First Report of Systemic Downy Mildew of Opium Poppy Caused by Peronospora somniferi in Australia
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Thangavel, T and Wilson, CR and Jones, S and Scott, JB and Voglmayr, H, First Report of Systemic Downy Mildew of Opium Poppy Caused by Peronospora somniferi in Australia, Plant Disease, 101, (2) pp. 392-392. ISSN 0191-2917 (2017) [Letter or Note in Journal]
© The American Phytopathological Society.Opium poppy (Papaver somniferum) is a highly valuable crop grown for its opiate alkaloid content, primarily morphine, thebaine, and codeine. Australia is the world’s largest producer of licit opiates, cultivating ∼50% of world poppy production, with an estimated farm gate value of $60 million. Downy mildew has been a major constraint to poppy production since it was first recorded in 1996 (Cotterill and Pascoe 1998; Scott et al. 2004). The pathogen was recently reclassified as Peronospora meconopsidis (Voglmayr et al. 2014). This downy mildew species produces vein-delimited, angular, localized necrotic lesions with sparse sporulation on abaxial leaf surfaces. A second downy mildew species, P. somniferi, has been recorded to produce systemic infections, resulting in stunting and deformation of opium poppy in Europe (Voglmayr et al. 2014). In the 2013/14 season, stunted poppy plants with chlorotic distorted leaves, little or no necrosis, and profuse abaxial sporulation were observed within commercial crops in Tasmania, Australia, for the first time. Affected plants also had strongly distorted stems. These symptoms were characteristic of systemic downy mildew infection. In the 2014/15 season, the incidence of plants with systemic downy mildew symptoms was widespread and resulted in complete crop loss in some fields. Pathogen samples were collected from leaves with systemic symptoms. Microscopic examination revealed the presence of hyaline conidiophores and conidia typical of Peronospora. Conidiophores (n = 10) were 290 to 530 μm long, with bifurcating branches. Paired terminal branchlets (n = 24) were 4.2 to 15.9 μm long and straight to slightly curved. Ovoid, hyaline conidia (n = 24) were 17.8 to 23.8 μm long and 14.3 to 17.2 μm wide, with length/width ratios between 1.19 and 1.47. Leaves with systemic symptoms were collected from a commercial field at Gawler in December 2015. Conidial suspensions were collected from leaves by rinsing with sterile deionized water and used to inoculate 6- to 8-week-old poppy seedlings. Seedlings were maintained in a growth chamber (16 to 21°C, 10:14 h dark/light regime; relative humidity 70 to 90%). Systemic symptoms of distorted, chlorotic leaves and stunted plants were observed after 14 to 21 days. Disease development was acropetal, with symptomless lower leaves and obvious symptoms on upper leaves. DNA was extracted from infected leaf tissues and extracts tested by PCR using primers targeting conserved regions of the coxI (Robideau et al. 2011) and coxII (Hudspeth et al. 2000) genes in Peronospora spp. Amplicons of 702 and 603 bp were obtained for the coxI and coxII gene regions, respectively. These were sequenced (GenBank accession nos. KX242325 and KX242326) and compared with published sequences (Voglmayr et al. 2014). Maximum likelihood phylogenetic analysis using a concatenate alignment of these two gene regions confirmed that systemic symptoms on Tasmanian opium poppy crops were caused by P. somniferi. This is the first record of P. somniferi in Australia and represents a major new threat to poppy production in this country.
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