Global PPR Status
PPR infection was first described in Côte d’Ivoire West Africa in 1942. In 1987, PPR appeared in the Middle East and has since then been confirmed in Arabia (Abu-Elzein et al., 1990), Jordan (Lefevre et al., 1991), southern India (Shaila et al., 1989, Nanda et al., 1996), Bangladesh (Sil et al., 1995), Pakistan (Amjad et al., 1996), Iraq (Barhoom et al., 2000), Afghanistan (Abdollahpour et al., 2006), Turkey (Ozkul et al., 2002; Toplu, 2004; Anderson and Sammin, 2005; Yesilbag et al., 2005), Kazakhstan (Lundervold et al., 2004) and Tajikistan (Kwiatek et al., 2007), Nepal (Banyard et al., 2010), China (Wang et al., 2009) and Bhutan (Banyard et al., 2010). PPR has received a growing attention because of its continuing spread and economic impacts (Lefevre and Diallo, 1990). As per May 2019, among the 198 countries recognized by the United Nations, 57 have already have PPR-free status according to OIE Standards, while 67 are infected and 74 have never reported PPR (FAO/OIE, 2015). Although the primary hosts of PPR are goats and sheep, the host range of PPR has been continuously expanding and reported to infect various animal hosts over the last decades, which could bring a potential challenge to effectively control and eradicate PPR globally (Dou et al., 2020).
PPR is caused by PPR virus (PPRV) which belongs to the genusMorbillivirus of the family Paramyxoviridae (sub familyParamyxovirinae ) under the order Mononegavirales , like Measles virus, Rinderpest virus, Distemper virus and Newcastle disease (ND) virus (Salami et al., 2014). PPRV has a tropism for both epithelial and lymphoid cells (Kumar et al., 2014). Clinical signs in small ruminants typically start with dullness and fever, progressing to mucopurulent oral, ocular and nasal discharge, followed by oral lesions, bronchopneumonia and diarrhoea (Albina et al., 2013; Balamurugan et al., 2014; Kumar et al., 2014). Animals can excrete PPRV prior to the onset of clinical signs (OIE, 2016; Parida et al., 2015), with large quantities of PPRV excreted in discharges from infected animals. However, PPRV is not stable in the environment and requires direct transmission in fluids for infectious spread (OIE, 2016; Parida et al., 2015). The extent of clinical signs, morbidity and mortality can depend on the viral strain, the environment and the immune status of the animal (Parida et al., 2015; Ratta et al., 2016; Santhamani et al, 2016). The virus has a high morbidity and mortality, reaching to 100% and over 90% in naïve herds, respectively (Parida et al., 2015). Mortality occurs between 5 and 10 days of onset of infection, with the few recovering animals developing strong lifelong immunity (OIE, 2016; Parida et al., 2015). Phylogenetically, based on the fusion (F) and nucleocapsid (N) genes, PPRV can be classified into four distinct lineages. PPRV lineages I and II are exclusively isolated from the countries in West Africa where PPRV originated. Lineage III is restricted to the Middle East and East Africa. Lineage IV is currently most prevalent in Asian countries and becoming overwhelmed lineage in Africa. (Munir et al., 2013; Banyard et al., 2010; Dhar et al., 2002; Dundon et al., 2014; Muniraju et al., 2016; OIE, 2016). Lineage IV historically only affected Asia, although has spread into Western and central Africa over the last two decades and northern Africa with PPRV described in Morocco 2008 and 2015, Algeria 2010 (OIE, 2016; Parida et al., 2015). PPRV Lineage III has also been described in the Middle East (OIE, 2016).