Smallpox is caused by a virus that may be airborne or spread by direct contact. After an incubation period of about two weeks, fever, aching, and prostration occur, lasting two or three days. An eruption then appears and spreads over the entire body; the lesions become blisterlike and pustular within a week. The lesions then open and crust over, causing itching and pain. When the crusts fall off, usually in another one or two weeks, the extent of permanent damage to the skin (pockmarks) becomes evident. There is no specific treatment for smallpox; an antibiotic may be administered to prevent secondary bacterial infection.
A crude vaccination method began with Emanuel Timoni, a Greek physician, in the early 18th cent. Edward Jenner modified the procedure (1796) by using the related cowpox virus to confer immunity. By 1977, vaccination programs, such as those by the World Health Organization (WHO), had eliminated the disease worldwide.
After 1980, when WHO officially declared smallpox eradicated as a disease, scientists retained some samples of the virus in laboratories for study. They mapped the genetic sequence of three strains of smallpox, and the destruction of the remaining samples of the live virus was scheduled and postponed several times. Owing to fears of a new natural outbreak or of the potential use of smallpox as a terrorist weapon against populations no longer vaccinated, research with the virus continued. The last declared samples of live virus are now stored by the U.S. and Russian governments under strict security, but it is believed that some nations may have secret stores of the virus that they could use as biological weapons. Responding to these concerns, WHO postponed the scheduled 1999 destruction of all remaining stocks of the smallpox virus until 2002. The 2001 bioterror attacks in the United States with anthrax led the United States and other nations to stockpile doses of smallpox vaccine out of concern that the smallpox virus might be used by terrorists, and WHO agreed to delay the destruction of virus stocks beyond 2002 to allow for the development of new vaccines. In 2002, because of bioterrorism concerns, the G. W. Bush administration decided to vaccinate frontline military personnel and health-care and emergency workers against smallpox.
See E. A. Fenn, Pox Americana: The Great Smallpox Epidemic of 1775-1782 (2001), and J. B. Tucker, Scourge (2001).
Smallpox is an infectious disease unique to humans, caused by either of two virus variants named Variola major and Variola minor. The disease is also known by the Latin names Variola or Variola vera, which is a derivative of the Latin varius, meaning spotted, or varus, meaning "pimple". The term "smallpox" was first used in Europe in the 15th century to distinguish variola from the great pox (syphilis).
Smallpox localizes in small blood vessels of the skin and in the mouth and throat. In the skin, this results in a characteristic maculopapular rash, and later, raised fluid-filled blisters. V. major produces a more serious disease and has an overall mortality rate of 30–35%. V. minor causes a milder form of disease (also known as alastrim, cottonpox, milkpox, whitepox, and Cuban itch) which kills ~1% of its victims. Long-term complications of V. major infection include characteristic scars, commonly on the face, which occurred in 65–85% of survivors. Blindness resulting from corneal ulceration and scarring, and limb deformities due to arthritis and osteomyelitis are less common complications, seen in about 2–5% of cases.
Smallpox is believed to have emerged in human populations about 10,000 BC. The disease killed an estimated 400,000 Europeans each year during the 18th century (including five reigning monarchs), and was responsible for a third of all blindness. Between 20 and 60% of all those infected—and over 80% of infected children—died from the disease.
During the 20th century, it is estimated that smallpox was responsible for 300–500 million deaths. As recently as 1967, the World Health Organization (WHO) estimated that 15 million people contracted the disease and that two million died in that year. After successful vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in December 1979. To this day, smallpox is the only human infectious disease to have been completely eradicated.
Smallpox is caused by infection with variola virus, which belongs to the genus Orthopoxvirus, the family Poxviridae, and subfamily chordopoxvirinae. It affects mostly babies and young children. Variola virus is a large brick-shaped virus measuring approximately 302 to 350 nanometers by 244 to 270 nm, with a single linear double stranded DNA genome consisting of 186 kilobase pairs (kbp) and containing a hairpin loop at each end. The two classic varieties of smallpox are variola major and variola minor. The closest viral relative is molluscum contagiosum, which like smallpox, infects only humans. However, unlike variola species, molluscum infection is benign. The lifecycle of poxviruses is complicated by having multiple infectious forms, with differing mechanisms of cell entry. Poxviruses are unique among DNA viruses in that they replicate in the cytoplasm of the cell rather than in the nucleus. In order to replicate poxviruses produce a variety of specialized proteins not produced by other DNA viruses, the most important of which is a viral-associated DNA-dependent RNA polymerase. Both enveloped and unenveloped virions are infectious. The viral envelop is made of modified Golgi membranes containing viral-specific polypeptides, including hemagglutinin. Infection with either variola major and variola minor confers immunity against the other.
Four orthopoxviruses cause infection in humans: variola, vaccinia, cowpox, and monkeypox. Variola virus infects only humans in nature, although primates and other animals have been infected in a laboratory setting. Vaccinia, cowpox, and monkeypox viruses can infect both humans and other animals in nature.
Variola minor is a less common presentation of smallpox, and a much less severe disease, with historical death rates of 1% or less. Subclinical (asymptomatic) infections with variola virus have also been noted, but are not believed to be common.
The incubation period between contraction and the first obvious symptoms of the disease is around 12 days. Once inhaled, variola virus invades the oropharyngeal (mouth and throat) or the respiratory mucosa, migrates to regional lymph nodes, and begins to multiply. In the initial growth phase the virus seems to move from cell to cell, but around the 12th day, lysis of many infected cells occurs and the virus is found in the bloodstream in large numbers (this is called viremia), and a second wave of multiplication occurs in the spleen, bone marrow, and lymph nodes. The initial or prodromal symptoms are similar to other viral diseases such as influenza and the common cold: fever (at least ), muscle pain, malaise, headache, prostration, and as the digestive tract is commonly involved, nausea and vomiting and backache often occur. The prodrome, or preeruptive stage, usually lasts 2–4 days. By days 12–15 the first visible lesions—small reddish spots called enanthem—appear on mucous membranes of the mouth, tongue, palate, and throat, and temperature falls to near normal. These lesions rapidly enlarge and rupture, releasing large amounts of virus into the saliva.
Smallpox virus preferentially attacks skin cells, causing the characteristic pimples (called macules) associated with the disease. A rash develops on the skin 24 to 48 hours after lesions on the mucous membranes appear. Typically the macules first appear on the forehead, then rapidly spread to the whole face, proximal portions of extremities, the trunk, and lastly to distal portions of extremities. The process takes no more than 24 to 36 hours, after which no new lesions appear. At this point Variola major infection can take several very different courses.
By the sixth or seventh day, all the skin lesions have become pustules. Between 7 and 10 days the pustules mature and reach their maximum size. The pustules are sharply raised, typically round, tense, and firm to the touch. The pustules are deeply embedded in the dermis, giving them the feel of a small bead in the skin. Fluid slowly leaks from the pustules, and by the end of the second week the pustules deflate, and start to dry up, forming crusts (or scabs). By day 16-20 scabs have formed over all the lesions, which have started to flake off, leaving de-pigmented scars.
Ordinary smallpox generally produces a discrete rash, in which the pustules stand out on the skin separately. The distribution of the rash is densest on the face; more dense on the extremities than on the trunk; and on the extremities, more dense on the distal parts than on the proximal. The palms of the hands and soles of the feet are involved in the majority of cases. In some cases, the blisters merge together into sheets, forming a confluent rash, which begin to detach the outer layers of skin from the underlying flesh. Patients with confluent smallpox often remain ill even after scabs have formed over all the lesions. In one case series, the case-fatality rate in confluent smallpox was 62%.
In the early, or fulminating, form, hemorrhaging appears on the second or third day as sub-conjunctival bleeding turns the whites of the eyes deep red. Hemorrhagic smallpox also produces a dusky erythema, petechiae, and hemorrhages in the spleen, kidney, serosa, muscle, and, rarely, the epicardium, liver, testes, and bladder. Death often occurs suddenly between the fifth and seventh days of illness, when only a few insignificant skin lesions are present. A later form of the disease occurs in patients who survive for 8–10 days. The hemorrhages appear in the early eruptive period, and the rash is flat and does not progress beyond the vesicular stage. Patients in the early stage of disease show a decrease in platelets, prothrombin, and globulin, and an increase in circulating antithrombin. Patients in the late stage have significant thrombocytopenia; however, deficiency of coagulation factors is less severe. Some in the late stage also show increased antithrombin. This form of smallpox occurs in anywhere from 3–25% of fatal cases (depending on the virulence of the smallpox strain).
The clinical definition of smallpox is an illness with acute onset of fever greater than 101°F (38.3°C) followed by a rash characterized by firm, deep seated vesicles or pustules in the same stage of development without other apparent cause.
Microscopically, one sees Guarnieri bodies, which are aggregates of the virus. Guarnieri bodies appear as pink blobs. The absence of Guarnieri bodies cannot be used to rule out smallpox, however.
If a clinical case is observed, smallpox is confirmed using laboratory tests. The diagnosis of an orthopoxvirus infection can be made rapidly by electron microscopic examination of pustular fluid or scabs. However, all orthopoxviruses exhibit identical brick-shaped virions by electron microscopy. Definitive laboratory identification of variola virus involves growing the virus on chorioallantoic membrane (part of a chicken embryo) and examining the resulting pock lesions under defined temperature conditions. Strains may be characterized by polymerase chain reaction (PCR) or restriction fragment length polymorphism (RFLP) analysis. Serologic tests and enzyme linked immunosorbent assays (ELISA), which measure variola virus-specific immunoglobulin and antigen have also been developed to assist in the diagnosis of infection.
Chickenpox was commonly confused with smallpox in the immediate post-eradication era. Chickenpox and smallpox can be distinguished by several methods. Unlike smallpox, chickenpox does not usually affect the palms and soles. Additionally, chickenpox pustules are of varying size due to variations in the timing of pustule eruption: smallpox pustules are all very nearly the same size since the viral effect progresses more uniformly. A variety of laboratory methods are available for detecting chickenpox in evaluation of suspected smallpox cases.
In fatal cases of ordinary smallpox, death usually occurs between the tenth and sixteenth days of the illness. The cause of death from smallpox is not clear, but the infection is now known to involve multiple organs. Circulating immune complexes, overwhelming viremia, or an uncontrolled immune response may be contributing factors. In early hemorrhagic smallpox, death occurs suddenly about six days after the fever develops. Cause of death in hemorrhagic cases involved heart failure, sometimes accompanied by pulmonary edema. In late hemorrhagic cases, high and sustained viremia, severe platelet loss and poor immune response were often cited as causes of death. In flat smallpox modes of death are similar to those in burns, with loss of fluid, protein and electrolytes beyond the capacity of the body to replace or acquire, and fulminating sepsis.
Other complications include encephalitis (1 in 500 patients), which is more common in adults and may cause temporary disability; permanent pitted scars, most notably on the face; and complications involving the eyes (2% of all cases). Pustules can form on the eyelid, conjunctiva, and cornea, leading to complications such as conjunctivitis, keratitis, corneal ulcer, iritis, iridocyclitis, and optic atrophy. Blindness results in approximately 35% to 40% of eyes affected with keratitis and corneal ulcer. Hemorrhagic smallpox can cause subconjunctival and retinal hemorrhages. In 2% to 5% of young children with smallpox, virions reach the joints and bone, causing osteomyelitis variolosa. Lesions are symmetrical, most common in the elbows, tibia, and fibula, and characteristically cause separation of an epiphysis and marked periosteal reactions. Swollen joints limit movement, and arthritis may lead to limb deformities, ankylosis, malformed bones, flail joints, and stubby fingers.
No drug is currently approved for the treatment of smallpox. However, antiviral treatments have improved since the last large smallpox epidemics, and studies suggest that the antiviral drug cidofovir might be useful as a therapeutic agent. The drug must be administered intravenously, however, and may cause serious renal toxicity.
The earliest procedure used to prevent smallpox was inoculation (also known as variolation). Inoculation was allegedly first practised in India as early as 1000 BC, and involved either nasal insufflation of powdered smallpox scabs, or scratching material from a smallpox lesion into the skin. However, this idea has been challenged as none of the ancient Sanskrit medical texts of India described the process of inoculation. Accounts of inoculation against smallpox in China can be found as early as the late 10th century, and the procedure was widely practised by the 16th century, during the Ming Dynasty. If successful, inoculation produced lasting immunity to smallpox. However, because the person was infected with variola virus, a severe infection could result, and the person could transmit smallpox to others. Variolation had a 0.5–2% mortality rate; considerably less than the 20–30% mortality rate of the disease itself.
In 1796 Edward Jenner, a doctor in Berkeley, Gloucestershire, rural England, discovered that immunity to smallpox could be produced by inoculating a person with material from a cowpox lesion. Cowpox is a poxvirus in the same family as variola. Jenner called the material used for inoculation vaccine, from the root word vacca, which is Latin for cow. The procedure was much safer than variolation, and did not involve a risk of smallpox transmission. Vaccination to prevent smallpox was soon practised all over the world. During the 19th century, the cowpox virus used for smallpox vaccination was replaced by vaccinia virus. Vaccinia is in the same family as cowpox and variola but is genetically distinct from both. The origin of vaccinia virus and how it came to be in the vaccine are not known.
The current formulation of smallpox vaccine is a live virus preparation of infectious vaccinia virus. The vaccine is given using a bifurcated (two-pronged) needle that is dipped into the vaccine solution. The needle is used to prick the skin (usually the upper arm) a number of times in a few seconds. If successful, a red and itchy bump develops at the vaccine site in three or four days. In the first week, the bump becomes a large blister (called a “Jennerian vesicle”) which fills with pus, and begins to drain. During the second week, the blister begins to dry up and a scab forms. The scab falls off in the third week, leaving a small scar.
The antibodies induced by vaccinia vaccine are cross-protective for other orthopoxviruses (such as monkeypox, cowpox, and variola (smallpox) viruses). Neutralizing antibodies are detectable 10 days after first-time vaccination, and seven days after revaccination. Historically, the vaccine has been effective in preventing smallpox infection in 95% of those vaccinated. Smallpox vaccination provides a high level of immunity for three to five years and decreasing immunity thereafter. If a person is vaccinated again later, immunity lasts even longer. Studies of smallpox cases in Europe in the 1950s and 1960s demonstrated that the fatality rate among persons vaccinated less than 10 years before exposure was 1.3%; it was 7% among those vaccinated 11 to 20 years prior, and 11% among those vaccinated 20 or more years prior to infection. By contrast, 52% of unvaccinated persons died.
There are side effects and risks associated with the smallpox vaccine. In the past, about 1,000 people for every 1 million people vaccinated for the first time experienced serious, but non-life-threatening, reactions including toxic or allergic reaction at the site of the vaccination (erythema multiforme), spread of the vaccinia virus to other parts of the body, and to other individuals. Potentially life-threatening reactions occurred in 14 to 52 people out of every 1 million people vaccinated for the first time. Based on past experience, it is estimated that 1 or 2 people in 1 million (0.000198%) who receive the vaccine may die as a result, most often the result of postvaccinial encephalitis or severe necrosis in the area of vaccination (called progressive vaccinia).
Given these risks, as smallpox became effectively eradicated and the number of naturally-occurring cases fell below the number of vaccine-induced illnesses and deaths, routine childhood vaccination was discontinued in the United States in 1972. Routine vaccination of healthcare workers was discontinued in 1976, and among military recruits in 1990, though military members deploying to the Middle East have been known to receive it to this day. It is now primarily recommended for laboratory workers at risk for occupational exposure. Mass smallpox vaccination was abandoned in most European countries in the early 1970s as well.
The first hemisphere-wide effort to eradicate smallpox was made in 1950 by the Pan American Health Organization. The campaign was successful in eliminating smallpox from all American countries except Argentina, Brazil, Colombia, and Ecuador. In 1958 Professor Viktor Zhdanov, Deputy Minister of Health for the USSR, called on the World Health Assembly to undertake a global initiative to eradicate smallpox. The proposal (Resolution WHA11.54) was accepted in 1959. At this point, 2 million people were dying every year. Overall, however, progress towards eradication was disappointing, especially in Africa and in the Indian subcontinent. In 1967, the World Health Organization intensified the global smallpox eradication by contributing $2.4 million annually to the effort. An international team, the Smallpox Eradication unit, was formed under the leadership of an American, Donald Henderson.
To eradicate smallpox, each outbreak had to be stopped from spreading, by isolation of cases and vaccination of everyone who lived close by. This process is known as "ring vaccination". The key to this strategy was monitoring of cases in a community (known as surveillance) and containment. The initial problem the WHO team faced was inadequate reporting of smallpox cases, as many cases did not come to the attention of the authorities. The fact that humans are the only reservoir for smallpox infection, and that carriers did not exist, played a significant role in the eradication of smallpox. The WHO established a network of consultants who assisted countries in setting up surveillance and containment activities. Early on donations of vaccine were provided primarily by the Soviet Union and the United States, but by 1973, more than 80% of all vaccine was produced in developing countries.
The last major European outbreak of smallpox was in 1972 in Yugoslavia ,but only in Serbia, after a pilgrim from Kosovo returned from the Middle East, where he had contracted the virus.Some rumours says that smallpox outbreak in Serbia was case of biological terrorist attack. The epidemic infected 175 people, causing 35 deaths. Authorities declared martial law, enforced quarantine, and undertook massive re-vaccination of the population, enlisting the help of the WHO. In two months, the outbreak was over. Prior to this, there had been a smallpox outbreak in May–July 1963 in Stockholm, Sweden, brought from the Far East by a Swedish sailor; this had been dealt with by quarantine measures and vaccination of the local population.
By the end of 1975, smallpox persisted only in the Horn of Africa. Conditions were very difficult in Ethiopia and Somalia, where there were few roads. Civil war, famine, and refugees made the task even more difficult. An intensive surveillance and containment and vaccination program was undertaken in the spring and summer of 1977. The last naturally occurring case of indigenous smallpox (Variola minor) was diagnosed in Ali Maow Maalin, a hospital cook in Merca, Somalia, on 26 October 1977. The last naturally occurring case of the more deadly Variola major had been detected in October 1975 in a two-year-old Bangladeshi girl, Rahima Banu.
The global eradication of smallpox was certified, based on intense verification activities in countries, by a commission of eminent scientists on 9 December 1979 and subsequently endorsed by the World Health Assembly on 8 May 1980 as Resolution WHA33.3. The first two sentences of the resolution read: "Having considered the development and results of the global program on smallpox eradication initiated by WHO in 1958 and intensified since 1967 … Declares solemnly that the world and its peoples have won freedom from smallpox, which was a most devastating disease sweeping in epidemic form through many countries since earliest time, leaving death, blindness and disfigurement in its wake and which only a decade ago was rampant in Africa, Asia and South America."
In March 2004 smallpox scabs were found tucked inside an envelope in a book on Civil War medicine in Santa Fe, New Mexico. The envelope was labeled as containing the scabs and listed the names of the patients they came from. Assuming the contents could be dangerous, the librarian who found them did not open the envelope. The scabs ended up with employees from the CDC who responded quickly once informed of the discovery. The discovery raised concerns that smallpox DNA could be extracted from these and other scabs and used for a biological attack.
An outbreak of weaponized smallpox possibly occurred during testing in the 1970s. General Prof. Peter Burgasov, former Chief Sanitary Physician of the Soviet Army, and a senior researcher within the Soviet program of biological weapons described the incident:
Others contend that the first patient may have contracted the disease while visiting Uyaly or Komsomolsk, two cities where the boat docked.
The Antonine Plague that swept through the Roman Empire and Italy in 165–180 is also thought to be either smallpox or measles. A second major outbreak of disease in the Empire, known as the Plague of Cyprian (251–266), was also either smallpox or measles.
The next major epidemic believed to be smallpox occurred in India. The exact date is unknown. Around AD 400, an Indian medical book recorded a disease marked by pustules and boils, saying "the pustules are red, yellow, and white and they are accompanied by burning pain … the skin seems studded with grains of rice." The Indian epidemic was thought to be punishment from a god, and the survivors created a goddess, Sitala, as the anthropomorphic personification of the disease. Smallpox was thus regarded as possession by Sitala. In Hinduism the goddess Sitala both causes and cures high fever, rashes, hot flashes and pustules. All of these are symptoms of smallpox.
Smallpox did not definitively enter Western Europe until about 581 when Bishop Gregory of Tours provided an eyewitness account that describes the characteristic findings of smallpox. Most of the details about the epidemic that followed are lost, probably due to the scarcity of surviving written records.
The clearest description of smallpox from pre-modern times was given in the 9th century by the Persian physician, Muhammad ibn Zakarīya Rāzi (Rhazes), who was the first to differentiate smallpox from measles in a treatise on both diseases.
Smallpox was a leading cause of death in the 18th century. It killed an estimated 400,000 Europeans each year in the 18th century, including five reigning European monarchs. Most people became infected during their lifetimes, and about 30% of people infected with smallpox died from the disease.
The Franco-Prussian War triggered a smallpox pandemic of 1870–1875 that claimed 500,000 lives.
|1520–1527||Mexico, Central America, South America||Smallpox kills millions of native inhabitants of Mexico. Unintentionally introduced at Veracruz with the arrival of Panfilo de Narvaez on April 23, 1520 and was credited with the victory of Cortes over the Aztec empire at Tenochtitlan (present-day Mexico City) in 1521. Kills the Inca ruler, Huayna Capac, and 200,000 others and weakens the Incan Empire.|
|1561–1562||Chile||No precise numbers on deaths exist in contemporary records but estimates are that the natives lost between twenty and twenty five percent of their population. According to Alonso de Góngora Marmolejo so many Indian laborers died that the Spanish gold mines had to shut down. .|
|1617–1619||North America northern east coast||Killed 90% of the Massachusetts Bay Indians|
|1674||Cherokee Tribe||Death count unknown. Population in 1674 about 50,000. After 1729, 1738, and 1753 smallpox epidemics their population was only 25,000 when they were forced to Oklahoma on the Trail Of Tears.|
|1702–1703||St. Lawrence Valley, NY|
|1770s||West Coast of North America||Kills out 30% of the West Coast Native Americans|
|1830s||Alaska||Reduced Dena'ina Athabaskan population in Cook Inlet region of southcentral Alaska by half. Smallpox also devastated Yup'ik Eskimo populations in western Alaska.|
|1865–1873||Philadelphia, PA, New York, Boston, MA and New Orleans, LA||Same period of time, in Washington D.C., Baltimore, MD, Memphis, TN, Cholera and a series of recurring epidemics of Typhus, Scarlet Fever and Yellow Fever|
|1877||Los Angeles, CA|
After first contacts with Europeans and Africans, some believe that the death of 90–95% of the native population of the New World was caused by Old World diseases. It is suspected that smallpox was the chief culprit and responsible for killing nearly all of the native inhabitants of the Americas. For more than 200 years, this disease affected all new world populations, mostly without intentional European transmission, from contact in the early 1500s to until possibly as late as the French and Indian Wars (1754–1767).
In 1519 Hernán Cortés landed on the shores of what is now Mexico and was then the Aztec empire. In 1520 another group of Spanish arrived in Mexico from Hispaniola, bringing with them the smallpox which had already been ravaging that island for two years. When Cortés heard about the other group, he went and defeated them. In this contact, one of Cortés's men contracted the disease. When Cortés returned to Tenochtitlan, he brought the disease with him.
Soon, the Aztecs rose up in rebellion against Cortés and his men. Outnumbered, the Spanish were forced to flee. In the fighting, the Spanish soldier carrying smallpox died. After the battle, the Aztecs contracted the virus from the invaders' bodies. Cortes would not return to the capital until August 1521. In the meantime smallpox devastated the Aztec population. It killed most of the Aztec army and 25% of the overall population. A Spanish priest left this description: "As the Indians did not know the remedy of the disease…they died in heaps, like bedbugs. In many places it happened that everyone in a house died and, as it was impossible to bury the great number of dead, they pulled down the houses over them so that their homes become their tombs." On Cortés's return, he found the Aztec army’s chain of command in ruins. The soldiers who lived were still weak from the disease. Cortés then easily defeated the Aztecs and entered Tenochtitlán. The Spaniards said that they could not walk through the streets without stepping on the bodies of smallpox victims.
The effects of smallpox on Tahuantinsuyu (or the Inca empire) were even more devastating. Beginning in Colombia, smallpox spread rapidly before the Spanish invaders first arrived in the empire. The spread was probably aided by the efficient Inca road system. Within months, the disease had killed the Sapa Inca Huayna Capac, his successor, and most of the other leaders. Two of his surviving sons warred for power and, after a bloody and costly war, Atahualpa become the new Sapa Inca. As Atahualpa was returning to the capital Cuzco, Francisco Pizarro arrived and through a series of deceits captured the young leader and his best general. Within a few years smallpox claimed between 60% and 90% of the Inca population, with other waves of European disease weakening them further. A handful of historians argue that a disease called Bartonellosis might have been responsible for some outbreaks of illness, but this opinion is in the scholarly minority. The effects of smallpox were depicted in the ceramics of the Moche people of ancient Peru.
Even after the two mighty empires of the Americas were defeated by the virus and disease, smallpox continued its march of death. In 1561, smallpox reached Chile by sea, when a ship carring the new governor Francisco de Villagra landed at La Serena. Chile had previously been isolated by the Atacama Desert and Andes Mountains from Peru, but at the end of 1561 and in early 1562, it ravaged the Chilean native population. Cronicles and records of the time left no accurate data on mortality but more recent estimates are that the natives lost between twenty and twenty five percent of their population. The Spanish historian Marmolejo said that gold mines had to shut down when all their indian labor died. . Mapuche fighting Spain in Araucania regarded the epidemic as a magical attempt by Francisco de Villagra to exterminate them because he could not defeat them in the Arauco War..
In 1633 in Plymouth, Massachusetts, the Native Americans were struck by the virus. As it had done elsewhere, the virus wiped out entire population groups of Native Americans. It reached Mohawks in 1634, the Lake Ontario in 1636, and the lands of the Iroquois by 1679. During the 1770s, smallpox killed at least 30% of the West Coast Native Americans. The smallpox epidemic of 1780–1782 brought devastation and drastic depopulation among the Plains Indians. By 1832, the federal government of the United States established a smallpox vaccination program for Native Americans.
A particularly virulent sequence of smallpox outbreaks took place in Boston, Massachusetts. From 1636 to 1698, Boston endured six epidemics. In 1721, the most severe epidemic occurred. The entire population fled the city, bringing the virus to the rest of the Thirteen Colonies. In the late 1770s, during the American Revolutionary War, smallpox returned once more and killed an estimated 125,000 people. Peter Kalm in his Travels in North America, described how in that period, the dying Indian villages became overrun with wolves feasting on the corpses and weakened survivors.
Prominent families throughout the world often had several people infected by and/or perish from the disease. For example, several relatives of Henry VIII survived the disease but were scarred by it. These include his sister Margaret, Queen of Scotland, his fourth wife, Anne of Cleves, and his daughter, Elizabeth I of England in 1562 (as an adult she would often try to disguise the pockmarks with heavy makeup). A more distant relative, Mary Queen of Scots, contracted the disease as a child but had no visible scarring.
In Europe, deaths from smallpox often changed dynastic succession. Louis XV of France succeeded his great-grandfather Louis XIV through a series of deaths of smallpox or measles among those earlier in the succession line. He himself died of the disease in 1774. The only surviving son of Henry VIII, Edward VI, likely died from complications shortly after apparently recovering from the disease, thereby rendering his sire's infamous efforts to provide England with a male heir moot. (His immediate successors were all females.) William III lost his mother to the disease when he was only ten years old in 1660, and named his uncle Charles as legal guardian: her death from smallpox would indirectly spark a chain of events that would eventually lead to the permanent ousting of the Stuart line from the British throne.
Both George Washington and Abraham Lincoln, Presidents of the United States, contracted and recovered from the disease. Joseph Stalin, who was badly scarred by the disease early in life, often had photographs retouched to make his pockmarks less apparent. Crime figure Lucky Luciano contracted disease in 1907 at the age of ten, upon coming to New York from Sicily.
Indian actress Geeta Bali died of smallpox in 1965.
Turkish poet Aşık Veysel Şatıroğlu was blinded by smallpox at the age of seven.
Smallpox in history