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The last `Great’ Influenza pandemic occurred in 1918-19, and while estimates vary widely, it may have claimed as many as 100 million lives. A new strain of H1N1, it was known at the time as `Spanish Flu’.
The impact of this pandemic, however, varied greatly. In 2006, in a Lancet journal (doi:10.1016/S0140- 6736(06) 69895-4) article cited as much as a 30-fold difference in mortality rates around the world:
Christopher JL Murray , Alan D Lopez , Brian Chin , Dennis Feehan , Kenneth H Hill
Excess mortality ranged from 0·2% in Denmark to 4·4% in India. Since there was some under-registration of mortality in India, total pandemic mortality could have been even higher.
Indeed, in some the more remote regions of the world – such as among the Maori of New Zealand or the Eskimos of Alaska – the mortality rates were even higher.
The following account comes from Alaska’s pandemic history on http://1918.pandemicflu.gov/
In some areas, influenza decimated whole villages. A schoolteacher reported that in her immediate area “three [villages were] wiped out entirely, others average 85% deaths...Total number of deaths reported 750, probably 25% [of] this number froze to death before help arrived.”
One of the other striking features of the 1918 pandemic – aside from the high death toll – was the sparing of those over the age of 65 in the United States.
The infamous `W shaped curve’ of the 1918 pandemic clearly shows that the death rates among those in their teens, 20s, and 30s was much higher than was normally seen in previous influenza years.
This wide disparity in mortality rates – much of it based on anecdotal accounts – has long intrigued researchers. Today we’ve a new study from the Norwegian Institute of Public Health that attempts to answer some of these questions.
What they found was that the mortality rate varied nearly 100 fold between remote, rural regions and urban populations, and that in the more remote areas, older persons were just as susceptible to the virus as those who were younger.
First excerpts from the Press release, then a link to the study. I’ll return with some comments.
Large differences in mortality between urban and isolated rural areas
Published 27.04.2011 , updated: 27.04.2011, 12:30
Stikkord:
In urban communities, less than 1 in 100 inhabitants died from Spanish flu in 1918, but in isolated communities up to 9 out of 10 died. An important explanation for the differences is due to different exposure to influenza in the decades before the Spanish flu came. Those living in urban communities probably had a higher degree of pre-existing immunity that protected against illness and death in 1918 than those living in very isolated rural areas. This is shown in a new study from the Norwegian Institute of Public Health.
Previous studies have suggested that an important reason for the large regional differences in mortality must be that people living in cities were more frequently exposed to similar viruses to the one that caused the Spanish flu earlier in life than those living in rural and extremely isolated areas.
“It is not inconceivable that there was a different geographical spread of the virus in the 1800s and early 1900s, at a time when intercontinental communication networks were less developed" said Svenn-Erik Mamelund, a senior adviser in the Division of Infectious Disease Control at the Norwegian Institute of Public Health.
“No one knows exactly which influenza viruses circulated before 1918. But a leading theory is that there were H1-like viruses circulating in the period before the last major pandemic, the Russian pandemic of 1889-90. Some viruses circulating prior to 1889 may therefore have been related to the virus that caused the Spanish flu in 1918, A (H1N1). This would mean that some people who were older than 28-30 years in 1918 may have had some protection against severe infection and death from Spanish flu because of previous exposure to similar viruses," he said.
This study appears in the Journal Epidemics.
Geography May Explain Adult Mortality from the 1918–20 Influenza Pandemic
Original Research Article
Pages 46-60
Svenn-Erik Mamelund
The theory that a similar H1 virus circulated prior to 1890 – and that provided some immunity to those over the age of 30 – is bolstered by this study.
Young people, and those older people living in isolation during the 1880s had not been exposed, and were therefore more vulnerable to the 1918 virus.
But as the author points out, that alone is not likely to have accounted for the huge difference in mortality. From the abstract, the author writes:
Low exposure to H1-like viruses in adults could not alone explain the high total mortality in remote populations (up to 90%). A high concurrent disease load, crowding, low genetic variability, a lack of basic care, and infrequent exposure to other forms of influenza virus 1890–1917 may have played a role as well.
This form of immunological cross-protection from previous exposure to A-type influenza viruses other than H1N1 can only be explained as a consequence of cellular immunity against internal proteins that show less inter-strain variation than the surface proteins.
Our most recent pandemic experience, once again at the hands of the H1N1 virus, proved milder than feared probably for the same reasons.
As populations intermingle - we trade more viruses - and over time build up a certain level of immunity. And part of that immunity may be generic cellular immunity, as opposed to antibodies to specific pathogens.
And in this highly mobile world, that may bode well for the next pandemic – assuming it comes from a relative of a virus that we’ve seen in the recent past; an H1, H2, or H3 strain.
There are no guarantees, of course.
Should a less familiar strain emerge, however, no one knows how severe an impact it might have.
The H5N1 virus has – thus far – killed about 50% of its known victims. Far worse than the Spanish flu of 1918. The H7 and H9 avian strains, however, have produced generally mild illness and few fatalities in humans.
So there is obviously more to the influenza mortality and morbidity story than just being immunologically naive to a virus.
While today’s paper may not provide definitive answers to the questions surrounding the 1918 pandemic, it does give us more data to ponder and a plausible explanation for its divergent impact around the world.
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