Don’t Count Your Children Until They’ve Had the POX!- the story so far





They’ve had


P O X!




M.B. O’Hare


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© M. B. O’ Hare. 2018.

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Can We Now Count Our Children?
 Part One:
How was the War on Bugs Won?
Part Two:
Whatever happened the Bubonic Plague and what has Chickenpox got to
do with it
Part Three:
The Many ‘Typhoid Marys’
Part Four:
Typhus: Filling in the Gaps
Part Five:
Cholera: The Disease that Inspired Bram Stoker to Write Dracula?
Part Six:
Scarlet Fever Returns: but it is a lot less deadly
 Part Seven:
Don’t Count Your Children Before They Get The Pox
Part Eight:
Would we survive Smallpox if it escaped from a Lab today?
From the Plague to the Pox


 Can We Now Count Our Children?

Whatever happened to the Great Plague of the middle ages; a disease we never had any medical interventions for? Although, back in the day, protection was adopted by visiting doctors who attended the sick – the mask with the beak of a bird was filled with various herb potions and if the afflicted didn’t die from the plague, surely they would have died of fright at the sight of such a vision on one’s sick bed.


Fig. 1: Physician attire for protection from the Black Death by Paul Fürst; Source: (CC-BY), commons.wikimedia. Vaccine added by author.

Now imagine what would happen if the old Plague in its true original colours (the same genes as the original Plague) returned to our modern communities today? Would we begin to die in our millions, or a third of Ireland’s population and the same proportion in Europe be wiped out as before? And bear in mind that as it turns out,  black rats and their fleas may be innocent after all! Therefore, no amount of avoiding them, or cleaning up rat-infested cesspits, would limit the spread of the Plague to-day.


Fig. 2: Rats may be innocent after all! Designed by the author.

As it happens, we don’t need to panic as the actual same Plague that once killed millions has already escaped out into the public at large on a number of occasions not that long ago. And in one unusually fatal case, it not only killed a pet (it is usually cats that get it – but it is still very rare indeed), but it also killed its owner – who unwittingly spread it to the broader community including unsuspecting infants in a day-care centre where she worked and they didn’t even show as much as a sniffle.

Interestingly, as the Plague itself hasn’t changed over the past half a millennia or so, we now find that having something like Chickenpox or Cold sores may actually have a lot to do with why we aren’t currently dying in our millions in more modern times.

Similarly, we could ask: What if Smallpox returned in its old colours? We don’t even have a vaccine any more to protect us! You may remember hearing of the threat of bioterrorist attacks being imminent in the early 2000s, and efforts were made to produce safe and effective vaccines, with rather mixed results on both counts? Again,  as it turns out – there may not be a need for panic as some of the most virulent strains have already escaped – quite by accident – into the public arena. These all originated from several labs and again, the impact was surprisingly minor.

All in all, it looks like we may have become generationally and naturally, immune to these once significantly more deadly pathogens – the Plague and Smallpox. Now we don’t have detailed and accurate mortality data  for the former disease due to it being so old, but we do have such data for the latter disease from London and this is compared to Ireland where official records only began in 1864 – the year after compulsory vaccination was introduced here and elsewhere as seen below:

smallpox London and Ireland compared

Fig. 3: Reproduced from Fig. 5.4. Deaths from smallpox per 1000 deaths from all causes in London, from 1629 to 1900. (Data from Guy (1882) and the Registrar General’s Statistical Review of England and Wales.) in F. Fenner, D. A. Henderson, I. Arita, Z. Jezek, I. D. Ladnyi (1988) – Smallpox and its Eradication. World Health Organization (WHO) 1988. Online here at the WHO website with Irish original data superimposed.   F. Fenner, D. A. Henderson, I. Arita, Z. Jezek, I. D. Ladnyi (1988) – Smallpox and its Eradication. World Health Organization (WHO) 1988. Online here at the WHO website. Irish graph superimposed number of annual deaths since records began in 1864, one year after compulsory vaccination – significantly scaled down to make a comparison with London data. Data derived from “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link.

As you can see from the above graphs, and indeed, clearly illustrated repeatedly throughout this study using graphs and historical sources, when we combine this with our more recent insights into natural generational immunity, we begin to understand how Nature works in much more sophisticated and mysteriously molecular ways than we have hitherto appreciated.

For instance, our history books describe in terrifying detail what can happen when an isolated indigenous community was initially devastated when they had first encountered some foreign and unfamiliar pathogens. Interestingly, these isolated populations were some of the healthiest and fittest individuals and naturally pristine natives.

However, this phenomenon has been studied in more recent times and we can now see that the relatively rapid recovery – over a few generations from such an event – cannot be explained via our current genetic inheritance evolutionary model as this kind of rapid adaptation simply could not have occurred by Darwinian means. Instead, it seems that these communities recovered and became ancestrally resistant to these same pathogens and our more recent molecular insights help explain just how this highly adaptive, rapid robust resilience works.

In summary, Nature appears to have an incredibly long-term memory for such pathogen/host battles of the past – leaving us with something of immense value to pass on silently to our children. Therefore,  even if we had all but forgotten these devastations – thankfully, our immune cells haven’t.

The history of successive onslaughts throughout the generations of some of the deadliest contagions known to humankind is inscribed in the charts presented throughout this study which mainly focuses on Ireland, with comparative data from several other nations, thus, these charts and graphs illustrate, in real time, our shared ancestral battle with the bugs. The overarching picture is that the identified pattern is of a near-simultaneous rise and dramatic decline in death rates from the same contagions for broadly the same timeframe –  is that it is an almost universal phenomenon and follows the natural principle of, what goes up, must also come down.

Thankfully, as this study aims to demonstrate, it would appear that we can now count our children because our ancestors have had the Plague, the Pox and just about everything else that has ever circulated in the past.  Now, isn’t that a relief?

Read on to explore natural immunity within its historical context and the newly emerging molecular science behind it...



How was the War on Bugs Won?

Fig. 1Fig. 4: Comparative scaled charts for all annual number of deaths recorded for all the major epidemic diseases in Ireland since first officially recorded. Charts generated using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright

It is difficult to grasp just how many deaths occurred in Ireland from infectious disease over the course of time. As you can see from the above charts in Figure 4 (showing the relative scale of mortality), some diseases were significantly deadlier than others. Compare, for instance, the annual death toll at its peak from TB to Smallpox which is discussed in greater detail in their relevant topics within this series. Figure 5 shows a range of once that these, irrespective of whether they are viral or bacterial become significantly less deadly, particularly by the mid-20th Century.

Note that some diseases such as Tetanus, Chickenpox, Mumps and Rubella are not illustrated above, as their impact on populations was so minuscule.

Fig. 5: Comparative charts showing the annual number of deaths recorded for many major epidemic diseases – bacterial and viral in Ireland since first officially recorded. Note the significant decline post mid-20th Century. Charts generated using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright

The essential pattern from the above charts is that all infectious diseases became significantly less deadly over time – to the point where they no longer register on the graphs above. This dramatic decline in deaths is not of course peculiar to Ireland, as irrespective of which disease we are talking about, or in which region we are viewing in the developing world for a similar timeframe, this great mountain of historical devastation dramatically declined – essentially, as discussed here, this is without our intervention.

Twentieth Century Mortality Trends in England and Wales

“Infectious diseases have declined to low levels, with the epidemics of the early part of the century no longer occurring”.

Griffiths and Brock, (2003) Office for National Statistics [1]

For comparative graphs to those from Ireland, see Thomas McKeown’s publication for England and Wales: The Role of Medicine: Dream, Mirage, or Nemesis? (1979) [2].  Again, these same type diseases are seen to become significantly less deadly across the board in the U.S. as well as seen in the study, ‘Annual summary of vital statistics: trends in the health of Americans during the 20th century’.

Annual summary of vital statistics: trends in the health of Americans during the 20th century

the beginning of the 20th century, the leading causes of child mortality were infectious diseases, including diarrheal diseases, diphtheria, measles, pneumonia and influenza, scarlet fever, tuberculosis, typhoid and paratyphoid fevers, and whooping cough. Between 1900 and 1998, the percentage of child deaths attributable to infectious diseases declined from 61.6% to 2%.

Guyer et al. (2000)  Paediatrics [3]

For comparative graphs of the dramatic decline of deaths throughout the earlier part of the 20th Century in the U.S.  See: Trends in Infectious Disease Mortality in the United States During the 20th Century (1999) by Armstrong et al, for graphs [4]. Also graphs of the decline of infectious diseases, again relating to the U.S. Infectious Diseases and Human Population History, (1996) by  Dobson and Carper [5].

Certainly, judging by the above graphs and historical records in general, by the earlier part of the 20th Century, our developing nations were becoming significantly safer for infants in particular that they were some decades before. This and a very similar decline in highly infectious diseases for essentially the same diseases are also noted as far north as Iceland corresponding to a comparable timeframe.

The Development of Infant Mortality in Iceland, 1800–1920

The great epidemic infant and child killers of the nineteenth century, such as measles and whooping cough, had lost much of their virulence. Occasionally, they were even successfully coped with in individual places with quarantine measures. By 1920 Iceland had become relatively safe for infants and young children in comparison with the dreadful situation prevailing around the mid-nineteenth century.

Loftur Guttormsson and Ólöf Garðarsdóttir (2002) [6]

What is perhaps more remarkable, is the fact that this common pattern of deaths from once deadlier diseases behaved similarly within nations on the other side of the world such as Australia as indicated in the two excerpts that follow:

Death registration and mortality trends in Australia 1856–1906

The age-standardised rate of all-cause mortality peaked at around 2,000 per 100,000 population in 1860—a year of fearsome epidemics. An important turning point occurred in 1885, after which mortality declined steadily and with less annual variation. The death rate fell from 1,600 in 1885 to under 1,000 in 1906, a fall of one-third over two decades.

Michael Willem de Looper (2014), Abstract, p. iv [7]

Epidemiologic Transition in Australia: The last hundred years

Long-term changes in major causes of death Australia experienced substantial changes in cause-specific mortality over the period 1907 to 2012 … mortality from infectious diseases decreased substantially during the first half of the twentieth century: in 1907, infectious diseases accounted for 16 per cent of the total standardised mortality rate for males and 23 per cent for females, but by 1946 accounted for less than 6 per cent for both sexes, and decreased to insignificant levels by 1960.

Booth,  Tickle and  Zhao (2016) [8]


Fig. 6: Dramatic decline in deaths from some of the greatest killer infectious diseases (mainly affecting children) in the pre-vaccine era.- Ireland (chart generated by A. Parent using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright Fig, 1a: U.S. comparable data. Source: Tavia Gordon, Public Health Reports, (1896-1970), Vol. 68, No. 4 (Apr. 1953), figure. 3.  Link to PDF The charts above compare the actual deaths recorded officially for Ireland since records began with deaths per 100, 000 from the United States. Below are comparable charts relating to the same dramatic decline in these same diseases as recorded from England and Wales for infants and children.

Take for example Figure 6, comparing a few of such major diseases where deaths from these diseases declined throughout the 20th Century in as far-flung nations as Ireland and the U.S. Deaths from the Measles virus or the bacterial pathogens known as: Pertussis (whooping cough) and Scarlet Fever – the other great killers of the 19th and earlier 20th Century – particularly amongst children, similarly plummeted according to a near identical pattern irrespective of the diversity or geographical location of our developing nations.

When we compare the decline in deaths from Scarlet Fever, Whooping Cough (Pertussis) and Measles seen within the above charts from such diverse regions as Ireland and the U.S. with graphs generated from England and Wales, we find once again, a very similar pattern of decline as seen in Figure 7. The only real difference between them all is that of number or rate of deaths annually which of course scales according to population sizes between these respective regions. For instance, if we removed the number individual deaths (as all the Irish charts employ), or the rate of deaths (used by most other more populous nations – per 100,000 or sometimes per million if their population is very large), apart from scale, these graphs would be difficult to tell apart.


Fig. 7: Adapted graphs based upon figures: 4.15 (Scarlet Fever), 4.24 (Whooping Cough/Pertussis) and 4.18 (Measles) showing rates of annual death rates per 100,000 of the population in England and Wales from 1901 – 2000. The shaded area represents post-WWII, after,Smallman-Raynor, M, Cliff, A (2012), Atlas of Epidemic Britain: A Twentieth Century Picture, Oxford University Press, Oxford. p.50, figure 4:18 (Measles); p. 52, figure 4:24 (Whooping Cough); p.49, figure 4:15 (Scarlet Fever).

Regarding the commentary about the above charts adapted for the purposes of this study (Fig. 7), the following statistics corresponds in percentage terms (not actual numbers of deaths as England and Wales would have a much larger overall population size compared to Ireland for the same period) very closely to what we observe in the Irish charts for the same diseases over the same timeframe.

Atlas of Epidemic Britain: A Twentieth Century Picture

A total of 67, 791 deaths from scarlet fever were recorded in England and Wales during the twentieth century, with the overwhelming majority (over 99 percent) occurring in the period 1901-45…
A total of 274,347 deaths from measles were recorded in England and Wales during the twentieth century, with over 98 percent occurring in the period 1901-45…
A total of 233,698 deaths from whooping cough were recorded in England and Wales during the twentieth century, with 97 percent occurring in the period 1901-45…

Smallman-Raynor, M, Cliff, A (2012), pp. 50, 52, 49, [9]

Causes of Death: A Study of a Century of Change in England & Wales

It is interesting that 3%, 2% and 4% of the reduction in mortality rate between 1901 and 1971 was due to whooping cough, measles and scarlet fever, respectively, but none of the decline in the mortality rate after this period. This is because by 1971 the mortality rate from these diseases already was extremely low.

Baillie et al.  (2012), p.6. [10]

This is just an example of the commonality of the decline in deaths over the same period and by similar percentages of certain diseases: Measles, Pertussis and Scarlet Fever across far-flung nations.

Not by our interventions?

In Thomas McKeown’s study dating to the late 1970s, The Role of Medicine: Dream, Mirage, or Nemesis? [11] he proposes, based upon the statistics of declining deaths within the context of our historical record of medical practice, that our medical intervention cannot, for the most part, be the direct cause of this decline – as these interventions came either too late or were not available at all to account for the almost universal decline in deaths from almost all of these once deadlier contagions of the past.

For instance, almost all of the previously more deadly diseases declined most significantly throughout the first half of the 20th Century, where there was a near 99 percent reduction in deaths in many regions as discussed above from the beginning of the 1900s if not earlier in some cases, to almost zero per by 1945 or the end of the Second World War (WWII), a time when antibiotics were only becoming more widely available which could begin combating the deadlier effects of many diseases and some antibiotics came later still depending upon specific infections.

Antibiotics are also only useful in fighting a disease that is bacterial and therefore, even taking into account their relatively late availability, cannot explain in any way for the decline in deaths from viral diseases that are discussed throughout this study. Nor can many of our vaccine or inoculation interventions be correlated directly with either the most significant decline in deaths, or the final demise of all the diseases discussed here as they either came too late – after the fact – or were not implemented at all.

This, of course, begs the question as to what is the cause of such an almost universal phenomenon in terms of the dramatic decline in deaths from some of the most deadly diseases? Scholars such as Thomas McKeown, suggest that other factors such as economics, improved living standards, better nutrition and a cleaner environments (the hygiene hypothesis as it is sometimes referred to) have commonly been offered as possible driving factors in the overall decline in infectious disease, as it now looks very like our medical interventions played a, perhaps surprisingly, small part in the historical and most major decline of deaths throughout the 20th Century – which is essentially the finding of this present study.

However, although this present study broadly supports McKeown’s conclusions regarding the fact that our medical interventions did not directly cause the decline in deaths from infectious diseases throughout the past few hundred years, the evidence that emerged from this present investigation does not support the alternative proposal offered by McKeown and others to account for the significant and often dramatic decline in deadly contagions throughout so many diverse nations for approximately the same timeframe. Their proposal simply doesn’t fit the data, or the historical record when we dig deeper into the context, rise and fall pattern over the course of time for each of the major diseases under discussion throughout this Natural Immunity Series.

This study will offer instead, a natural biological explanation as it relates to generational immunity over the course of time that can explain the almost universal pattern of decline in deaths from some of our most deadly contagions clearly evidenced throughout our nations as they developed into the modern era.

These more recent insights into the dynamic and sophisticated interplay between pathogens and us as their hosts are well supported by the historical record and matches the overall pattern of death statistics in general than either the medical intervention or the hygiene/population dynamics offered by others as an alternative. This present study revisited historical accounts of each of these plagues of humanity in the light of the findings produced from several lines of molecular investigations and found that this matched the data much better than other proposals offered thus far.

References for Intro & Part One

1. Griffiths C and Brock A (2003) Twentieth Century Mortality Trends in England and Wales. Health Statistics Quarterly, Issue 18, pp. 5–17. [Available online as PDF]–18–summer-2003/twentieth-century-mortality-trends-in-england-and-wales.pdf
2 Mc Keown, T (1979) The Role of Medicine: Dream, Mirage, or Nemesis? Basil Blackwell, Oxford [Available online as PDF]
3 Guyer B, Freedman MA, Strobino DM, Sondik EJ. (2000) Annual summary of vital statistics: trends in the health of Americans during the 20th century, Pediatrics. Vol. 106, [6]: pp. 1307-17.
4. Gregory L. Armstrong, G.L, Conn L.A, Pinner, RW (1999) Trends in Infectious Disease Mortality in the United States During the 20th Century, JAMA. Vol. 281 [1]: pp.61-66. DOI: 10.1001/jama.281.1.61
5. Dobson, AP. and Carper, ER (1996) Infectious Diseases and Human Population History: Throughout history the establishment of disease has been a side effect of the growth of civilization, BioScience, 46, Issue [2,] pp. 115–126, DOI: 10.2307/1312814 [Available online as PDF]
6 Guttormsson, L and Garðarsdóttir, Ó (2002) The Development of Infant Mortality in Iceland, 1800–1920, Hygiea Internationalis, An Interdisciplinary Journal for the History of Public Health, Vol. 3 [1] pp. 151 – 176, PDF · [Available online as PDF] DOI: 10.3384/hygiea.1403-8668.0231151
7 De Looper, MW (2014) Death registration and mortality trends in Australia 1856–1906, Abstract, p. iv. PhD Thesis: The Australian National University [Available online as PDF]…/De%20Looper%20Thesis%202015.pdf
8 Booth, H, Tickle, L, Zhao, J (2016) Epidemiologic Transition in Australia: The last hundred years, Canadian Studies in Population Vol. 43, [1–2]: pp. 23–47.
9 Smallman-Raynor, M, Cliff, A (2012), Atlas of Epidemic Britain: A Twentieth Century Picture, Oxford University Press, Oxford. p.50, figure 4:18 (Measles); p. 52, figure 4:24 (Whooping Cough); p.49, figure 4:15 (Scarlet Fever).
10 Baillie, L. and Hawe, E. (2012) Causes of Death: A Study of a Century of Change in England & Wales, OHE (Office of Health & Economics) p.6.
11 Mc Keown, T (1979) The Role of Medicine: Dream, Mirage, or Nemesis? Basil Blackwell, Oxford [Available online as PDF]


Whatever happened the Bubonic Plague and what has Chickenpox got to do with it?

BBC History

‘there were hardly enough living to care for the sick and bury the dead’
…scarcely a tenth of mankind was left alive.
James, 2011, ‘Black Death: The lasting impact’  

A plague tsunami swept across Europe in the year 1348 wiping out more than a third of its population. By the late summer, the Black Death descended upon Irish shores with a particularly harsh impact in the urban centres which took its greatest toll in the dead of winter. Spreading out in a second wave reaching its tentacles beyond to the most desolate hills in search of fresh victims, this plague knew no social boundaries as Nobles, Clergy, Merchants and Peasants either survived the disease – gaining immunity, or succumbed and died.

‘1348: A Medieval Apocalypse – The Black Death in Ireland’

1348 was one of the darkest years in European history. The most deadly of all diseases – the Black Death – swept across the continent reaching Ireland in the late summer. Within twelve months over one-third of the population had died. Towns and villages were abandoned.
Dwyer, 2016. Book Synopsis 

…But, Rats and their fleas may not be guilty after all…

rat heap

Fig. 1: The Grime Reaper Rat on a pile of rat corpses. Illustration of what archaeologists should have found, but didn’t – thus indicating that rats and their fleas may be innocent in being the true cause of the rapid and widespread devastation of the Plague during the middle ages.

Now looking at the archaeological evidence, as it turns out, there is a serious lack of evidence for great heaps of dead black rats.

‘Black Death? Rats and fleas finally in the clear’

…Archaeologists and forensic scientists … have examined 25 skeletons … Analysis of the bodies and of wills registered in London at the time has cast serious doubt on “facts” that every school child has learned for decades: that the epidemic was caused by a highly contagious strain spread by the fleas on rats…
Mortality continued to rise throughout the bitterly cold winter, when fleas could not have survived, and there is no evidence of enough rats… In sites beside the Thames, where most of the city’s rubbish was dumped and rats should have swarmed, and where the sodden ground preserves organic remains excellently, few black rats have been found.
Thorpe, 2014, 

As noted above, we also know that the plague was spectacularly lethal during the winter months and the fleas that are supposed to be the culprits in spreading it via black rats, would not have been able to survive in this late season. Similarly, this was also the case in Ireland judging by the historical records.

‘Unheard of mortality’ The Black Death in Ireland

The plague raged in Dublin between August and December, setting a pattern for the terror it would spread through other parts of the country…
Thorpe 2014, ‘Black Death? Rats and fleas finally in the clear’

So if no amount of cleaning up rat infestations could have curtailed the spread – as the rats and their fleas now appear to be off the hook, what caused such a devastatingly rapid and severe spread of this great pestilence?

A clue might lie in the following. If anyone is old enough to remember actually singing this little rhyme below, having no idea whatsoever what we were singing about, then you might be interested to know what it was all about.

Ring a’ ring a rosies,

A pocket full of posies,

A Tishoo,a tishoo,

We all fall down.

Bugl, 2008, 8, ‘History of Epidemics and Plagues’ 

Apparently, according to Bugl in the History of Epidemics and Plagues’, the common interpretation of the Rosies refers to rosary beads (the religious item used for prayer – presumably in the hope that this would provide protection from the plague and imminent death) and the part of the rhyme when the children hold hands, forming a circle, presumably indicates the ring.

It seems that the pocket full of posies suggests wildflowers to mask the odour of plague victims. However, further research on the medical interventions of the era would indicate that flowers and herbs (posies) may have been used as protection as well. But, perhaps the most interesting part of the rhyme which gives us the big clue, is that last line (the fun part for children if you didn’t know any better, as they all collapse unto the ground in a giggle at the end), relates to a mock sneezing “A Tishoo, A Tishoo,” – which strongly points to the pneumonic (lung) form of transmitting the plague rather than the bubonic means of transmission, as they all fall down after being sneezed on.

As the article excerpt below indicates, the pneumonic and bubonic plague are essentially the same disease; and are simply manifested in different ways within the body.

Risk of Person-to-Person Transmission of Pneumonic Plague

Bubonic plague never spreads directly from one person to another. The bacteria may reach the lungs of people through hematogenous spread… Pneumonic plague is the only form of plague that can be transmitted from human to human.
Kool and Weinstein, 2005

Therefore, the sneezing form (pneumonic) can originate from the bubonic plague by making its way into the lungs via the bloodstream (hematogenous – meaning to spread by the blood) (see below),, as suggested above. This lends greater support to the means by which the Plague could have spread with such initial devastation – now having a way to directly pass from person-to-person. In other words, we do not necessarily require rats and their fleas to explain the wildfire type spread of this disease, at least during the Middle Ages.



1. Producing blood.

2. Originating in or spread by the blood.

Stedman’s Medical Dictionary (2002)

We can now begin to imagine how the Plague could have possibly arisen  and gotten a foothold – at least initially via infected rats in its bubonic form (hence the term Black Death in some cases), and if it had found a way of entering the bloodstream which, we now know is medically possible and common enough judging by modern studies, we can see just how more easily spreadable the pneumonic form (via sneezing etc) would be compared to the rat/flea-borne bubonic plague form – which would have been more easily spotted than the sneezing form.

We could, therefore, suggest that the flea-infested rats may have been the spark, but the uninitiated population (new virgin hosts for the pathogen) provided the kindling and it all went up like a tinderbox as the growing European shipping commerce fanned the flames of the burgeoning metropolitan centres during the Middle Ages.

However, the good news is that, just as rapidly as this devastation spread, it also appears to have burnt itself out almost as swiftly. Seemingly, it had consumed just about all that it could find in its path and those that remained standing would have become immune because of it.

The Black Death in Ireland


Today we have the benefit of hindsight. We know, as fourteenth-century people suspected, that the mortality caused by the bubonic plague of the Black Death was the worst demographic disaster in the history of the world. We also know that the mortality came to an end in the first outbreak soon after 1350; contemporaries could not have known this would happen – so far as they were concerned everyone might well die…
Kelly, 2001, ‘Unheard-of Mortality’ 

As the plague was virtually unheard of after the 1350s in Ireland and most other parts of Europe, one might wonder where it went and would we survive the Plague if it rekindled itself? As it turns out, it did come back within historical living memory as documented for Ireland as we prepared for its reemergence as described below:

1900: Ireland’s last bubonic plague scare

While bubonic plague evokes images of the Middle Ages, Ireland has had more than one brush with the dreaded disease. As recently as the year 1900, ports across Ireland prepared for an imminent outbreak of the Black Death…
…The last great plague scare in Ireland began after the illness broke out in Glasgow in August 1900. Ireland with its constant and frequent traffic with the Scottish port was immediately at risk of infection… As the death toll in Glasgow reached 13 by September 8th 1900, petty politics in Ireland hamstrung preparations to prevent an outbreak… Nevertheless in spite of such attitudes all vessels arriving in Ireland from Glasgow continued to be subjected to rigorous checks. Meanwhile the Glaswegian authorities, not only isolated those who contracted the disease but also those who lived in close proximity to them. This drastically reduced contagion and by the end of September there was a dwindling number of new cases.
Dwyer  2016, ‘1900: Ireland’s last bubonic plague scare’

Fortunately, the new cases began to quickly fade as indicated above, and perhaps it was to do with the containment measures, but more recent outbreaks would suggest otherwise. For instance, modern-day incidences and more recent historical experiences with outbreaks are rather puzzling as the Plague itself, even in its pneumonic form doesn’t appear to have the great impact that it once had. I.e., even if it does escape out into the unsuspecting public, which it has done on a number of occasions in more recent times, it has thankfully turned out to be surprisingly tame.

Plague has received much attention because it may be used as a weapon by terrorists. Intentionally released aerosols of Yersinia pestis would cause pneumonic plague. In order to prepare for such an event, it is important, particularly for medical personnel and first responders, to form a realistic idea of the risk of person-to-person spread of infection…
The disease resulting from direct infection of the airways is usually called primary pneumonic plague. This form would also occur after an intentional release of aerosolized Yersinia pestis…
Since 1925, person-to-person transmission of pneumonic plague has not been documented in the United States. From 1925 to 2003, there were 447 cases of plague reported to the CDC, and 48 developed into secondary pneumonic plague. Thirteen cases of primary pneumonic plague were reported in the same period; 5 of these were caused by cats with plague pneumonia, 1 was associated with caring for a sick dog, and 3 cases were laboratory-acquired.
In 4 cases, the origin of the infection remained unknown (CDC; unpublished data) … None of the contacts of these 61 patients with pneumonic plague seem to have developed the disease.
Kool and Weinstein,  2005  

One of these cases is worth reviewing in order to demonstrate just how tame the plague appears to have become compared to when it was circulating in the Middle Ages. For instance, although its only victim did unfortunately die, it was discovered after the fact that she had the real pneumonic Plague form – (they thought she had actual pneumonia at first as Plague is so rare these days) and it was sometime later when she had already exposed quite a number of people, including small infants in the day-care centre where she worked, that the penny finally dropped when the medical people realised what had just happened. This is described in the excerpted article below:

Discover Magazine

‘Will the Black Death Return?’

On October 2, 1980, a 47-year-old woman from south lake Tahoe, California, lost her 9-month-old pet cat to an acute infection. Three days later, the woman’s own temperature shot up, but she still went to her job at a day-care center. The fever worsened; she developed chest pains and shortness of breath. Two days later she drove herself to the hospital. The diagnosis was pneumonia, and she was treated with tetracycline. Shortly afterward the woman died.
Not until four days later did anyone realize that the woman had died of plague…
….Fearing that treatment might arrive too late, doctors rushed prophylactic antibiotics to the children and staff at the day-care center.. Luckily, no one exposed to the woman fell ill.
Orent, 2001

Under the same conditions of the Middle Ages, those around the infected and caring for the sick died in large numbers and the Plague spread rapidly to hundreds more, leading to thousands and ultimately millions, yet, in our more recent era, it is thankfully a completely different story.

Of course, this then raises the question: well, the plague must have changed somehow, as we know those clever bacteria can adapt very rapidly, unlike our relatively fixed genetic code. Perhaps this wasn’t the once deadly plague? Maybe it had become tamer over the centuries? This very question has recently been answered by extracting DNA from the original once deadly Plague:

Black Death? Rats and fleas finally in the clear’ Discovery Magazine

By extracting the DNA of the disease bacterium, Yersinia pestis,.. [T]o their surprise, the 14th-century strain, the cause of the most lethal catastrophe in recorded history, was no more virulent than today’s disease. The DNA codes were an almost perfect match…
Thorpe, 2014

Just think about that for a moment. This is the same once lethal plague that once killed millions some few hundred years previously and now, even if some mad terrorists release it into the public, we might not even notice that it is the pneumonic form of the Plague at all as no one would have black bubonic type lumps to say otherwise. Of course, this is really good news for most of us – I am sure we wouldn’t all escape, but we simply shouldn’t worry too much about such an event in our day and age.

However, it still doesn’t explain how we became so resistant to such previously deadly contagions like the Plague in the first place, and especially, because it hasn’t changed (genetically speaking) one jot since its devastation of the Middle Ages. A clue lies in the following excerpt.

Scientific America

How Black Death Kept Its Genes but Lost Its Killing Power

The newly sequenced genome of the plague-causing bacterium Yersinia pestis suggests human adaptations are what have kept this disease in check… The global population has likely built up some immunity from centuries of exposure to the pathogen.
Harmon, 2011 ‘How Black Death Kept Its Genes but Lost Its Killing Power’ [Video], 

Seemingly we have become immune over the centuries and the mechanism may lie in a very unlikely source: another friendlier pathogen in the form of some familiar viral characters that most of us have had some experience with over the generations. This is where Chickenpox and its relatives come into the saga of explaining whatever happened to the Plague per se.

For instance, recent molecular studies have revealed something rather surprising about the fate of the once much more lethal Plague. In essence, scientists are now finding that if mice can combat the deadly form of the PLAGUE with common viruses most of us are already infected with, it is quite possible and highly likely, that we do the same.

The Good Thing About Herpes

     The herpes family of viruses can have a surprising upside–it can protect against the bubonic plague and other bacterial contagions, at least in mice. …Nearly all humans become infected with multiple herpes virus family members during childhood. These germs not only include the herpes simplex viruses, which lead to cold sores and possibly genital herpes, but also the diseases responsible for chickenpox and “mono,” as well as several less well-known ailments. Herpes infections have bedeviled animals for more than 100 million years…
…The scientists discovered latent infections with these viruses could protect mice from bacterial infections, including Yersinia pestis, which causes bubonic plague… findings detailed in the May 17 issue of the journal Nature. The herpes viruses spur the immune system to boost levels of a protein hormone called interferon gamma “that in effect puts some immune system soldiers on yellow alert, causing them to patrol for invaders with their eyes wide open and defense weapons ready,” Virgin said. As a result, the bacteria grew more slowly and were less likely to kill the mice.
Choi, 2007

The Herpes family of viruses are, as noted above, very common and most of us already have these living inside us. Essentially, it looks like the host (that’s us) learns to defend itself making it impossible for critters to continue their destruction and it does this by slowing down the virus’ s ability to replicate in the highjacked cells and stave off the worst effects of the bacterial Plague, giving our own immune systems time to respond. The more the immune system does this: the more efficient it becomes and it does this, apparently, via the boosting of our immunity through simple exposure to things such as Chickenpox.

Basically, the Plague bacteria have to adapt or suffer the consequences of our mighty defence. They usually learn to behave themselves and become less invasive and quite tame. This immunity comes essentially from allowing the typically benign childhood disease of Chickenpox, for example, to circulate naturally so that all ages keep boosting their immune systems as you will see in the article below.

As Chickenpox is part of this family that seems to be implemented in the reason why we no longer are dying in our millions from the plague, it may be important to keep it around as it now appears that it is quite important to let it circulate naturally for the reasons outlined below. The article relates to the fact that the UK is considering introducing a vaccine into the childhood schedule to tackle Chickenpox and looking to the experience in the U.S. where the vaccine has been included in the infant and childhood schedule for some time now. The situation in Ireland is somewhat similar to that of the UK as we have never had a routine vaccine given for Chickenpox.

Chickenpox, chickenpox vaccination, and shingles

Chickenpox in the United Kingdom, where vaccination is not undertaken, has had a stable epidemiology for decades and is a routine childhood illness. Because of vaccination, chickenpox is now a rarity in the USA. In the UK vaccination is not done because introduction of a routine childhood vaccination might drive up the age at which those who are non‐immune get the illness (chickenpox tends to be more severe the older you are), and the incidence of shingles may increase. The United Kingdom is waiting to see what happens in countries where vaccination is routine.
…We know that exposure to chickenpox can significantly prevent or delay shingles (by … boosting of immunity)… Increased annual chickenpox rates in children under 5 are associated with reduced shingles in the 15–44 age group. Having a child in the household reduced the risk of shingles for about 20 years, the more contact with children the better, and general practitioners and paediatricians have a statistically significant lowering of risk,.. possibly because of their contact with sick children (teachers did not have a significantly reduced rate)…
If there is less chickenpox in children then there will be no boosting of immunity by exposure to chickenpox for middle and older aged people and thus there will be more shingles, at least until all the elderly have been vaccinated as children but this assumes that immunity conferred by vaccination is lifelong… The greater the chickenpox vaccination rates the higher the initial incidence of shingles would be until everyone was vaccinated (in other words until those of us my age who harbour varicella zoster virus in our nervous ganglia die off). It may be that a less than 100% cover by vaccination might reduce the combined chickenpox and shingles morbidity by allowing the virus to circulate in the population with only minor increases in the age of chickenpox while boosting immunity to shingles…
The extent of decline in vaccination induced immunity to chickenpox over future years is not, of course, known and neither is the proportion of those vaccinated in the USA from 1995 that will become susceptible to “geriatric chickenpox.”
Welsby, 2006, 351-52 


Remember that, based upon the above evidence, all in all, it now appears that no amount of capturing rats and cleaning up flea infestations would have helped reduce the death toll of the disease even in our modern era, as the evidence now strongly supports the black rat’s innocence – along with their flea companions – in being the harbingers of death and destruction during the Middle Ages.

Furthermore, our medical interventions cannot account for the rapid decline of deaths in such a short space of time in most regions as we never had a vaccine to try to eradicate the disease or antibiotics back then. And I don’t think the plague doctors going around with prodding sticks and bird mask with beak filled with herbs and poisons did anything other than protecting them against getting the disease itself – if it protected them at all – we don’t know. Seemingly, the plague resolved itself naturally as there are still cases in parts of the U.S. annually that typically don’t end in death and their contacts are not falling down in their millions after going: “A Tishoo…A Tishoo…” thinking it was a bad cold or the flu that turned to a case of pneumonia.

It looks like Nature has tamed this once much more deadly beast which – although it is the same disease as that of the Middle Ages (genetically speaking) that once killed millions, in more modern times via our exposure to natural viral infections with the Herpes Family over many generations  our defences against the Plague have gotten fairly robust. This seems a reasonable trade-off as it beats having the Plague compared to providing a home for something as benign (for the most part) as cold sores (just don’t go kissing any new-born infants), or childhood Chickenpox.

Perhaps, therefore, we are very fortunate here in Ireland and indeed, the UK and the other regions in Europe where they do not currently have the Chickenpox vaccine along with several boosters in the childhood schedule, as most children still  get the disease naturally, gaining life-long immunity (which is incredibly long compared to the much more variable and significantly shorter immunity we now know that all vaccines studied can offer).

Exposure to the real Herpes Family disease seems a much more beneficial option all round, as having something like Chickenpox, not only seemingly boosts natural resistance to the potential latent virus eruption later in life in the form of fairly painful Shingles but, by allowing the disease to circulate naturally, we also expose children at the appropriate age – thus reducing complications and confer life-long immunity against ever having Chickenpox again. Perhaps, of greatest importance, we may be most fortunate in allowing the Herpes Family of viruses, (of which Chickenpox is one member) to circulate naturally as it seems to be doing a fairly good job at keeping the more lethal impact of the Plague at bay.

So, if the Plague does escape from the lab again, as it has done on a number of cases in the past, try to find some children having a pox party and see if they’ll let you in.

References to Part Two

[1] James, T. (2011) Black Death: The lasting impact, BBC, (17th Feb, 2011).[Available online at]
[2] Dwyer, F (2016) 1900: Ireland’s last bubonic plague scare (5th Jan, 2016), Irish History Podcast [Available online from]
[3] Thorpe, V. (2014) Black Death? Rats and fleas finally in the clear, (30th March 2014). [Available online at],
[4] Thorpe, V. (2014) Black Death? Rats and fleas finally in the clear, (30th March 2014). [Available online at],
[5] Bugl, P (2008) History of Epidemics and Plagues’ p.8. [Available online at as PDF]]
[6] Kool, J.L., and Robert A. Weinstein R.A (2005) Risk of Person-to-Person Transmission of Pneumonic Plague, Clinical Infectious Diseases, Vol.40, Issue 8, (15 April 2005), Pp. 1166–1172, [Available online ]
[7] Stedman’s Medical Dictionary (2002) Definition of ‘hematogenous’,  American Heritage, Houghton Mifflin Company, U.S.A. [Available online at Link]
[8] Kelly, M. (2001) Unheard-of Mortality….The Black Death in Ireland, History Ireland: Issue 4 (Winter 2001), Medieval History (pre-1500), Vol. 9, [Available onlin at]
[9] James, T. (2011) Black Death: The lasting impact, BBC, (17th Feb, 2011) [Available online at]
[10] Findwyer (2016) 1900: Ireland’s last bubonic plague scare (5th Jan, 2016), Irish History Podcast [Available online from]
[11] Orent, W. (2001), Will the Black Death Return?, Discover Magazine, (1st Nov, 2001), [Available online at]
[12] Thorpe, V. (2014) Black Death? Rats and fleas finally in the clear, (30th March 2014). [Available online at],
[13] Harmon, K (2011), How Black Death Kept Its Genes but Lost Its Killing Power, Scientific America, (12th Oct. 2011), [Available online at Video]
[14] Choi, C.Q. (2007) The Good Thing About Herpes, Live Science (16th May 2007), [Available online from livescience]
[15] Welsby, P. D. (2006). Chickenpox, chickenpox vaccination, and shingles. Postgraduate Medical Journal, Vol. 82, [967], pp. 351–352. [Available online].


The Many ‘Typhoid Marys’

Typhoid fever facts, information, pictures | articles about typhoid fever

Typhoid fever is passed from person to person through poor hygiene, such as incomplete or no hand washing after using the toilet. Persons who are carriers of the disease and who handle food can be the source of epidemic spread of typhoid. One such individual gave her name to the expression “Typhoid Mary,” a name given to someone whom others avoid.
 Gale, T. (2006)
Typhoid Fever, Gale Encyclopedia of Medicine, 3rd ed.

But, as it turns out, Mary Mallon, the silent carrier of Typhoid Fever, was not actually as deadly as her infamy would lead us to believe. It is simply that her case was the most publicised at the time.


“Mary Mallon was born in 1869 in Cookstown, Co Tyrone. She emigrated from Ireland to the United States in 1884.

Mallon became the focus of one of the best-known episodes in the history of communicable disease when U.S. health officials identified her as a healthy carrier of the organism causing typhoid fever. Mallon, who refused to acknowledge her role in spreading the disease as a cook, is known to have infected at least 53 people, resulting in three deaths. Unable to stop her from cooking for others, New York City authorities confined her for 26 years…”
Stair na hÉireann/History of Ireland (2014)

I am sure if we could explain to Mary back then (but no one knew at that time), that she simply could not feed anyone uncooked food – no matter how delicious her recipe for frozen peaches was, and still would have been able to maintain herself through work and not spend more than a quarter of her life in captivity with threats of removing her gallbladder.

Mary mostly cooked for wealthy families, some of which she inadvertently infected, and as you will see below, she also infected other well-scrubbed and well-fed individuals such as, doctors, nurses and medical staff at a maternity hospital. Essentially, people who would have had the least exposure from their environment of such a pathogen.

Refusing Quarantine: Why Typhoid Mary Did It

Health officials lost track of her for a few years, but found her again in the midst of another typhoid outbreak, this time at a Manhattan maternity hospital where 25 people, mostly doctors and nurses, were infected. Mary had been cooking there under a fake name, but fled before health officials could catch her. They traced her to a house in Queens, where they had to sneak in through a second-story window, using a ladder, to apprehend her, according to the Times report on the event.
Latson, J (2014) , Time Magazine (Nov., 11th 2014)

In some ways, as tragic as the few deaths were that Mary inadvertently caused, look how many people she infected (particularly the most hygienic health professionals as they probably had managed to avoid such an unhygienic infection up to this point in their lives), and did survive to tell the tale, thus leaving them with immunity from the disease for life. Moreover, her spate of silently spreading the disease to previously unexposed individuals should be viewed in the context of the bigger picture of the devastation the disease itself had caused amongst populations both within Ireland, her homeland, and across the Atlantic.

Typhoid Fever Mortality Ireland

Fig. 1: Chart of the annual number of deaths in Ireland from Typhoid Fever since records for this disease began. Note the dramatic decline throughout the late 19th Century through to the mid 20th Century. Source: Chart generated using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright

When the rate of annual deaths from Typhoid Fever are compared between the U.S. and Ireland we find a near identical decline for a similar timeframe where the main difference is simply a matter of scale. I.e., the U.S. population being much greater than that of a tiny country like Ireland, the proportions of deaths per population from Typhoid would have been similar, but of course the actual total numbers of deaths per year in the U.S would have been in the tens of thousands.

For instance, a graph [4], Figure 16, p. 82, Vital Statistics Rates, Death rates for Typhoid Fever: Death –registration States, 1900-32, and United States, 1933-60, based upon rates per 100,000 population show that at its height,  there were 32 deaths per 100,000 per year starting at 1900 (in a population of a couple of hundred million, that’s a lot of deaths) and declining to less than 20 deaths per 100,000 dramatically dropping from 1910 onwards and from the 1920s, this downward trend continues until deaths from Typhoid Fever becomes very rare by the 1960s.

In Ireland, (See Fig. 1), the deaths per year from Typhoid Fever had become almost a rarity by the 1920s and 30s, with a slight peak in the 1940s and then practically unheard of after this period. The Irish had seemingly won their battle against the disease, as did Americans. In other words, in the scheme of things, Typhoid Mary was a drop in the Atlantic Ocean when it comes to being responsible for the spread of Typhoid Fever in the States.

By the time Mary Mallon had landed as an Irish immigrant on the U.S. shores, deaths from Typhoid Fever were already on the brink of free-fall, suggesting that the vast majority of people were well on their way to becoming immune to the disease already. Almost everyone had most likely already been exposed to the Typhoid, whether they knew it or not, and had become immune for life. This is reflected in the statistical data, indicating that generations had already become resilient and hardened to the disease, making it increasingly more difficult for the pathogen to gain a foothold in these populations as a whole. Was Mary alone in not remembering that she had the disease, or perhaps she was correct when she said she never had any symptoms at all?

As it turns out, she was not the only ‘Typhoid Mary’ type – apparently there were many others just like her, but of course, they weren’t all called Mary. Although her case is certainly the most famous, being a silent, or latent carrier of Typhoid was not actually that uncommon.

Typhoid and Paratyphoid Fever

About 1 in 300 people infected with typhoid fever may have a low-grade infection.
They may not develop any significant symptoms, and then become carriers of the disease’.
Tidy, C. (2018)

That’s not taking into account the ones that were infected but didn’t know it for some time after as symptoms develop late in this disease as also indicated in the rest of the article excerpted above. So you can perhaps begin to imagine how much of the population in both Ireland and the United States had already had exposure to the disease and built up community immunity from having survived it.

This begins to make sense of the steep decline in deaths in both nations over a similar course of time, and how the pathogen was dramatically losing its grip on the population as a whole – it was running out of options to colonise new hosts – fresh victims now only remained in small pockets of previously unexposed individuals. But what if we imaged for a moment that Mary was put on a boat and set out to sea, maybe to keep her company they gathered up all the known silent carriers. ‘Typhoid Mary’ and her merry band of exiles, although, not as lethally infectious in the scheme of things back home, due to so many having already built up resistance, if they happened upon a previously naive native population who had absolutely no immune resistance or experience to these foreign pathogens, their arrival would be devastating, at least initially.

The vessel carrying the bunch of ‘Typhoid Mary’ types, would not be that different from what has been all too commonly documented historically, particularly when explorers and colonisers of the so-called New Worlds of the Americas and Southern Latitudes arrived as silent carriers showing no signs of diseases or particular ill-health themselves, yet little did anyone know until the previously uninfected Indigenous Peoples begin dying in great numbers that what had happened began to sink in – old pathogens within previously exposed and now resilient populations had found new virgin territory to colonise.

Charles Darwin – the great evolutionist, directly quotes and comments on such incidences in relation to his own experience whilst on his adventures to the South seas in the Beagle.

CHAPTER XIX Australia in 1836:

The Rev. J. Williams, in his interesting work, … says, that the first intercourse between natives and Europeans, “is invariably attended with the introduction of fever, dysentery, or some other disease, which carries off numbers of the people.” Again he affirms, “It is certainly a fact, which cannot be controverted, that most of the diseases which have raged in the islands during my residence there, have been introduced by ships; … and what renders this fact remarkable is, that there might be no appearance of disease among the crew of the ship which conveyed this destructive importation.”
This statement is not quite so extraordinary as it at first appears; for several cases are on record of the most malignant fevers having broken out, although the parties themselves, who were the cause, were not affected.
Darwin, C (1839)
In :Alice Bergfeld – Rolf Bergmann – Peter v. Sengbusch BOTANY Online – The Internet Hypertextbook 2004.

Historically, this was an all too common phenomenon, but thankfully, it would seem that most of the world has had experience with many of these much deadlier infectious contagions and they are now incredibly rare, at least in our more developed nations. Interestingly, there is an indication from the literature in general that these same diseases are becoming rarer in less developed nations too. It looks like Nature is on the case and as you will see below, there is strong evidence to suggest they too will soon be looking back at their mortality statistics and seeing a similar pattern of plummeting deaths as we have thankfully experienced now in the developed world.

For example, the article excerpt below describes the historical devastation from Europeans – who were like Typhoid Mary and her band of silent carriers of plague-like proportions as given in accounts from when these new settlers and adventures began to colonise the Americas from the 16th Century onwards. However, it also offers hope, as it describes the natural resilience that can come about from having exposure to such pathogens circulating in general.

Rationalizing epidemics: meanings and uses of American Indian mortality since 1600

Europeans encountered new populations, in Hispaniola and Mexico in the 1500s, in New England and Quebec in the 1600s, and even in Alaska and the Amazon in the 1900s, they witnessed terrible mortality. Epidemics of smallpox, measles, and influenza took the highest toll. These diseases, endemic in Europe, had not been present in the Americas before European arrival. Europeans, exposed as children, developed immunity that protected them as adults. American Indians, without this immunity from prior exposure, and stressed by the chaos of European colonization, were dangerously vulnerable. They died in great numbers…
 Jones, D.S. (2004)
Rationalizing Epidemics: Meanings and Uses of American Indian Mortality since 1600. Cambridge: Harvard University Press, p. 26

The above excerpt reveals that seemingly, the Europeans themselves, due to exposure as children had become rather resilient to such previously devastating plagues, to the point where they all became ‘Typhoid Mary’ types, and although it was initially devastating to the previously unexposed natives, there is actually a positive side to this story as that surely, if the Europeans had become immune generations before, then so could the natives themselves. The Europeans would have once been in the same boat generations before. The article excerpt below lends some support to this idea:

Immune Aspects of First Contact Epidemics

Isolated island populations were clearly subject to disastrous outcomes when new infectious diseases were first introduced, but this often did not extend to subsequent epidemics by the same pathogen…
Mathematic models make it clear that whatever the reason the extreme mortality rapidly decreased after the first-contact epidemics on Pacific islands, it was not due to Darwinian selection of disease-resistance genes. The time interval of only 2–3 generations is simply too short to involve such putative disease-resistance genes.
Shanks, G.D. (2016)
Am J Trop Med Hyg. 2016 Aug 3; 95(2): 273–277. doi: 10.4269/ajtmh.16-0169
Lethality of First Contact Dysentery Epidemics on Pacific Islands

We have only in more recent times began to gain more insight into just how adaptable and responsive the immune system actually is. Seemingly, just about every living thing can rapidly respond and defend itself from danger and threats, particularly disease, without having to wait around for millions of years in hope that we might end up with the lucky genes that will save us in the end. In other words, as indicated in the excerpt above, adaptation and resistance to disease can be handed down through generations and goes directly against our current dogma of genetically-driven adaptation as the following excerpt title highlights:

Your Immune System Is Made, Not Born

New research dispels the belief that the strength of the body’s defense system is genetically programmed
…genes themselves need instructions for what to do … Those instructions are found not in the letters of the DNA itself but on it, in an array of chemical markers and switches, known collectively as the epigenome, that lie along the length of the double helix. These epigenetic switches and markers in turn help switch on or off the expression of particular genes. Think of the epigenome as a complex software code, capable of inducing the DNA hardware to manufacture an impressive variety of proteins, cell types, and individuals.
Landhuis, E. (2015)

You see, Nature may not be in the business of only allowing the fittest to survive, but ensuring that we all survive via a very different flexible non-genetic epi-genetic code and one of the ways this is done in via our mothers.

Immune Priming: Mothering Males Modulate Immunity

Non-genetic transfer of immunity from mother to offspring is a well-recognized phenomenon known as transgenerational immune priming. Mammals, for instance, exchange immunological information on abundance and composition of pathogens to offspring via the placenta and antibody-rich mother’s milk…
The paradigm is that offspring who are destined to be raised in a similar disease environment to their mothers will benefit from a maternal enhancement of offspring immunity that reflects the current environmental challenges.
Keightley M.C., Wong B.B.M, and G J. Lieschke (2013)

It also now looks like we can inherit this hard-fought-for immunity, not just from our mother’s directly, but from their mother’s and perhaps generations of mothers before them as suggested by the following study – at least in pigeons.

Grandmothers can pass immunity to their grandchildren, at least in pigeons

At the moment of birth, a newborn leaves behind its safe protective environment and enters a world teeming with bacteria, parasites, viruses, and infectious agents of all sorts. However, the babies do have one trump card: antibodies and immune compounds passed across the placenta from their mothers. These short-lived molecules can dip into mom’s immunological experience to protect the newborn until the immune system gets up to speed. Now, a new study in pigeons suggests that some baby birds owe their early immunity not just their mothers, but to their grandmothers as well.
…previous research has suggested that these early maternal immune compounds may have “educational effects” on the newborn’s developing immune profile—that they may somehow be priming the system to be on the lookout for common local diseases or parasites…
Shultz. D (2015)

In other words, it is now looking quite likely that our immune systems can memorise past battles with pathogens – epigenetic imprinting which is generational – i.e. these adaptations can be inherited along with your genes and we can pass those experiences and expertise gleaned from the battles to our offspring.

You see, your immune system, as we are coming to appreciate in more recent times, as we gain more insights into tiny biochemical and molecular world beyond the relatively fixed and unchanging genes, is just as clever and flexible as the pathogens themselves.  Most of us have heard of antibiotic-resistant strains of bacteria and how bugs can become superbugs due to their rapid adaptation to our efforts to eradicate them? Well, our immune systems also adapt rapidly to pathogens, it is just that we are more complex and bigger than bacteria so it might take us a few generations for the whole community to become robustly immune as suggested by the mathematically model study highlighted earlier.

Unfortunately, there are casualties, particularly when a pathogen that our immune systems are not familiar with gains a foothold, as illustrated by the large number of deaths from Typhoid Fever in the earlier days since records began as seen in the Irish chart and discussed for the U.S. Our immune systems are built to adapt to and withstand all sorts of pathogens as illustrated so clearly, not just in the mortality charts for Typhoid, but for all the other highly infectious disease that were once significantly more deadly as the record clearly shows.

Therefore, it seems that the more the immune system is exposed to the pathogen, directly, or indirectly as it silently circulates in the natural background (bear in mind that the Typhoid causing pathogen never went extinct, it is still with us today), the more adept our immune system becomes at defending us. In effect, each exposure – even if we are not sometimes aware of the pathogen circulating, trains and educates our immune systems to deal with just about everything in the end.  And now, it looks like this immunity is not just for life if you survive the ordeal, or even have to experience the disease directly to gain general resistance,  but that immunity may be inherited as well.

And just one more point on this long-term, non-genetic generational immunity. This means that there is hope for us even today, if for some reason one of these much deadlier contagions did erupt out into our modern-day world (perhaps via an intentional bioweapon), we may not have to fall about dying to build up community immunity all over again. This is supported in the following excerpt, which suggests that the disease doesn’t even need to be circulating in an obvious way for us to still build up and retain resistance to it. In other words, we may have now forgotten those diseases, but our immune systems have not.

Rethinking the Origin of Chronic Diseases

Some modern-day diseases reflect the capacity of organisms to “memorize” responses to external signals and transmit them across generations; …
 the original causative agent may not be extant today, but “memory” of the infection has persisted.
Shoja, M.M  et al, (2012)
BioScience, Volume 62, Issue 5, 1st May 2012,

So perhaps now you might see Mary Mallon’s story with a slightly different lens when we realise that being exposed to pathogens, in the broader scheme of things, although tragic for the few that lost their lives, there is actually a positive aspect underlying this means of infection via a healthy silent carrier of the disease.

It seems that we have our ancestors to thank for taking the greatest hit for us. Recall that each person who Mary infected (remember most survived), not only gained life-long immunity, but they gained something of even greater value – generationally immunity that they could then pass on to their own offspring for the future. We are that future.


References to Part Three

[1]  Gale, T. (2006) Typhoid fever facts, information, pictures, Gale Encyclopedia of Medicine, 3rd ed. [Available online]
[2]  Stair na hÉireann/History of Ireland (2014)  1938 – Death of Mary Mallon (Born in Cookstown, County Tyrone), Also known as Typhoid Mary [Available online]
[3Latson, J (2014) Refusing Quarantine: Why Typhoid Mary Did It, Time Magazine (Nov., 11th 2014) [Available online]
[4], Grove, R.D. and Hetzel, A.M.  (1968) Vital Statistic Rates in the United States, 1940-1960, U.S. Department of Health Education, and Welfare Public Health Service, Washington D.C. National Centre for Health Statistics (Figure 16, p. 82 Vital Statistics Rates, Death rates for Typhoid Fever: Death –registration States, 1900-32, and United States, 1933-60), [Available Online].
[5] Tidy, C. (2018), Typhoid and Paratyphoid Fever [Available online]
[6] Bergfeld, A, Bergmann R. and Sengbusch, P.V. (2004), Charles Darwin (1839), CHAPTER XIX :Australia in 1836,  BOTANY Online – The Internet Hypertextbook 2004.[Available online]
[7] Jones, D.S. (2004)  Rationalizing Epidemics: Meanings and Uses of American Indian Mortality since 1600. Cambridge: Harvard University Press, p. 26
[8] Shanks, G.D. (2016) Immune Aspects of First Contact Epidemics, Lethality of First Contact Dysentery Epidemics on Pacific Islands, Am J Trop Med Hyg. Vol. 95 [2], pp. 273–277. doi: 10.4269/ajtmh.16-0169 [Available Online]
[9] Landhuis, E. (2015), Your Immune System Is Made, Not Born, Discovery Magazine (Jan., 29th 2015)  [Available online]
[10] Keightley M.C., Wong B.B.M, and G J. Lieschke (2013) Immune Priming: Mothering Males Modulate Immunity, Current Biology, Vol. 23, [2] pp. 76-78 [Available online] doi:org/10.1016/j.cub.2012.11.050
[11Shultz. D (2015) Grandmothers can pass immunity to their grandchildren, at least in pigeons, (Nov. 10th 2015), [Available Online]
[12]Shoja, M.M  et al, (2012), Rethinking the Origin of Chronic Diseases, BioScience, Vol, 62, [5], [Available online]


Typhus: Filling in the Gaps

Typhus’ Rise to Prominence

Typhus deaths Ireland

Fig. 1: Chart of the annual number of deaths in Ireland officially recorded from Typhus Fever since records began for this disease. Note the large spike at the beginning.  Source: Chart generated using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright

The death toll from Typhus may have been significantly greater prior to 1864 in Ireland. This is indicated by the rather large spike at the beginning of the graph above (Fig. 1). This spike accounts for some 2000 officially recorded deaths from Typhus and may just be the tip of the iceberg, or, in other words, the very tame tail-end of a much more devastating disease of the decades preceding it.

For instance, as Peterson has suggested  –

“…Mortality is incredibly high under epidemic conditions, nearing 100%…” (2018, 156) [1].

– and now we can perhaps begin to make a stab at the real impact of Typhus preceding 1864 by applying the estimates given in the following for what seems to be Ireland’s first major encounter with epidemic Typhus going back to 1816.


Typhus had been recognized in Ireland as early as 1652, but it was not until 1816 that a major epidemic of the disease produced 700,000 cases out of a population of 6,000,000. Three more major epidemics thereafter, in 1821 and 1836, accompanied harvest failures.
Conlon, J. M., (2007, 13)

In an attempt to fill in the historical gaps, we can extrapolate the proposed fatality rate from Typhus (see Peterson, 2018, 156) and apply it to the figure of well over half a million cases estimated for the initial devastation of the 1816 Irish epidemic. Now, in the context of a total population of about six million, this means that Typhus may have been much more deadly than previously recognised. Almost one person out of every six of the entire population of six million had seemingly been infected and most of them probably didn’t survive. This begins to echo the scale of deadly impact within a naive population that is unfamiliar with a particular pathogen as discussed previously.

However, as also discussed thus far, in the case of any previously unexposed population, as devastating as a population’s initial encounter with an unfamiliar pathogen, it also appears to be the case that these same populations rapidly adapt to even the most deadly of pathogens and within a few short generations, become effectively resistant, and ultimately immune – via general background exposure (rebalance has been achieved perhaps?). ( See, previous discussion here).

Typhus, it seems, is no different as we are encouraged to see that when we look at the official data of recorded deaths annually in Ireland from this once mighty pathogen, we can clearly see that the annual number of deaths dropped dramatically from around 2000 deaths to an average of 500 deaths annually after the large spike of 1864, followed by a little rise again and then its fatality within the population as a whole becomes significantly less throughout the rest of the 19th Century. Finally, deaths from Typhus becomes a rarity by the first quarter of the 20th Century, never to be heard of again in this country (Fig. 1).

Once again, we seem to be looking at a natural rise and fall pattern of deaths from a previously much more deadly contagion. This is well supported by the historical accounts of the disease as you will see throughout the discussion that follows. But first, we will explore some other proposals, that are commonly offered as explanations for such devastating epidemic outbreaks and their ultimate resolution.

One suggestion is given above (see Conlon, 2007, 13),  in terms of the disease coming in most fiercely on the back of harvest failures. This would seem a reasonable suggestion, however, when we drill down to the details, it doesn’t quite stand up to scrutiny as history has shown as argued by Dirks 1993, and Carmichael 1983:

“It should be pointed out that recent research has questioned the widely held assumption that malnutrition inevitably leads to increased susceptibility to infection.” (in Mokyr, J., and Ó Gráda, C., 2002, 21). [3].

This insight is further reiterated by other researchers who have concluded something similar regarding this widely held assumption, and also support the general proposal presented here in pointing out that the pattern of disease can best be explained from a biological perspective:

Famine, Mortality, and Epidemic Disease in the Process of Modernization

Chambers carried his case to the point of questioning the medical concept that under-nutrition and malnutrition interfere with the ability to resist infectious contagion, acknowledging, however, that nutritional deficiencies will exacerbate endemic illnesses …
Since European famines were not invariably followed by serious epidemics, it is possible that plague and similar crises of public health were essentially biological in origin and not directly related to problems of subsistence.
Thus Fernand Braudel has stated that “every disease has its own autonomous life, independent of the endless correlations” historians suggest, and that correlations with economic crises are “at most only minor accidents in a history linked with other factors”…
Post, J.D., (1975, 14)

As highlighted above, seemingly outbreaks of any of the major contagious diseases within such widely disparate regions, do not necessarily correlate with famine, crop failures or malnutrition in general when viewed together and within the broader context of the impact and spread of the disease itself.

For instance, famines or crop failures are noted a number of times as occurring within Ireland at around the same time as various epidemic eruptions, including such diseases as Typhus (See Creighton, 1894) [5]. However, as highlighted above, this may not actually be causal to either its rise or its demise, but merely a coincidental historical observation.

For instance, the United States did not have any particular crop failures when it experienced its first major Typhus outbreak of the 1830s, around the same time as Ireland was experiencing its own Typhus epidemic, nor did many parts of Europe that experienced near-simultaneous Typhus outbreaks have corresponding widespread crop shortages.

Now, take, for example, London (see excerpt below), where it also seems that although a major Typhus epidemic was underway at around this time as the Irish epidemic of the 1830s,  crop failure is not the main factor in its eruption or spread?

Health and Hygiene in the Nineteenth Century

In the 1830s the “new fever,” typhus, was isolated. During its worst outbreak, in 1837-38, most of the deaths from fever in London were attributed to typhus, and new cases averaged about sixteen thousand in England in each of the next four years.
Douglas, L., (Victorian Web, 11th Oct., 2002)

Another example that famine wasn’t a major factor in, or direct cause of, the rise of Typhus is highlighted in the following in relation to Scotland, which experienced the same type of epidemic Typhus of the same general period and experienced fairly large death tolls as Ireland; yet, as the excerpt points out:

A History of Epidemics in Britain, Volume II

“The increase of fever in Glasgow,” says Cowan, “during the seven years prior to 1837, had taken place, not in years of famine or distress, but during a period of unexampled prosperity, when every individual able and willing to work was secure of steady and remunerating employment.
Creighton, C., (1894, 191)

The evidence presented above lends good support to the idea that Typus was what we would call pandemic, i.e., it hit a great many nations, on different continents of the world, at about the same time, with a similar virulence. Thus, a localised crop failure in one region cannot possibly explain the similar eruptions in other nations not suffering a similar plight.

Therefore, as resultant malnutrition are not necessarily linked directly to massively increased deaths from highly infectious diseases such as Typhus, instead – perhaps indirectly, the common body louse has been implicated in the disease – and by association – its spread as indicated below:

Epidemic Diseases of the Great Famine

It is now known that the vector of fever was not famine, nor social distress… but pediculus humanus, the human body louse.
Geary L., (Spring 1996, History Ireland Magazine)

Does that mean that crowded conditions and lice infections were the cause? Perhaps not entirely either, as another historical reference suggests.

A History of Epidemics in Britain, Volume II

The lesson of the history is unmistakable: with all the inducements to typhus from neglect of sanitation in the midst of rapidly increasing numbers, there was surprisingly little of the disease…
Creighton, C., (1894, 167)

It is therefore fairly unlikely that this pattern of disease within populations can be directly caused by any of the main factors that we would normally attribute to such spread and high mortality from such contagions.

The idea that neither famine, starvation, nor necessarily overcrowding and generally lousy conditions can fully explain the initial devastation of Typhus in its plague-like devastation is further supported by the evidence emerging from historical accounts of what is often referred to as the Great Irish Famine of the mid-1840s. (it was much more socially and politically complex than simply crop failure, but that is another story).

For instance, the estimates of deaths from Typhus at this time from the so-called famine relief workhouses (that kept fairly comprehensive records for the main famine years) are rather low relative to the high mortality from all the other famine-related causes of death – particularly, considering that the workhouses would have been hotbeds for body lice makes the following figures even more surprising.


Approximately 190,000 Irish citizens died from typhus contracted in the louse-infested workhouses they were forced to inhabit….
Conlon, J. M., (2007, 13)

No other circumstances should have been more conducive to encouraging the ravages of Typhus and other widely infectious diseases than this. But, as suggested in the figures given above (almost 200,000 deaths from Typhus over the course of the few years of the Great Famine which, broadly speaking would average out to less than 50, 000 deaths from Typhus over each of the famine years), is still significantly lower than the estimated death toll for the initial epidemic of 1816 (perhaps as much as half a million in a single outbreak) when living conditions were significantly better than during the Famine years of the mid 1840s onwards.

In other words, it looks like the later outbreaks of Typhus – (post-early 1800s), the widespread Typhus pandemics of the 1830s, and onwards until the Great Irish Famine era (even at the height of great famine,  pestilence and recorded louse infestations) and certainly after this point, Typhus, as a harbinger of near-certain death in the early days to an estimated one in every six of the entire population of relatively healthy and hardy people, had become increasingly tame over the decades that followed; even during the nation’s most dreadful famine years of the mid to late-1840s.

Indeed, there are historical accounts that support the taming of this once more deadly disease of Typhus, as supported in the following:

A History of Epidemics in Britain, Volume II

It was from 1830 to 1834 that a change in the reigning type of fever began to be remarked in London, Dublin, Edinburgh and Glasgow, the new type becoming more and more evident as fevers became more prevalent in the ‘ thirties ‘ and ‘forties.’
Relapsing Fever the common type in 1847, …
Mayo and Galway, and in Gweedore, Donegal, not more than one in a hundred cases of relapsing fever proved fatal. In Limerick the mortality was ” very small.” In many places it is given at three in the hundred cases, in some places as high as six in the hundred. When deaths occurred, they were often sudden and unexpected…
Creighton, C., (1894, 189)

Relapsing Fever as it turns out is actually the less lethal form of Typhus and it is notable that this phenomenon is near-simultaneous – from the 1830s onwards – throughout many regions, including  Ireland. The fatalities indicated in the excerpt above for those that got the relapsing form of the fever are significantly less (one or as many as six per hundred of cases of the disease and the cases themselves do not seem to be that many) than those estimated for the initial 1816 epidemic.

Interestingly, although communities were finally starting to sigh a breath of relief as Typhus (relapsing fever) was seemingly becoming less deadly, after the mid 19th Century, people on the ground – so to speak, were beginning to feel its replacement in the form of another contagion: namely, Enteric Fever, which is another name for Typhoid Fever (see previous article here) as referenced below:

A History of Epidemics in Britain, Volume II

The cases of enteric fever increased decidedly after 1865… ….The disappearance, during the last twenty years, of typhus and relapsing fevers from the observation of all but a few medical practitioners in England, Scotland and Ireland, is one of the most certain and most striking facts in our epidemiology.
…Still more recently, the relative proportions of typhus and enteric fever have been reversed, so that there have been years with little or no typhus but with a good deal of enteric fever… Typhus declined, and typhoid rose…
Creighton, C., (1894, 202)

Typhus and Typhoid deaths Ireland compared                              

Fig. 2: Chart of the annual number of deaths in Ireland from Typhus Fever (black) compared to the annual number of deaths officially recorded from Typhoid Fever (light grey and translucent) in Ireland since records for these diseases began. Source: Chart generated using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright

Figure. 2 above, clearly shows this rise in deaths of Enteric Fever (Typhoid) as deaths from Typhus decline. Now we know why the deaths from Typhoid Fever were only recorded from 1881 onwards, as Typhoid hadn’t much hope of getting in while Typhus was wrecking havoc. It also puts the comparatively small number of deaths from Typhoid annually in Ireland into some sharp relief when we begin to calculate the estimated mass devastation that Typhus seems to have caused at its height – prior to when official records began. The graph above (Fig. 2) also clearly illustrates the dramatic and ultimate decline in deaths from both diseases in the end.

This historical investigation into the fate of Typhus revealed that this once mighty disease soon lost its grip throughout much of the 19th Century in Ireland and elsewhere and this is strongly indicated by the historical estimates as well as the documented observations of a  shift from the more deadly form of Typhus to what came to be known as relapsing fever (the less deadly form). This evidence is indicative of natural resistance to the pathogen due to exposure over generations, even in the greatest years of hunger and destitution, which finds further support in the excerpts that follow.

A History of Epidemics in Britain, Volume II

… The best illustrations of the greater severity and fatality of typhus among the well to do come from Ireland, in times of famine…
But it may be said here, so that this point in the natural history of typhus fever may not be suspected of exaggeration, that the enormously greater fatality of typhus (of course, in a smaller number of cases) among the richer classes in the Irish famines, who had exposed themselves in the work of administration, of justice, or of charity, rests upon the unimpeachable authority of such men as Graves, and upon the concurrent evidence of many…
Creighton, C., (1894, 189)

This historical excerpt begins to explain the possible reason why the death toll was not much more massive during the Irish Famine of the 1840s, as it seems that most of the Irish who were impacted the greatest by malnutrition and just about everything else that could be thrown at them, were for the most part, essentially resilient to Typhus’ worst effects  (and those that did survive had to face the onslaught of  an unfamiliar pathogen that was implicated in Typhoid).

On the other hand, as reiterated below, those who were the least exposed to such conditions – the most hygienic, best-fed and generally healthiest individuals – the professionals and philanthropists trying to care for the destitute Irish, were the most vulnerable to Typhus’ worst effects.

Epidemic Diseases of the Great Famine

“During the Great Famine, relapsing fever was the prevalent disease among the general population, while the higher social classes tended to contract the more deadly typhus fever, especially those who were most exposed to infection, notably clergymen, doctors, members of relief committees and those connected with the administration of the poor law. The mortality rate from typhus was also more pronounced among the middle and upper classes than it was among the poor, who may have developed some immunity through long-term exposure”.

Geary L., (Spring 1996, History Ireland Magazine)

It seems that it is the less well-washed and most exposed to body lice populations that were able to build up the most formidable resistance to the disease, whilst, unfortunately, it was the people who had the least resistance that ended up with the poorest immunity, those with the greatest intentions, that ended up more frequently with the decidedly deadlier form of Typhus than those they were trying to help.

The key point from this historical investigation is that it is obviously quite important to be exposed to such pathogens in the first place in order to build up familiarity and ultimate immunity, particularly as our ancestors have seemingly already taken the hit for us. Thus, by not being too squeaky clean and allowing a little clean dirt into our lives, we are actually building up robust resistance to all sorts of pathogens – whether we know it or not.

Remember, just like the pathogen that appears to trigger Typhoid or, the pathogen implicated in the Plague, these microbes never actually went anywhere – they still exist all around us today and can, very occasionally, find a little chink in our armour. And particularly under extreme conditions that can and have sometimes erupted in later history into sporadic epidemics – but nowhere ever on the scale of previous times. Nor, has the common body louse and its own particular parasite that is supposed to be the main cause of  Typhus gone extinct  – it still exists today.  

So, obviously, it helps not to invite the return of such critters to test just how robust our ancestral immunity may actually be, but, as we generally do not – thankfully – hear much about Typhus in our own developing nations these days, perhaps we are more generationally resistant to it than we realise. At this stage, after two major world wars and the amount of travelling that we have done over the past few generations, I would say that our immune systems are all pretty much now familiar with the Typhus pathogen. The fact that we do not often hear about the disease, is probably due to our immune systems doing such a good job all these years. Long may it continue. And presumably, the less developed nations currently having their own battle with such pathogens, as we once did not that many generations ago, will soon follow suit in terms of their own more robust immunity.

Hopefully, this has filled in some of the gaps in our knowledge regarding Typhus.

References for Part Four

[1] Peterson, K.D., (2018) Typhus, Entomology Group Insects, Disease, and History, Montana State University, p.156. [Available online]
[2] Conlon, J. M., (2007) The Historical Impact of Epidemic Typhus, Entomology. Montana Education, History of the Bug, p. 13. [Available Online Google].
[3] Mokyr, J., and Ó Gráda, C., (2002) Famine Disease and Famine Mortality: Lessons from the Irish Experience, 1845-50. in: eds., Tim Dyson & Cormac Ó Gráda. Famine Demography: Perspectives from the Past and Present, Oxford University Press, p. 21. [Available Online]
[4] Post, J.D., (1976) Famine, Mortality, and Epidemic Disease in the Process of Modernization, The Economic History Review. Vol. 29, [1], pp. 14-37 [Available online at JSTOR.ORG ]
[5] Creighton, C., (1894) A History of Epidemics in Britain, Volume II, Cambridge, University Press. [Available online at ]
[6] Douglas, L., (2001) Health and Hygiene in the Nineteenth Century, The Victorian Web (11th Oct., 2002),
[7] Creighton, C., (1894) A History of Epidemics in Britain, Volume II, p. 191, Cambridge, University Press. [Available online at ]
[8] Conlon, J. M., (2007) The Historical Impact of Epidemic Typhus, Montana Education, History of Bugs. p. 13 [Available online as PDF from ]
[9] Geary L., (1996) 18th – 19th Century History/Epidemic Diseases of the Great Famine.., History Ireland Magazine, Vol. 4. [1] (Spring 1996) [Available online ]
[10] Creighton, C., (1894) A History of Epidemics in Britain, Volume II, p. 167, Cambridge, University Press. [Available online at ]
[11] Creighton, C., (1894) A History of Epidemics in Britain, Volume II, p. 167, Cambridge, University Press. [Available online at ]
[12] Creighton, C., (1894) A History of Epidemics in Britain, Volume II, p. 189, Cambridge, University Press. [Available online at ]
[13] Creighton, C., (1894) A History of Epidemics in Britain, Volume II, p. 202, Cambridge, University Press. [Available online at ]
[14] Geary L., (1996) 18th – 19th Century History/Epidemic Diseases of the Great Famine.., History Ireland Magazine, Vol. 4. [1] (Spring 1996) [Available online ]


Cholera: The Disease that Inspired Bram Stoker to Write Dracula? And a Tale of Two Pathogens 

The Lancaster County Cholera Epidemic of 1854 …

Cholera, which was endemic to India, escaped the subcontinent in 1817, striking Moscow in September 1830. It then spread westward across Europe, reaching England in 1831 and North America in 1832. The pandemic would return to Europe and America in 1849, 1854, and 1866, each time filling the population with terror and revulsion; the mystery surrounding the cause of the disease only exacerbated the situation. Its effects were both rapid and devastating, and death was agonizing to those who succumbed to the disease…
Osborne, J.D., (2009)

A disease that becomes pandemic (impacts nations world-wide often with deadly impact) is obviously one that can be passed from person to person. And Ireland, on the edge of Europe, was certainly not immune to Cholera’s devastation as highlighted in the following excerpt:

Why does cholera have such a reputation?

Cholera was once one of the biggest killers in Irish society. The 1832 epidemic killed 30,000 people… Folk memories of the cartloads of bodies during the 1832 epidemic helped inspire Bram Stoker to write the novel ‘Dracula’.
MedMedia Group (2018)

30,000 deaths in a single Cholera outbreak of the 1830s pandemic in Ireland (the first and seemingly, the worst), although not as major in terms of the death toll estimated for the initial impact of Typhus in the early days (which could have been well over half a million in a population of only 6 million), is still a massive impact to a community of several million at this time. Take, for example, just one well-documented experience within a single county in the whole country of Ireland, as outlined in the following:

The Sligo epidemic that stoked Bram’s interest in all things

Stoker’s mother, Catherine Thornley, came from Sligo town, and witnessed at first hand the devastating cholera epidemic that swept the county in 1832. Bram — or Abraham, as he was christened — would avidly listen to Catherine’s sobering accounts of what she had witnessed in Sligo before he was born…
And Stoker experts believe Catherine’s vivid descriptions of the suffering she had seen stayed with young Stoker and helped fuel his macabre novel later on in life…
It’s not known how it started but the first signs of the disease were noted shortly after a heavy thunderstorm. A market was being held that day and thanks to the large concentration of people in a comparatively contained space, it struck with a brutal swiftness.
A farmer was infected as he mounted his horse on one side of the town and was dead by the time he reached the other. Another man who attended the funeral of an employee in the morning became ill during the burial and was dead by evening. One family saw six of its members die in the course of a single night. The death rate was so rampant that carpenters ran out of wood for making simple coffins and the dead had to be wrapped in pitched sheets and rolled into mass graves.
Local legend has it that some people were buried alive, so great was the haste to dispose of the corpses. The scenes at night around Sligo only served to heighten the sense of dread in the town. Tar barrels were lit in the streets in a misguided attempt to purify the air…
Doctors valiantly attempted to stem the outbreak, and had to contend with widespread ignorance about the disease. There was also suspicion that the medics themselves may have brought the disease upon the town — they had conducted tests on the water to see if the epidemic had started there, and word spread that the water had been tampered with. Even when five of the doctors contracted cholera and died, the allegations continued.
Some 15,000 people were forced to flee the county and it is thought more than 1,500 people died from the epidemic. The events of 1832 would scar Sligo for generations, and the suffering of those who survived would be exacerbated by the Great Potato Famine, which struck just 13 years later.
John Meagher, J., (Independent, Apr., 22nd 2012)

The most revealing part of this narrative is perhaps the swiftness of the spread of Cholera – seemingly person to person – with no particular trigger such as the locals all drinking contaminated water (note that Cholera is supposed to be a waterborne disease). We have other historical documentation to support this very point as seen in the excerpt below. It relates to a later pandemic of 1854 as Cholera broke out in a small pocket of Columbia, U.S.

The Lancaster County Cholera Epidemic of 1854 and the Challenge to the Miasma Theory of Disease

September 6, 1854, when two German immigrants, sick with cholera, were left at the railroad terminus in Columbia while their party continued west. The men died the next day. Four Columbians who had tried to aid them came down with cholera and died shortly thereafter…
By September 9, cholera had spread to almost every section of the town, and 30 people had died, many of whom had visited the stricken immigrants. Physicians had no doubt that the disease that they were witnessing was cholera. The virulence of the epidemic that struck Columbia caused Jackson to observe that two-thirds of the victims died within five hours of showing symptoms of the disease…
Although only 127 victims died in Columbia—out of a population of five thousand—Dr. Wilson Jewell of the College of Physicians of Philadelphia and president of the Philadelphia Board of Health estimated that if a similar outbreak had occurred in Philadelphia, it would have killed 75 people an hour.
Osborne, J.D., (2009)

This third recorded Cholera pandemic of 1854 strongly suggests that no amount of cleaning up sewers could have stopped the disease in its tracks, at least not at a national and transnational level once it had found a means of jumping from person to person, as also implied by the title of article excerpt above. And supporting this concept, as noted at the beginning – the very nature of pandemics goes against the idea that Cholera was spread due to the level of hygiene within any of our far-flung and emerging nations.

 In other words,  although this goes against our commonly and firmly held belief that Cholera and other old diseases like it, came to prominence and ultimately declined due to our level of cleanliness, does not appear to fit the historical facts. A case in point is documented in the following:

No better example of this belief exists than in the now famous case of the Broad Street pump incident as outlined below:

John Snow and the Broad Street Pump: On the Trail of an Epidemic

The first cases of cholera in England were reported in 1831, about the time Dr. Snow was finishing up his medical studies at the age of eighteen…
Dr. Snow believed sewage dumped into the river or into cesspools near town wells could contaminate the water supply, leading to a rapid spread of disease.
In August of 1854 Soho, a suburb of London, was hit hard by a terrible outbreak of cholera. Dr. Snow himself lived near Soho, and immediately went to work to prove his theory that contaminated water was the cause of the outbreak.
“Within 250 yards of the spot where Cambridge Street joins Broad Street there were upwards of 500 fatal attacks of cholera in 10 days,”
…Officials contended there was no way sewage from town pipes leaked into the pump and Snow himself said he couldn’t figure out whether the sewage came from open sewers, drains underneath houses or businesses, public pipes or cesspools.
The mystery might never have been solved except that a minister, Reverend Henry Whitehead, took on the task of proving Snow wrong.
… Reverend Whitehead interviewed a woman, who lived at 40 Broad Street, whose child who had contracted cholera from some other source.  The child’s mother washed the baby’s diapers in water which she then dumped into a leaky cesspool just three feet from the Broad Street pump, touching off what Snow called “the most terrible outbreak of cholera which ever occurred in this kingdom.”
A year later a magazine called The Builder published Reverend Whitehead’s findings along with a challenge to Soho officials to close the cesspool and repair the sewers and drains because “in spite of the late numerous deaths, we have all the materials for a fresh epidemic.”  It took many years before public officials made those improvements.
Tuthill, K., (2003)

Although the Broad Street outbreak may have greatly exacerbated the ongoing pandemic of 1854 at a local level within this tiny area of the London suburb, I think we can safely say that this episode cannot account for the pattern of deaths from Cholera – the same pandemic of 1854 – experienced simultaneously throughout our diverse nations.

Recalling that it took years for the contaminated sewer leak at Broad Street, London to be repaired, it is also worth noting that such hygiene measures and attempts to control the spread of Cholera were not always successful,  or, even necessarily viewed as a good thing as encapsulated in the excerpt from a letter to the ‘Times’ around the time of the 1854 pandemic.

Letter to the ‘TIMES’ 1854

‘ We prefer to take our chance with cholera than be bullied into health. There is nothing a man hates so much as being cleansed against his will or having his floor swept, his hall whitewashed, his dung heaps cleared away and his thatch forced to give way to slate. It is a fact that many people have died from a good washing.’
Child, J and Shuter, P. (1992, 101)

Obviously, some people were willing to take their chances with the disease itself, which appears by all historical accounts to be becoming significantly less deadly as time went on – and certainly, from the time when Cholera first impacted our developing nations around the 1830s.

Perhaps that is why people were beginning to get a little irked by this zealous cleanliness as I am sure that many people on the ground knew quite well that the Cholera that had, not that long ago, swept across their homelands (certainly in living memory) was becoming relatively tame compared to the earlier days of the deadlier Cholera of plague-like proportions that swiftly spread devastatingly from person to person and the fact that people may have noticed that the limp corpses of entire families  being tossed unto cartloads of putrifying wretched bodies to be buried alive or dead amidst the tar filled sulphur piles, were not a common sight in the Cholera outbreaks of 1854.

An indication of this relative tameness of later Cholera pandemics, is already clear when we look to the preceding pandemic recorded a few years earlier dating to the late 1840s – generally known as Asiatic Cholera. What is interesting about this particular pandemic in the context of Ireland, is that it erupted on the heels of what is commonly referred to as the Great Hunger (or Irish Famine) of the 1840s.

One would think that this would have greatly increased the numbers dying from the disease, given our very poor nutritional status and overall dreadful living conditions, however,  as it turns out, seemingly, starvation, famines and overall impoverishment and squalid conditions do not appear to have played a major role in increasing the death toll as one might expect; although, it certainly didn’t help matters as indicated in the excerpt that follows:

History Ireland

Epidemic Diseases of the Great Famine

The arrival of Asiatic cholera as a pandemic in 1848-49 exacerbated the situation. This fearsome disease added to the physical and mental suffering of the beleaguered population and increased the overall mortality.
Greary, L., (1996)

Instead, it actually looks like Cholera is losing its grip – even at the height of the Great Irish Famine of the mid-1840s, as indicated by the data recorded in the following excerpt based upon the national census over the course of the main famine years:

Famine Disease and Famine Mortality: Lessons from the Irish Experience, 1845-50

… the census reported a total of 1,376 cholera deaths in the years 1841-47 (plus a further 2,502 in 1848).
Mokyr, J., and Ó Gráda, C., (1999, 7)

Therefore, if we compare the Cholera pandemic of this Asian type of the late 1840s, with the first major and preceding Cholera pandemic of the early 1830s, we can clearly see that the estimated 30,000 deaths, in a single outbreak of Cholera in Ireland alone, compared to the incredibly reduced estimates – even with all its inaccuracies and difficulties – reported from the Irish census of a few thousand deaths from Cholera over the worst of the Famine years ever recorded in this small nation, we truly begin to see that starvation, poverty and dreadfully stressful conditions all round does not necessarily lead directly to increased mortality from Cholera circulating as part of a broader pandemic at the time.

Moreover, this significant taming of Cholera is clearly seen from statistics recording deaths from the final major pandemic of Cholera – which occurs simultaneously throughout our developing nations in 1866. This is the first Cholera pandemic captured by the official statistics of deaths from Ireland which began two years previously (Fig. 1). The death figures for the 1866 pandemic in Ireland shows a significant decline in the number of deaths for several decades when it re-erupts briefly for another decade – but is not as deadly, and is suddenly never heard of again (Fig. 1). 

Cholera deaths Ireland

Fig. 1: Chart of the annual number of deaths in Ireland from Cholera since records for this disease began in Ireland. Source: Chart generated using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of: An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright

Once again, we may be looking at natural resistance to the disease over generations of exposure as indicated in a more modern assessment of the disease of Cholera as seen in the more recent excerpt given in the following.

Etiology and Epidemiology of Cholera

When cholera first appears in epidemic form in an unexposed population, it can affect all age groups. In contrast, in areas with high rates of endemic disease, most of the adult population have gained some degree of natural immunity because of illness or repeated asymptomatic infections.
CDC (1999, 39)

In other words, Cholera, and such diseases that are typically viewed as hygiene preventable, appear to be marginally impacted by any of our regional hygienic responses and attempts at intervening in the natural circulation of this pathogen –  except perhaps at a local level.

The historical archives and the statistical data presented above indicate a very similar natural patterning over national boundaries for corresponding timeframes for the fate of Cholera. We see the near-simultaneous rise of Cholera to deadly prominence in pandemic proportions, rapidly spreading from person to person, but within a few short generations – the massive devastation  as epitomised by the macabre accounts of the initial pandemic of the 1830s, just as quickly lost its lethal grip on our fledgling nations to become a relatively benign disease once again.

Cholera, a waterborne pathogen still exists. It never went extinct, but instead, it seems that we have built up natural resistance and immunity to this pathogen via generational exposure and as such, this pattern is indicative of a natural biological interplay between the pathogen itself and us as its host.

This brings us to another interesting pattern as seen in the following section which lends further support for the ultimate demise of Cholera from its much deadlier impact in the earlier part of the 19th Century, which can be seen from the interplay between the pathogens themselves, attempting to compete with each other for us as their own particular host.

A Tale of Two Pathogens

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Fig. 2: Chart of the annual number of deaths in Ireland from Cholera and Dysentery since records for this disease began. Note the large spike at the beginning, (from when records for both these diseases first began). These diseases decline somewhat thereafter, only to erupt again during the 1880s (Dysentery first, and then Cholera takes prominence from 1900 for almost a decade),– but both diseases stop abruptly with the first decade of the 20th Century. Source: Chart generated using annual statistics reports since records began – “Annual Reports on Marriages, Births and Deaths in Ireland, from 1864 to 2000” courtesy of An Phríomh-Oifig Staidrimh, Central Statics Office CSO, link. © Copyright

Notice from Figure 2, that there is a dramatic drop in deaths from Cholera (Dark Grey) just after the 1866 pandemic (shortly after official records began to record deaths from this disease). Note that deaths from Dystentery (Light Grey) since official records began, fill the space where Cholera seems suppressed somewhat by the predominance of Dysentery for a number of decades.  Note also, the slight gap in the graph that shows very few deaths from either Cholera or Dysentery compared to their loftier heights before records began as significantly more deadly diseases. As it turns out, this void of pathogen destruction appears to be filled by deaths from Typhus  (see the previous discussion on this disease) (Fig, 2).

Taking a closer look at Dysentery, we can see from (Fig.  2) that the deaths registered from this disease stop abruptly in 1900. Like Cholera, and all the other diseases discussed thus far in the context of our now developed nations, the historical records clearly show that Dysentery had a much deadlier beginning within our developing nations of the past.

Now, if we inspect the fate of Cholera (Fig. 2), we can now perhaps see what stopped Dysentery in its tracks. But even so, Cholera’s final reign only lasts a further decade before it too suddenly became an awful lot less deadly (note that these figures do not go beyond 1910, as there were simply no deaths officially being recorded annually in the register).

This interplay between the rise and fall of these two diseases is supported by the historical reference from the closing decade of the 19th Century as seen in the excerpt below. Note, however, that when this observation was written, little did the author know that even Cholera would also, like its older country cousin, be a thing of past just over a decade later.

A History of Epidemics in Britain, Volume II

Dysentery, the old ” country disease,” has steadily declined to about a hundred deaths in the year, while the considerable mortality from diarrhoea, nearly two thousand deaths in a year, is nearly all from the cholera infantum or summer diarrhoea of children in the large towns.
Creighton, C., (1894, 296)
[10] ]

As investigated in the previous sections on Typhus and Typhoid, a similar interplay of the rise and fall seen in the graphs as the predominance of one disease over the other presumably reflects their attempts to opportunistically colonise us as their hosts.  This pattern strongly suggests a biological cause – more to do with the vying for dominance between the pathogens themselves – than any hygiene measures that our particular developing nations may have (or not) implemented at any given time, within any particular region to try and prevent these pathogen’s bid for dominance.

Irrespective of this interesting interplay of pathogens fighting amongst themselves for top dog position, it seems that our own mighty immune systems won the day and managed to bring them all under control in the end. 

References to Part Five
[1] Osborne, J.D., (2009) The Lancaster County Cholera Epidemic of 1854 and the Challenge to the Miasma Theory of Disease, Edward Hand Medical Heritage Foundation [Available online at]
[2] MedMedia Group (2018) Why does cholera have such a reputation? Irish Health, [Available Online ]
[3] Meagher, J., (2012) The Sligo epidemic that stoked Bram’s interest in all things, Independent, (Apr., 22nd 2012) [Available online
[4] Osborne, J.D., (2009) The Lancaster County Cholera Epidemic of 1854 and the Challenge to the Miasma Theory of Disease, Edward Hand Medical Heritage Foundation [Available online at]
[5] Tuthill, K., (2003) John Snow and the Broad Street Pump: On the Trail of an Epidemic, Cricket Magazine, Cricket Vol, 31, [3], pp. 23-31, (Nov. 2003); Carus Publishing Company. [Available online republished with permission in full online: ]
[6] Child, J and Shuter, P. (1992, 101), Letter to the ‘TIMES’ 1854, Understanding History, Vol. 2, Heinemann [Available Online on Google Books ]
[7] Geary L., (1996) 18th – 19th Century History/Epidemic Diseases of the Great Famine.., History Ireland Magazine, Vol. 4. [1] (Spring 1996) [Available online ]
[8] Mokyr, J., and Ó Gráda, C., (1999) Famine Disease and Famine Mortality: Lessons from the Irish Experience, 1845-50. PDF, p. 7. [Available Online as PDF at ]]
[9] CDC (1999) Etiology and Epidemiology of Cholera, in, Laboratory Methods for the Diagnosis of Epidemic Dysentery and Cholera, Centers for Disease Control and Prevention, Atlanta, Georgia, Chapt., 5, p. 39. [Available online as PDF ]
[10] Creighton, C., (1894) A History of Epidemics in Britain, Volume II, p. 296, Cambridge, University Press. [Available online at ]

Next Episode: Part Six: Scarlet Fever Returns, but it is a lot less deadly.

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