Date: Sat 13 Jan 2001
From: Ray Bradley <r.bradley@vla.maff.gov.uk> , <raybradley@btinternet.com>
All world authorities are satisfied that bovine semen is safe. Even UK semen
can be exported to Australia and New Zealand. The OIE has semen on its list
of commodities that can be freely traded even from countries with BSE as
stated in the OIE International Animal Health Code chapter on BSE:
"Regardless of the BSE status of the exporting country, Veterinary
Administrations should authorise without restriction the import or transit
through their territory of the following commodities: a) milk and milk
products, b) semen." (There follows a list of other safe commodities).
There is a considerable literature on the subject (see ref. below). The main
evidences come from the absence of transmission studies of BSE via semen or
any male reproductive tissue inoculated i/c into mice and epidemiological
studies in the field (that endorses the safety of commercial semen for AI).
I know of no link between the introduction of AI and the occurrence of BSE.
(Any concern would not be) from the semen itself but rather from
constituents of the diluent, if they were of animal origin and not sourced
appropriately, or became contaminated with BSE agents in any way. The same
goes for instruments if they got contaminated and were re-used. For the most
part disposable instruments are used for other reasons than BSE control.
AI does not involve the use of bovine pituitary derived hormones. There have
been no reports to my knowledge or evidence of iatrogenic transmission of
BSE into any species by the use of medicinal or biological products.
Pituitrin is now synthetic anyway. Pituitary gonadotrophins if prepared from
bovine pituitaries are prepared from safe sources otherwise they would not
be licensed.
I am not aware that studies have been published on the presence or absence
of PrP C in male reproductive tissues. The question is irrelevant however
since PrP C is expressed in a wide range of animal tissues (including muscle
and heart for example) in which no detectable infectivity is found in
diseased individuals. Every cell in the body has the genetic capability to
produce PrP C so that is why I think the question is irrelevant.
I am not aware of any publication that indicates that freezing/thawing
converts PrP C into an infectious form. If it did I do not think I would
like to go out on cold days or get things from the fridge! BSE is not a
familial disease. In fact, there is no animal TSE that is the direct
equivalent of familial CJD in man. The epidemio-logical studies referred to
above indicate clearly that even bulls that develop BSE have a similar
incidence of BSE in their adult female offspring as do healthy bulls without
BSE. BSE is a largely or entirely a feed-transmitted disease.
I cannot believe that in this era anyone can propose that semen transmits
BSE, even though there are no controls on it (other than that semen from
bulls that get BSE is destroyed along with the bull) yet there are controls
on feed, and where these are properly enforced (UK and Switzerland) the BSE
epidemic is in continuous decline; yet where they are not, or have not been
until recently, (Germany, Spain, France, Ireland, Portugal) the epidemics
are increasing. I really do believe that at this time countries should put
in the greatest of efforts to secure the safe feeding of ruminant and other
species rather than worry too much about semen. Ours from the UK has gone
all over the world!
It also may be of interest that bulls kept for commercial AI do not return
to stud until around 6 years old after the results of progeny testing are
complete. Since the mean incubation period of BSE is 5 years it is
improbable that a bull will develop develop clinical signs of BSE whilst at
stud and collections are being made.
(The hypothesis could be tested) by introducing high titre infected BSE
brain material into the uterus of a BSE free heifer and waiting for 7 years
to see if BSE develops and if the incubation period is longer or shorter
than if the same dose is given by the oral route. However, this is a purely
academic exercise of no practical value.
---
Ray Bradley
Ministry of Agriculture, Fisheries & Food
London, UK
<r.bradley@vla.maff.gov.uk>
<raybradley@btinternet.com>
Reference:
------------
Bradley R and Wilesmith JW (1993). B Med Bull 49, 932-959 Opinions of the
EC Scientific Steering Committee (visit their website) Wrathall A E (2000).
Livestock Production Science 62, 287 - 316 (10 columns of references in
this).
--
ProMED-mail
<promed@promedmail.org>
[Apropos, I received among other comments similar to Ray´s but in less
detail. The following was received from Ralph Blanchfield:
Wilesmith et al, Bovine spongiform encephalopathy: Epidemiological Studies,
Vet Record, 1988, 123, 638-644.
On checking that paper, I found my recollection was correct that AI played
no part in BSE:
"The analysis of the records of purchases of animals and the investigation
of the pedigrees of the sires used, particularly in closed herds, provided
conclusive evidence that BSE was not introduced into Great Britain by
imported cattle or disseminated via semen". - MHJ]
.
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