Smallpox in Australia facts for kids

The arrival of Europeans in Australia brought many new diseases. The original inhabitants, Aboriginal people, had never been exposed to these illnesses before. Diseases like colds, influenza, tuberculosis (TB), and measles became major killers. These diseases greatly harmed Aboriginal populations, weakened their cultures, and made it hard for them to resist the new settlers.

Within about six months of the First Fleet arriving, diseases were already a big problem for local Aboriginal groups. But the first major disease to cause a huge drop in the Aboriginal population around Sydney was the 1789 outbreak. This happened about 16 months after the Fleet arrived. Governor Phillip and others called it "smallpox." A captain named Watkin Tench wrote that the bodies were covered in spots like those from smallpox. He found it hard to understand how a disease they had never seen before could spread so quickly.

There were two main types of smallpox outbreaks in Australia. The first type included three "Aboriginal" epidemics. These outbreaks badly affected Aboriginal people but mostly spared the European colonists. Two happened in New South Wales: in 1789 and 1830. A third, longer outbreak happened in the 1860s. It spread across much of Northern and Western Australia, reaching down to the Great Australian Bight in the south.

The second type of outbreaks involved six major ones brought by ships in the 1800s (1857, 1868-1869, 1871, 1881-1882, 1884-1886, 1887, and 1893). These were kept mostly within port cities and mainly affected European colonists. After these, any new cases of imported smallpox were minor.

Even though the electron microscope (which lets doctors see viruses) wasn't available until the 1940s, experts are quite sure the second group of outbreaks was true smallpox. They had the typical death rate of about one in four infected people. They also spread relatively slowly. These outbreaks did not only kill Aboriginal people, and their origin was clear. In total, this second group killed about 100 people.

The first group of outbreaks, which mainly affected non-Europeans, was much deadlier. They spread faster and had a much bigger impact on Australia's history and the lives of its Aboriginal people today. Historian Judy Campbell said that between 1780 and 1870, smallpox was the main cause of Aboriginal deaths. She added that the effects of smallpox on Aboriginal people are a key part of modern Australian history.

The 1789 outbreak, in particular, has been much discussed. Some medical experts and anthropologists have argued it wasn't smallpox. They think it was probably chickenpox. Chickenpox is very contagious and has similar symptoms, but Europeans had some immunity to it, while Aboriginal people did not. The famous virologist Frank Fenner, who helped get rid of smallpox worldwide, said in 1985:

It's always hard to figure out what disease caused outbreaks in the distant past. We can never be sure if the 1789 outbreak was smallpox or chickenpox. But the little information we have seems to point to smallpox, even though we don't know how it started.

Since Fenner's comments in 1985, more historical evidence has appeared, and opinions have become stronger. Medical experts Ford and Carmody say that because the 1789 outbreak didn't affect Europeans (even though there were many chances), it couldn't have been smallpox. Yet, most historians still believe it was smallpox. The journals of the First Fleet's surgeons are missing, but historians guess they, like Governor Arthur Phillip, called it smallpox. It's not clear how much smallpox and chickenpox were seen as separate diseases in 1789.

Among those who believe the disease was smallpox, there are two main ideas. One is that it came from Sulawesi in Indonesia, brought by Macassan traders. The other is that it was brought directly to south-eastern Australia by European ships. Some, like independent scholar Christopher Warren, believe it was smallpox and that British colonists probably released it on purpose as an act of biological warfare. This idea has been supported by some Aboriginal leaders, including professors Maynard and Langton, and Dr Mark Wenitong. However, historians Henry Reynolds, Peter Dowling, and Cassandra Pybus still see this theory as unproven.

The 1789 Outbreak: A Closer Look

This disease quickly caused huge damage to the local Eora Aboriginal population. Most of those not infected fled the area. The epidemic likely started in March 1789 and "slowed down by early May." In early April 1789, British observers noticed that "native canoes" had suddenly disappeared from the harbor's many coves. They investigated and found sick or dying Aboriginal people in terrible conditions.

Naval officer William Bradley, who sailed into Sydney on May 9, 1789, was shocked by the "havoc." He saw that some people left in rock shelters seemed to have died of thirst because they were too sick to find water. Children often died next to a dead parent. Another naval officer, John Hunter, agreed that thirst or hunger increased deaths. This happened because sick people were "immediately deserted by their friends and left to perish." Judy Campbell, in her 2002 book Invisible Invaders, said that the disease's first impact in 1789 "was especially severe because of shock, flight, and fear, as well as the virus itself."

Bradley, unlike Tench, wondered if Aboriginal people had seen smallpox before. Lieutenant King was sure they had not. This is still a point of debate among historians. Most point to the lack of visible scars when Europeans first met Aboriginal people. But some, like Robert Barnes and Alan Frost, think that since three observers (King, Hunter, and Collins) said Aboriginal people had a name for it, the disease was probably a pre-existing, though rare, visitor.

It's hard to know exactly how many Aboriginal people died. Governor Phillip guessed that perhaps half had died. The Aboriginal man Bennelong also believed that half the Eora people in the Sydney area had died. After a few weeks, the canoes returned. Twenty were seen passing Sydney Cove on June 2, 1789. But Phillip's trips in the following months showed him that the disease, if it started near Sydney, had quickly moved on to nearby Aboriginal tribes.

Aboriginal people did not seem to connect this disease with the settlement. In mid-1788, they had shown strong anger towards the colony, with several spearings. But by 1791, they had become regular, peaceful visitors, even to the Governor's House. John Hunter noted that "before I left Port Jackson, the natives became very familiar and intimate with every person in the settlement." Many even slept in the gentlemen's houses. Yet, in 1789, the outbreak reduced not only the number of Aboriginal people living near the new settlement but also their ability to fight. It likely lowered their confidence in their culture. Historian Peter Dowling argues that it probably ended any chance of Aboriginal people attacking and destroying the colony in its early years.

Like smallpox, this outbreak caused many small spots that often left permanent scars on survivors. Other diseases had likely been introduced recently, but this spotty disease was clearly the main killer of Aboriginal people. Carmody and Hunter calculated in 2014 that if the disease was truly smallpox, it would have caused about 30 to 50 recorded cases within the colony, especially among the 84 children. Those who believe it was smallpox argue that in early 1789, there simply wasn't enough contact with the colonists for the disease to reach them.

Some have pointed to official letters where Governor Arthur Phillip regretted not being able to contact Aboriginal people. Yet, the memoirs of the colony's Lieutenant Governor David Collins suggest that convicts and some children might not have had the same problem. He described "large parties of the convicts of both sexes" holding regular parties with friendly Aboriginal people in a nearby cove. They "danced and sung with apparent good humour." Collins also said:

Even though Sydney Town was full of children at this time, many of whom visited the natives who were sick with this disorder, not one of them caught it. However, a North-American Indian sailor from Captain Ball's ship [the Supply] got sick with it and died.

This sailor, Joseph Jeffries, died on May 2, 1789, without, as Dowling notes, passing it to any of his shipmates. Phillip twice found groups of sick or dying Aboriginal people. He had them brought back to the colony and treated by surgeons. In each case, the adults died, but a child survived and was later adopted by a colonist family. No Europeans seemed to catch the disease from these patients. However, an Aboriginal man living in the colony, Arabanoo, who helped care for the sick Aboriginal patients, caught the disease and died. This evidence led to the 1985 debate between Fenner and Hingston (see below) about whether the 1789 disease could really have been smallpox.

The epidemic also changed how Europeans saw Aboriginal people. Surgeon George Bouchier Worgan had written that the local Eora Aboriginal people "seemingly enjoy uninterrupted Health, and live to a great Age." But as TB, influenza, and pneumonia began to affect Aboriginal people, they started to be seen as a diseased and even a dying race. Looking back around 1970, poet Les Murray wrote about how "The thoughtful savage with Athenian flanks/ fades from the old books." He described how Aboriginal people, no longer seen as a threat or rivals for land, began to be seen as sad and exotic, "pathetic with sores." Thomas Keneally's 1967 novel Bring Larks and Heroes, based loosely on the Sydney settlement, uses smallpox (which he says affected both races) as a symbol of the settlement's spiritual sickness.

Later Outbreaks: 1830s and 1860s

The outbreaks in the 1830s and 1860s might have started earlier and lasted longer than written records show. Dowling, for example, prefers to list the 1830-31 outbreak as 1828-1832. It's also possible that if the 1789 outbreak was the first infection, later ones were flare-ups of a disease that was now always present somewhere in Australia.

These later outbreaks don't have to be the same disease as the 1789 one, but some arguments link them. In 1831, surgeon John Mair reported that several people he spoke to believed that Aboriginal people with scars from a much older epidemic were immune to the current one. So, the debate between surgeons Mair and Busby (see below) about whether the 1830-1831 outbreak was smallpox or chickenpox also affects ideas about the 1789 epidemic.

The 1860s outbreak(s) haven't always been seen as a huge event in "settlement history." Yet, they caused a fairly high death rate, again mostly among Aboriginal people. Like the two earlier outbreaks, these were recorded as spreading quickly, but this time much more widely. It's generally believed they entered Australia in the tropical North. Then they spread south and west across much of the continent. If they were smallpox, as commonly believed, their rapid spread might support those who argue that the 1789 outbreak could also have been smallpox. This would mean it was brought to Northern Australia from Indonesia in the 1780s and then traveled overland to Sydney.

However, Cumpston records a Northern Territory Medical Officer wondering in 1906 why historical records of smallpox coming from the North and reaching "Central Australia" didn't match how smallpox behaved in his day. He added, "No satisfactory explanation offers itself." Carmody and Hunter, who argue the 1789 outbreak was chickenpox, don't specifically comment on these later outbreaks. But they say, as a general rule, that "Chickenpox is about five times more infectious than smallpox... and so fast nationwide transmission is more believable for chickenpox."

Ending Smallpox in Australia

The smallpox vaccine began to be made in Australia in 1917. In 1932, public immunization for the community started. The last reported smallpox case in Australia was in 1938. Smallpox vaccination stopped in 1980 after smallpox was officially declared eradicated worldwide in 1979.

Smallpox from Macassan Ships: A Theory

The idea that smallpox first came to northern Australia from Indonesia, probably with Macassan traders and fishers, and then reached southern Australia along Aboriginal trade routes, has been a major alternative to the "brought/released by the British" and chickenpox theories. Over time, debates about these theories have gone back and forth. Supporters of each theory often create new versions of their own ideas, while saying the opposing theories are unlikely.

Medical scientists like Sir Edward Stirling and Sir John Cleland published books and articles between 1911 and 1966. They suggested that smallpox arrived in Northern Australia from an Asian source. Later scholars usually connected this idea to Makassan contact with Australia. While there were smallpox cases in the city of Macassar in Sulawesi in 1789, there are no reports of it before that time. However, smallpox had been present in other islands of South East Asia for a long time, possibly as early as the 4th century, according to virologist Frank Fenner. There were smallpox outbreaks on the islands of the Indonesian archipelago throughout the 18th century. These included major epidemics in the Sultanate of Tidore (in the Moluccas) in the 1720s, the Sultanate of Banjar (South Kalimantan) in 1734, 1750–51, 1764–65, and 1778–79. There were also outbreaks in southern Sumatra in the 1750s, 1770s, and 1786. Macassans had contact with these areas directly and indirectly.

The Macassan theory was also considered in 1914 by Dr J. H. L. Cumpston, director of the Australian Quarantine Service. He wrote The History of Small-pox in Australia from 1788 to 1908. Cumpston was less sure about the earlier outbreaks. But he argued that the Macassan theory best explained the source and paths of the 1860s outbreak(s).

Professor Noel Butlin, while suggesting his own theory that smallpox was released in 1789 near Sydney, rejected the Macassan theory. In 1983, he argued that while Macassan fishermen could possibly "have landed the virus on the Australian mainland," their ability to do so was limited. He thought it highly unlikely that this virus would have traveled from the Gulf of Carpentaria to appear just 15 months after the First Fleet landed. He also argued that the time it took for Macassan voyages (more than seven to eight weeks), the type of boats, the limited contact between Aboriginal people and fishermen, the lack of clothing as a carrier, and the fact that the virus is destroyed by salt water, made the Macassan theory very unlikely. He thought infected Macassans would be "either dead or fully recovered long before reaching the Gulf of Carpentaria." Instead, he thought it more likely that in 1789, the virus had somehow escaped from inoculation kits carried by the First Fleet's surgeons.

In 1986, C. C. Macknight, an expert on the long history of contact between Indigenous Australians and people from Makassar (Sulawesi, now part of Indonesia), disagreed. He brought back the theory that smallpox was introduced to Australia by Macassan sailors visiting Arnhem Land. In 1993, Butlin seemed to change his mind about Macassan transmission being impossible. He wrote that smallpox had "certainly been delivered to parts of northern Australia and possibly more widely from Macassan praus."

In her 2002 book, Invisible Invaders, historian Judy Campbell, advised by Fenner, looked at reports of disease among Aboriginal people from 1780 to 1880. This included the smallpox epidemics of 1789–90, the 1830s, and the 1860s. Campbell argues that the evidence shows that while many diseases like tuberculosis were brought by British colonists, smallpox was not. She believes that other historians' ideas about British responsibility were based on weak evidence. This was mostly just the coincidence that the 1789–90 epidemic was first seen affecting Aboriginal people not long after the first British settlement. Campbell argues instead that the north–south path of the 1860s epidemics (which is generally agreed upon) also applied to the earlier ones. She is confident that all three were smallpox.

Campbell notes that fast Macassan fishing vessels, pushed by monsoon winds, reached Australia after being at sea for as little as 10 to 15 days. This is well within the time it takes for smallpox to develop. The large number of people traveling in the fleets was enough to keep smallpox going for long periods without it "burning out." The Macassans spent up to six months fishing along the northern Australian coast. Aboriginal people had "day-to-day contact with the islanders. Aboriginals visited the praus and the camps the visitors set up on shore, they talked and traded...." She also notes that Butlin, writing in 1983, "did not recognize that Aboriginals were ‘great travellers,’ who spread infection over long distances." She believes smallpox spread through their wide social and trading contacts, as well as by Aboriginal people fleeing the disease. Campbell also mentions British historian Charles Wilson, who used "medical microbiology" to disagree with Butlin about the 1789 outbreak's origins. Wilson "doubted his estimates of its demographic impact." Also, "First Fleet historian Alan Frost also disagreed with Butlin's views."

Two supporters of the deliberate release idea, Craig Mear (2008) and Michael J. Bennett (2009), have disagreed with Campbell's Macassan hypothesis, at least for the 1789 outbreak. However, Macknight re-entered the debate in 2011, stating: "It's overwhelmingly probable that it [smallpox] was introduced, like the later epidemics, by [Macassan] trepangers on the north coast and spread across the continent to arrive in Sydney quite independently of the new settlement there." In 2013, Macknight suggested that "substantial contact" between Macassan trepangers and Aboriginal people in Northern Australia began "around 1780." This makes the disease's appearance near Sydney in 1789 entirely possible. In his view, for the Sydney region, it was "a completely new event, without the effect of previous epidemics."

Independent scholar Christopher Warren (2014), in a longer explanation of his case that smallpox was deliberately released by the Royal Marines in 1789, rejected the idea that the 1789 epidemic came from Macassar. He claimed there was no evidence of a major smallpox outbreak in Macassar before 1789. He also said there were no Indigenous trade routes that would have allowed overland spread from Arnhem Land to Port Jackson. He argued that the Macassan theory went against Aboriginal oral tradition. He also said that 1829 was the earliest point where there was possible evidence that Macassans had caused a smallpox outbreak. Macknight, replying in The Canberra Times on December 18, 2021, and again on December 29, 2021, to a letter by Christopher Warren on "The Smallpox Debate", said that "Many such historical issues are judgments of probability and require a full reading of all the relevant literature." But he said Warren's alternative theory of deliberate infection by the Royal Marines was "very, very probably wrong."

Smallpox and Chickenpox: How They Were Confused

People trying to identify "smallpox" or "chickenpox" in Australia's early colonial documents face a problem. These terms might not have meant the same thing then as they do now. Today, the Germ theory of disease is widely known and accepted in science. This theory tells infectious diseases apart by the tiny germs that cause them. When the same germ causes different effects, modern doctors often suggest that different groups of people have different levels of immunity.

However, surgeons before the mid-1800s didn't often think about this. When they diagnosed a "disease," they were identifying a syndrome. This was a set of symptoms or "disorders," rather than a specific germ. To the English doctor Richard Morton, writing in 1694, "chickenpox" was just a common name for the "most benign" (meaning least harmful) forms of smallpox. So, as two modern virologists put it, "chickenpox (Varicella) was confused with smallpox until the 1800s, when both illnesses became better understood." But they note that good lab tests to tell the difference between Variola (smallpox) and Varicella (chickenpox) infections weren't available until the 1890s.

While all people seem at risk from smallpox, some have good immunity to the chickenpox virus. Among Europeans, chickenpox often causes just a short but painful childhood illness. Yet, early surgeons couldn't rely on its usually milder symptoms to tell it apart from smallpox. One reason is that smallpox itself varied. Even when caused by Variola major (the deadlier of the two types of "true" smallpox), smallpox still had at least four different "presentations," with very different levels of severity and death rates.

It was only in the mid-1900s, when doctors could definitely tell the difference between Variola and Varicella viruses, that chickenpox's behavior could be fully separated from smallpox. We now know that chickenpox is much more infectious than smallpox. It can actually be deadly, especially in a virgin soil epidemic (a term only used in medicine since 1976). It is also more dangerous to adults than to children (the opposite of smallpox). In contrast, smallpox, which spreads mainly by "respiratory droplets," is most often passed on after moderately long close contact, usually indoors. We also know, since 1888, that the chickenpox virus stays in the body permanently. It can break out again during times of stress or poor nutrition as "shingles," with infectious spots. So, there's no problem explaining how this virus reached the colony, as almost every adult colonist unknowingly carried it.

However, 20th-century virology also made the situation more complex. It introduced a difference between two types of "true" smallpox. Variola major, the more common and deadlier type, was now separated from Variola minor, also known as Alastrim. Alastrim was less severe and, on average, much less deadly, with death rates more like 1%. This is up to 30 times lower than Variola major's 25%-30% death rate. Before the electron microscope, there was debate about whether alastrim should be called "smallpox" and if it belonged in the Variola group. So, J. H. L. Cumpston and F. McCallum, in their 1923 book The History of Smallpox in Australia 1909-1923, noted a worldwide debate about "an exceptionally mild form of the disease." They said that some wanted to see alastrim as just a form of variola, while others believed it was a separate species. The fact that these two viruses eventually proved to be closely related, plus the belief that infection with one gave lifelong immunity to the other, led both to be classified as Variola and called smallpox.

However, the possibility that Variola minor might have much less severe effects on a "virgin soil" population than chickenpox (Varicella zoster) adds to the difficulty of understanding historical accounts. For example, if the deadly 1789 epidemic is believed to be Variola major, then it's possible that the less deadly 1830-31 epidemic of "aggravated" Varicella (as diagnosed by surgeon George Busby in 1831) might be neither chickenpox nor a continuation of the 1789 epidemic, but a separate outbreak of Variola minor.

Carmody has suggested that Governor Arthur Phillip's use of the word "smallpox" instead of "chickenpox" might simply mean he recognized the 1789 outbreak as severe. On the other hand, as early as 1767, the British physician William Heberden presented a paper On the Chickenpox to the Royal College of Physicians of London. In this paper, he argued that smallpox and chickenpox were separate diseases, and recovering from one did not give immunity to the other. Yet, despite the fact of separate immunities, doctors for some time found it hard to tell chickenpox cases from milder attacks (or possibly mild recurrences) of smallpox. (Modern medical opinion, however, is that smallpox does not recur.)

Heberden's view eventually won out. It was carefully supported by David Craigie in 1836 in his important book Elements of the practice of physic. Even so, Craigie noted chickenpox's close resemblance to smallpox, "with which it was always considered as allied, to which it probably bears an intimate relation, and with which it has been often confounded." It's not known if the 1789 surgeons (who were not university-trained doctors but qualified through apprenticeships) had read Heberden's paper or what they thought of it. But four decades later, during the 1830-31 outbreak, there was a strong debate among the colony's surgeons about their diagnoses.

The 1831 Mair-Busby Debate

In 1831, the Governor sent John Mair, a skilled young army surgeon, to the Bathurst region to investigate the 1830-1831 epidemic. Mair sent back alarming news: it was almost certainly smallpox. Mair noted that the disease "was very similar in its symptoms to smallpox." He added that the death rate varied "from one in three to one in five or six, but might have been less" if patients had had shelter and medical care. (This is less than the 50% death rate that Phillip and Bennelong estimated for the 1789 outbreak.) Mair also said that vaccination seemed to control it. He noted that "three blacks who had been successfully vaccinated, although equally exposed to the disease, escaped infection." (A supply of cowpox serum, allowing for true vaccination, had been brought to Sydney in 1804, six years after Jenner's successful experiment in 1796. With official support, it had been widely distributed.)

However, George Busby, the surgeon in charge of the Bathurst hospital, disagreed with Mair's diagnosis. Busby, supported by the colony's senior surgeon James Bowman, told the Governor that the outbreak appeared to be chickenpox. Busby also reported that when he examined two Aboriginal men, he was unsure of his diagnosis. But later, when he saw the full course of the disease while treating a European man who had caught the disease from an Aboriginal housemate who died of it, he diagnosed chickenpox. In his words:

[V]aricella, showing itself in a more severe form than it usually does, but by no means deadly or unstoppable. It was not likely, with normal comfort and care in civilized society, to be fatal in more than a few cases.

Busby also remarked:

Everyone who helped them [Aborigines] agrees that in every case, even the worst kind, where a little salts were given, and a little food, like tea or milk, was provided, along with protection from bad weather, they all recovered.

Busby did not think there was a difference in immunity between Aboriginal people and Europeans. He blamed the higher Aboriginal death rate on their nomadic lifestyle and lack of proper care.

Dr J. H. L. Cumpston, in his 1914 book The History of Small-Pox in Australia 1788–1908, quoted Busby's arguments at length, while seeming to dismiss them. Yet Cumpston noted that a repeated theme in his History was the long debate in Australian medical journals. Doctors like Busby insisted that a case or an outbreak was severe chickenpox, not smallpox. The common view was that if the pox disease, on its own, was causing deaths, then it must be smallpox. He cited Richard Quain's 1882 Dictionary of Medicine: "no physician has recorded a fatal case of chicken-pox." Cumpston leaned towards the second view: "It is a matter of common knowledge that chicken-pox is very rarely fatal." Yet he immediately after cited statistics that in Victoria, between 1857 and 1910, 70 deaths were blamed on chickenpox, versus 27 on smallpox. He also commented that such frequent debates and confusions "make one wonder to what extent the officially reported outbreaks of small-pox represent the real incidence of the disease." He remarked that, except for the cases Mair and Busby described, "there is no definite record of the existence of small-pox amongst Europeans in New South Wales before... 1874."

Peter Dowling, in his 2021 book Fatal Contact, notes that the Governor and Council accepted Busby's and Bowman's advice. However, Dowling dismisses Busby's diagnosis. He claims that the European patient's symptoms were what would be expected in a recurrence of smallpox. Dowling claims this is possible when the earlier infection was Variola minor not Variola major. He lists his account under "Busby, George (Dr)... chickenpox, misdiagnosis of."

Dowling mentions that the outbreak killed two Europeans in families that had taken in sick Aboriginal people. Also, Mair noted that the 1831 outbreak was more dangerous to adults, being "chiefly fatal to adults and old people, seldom to children." This pattern is typical of chickenpox outbreaks, but not smallpox, according to modern medical experts.

The 1985 Fenner-Hingston Debate

One hundred and fifty-four years later, in February 1985, there was an exchange of letters in the Medical Journal of Australia. Professor Frank Fenner had written an article on getting rid of smallpox. Richard Hingston, a doctor who had faced a deadly chickenpox epidemic in rural Papua with symptoms "clinically similar to smallpox," praised the article. But he criticized Fenner for suggesting the 1789 outbreak had been smallpox:

Everyone agreed that smallpox was absent in Europeans, both before and after arriving in the colony. A sailor from the Supply caught it [the 1789 outbreak] from the Aborigines, but he was a North-American Indian. Europeans think chickenpox is a minor childhood disease, but it looks very different in populations with no previous immunity. [...] Chickenpox in members of the First Fleet probably wouldn't have been reported, for the same reason it's not news today. The same infection, passed to Aborigines, wouldn't have been recognized because of its different symptoms.

Fenner, in his reply, agreed that Hingston had a point: "Chickenpox is a possible alternative diagnosis for the 1789 epidemic among the Aborigines of eastern Australia... but I prefer the more common opinion that the disease was smallpox." He also admitted, as noted above, that "We can never be sure whether the 1789 outbreak was due to smallpox or chickenpox." However, Fenner offered several arguments that he believed, together, justified his preference for the smallpox theory.

One argument involves evidence that the 1789 and 1830–1831 epidemics were the same disease. Fenner cited Mair's report that the 1830-1831 outbreak was smallpox. He linked this to Mair's strong suspicion that Aboriginal people with scars from a much older epidemic (perhaps the 1789 one) might now be immune. However, later research by Dowling (a strong supporter of the smallpox theory) seems to weaken this argument. Dowling found that Mair arrived too late to see any active cases of the disease. Also, as mentioned, the local surgeon, George Busby, disagreed and diagnosed chickenpox.

Dowling also recognizes the importance of Lieutenant Governor David Collins's memoir. He cites parts of it that may go against two of Fenner's other suggestions: that there weren't enough children in the colony to keep a chickenpox outbreak going, and that there wasn't enough contact with Aboriginal people for the colonists to have caught smallpox from them. However, the children Collins mentions visiting sick Aboriginal people in 1789 without catching the disease would have been born in the UK. Many may have already been immune to chickenpox.

Fenner also argued that the frequent reports of scarring on survivors suggested smallpox. He understood the importance of "hygiene" in preventing infection of the open spots of either disease. But he said that even in more recent chickenpox outbreaks among Somali nomads (whose hygiene he thought was probably "similar to that of the Aborigines in 1789"), serious scarring after chickenpox was very rare: 2.4% of cases were seen one year after the attack, compared with 85% from smallpox. However, when Christopher Warren used a version of this argument on Ockham’s Razor in April 2014, Carmody argued in reply that the severity of the virus attack could not be figured out later from the amount of scarring. This was "in part because there would have been a great deal of bacterial infection of the skin lesions, which would have worsened the scarring."

The debate in the medical journal in 1985 was not continued. Fenner's "favoring" of the smallpox theory was helpful to its supporters, but it was weakened by his clear statements that chickenpox could not be ruled out.

However, some smallpox supporters have presented this debate as a crushing defeat for the chickenpox theory. Christopher Warren has stated, for instance, "The chickenpox story is an old theory that has been dealt with. It was suggested by Richard Hingston in the Australian Medical Journal in 1985 and was immediately disproven by a leading virologist, Professor Frank Fenner." Warren has also claimed that Fenner's 1985 argument about Mair is final. In 2021, when Carmody criticized a reviewer for assuming the 1789 epidemic was smallpox, she responded: "Richard Hingston suggested the chickenpox theory in 1985, but this was disproven by virologist Frank Fenner."

Dowling, in his 1997 ANU PhD thesis "A Great Deal of Sickness", offered a new version of Fenner’s remark that the little data means that "we can never be sure" which disease it was. Dowling stated, "The little evidence we have about the 1789 epidemic in the Sydney region has left some historians and medical writers (Crosby 1986; Cumpston 1914; Curson 1985; Hingston 1985: 278) with doubts as to whether it was smallpox." Twenty-eight years later, in the chapter on smallpox in his 2021 book Fatal Contact, Dowling more strongly rejected the chickenpox theory. He again expressed admiration for Fenner and implied that his own views are similar to Fenner's. In a short section called "Disproving the doubters," Dowling does not describe the arguments or mention the names of Cumpston, Curson, Hingston, Carmody, Ford, Wright, and others who have supported the chickenpox theory. But he does offer a series of arguments against chickenpox. These are very similar to the arguments Fenner used in his debate with Hingston, but with significant additions to some points, especially the argument about scarring.

The Chickenpox Theory

Cumpston, in his 1914 History, mentions many medical discussions of the once-common term "native pock." It seems to have meant different things to different people, but sometimes sounds like Busby's "aggravated" varicella. For example, he quotes an unnamed doctor observing in a medical journal in 1846:

So far, this colony has been free from smallpox. We know that a disease which has appeared and caused many deaths among the Aboriginal tribes at various times is thought to be smallpox, but there is no clear evidence on that point. If it were, it would be a strange question to figure out how it got among them, and how it didn't spread to the white population. A large part of the white population, lacking vaccination, would have been very open to catching it. The condition known as "native pock" is certainly a smallpox-like disease, but it looks more like a severe form of varicella [i.e., chickenpox] than true smallpox.

The first clear statement that at least one of the major outbreaks was chickenpox may be Busby's in 1831. Cumpston shows that for some decades after that, both Busby and Mair had their supporters in medical journals.

Moodie, in 1973, argued that since the 1789 outbreak spared Europeans, it might have been a particularly severe form of chickenpox.

In the 1980s, growing awareness of how diseases affect populations with no prior immunity led to the chickenpox theory coming back. It was suggested carefully by Peter Curson in 1983, then more confidently by Hingston (1985) and Barry Wright (1987).

For the next 20 years, the chickenpox theory was mentioned less often. However, in 2010, John Carmody, a professor of medicine, strongly brought it up again on Robyn Williams's Ockham’s Razor program on ABC Radio National. Carmody claimed that the 1789 epidemic could not have been smallpox and was almost certainly chickenpox. He argued that smallpox, being much less infectious than chickenpox, could not have spread so quickly from tribe to tribe around Sydney (nor from Arnhem Land to the Sydney region). But if it had been present, it would certainly have infected some European colonists: "If it had really been smallpox, I would have expected about 50 cases amongst the colonists." Carmody said this would have caused several recorded deaths, since smallpox has about a 30% death rate. However, he said, the only non-Aboriginal person reported to have died in this outbreak was a sailor named Joseph Jeffries, who was recorded as being "a North American Indian." Carmody also remarked that if the virus had been smallpox and came from the surgeons' inoculation jars, it would have "had to last three summers before that 1789 outbreak."

Carmody noted that chickenpox can severely affect populations with little natural or acquired immunity. He also said it was certainly present in the colony. Regarding how smallpox could have reached the colony, Carmody later said: "There is absolutely no evidence to support any of the theories, and some of them are imaginative and far-fetched." In response, Christopher Warren rejected suggestions that chickenpox caused the 1789 epidemic. He also said it was not imaginative to think that the smallpox virus could have survived so long in dried scabs. Warren had already suggested in 2008 that Campbell was wrong to assume that high temperatures would have sterilized the British supply of smallpox. However, H. A. Willis (2010), in a review of the literature discussed above, supported Campbell's argument. In response, Warren (2011) suggested that Willis had not considered research on how heat affects the smallpox virus, as cited by the WHO. Willis (2011) replied that his position was supported by a closer reading of Frank Fenner’s report to the WHO (1988) and invited readers to consult that report online.

Carmody's argument on the Science Show was not followed by a scholarly paper for some time, and many historians ignored it. However, another medical researcher working on diseases among Aboriginal people in the early colonial era (this time not on the Eora but on nearby groups to the North West), G. E. Ford, stated in late 2010 that he had previously and independently reached Carmody's conclusions: "In a project applying a specialist understanding of disease and epidemiology from my own previous professional life as a pathobiologist, I had verified that the small pox was not Smallpox but was Chicken Pox brought to the colony in a latent form later known as Shingles." Ford also said that he had "identified a likely convict carrier and the means by which the chicken pox infection spread through the population."

However, Ford admits that neither he nor Carmody can claim to be the first with this theory since: "In 1985, a teacher of 'medical geography,' Peter Curson of Macquarie University, presented a good case based on historical evidence that the disease was chickenpox." Ford added that at a conference in 1987, archaeologist Barry Wright presented similar arguments and conclusions. To stay consistent with earlier historical accounts, Ford refers to "the small pox epidemic" of 1789–1791. But he writes "small pox" as two words and reminds the reader that he believes the "small pox" in question was "Chicken Pox, a small pox other than Smallpox."

In a conference paper in February 2014 on historical Aboriginal population numbers, Boyd Hunter of the Australian National University joined with Carmody. They argued that the recorded behavior of the 1789 epidemic rules out smallpox and points to chickenpox. In 2021, Carmody summarized the case against smallpox:

The truth was that not one of the British settlers got the disease (especially no children, who are very vulnerable to smallpox), even though some of them had very close contact with the victims. That result would have been impossible if the illness had really been smallpox. The much more likely diagnosis would have been chickenpox, which almost every colonist would have carried in their nervous system from a childhood infection. When some of them, under the stress of daily colonial life, developed ‘shingles,’ the children would have developed chickenpox and then passed it into the Aboriginal community, which, most likely, had no previous experience with that disease.

Yet, despite Ford's and even Fenner's agreement that chickenpox must eventually have entered the colony via shingles and was then very likely to spread fast and prove deadly to Aboriginal people, there is no strong evidence that it had actually appeared by April 1789. (The surviving part of Chief Surgeon John White’s journal suggests it had not been noticed by November 1788).

There is also some disagreement between Hingston's idea, where the surgeons recognized and ignored childhood chickenpox as unimportant, and Carmody's. Carmody doubts that the surgeons in 1789 believed there was a difference between the two diseases. But he implies they may not have noticed a child or children who carried a chickenpox infection, from an adult with shingles, to Aboriginal children with whom they played. No surviving records mention "smallpox" inside the colony, even though Tench and others were wondering how it reached the Aboriginal people.

Unanswered Questions in the Chickenpox Debate

However, the same difficulty in documenting the first appearance of chickenpox in Australia may also complicate the ideas of those who are quite sure that the 1789 outbreak was not chickenpox. Chickenpox, as Fenner and Hingston agreed, is a proven killer of populations with no prior immunity. None of the experts who favor smallpox has yet argued that Aboriginal people had immunity to chickenpox. If the sharp increase in Aboriginal deaths in 1789 cannot be blamed on the arrival of chickenpox, then chickenpox's first impact on Aboriginal populations still needs to be documented. Colin Tatz, in his Genocide in Australia: By Accident or Design?, puts chickenpox ahead of smallpox at the top of a list of major "settler-introduced diseases," but does not provide details.

Yet Fenner, in his 1985 debate with Hingston, gives reasons to doubt that chickenpox in 1789-1790 could have caused the death rates or scarring that the records suggest. The common Aboriginal custom of living and sometimes sleeping on bare earth around their campfires is well documented. This might have worsened the scarring, as Carmody suggests, through bacterial infection of open spots. Yet Fenner’s striking statistic about a deadly chickenpox epidemic causing only a 2.4% rate of serious scarring among its survivors seems a potential problem for the chickenpox explanation of the 1789 epidemic.

Governor Phillip’s rough estimate of a 50% death rate is much more like that of smallpox than chickenpox, though unusually high for either disease. Carmody and Hunter cite "a very severe epidemic" of chickenpox in the French Cameroons in 1936 that killed 19.3% of clinical cases (cases that received some medical treatment). They themselves estimate a likely death rate among Aboriginal people in 1789 of about 30%. This, they recognize, is still "substantially lower than most of the smallpox-based assumptions in Butlin's research." However, they argue that other health problems may have meant that Aboriginal people were actually suffering from "multiple epidemics." The pox disease, with its dramatic skin eruptions, took all the blame. The Aboriginal public health expert Dr Mark Wenitong has rejected such arguments, telling the ABC in 2021: "It looked like smallpox and acted like smallpox, and the outcomes were high death rates like smallpox."

The speed with which the 1789 disease spread does not necessarily prove it was chickenpox. Unknown cultural factors or behaviors might have helped it spread. Dowling says that it was common for smallpox to become highly contagious "in a virgin soil population." Very little or nothing is known about how much the behavior of either disease may have changed in a truly "virgin soil" Aboriginal population in 1789. The failure to infect and kill Europeans remains the clearest argument that it was not smallpox.

Some supporters of the smallpox theory, however, turn this argument around. They claim that smallpox failed to infect Europeans precisely because they were already immune to it. Carmody and Hunter (2014) agree that those colonists who had suffered smallpox were now immune. But they argue that smallpox's epidemic behavior in Britain, with its "impressively constant" rates of infection and death, proves the population as a whole was far from immune. They calculate that about half of the colonists, including almost all the younger children, were vulnerable. Dowling agrees that many of the roughly one thousand colonists would not have been immune to smallpox, especially the children. However, he doubts that there was enough contact with Aboriginal people.

To accept the 1789 "smallpox epidemic" as the work of chickenpox would mean a large-scale re-evaluation of the history of such epidemics. All supposed epidemics of "smallpox" recorded before 1800—especially if they moved quickly, and if they affected populations never exposed before—might be suspected of being the more infectious chickenpox. The entire history and spread of smallpox in the Americas might need to be re-examined. In Australia, too, there would be new things to research. For instance, Carmody and Hunter remark that it is "reasonable to assume that chickenpox then [i.e., after 1789] spread relatively quickly across the continent from Port Jackson [Sydney] because it has a very high infection rate."

In Europe and Asia, many long-running debates about what caused past plagues, such as the Black Death, have supposedly been solved in the 21st century by DNA evidence. To date, no DNA evidence has been offered on the 1789 epidemic.

Theories of Deliberate Release in 1789

Although the First Fleet itself did not arrive with any known carriers of the disease, the appearance of an epidemic about 16 months after the colony was set up has led to ideas that the Fleet itself brought this disease to Australia. The surgeons carried sealed samples of dried smallpox scabs to use in variolation. Some historians have suggested that the disease was later released from the surgeons' medical supplies, either by accident (perhaps through theft) or on purpose.

Variolation, a type of inoculation with dried smallpox scab, was a well-known medical practice. It was used up until, and even after, the process of smallpox vaccination (with cowpox) was successfully shown by Edward Jenner in 1796. Variolation was a risky procedure, as people sometimes died from the infection or spread it to others. Yet, during severe epidemics, it seemed to offer significant protection. This was perhaps because the patient received only a small infection from the dried scab and was then immune. Dried smallpox scab was commonly stored in glass containers as part of a surgeon's remedies. Successful variolation produced a single, localized mark called a papule at the infection site. So, surgeons would normally know if their scab samples were still good.

There is no record of the surgeons using this material. No First Fleet members had suffered from the disease on the voyage, and no cases had been recorded since. So, smallpox's sudden appearance among the Aboriginal people was a puzzle. As mentioned, Watkin Tench noted that the marks on the bodies were "similar" to those caused by smallpox. Tench then wondered if the disease might be native to the country. Or if it had been brought to the colony by the French expedition of Lapérouse a year before. Or if it had traveled across the continent from the West where Europeans had previously landed. Or if it was brought by the expedition of James Cook. Or indeed, if it arrived with the first British settlers at Sydney. "Our surgeons brought out variolous matter in bottles," he wrote, "but to think it came from this cause would be such a wild idea as to be not worth considering."

However, Dowling finds evidence that by 1830, with the help of well-meaning settlers, many Aboriginal people seem to have been either vaccinated (with cowpox) or "inoculated" (meaning variolated). This method would seem to have risked spreading either smallpox (Variola major or Variola minor) or its partial lookalike, chickenpox.

In later years, most historians assumed that the 1789 epidemic was smallpox. Several of them wondered how smallpox might have traveled from Indonesia via Macassan traders and then overland to southern Australia. However, in 1914, Dr J. H. L. Cumpston, while not ruling out this possibility, nor the possibility that it was chickenpox, put forward a competing theory. He suggested that smallpox somehow reached NSW in 1789 via British settlers. He did not believe smallpox infections could have gone unnoticed. So he thought that the "variolous matter" mentioned by Watkin Tench "cannot be dismissed lightly as a possible source of the epidemic. It is at least as likely a theory as that of the introduction by the French sailors." However, Cumpston thought that "this question can never be settled unless some previously undiscovered records come to light."

This theory was brought back and expanded in 1983 when Professor Noel Butlin, an economic historian, suggested: "it is possible and, in 1789, likely, that infection of the Aboriginal people was a deliberate act to wipe them out." Butlin did not say how the virus was released. But (having argued that the Macassan/overland theory was unlikely) he suggested that the most likely explanation for smallpox's appearance in 1789 was that it had been transferred somehow, by theft, accident, or similar, from scab originally stored in glass containers carried by just one of the seven medical officers on the first fleet.

Several historians after that mentioned this possibility. They debated if this was more believable than overland transmission. David Day (2001) repeated Butlin's argument and suggested that members of Sydney's Royal Marines garrison may have tried to use smallpox as a biological weapon in 1789. The next year, however, John Connor stated that Day's theory was "unsustainable." Historian Henry Reynolds in 2001 repeated Butlin's claims and wrote: "one possibility is that the epidemic was deliberately or accidentally let loose by someone in the settlement at Sydney Cove."

However, renewed arguments for overland transmission were put forward by Judy Campbell in her 2002 book Invisible Invaders, and by Macknight (1986 and 2011). H. A. Willis complained in 2010 that Butlin's supporters had ignored the fact that his study "was confined to the period before 1850. Yet the 1860s epidemic shows that smallpox could and did travel overland from northern Australia." There was also, in the 1980s, a return of the competing chickenpox theory.

Independent scholar Christopher Warren (2007, 2014) became a strong supporter of the view that smallpox was deliberately released from the surgeon's inoculation jars as an act of germ warfare. This led him into complex debates with Fenner, Carmody, Willis, and others about whether these inoculation samples could have been protected from heat enough to still be active in April 1789. However, in 2014, he presented a detailed argument that the colony in April 1789 was in a very weak military position against the Aboriginal people. He suggested that the release of smallpox was a response to this by one or more of the colonists, perhaps without the Governor's knowledge. Warren also cited a story from the Balmoral region of North Sydney, reported in 2001 by Aboriginal academic Dennis Foley: "According to Foley, an Aboriginal oral tradition reported that, at Balmoral, there were blankets with red markings, a stripe of words or a crown, and that those who took the blankets died a horrible death of fire under their skin and the pus of a thousand festering sores." Warren suggests that concentrations of Aboriginal remains around Sydney "are consistent with a release of smallpox at Balmoral and at Botany Bay [south of Sydney] with some natives dying as they fled north and south." In 2021, Warren claimed that "the British had no other option than to use smallpox against local Aborigines in 1789 because they had no ammunition for their muskets."

While acknowledging Carmody's and Ford's argument that chickenpox was present on the First Fleet and would have become infectious via shingles, Warren argued in his 2014 article that it was suspicious that in April 1789, a smallpox epidemic "was reported amongst the Port Jackson Aboriginal tribes who were actively resisting settlers from the First Fleet." When the Ockham’s Razor radio program for April 13, 2014, invited Warren to restate these arguments, Carmody responded briefly on the same program. He claimed that there was in fact "no hard medical evidence" that the 1789 outbreak was smallpox. He also said that the surgeons' inoculation samples would have been inactive by April 1789.

Deliberate Release: North American Comparisons

However, Warren and others argue that the British had already used smallpox in this way in North America:

In the 18th century, British forces using smallpox was not new. This tactic was promoted by Major Robert Donkin. It was started by General Jeffrey Amherst in 1763. Smallpox-laden blankets and a handkerchief were given out from Fort Pitt near the Great Lakes in North America.

In June 1763, during Pontiac's War, Colonel Henry Bouquet ordered smallpox blankets to be given to a Delaware delegation when they laid siege to Fort Pitt. Yet, A. R. Rao's careful research in the 1960s found little truth in the traditional belief that smallpox can be spread from a distance through infected clothing or bedding. There is independent evidence that Bouquet's attempt, even with very fresh material from the smallpox epidemic inside their own fort, was unsuccessful.

The comparison with the Sydney colony is not perfect. Smallpox had long been a problem in North America. But in Australia, the British would have been infecting their new territory with a deadly disease from which it (and its new colonists) had been free. Henry Reynolds commented in 2001: "Not surprisingly, this is a very controversial idea. If true, it would clearly fall under the Genocide Convention." Seth Carus of the National Defense University in the US wrote in 2015 that: "Ultimately, we have a strong circumstantial case supporting the theory that someone deliberately introduced smallpox into the Aboriginal population." However, Colin Tatz, in his 2011 book Genocide in Australia: By Accident or Design?, rejects as absurd the idea that the British would have deliberately released a disease in Australia that they had so much reason to fear.

Several historians, while sticking with the traditional diagnosis of smallpox, have remained undecided about how it reached the Sydney region in 1789. In 2020, Professor Henry Reynolds told the ABC that how smallpox got to Sydney remained and might always remain "a real mystery." Also, in August 2021, historian Cassandra Pybus, in a review of Peter Dowling’s 2021 book Fatal Contact: How Epidemics Nearly Wiped Out Australia’s First People, rejected the suggestion that smallpox was deliberately released from the surgeons' "variolous matter" as "very circumstantial." She pointed to "David Collins' observation that the only non-Indigenous person to be affected by the disease was a Native American." She suggested that if the disease was smallpox, "it was more likely to have come from the American whalers who came to and went from Sydney Cove before and during 1788–1789. No one really knows." Dowling, who does not propose the whaler idea, is not satisfied with any explanation of how smallpox first reached the Sydney region. He wrote in 2021 that: "no one author or theory has in the end prevailed over the others. The question of the origin of the 1789 smallpox epidemic among the Australian Aboriginal people has remained unresolved."

The "History Wars" and the Smallpox Debate

The History Wars in Australia involve debates about unfair treatment that Aboriginal people suffered from European settlers. It is likely that these "History Wars" have influenced discussions or investigations of smallpox in the colonial era.

The fact that the three main smallpox outbreaks affected Aboriginal people rather than settlers has not been proven to be due to anyone's deliberate or harmful action. Yet, to some Aboriginal people, it seems to symbolize the many injustices and disadvantages they have suffered. In the view of Dr Mark Wenitong, it is potentially suspicious. Some Aboriginal people and their supporters have implied that they feel the pattern of Australian history will be incomplete until evidence can be found that the smallpox outbreaks were in some way a deliberate plot introduced by British colonists. On the other hand, some supporters of the Macassan or chickenpox theories imply that they see social value or historical fairness in ruling out conspiracy theories. Judy Campbell, for instance, wrote in her book Invisible Invaders that she hoped to help reconciliation by answering an Aboriginal protester who claimed, "You gave us smallpox." Professor Carmody told a journalist in 2013 that another reason for doubting that the 1789 plague was smallpox released by the surgeons was that he had read their surviving records and, "They all struck me as being of really ethical character and I simply can't believe any of them would do that."

What is not in doubt is that the early "smallpox" epidemics caused immense harm to Aboriginal people. They had major effects on the balance of power between Aboriginal people and the colonists. Each of the three best-supported theories about the epidemics may lead to different, yet important, moral criticisms of the settlers' behavior. For instance, if the Macassan theory were proved true, and it was Macassans, not Europeans, who brought smallpox to Australia, it would still be true that it was settlers and squatters from Europe who took advantage of smallpox (and other new diseases) to take over Aboriginal lands. However, if it could be proved that British colonial settlement was made easier in 1789 by a conscious act of germ warfare, the morality and rightfulness of the colonization of Australia would be questioned more severely.