The outbreak of (Andean) Hantavirus on board the Dutch eco-adventure ship Hondius clearly is a matter of concern; and is not being played well by the experts who tell us one rather soothing thing about it only being transmitted through intimate contact, but then show up in the highest grade of Hazmat suit when evacuating people from the ship.

See this story Where did the hantavirus outbreak start, and where has it spread? from Al Jazeera (11 May 2026) and this Inside Story episode: Should we be worried about the hantavirus outbreak? (Al Jazeera 9 May 2026, and here on YouTube).

We keep hearing about the established history of the virus in southern South America, whereas we need to get a handle on the possibly quite different future of the hantavirus. This zoonotic virus has probably already changed; or it may have found an environment in which it is possible (or even necessary) to behave differently from the way it behaves in its endemic South American setting.

Around 16 minutes into the program, interviewer James Bayes asks: "This particular ship … is not your typical cruise ship. They describe it as an 'expedition ship, often with scientific, wildlife or geopolitics lecturers on board'. … I am told that the experience of previous passengers is that they have very strict safety protocols because of the places they visit, mainly for biodiversity reasons. Previous passengers have recalled sniffer dogs and having to wear sanitised boots. If it can happen on a ship like that, do you have concerns in general? … Are cruises incubators for disease? Would you go on a cruise holiday?" (The subsequent answers, by experts, trivialised this important question.)

The Hondius was as sterile as any ship could possibly be. Could the human-human transmission on board that ship be because of that sterility, rather than despite the sterile shipboard environment? In a sterile environment, a virus which has already infected an embarking passenger has no soil or other muck that it can transmit to; rather, the least sterile life-forms available are the other people on board. Hence an unusually sterile environment may be the counterintuitive cause of human-human transmission of a virus which 'prefers' other options.

Evolutionary variation of any life-form can arise in three ways: because of selection in favour of one existing variant over another; because of a mutation creating a favourable new variant; or because of a hybridisation of two quite different variants creating a genuinely novel form. The first of these three mechanisms of variation may have been enough to create a humanly-transmissible form of the Andean hantavirus. (We note that Covid19 was significant because it was transmitted by a novel virus; transmission of coronaviruses has been widespread throughout our lifetimes.)

This would be a nightmare scenario. Such a new-variant virus – maybe a novel virus – would still be lethal, would still have a long incubation period, would have an unknown duration of infectiousness before symptoms emerge, and an unknown rate of transmission.

The Black Death in Europe: 1346 to 1353

This historically famous pandemic reduced the population of Europe by about forty percent. It is generally attributed to a disease called Plague (aka Yersinia pestis), which comes in several forms, the best known being bubonic plague. The Plague pathogen – Yersinia pestis bacteria – was identified by Alexandre Yersin and Kitasato Shibasaburō during a much more recent pandemic; a pandemic which impacted seaports all around the world in the decade after 1894 (including Sydney and Auckland in 1900).

This disease – linked to rats and fleas – looked like a good fit for the Black Death; the descriptions of the symptoms were a good match. So, the Black Death narrative came to incorporate Yersinia pestis as the culprit. This pathogen is endemic today in some parts of the world, including the southwest of the United States, but generally confines its lethal mayhem to rodents. People die of it most years. The good news for later twentieth century human populations was that bubonic plague is treatable with antibiotics.

However, especially around the early twenty-first century, the 'Yersinia pestis as the culprit' thesis was substantially questioned. (See A plague on all your houses, The Guardian, 14 Aug 2004; I have read Return of the Black Death: The World's Greatest Serial Killer by Susan Scott and Christopher Duncan.) This questioning has subsided of late, because of the discovery of Yersinia pestis DNA in the bodies of known victims of the Black Death. James Belich, author in 2022 of The World the Plague Made: The Black Death and the Rise of Europe, argues that those sceptical narratives were an important part of the scientific process, but settles on Yersinia pestis, based on subsequent DNA evidence.

Nevertheless, I was persuaded by aspects of Susan Scott's argument. She agrees that bubonic plague was significantly present in Europe – especially in Mediterranean ports – in the late 1340s. Essentially, her argument is that there was another disease present at that time in Europe, and that this other disease played a greater role than bubonic plague in the lived experience of pandemic plague in the period from the 1340s to the 1590s. Scott made her argument using village studies which suggested that the three main epidemic parameters – transmissibility (especially from humans to humans), incubation, and duration of infectiousness – were a poor fit for the known information about Yersinia pestis. (We may also note that there is a variation of bubonic plague known as pneumonic plague, which is human-human transmitted, looks a more plausible fit for the 1340s to the 1590s than rat-flea transmission. But the parameters of pneumonic plague don't fit, either.)

In Scott's thesis the principal agent of the Black Death was what she calls Haemorrhagic Plague. It is well known today that there is a family group of lethal zoonotic viruses which cause haemorrhagic fevers in humans; these include ebola and hantavirus. For the vast majority of human cases, they are transmitted to humans from animal incubators. Her argument is that the majority of Black Death deaths were caused by one of these viruses, not by Yersinia pestis bacteria. The parameters she calculated from the historical data match haemorrhagic fevers rather well.

The pneumonic symptoms of the two diseases could be similar (albeit more blue than black). Indeed the 1918 influenza pandemic was known, at least in New Zealand, as the Black Flu. Plague is bacterial, treatable by antibiotics. Haemorrhagic fever is not treatable, except at the margins; it's a viral illness.

We may also note that it's rare to have two simultaneous epidemics. One epidemic of a viral disease tends to pre-empt another viral pathogen. However, simultaneous epidemics – even pandemics – of bubonic plague and haemorrhagic fever seem entirely plausible. Because the pathogens are so different, even if the end states of both diseases are quite similar. And we note that the stresses arising from one lethal illness may create malnutrition and other states of being likely to make us more vulnerable to a second quite different pathogen doing the rounds.

We should also note that, after much trial and error, the Black Plague could be contained by quarantine; isolation for forty days. Quarantines are particularly effective for human-human transmissible diseases. Presumably less effective at containing burrowing rodents (or mosquito-borne diseases for that matter). Rats don’t carry passports.

Warning

Susan Scott was particularly concerned about modern complacency towards the Black Death. The widespread perception in modern infectious diseases studies is that bubonic plague is treatable, and that the rodent-flea transmission mechanism is less plausible in modern more-sterile environments, reflecting the perception that modern cleanliness and bubonic plage are incompatible. (And noting James Bayes' presumption that if hantavirus can transmit human-to-human on a sterile ship, then it must be able to so transmit anywhere.)

There is no complacency towards haemorrhagic fevers such as ebola (hence the PPE); although it's still widely understood to be – in a sense, dismissed as – a 'third world' disease. Susan Scott was concerned that complacent modern public health systems would leave us completely unprepared for a pandemic involving a haemorrhagic virus, such as hantavirus; indeed, I did not sense sufficient concern among the panel of interviewees on Inside Story.

Even if it can be proved that Scott's thesis about the Black Death is completely wrong, then nevertheless her research still represented an important warning to the world about what the next really lethal pandemic might look like. At the very least, the present hantavirus scare should be understood as an important wake-up call.

If we had learned much more about the history of coronaviruses – viruses which were known to have been long-circulating as 'common cold' viruses – after the 2003 SARS1 panic, we might have been much more prepared for the SARS2 Covid19 pandemic in 2020. Scientists should not be too quick to dismiss Susan Scott's hypothesis about the causes of the 'great levelling' event which came to be called the Black Death.

A lethal transmissible disease which is asymptomatic for six weeks, and which is infectious before symptoms occur, is one of our worst public health nightmares. The present scare should remind us of that.

How can we cooperate through pandemics when we are too busy waging hot and cold wars? The 1918 novel influenza virus was forged on the battlefields of France; a hybrid of influenza strains from Asia and America. In the end, it killed as least as many people as were killed on the 1918 battlefields.

We should learn to question prevailing narratives. Experts – whether epidemiologists, economists, or geopoliticians – don't have all the answers; too often they pontificate from professional scripts while ignoring inconvenient evidence. People, especially those with a modicum of power, should exercise their influence with more humility and less sureness.

The world is becoming more vulnerable; too vulnerable for badheads and hotheads and sureheads (such as Christopher Luxon) and bombastic appeasers (such as Keir Starmer) who cannot broach alternative explanations or strategies. These people simply 'double-down' when the evidence is that what they are doing is harmful or counter to their stated objectives.

Pestilence follows deprivation, closed-mindedness, and stupidity. These qualities are not confined to the uncivilised. Our environments fight back, often in ways that we least expect, often in places where we do not look.

Keith Rankin (keith at rankin dot nz), trained as an economic historian, is a retired lecturer in Economics and Statistics. He lives in Auckland, New Zealand.

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