Baptismal record for Laers, son of Truels Laersen, living at Bruk 4 of Broe, from the Kirkebok for Rennesøy Palm Sunday 24 March 1771.

While I was researching and writing “The Early Years” segment of the book I have been writing about my great-great-great-grandfather Nils Trulsen Bru, I needed to look at his family of origin. What could be learned about his parents and siblings which might shed light on the course his life followed?

I had previously recorded data about his parents and the names and dates for his sister Malena and for two brothers, both named Lars. I knew that the first “Lars” died as a baby and that it was fairly common practice in those days to name a later child after one which had been lost. In fairness, I had never paid much attention to the death of the older Lars, who was baptized 24 March 1771 and buried later that year (on 10 November).

Losing a baby or two during the eighteenth century was unremarkable. Even a century later my great-grandmother Carrie Hanson lost, in infancy or childhood, five of the 17 children she bore. In any event, I went to the Church Book (Kirkebok, Rennesøy Parish, Stavanger amt, Norway) to see if there was more to learn.

I was stunned to look at the Kirkebok and see that the entries for burials just before and then following the record for Lars were all of babies and children. I had never before noticed anything like this. What was going on?

The next burial of a person over 21 did not occur until nearly six months later, on 18 January 1772.

This strange circumstance appeared to have begun in late July 1771. On 22 July, an “old” person – 66-year-old Anna Norbøe – was buried. The next burial of a person over 21 did not occur until nearly six months later, on 18 January 1772. In the meantime, the babies and youth of Rennesøy were dying as if in the grip of a miasma. In the period I examined, starting on 28 July 1771 and ending 15 February 1772, burials were recorded for 67 souls fifteen years of age and younger. In the same period there were only three burials of persons over 21 years of age. The pestilence appeared to end almost as suddenly it had begun. After 15 February 1772, the list of burials returned to a much more customary distribution.

Of the 67 burials, fifty-two were for children five years of age and younger. When I compared the baptismal (Døpte) register for the five years preceding the epidemic with the burial records (Gravlagte), the death rate approximated 30%.

This was a strange and terrifying discovery. I cannot comprehend the anguish and fear of the people of Rennesøy as they watched the neighboring children, their nieces and nephews, and their very own children die as they stood by and watched helplessly.

What was the origin of this epidemic? Historians suggest that “plagues” in the eighteenth century were customarily caused by dysentery, typhus and typhoid fevers, or by smallpox. Famine was a killer, too, but less so on the West Coast of Norway, where fish supplemented a diet mostly of oats. I discounted famine as a cause even though the fishing in the winter of 1771-72 was tenuous and crops partially failed the next year. In a famine the deaths would have been expected to include older people who had been in poor health, and certainly would not have begun so suddenly and ended so abruptly.

The phenomenon of clustered deaths in this period has been examined.

The phenomenon of clustered deaths in this period has been examined. In his account of European demography for this period, John D. Post wrote, “The major change in the trend of the population growth rates of the English and Continental populations took place during the European food shortages and mortality crises of the early I770s.”[1]

The food shortages and mortality crises of the early I770s are an outstanding fact of European population history. The regions of northern, central, and western Europe all experienced elevated food prices and death rates.[2] By the end of 1772, however, famine conditions had developed and epidemics of typhus fever and dysentery had become rife in the Norwegian dioceses.[3]

Notwithstanding Professor Post’s research, I am inclined to believe the 1771-72 epidemic on Rennesøy was smallpox for the following reasons:

1. The uniformity of age … no one over 21 died during the course of the epidemic;
2. Dysentery or fever would likely have killed at least a few adults;
3. Even the bad fishing of the winter of 1771 and a poor harvest the following year would not have precipitated an epidemic in fishing areas;
4. The sudden start and abrupt end eliminate famine as a cause;
5. The population was spread over several islands and many farms, each with their own water supplies and sanitary practices, which argues against water borne diseases or those caused by lack of good sanitary practices;
6. The specificity of deaths suggests a lack of immunity among the victims;
7. Those who escaped the contagion may have benefited from a degree of immunity given previous exposure to smallpox. Dysentery and fevers can pay a return visit; smallpox was a one-time experience;
8. Church services when the populace went from island to island were a probable vector; no other means of transmission seems as probable.

Did Nils Trulsen grow up experiencing an idyllic life in eighteenth-century Norway? The island farm, the sea for swimming and boating, the family connections, and peace all argue yes. The contagion of 1771-72 most decidedly represented a very imperfect part of life at the time.

As we, in our own time, fret about a global pandemic of yet another virus afflicting the human species, we confidently expect that twenty-first-century medicine will save us from the outcome experienced by my ancestors in coastal Norway 250 years ago. We also take comfort in the eradication of smallpox and knowing that the only traces of smallpox (variola virus) in existence are in secure labs. We hope Covid-19 joins variola virus in the deep freeze sometime soon.

Notes

[1] John D. Post, “The Mortality Crises of the Early 1770s and European Demographic Trends,” The Journal of Interdisciplinary History 21: 1 [1990]: 29-62 at 36; https://www.jstor.org/stable/204917?seq=1.

[2] Ibid., 37.

[3] Ibid., 50.