Thanks Paul for your thought-provoking comments. I believe that PPR existed long before outbreaks were recorded/reported. In west Africa although the disease was  reported by Gargadenec and Lallane in !942 from Cote d'Ivoire , it took about 25 years later for the disease to be recognized in Nigeria. with the re-emergence of rinderpest in Africa a very effective networked laboratory diagnostic capability was established, sustained by PARC and this made us think rinderpest, rinderpest and rinderpest. We had very robust and easy to perform tests that could differentiate RP from PPR. The more we did this the more we were able to also see PPR . 
Remember that natural rinderpest was reported in sheep grazed with infected cattle in Nigeria by Johnson 1958. In India outbreaks involving only sheep and goats but later spreading to cattle were reported  (Narayanaswamy and Ramani, 1973). You may wish to refer to our serological studies with PPR and Rinderpest viruses in sheep and goats (Obi, Rowe and Taylor 1984). Although neutralizing antibodies against the two viruses  were detected, parallel titration of samples which neutralized both viruses indicated primary infection with the PPR virus. Some samples which failed to neutralize PPRV neutralized RPV indicating some low level rinderpest virus activity in small ruminants. But I don't think the population of antibody positive population in sheep and goats was high enough to suppress PPR. 
In Nigeria control of PPR by vaccination using formerly TCRV and later homologous PPR vaccine has been largely neighter coordinated nor sustained resulting in an endemic situation. We should not adopt a live-with it option. We need better coordination using appropriate vaccine and should not be free as I suggested in my first contribution. I equally agree PPR control should be packaged into a small ruminant health programme to make it more attractive to funding organizations.
Prof. Timothy Obi

Date: Sun, 9 Feb 2014 18:14:34 +0000
From: [log in to unmask]
Subject: (1)Did PPR benefit from rinderpest eradication? (2). PPRV in cattle.  Moderator's input
To: [log in to unmask]

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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