Above is the most celebrated insect illustration – the flea, from Robert Hooke’s Micrographia (1665): a classic of microscopy, it is reproduced in many historical studies. 1665 was the year of the “great plague” in London, but the flea aroused no suspicion then as an agent of bubonic plague spread – nor did it, until the 1890s. It is now common knowledge, purveyed by specialist and popularising works alike, that fleas transmit plague from rats or other infected species to humans. But far from commonly known and sparsely mentioned, are the investigations which elucidated the flea’s role in epidemic plague.
In Asia, outbreaks of plague have probably continued regularly since the fourteenth century “Black Death”. Sylvatic animal reservoirs of infection exist, for instance in gerbils, whose underground habitats serve to perpetuate the disease. (The same is true of ground squirrels in California, where sporadic human plague cases continue to occur.) Even major Asian epidemics were unlikely to excite much European interest, until spread into Hong Kong and India in the late nineteenth century generated huge volumes of literature from plague commissions sent from many European countries. When India and Hong Kong were engulfed, they were seen as extensions of Europe, so a third “world pandemic” was now announced. Prolific sea trade threatened Europe itself, for the first time in over two centuries. It was known that rat deaths coincided with human plague, but nobody causally connected the two until the 1890s. It now seems obvious that fleas jumping from sick rats to healthy humans are likely plague vectors: but experiments showing this were ignored – worse, denounced by the “scientific” establishment, especially in England.
A Japanese physician working in Formosa, Ogata Masanori, demonstrated in 1897 that fleas harboured plague bacilli. The implications for transmission to man were obvious, and should have been further examined immediately. That was not the case, and only one established researcher paid attention. Paul-Louis Simond, working for the Pasteur Institute, in 1897 took over a post in Bombay vacated by Alexandre Yersin (co-discoverer of the plague bacillus in 1894 in Hong Kong), and worked on plague vaccines. The following year he moved to Karachi, and while there, he demonstrated that plague from sick rats transferred to healthy rats in adjacent cages. The most likely mechanism was the flea, which Simond was convinced was the responsible agent. It was an obvious conclusion, given Ogata’s observations: but exact transmission details were yet to be demonstrated, so the flea theory, however persuasive, was still “only a hypothesis”. In 1901, the British Plague Commission in India dismissed Simond’s work, thus:
“It will have become manifest that the process of induction by which Dr. Simond endeavours to establish the proposition that suctorial insects play an important part in the transference of plague from sick to healthy animals is so weak as to be hardly deserving of consideration.”
This was metaphysics, not biology – the key term being “induction”: Simond offered a hypothesis, but suspect French speculation transgressed English methodological Holy Writ, fortified by Newton’s dislike of hypotheses and firmly consolidated by Whewell and Mill in the 19th century. Induction, not hypothesis and deduction, was to be practised (and this orthodoxy demanded that evidence was to be ignored, as necessary).
Meantime, plague was spreading round the world – and it was on its way to Sydney. The Australian and Tasmanian Intercolonial Plague Conference, meeting in Melbourne in April 1900, declared that,
“The danger threatening Australia is more terrible than war.”
Busy port cities all over the world were vulnerable. When plague reached Sydney in 1900, John Ashburton Thompson, president of the NSW Board of Health, accepted the logic of flea transmission. Some human cases displayed signs of flea bites in the lower limbs: as Thompson said:
“I am unable to imagine any plausible explanation ……. which does not include some means of communication between them and the plague-rats which is complete in itself, endowed with locomotive powers, attracted to man by instinct, and more likely to reach this than any other part of the body. These requirements betoken an insect, and the insect which best meets them appears to me to be the flea.”
Thompson managed the outbreak on that basis, but could not prevent politicians from evicting residents of the Rocks area of Sydney, demolishing their houses, and incarcerating so-called “contacts” in quarantine at North Head – measures whose validity were denied by Thompson. When a second outbreak occurred in 1902, Thompson got his way, cutting out such senseless measures – thereby saving a large amount of human distress and public money. A landmark had been passed – twice – namely, management of bubonic plague on what are now recognised as correct measures. But the rest of the world seems to have paid no attention.
In terms of laboratory investigation, the jigsaw piece missing from Simond’s work had been supplied well before 1900, by a young member of the Indian Medical Service, William Glen Liston. Liston’s elegant work involved placing fleas from plague infected rats in tubes sealed with muslin, through which they could bite but not escape: healthy rats were infected by their bites. He also demonstrated that fleas from plague stricken rats had blocked digestive tracts, clogged by proliferating bacilli. Hence, when they bit, instead of sucking blood, they regurgitated plague bacteria into the skin of healthy victims. Astonishingly, the various Indian Plague Commissions ignored his research. He went unrecognised until 1971, when the American Vetinary Epidemiological Society posthumously awarded him its Golden Headed Cane for his pioneering studies: the citation reads,
“On the basis of his work, plague control became possible, thus saving countless millions from this dread disease.”
Thompson, in 1900, was unaware of Liston’s work, but – convinced that Simond was right – he was first in the world to put the correct theory into public health practice. It was, of course, not possible to take wholesale measures against fleas. Rat-catching gangs were paid to hunt down the rodents: but, as Thompson saw, building regulations designed to exclude rats from human habitation were prophylactic, so he instituted appropriate regulations. Likely places where rats might gain entry via openings for pipes – kitchens, bathrooms and lavatories – were required to have thick cement floors, something which persists to this day in our planning laws.
Sporadic outbreaks continued in Australia until 1921, when the last couple of cases occurred in South Australia. In 1900, a Sydney diarist noted “extraordinary devices to prevent [rats] from leaving the ships”. I assume this refers to discs on mooring lines, which, from the diary, seem to have been new at the time, at any rate in Sydney. I’ve been unable to discover whether these were invented here: perhaps a reader can enlighten me.