Citrus canker is a disease affecting Citrus species caused by the bacterium Xanthomonas axonopodis. Infection causes lesions on the leaves, stems, and fruit of citrus trees, including lime, oranges, and grapefruit. While not harmful to humans, canker significantly affects the vitality of citrus trees, causing leaves and fruit to drop prematurely; a fruit infected with canker is safe to eat, but too unsightly to be sold.
The disease, which is believed to have originated in Southeast Asia, is extremely persistent when it becomes established in an area. Citrus groves have been destroyed in attempts to eradicate the disease. Brazil and the United States are currently suffering from canker outbreaks.
Xanthomonas axonopodis is a rod-shaped Gram-negative bacterium with polar flagella. The bacterium has a genome length around 5 megabase pairs. A number of types of citrus canker diseases are caused by different pathovars and variants of the bacterium:
The Asiatic type of canker (canker A), X. axonopodis pv. citri, caused by a group of strains originally found in Asia, is the most widespread and severe form of the disease.
Cancrosis B, caused by a group of X. axonopodis pv. aurantifolii strains originally found in South America is a disease of lemons, key lime, bitter orange, and pomelo.
Cancrosis C, also caused by strains within X. axonopodis pv. aurantifolii, only infects key lime and bitter orange.
Plants infected with citrus canker have characteristic lesions on leaves, stems, and fruit with raised, brown, water-soaked margins, usually with a yellow halo or ring effect around the lesion. Older lesions have a corky appearance, still in many cases retaining the halo effect. The bacterium propagates in lesions in leaves, stems, and fruit. The lesions ooze bacterial cells that, when dispersed by windblown rain, can spread to other plants in the area. Infection may spread further by hurricanes. The disease can also be spread by contaminated equipment, and by transport of infected or apparently healthy plants. Due to latency of the disease, a plant may appear to be healthy, but actually be infected.
Citrus canker bacteria can enter through a plant's stomata or through wounds on leaves or other green parts. In most cases, younger leaves are considered to be the most susceptible. Also, damage caused by citrus leaf miner larvae (Phyllocnistis citrella) can be sites for infection to occur. Within a controlled laboratory setting, symptoms can appear in 14 days following inoculation into a susceptible host. In the field environment, the time for symptoms to appear and be clearly discernible from other foliar diseases varies; it may be on the order of several months after infection. Lower temperatures increase the latency of the disease. Citrus canker bacteria can stay viable in old lesions and other plant surfaces for several months.
The disease can be detected in groves and on fruit by the appearance of lesions. Early detection is critical in quarantine situations. Bacteria can be tested for pathogenicity by inoculating multiple citrus species with them. Additional diagnostic tests (antibody detection, fatty-acid profiling, and genetic procedures using polymerase chain reaction can be conducted to confirm diagnosis and may help to identify the particular canker strain. Clara H. Hasse was the woman responsible for finding the cause of the citrus canker, her research was published in the Journal of Agricultural Research in 1915. Her research played a major part in saving citrus crops in multiple states.
Not all species and varieties of citrus have been tested for citrus canker. Most of the common species and varieties of citrus are susceptible to it. Some species are more susceptible than others, while a few species are resistant to infection.
To many farmers concern, at this moment in time, scientists have not been able to come up with a proper system and a way to help these farmers. If this disease continues to spread on and on, farming citrus will become very costly and difficult too.
Citrus canker is thought to have originated in the area of Southeast Asia-India. It is now also present in Japan, South and Central Africa, the Middle East, Bangladesh, the Pacific Islands, some countries in South America, and Florida. Some areas of the world have eradicated citrus canker and others have ongoing eradication programs, but the disease remains endemic in most areas where it has appeared. Because of its rapid spread, high potential for damage, and impact on export sales and domestic trade, citrus canker is a significant threat to all citrus-growing regions.
The citrus industry is the largest fresh-fruit exporting industry in Australia. Australia has had three outbreaks of citrus canker, all of which have been successfully eradicated. The disease was found twice during the 1900s in the Northern Territory and was eradicated each time. In 2004, an unexplained outbreak occurred in central Queensland. The state and federal governments ordered all commercial groves, all noncommercial citrus trees, and all native lime trees (C. glauca) in the vicinity of Emerald to be destroyed rather than trying to isolate infected trees. Eradication was successful, with permission to replant being granted to farmers by the biosecurity unit of the Queensland Department of Primary Industries in early 2009.
Citrus is an important domestic and export crop for Brazil. Citrus agriculture is the second-most important agricultural activity in the state of São Paulo, the largest sweet orange production area in the world. Over 100,000 groves are in São Paulo, and the area planted with citrus is increasing. Of the estimated 2 million trees, greater than 80% are a single variety of orange, and the remainder is made up of tangerine and lemon trees. Because of the uniformity in citrus variety the state has been adversely affected by canker, causing crop and monetary losses. In Brazil, rather than destroying entire groves to eradicate the disease, contaminated trees and trees within a 30-m radius are destroyed; by 1998, over half a million trees had been destroyed.
Citrus canker was first found in the United States in 1910 not far from the Georgia – Florida border. Subsequently, canker was discovered in 1912 in Dade County, more than 400 mi (600 km) away. Beyond Florida, the disease was discovered in the Gulf states and reached as far north as South Carolina. It took more than 20 years to eradicate that outbreak of citrus canker, from 1913 through 1931, $2.5 million in state and private funds were spent to control it—a sum equivalent to $28 million in 2000 dollars. In 26 counties, some 257,745 grove trees and 3,093,110 nursery trees were destroyed by burning. Citrus canker was detected again on the Gulf Coast of Florida in 1986 and declared eradicated in 1994.
The most recent outbreak of citrus canker was discovered in Miami, Dade County, Florida, on Sept. 28, 1995, by Louis Willio Francillon, a Florida Department of Agriculture agronomist. Despite eradication attempts, by late 2005, the disease had been detected in many places distant from the original discovery, for example, in Orange Park, 315 miles (500 km) away. In January 2000, the Florida Department of Agriculture adopted a policy of removing all infected trees and all citrus trees within a 1900-ft radius of an infected tree in both residential areas and commercial groves. Previous to this eradication policy, the department eradicated all citrus trees within 125 ft of an infected one. The program ended in January 2006 following a statement from the USDA that eradication was not feasible.
Citrus canker is a disease of cultivated citrus plants caused by nonindigenous bacterial pathogen Xanthomonas axonopodis pv. citri ('Xac').Genus Xanthomonas consists of gram-negative, rod-shaped, polarly-flagellated bacteria whose members commonly occur as serious plant pathogens. Colonies are typically yellow in color due to the presence of a particular carotenoid pigment identified through relatively simple screening procedures and generally indicative of the genus (Starr and Stephens 1964).The pathogen expresses itself in infected citrus plants as brown, raised lesions on leaves and fruits with oily, water soaked and necrotic margins and a surrounding yellow halo. Affected areas of leaves may fall out in time, leaving holes. Microscopic examination of tissue sliced from the edges of active lesions on infected plants reveals streaming masses of rod-shaped bacteria (DACS 2002, ISSG).
Citrus canker is likely native to southeast Asia and India, but has now spread worldwide into to warm, moist, citrus-growing coastal regions. The pathogen is now also established in Australia, Japan, the Middle East, Africa, Papua New Guinea and elsewhere in the Pacific, and the Americas (Gotwald et al. 2002, Kumar et al. 2004).In Florida, citrus canker had been reported from 24 counties as of January 2006. Recent northward spread of citrus canker into central Florida is believed to be a consequence of the hurricanes of 2004 and 2005 (Gaskalla 2006). As of January 2006, citrus canker had been reported in the India River Lagoon region from Brevard, Indian River, St. Lucie, Martin, and Palm Beach counties (Gaskalla 2006). Most reports of citrus canker in the India River Lagoon region north of Martin County did not occur until after the 2004 hurricanes.
There are multiple strains or pathotypes of the Xanthomonas spp. citrus canker bacterium. The most devastating of these is X. axonopodis pv. citri pathotype A, also known as Asiatic citrus canker. Also present in Florida are pathotypes B and C of X. aurantifolia pv. aurantifolia and at least two pathotypes of the congeneric bacterium X. campestris, responsible for bacterial leaf spot disease in citrus (Integrated Plant Genetics Inc. undated, ISSG). An outbreak of bacterial leaf spot disease in Florida in 1984 was previously misidentified as a citrus canker outbreak (ISSG).Recent molecular studies have suggested that X. aurantifolii pv. citri should be reinstated to species status as X. citri.Florida citrus trees are now additionally under threat from citrus greening disease (also called huanglongbing, HLB, or yellow dragon disease), also a bacterial disease, that is believed to be capable of worse damage than canker. The responsible pathogen (unnamed as of 2007) is also not native to the U.S., and is considered by some to be the most serious worldwide citrus disease. Citrus greening disease was first reported from Florida in 2005. Disease symptoms are dissimilar to those of citrus canker, and include yellowing of shoots, leaf mottling or discoloration, and the production of lopsided poor-quality fruit.
The larval form of a moth known as the Asian citrus leaf miner (Phyllocnistis citrella), non-native in Florida, facilitates spread of the citrus canker bacterium through its leaf-burrowing activities which expose disease-causing X. axonopodis pv.citri to transport through wind and rain.Invasion History: Citrus canker was first identified in Florida approximately a century ago in 1910. Aggressive measures were taken to combat the disease and it was declared eradicated from the state in 1933. After an apparent absence of more than 50 years, citrus canker was again detected in Florida, in Manatee County in 1986. Once again, steps were taken to contain the disease and it was in 1994 again declared eradicated (Gaskalla 2006).Canker-infected plants were in 1995 again reported from south Florida, in the vicinity of Miami International Airport. An aggressive USDA-administered eradication program was established but proved unsuccessful. The Florida 2004 and 2005 hurricanes facilitated the spread of citrus canker in the state to the point that eradication was no longer deemed possible. Federal funds for eradication were withdrawn in 2006 and the response strategy shifted to a management and containment plan (Gaskalla 2006).Although individual plant quarantines have been eliminated, a USDA statewide quarantine remains in effect which places restrictions on the transport of harvested citrus or plant stocks out of the state. Transport of material to other citrus-producing states is prohibited. Prior to the 2006 lifting of individual quarantines, more than 600,000 ha of Florida land had been placed under enforced quarantine (FDOACS undated, Gaskalla 2006).The citrus canker pathogen was first reported in Palm Beach County in 1999 and in Martin County from a commercial citrus grove in 2001. Citrus canker in the IRL region north of Martin County largely did not occur until after the 2004 hurricanes. The post-hurricane appearance of canker was first reported from St. Lucie County in December 2004, from a sentinel survey site in Port St. Lucie. The first reports from Indian River County were post-hurricanes, December 2004, in a grove near the Indian River/St. Lucie county line. Confirmed reports of the disease in Brevard County as of 2005 were confined to a handful of residential sites.The citrus canker pathogen has been spread through the transport of fruit, plants, and equipment, and dispersal appears to be greatly facilitated by wind and rain. Overhead irrigation systems may also facilitate movement of citrus canker as does the leaf-burrowing activity of larval P. citrella. Potential to Compete With Natives: The biological impact of X. aurantifolii pv. citri is primarily as a plant pathogen; competition with native microbial species remains unreported. Possible Economic Consequences of Invasion: X. aurantifolii pv. citri is a serious disease agent of citrus crops in Florida and elsewhere. Infected trees exhibit a gradual decline in health and fruit production until they eventually succumb to the disease. As of January 2006, more than 15 million commercial trees in groves and nurseries had been destroyed in Florida as a result of efforts to eradicate citrus canker. Nearly 1 million residential trees were destroyed as well (Gaskalla 2006).Transport of live citrus plants in and out of Florida is currently prohibited. Homeowners who wish to plant citrus trees must purchase certified symptom-free citrus plants through nurseries registered with the state (FDOACS 2006).
Reproduction in genus Xanthomonas is similar to that of other bacteria, occurring through asexual binary fission in which each dividing clonal daughter cell receives an identical copy of the parental genome (Campbell et al. 1999).