Crazy cows and missiles… What could go wrong?

Crazy cows and missiles… What could go wrong?

While they never quite left us… during the last weeks seem that the crazy cows as dark swallow come back with their tails in our windows to knock. As the poet would say...

The new case confirmed for Brazil some weeks ago comes on top to previous ones from last February in Holland and Spain, and to the repeated alerts over practically all the previous years.

While, thanks to learnt since the beginning of the crisis at 90’s, today we know that fortunately all these recent cases correspond to the variants called “atypicals”; mainly the H, whose would appear spontaneously and about doesn’t exist, until now, any evidence respects to their relation to the consumption of feed contaminated by part of the affected animals.

All this takes on a special dimension when the war in Ukraine has severely affected the supply chains of various raw materials for feed production, raising their prices in general and hindering, directly and indirectly in others, their availability. Creating a situation conducive to the appearance of irregularities, especially after the recent recovery of "normality" in the use of proteins of animal origin in feed, as we will analyze later.

Briefly, since it is not the objective of this short article, for a better understanding of the BSE origin, let us remember that this pathology is caused for proteins of the cell membrane of neurons, which receive the specific name of prions.

Prions, simplifying the matter, it could be said that, like other proteins, they acquire their biological function based on their folding, a process in which they roll and fold on themselves. As the culmination of AlphaFold2 recently made fashionable, an AI capable of predicting the folding of proteins.

When this folding, due to mutations and / or various cofactors, changes its three-dimensional shape, they become pathological, as in the case of PrPSc of the EBB.?The prion of mad cows to understand us...

Affected animals ingest these malignant prions through the food or fluids of other affected animals, reaching the intestine where through the bloodstream they achieve the brain; once in which, by processes not yet fully understood, they cause normal prions to become malignant versions in a process similar to a contagion. These malignant prions (abnormal proteins) accumulate in neurons causing a neurodegenerative process without the induction of any immune response.

Looking back a little, the vast majority will remember that BSE (bovine spongiform encephalopathy) made its stellar appearance in the early 90s in the UK, and soon after, a new variant of Creutzfeldt-Jakob disease caused by exposure to EBB prions was identified.

It should be clarified that the variant of Creutzfeldt-Jakob disease, i.e. the human "version" of the disease caused by BSE, is mainly caused by the consumption of meat or derivatives of affected beef. And that in the same way cattle, contract the disease by ingesting feed contaminated with BSE prions, or the disease that caused it: Scrapie; a transmissible spongiform encephalopathy (ETT) of sheep and goats, old known in the United Kingdom country in which there are reports since 1732, coincidentally origin of BSE.[1]

That is, although it is not common to find it defined as a foodborne disease, the truth is that it is in both humans and animals.

Surely to many will sound this jump from a disease of animal origin to humans, come on ... What we call zoonoses for short. COVID-19, with an unprecedented impact on contemporary history, seems to have discovered new situations that really are not at all and from which we would sometimes seem to have learned little.

The truth is that since 1996 in which the European authorities banned the export of British beef to prevent the spread of EBB, the disease spread throughout Europe, giving rise directly and indirectly to a truly devastating situation.

Some years later, between 2000 and 2001, from a greater knowledge of the problem, control and prevention measures were "consolidated" and together with an increase in restrictions on international trade in products likely to act as a vector of the disease, and the prohibition to use meals of animal origin, in force since 1994 for ruminants, was extended (EC Regulation No. 999/2001) , with the specific exception of fishmeal, to the manufacture of feedingstuffs for all types of animals for human consumption.

The European Union (EC Regulation No. 381/1994) has had from the outset an obvious desire to repeal the total ban, adopted temporarily and initially for six months. Despite this, after several revisions, it has been extended for almost 20 years, until its definitive repeal on August 17, 2021 with the publication of EC Regulation No. 1372/2021.

These measures have proved effective by keeping the official disease risk status negligible throughout Europe, except for Greece with controlled risk.

In this situation, although we could say that the classic variant is controlled, it is no less true that new "atypical" variants have been identified for which there is no evidence of risk to humans. Despite this, there are authors [2],[3],[4],[5] who have reported the lack of sufficient knowledge to make a decision beyond doubt. Therefore, while the position adopted by EFSA and other authorities is understandable, as well as the information disseminated regarding the non-transmission capacity to humans via food (https://www.efsa.europa.eu/en/topics/topic/bovine-spongiform-encephalopathy-bse#, literally: "Classical BSE is the only form that can be transmitted to humans through the consumption of contaminated meat "), it would be more accurate to state the current absence of evidence to the contrary.

In special attention, as I pointed out earlier, COVID-19 has reminded us that the crossing of inter-species barriers, by feeding non-ruminants with atypical BSE prions without adequate control, for example, could lead to the emergence of new zoonotic prions as various evidences suggest occurred in the case of the BSE-C or "classic" prion from Scrapie prions from goats or sheep.

Especially since, in practice, the situation of the "control" of feed with proteins derived from animals, which gave rise to the total ban, has not changed much despite the validation of different molecular techniques for the detection of material derived from ruminants and non-ruminants, as cited in their justification the corresponding repealing European regulations.

It is worth reflecting, or rather we could say that a reflection is necessary, on the sufficiency of the actual use of these analytical techniques, despite their availability, on which the derogations from the bans on the use of proteins of animal origin in feedingstuffs were based.

Additionally, decreeing the prohibition of feed or protein for its manufacture, regardless of the animals to which they were intended, in the event that any prion variant of BSE was detected, could constitute a prudent and effective preventive measure and of an acceptable impact in light of the observed prevalence. At least with the control pressure to which I alluded in previous paragraphs.

For all these reasons, it would seem prudent not to lower our guard, but on the contrary to update at least the self-control and official programs, effectively applying the verification of species according to the destination of feed, and also including the detection of all prion variants, using techniques also available today, precise and viable as immuno-PCR. About we probably talk in a new article soon.

Controls that are especially relevant when the armed conflict in Ukraine has generated a global geopolitical and economic situation that has caused a notable increase in prices of raw materials for animal feed, which could lead to a dangerous increase in fraud as has been clearly identified in food for human consumption already as a result of the COVID-19 pandemic.

References

[1]?Poser C.M. Notes on the history of the prion diseases. Part I.?Clin. Neurol. Neurosurg.? 2002;104:1–9. doi:?10.1016/S0303-8467(01)00186-X.

[2] Comoy?EE, Casalone?C, Lescoutra-Etchegaray?N, Zanusso?G, Freire?S, et al. (2008)?Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLOS ONE 3(8): e3017.?https://doi.org/10.1371/journal.pone.0003017

[3] Kong Q, Zheng M, Casalone C, Qing L, Huang S, Chakraborty B, Wang P, Chen F, Cali I, Corona C, Martucci F, Iulini B, Acutis P, Wang L, Liang J, Wang M, Li X, Monaco S, Zanusso G, Zou WQ, Caramelli M, Gambetti P. Evaluation of the human transmission risk of an atypical bovine spongiform encephalopathy prion strain. J Virol. 2008 Apr;82(7):3697-701. doi: 10.1128/JVI.02561-07. Epub 2008 Jan 30. PMID: 18234793; PMCID: PMC2268471.

[4] Costassa EV, Iulini B, Mazza M, Acutis P, Maurella C, Meloni D, Pautasso A, Capucci L, Bozzetta E, Simmons MM, Zanusso G, Pocchiari M, Corona C, Casalone C. Pathogenesis and Transmission of Classical and Atypical BSE in Cattle. Food Saf (Tokyo). 2016 Dec 7;4(4):130-134. doi: 10.14252/foodsafetyfscj.2016018. PMID: 32231917; PMCID: PMC6989206.

[5] Marín, B., Otero, A., Lugan, S.?et al.?Classical BSE prions emerge from asymptomatic pigs challenged with atypical/Nor98 scrapie.?Sci Rep?11, 17428 (2021). https://doi.org/10.1038/s41598-021-96818-2