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Claudia Schulz,1 Christine Fast, Kore Schlottau, Bernd Hoffmann, Martin Beer Eradication of small ruminant morbillivirus (PPRV) is target- ed for 2030.

PPRV lineage IV is found in much of Asia and Africa. We used PPRV lineage IV strain Kurdistan/2011 in transmission trials to investigate the role of pigs, wild boar, and small ruminants as PPRV reservoirs. Suids were a pos- sible source of infection. Peste des petits ruminants is one of the most serious (economically and clinically) transboundary animal diseases (1C3). Of

4 lineages, small ruminant morbilli- virus (previously called peste des petits ruminants virus;

PPRV) lineage IV (PPRV-LIV) has spread the most widely in the past decade, particularly in Asia, and increasingly dominates the PPRV lineages in Africa (2,4). Morbidity and mortality rates for goats are high, up to 100%;

how- ever, sheep can be subclinically infected and play a ma- jor role in the silent spread of PPRV over large distances and across borders (3). The role of other wild and domestic Artiodactyls in the epidemiology of PPRV is unknown or insufficiently understood (3). Pigs are considered dead-end hosts for PPRV (5). In an experimental infection study, pigs infected with PPRV lineage II (LII) strains did not trans- mit PPRV to goats, but they can transmit the closely re- lated Rinderpest morbillivirus to cattle (6). To determine the pathogenesis of PPRV-LIV infection in pigs and wild boar and the capability of these suids to transmit PPRV in comparison with that of goats and sheep, we conducted

4 independent transmission trials during 2015C2016. The ex- perimental protocol was reviewed by a state ethics com- mission and approved by the State Office for Agriculture, Food Safety and Fisheries of Mecklenburg-Vorpommern, Rostock, Germany (LALLF M-V/TSD/7221.3-1-018/14). The Study In

4 trials (trials 1C4;

Table), we intranasally inoculated suids with a recent PPRV-LIV strain (Kurdistan/2011 [7,8]). Contact control animals were added

2 days later. We recorded clinical signs and temperature regularly and collected samples to evaluate the suitability of different virologic, serologic, and pathological methods for detect- ing PPRV infection. We conducted statistical analyses to calculate whether PPRV RNA loads in secretions and ex- cretions (oral, nasal, and fecal swab samples) collected over time from pigs, wild boar, goats, and sheep differed significantly and to determine correlations between the results of virus isolation and PCR assays by using swab samples and purified leukocytes as sample materials (on- line Technical Appendix, https://wwwnc.cdc.gov/EID/ article/24/12/18-0507- Techapp1.pdf). As expected, goats showed the typical moderate to severe clinical signs (trials

1 and 3) reported previously (7C9). Clinical signs in PPRV-infected sheep (trial 4) were generally mild to moderate, as previously described (3,8). Contact controls showed similar clinical signs. One PPRV- infected sheep showed severe clinical signs similar to those of the goats. Surprisingly, all PPRV infected pigs and wild boar (trials 1C3) showed various mild to moderate clinical signs, including fever and reduced general condition (all suids), diarrhea (pig 1, boar 1C4), and ocular (pigs 1C3) and nasal (boar 4) discharge typical for PPRV infection (Fig- ure 1;

Figure 2, panels ACC;

online Technical Appendix). PPRV-induced immunosuppression may predispose af- fected animals to secondary infections (3,9) as reflected by distinct severe leukocytopenia in pigs and goats a few days after inoculation. Different expressions of clinical signs af- ter PPRV infection might have been caused by concurrent infections with other pathogens or differences in individual resistance to PPRV infection (9). In the