Farmer spraying an insecticide on a cashewnut tree in Tanzania
Insecticides are substances used to kill insects. They include ovicides and larvicides used against insect eggs and larvae, respectively. Insecticides are used in agriculture, medicine, industry
and by consumers. Insecticides are claimed to be a major factor behind
the increase in the 20th-century's agricultural productivity.
Nearly all insecticides have the potential to significantly alter
ecosystems; many are toxic to humans and/or animals; some become
concentrated as they spread along the food chain.
Insecticides can be classified into two major groups: systemic
insecticides, which have residual or long term activity; and contact
insecticides, which have no residual activity.
Furthermore, one can distinguish three types of insecticide. 1. Natural insecticides, such as nicotine, pyrethrum and neem
extracts, made by plants as defenses against insects. 2. Inorganic
insecticides, which are metals. 3. Organic insecticides, which are organic chemical compounds, mostly working by contact.
The mode of action
describes how the pesticide kills or inactivates a pest. It provides
another way of classifying insecticides. Mode of action is important in
understanding whether an insecticide will be toxic to unrelated species,
such as fish, birds and mammals.
Insecticides may be repellent or non-repellent. Social insects
such as ants cannot detect non-repellents and readily crawl through
them. As they return to the nest they take insecticide with them and
transfer it to their nestmates. Over time, this eliminates all of the
ants including the queen. This is slower than some other methods, but
usually completely eradicates the ant colony.
Insecticides are distinct from non-insecticidal repellents, which repel but do not kill.
Type of activity
Systemic insecticides become incorporated and distributed
systemically throughout the whole plant. When insects feed on the plant,
they ingest the insecticide. Systemic insecticides produced by transgenic plants are called plant-incorporated protectants (PIPs). For instance, a gene that codes for a specific Bacillus thuringiensis biocidal protein was introduced into corn (maize) and other species. The plant manufactures the protein, which kills the insect when consumed.
Contact insecticides are toxic to insects upon direct contact.
These can be inorganic insecticides, which are metals and include the
commonly used sulfur, and the less commonly used arsenates, copper and fluorine
compounds. Contact insecticides can also be organic insecticides, i.e.
organic chemical compounds, synthetically produced, and comprising the
largest numbers of pesticides used today. Or they can be natural
compounds like pyrethrum, neem oil etc.
Contact insecticides usually have no residual activity.
Efficacy can be related to the quality of pesticide application, with small droplets, such as aerosols often improving performance.
Biological pesticides
Many organic compounds are produced by plants for the purpose of
defending the host plant from predation. A trivial case is tree rosin, which is a natural insecticide. Specifically, the production of oleoresin by conifer species is a component of the defense response against insect attack and fungal pathogen infection. Many fragrances, e.g. oil of wintergreen, are in fact antifeedants.
Transgenic crops that act as insecticides began in 1996 with a genetically modified potato that produced the Cry protein, derived from the bacterium Bacillus thuringiensis, which is toxic to beetle larvae such as the Colorado potato beetle. The technique has been expanded to include the use of RNA interference RNAi that fatally silences crucial insect genes. RNAi likely evolved as a defense against viruses.
Midgut cells in many larvae take up the molecules and help spread the
signal. The technology can target only insects that have the silenced
sequence, as was demonstrated when a particular RNAi affected only one
of four fruit fly species. The technique is expected to replace many other insecticides, which are losing effectiveness due to the spread of pesticide resistance.
Biosynthesis of antifeedants by the action of myrosinase.
The myrosinase is released only upon crushing the flesh of
horseradish. Since allyl isothiocyanate is harmful to the plant as well
as the insect, it is stored in the harmless form of the glucosinolate,
separate from the myrosinase enzyme.
A
major emphasis of organic chemistry is the development of chemical
tools to enhance agricultural productivity. Insecticides represent a
major area of emphasis. Many of the major insecticides are inspired by
biological analogues. Many others are completely alien to nature.
Organophosphates
are another large class of contact insecticides. These also target the
insect's nervous system. Organophosphates interfere with the enzymesacetylcholinesterase and other cholinesterases, disrupting nerve impulses and killing or disabling the insect. Organophosphate insecticides and chemical warfare nerve agents (such as sarin, tabun, soman, and VX)
work in the same way. Organophosphates have a cumulative toxic effect
to wildlife, so multiple exposures to the chemicals amplifies the
toxicity. In the US, organophosphate use declined with the rise of substitutes.
Carbamate
insecticides have similar mechanisms to organophosphates, but have a
much shorter duration of action and are somewhat less toxic.
Pyrethroids
Pyrethroid pesticides mimic the insecticidal activity of the natural compound pyrethrum, the biopesticide found in pyrethrins.
These compounds are nonpersistent sodium channel modulators and are
less toxic than organophosphates and carbamates. Compounds in this group
are often applied against household pests.
Neonicotinoids
Neonicotinoids are synthetic analogues of the natural insecticide nicotine (with much lower acute mammalian toxicity and greater field persistence). These chemicals are acetylcholine receptor agonists.
They are broad-spectrum systemic insecticides, with rapid action
(minutes-hours). They are applied as sprays, drenches, seed and soil treatments. Treated insects exhibit leg tremors, rapid wing motion, stylet withdrawal (aphids), disoriented movement, paralysis and death. Imidacloprid may be the most common. It has recently come under scrutiny for allegedly pernicious effects on honeybees and its potential to increase the susceptibility of rice to planthopper attacks.
Ryanoids
Ryanoids are synthetic analogues with the same mode of action as ryanodine, a naturally occurring insecticide extracted from Ryania speciosa (Flacourtiaceae). They bind to calcium channels
in cardiac and skeletal muscle, blocking nerve transmission. The first
insecticide from this class to be registered was Rynaxypyr, generic name
chlorantraniliprole.
Insect growth regulators
Insect growth regulator (IGR) is a term coined to include insect hormone mimics and an earlier class of chemicals, the benzoylphenyl ureas, which inhibit chitin (exoskeleton) biosynthesis in insects. Diflubenzuron is a member of the latter class, used primarily to control caterpillars that are pests. The most successful insecticides in this class are the juvenoids (juvenile hormone analogues). Of these, methoprene is most widely used. It has no observable acute toxicity in rats and is approved by World Health Organization (WHO) for use in drinking water cisterns to combat malaria. Most of its uses are to combat insects where the adult is the pest, including mosquitoes, several fly species, and fleas. Two very similar products, hydroprene and kinoprene, are used for controlling species such as cockroaches and white flies.
Methoprene was registered with the EPA in 1975. Virtually no reports of
resistance have been filed. A more recent type of IGR is the ecdysone agonist tebufenozide (MIMIC), which is used in forestry
and other applications for control of caterpillars, which are far more
sensitive to its hormonal effects than other insect orders.
Environmental harm
Effects on nontarget species
Some
insecticides kill or harm other creatures in addition to those they are
intended to kill. For example, birds may be poisoned when they eat food
that was recently sprayed with insecticides or when they mistake an
insecticide granule on the ground for food and eat it.
Sprayed insecticide may drift from the area to which it is applied and
into wildlife areas, especially when it is sprayed aerially.
DDT
The development of DDT was motivated by desire to replace more
dangerous or less effective alternatives. DDT was introduced to replace
lead and arsenic-based compounds, which were in widespread use in the early 1940s.
DDT was brought to public attention by Rachel Carson's book Silent Spring.
One side-effect of DDT is to reduce the thickness of shells on the eggs
of predatory birds. The shells sometimes become too thin to be viable,
reducing bird populations. This occurs with DDT and related compounds
due to the process of bioaccumulation, wherein the chemical, due to its stability and fat solubility, accumulates in organisms' fatty tissues. Also, DDT may biomagnify, which causes progressively higher concentrations in the body fat of animals farther up the food chain. The near-worldwide ban on agricultural use of DDT and related chemicals has allowed some of these birds, such as the peregrine falcon, to recover in recent years. A number of organochlorine pesticides have been banned from most uses worldwide. Globally they are controlled via the Stockholm Convention on persistent organic pollutants. These include: aldrin, chlordane, DDT, dieldrin, endrin, heptachlor, mirex and toxaphene.
Pollinator decline
Insecticides can kill bees and may be a cause of pollinator decline, the loss of bees that pollinate plants, and colony collapse disorder (CCD), in which worker bees from a beehive or Western honey bee colony abruptly disappear. Loss of pollinators means a reduction in crop yields. Sublethal doses of insecticides (i.e. imidacloprid and other neonicotinoids) affect bee foraging behavior. However, research into the causes of CCD was inconclusive as of June 2007.
Bird decline
Besides
the effects of direct consumption of insecticides, populations of
insectivorous birds decline due to the collapse of their prey
populations. Spraying of especially wheat and corn in Europe is believed
to have caused an 80 per cent decline in flying insects, which in turn
has reduced local bird populations by a third to two thirds.
Alternatives
Instead
of using chemical insecticides to avoid crop damage caused by insects,
there are many alternative options available now that can protect
farmers from major economic losses. Some of them are:
Breeding crops resistant, or at least less susceptible, to pest attacks.
Spread of the Black Death in Europe and the Near East (1346–1353)
The Black Death, also known as the Great Plague or the Plague, or less commonly the Black Plague, was one of the most devastating pandemics in human history, resulting in the deaths of an estimated 75 to 200 million people in Eurasia and peaking in Europe from 1347 to 1351. The bacteriumYersinia pestis, which results in several forms of plague, is believed to have been the cause. The Black Death was the first major European outbreak of plague, and the second plague pandemic. The plague created a number of religious, social and economic upheavals which had profound effects on the course of European history.
The Black Death is thought to have originated in the dry plains of Central Asia, where it travelled along the Silk Road, reaching Crimea by 1343.[6] From there, it was most likely carried by fleas living on the black rats that traveled on all merchant ships, spreading throughout the Mediterranean Basin and Europe.
The Black Death is estimated to have killed 30% to 60% of Europe's population. In total, the plague may have reduced the world population from an estimated 450 million to 350–375 million in the 14th century. It took 200 years for the world population to recover to its previous level. The plague recurred as outbreaks in Europe until the 19th century.
Chronology
Origins of the disease
The plague disease, caused by Yersinia pestis, is enzootic (commonly present) in populations of fleas carried by ground rodents, including marmots, in various areas including Central Asia, Kurdistan, Western Asia, North India and Uganda. Due to climate change in Asia, rodents began to flee the dried out grasslands to more populated areas, spreading the disease. Nestorian graves dating to 1338–1339 near Issyk-Kul in Kyrgyzstan
have inscriptions referring to plague and are thought by many
epidemiologists to mark the outbreak of the epidemic, from which it
could easily have spread to China and India. In October 2010, medical geneticists suggested that all three of the great waves of the plague originated in China.
The 13th-century Mongol conquest of China
caused a decline in farming and trading. However, economic recovery had
been observed at the beginning of the fourteenth century. In the 1330s,
a large number of natural disasters and plagues led to widespread
famine, starting in 1331, with a deadly plague arriving soon after.
Epidemics that may have included plague killed an estimated 25 million
Chinese and other Asians during the fifteen years before it reached Constantinople in 1347.
The disease may have travelled along the Silk Road with Mongol armies and traders or it could have come via ship. By the end of 1346, reports of plague had reached the seaports of Europe: "India was depopulated, Tartary, Mesopotamia, Syria, Armenia were covered with dead bodies".
Plague was reportedly first introduced to Europe via Genoese traders from the port city of Kaffa in the Crimea in 1347. During a protracted siege of the city by the Mongol army under Jani Beg, whose army was suffering from the disease, the army catapulted infected corpses over the city walls of Kaffa to infect the inhabitants. The Genoese traders fled, taking the plague by ship into Sicily and the south of Europe, whence it spread north.
Whether or not this hypothesis is accurate, it is clear that several
existing conditions such as war, famine, and weather contributed to the
severity of the Black Death.
European outbreak
The seventh year after
it began, it came to England and first began in the towns and ports
joining on the seacoasts, in Dorsetshire, where, as in other counties,
it made the country quite void of inhabitants so that there were almost
none left alive.... But at length it came to Gloucester, yea even to
Oxford and to London, and finally it spread over all England and so
wasted the people that scarce the tenth person of any sort was left
alive. Geoffrey the Baker, Chronicon Angliae
There appears to have been several introductions into Europe. The plague reached Sicily in October 1347, carried by twelve Genoese galleys, and rapidly spread all over the island. Galleys from Kaffa reached Genoa and Venice in January 1348, but it was the outbreak in Pisa
a few weeks later that was the entry point to northern Italy. Towards
the end of January, one of the galleys expelled from Italy arrived in Marseille.
From Italy, the disease spread northwest across Europe, striking
France, Spain, Portugal and England by June 1348, then turned and spread
east and north through Germany, Scotland and Scandinavia from 1348 to
1350. It was introduced in Norway in 1349 when a ship landed at Askøy, then spread to Bjørgvin (modern Bergen) and Iceland.
Finally it spread to northwestern Russia in 1351. The plague was
somewhat less common in parts of Europe that had smaller trade relations
with their neighbours, including the majority of the Basque Country, isolated parts of Belgium and the Netherlands, and isolated alpine villages throughout the continent.
Modern researchers do not think that the plague ever became
endemic in Europe or its rat population. The disease repeatedly wiped
out the rodent carriers so that the fleas died out until a new outbreak
from Central Asia repeated the process. The outbreaks have been shown to
occur roughly 15 years after a warmer and wetter period in areas where
plague is endemic in other species such as gerbils.
Middle Eastern outbreak
The plague struck various regions in the Middle East during the pandemic, leading to serious depopulation and permanent change in both economic and social structures. It spread from China with the Mongols to a trading post in Crimea, called Kaffa, controlled by the Republic of Genoa.
As infected rodents infected new rodents, the disease spread across the
region, entering also from southern Russia. By autumn 1347, the plague
reached Alexandria in Egypt, through the port's trade with Constantinople, and ports on the Black Sea. During 1347, the disease travelled eastward to Gaza, and north along the eastern coast to cities in Lebanon, Syria and Palestine, including Ashkelon, Acre, Jerusalem, Sidon, Damascus, Homs, and Aleppo. In 1348–1349, the disease reached Antioch. The city's residents fled to the north, but most of them ended up dying during the journey.
Mecca became infected in 1349. During the same year, records show the city of Mawsil (Mosul) suffered a massive epidemic, and the city of Baghdad experienced a second round of the disease.
An inguinal bubo on the upper thigh of a person infected with bubonic plague. Swollen lymph glands (buboes) often occur in the neck, armpit and groin (inguinal) regions of plague victims.
Contemporary accounts of the plague are often varied or imprecise. The most commonly noted symptom was the appearance of buboes (or gavocciolos) in the groin, the neck and armpits, which oozed pus and bled when opened. Boccaccio's description:
In men and women alike it first betrayed itself by the emergence of certain tumours
in the groin or armpits, some of which grew as large as a common apple,
others as an egg ... From the two said parts of the body this deadly gavocciolo soon began to propagate and spread itself in all directions indifferently; after which the form of the malady
began to change, black spots or livid making their appearance in many
cases on the arm or the thigh or elsewhere, now few and large, now
minute and numerous. As the gavocciolo had been and still was an
infallible token of approaching death, such also were these spots on
whomsoever they showed themselves.
The only medical detail that is questionable in Boccaccio's
description is that the gavocciolo was an "infallible token of
approaching death", as, if the bubo discharges, recovery is possible.
This was followed by acute fever and vomiting of blood. Most victims died two to seven days after initial infection. Freckle-like spots and rashes, which could have been caused by flea-bites, were identified as another potential sign of the plague.
Some accounts, like that of Lodewijk Heyligen, whose master the Cardinal Colonna died of the plague in 1348, noted a distinct form of the disease that infected the lungs and led to respiratory problems and is identified with pneumonic plague.
It is said that the plague takes
three forms. In the first people suffer an infection of the lungs, which
leads to breathing difficulties. Whoever has this corruption or
contamination to any extent cannot escape but will die within two days.
Another form ... in which boils erupt under the armpits, ... a third
form in which people of both sexes are attacked in the groin.
Causes
The Oriental rat flea (Xenopsylla cheopis) engorged with blood. This species of flea is the primary vector for the transmission of Yersinia pestis, the organism responsible for spreading bubonic plague in most plague epidemics. Both male and female fleas feed on blood and can transmit the infection.
Oriental rat flea (Xenopsylla cheopis) infected with the Yersinia pestisbacterium which appears as a dark mass in the gut. The foregut (proventriculus) of this flea is blocked by a Y. pestisbiofilm; when the flea attempts to feed on an uninfected hostY. pestis is regurgitated into the wound, causing infection.
Yersinia pestis (200x magnification), the bacterium which causes bubonic plague
Medical knowledge had stagnated during the Middle Ages. The most authoritative account at the time came from the medical faculty in Paris in a report to the king of France that blamed the heavens, in the form of a conjunction of three planets in 1345 that caused a "great pestilence in the air".
This report became the first and most widely circulated of a series of
plague tracts that sought to give advice to sufferers. That the plague
was caused by bad air became the most widely accepted theory. Today,
this is known as the miasma theory. The word plague
had no special significance at this time, and only the recurrence of
outbreaks during the Middle Ages gave it the name that has become the
medical term.
The importance of hygiene
was recognised only in the nineteenth century; until then it was common
that the streets were filthy, with live animals of all sorts around and
human parasites abounding. A transmissible disease will spread easily in such conditions. One development as a result of the Black Death was the establishment of the idea of quarantine in the city-state of Ragusa (modern Dubrovnik, Croatia) in 1377 after continuing outbreaks.
The dominant explanation for the Black Death is the plague theory, which attributes the outbreak to Yersinia pestis,
also responsible for an epidemic that began in southern China in 1865,
eventually spreading to India. The investigation of the pathogen that
caused the 19th-century plague was begun by teams of scientists who
visited Hong Kong in 1894, among whom was the French-Swiss
bacteriologist Alexandre Yersin, after whom the pathogen was named. The mechanism by which Y. pestis was usually transmitted was established in 1898 by Paul-Louis Simond and was found to involve the bites of fleas whose midguts had become obstructed by replicating Y. pestis
several days after feeding on an infected host. This blockage results
in starvation and aggressive feeding behaviour by the fleas, which
repeatedly attempt to clear their blockage by regurgitation,
resulting in thousands of plague bacteria being flushed into the
feeding site, infecting the host. The bubonic plague mechanism was also
dependent on two populations of rodents: one resistant to the disease,
which act as hosts, keeping the disease endemic,
and a second that lack resistance. When the second population dies, the
fleas move on to other hosts, including people, thus creating a human epidemic.
The historian Francis Aidan Gasquet wrote about the Great Pestilence in 1893
and suggested that "it would appear to be some form of the ordinary
Eastern or bubonic plague". He was able to adopt the epidemiology of the
bubonic plague for the Black Death for the second edition in 1908,
implicating rats and fleas in the process, and his interpretation was
widely accepted for other ancient and medieval epidemics, such as the Justinian plague that was prevalent in the Eastern Roman Empire from 541 to 700 CE.
An estimate of the mortality rate for the modern bubonic plague, following the introduction of antibiotics, is 11%, although it may be higher in underdeveloped regions. Symptoms of the disease include fever of 38–41 °C (100–106 °F), headaches, painful aching joints, nausea and vomiting, and a general feeling of malaise. Left untreated, of those that contract the bubonic plague, 80 percent die within eight days. Pneumonic plague has a mortality rate of 90 to 95 percent. Symptoms include fever, cough, and blood-tinged sputum. As the disease progresses, sputum becomes free-flowing and bright red. Septicemic plague is the least common of the three forms, with a mortality rate near 100%. Symptoms are high fevers and purple skin patches (purpura due to disseminated intravascular coagulation).
In cases of pneumonic and particularly septicemic plague, the progress
of the disease is so rapid that there would often be no time for the
development of the enlarged lymph nodes that were noted as buboes.
A number of alternative theories – implicating other diseases in
the Black Death pandemic – have also been proposed by some modern
scientists (see below – "Alternative Explanations").
DNA evidence
Skeletons in a mass grave from 1720–1721 in Martigues, France, yielded molecular evidence of the orientalis strain of Yersinia pestis,
the organism responsible for bubonic plague. The second pandemic of
bubonic plague was active in Europe from 1347, the beginning of the
Black Death, until 1750.
In October 2010, the open-access scientific journal PLoS Pathogens published a paper by a multinational team who undertook a new investigation into the role of Yersinia pestis
in the Black Death following the disputed identification by Drancourt
and Raoult in 1998. They assessed the presence of DNA/RNA with polymerase chain reaction (PCR) techniques for Y. pestis from the tooth sockets
in human skeletons from mass graves in northern, central and southern
Europe that were associated archaeologically with the Black Death and
subsequent resurgences. The authors concluded that this new research,
together with prior analyses from the south of France and Germany, "ends the debate about the cause of the Black Death, and unambiguously demonstrates that Y. pestis was the causative agent of the epidemic plague that devastated Europe during the Middle Ages".
The study also found that there were two previously unknown but related clades (genetic branches) of the Y. pestisgenome
associated with medieval mass graves. These clades (which are thought
to be extinct) were found to be ancestral to modern isolates of the
modern Y. pestis strains Y. p. orientalis and Y. p. medievalis, suggesting the plague may have entered Europe in two waves. Surveys of plague pit remains in France and England indicate the first variant entered Europe through the port of Marseille
around November 1347 and spread through France over the next two years,
eventually reaching England in the spring of 1349, where it spread
through the country in three epidemics. Surveys of plague pit remains
from the Dutch town of Bergen op Zoom showed the Y. pestis genotype responsible for the pandemic that spread through the Low Countries
from 1350 differed from that found in Britain and France, implying
Bergen op Zoom (and possibly other parts of the southern Netherlands)
was not directly infected from England or France in 1349 and suggesting a
second wave of plague, different from those in Britain and France, may
have been carried to the Low Countries from Norway, the Hanseatic cities or another site.
The results of the Haensch study have since been confirmed and amended. Based on genetic evidence derived from Black Death victims in the East Smithfield
burial site in England, Schuenemann et al. concluded in 2011 "that the
Black Death in medieval Europe was caused by a variant of Y. pestis that may no longer exist." A study published in Nature in October 2011 sequenced the genome of Y. pestis
from plague victims and indicated that the strain that caused the Black
Death is ancestral to most modern strains of the disease.
DNA taken from 25 skeletons from the 14th century found in London have shown the plague is a strain of Y. pestis that is almost identical to that which hit Madagascar in 2013.
Alternative explanations
The plague theory was first significantly challenged by the work of
British bacteriologist J. F. D. Shrewsbury in 1970, who noted that the
reported rates of mortality in rural areas during the 14th-century
pandemic were inconsistent with the modern bubonic plague, leading him
to conclude that contemporary accounts were exaggerations.
In 1984, zoologist Graham Twigg produced the first major work to
challenge the bubonic plague theory directly, and his doubts about the
identity of the Black Death have been taken up by a number of authors,
including Samuel K. Cohn, Jr. (2002 and 2013), David Herlihy (1997), and Susan Scott and Christopher Duncan (2001).
It is recognised that an epidemiological
account of the plague is as important as an identification of symptoms,
but researchers are hampered by the lack of reliable statistics from
this period. Most work has been done on the spread of the plague in
England, and even estimates of overall population at the start vary by
over 100% as no census was undertaken between the time of publication of
the Domesday Book and the year 1377. Estimates of plague victims are usually extrapolated from figures from the clergy.
In addition to arguing that the rat population was insufficient
to account for a bubonic plague pandemic, sceptics of the bubonic plague
theory point out that the symptoms of the Black Death are not unique
(and arguably in some accounts may differ from bubonic plague); that
transference via fleas in goods was likely to be of marginal
significance; and that the DNA results may be flawed and might not have
been repeated elsewhere or were not replicable at all, despite extensive samples from other mass graves.
Other arguments include the lack of accounts of the death of rats
before outbreaks of plague between the 14th and 17th centuries;
temperatures that are too cold in northern Europe for the survival of
fleas; that, despite primitive transport systems, the spread of the
Black Death was much faster than that of modern bubonic plague; that
mortality rates of the Black Death appear to be very high; that, while
modern bubonic plague is largely endemic as a rural disease, the Black
Death indiscriminately struck urban and rural areas; and that the
pattern of the Black Death, with major outbreaks in the same areas
separated by 5 to 15 years, differs from modern bubonic plague—which
often becomes endemic for decades with annual flare-ups.
McCormick has suggested that earlier archaeologists were simply
not interested in the "laborious" processes needed to discover rat
remains.
Walløe complains that all of these authors "take it for granted that
Simond's infection model, black rat → rat flea → human, which was
developed to explain the spread of plague in India, is the only way an
epidemic of Yersinia pestis infection could spread", whilst pointing to several other possibilities. Similarly, Green has argued that greater attention is needed to the range of (especially non-commensal) animals that might be involved in the transmission of plague.
A variety of alternatives to Y. pestis have been put forward. Twigg suggested that the cause was a form of anthrax, and Norman Cantor
thought it may have been a combination of anthrax and other pandemics.
Scott and Duncan have argued that the pandemic was a form of infectious
disease that they characterise as hemorrhagic plague similar to Ebola.
Archaeologist Barney Sloane has argued that there is insufficient
evidence of the extinction of a large number of rats in the
archaeological record of the medieval waterfront in London and that the
plague spread too quickly to support the thesis that Y. pestis was spread from fleas on rats; he argues that transmission must have been person to person.
This theory is supported by research in 2018 which suggested
transmission was more likely by body lice and human fleas during the
second plague pandemic.
However, no single alternative solution has achieved widespread acceptance. Many scholars arguing for Y. pestis
as the major agent of the pandemic suggest that its extent and symptoms
can be explained by a combination of bubonic plague with other
diseases, including typhus, smallpox
and respiratory infections. In addition to the bubonic infection,
others point to additional septicemic (a type of "blood poisoning") and
pneumonic (an airborne plague that attacks the lungs before the rest of
the body) forms of the plague, which lengthen the duration of outbreaks
throughout the seasons and help account for its high mortality rate and
additional recorded symptoms. In 2014, Public Health England
announced the results of an examination of 25 bodies exhumed in the
Clerkenwell area of London, as well as of wills registered in London
during the period, which supported the pneumonic hypothesis.
There are no exact figures for the death toll;
the rate varied widely by locality. In urban centres, the greater the
population before the outbreak, the longer the duration of the period of
abnormal mortality. It killed some 75 to 200 million people in Eurasia. According to medieval historian Philip Daileader in 2007:
The trend of recent research is
pointing to a figure more like 45–50% of the European population dying
during a four-year period. There is a fair amount of geographic
variation. In Mediterranean Europe, areas such as Italy, the south of
France and Spain, where plague ran for about four years consecutively,
it was probably closer to 75–80% of the population. In Germany and
England ... it was probably closer to 20%.
A death rate as high as 60% in Europe has been suggested by Norwegian historian Ole Benedictow:
Detailed study of the mortality
data available points to two conspicuous features in relation to the
mortality caused by the Black Death: namely the extreme level of
mortality caused by the Black Death, and the remarkable similarity or
consistency of the level of mortality, from Spain in southern Europe to
England in north-western Europe. The data is sufficiently widespread and
numerous to make it likely that the Black Death swept away around 60
per cent of Europe's population. It is generally assumed that the size
of Europe's population at the time was around 80 million. This implies
that around 50 million people died in the Black Death.
The most widely accepted estimate for the Middle East, including
Iraq, Iran and Syria, during this time, is for a death rate of about a
third. The Black Death killed about 40% of Egypt's population. Half of Paris's population of 100,000 people died. In Italy, the population of Florence was reduced from 110,000–120,000 inhabitants in 1338 down to 50,000 in 1351. At least 60% of the population of Hamburg and Bremen perished, and a similar percentage of Londoners may have died from the disease as well. In London approximately 62,000 people died between 1346 and 1353.
While contemporary reports account of mass burial pits being created in
response to the large numbers of dead, recent scientific investigations
of a burial pit in Central London found well-preserved individuals to
be buried in isolated, evenly spaced graves, suggesting at least some
pre-planning and Christian burials at this time. Before 1350, there were about 170,000 settlements in Germany, and this was reduced by nearly 40,000 by 1450.
In 1348, the plague spread so rapidly that before any physicians or
government authorities had time to reflect upon its origins, about a
third of the European population had already perished. In crowded
cities, it was not uncommon for as much as 50% of the population to die.
The disease bypassed some areas, and the most isolated areas were less
vulnerable to contagion. Monks, nuns and priests were especially
hard-hit since they cared for victims of the Black Death.
Persecutions
Inspired by the Black Death, The Dance of Death, or Danse Macabre, an allegory on the universality of death, was a common painting motif in the late medieval period.
Renewed religious fervour and fanaticism bloomed in the wake of the
Black Death. Some Europeans targeted "various groups such as Jews,
friars, foreigners, beggars, pilgrims", lepers, and Romani, thinking that they were to blame for the crisis. Lepers, and other individuals with skin diseases such as acne or psoriasis, were singled out and exterminated throughout Europe.
Because 14th-century healers were at a loss to explain the cause,
Europeans turned to astrological forces, earthquakes, and the poisoning
of wells by Jews as possible reasons for the plague's emergence.
The governments of Europe had no apparent response to the crisis
because no one knew its cause or how it spread. The mechanism of
infection and transmission of diseases was little understood in the 14th
century; many people believed the epidemic was a punishment by God for
their sins. This belief led to the idea that the cure to the disease was
to win God's forgiveness.
There were many attacks against Jewish communities. In the Strasbourg massacre of February 1349, about 2,000 Jews were murdered. In August 1349, the Jewish communities in Mainz and Cologne were annihilated. By 1351, 60 major and 150 smaller Jewish communities had been destroyed.
These massacres eventually died out in Western Europe, only to continue
on in Eastern Europe. During this period many Jews relocated to Poland,
where they received a warm welcome from King Casimir the Great.
Recurrence
The Great Plague of London, in 1665, killed up to 100,000 people.
The plague repeatedly returned to haunt Europe and the Mediterranean throughout the 14th to 17th centuries. According to Biraben, the plague was present somewhere in Europe in every year between 1346 and 1671. The Second Pandemic
was particularly widespread in the following years: 1360–1363; 1374;
1400; 1438–1439; 1456–1457; 1464–1466; 1481–1485; 1500–1503; 1518–1531;
1544–1548; 1563–1566; 1573–1588; 1596–1599; 1602–1611; 1623–1640;
1644–1654; and 1664–1667. Subsequent outbreaks, though severe, marked
the retreat from most of Europe (18th century) and northern Africa
(19th century). According to Geoffrey Parker, "France alone lost almost a million people to the plague in the epidemic of 1628–31."
In England, in the absence of census figures, historians propose a
range of pre-incident population figures from as high as 7 million to
as low as 4 million in 1300, and a post-incident population figure as low as 2 million.
By the end of 1350, the Black Death subsided, but it never really died
out in England. Over the next few hundred years, further outbreaks
occurred in 1361–1362, 1369, 1379–1383, 1389–1393, and throughout the
first half of the 15th century.
An outbreak in 1471 took as much as 10–15% of the population, while the
death rate of the plague of 1479–1480 could have been as high as 20%. The most general outbreaks in Tudor and Stuart England seem to have begun in 1498, 1535, 1543, 1563, 1589, 1603, 1625, and 1636, and ended with the Great Plague of London in 1665.
Plague Riot in Moscow in 1771: during the course of the city's plague, between 50,000 and 100,000 people died, 17–33% of its population.
In 1466, perhaps 40,000 people died of the plague in Paris. During the 16th and 17th centuries, the plague was present in Paris around 30 per cent of the time.
The Black Death ravaged Europe for three years before it continued on
into Russia, where the disease was present somewhere in the country 25
times between 1350 and 1490. Plague epidemics ravaged London in 1563, 1593, 1603, 1625, 1636, and 1665, reducing its population by 10 to 30% during those years. Over 10% of Amsterdam's population died in 1623–1625, and again in 1635–1636, 1655, and 1664. Plague occurred in Venice 22 times between 1361 and 1528. The plague of 1576–1577 killed 50,000 in Venice, almost a third of the population. Late outbreaks in central Europe included the Italian Plague of 1629–1631, which is associated with troop movements during the Thirty Years' War, and the Great Plague of Vienna in 1679. Over 60% of Norway's population died in 1348–1350. The last plague outbreak ravaged Oslo in 1654.
In the first half of the 17th century, a plague claimed some 1.7 million victims in Italy, or about 14% of the population. In 1656, the plague killed about half of Naples' 300,000 inhabitants. More than 1.25 million deaths resulted from the extreme incidence of plague in 17th-century Spain. The plague of 1649 probably reduced the population of Seville by half. In 1709–1713, a plague epidemic that followed the Great Northern War (1700–1721, Sweden v. Russia and allies) killed about 100,000 in Sweden, and 300,000 in Prussia. The plague killed two-thirds of the inhabitants of Helsinki, and claimed a third of Stockholm's population. Europe's last major epidemic occurred in 1720 in Marseille.
Worldwide distribution of plague-infected animals, 1998
The Black Death ravaged much of the Islamic world. Plague was present in at least one location in the Islamic world virtually every year between 1500 and 1850. Plague repeatedly struck the cities of North Africa. Algiers lost 30,000–50,000 inhabitants to it in 1620–1621, and again in 1654–1657, 1665, 1691, and 1740–1742. Plague remained a major event in Ottoman
society until the second quarter of the 19th century. Between 1701 and
1750, thirty-seven larger and smaller epidemics were recorded in Constantinople, and an additional thirty-one between 1751 and 1800. Baghdad has suffered severely from visitations of the plague, and sometimes two-thirds of its population has been wiped out.
Third plague pandemic
The third plague pandemic (1855–1859) started in China in the
mid-19th century, spreading to all inhabited continents and killing 10
million people in India alone.
Twelve plague outbreaks in Australia between 1900 and 1925 resulted in
well over 1,000 deaths, chiefly in Sydney. This led to the establishment
of a Public Health Department there which undertook some leading-edge
research on plague transmission from rat fleas to humans via the
bacillus Yersinia pestis.
Modern treatment methods include insecticides, the use of antibiotics, and a plague vaccine. The plague bacterium could develop drug resistance and again become a major health threat. One case of a drug-resistant form of the bacterium was found in Madagascar in 1995. A further outbreak in Madagascar was reported in November 2014. In October 2017 the deadliest outbreak of the plague in modern times hit Madagascar, killing 170 people and infecting thousands.
Names
The phrase "black death" (mors nigra)
was used in 1350 by Simon de Covino or Couvin, a Belgian astronomer,
who wrote the poem "On the Judgment of the Sun at a Feast of Saturn" (De judicio Solis in convivio Saturni), which attributes the plague to a conjunction of Jupiter and Saturn.
In 1908, Gasquet claimed that use of the name atra mors for the 14th-century epidemic first appeared in a 1631 book on Danish history by J. I. Pontanus: "Commonly and from its effects, they called it the black death" (Vulgo & ab effectu atram mortem vocatibant).
The name spread through Scandinavia and then Germany, gradually
becoming attached to the mid 14th-century epidemic as a proper name.
However, atra mors is used to refer to a pestilential fever (febris pestilentialis) already in the 12th-century On the Signs and Symptoms of Diseases (Latin: De signis et sinthomatibus egritudinum) by French physician Gilles de Corbeil. In English, the term was first used in 1755. Writers contemporary with the plague described the event as "great plague" or "great pestilence".