zoo primates: horrible BSE news

[Guest guest]

Subj: zoo primates: horrible BSE news

Date: 3/28/99 2:53:45 PM Eastern Standard Time

From: tom@... (tom)

Sender: BSE-L@... (Bovine Spongiform Encephalopathy)

Reply-to: BSE-L@... (Bovine Spongiform Encephalopathy)

To: BSE-L@... (Multiple recipients of list BSE-L)

The 30 Mar 99 issue of PNAS 96:4046-4051, which is still not quite posted,

carries an explosive French study of very high experimental standards (with a

Nobel lauriate co-author) about TSE in primates in French zoos using BSE-

tainted feed supplements through June, 1996. This is a huge scandal because

it potentially affects the survival of many of the world's primate species.

In my opinion, it also suggests very strongly that the nvCJD epidemic will

indeed be of 'biblical proportions'.

[The primates showed contamination of the tonsils, esophagus, gastric glands,

duodenum, walls of lymph and blood vessels, Peyer's patches, and spleen, in

addition to dorsal and ventral root ganglian, spinal chord and brain. 14 of

26 non-experimental primates had neurological signs; 5/6 autopsies were

positive, indicating very high dietary penetrance in a variety of primates.]

Shockingly, the British manufacturer had continued to manufacure and

distribute this speciality product, possibly to hundreds of zoos on the

Continent and possibly worldwide, for 10 years after zoo ungulates and

carnivores were diagnosed in England. British zoos apparently continue to

export carrier animals worldwide.

Equally shocking, French zoos continued to use this feed despite knowning its

contaminated source, even though nearly every one of the 234 species of

primate is endangered in the wild, zoos are often used to sustain

populations, and breeding facilities provide animals for human medical

research. Only 8 French zoos and primate breeding facilities out of 89 agreed

to cooperate with this study, which simply asked about primate neurological or

unexplained deaths and dietary practices. A zoo in Lille acknowledged 3

primate deaths with TSE-like neurological illness.

It is highly questionable not to autopsy [or save samples] from valuable

animals with unexplained neurological deaths fed known BSE feed, yet this is a

big step up from non-cooperation. It seems that French veterinary ethics have

a similar standard to those of French medicine (AIDS and hepatitis).

But is the problem limited to France and primates? We all know that English

zoos have been lying through their teeth [MAFF interfered with kudu and dogs

according to the Inquiry, did it stop there: the list of species affected

never made any sense given the prion sequences involved]. Whose protein

supplement did English zoos use for primates if not the local company's? Why

would only French primates go down with TSE? (Explanation: Max the cat was

bad enough, how could the UK resume beef exports if they announced Charlie the

chimpanzee had BSE?)

The products are identified as " Singe 107, MP, or Marex. " Singe 107 (UAR,

Paris, France) was previously described as containing " products declared fit

for human consumption. " The present article does not identify the companies

by name but says, " according to the manufacturers, this food contained

various items, including gross protein, fats, corn, soya, carob bean, alfalfa,

minerals, yeast, vitamis A, C, D3, and E, and cracklings (the so-called 'fifth

quarter of beef' suitable for human the same French distributor.

The British manufacturer 'which distributes nutritional supplements to zoos

and animal breeding facilities through a French company [and possibly others

in other countries]) announced in June, 1996 that it ceased to use beef in its

nutritional supplements' which the authors take to mean that they had used

beef prior to 'ceasing'. On 6 July 1996, an article appeared in Lancet

documenting non-experimental transmission of BSE to primates (in a rhesus

monkey that had died in 1992).

The 79 primates of 11 species were feed 20-40 gm/kg of these feeds in addition

to their usual fruits and vegetables. For a 60 kg human, this works out to

1200-2400 gm.

In July 1996, Bons et al. published that a rhesus monkey and two lemurs at the

Montpellier zoo had died of TSE. Here they look at an additional 20 lemurs

and macaques from 3 French zoos. The zoos had to kill these lemurs anyway

because they were primate hybrids, now illegal in France. Two lemurs were

symptomatic, 18 were not: all were definitely positive for prion disease.

Lemurs and macaques can live for 20+ years, so what this implies is that a

great many primates in French zoos are not yet symptomatic but are slowly

incubating BSE-based prion disease.

We could ask whether the facilities are thoroughly contaminated (like the ones

in Colorado), whether only primates are affected, whether only French zoos are

affected, whether food 'fit for human consumption' ended up in the human food

chain, and indeed, wonder whether there is much of a species barrier at all to

humans, given that 5 other species of primate have gone down via the oral

route.

Corresponging author: ephemcb@...

Species used in study:

Microcebus murinus# [strepsirhini (prosimians) small, short-lived mouse lemur

exposed to BSE brain orally]

Eulemur fulvus mayottensis# [prosimian, lemur]

Eulemur fulvus albifrons# [prosimian, lemur]

Eulemur mongoz# [prosimian, lemur]

Eulemus macaco# [prosimian, lemur]

Lemur catta# [prosimian, (ring-tailed lemur]

Varecia variegata varigata# [prosimian, ruffed lemur]

Varecia variegata rubra [prosimian, ruffed lemur]

Macaca mulatta#* [old world monkey]

Macaca sylvanus* [old world monkey]

Macaca fuscata* [old world monkey]

Saimiri sciureus#* [new world monkey]

#one or more non-experimental BSE-food exposed animal suspected or confirmed.

*sequence of prion gene known. 35 other individuals pending further study.

=-=-=-=-=-=-=-=-=

Spontaneous spongiform encephalopathy in a young adult rhesus monkey

The Lancet Volume 348, Number 9019 - Saturday 6 July 1996

Noelle Bons, Nadine Mestre-Francois, Yves Charnay, Fabrizio Tagliavini

Sir--Although human and animal prion diseases have been experimentally

transmitted to various monkey species, spontaneous occurrence of a spongiform

encephalopathy in non-human primates has not been reported. We describe the

development of a spongiform encephalopathy without

known cause in a rhesus monkey (Macaca mulatta).

The monkey was born in 1982 and was acquired from Ravensden zoo, Rushend,

Northants, UK, in October, 1986, by the zoological park in Montpelier, France

where it was housed in the primate colony. In Montpelier, the monkey was fed

standard monkey feed including Singe 107 (UAR, Paris, France) which contains

meat products declared fit for human consumption. In summer, 1991, aged 9, the

previously healthy monkey became

lethargic and developed mood changes, in particular, aggressiveness. The

monkey became isolated from its companions and hid itself away. In June, 1992,

the monkey was anaesthetised...

-=-=-=-

Oral transmission of BSE to primates

Thew Lancet Volume 348, Number 9035 - Saturday 26 October 1996

R M RIdley, H F Baker

MRC Comparative Cognition Team, Department of Experimental Psychology UK

Sir--In a report to the European Union Commission, Prof C Weissmann of Zurich

University

has recommended that experiments be set up to investigate oral transmission of

BSE to

primates to see whether human beings are at risk from eating beef products.1

Bovine

spongiform encepholopathy (BSE) has already been transmitted to primates by

intracerebral

injection of infected brain tissue homogenate2 so the " species barrier "

between cattle and

primates is not absolute. BSE has also been transmitted by feeding infected

brain to mice3 so

clearly transmission of this agent by the oral route is possible. During the

BSE epidemic not

only were cattle fed on contaminated, rendered material, but large numbers of

other species in

zoos, farms, and domestic ownership were also fed on pelleted food containing

rendered

material. A few animals of several species of antelope and cat4 but not

monkeys5 became

affected despite these monkeys being fed for many years on pellets which

contained up to four

times the amount of the implicated, rendered meat and bone meal that was

included in cattle

pellets. Thus a " species barrier " of some sort exists between cattle and

primates. But will

Weissmann be able to quantify this in a way which will have public health

implications?

In 10 years' time he may be able to determine the smallest amount of raw cow

brain necessary

to cause disease if fed to perhaps a few dozen monkeys. But what will this

tell us about the

maximum quantity of bovine-derived material (from which specified offals have

been

removed) which can be consumed without causing illness when the sample size

could be up to

50 million people in the UK? As every drug company knows, extensive tests in

clinical trials

in large numbers of people cannot ensure that a new drug, when available on

general

prescription, will not cause serious illness in a handful of patients such

that the drug has to

be withdrawn. At best Weissmann's experiments will be irrelevant; at worse

they will

provide a degree of reassurance which is unwarranted. There is nothing that

can be done to

reduce any risk to which people have been exposed in the past, and there is

now no alternative

but to do the best we can to eliminate BSE entirely.

Failure to transmit bovine spongiform encephalopathy to marmosets with

ruminant-derived meal

Lancet letter R M Ridley, H F Baker, C P Windle

Sir--We have kept a large breeding colony of common marmosets (Callithrix

jacchus) for

use in neuropsychological research for almost 20 years. This primate species

develops

spongiform encephalopathy with an incubation period of 3÷5 or 4 years after

intracerebral

injection of scrapie-affected or bovine spongiform encephalopathy

(BSE)-affected brain

homogenate.1 The majority of marmosets in the colony are used for experimental

purposes

and are killed when under 3 years of age, but the breeding animals are aged

3«10 years and a

small number of animals have been kept for up to 15 years in an investigation

of ageing.2

All animals are fed a daily diet of egg sandwiches, fruit, and a proprietary

brand of

UK-produced New World monkey pellets. According to the manufacturers these

pellets

contained a 20% inclusion of ruminant-derived meat-meal protein until April

1996

(cattle-feed supplements before 1988 contained about 4% of meat and bone

meal). From

1985 onwards, ruminant-derived feed probably contained increasing amounts of

BSE agent

from affected cattle and although the Ruminant Feed Ban of 1988 prohibited the

feeding of this

material to ruminants, its use in other animal feeds was legal until April

1996.

We estimate that more than 100 marmosets born in our colony between 1980 and

1990 lived

for more than 5 years and were exposed to ruminant-derived protein in their

diet for their

entire life. Each adult marmoset (weight 350 g) was fed about 2 g meat meal

per day. It seems

likely, therefore, that the mature monkeys in our colony were exposed to

significant amounts

of infective agent for more than 5 years and in some cases for up to 10 years.

With the

exception of those animals which were injected intracerebrally with infected

brain in our

primary transmission studies, no animal in our colony has ever developed

spongiform

encephalopathy. As part of general husbandry all animals are monitored daily

for signs of

ill-health and any with severe illness or persistent poor condition are

killed.