Causal agent of sugarcane leaf scald. Prolonged latent infection can occur, necessitating detection by isolation or sensitive molecular assays. Produces albicidin toxins that block prokaryotic DNA replication and plastid development, causing chlorosis in emerging leaves. Albicidins interfere with host resistance mechanisms, allowing systemic invasion.
Strains vary in virulence.
Eradication is impractical because of alternative hosts. Measures to reduce inoculum sources and transmission can reduce losses. Long-term control requires sugarcane varieties with introgressed resistance, thus limiting gains from breeding. Characteristic white pencil lines and extensive chlorosis of emerging leaves in the chronic form of sugarcane leaf scald disease, and side shoots on a more severely diseased plant.