Distribution, host range, and control of St. Augustine Decline1
- R. W. Toler
St. Augustine Decline was first observed in 1966 by lawn service operators in South Texas. The disease spread to 56 counties in the state of Texas by 1972, and has been observed in Louisiana and Mexico. In 1968 the disease agent was transmitted to St. Augustinegrass (Stenotaphrum secundatum Walt. Kuntz) and [Setaria italica (L.) Beauv.] millet. The symptoms developed earlier on millets (7 to 14 days) than on St. Augustinegrass (21 to 30 days). Transmission and in vitro studies determined the disease was caused by a strain of Panicum mosaic virus. Host range includes Proso (Panicum miliaceum L.), Pearl (Pennisetum glaucum (L.) R. Br.), and Foxtail (Setaria italica (L.) Beauv.) millets, as well as crabgrass (Digitaria sangiunalis (L.) Scop) and St. Augustinegrass. The symptoms on Proso were severe mosaic and necrosis, on Pearl millets terminal necrosis, and on Foxtail a uniform mottling. Symptoms on crabgrass were mottling and reddening, and on St. Augustinegrass mosaic, yellowing and necrosis. Inoculation techniques were developed to screen for sources of resistance in 1968. Of the genetic materials observed, Florida accession FA 110 had the highest level of resistance to the virus causing St. Augustine Decline. Additional index words: St. Augustinegrass, St. Augustine Decline, Alternate Hosts, Susceptibility, Floratam, Panicum mosaic virus SAD strain.Please view the pdf by using the Full Text (PDF) link under 'View' to the left.
Copyright © 1974. . Copyright 1974 by the American Society of Agronomy, Inc. and the Crop Science Society of America, Inc., 5585 Guilford Rd., Madison, WI 53711 USA