrictive effects on medieval population growth than the plague (Keil 1993).

Contemporary medical compendiums, such as Saint Hildegard of Bingen's Causae et curae, written in the 1150s, were quite familiar with tertian, quartan and quotidian fevers. The Danish physician Henrik Harpestræng (d. 1244?) was acquainted with 25 remedies against different fevers, most of them tertian, quartan or quotidian ones, characterised as shiverings ('rithæ') or chilling sickness ('kaldæ sot') (Meineke & Schier 1995; Møller-Christensen 1959). In Bremen the patrician Arnoldus Doneldey differentiated in 1382 between cold fevers and burning fevers, the latter being identified as the newly arrived bubonic plague. Apparently, the doctors from whom he copied his recipes were very experienced in treating malaria. They knew duplicated malaria infections and spring relapses, which were considered not nearly so lethal as autumnal infections, and they described the rare blackwater fever (haemoglobinuria): a lethal complication among patients suffering from G6PD deficiency or severe tropical malaria, expressing itself in bloody urine (cited in Knottnerus 1999:32).

Although it is possible that these recipes merely reflected the lessons of Salernian medicine, it is more likely that its authors had learned about malaria from their own experience (Cameron 1993:54-55). Indeed, malaria has been so common in the 14th century that a Hamburg Bible translator automatically imagined Christ not to expel an ordinary fever, but a cold fever ('dat kalde') from a patient (cited in Knottnerus 1999:33, after Luke 4:38).


High-days (1500-1750)

Still, the high-days of malaria were in the Early Modern Age (Reiter 2000; Wernsdorfer & McGregor 1988:943). Although the general drop in temperatures should have reduced disease frequencies, increasing human efforts to exploit the coastal niche had an adverse effect on living conditions. Intensified traffic increased the risks of contagion, whereas hydraulic innovations fostered waterways and ditches to salt up. Newly built floodgates, harbours and canals, meant to facilitate shipping-transport, enabled seawater to seep in more easily. Moreover, during summertime floodgates were often deliberately opened as to prevent river-crafts from running aground, while allowing rushing in seawater to drive up fresh waters into the scorched pastures.

Since the 14th century circumstances were deteriorating all over because of the salting up of bays, creeks and rivers, such as the Zuyder Sea, the Dollard and Jade estuaries, which affected the water qualities on the land side of the dikes. Although the existing dikes were strengthened and large tracts of salt-marsh were reclaimed from the sea, new embankments provided the mosquitoes with an even more favourable habitat. In addition, the artificial reclamation of vast lakes fostered the percolation of brackish ground-water from underlying salt-water domes. Frequent storm surges and wartime inundations had a detrimental effect on water qualities too.

Hence, mosquito populations must have been increasing, thereby boosting the risk of malaria. Acid waters leaking from the inland bogs might have curtailed the mosquito scourge, but for agricultural reasons these waters were kept at bay and - whenever possible - conveyed to the sea as soon as possible. Additionally, the relocation of settlements from the artificial mounds to the embanked polderlands must have intensified health risks too. Only the silting up of inland river-beds due to excessive grazing and forest clearance had an opposite effect, since the salt water border was driven back seaward. Already at the closure of the 18th century death rates on the Lower Weser river banks barely outstripped the inland figures (Hinrichs & al. 1988:21-22).

This is not the appropriate place for exhibiting a catalogue of malaria reports. Nevertheless, we may conclude that they were extant in almost every coastal district (De Baets 1998; Priester 1998:37, 60-66; Dobson in Bynum & Fantini 1994:35-60; Norden 1984:85-95; Brouwer 1983; Schuberg 1927; Lemaire 1922; Wesenberg-Lund 1920-21; Schouten 1920; Trautman 1913; Nuttall & al. 1901; Focke 1889; Haeser 1875-82; Hirsch 1883-86). Everywhere we find abundant remarks in parish registers, regional monographs and medical reports, which might prove our point. Topical expressions, such as Fenland ague, Polder fever, Northern 'stier', Zealand fever, Dutch pip, Holstein marsh sickness or Eiderstedt stubble fever have terrified medical practitioners for centuries. Strangers were scared off, whereas newcomers had to fear for their lives.

Moreover, a 3-500 km zone in which malaria had a more incidental character surrounded the coastal districts. Here hyperendemicity was largely restricted to isolated pockets of marshland in which A. messae were abundant. Lack of cattle as an alternative host, as well as poverty and malnutrition were the main causes for maintaining secondary hotbeds of malaria. Particularly in the Netherlands, Northern Germany, Denmark and Scotland many inhabitants of scattered swamps, bogs and river valleys were infected. Peddlers and seasonal workers returning from the coastal districts as well as travellers from Southern Europe may have been responsible for spreading the disease. But eventually many secondary centres held out on their own. Malaria has also been endemic in many other wetland areas, from the Upper Rhine, Bavaria and Thuringia up to the Baltic. Heavily inflicted were the salt mining towns, where A. atroparvus found appropriate breeding sites.

Notwithstanding, the coastal districts stood at the heart of every major malaria epidemic. According to an 18th-century physician from Friesland "the autumnal bilious fevers are our main national disease". Although few patients died, many fell seriously ill. One of his colleagues stated that the disease was so well-known that it needed no further description. A medical survey concluded in 1824 that probably no country in Europe, except for Italy, had been so badly afflicted by malicious intermittent fevers as Holland (Seventer 1969:9). Similar reports can be cited from almost every corner of the North Sea, particularly from low-lying islands and peninsulas that were surrounded by the sea. Regional monographs abounded in the 19th century until there was hardly a region, which did not have its own malaria literature. The reports were then collected and incorporated into medical surveys, whereupon they have been largely forgotten.

Repercussions on coastal society

The significance of malaria for the social history of the North Sea coastal marshes can be summarized into four statements:

Firstly, the geography of malaria is delineated by enhanced mortality rates. Hence, its spatial distribution can be largely determined with the help of mortality statistics. Unfortunately, only scattered figures have been published. As a reasoned guess, we would expect coastal death rates in the 16th, 17th and 18th centuries to have amounted to at least 30 to 50 per 1,000 as against 20 to 30 per 1,000 for inland districts (table 1). Hence, every fourth or fifth death was indirectly caused by malaria or related diseases. To demarcate the importance of malaria as against other typical wetland diseases, subsequent data on the extent of salination are required. Incidentally, however, endemic malaria may have been conveyed to fresh water areas as well. Especially heathland villages bordering on the saltmarsh could become infected by mosquitoes bred in neighbouring low-lying ponds.

For the second half of the 18th century enhanced mortality rates have been reported in a wide range of coastal districts from Furnes to Ribe and beyond (Knottnerus 1999:35). The excessive mortality was sufficient for restricting natural population growth, therefore causing several marsh regions to become dependent on immigration. Moreover, the step-by-step concentration of landholding into the hands of large farmers which can be observed in many marsh districts, was furthered by the enhanced mortality rates.

Secondly, the chronology of malaria may coincide with storm surges, high summer temperatures and summer drought. Therefore, data on epidemics and death rates must be connected with climatic observations. We may assume that most epidemic outbreaks after storm surges or during prolonged periods of drought and heath can be largely explained by malaria. Preliminary findings suggest that this is indeed the case. Moreover, there are many indications that epidemics in different coastal districts took a synchronous course. Hence, it seems justifiable to interpolate our scattered data into prolonged series for the entire southern North Sea coast, and maybe for the British marshlands as well (Dobson 1987; Fraatz 1929; Hanssen 1925; Lersch 1896; Creighton 1891-94).

Thirdly, the social topography of malaria implies that its impact on the poor was more pronounced than on the well-to-do. Malaria is known to be transmitted more effectively when people are insufficiently dressed, sheltered and nourished. Not only were members of poor families more frequently exposed to mosquito bites, also their general health condition made them more susceptible to the infection. Once fallen ill, their chances of recovery were lower because they could not afford medical treatment. Moreover, they were not able to compensate for the loss of income and working-day's. There have even been sporadic reports of poor people who tried to avoid the risk by tarring their legs before working into the submersed fields. But such preventive measures seem to have been quite exceptional, at least in the 18th and 19th centuries when most adult males owned boots and shoes.

Extremely susceptible to malaria were the tens of thousands of seasonal workers from inland districts who did much of the mowing, digging and reaping in the coastal marshes. Though they did not have the immunity of the indigenous population, they often slept in outdoor shelters or tents, drinking infected ditch-water and eating rancid bacon. Eighteenth-century estimations claim that a quarter to a third of them had caught an intermittent fever before returning to their villages. In several Westphalian districts special sick-transports have been organized to take them home (Knottnerus 1999:36).

Fourthly, the cultural reflection upon malaria risks led to various preventive measures and curative remedies. But these did not always reduce actual exposure. In Britain as well as on the Continent most people were convinced that living near the sea-shore was hazardous. In accordance with current medical doctrine the medieval fear of the sea was transposed into a novel concern for miasmatic emanations. Early-modern man did not know about the role played by mosquitoes in transmitting malaria. Instead he believed that his disorders were caused by the hazes ascending from salt-marshes, swamps and ditches. Particularly in Germany and Denmark people thought they were better off in their heated parlors. It is questionable whether such a preventive strategy was effective at all. Mosquitoes may actually have preferred the stuffy living quarters, whereas they were scared off by the open fire places which were common in Holland and Britain (Knottnerus 1997:163-64).

Some traditional remedies may have been quite effective. Tobacco smoke for instance must have acted as a powerful mosquito repellent. In the coastal districts smoking a pipe was quite fashionable in the 17th and 18th century, not only among men, rich as well as poor, but also among married women (Knottnerus 1997:155). Several traditional drugs had antiseptic properties, such as pennyroyal (Mentha pulegium), already mentioned in Anglo-Saxon sources. Others might serve as a mosquito repellant (yarrow, achillea millefolium), they may have prevented renal failure (bogbean or 'fever herb', Menyanthes trifoliata) or they actually helped against diarrhea (creeping cinquefoil, Potentilla reptans). The painter Albrecht Dürer, who catched a malaria fever in Zealand in the 1520s, took swallowwort (Chelidoneum majus) as a medicine. Distinct members of the Artemisia family, particularly wormwood (A. absinthum) and sea wormwood (A. maritima), have been used against malaria too. Possibly, they contain small doses of artemissinin as their Chinese counterpart A. annua does. Sea wormwood is proven to be effective against liver damage (Dobson 1998; Tunón 1995; Janbaz & Gilani 1995; Cameron 1993:117-29; Winkle 1997:755, 1292).

Nonetheless, many remedies reverted to magic. Magical spells were common, as were the holy trees on which a fever could be tied. Some of these trees held out until the 20th century. Specific kill or cure remedies and bitter-tasting medicines were preferred because of their supposed capacities to expel evil. Expressions such as Flemish 'Noordsche stier' (Northern tribute), Frisian 'tjinst' (bond, bondage) and North Frisian 'thwung' (coercion) suggest that malaria fevers have been associated with possession by evil spirits until fairly recently. Obviously, people identified the haze as the agent of disease. Originally these expressions may have meant that the patient was paying tribute to the evil powers from the Northern seas (Knottnerus 1997:148, 155, 170; De Baets 1998).

Most of the remedies concerned were favoured because of their supposed ability to drive out the chills associated with malaria fevers. Liquor and wine were consumed in large quantities. Tropical products, such as tobacco, coffee and tea, were said to prevent illness. In the 19th-century Fenlands opium was used to comfort ailing children (Dobson 1980:370). Another drug which was said to avert fever was the sweet-flag (Acorus calamus), often used in liquor or a kind of tea. After being imported from Turkey in the sixteenth century, its proliferation in the coastal marshes may have been encouraged by medical beliefs. Purgatives were popular as well: in Holland the well-known Haarlemmer Oil, a forceful mixture of linseed-oil and turpentine, was considered as one of the most effective remedies against intermittent fevers and diarrhea (Knottnerus 1999:37).

Medical progress did not always lead to appropriate answers. Though Peruvian bark or Cinchona has been widely used in coastal medicine since the end of the 17th century, the medical profession had many reservations. The drug was introduced by Spanish Jesuits in the 1639 and became known in Britain, Belgium and Holland in the 1650s. Soon afterwards medical practitioners began to prescribe it against all kinds of intermittent fevers (Dobson 1998; Wernsdorfer & McGregor 1988:16-19). In 18th-century Holland Cinchona was processed into several popular theriaca and sold in local shops as a panacea. Medical science, however, especially in Germany, turned away from Cinchona, as the usual doses were often too small to be effective, whereas many other diseases falsely diagnosed as malaria did not respond at all. Moreover, its bitter taste and its supposedly hot properties did not fit into the Galenian system. As an official drug, it only made a comeback after the 1820s, as the cheaper and more concentrated derivative quinine became available in drugstores and grocery shops. Since the 1860s many households kept their own stocks of quinine (Swellengrebel and De Buck 1938:11, 26-27; Schouten 1920:12; Roth 1906:60, 80; Focke 1889:12-13, 19).

Indeed, it is striking to see how medical science slowly went astray, as it was searching for more adequate solutions. Since mid-17th century many physicians began to downplay the risk of intermittent fevers. Instead, they became more concerned with a novel disease called 'land scurvy'. In spite of its name, land scurvy had hardly anything to do with the vitamin deficiencies among urban populations, which had been observed in the 16th century. Rather its symptoms, such as anaemia, hydrops and splenomegaly, largely coincided with the protracted effects of malaria. Case histories often began with a complicated quartan fever which triggered many other complaints not necessarily connected with malaria. As R. Elwyn Hughes rightly observed, "scurvy or 'the scorbute' suddenly became a convenient nosological safety net for the not inconsiderable diagnostic failures of the period" (Hughes 1990:57; Knottnerus 1997:157-59).

Thus, land scurvy came to be seen as the archetypical scourge of all coastal districts. It was said to be endemic in Britain, Holland and Northern Germany as well as in Scandinavia. According to Thomas Bartholinus' De medicina Danorum domestica (1666), scurvy and fever were the only two diseases which mattered in Denmark. Scurvy was above all a moral condition: its sufferers were not treated as victims but as individuals who had exposed themselves to the disease. The inhabitants of the prosperous coastal districts were said to be inflicted because of their immodest life-style. Moreover, nobody was entirely free from the affliction. In fact, the theory of scurvy was closely bound up with religious revival movements which gained ground in Britain and Holland. German physicians, on the other hand, argued that scurvy was an epidemic disease which affected any foreigner visiting the coastal districts. They suspected the Dutch had introduced it from abroad (Knottnerus 1997:164). Both views reflected the actual situation, in which the coastal population was accustomed to malaria, whereas newcomers fell ill.

Retreat (1750-1950)

The retreat of malaria has not yet been sufficiently explained. During the 18th century mortality rates in some regions were falling rapidly, whereas in others they remained largely the same. Particularly in Southeast England and the western districts bordering the Wadden Sea (Friesland, Groningen and East Friesland) population growth started early. But in Holland, Zealand and many German districts figures remained stagnant until the 19th century, whereas mortality rates were high up to the 1850s (Dobson 1998:81-159; Knottnerus 1997:38; Norden 1984). Moreover, in the German Lower Rhineland as well as in the Baltic unprecedented outbreaks of malaria took place during the first half of 19th century (Jaenson & al. 1986; Anderson 1980; Kortenhaus 1928; Wesenberg-Lund 1920-21:172). In general, tertian fevers got a more epidemic character instead of remaining endemic, whereas quartan fevers tended to become rare. As malaria outbreaks became more uncommon, seasonal peaks shifted from late summer to early spring (Swellengrebel and De Buck 1938; Seventer 1969).

There are at least five possible explanations for the retreat of malaria (Seventer 1969; Schuberg 1927:361-72; Focke 1889:17-25).

1. Medical progress: the massive use of Cinchona in Britain and the Netherlands may have mitigated disease transmission allready in the 18th century. The subsequent introduction of quinine in the 1820s then made a further reduction possible.

2. Agricultural innovations: The introduction of the potato and the subsequent expansion of pig-breeding by cotters and agricultural labourers during the second half of the 18th century had a health-improving effect. Potato-growing not only improved general health by providing a nutritious diet to humans and their livestock. The supplement of vitamin C may also have been important to reduce the effects of anaemia (Green and Danubio 1997:223-24; Cameron 1993:17-18, 182). Moreover, pig-breeding has diminished the risk of mosquito bites, as A. atroparvus prefers to feed on pigs (Jetten & Takken 1994:49-50). The 19th-century shift from traditional hairy swines to naked Chinese pigs must have reduced mosquito risks even more. Finally, the 20th-century introduction of modern byres and pig-sties led to a spectacular fall in mosquito populations.

3. Improved water management: Reduced water-levels and the replacement of field-drains by draining-pipes have reduced the number of breeding-places for mosquitoes (Schouten 1920:49). The introduction of Americal river-weed (Elodea canadensis) since the 1870s, the eutrofication of surface water and the subsequent spread of duck-weed (Lemna gibba) may have had a supplementary effect (Seventer 1969:40; Focke 1889:23-24). Heightened dikes, larger canals and more effective sluices have reduced salt-water leakage and inundation risks, thereby destroying the natural habitat of A. atroparvus. The introduction of DTT has reduced the remaining populations even more.

4. Rising standards of living: The living conditions for cotters and farmhands have gradually improved during the 19th and 20th centuries: better and dryer housing, adequate clothing and sufficient fuel. These may have reduced the effectiveness of existing mosquito vectors. Traditional farm-buildings in which human living quarters, byres and pig-sties were found together under the same roof, have largely disappeared.

5. Parasitical evolution: Possible genetic variations in the virility of existing malaria-strains might have reduced malaria risks. Nowadays, even in heavily afflicted Indian communities, P. vivax is not a lethal disease. It may be, however, that its effects would be more detrimental, if had it not been accompanied by P. falciparum (cf. Wernsdorfer & McGregor 1988:715).

We are inclined to the conclusion that the combined agricultural and hydrological innovations were decisive. In many districts where drainage efforts were delayed malaria was active for much longer. The Western provinces of the Netherlands, for instance, had higher death-rates than the North until the 1870s. The same holds true for Germany, where hydrological measures and housing improvements had to wait much longer. But other factors should not be ruled out, as they helped to change the balance between humans and mosquitoes to the latter's disadvantage. Apparently, all the causes combined have pushed the risk of contagion below a certain threshold, under which the disease could not be transmitted successfully. The existing degree of communal immunity may have acted as a supplementary warrant against reintroduction of the disease (Dobson 1980:385).


Is long-term climatic change relevant for explaining the history of malaria in Western Europe? As we have indicated, on the long range human interventions may have been more important than temperature fluctuations. Moreover, malaria incidence is largely dependent on summer temperatures. To a substantial extent the impact of global temperature fluctuations on Western European summer temperatures is muted by the shifting balance between continental and maritime climates (cf. Buisman 1995-98, vol 3:738). Regional differences in mean summer temperatures, ranging from 14°C in Scotland to 17.5°C in the Rhine valley, were far more pronounced than long-term historical trends.

Indeed, the rise and fall of tertian malaria in Western Europe does not seem to correspond with temperature changes. Only the arrival of quartan malaria may have coincided with the medieval climatic optimum. Nevertheless, we might get another picture if we concentrate on 25-year periods or even decades. Here the peaks of malaria incidence seem to coincide with periods of high summer temperatures. Critical periods, such as the 1550s, the 1720s and the 1820s all have been characterized by warm summers, even when the winters were cold. Finally, we must consider the frequency of warmer summers: as soon as intermediate periods lasted long enough (at least four years), the chain of transmission could be interrupted. As a consequence, the next outbreak of tertian malaria might become epidemic. This mechanism may have been responsible for the epidemics of the 1820s.

Will malaria return in Western Europe as a result of rising temperatures? Most epidemiologists agree that this is highly improbable. Even if A. atroparvus populations will expand spectacularly, due to global warming and rising sea levels, the accessibility of medical services in 21th-century society are such, that infections will not remain unnoticed for long (Reiter 2000; Jetten & Takken 1994:55-58).


This paper has also been presented at the Third European Social Science History Conference, Amsterdam, April 12-15, 2000. I am thankful to Wiet Koren for his comments.

Table 1: Crude Death Rates per 1,000 inhabitants in different districts

Sources: Norden 1984; Hinrichs et al. 1988; Lorenzen-Schmidt 1987.


Pastoral sea marsh


(n) = number of parishes

Arable sea marsh

(Marne, Dithmar­schen)



(Bockhorn, Oldenburg)




42 (2)




34 (3)




55 (4)




48 (6)




101 (1)




44 (9)




45 (9)




21 (7)




51 (9)




30 (9)





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