Xanthomonas campestris pv. campestris

Members of the plant family Brassicaceae (Cruciferae), which includes cabbage, broccoli, cauliflower, kale, turnip, oilseed rape, mustard, radish, and the model organism Arabidopsis thaliana are affected by black rot.^{[4][9][10][11][5]}

Host infection by Xcc causes V-shaped chlorotic to necrotic foliar lesions, vascular blackening, wilting, stunted growth, and stem rot symptoms.^[4] As the pathogen proceeds from the leaf margins towards the veins, water stress and chlorotic symptoms develop due to occlusion of water-conducting vessels by bacterial exopolysaccharides and components of degraded plant cell walls.^[4][9] The darkening of vascular tissues following bacterial invasion gives the black rot disease its name.^[5] Lesions produced by Xcc may serve as portals of entry for other soft-rot pathogens such as Pectobacterium carotovorum (formerly Erwinia carotovora) and Pseudomonas marginalis.^[4][5][11]

These symptoms may be confused with fusarium wilt of cabbage (fusarium yellows), caused by the fungus Fusarium oxysporum f. sp.Tooltip forma specialis conglutinans. In contrast to black rot, in which the pathogen invades leaf margins and causes chlorotic to necrotic symptoms that progress downwards in the plant, fusarium wilt symptoms first develop in the lower portions of the plant and move upwards.^[12] Furthermore, leaf veins invaded by Xcc turn black compared to the dark brown vein discoloration found in fusarium wilt.^[12][13]

Symptoms of black rot may vary widely among different species of crucifers. On cauliflower, Xcc infection via stomata causes black or brown specks, scratched leaf margins, black veins, and discolored curds.^[14] Additionally, the severity of symptoms and aggressiveness of the disease varies between different strains of the Xcc pathogen.^[4] The isolates can be differentiated into races based on the reaction of several Brassica lines after inoculation. A race structure including five races (0 to 4) was first proposed in 1992;^[15] a revised classification model with six races was proposed in 2001^[16] and, more recently, the model was expanded to include nine races.^[3][17]

The primary source of inoculum is Xcc infected seed.^[4] During germination, the seedling becomes infected through the epicotyl^[4] and cotyledons may develop blackened margins, shrivel, and drop.^[9] The bacteria progress through the vascular system to the young stems and leaves, where the disease manifests as V-shaped chlorotic to necrotic lesions extending from the leaf margins. Under humid conditions, bacteria present in guttation droplets can be spread by wind, rain, water splashes, and mechanical equipment to neighboring plants.^[4][9]

The natural route of invasion by Xcc is through the hydathodes, though leaf wounds caused by insects and plant roots may also be portals of entry.^[4] Occasionally, infections occur through stomata. Hydathodes provide the pathogen a direct path from the leaf margins to the plant vascular system and thus systemic host infection. Invasion of the suture vein leads to production of Xcc infected seed.^{[citation needed]}

Xcc can survive in plant debris in soil for up to 2 years, but not more than 6 weeks in free soil.^[4] Bacteria present in plant debris can serve as a source of secondary inoculum.^{[citation needed]}

Warm and wet conditions favor plant infection by Xcc and the development of disease.^[9][11] Free moisture is required for host invasion, considering that the natural route of infection is through the hydathodes.

The optimum temperature range for bacterial growth and host symptom development is between 25° and 30 °C. A slower rate of growth is observed at temperatures as low as 5 °C and up to 35 °C.^[9] However, infected hosts are symptomless below 18 °C.^[18]