Citrus Canker: Pathogen, Xanthomonas

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n 1910 Citrus Canker was introduced to the United States on trifoliate rootstock seedlings that were imported Japan. The disease spread rapidly around the Gulf Coast. Starting in Texas, it made it’s way east to Florida, then north to South Carolina. The pathogen, Xanthomonas axonopodis has two pathovars known to cause Canker; one being citri, and the other being aurantifolii. These can affect all citrus cultivars and even some citrus relatives. This bacterium is not known to be harmful to humans or other animals.

Xanthomonas axonopodis is classified as a gram negative Protobacteria. Because the bacterium are gram negative, they all have an outer membrane of lipopolysaccharide (LPS) and a phospholipid inner membrane.They are aerobic and rod
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There are three known forms; Asiatic Canker (A), Canker B, and Canker C. Asiatic is the most known and widespread variety of Citrus Canker. This type of canker accounts for most of the damage done to a large variety of citrus trees. Canker B is mostly known to be a problem for lemons in South America. Canker C is primarily known to effect the “Mexican” lime in Brazil. Xanthomonas axonopodis resides on the surface of leaves and above ground tissues. The source of primary inoculum are the erupting pustules. Wind and rain are the primary modes of transportation for this bacterium; entering mostly through injuries or stomates. Citrus Canker starts from spots that can attain a maximum size of 2-10 mm in diameter. The size depends on the age of the host tissue at the time of infection and on the type of citrus cultivar (Gottwald et al). After infection, there is a 7 to 10 day period before the lesion becomes visible. The lesions always start on the underside of the leaf and then appear on the upper surface. The lesions turn gray to tan brown as they age. These raised, corky tissues are usually surrounded by a yellow halo. Lesions on twigs and branches can persist for several years with bacteria living inside them. Severely blemished fruits can drop prematurely, while the internal quality of mature fruit is unaffected by individual lesions. Some lesions may penetrate deeper into the rind and expose the flesh to secondary infection by decay

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