Rhizomania     The first Rhizomania citing was described in Italy in1952. Movement of infested soil apparently spread it. Rhizomania subsequently was reported in Japan in 1969; California in 1983; Texas in 1986; and Idaho, and Nebraska in 1992.  The spreading agent wasn’t known until 1973 when Japanese plant pathologists showed rhizomania was caused by a virus, and that a common soil borne fungus served as the vector of the virus.  Symptoms vary greatly, with some infected plants occasionally appearing healthy. Classical root symptoms following early infection include a mass of fine, hairy secondary roots, mostly dead, that give the taproot a beard-like appearance.  With slightly later infection, the storage root often is rotted and constricted, becoming much broader near the crown resembling the shape of a wine glass. Infected roots occasionally rot. Very late infections may result in no obvious symptoms.  Diseased plants usually occur in patches or areas of the field and not as scattered individual plants dispersed throughout the field.  Because a vector that thrives in moist areas carries the virus, disease severity usually is greatest in depressions poorly drained portions of the field that collect water and stay wet.  Control measures are limited because the virus may stay dormant in spore stage for many years.  The use of soil-applied fungicides has not been effective for rhizomania control in infested fields.  Resistant varieties of sugar beet are currently the best option.  This virus is a particular concern to the sugar beet industry of Western Nebraska.