Dear Satya,
thanks for this experiment with the PPR vaccine. I can confirm that during the development on the current attenuated vaccine PPR 75/1, I did the same experiment : vaccination of goats. In-contact naive animals remained negative by serology and virus isolation. this is not the same case when goats/ sheep are infected with virulent strain of PPRV. In-contact animals are infected with expression of clinical signs.
Regards
E. Couacy-Hymann
Date: Mon, 10 Feb 2014 20:36:44 +0000
From: [log in to unmask]
Subject: Re: (1)Did PPR benefit from rinderpest eradication? (2). PPRV in cattle. Moderator's input
To: [log in to unmask]
Dear Paul,
Please find answer to your query “All the original laboratory work showed that vaccinated cattle did
not shed tissue culture rinderpest virus. (It might have been better if they did because we would have had a much easier task of achieving high herd immunity rates thereby eradicating rinderpest earlier. Perhaps this is another challenge for the laboratories
– please can we have a safe vaccine against PPR that transmits itself a little bit?).”
Answer: Two months before I had done a PPR vaccine challenge experiment in Pirbright Isolation unit and from the eye swab of vaccinated goats I was able to revive the vaccine
virus on 8 days post vaccination. However I kept two naïve goats with these vaccinated animals to check the transmission and could not find any PPR specific antibody in these two animals on 28 days post-vaccination. May be the amount of vaccine virus excreted
through tears (eye swabs) are not sufficient to infect these naïve animals as we recovered these virus after second passage in many animals and 1st passage in few animals. In contrast the infected goats without vaccinenation excretes a large quantity
of virus and almost all eye swabs were positive for virus isolation. Therefore there is a chance that these infected unvaccinated goats may transmit virus to other naïve sheep, goats and cattle live together.
Best regards
Satya
From: Establishment of a PPR Global Research and Expertise Network
(PPR-GREN) [mailto:[log in to unmask]] On Behalf Of Paul Rossiter
Sent: 09 February 2014 18:15
To: [log in to unmask]
Subject: (1)Did PPR benefit from rinderpest eradication? (2). PPRV in cattle. Moderator's input
Dear Colleagues,
(1) Thanks to those of you who sent in answers to Dr Ithondeka’s question. I am not sure that we have fully answered it and, since one of my jobs as
moderator is to stimulate discussion or stir things up a bit, I am going to put my head on the block with a few thoughts on the subject.
The original question relates to the apparent upsurge in the distribution of PPR in many parts of the Old World at or just after the eradication of rinderpest
from the same territories. What I think is the underlying concern is whether or not the upsurge of PPR, especially in East Africa, was just a coincidence or was in some way aided or even caused by the eradication of rinderpest (see other comments on this
from Drs Richard Kock, Ashley Banyard and Tim Obi). If the eradication of rinderpest did play a role then we should understand how this came about in order to avoid repeating it. To me, it would mean that the presence of rinderpest must have been suppressing
the transmission of PPRV in sheep and goats. Could this have been due to the virus itself immunizing nearby small ruminants or to rinderpest control measures especially vaccination?
Considering the possible immunizing potential of virulent RPV, we know from historical records and more recent serology that outbreaks of rinderpest in
cattle did transmit infection to sheep and goats and other species. But the published data on antibody prevalences in sheep and goats never remotely approached what might be considered sufficiently high levels of herd immunity capable of protecting whole
populations against infection with PPRV. Furthermore, even if this was a workable mechanism, the amount of clinical rinderpest actually circulating in cattle in Africa and most of Asia since the mid to late 1980s was far too low to trigger much immunization
of sheep and goats and certainly not of populations. In fact the sheep and goats into which PPR spread were nearly all born long after any rinderpest circulated in their vicinity. So I don’t think that virulent RPV immunization caused the “upsurge”.
Similarly, I doubt that the vaccination of cattle with live RPV vaccine could have immunised nearby sheep and goats against PPR. All the original laboratory
work showed that vaccinated cattle did not shed tissue culture rinderpest virus. (It might have been better if they did because we would have had a much easier task of achieving high herd immunity rates thereby eradicating rinderpest earlier. Perhaps this
is another challenge for the laboratories – please can we have a safe vaccine against PPR that transmits itself a little bit?). If the vaccine couldn’t immunise other cattle by contact I cannot see how it would immunise sheep and goats to protective levels
of herd immunity against PPRV.
Another possibility is that RPV vaccine, especially when being withdrawn from use in cattle, was more widely used to protect sheep and goats against PPR
than was accounted for. Although this may have occurred in a few places I believe that most veterinary departments withdrew RPV vaccine from the field when cattle vaccination ceased and I think this is also unlikely to account for the epidemic surge of PPR
through East Africa and other places.
So, in answer to Dr Ithondeka’s question I don’t think that the upsurge in PPR was due to the eradication of rinderpest and I suspect that the real reason
lies in a combination of factors such as those described by Dr Libeau and other contributors. But…..
(2) Considering the reverse scenario of PPRV infecting cattle, buffaloes and other species, a subject raised in several contributions to the conference
including one from Dr Balamurugan, we know that nature is supposed to hate a vacuum. It is easy to imagine PPRV trying to grasp the opportunity of occupying the vacant niche or “natural vacuum” (cattle) left by the eradication of RPV. Fortunately, the evidence
from published studies and contributions to this conference is that although PPRV continues to have plenty of chances to fill this niche it has not yet succeeded in becoming “bovine PPRV” a virus (probably accompanied by a disease to facilitate transmission)
that is maintained independently of sheep and goats. Occasional jumps by RPV from cattle into sheep and goats did not lead to self-sustaining small ruminant rinderpest and did not affect the eradication of RPV. I don’t think occasional, self-limiting (no
or very little clinical disease, no transmission of virus) transmissions to cattle will affect our plans to eradicate PPRV, at least not at present. Whether or not this might become a problem in the future is another story and may depend on what we achieve
in sheep and goats - and some surveillance of cattle and other species.
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