History, biology and management of the plum pox virus
Editor’s note: This article is from the archives of the MSU Crop Advisory Team Alerts. Check the label of any pesticide referenced to ensure your use is included.
The stone fruit disease plum pox was confirmed for the first time in Michigan in July 2006. Plum pox was first found in North America in Pennsylvania in September 1999. The Michigan Department of Agriculture (MDA) has participated in a national surveillance program for plum pox virus (PPV) since 2000. The discovery of PPV in southwestern Michigan was the result of this ongoing survey. The USDA‘s Animal Plant Health Inspection Service (APHIS) is also involved in the detection effort and determining the spread of plum pox in the United States.
The virus causes chlorotic rings on the fruit and leaves of infected plants. Fruit of infected plants may be of poorer quality and distorted. Symptoms vary depending on the plant type, variety, condition of the plant, time of year, and the length of time the plant has been infected. Many trees may not show symptoms for the first few years following first infection. Symptoms on mature peach fruit consist of chlorotic rings or line patterns. Apricot and plum fruit will often be bumpy. European plum varieties can develop red discolored areas and drop prematurely whereas Japanese plums show ring spot symptoms. The D strain can cause severe necrotic spots on leaves of some plum varieties; peaches may have chlorotic spots and streaks, and apricot leaves typically show only mild symptoms. Leaf symptoms are more easily seen in spring.
PPV symptoms are sometimes difficult to distinguish from other diseases and may be confused with rusty spot of peaches and nectarines as well as insect-related problems such as damage from thrips, white apple leafhopper and San Jose scale.
Plum pox, also called Sharka, is considered one of the most serious virus diseases of stone fruit in Europe. The cradle of the disease is southeastern Europe. Early reports indicate Macedonia (part of former Yugoslavia) as the place where the first disease symptoms were observed as early as 1910. Growers in Bulgaria started reporting seeing pox on the plums during 1915-18. Bulgarian researcher Atanasoff was the first to write about the disease and its virology in his report ‘Sarka po slivite’ (Pox of Plums) in 1932. Since then, the disease spread slowly until after World War II. By the mid 1980’s, it had spread to most of Europe with the exception of Netherlands, Belgium and Switzerland where it was presumably eradicated. By the late 1980’s it had spread to Cyprus, Egypt, Syria and India. In Europe, there are some 100 million trees infected presenting a serious economic problem. Susceptible varieties can have up to 100 percent crop loss due to diminished quality or massive fruit drop about 10 days prior to harvest. In 1992, it was found in Chile in the Western Hemisphere.
Plum pox was first found in North America in Pennsylvania in October 1999. The USDA launched an extensive survey and eradication effort that eventually stretched over three counties. Plum pox was discovered in eastern Ontario and Nova Scotia in 2000, and western New York in early July 2006. PPV has apparently been eradicated from Nova Scotia. The USDA has pursued a vigorous policy of detection and eradication in the United States.
What is plum pox?
Plum pox is caused by a virus from the genus Potyvirus, one of the largest groups of plant viruses. It is the only known potyvirus infecting stone fruit Prunus sp. Four strains of PPV have been identified in the world. These strains are: PPV-M, PPV-EA, PPV-C and PPV-D. The most prevalent strain in central, eastern and southern Europe is strain M that infects peaches, plums and apricots. It is easily transmitted by aphids and, in certain varieties, by seed as well. It is considered to be the epidemic strain of the virus.
Strain EA is known to exist only in northern Africa. It will infect apricots. Strain C is probably the most devastating strain due to the wide range of species that can be infected. It is known as “cherry strain” since the natural host range includes sweet and sour cherries. It was isolated from the sour cherry trees in Moldova. It could be very easily transmitted onto other Prunus sp. by inoculation. It was wide spread in central and eastern Europe.
PPV-D strain is widely spread throughout western Europe. This is the only strain found in the Western Hemisphere, first in Chile, then in Pennsylvania and consequently in Canada, New York and Michigan. This Dideron or “D” strain of the virus infects peach, nectarine, plum, and apricots but not cherries. Research has shown that it is not seed-transmitted. The D strain is less aggressive than the M and EA strains. Numerous cultivated and weed annual plants can become artificially infected with PPV, but never have been shown to be a risk to stone fruit. Extensive surveys in Pennsylvania in areas adjacent to PPV-infected orchards provided no evidence that PPV has moved into wild species.
Infected peach, nectarine, plum and apricot trees are the primary source of PPV inoculum. The virus is spread to new areas by moving uncertified infected plant material through budding, grafting and transplanting, and by migrating aphids. Aphids are effective for spreading PPV within a tree and to adjacent trees. Aphids have several generations per year and have winged forms for movement from tree to tree.
Spread by aphids over long distances is less common. Natural barriers such as hills and woods help to restrict spread. Several aphid species can serve as carriers for PPV. Among the most important species are the green peach aphid (Myzus persicae), leaf curling plum aphid (Brachycaudus helichrysi), peach leafroll aphid (Myzus varians), damson-hop aphid (Myzus humili), thistle aphid that overwinters on plums (Brachycaudus cardui) and the spirea aphid (Aphis spiraecola) as well as many less commonly found in commercial stone fruit orchards.
Aphids common in stone fruit orchards generally have two to three generations per year and tend to be most abundant on lush foliage shortly after shuck split, especially during cool and wet springs. It is important to realize that some aphids such as cherry aphid (Myzus cerasi), mealy plum aphid (Hyalapterus pruni), and non-aphid arthropods such asleafhoppers (Edwardsonia plebei), lecanium scale (Lecanium corni) andplant bug (Lygus pratensis) are not capable of transmitting the virus.
Aphids obtain the virus while probing and feeding on infected plant tissue with a straw-like stylet for sucking up plant sap. The highest concentration of the virus is found in the cell sap of the leaf epidermal cells. When the aphid penetrates with its stylet into one of those cells, the virus is pulled into the stylet where it remains. Plum pox is a non-persistent virus, meaning that the aphid retains the virus in its mouthparts and foregut until its next feeding probe, usually less than one hour, and rarely as long as several hours. The virus is transmitted as soon as the aphid spears the cell with its stylet containing sufficient amount of virus obtained by the previous probing. An important point is that the virus does not circulate within the aphid, and it does not replicate itself while in the aphid’s body. Infections spread slowly cell-to-cell within plant tissue from the point of initial aphid feeding. Gradually, the infection spreads throughout the entire tree, especially if aphids continue to feed on the tree.
When the disease is first introduced to an orchard, the spread from tree-to-tree is slow, because of the low probability that a feeding aphid will encounter the virus. The speed of PPV spread in an orchard increases greatly as the number of aphids and number of infected trees increases.
Management strategies of plum pox are aimed primarily at preventing introduction by use of virus-tested clean nursery stock. Once detected, strict quarantine, eradication and ongoing surveys are the only useful strategies because a tree, once infected, will never be free of the disease.
Insecticide management strategies that keep aphid populations low may help to slow PPV movement in areas where PPV is rare, but may not be a good idea in some situations. Insecticide treatment can sometimes cause winged forms of the aphids to leave treated areas, taking the virus with them to infect new hosts.
Atanasoff, D. (1932). J. Univ. of Sofia Agr. Faculty 11: 49.Brunt ,A.A. et al. (1996). Plant Viruses Online.
Jordović,M. (1965). Zastita Bilja. 85-88: 353-355.
Jordović,M. (1967). Zastita Bilja. 96-97: 332-336.
Jordović,M. (1968). Zastita Bilja. 100-101: 273-277.
Jordović,M. (1969). Zastita Bilja. 104: 123-130.
Jordović,M., Ranković, M and Festić,H. (1970). Zastita Bilja. Ann. De Pathologie.71-72: 179-184.
Jordović,M, and Ranković,M. (1972). J.of Yugoslav Pomology. 21-22: 797-802.
Levy,L., Demsteegt, V., Scorza, R. and Kölber, M. (2000). APSnet. 3/1-31.
Nemeth, M. and Kolber,M. (1983). Acta Horticulturae. 130:293.
Ranković, M. and Jordović, M. (1970). Zastita Bilja. 21:109: 195-199.