Routine establishment of epidemics of systemic disease of Canada thistle (Cirsium arvense) caused by the rust fungus Puccinia punctiformis

Authors: Berner, Dana; Smallwood, Emily; Cavin, Craig; KASHEFI, JAVID - American Farm School; LAGOPODI, ANATASTIA - Aristotle University Of Thessaloniki

Submitted to: APS Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 3/14/2012
Publication Date: 6/1/2012
Citation: Berner, D.K., Smallwood, E.L., Cavin, C.A., Kashefi, J., Lagopodi, A. 2012. Routine establishment of epidemics of systemic disease of Canada thistle (Cirsium arvense) caused by the rust fungus Puccinia punctiformis [abstract]. APS Annual Meeting. 102:S31.

Interpretive Summary:

Technical Abstract: Because of observed effectiveness in eliminating Canada thistle (Cirsium arvense) patches, the rust fungus Puccinia punctiformis was proposed as a biological weed control agent in 1893. Since then, there has been considerable documentation on the effectiveness of the rust in controlling Canada thistle, but establishment of epidemics of the systemic state of the rust in disease-free thistle patches has not been accomplished. The reason for this failure has been lack of understanding of the disease cycle and the close synchrony between life stages of the host and the rust. We now understand the disease cycle much better and have used this knowledge to establish rust epidemics in fields in Maryland, USA and Greece. In the spring, systemically diseased shoots arise from roots infected with the fungus. The first signs of the fungus on these shoots are orange haploid pycnia (spermagonia) that cross fertilize to form haploid dikaryotic aeciospores. These spores infect leaves of nearby plants, producing local lesions, which give rise to uredinia that produce haploid dikaryotic urediniospores that, in turn, infect other leaves. In the late summer the uredinia transform into telia which undergo nuclear fusion (karyogamy). Through mitotic division the telia give rise to two-celled diploid teliospores. In the late summer and fall, the plants that emerged in the spring senesce and diseased leaves bearing telia dehisce onto newly emerging rosettes. Under conditions of adequate dew the teliospores undergo meiosis and germinate into haploid basidiospores that infect the rosettes. The fungus then develops hyphae that grow into the stem, and ultimately down into the roots of the rosettes where it survives the winter. Systemically diseased shoots emerge from this rootstock the following spring. Inoculating rosettes in the fall with teliospore-bearing leaves is a practical means of producing systemically diseased plants the following spring and initiating a disease epidemic.