Dear Timothy

 

Paul’s arguments are very reasonable and suggest that it is harder to explain emergence of PPR than a simple ecological niche argument or the loss of cross protection from RPV virus or the vaccine might suggest. There is also your valid argument that the emergence might relate simply to improved detection methods. However this does not stand for the apparent movement of virus into buffalo populations in Uganda between 2002 and 2004. Here antibody baselines in buffalo population were negative in 2002 and then when these same populations were resampled in 2004 there was seroconversion of between 25 – 45% of the populations. Coincidentally the first cases in Uganda in livestock were reported (see AU IBAR ARIS reports in 2004) albeit in only one location Soroti (official reports to OIE only noted PPR in 2007). We were able to also show significant seroconversions in buffalo across several protect areas throughout the country simultaneously. Unless these data represent false positives (and the Soroti data suggest they are probably correct) this is highly suggestive of a rapid spread of virus over a year or two across Uganda. And if this was indicative of an overall trend in virus movement at that time this explains also the epidemics in Kenya in 2006 which were severe, suggesting naïve populations. In West Central and Ethiopia spill over antibody in wildlife has been detected in areas of known endemic PPR for some years before this. As indicators, wildlife appear to be useful and in the case of East Africa supporting evidence of true emergence although the reasons remain unexplained! We have also detected antibody in tiang antelope in South Sudan at a seroprevalence suggestive of true virus circulation similar to what we experienced with RPV in buffalo in the 1990s which is also highly interesting and will follow this up over this year to determine the epidemiology in this large population if possible.

 

I hope very much that the wildlife data shows that we need not consider them as an epidemiological threat but before we can do this we must confirm and understand these earlier findings. Widespread coordinated vaccination before this is done will be premature…and probably should only be directed at vulnerable populations which can be protected efficiently – where virus is circulating strongly there is probable little point as the virus will do the job for you.

 

We are currently planning our first sampling missions under IUEPPR funding in Uganda Tanzania to look at populations of wildlife, and we should be able to confirm these earlier data as animals alive at that time will still be present in Uganda buffalo populations. We will also see if there is evidence for similar spill over events in Tanzania. Random sampling so far from Kenya and Tanzania wildlife over the period of emergence 2006-present have not shown positives which is also perplexing but could be explained by contact probabilities given samples were note taken in outbreak areas specifically. We will also initiate studies in South Sudan and in other countries. For more detail please contact Satya at Pirbright who is also involved in this forum.

 

More anon..

 

All best

 

 

Richard Kock

Professor Wildlife Health and Emerging Diseases

Department of Pathology and Infectious Diseases

The Royal Veterinary College

Hawkshead Lane

North Mymms

Hertfordshire, AL9 7TA

England

Tel: +44(0)170766 6396 (Office)

Tel: +44(0)7903392359 (Mobile)

Email:   [log in to unmask]

 

Adjunct Prof. Faculty of Veterinary Medicine, University of Tufts, Grafton Mass. USA

Co-Chair IUCN Species Survival Commission - Wildlife Health Specialist Group

 

 

 

 

From: Establishment of a PPR Global Research and Expertise Network (PPR-GREN) [mailto:[log in to unmask]] On Behalf Of Timothy Obi
Sent: 10 February 2014 13:43
To: [log in to unmask]
Subject: Re: (1)Did PPR benefit from rinderpest eradication? (2). PPRV in cattle. Moderator's input

 

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.

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