POD: A devastating soybean blight causes oilseed prices to more than double in 1985. Feedlot beef and milk producers (who are also ultimately beef producers) worldwide are universally and rapidly forced to switch to using bone meats and meal as a protein supplement for their cattle (whereas previously it was more economical to sell it on for other uses, and feed their cows oilseeds for protein).(1)
Bovine spongiform encephalopathy a.k.a. mad cow disease spreads rapidly in the animal population: once a single infected animal enters the food-chain the disease rapidly spreads across the whole industry.(2) By 1990 infection rates among feedlot cows in Europe and North America have surpassed 50% and approach 90% by 1992.(3)
The vast majority of cows – including dairy cows – are slaughtered before they become visually symptomatic. A small number will progress more rapidly(4), and this will be noticed, and likely attributed to a disease analogous to scrapie (the prion disease of goats and sheep), but it will be dismissed as economically insignificant, and not a threat to human health (scrapie, then the only animal prion disease known, being common throughout history, isn’t transmissible to people). These symptomatic animals, deemed not fit for human consumption, are instead rendered in whole into animal feed; there being no understanding of the transmission mechanism of prion disease (in fact, no knowledge of the existence of prions at all)
In 1995 epidemiologists begin to notice a sharp rise in CJD cases (which occurs naturally and spontaneously in a tiny fraction of the population at a heretofore stable rate). It takes only a few months to connect the dots between the growing number of people coming down with fatal neural wasting disease, the silent decade-long epidemic of a similar disease among cows, and the little known ‘kuru’ disease endemic among cannibals in New Guinean. By this time over 95% of the population of Western Europe and North America (and smaller percentages elsewhere) has been persistently exposed to BSE-infected meat products for a decade, and around 5% of them will eventually develop and die of vCJD.(5)
Re-examination of dusty Australian colonial-era studies of kuru show that that prion disease has a frighteningly long incubation period, in some cases exceeding 30 years between initial infection and the onset of symptoms. It dawns on a horrified public that upwards of 50 million people, concentrated mostly in and split roughly between Europe and North America, will die of this disease: for which there is no cure nor any way to diagnose infection until symptoms have set in. vCJD’s prognosis is truly terrifying: over the course of around a year, the patients brain turns to swiss-cheese, causing first emotional changes, then progressive paralysis, and ultimately death.
So…. what’s the effect? Beyond a radical re-think of food production, does the dread of not-knowing cause an outbreak of fatalism and nihilism in the West? Does the stress lead to widespread depression and suicide? As the deaths reach a peak around the turn of the millennium how does society deal with so many helpless dying people?
If this is even half-plausible it’s pretty damn frightening!
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1. Mad cow became epidemic in Europe and not elsewhere because of marginally higher local oilseed prices due to poor growing conditions IOTL
2. Either the founder cases are spontaneous (a very small percentage of mammals will develop prion disease spontaneously) or are introduced from wild ruminants with endemic BSE.
3. IOTL BSE infections in Britain probably didn’t exceed 1%, but it’s not uncommon for many mammal populations to have prion infection rates approaching 100%, particularly among carnivores, which these cows have in effect become
4. BSE becomes symptomatic over time in something of a bell-curve distribution, with a peak in cows at about 10 years, while commercially raised cows rarely live past 4 years
5. Animal studies show infection rates increase exponentially with exposure, so there’s an exponential rise in infections with nearly universal mad-cow in this scenario versus the less-than-one-percent in OTL Britain.
Bovine spongiform encephalopathy a.k.a. mad cow disease spreads rapidly in the animal population: once a single infected animal enters the food-chain the disease rapidly spreads across the whole industry.(2) By 1990 infection rates among feedlot cows in Europe and North America have surpassed 50% and approach 90% by 1992.(3)
The vast majority of cows – including dairy cows – are slaughtered before they become visually symptomatic. A small number will progress more rapidly(4), and this will be noticed, and likely attributed to a disease analogous to scrapie (the prion disease of goats and sheep), but it will be dismissed as economically insignificant, and not a threat to human health (scrapie, then the only animal prion disease known, being common throughout history, isn’t transmissible to people). These symptomatic animals, deemed not fit for human consumption, are instead rendered in whole into animal feed; there being no understanding of the transmission mechanism of prion disease (in fact, no knowledge of the existence of prions at all)
In 1995 epidemiologists begin to notice a sharp rise in CJD cases (which occurs naturally and spontaneously in a tiny fraction of the population at a heretofore stable rate). It takes only a few months to connect the dots between the growing number of people coming down with fatal neural wasting disease, the silent decade-long epidemic of a similar disease among cows, and the little known ‘kuru’ disease endemic among cannibals in New Guinean. By this time over 95% of the population of Western Europe and North America (and smaller percentages elsewhere) has been persistently exposed to BSE-infected meat products for a decade, and around 5% of them will eventually develop and die of vCJD.(5)
Re-examination of dusty Australian colonial-era studies of kuru show that that prion disease has a frighteningly long incubation period, in some cases exceeding 30 years between initial infection and the onset of symptoms. It dawns on a horrified public that upwards of 50 million people, concentrated mostly in and split roughly between Europe and North America, will die of this disease: for which there is no cure nor any way to diagnose infection until symptoms have set in. vCJD’s prognosis is truly terrifying: over the course of around a year, the patients brain turns to swiss-cheese, causing first emotional changes, then progressive paralysis, and ultimately death.
So…. what’s the effect? Beyond a radical re-think of food production, does the dread of not-knowing cause an outbreak of fatalism and nihilism in the West? Does the stress lead to widespread depression and suicide? As the deaths reach a peak around the turn of the millennium how does society deal with so many helpless dying people?
If this is even half-plausible it’s pretty damn frightening!
-------------
1. Mad cow became epidemic in Europe and not elsewhere because of marginally higher local oilseed prices due to poor growing conditions IOTL
2. Either the founder cases are spontaneous (a very small percentage of mammals will develop prion disease spontaneously) or are introduced from wild ruminants with endemic BSE.
3. IOTL BSE infections in Britain probably didn’t exceed 1%, but it’s not uncommon for many mammal populations to have prion infection rates approaching 100%, particularly among carnivores, which these cows have in effect become
4. BSE becomes symptomatic over time in something of a bell-curve distribution, with a peak in cows at about 10 years, while commercially raised cows rarely live past 4 years
5. Animal studies show infection rates increase exponentially with exposure, so there’s an exponential rise in infections with nearly universal mad-cow in this scenario versus the less-than-one-percent in OTL Britain.
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