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MALARIA
Settlement also brought malaria. ‘There is no doubt’, judged the distinguished Australian immunologist, Macfarlane Burnet (1899–1985), ‘that malaria has caused the greatest harm to the greatest number’ – not through cataclysms, as with bubonic plague, but through its continual winnowing effect. First in sub-Saharan Africa and elsewhere since, conversion of forests into farmland has created environments tailormade for mosquitoes: warm waterholes, furrows and puddles ideal for rapid breeding. Malaria is worth pausing over, since it has coexisted with humans for thousands of years and remains out of control across much of the globe.
The symptoms of malarial fevers were familiar to the Greeks, but were not explained until the advent of tropical medicine around 1900. They are produced by the microscopic protozoan parasite Plasmodium, which lives within the body of an Anopheles mosquito, and is transmitted to humans through mosquito bites. The parasites move through the bloodstream to the liver, where they breed during an incubation stage of a couple of weeks. Returning to the blood, they attack red blood cells, which break down, leading to waves of violent chills and high fever.
Malarial parasites have distinct periodicities. Plasmodium vivax, the organism causing benign tertian malaria, once present in the English fenlands, has an incubation period of ten to seventeen days. The fever lasts from two to six hours, returning every third day (hence ‘tertian’); marked by vomiting and diarrhoea, such attacks may recur for two months or longer. In time, as Greek doctors observed, the spleen enlarges, and the patient becomes anaemic and sometimes jaundiced. Quartan malaria, caused by Plasmodium malariae, is another mild variety.
Malignant tertian malaria, caused by Plasmodium falciparum, is the most lethal, producing at least 95 per cent of all malarial deaths. The incubation period is shorter but the fever more prolonged; it may be continuous, remittent or intermittent. Plasmodium falciparum proliferates fast, producing massive destruction of red blood cells and hence dangerous anaemia; the liver and spleen also become enlarged.
Malaria may sometimes appear as quotidian fever, with attacks lasting six to twelve hours – the result of multiple infection. Patients may also develop malarial cachexia, with yellowing of the skin and severe spleen and liver enlargement; autopsy shows both organs darkened with a black pigment derived from the haemoglobin of the destroyed red blood cells. What the ancients called melancholy may have been a malarial condition.
Malaria shadowed agricultural settlements. From Africa, it became established in the Near and Middle East and the Mediterranean littoral. The huge attention Graeco-Roman medicine paid to ‘remittent fevers’ shows how seriously the region was affected, and some historians maintain the disease played its part in the decline and fall of the Roman empire. Within living memory, malaria remained serious in the Roman Campagna and the Pontine marshes along Italy’s west coast.
Coastal Africa was and remains heavily malarial, as are the Congo, the Niger and hundreds of other river basins. Indigenous West African populations developed a genetically controlled characteristic, the ‘sickle-cell’, which conferred immunity against virulent Plasmodium falciparum. But, though protective, this starves its bearers, who are prone to debility and premature death: typical of such evolutionary trade-offs, gains and losses are finely balanced.
India was also ripe for malarial infection. Ayurvedic medical texts (see Chapter Six) confirm the antiquity of the disease in the subcontinent. China, too, became heavily infected, especially the coastal strip from Shanghai to Macao. And from the sixteenth century Europeans shipped it to Mesoamerica: vivax malaria went to the New World in the blood of the Spanish conquistadores, while falciparum malaria arrived with the African slaves whom the Europeans imported to replace the natives they and their pestilences had wiped out.
Malaria was just one health threat among many which set in with civilization as vermin learned to cohabit with humans, insects spread gastroenteric disorders, and contact with rodents led to human rickettsial (lice-, mite- and tick-borne) arbo diseases like typhus. Despite such infections encouraged by dense settlement and its waste and dirt, man’s restless inventive energies ensured that communities, no matter how unhealthy, bred rising populations; and more humans spawned more diseases in upward spirals, temporarily and locally checked but never terminated. Around 10,000 BC, before agriculture, the globe’s human population may have been around 5 million; by 500 BC it had probably leapt to 100 million; by the second century AD that may have doubled; the 1990 figure was some 5,292 million, with projections suggesting 12 billion by 2100.
Growing numbers led to meagre diets, the weak and poor inevitably bearing the brunt. But though humans were often malnourished, parasite-riddled and pestilence-smitten, they were not totally defenceless. Survivors of epidemics acquired some protection, and the mechanisms of evolution meant that these acquired sophisticated immune systems enabling them to coexist in a ceaseless war with their microbial assailants. Immunities passed from mothers across the placenta or through breast-feeding gave infants some defence against germ invasion. Tolerance was likewise developed towards parasitic worms, and certain groups developed genetic shields, as with the sickle-cell trait. Biological adaptation might thus take the edge off lethal afflictions.
THE ERA OF EPIDEMICS
Some diseases, however, were not so readily coped with: those caused by the zoonoses (animal diseases transmissible to man) which menaced once civilization developed. By 3000 BC cities like Babylon, with populations of scores of thousands, were rising in Mesopotamia and Egypt, in the Indus Valley and on the Yellow River, and later in Mesoamerica. In the Old World, such settlements often maintained huge cattle herds, from which lethal pathogens, including smallpox, spread to humans, while originally zoonostic conditions – diphtheria, influenza, chickenpox, mumps – and other illnesses also had a devastating impact. Unlike malaria, these needed no carriers; being directly contagious, they spread readily and rapidly.
The era of epidemics began. And though some immunity would develop amongst the afflicted populations, the incessant outreach of civilization meant that merchants, mariners and marauders would inevitably bridge pathogen pools, spilling diseases onto virgin susceptibles. One nation’s familiar ‘tamed’ disease would be another’s plague, as trade, travel and war detonated pathological explosions.
The immediate consequence of the invasion of a town by smallpox or another infection was a fulminating epidemic and subsequent decimation. Population recovery would then get under way, only for survivors’ heirs to be blitzed by the same or a different pestilence, and yet another, in tide upon tide. Settlements big enough to host such contagions might shrink to become too tiny. With almost everybody slain or immune, the pestilences would withdraw, victims of their own success, moving on to storm other virgin populations, like raiders seeking fresh spoils. New diseases thus operated as brutal Malthusian checks, sometimes shaping the destinies of nations.
Cities assumed a decisive epidemiological role, being magnets for pathogens no less than people. Until the nineteenth century, towns were so insanitary that their populations never replaced themselves by reproduction, multiplying only thanks to the influx of rural surpluses who were tragically infection-prone. In this challenge and response process, sturdy urban survivors turned into an immunological elite – a virulently infectious swarm perilous to less seasoned incomers, confirming the notoriety of towns as death-traps.
The Old Testament records the epidemics the Lord hurled upon the Egypt of the pharaohs, and from Greek times historians noted their melancholy toll. The Peloponnesian War of 431 to 404 BC, the ‘world war’ between Athens and Sparta, spotlights the traffic in pestilence that came with civilization. Before that war the Greeks had suffered from malaria and probably tuberculosis, diphtheria and influenza, but they had been spared truly calamitous plagues. Reputedly beginning in Africa and spreading to Persia, an unknown epidemic hit Greece in 430 BC, and its impact on Athens was portrayed by Thucydides (460 – after 404 BC). Victims were poleaxed by headaches, coughing, vomiting, chest pains and convulsions. Their bodies became reddish or livid, with blisters and ulcers; the malady often descended into the bowels before death spared sufferers further misery. The Greek historian thought it killed a quarter of the Athenian troops, persisting on the mainland for a further four years and annihilating a similar proportion of the population.
What was it? Smallpox, plague, measles, typhus, ergotism and even syphilis have been proposed in a parlour game played by epidemiologists. Whatever it was, by killing or immunizing them, it destroyed the Greeks’ ability to host it and, proving too virulent for its own good, the disease disappeared. With it passed the great age of Athens. Most early nations probably experienced such disasters, but Greece alone had a Thucydides to record it.
Epidemics worsened with the rise of Rome. With victories in Macedonia and Greece (146 BC), Persia (64 BC) and finally Egypt (30 BC), the Roman legions vanquished much of the known world, but deadly pathogens were thus given free passage around the empire, spreading to the Eternal City itself. The first serious outbreak, the so-called Antonine plague (probably smallpox which had smouldered in Africa or Asia before being brought back from the Near East by Roman troops) slew a quarter of the inhabitants in stricken areas between AD 165 and 180, some five million people in all. A second, between AD 211 and 266, reportedly destroyed some 5,000 a day in Rome at its height, while scourging the countryside as well. The virulence was immense because populations had no resistance. Smallpox and measles had joined the Mediterranean epidemiological melting-pot, alongside the endemic malaria.
Wherever it struck a virgin population, measles too proved lethal. There are some recent and well-documented instances of such strikes. In his Observations Made During the Epidemic of Measles on the Faroe Islands in the Year 1846, Peter Panum (1820–85) reported how measles had attacked about 6,100 out of 7,864 inhabitants on a remote island which had been completely free of the disease for sixty-five years. In the nineteenth century, high mortality was also reported in measles epidemics occurring in virgin soil populations (‘island laboratories’) in the Pacific Ocean: 40,000 deaths in a population of 150,000 in Hawaii in 1848, 20,000 (perhaps a quarter of the population) on Fiji in 1874.
Improving communications also widened disease basins in the Middle East, the Indian subcontinent, South Asia and the Far East. Take Japan: before AD 552, the archipelago had apparently escaped the epidemics blighting the Chinese mainland. In that year, Buddhist missionaries visited the Japanese court, and shortly afterwards smallpox broke out. In 585 there was a further eruption of either smallpox or measles. Following centuries brought waves of epidemics every three or four years, the most significant being smallpox, measles, influenza, mumps and dysentery.
This alteration of occasional epidemic diseases into endemic ones typical of childhood – it mirrors the domestication of animals – represents a crucial stage in disease ecology. Cities buffeted by lethal epidemics which killed or immunized so many that the pathogens themselves disappeared for lack of hosts, eventually became big enough to house sufficient non-immune individuals to retain the diseases permanently; for this an annual case total of something in the region of 5,000–40,000 may be necessary. Measles, smallpox and chickenpox turned into childhood ailments which affected the young less severely and conferred immunity to future attacks.
The process marks an epidemiological watershed. Through such evolutionary adaptations – epidemic diseases turning endemic – expanding populations accommodated and surmounted certain once-lethal pestilences. Yet they remained exposed to other dire infections, against which humans were to continue immunologically defenceless, because they were essentially diseases not of humans but of animals. One such is bubonic plague, which has struck humans with appalling ferocity whenever populations have been caught up in a disease net involving rats, fleas and the plague bacillus (Yersinia pestis). Diseases like plague, malaria, yellow fever, and others with animal reservoirs are uniquely difficult to control.
PLAGUE
Bubonic plague is basically a rodent problem. It strikes humans when infected fleas, failing to find a living rat once a rat host has been killed, pick a human instead. When the flea bites its new host, the bacillus enters the bloodstream. Filtered through the nearest lymph node, it leads to the characteristic swelling (bubo) in the neck, groin or armpit. Bubonic plague rapidly kills up to two-thirds of those infected. There are two other even more fatal forms: septicaemic and, deadliest of all, pneumonic plague, which doesn’t even need an insect vector, spreading from person to person directly via the breath.
The first documented bubonic plague outbreak occurred, predictably enough, in the Roman empire. The plague of Justinian originated in Egypt in AD 540; two years later it devastated Constantinople, going on to massacre up to a quarter of the eastern Mediterranean population, before spreading to western Europe and ricocheting around the Mediterranean for the next two centuries. Panic, disorder and murder reigned in the streets of Constantinople, wrote the historian Procopius: up to 10,000 people died each day, until there was no place to put the corpses. When this bout of plague ended, 40 per cent of the city’s population was dead.
It was the subsequent plague cycle, however, which made the greatest impact. Towards 1300 the Black Death began to rampage through Asia before sweeping westwards through the Middle East to North Africa and Europe. Between 1346 and 1350 Europe alone lost perhaps twenty million to the disease. And this pandemic was just the first wave of a bubonic pestilence that raged until about 1800 (see Chapter 5).
Trade, war and empire have always sped disease transmission between populations, a dramatic instance being offered by early modern Spain. The cosmopolitan Iberians became subjects of a natural Darwinian experiment, for their Atlantic and Mediterranean seaports served as clearing-houses for swarms of diseases converging from Africa, Asia and the Americas. Survival in this hazardous environment necessitated becoming hyper-immune, weathering a hail of childhood diseases – smallpox, measles, diphtheria, gastrointestinal infections and other afflictions rare today in the West. The Spanish conquistadores who invaded the Americas were, by consequence, immunological supermen, infinitely more deadly than ‘typhoid Mary’; disease gave them a fatal superiority over the defenceless native populations they invaded.
TYPHUS
Though the Black Death ebbed away from Europe, war and the movements of migrants ensured that epidemic disease did not go away, and Spain, as one of the great crossroads, formed a flashpoint of disease. Late in 1489, in its assault on Granada, Islam’s last Iberian stronghold, Spain hired some mercenaries who had lately been in Cyprus fighting the Ottomans. Soon after their arrival, Spanish troops began to go down with a disease never before encountered and possessing the brute virulence typical of new infections: typhus. It had probably emerged in the Near East during the Crusades before entering Europe where Christian and Muslim armies clashed.
It began with headache, rash and high fever, swelling and darkening of the face; next came delirium and the stupor giving the disease its name – typhos is Greek for ‘smoke’. Inflammation led to gangrene that rotted fingers and toes, causing a hideous stench. Spain lost 3,000 soldiers in the siege but six times as many to typhus.
Having smuggled itself into Spain, typhus filtered into France and beyond. In 1528, with the Valois (French) and Habsburg (Spanish) dynasties vying for European mastery, it struck the French army encircling Naples; half the 28,000 troops died within a month, and the siege collapsed. As a result, Emperor Charles V of Spain was left master of Italy, controlling Pope Clement VII – with important implications for Henry VIII’s marital troubles and the Reformation in England.
With the Holy Roman Empire fighting the Turks in the Balkans, typhus gained a second bridgehead into Europe. In 1542, the disease killed 30,000 Christian soldiers on the eastern front; four years later, it struck the Ottomans, terminating their siege of Belgrade; while by 1566 the Emperor Maximilian II had so many typhus victims that he was driven to an armistice. His disbanded troops relayed the disease back to western Europe, and so to the New World, where it joined measles and smallpox in ravaging Mexico and Peru. Typhus subsequently smote Europe during the Thirty Years War (1618–48), and remained widespread, devastating armies as ‘camp fever’, dogging beggars (road fever), depleting jails (jail fever) and ships (ship fever).
It was typhus which joined General Winter to turn Napoleon’s Russian invasion into a rout. The French crossed into Russia in June 1812. Sickness set in after the fall of Smolensk. Napoleon reached Moscow in September to find the city abandoned. During the next five weeks, the grande armée suffered a major typhus epidemic. By the time Moscow was evacuated, tens of thousands had fallen sick, and those unfit to travel were abandoned. Thirty thousand cases were left to die in Vilna alone, and only a trickle finally reached Warsaw. Of the 600,000 men in Napoleon’s army, few returned, and typhus was a major reason.
Smallpox, plague and typhus indicate, how war and conquest paved the way for the progress of pathogens. A later addition, at least as far as the West was concerned, was cholera, the most spectacular ‘new’ disease of the nineteenth century.
COLONIZATION AND INDUSTRIALIZATION
Together with civilization and commerce, colonization has contributed to the dissemination of infections. The Spanish conquest of America has already been mentioned; the nineteenth-century scramble for Africa also caused massive disturbance of indigenous populations and environmental disruption, unleashing terrible epidemics of sleeping sickness and other maladies. Europeans exported tuberculosis to the ‘Dark Continent’, especially once native labourers were jammed into mining compounds and the slums of Johannesburg. In the gold, diamond and copper producing regions of Africa, the operations of mining companies like De Beers and Union Minière de Haute Katanga brought family disruption and prostitution. Capitalism worsened the incidence of infectious and deficiency diseases for those induced or forced to abandon tribal ways and traditional economies – something which medical missionaries were pointing out from early in the twentieth century.
While in the period after Columbus’s voyage, advances in agriculture, plant-breeding and crop exchange between the New and Old Worlds in some ways improved food supply, for those newly dependent upon a single staple crop the consequence could be one of the classic deficiency diseases: scurvy, beriberi or kwashiorkor (from a Ghanaian word meaning a disease suffered by a child displaced from the breast). Those heavily reliant on maize in Mesoamerica and later, after it was brought back by the conquistadores, in the Mediterranean, frequently fell victim to pellagra, caused by niacin deficiency and characterized by diarrhoea, dermatitis, dementia and death. Another product of vitamin B1 (thiamine) deficiency is beriberi, associated with Asian rice cultures.
The Third World, however, has had no monopoly on dearth and deficiency diseases. The subjugation of Ireland by the English, complete around 1700, left an impoverished native peasantry ‘living in Filth and Nastiness upon Butter-milk and Potatoes, without a Shoe or stocking to their Feet’, as Jonathan Swift observed. Peasants survived through cultivating the potato, a New World import and another instance of how the Old World banked upon gains from the New. A wonderful source of nutrition, rich in vitamins B1 B2 and C as well as a host of essential minerals, potatoes kept the poor alive and well-nourished, but when in 1727 the oat crop failed, the poor ate their winter potatoes early and then starved. The subsequent famine led Swift to make his ironic ‘modest proposal’ as to how to handle the island’s surplus population better in future:
a young healthy Child, well nursed is, at a Year old, a most delicious, nourishing and wholesome Food; whether Stewed, Roasted, Baked, or Boiled; and, I make no doubt, that it will equally serve in a Fricassee, or Ragout … I grant this Food will be somewhat dear, and therefore very proper for Landlords.
With Ireland’s population zooming, disaster was always a risk. From a base of two million potato-eating peasants in 1700, the nation multiplied to five million by 1800 and to close on nine million by 1845. The potato island had become one of the world’s most densely populated places. When the oat and potato crops failed, starving peasants became prey to various disorders, notably typhus, predictably called ‘Irish fever’ by the landlords. During the Great Famine of 1845–7, typhus worked its way through the island; scurvy and dysentery also returned. Starving children aged so that they looked like old men. Around a million people may have died in the famine and in the next decades millions more emigrated. Only a small percentage of deaths were due directly to starvation; the overwhelming majority occurred from hunger-related disease: typhus, relapsing fevers and dysentery.
The staple crops introduced by peasant agriculture and commercial farming thus proved mixed blessings, enabling larger numbers to survive but often with their immunological stamina compromised. There may have been a similar trade-off respecting the impact of the industrial Revolution, first in Europe, then globally. While facilitating population growth and greater (if unequally distributed) prosperity, industrialization spread insanitary living conditions, workplace illnesses and ‘new diseases’ like rickets. And even prosperity has had its price, as Cheyne suggested. Cancer, obesity, gallstones, coronary heart disease, hypertension, diabetes, emphysema, Alzheimer’s disease and many other chronic and degenerative conditions have grown rapidly among today’s wealthy nations. More are of course now living long enough to develop these conditions, but new lifestyles also play their part, with cigarettes, alcohol, fatty diets and narcotics, those hallmarks of life in the West, taking their toll. Up to one third of all premature deaths in the West are said to be tobacco-related; in this, as in so many other matters, parts of the Third World are catching up fast.
And all the time ‘new’ diseases still make their appearance, either as evolutionary mutations or as ‘old’ diseases flushed out of their local environments (their very own Pandora’s box) and loosed upon the wider world as a result of environmental disturbance and economic change. The spread of AIDS, Ebola, Lassa and Marburg fevers may all be the result of the impact of the West on the ‘developing’ world – legacies of colonialism.
Not long ago medicine’s triumph over disease was taken for granted. At the close of the Second World War a sequence of books appeared in Britain under the masthead of The Conquest Series’. These included The Conquest of Disease, The Conquest of Pain, The Conquest of Tuberculosis, The Conquest of Cancer, The Conquest of the Unknown and The Conquest of Brain Mysteries, and they celebrated ‘the many wonders of contemporary medical science today’. And this was before the further ‘wonder’ advances introduced after 1950, from tranquillizers to transplant surgery. A signal event was the world-wide eradication of smallpox in 1977.
In spite of such advances, expectations of a conclusive victory over disease should always have seemed naive since that would fly in the face of a key axiom of Darwinian biology: ceaseless evolutionary adaptation. And that is something infectious disease accomplishes far better than humans, since it possesses the initiative. In such circumstances it is hardly surprising that medicine has proved feeble against AIDS, because the human immunodeficiency virus (HIV) mutates rapidly, frustrating the development of vaccines and antiviral drugs.
The systematic impoverishment of much of the Third World, the disruption following the collapse of communism, and the rebirth of an underclass in the First World resulting from the free-market economic policies dominant since the 1980s, have all assisted the resurgence of disease. In March 1997 the chairman of the British Medical Association warned that Britain was slipping back into the nineteenth century in terms of public health. Despite dazzling medical advances, world health prospects at the close of the twentieth century seem much gloomier than half a century ago.
The symbiosis of disease with society, the dialectic of challenge and adaptation, success and failure, sets the scene for the following discussion of medicine. From around 2000 BC, medical ideas and remedies were written down. That act of recording did not merely make early healing accessible to us; it transformed medicine itself. But there is more to medicine than the written record, and the remainder of this chapter addresses wider aspects of healing – customary beliefs about illness and the body, the self and society – and glances at medical beliefs and practices before and beyond the literate tradition.
