My super-smart partner and I meet: Prion disease in Algerian camels

Amy says I shouldn’t cut-and-paste so much and that I’m better when I just write my own stuff.

Howard Stern’s wife said that to him, at least according to the movie version in Private Parts, 1997, but I counter with I only cut-and-paste the really interesting stuff.

Algeria, French and prions, we’re in a zone.

Everyone else is recall.net, where the copy is provided by 100K-a-year hacks who write and vomit press releases.

Journalism used to be a viable activity.

No worries, story-telling about the Tom-Wolfe-styled-vanities of the food safety privileged retain currency. And those stories are what I have been working on,

I’ll go with a Paul Giamatti,-style, who I am enjoying in Billions and was great in John Adams, Cinderella Man, American Splendor, and so on.

Everyone needs a Paul.

Or an Amy.

Her accomplishments over the seven years since we moved to Australia, including caretaking me and Sorenne, have been extraordinary.

Much love.

Prion disease in Dromedary camels, Algeria

6 June 2018

Emerging Infectious Diseases Vol 24, no 6

Baaissa Babelhadj, Michele Angelo Di Bari, Laura Pirisinu, Barbara Chiappini, Semir Bechir Suheil Gaouar, Geraldina Riccardi, Stefano Marcon, Umberto Agrimi, Romolo Nonno, and Gabriele Vaccari

https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article

Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE).

After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions.

We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals.

Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie.

Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.

 

 

Atypical BSE in Alabama cow

The U.S. Department of Agriculture (USDA) announced an atypical case of Bovine Spongiform Encephalopathy (BSE), a neurologic disease of cattle, in an eleven-year old cow in Alabama.  This animal never entered slaughter channels and at no time presented a risk to the food supply, or to human health in the United States.

USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Laboratories (NVSL) have determined that this cow was positive for atypical (L-type) BSE.  The animal was showing clinical signs and was found through routine surveillance at an Alabama livestock market. 

BSE is the form that occurred primarily in the United Kingdom, beginning in the late 1980’s, and it has been linked to variant Creutzfeldt-Jakob disease (vCJD) in people. The primary source of infection for classical BSE is feed contaminated with the infectious prion agent, such as meat-and-bone meal containing protein derived from rendered infected cattle. Regulations from the Food and Drug Administration (FDA) have prohibited the inclusion of mammalian protein in feed for cattle and other ruminants since 1997 and have also prohibited high-risk tissue materials in all animal feed since 2009.

Atypical BSE is different, and it generally occurs in older cattle, usually 8 years of age or greater. It seems to arise rarely and spontaneously in all cattle populations.

This is the nation’s 5th detection of BSE.  Of the four previous U.S. cases, the first was a case of classical BSE that was imported from Canada; the rest have been atypical (H- or L-type) BSE.