Origin │ Habitat and Spread │ Impacts │ Identification on Potatoes │ Identification on Tomatoes│ Prevention and Control │ Occurrences

Background

Late blight (Phytophythora infestans) is a disease that affects the stem, leaves, fruits, and tubers of potato and tomato crops. The disease was first discovered in the United States in the early 1840s where it caused devastation to many crop yields. Late blight is also responsible for causing the Irish potato famine in 1845. Phytophythora infestans is an oomycete pathogen.  In other words, it shares similar superficial characteristics with fungi, such as reproduction using spores produced in sporangia, but it is actually more closely related to brown algae.

Origin

Late blight is thought to have originated from central Mexico before appearing in the United States and Europe in the 1840s.  By the beginning of the twentieth century, the disease has been spread worldwide.

Habitat and Spread

Phytophythora infestans (late blight) grows and reproduces rapidly on host crops such as tomatoes and potatoes, but may be found on other plant species as well. In the United States, there have been occurrences on hairy nightshade (Solanum sarachiodes), bittersweet (Solanum dulcamara), and petunias (Petunia hybride).  Typically, environments with high moisture and moderate temperatures (60° and 80° F) are ideal for rapid reproduction.

Late bight can survive from season to season by living in infected potato tubers. Under favorable conditions, the pathogen may produce millions of spores that may spread in the air by wind or through the soil in wet conditions.  The disease may further be spread by infected seed potatoes, growths from previously diseases potatoes that were not harvested in the previous year, cull and compost piles, and also plant transplants from one field to another.

Impacts

It is very important to identity and control late blight. The disease is capable of wiping out entire crops even in commercial sized fields if the conditions are favorable. Not only will potato and tomato yields decrease in a given year, but infected tubers could reside in the soil to infect future crops if not managed properly. Late blight can have a large economic impact on a community through loss of tomato and potato yields, increased unemployment, as well as through the cost of control. A study by Guenthner et al. (2001) estimated the late blight cost to US growers to be over $287 million or $507 per hectare taking into account yield decrease, storage loss, decline in quality, price adjustment, and fungicide use. Additionally, fungicide application requires the use of machinery, which increases the amount of fuel needed. From an environmental standpoint, this may lead to decreases in energy supplies and increased pollution of the air and water (Haverkort et al. 2008).

Identification on Potatoes

Purple-brown lesions may occur on the surface of a tuber. If cut, the tuber will have rotted tissue that extends approximately one inch into the tuber and will appear reddish-brown. Observing symptoms may become difficult if the tuber, which was previously infected by late blight, becomes invaded from a second source, such as bacteria.

After wet periods, black, water-soaked lesions on leaves may be noticed within a week after becoming infected.  Whitish growths (spores and sporangia) may be seen in humid conditions at the edges of the lesion, but once the lesion dries and turns brown, the spores will not be visible.

Stems of infected potato plants may have brown, greasy lesions. Stem lesions are frequently found at the junctions between the steam and a leaf, or at the top of a stem near clusters of leaves.

Identification on Tomatoes

Lesions that occur on the stem and leaves of tomato plants will look similar to lesions found on potato plants.  The fruit of tomatoes however, will have greasy circular lesion that may eventually become leathery and dark brown that take over the entire fruit. Spore producing structures may be present under humid conditions.

If you are unsure if the plant is infected by late blight, placing suspected infected leaves in a moist chamber overnight may produce the whitish sporangia.

There are some plant pathogens that look like late blight. If you are unsure if what you are dealing with is late blight contact your local Cornell Cooperative Extension or submit the plant to a diagnostic clinic for identification. Some common late blight look-a-likes include:

• Gray Mold: Late blight occurs in living tissue whereas gray mold will first establish itself in dead plant tissue.  Growth will be fuzzier and gray or brownish (not white). Affected fruit will soften, but not brown.
• Drought stress: Occurs when part of the leaf tissue browns at leaf edges when dying from lack of water. No fuzzy pathogen growth.
• Early blight: Spots on all parts of the plant are smaller than late blight, which has concentric ring patterns in them.
• Septoria leaf spot: Smaller leaf and stem spots than late blight with a tan center. Fruits are not affected.
• Buckeye fruit rot: Leaves and stems are not affected. Affects fruit (usually those close to soil) by turning them brown with white spores forming. Fruit stays firm and smooth.

Prevention and Control

It is best to try and avoid sources of spores early in the season. Only plant healthy certified seed potatoes as well as avoid any transplants or imported fruit that could have come in contact with the disease. Before planting, make sure to examine the seed and only plant those that are healthy and blemish free. Unhealthy, potentially infected seed and plants should be destroyed or made sure to be completely decomposed. If you had previously infected plants last season, make sure to remove all new growth. To prevent spores in the soil from infecting the potato tubers, you can hill up the soil around the plant base. Also, vines should be dead or cut above the soil surface 2-3 weeks before harvesting.

There are some potato and tomato varieties that are showing some resistance to late blight (Chen et al. 2003).  Planting these may be an alternative to slow down the spread of late blight, but may not necessarily prevent the disease from occurring. To decrease the impact of late blight on communities, researchers are further investigating genetic modification of potatoes to decrease susceptibility to late blight (Haverkort et al. 2008).

If it is known that late blight is in your area and the growing season is wet, there are fungicides that may help protect your plants. These need to be applied before coming in contact with the disease. Late blight can infect plants at any time during the growing season, so continual application of the fungicide may be needed.  Fungicides with maneb, mancozeb, chlorothalonil, or fixed copper and has tomato and potato late blight on the label could be used. There are concerns that overuse of fungicides may lead to the evolution of pesticide resistance within late blight. It is best to contact your local Cornell Cooperative Extension for more information about how to use pesticides and which ones are approved organic before using them. As always, it is important to read the instructions on the label and use the pesticides accordingly.

It is recommended to inspect plants every week for symptoms. If you experience an outbreak or know of local occurrences, it is also best to inform and educate neighboring growers.

Occurrences

As part of prevention of late blight, it is important to stay up-to-date on where late blight has already occurred by checking out www.usablight.org/map

Origin | Introduction and Spread | Impacts | Identification and Symptoms | Prevention | Control | Occurrences

Background

The plum pox virus (PPV) or Potyvirus sp. is a viral disease that affects stone fruits, especially those in the Prunus genus, such as plums, peaches, nectarines, apricots, almonds, and cherries. Sharka disease is another common name for PPV. There are six strains of PPV, of which, the D strain or Dideron strain has been identified in New York State. The D strain primarily infects peaches, nectarines, apricots, and plums.

Origin

Plum pox virus (PPV) was first reported in 1910 in Bulgaria.

Introduction and Spread

Plum pox virus has spread to many countries worldwide. The virus may be spread long distance by the transplant of infected plant propagations, nursery stock, or illegal traffic. Insufficient monitoring of stone fruit before transporting the fruit from one location to another is also a cause for spread. Some fruit may appear symptomless initially and may accidentally pass inspection. Plum pox virus spreads over a short distance using aphid vectors when sucking the sap of an infected plant and transferring it to a healthy plant. The D strain of PPV is not known to be seed-transmitted.

Impacts

It is estimated that the plum pox virus will have a $600 million per year economic impact on the plum, peach, and apricot industry worldwide (Fuchs et. al. 2008). A study from 2006 estimates the economic loss in previous years to the peach industry from the PPV D-strain in the United States and Canada to be about 4.8 million euros (about $6.1 million USD) from the removal of 264,000 trees in Canada and 190,000 trees in Pennsylvania (Cambra et al. 2006). Widespread outbreaks of the virus could lead to increase cost for consumers due to a decline in production and exportation.

Identification and Symptoms

Symptoms of plum pox virus may vary depending the virus strain, cultivar and various environmental factors. Symptoms may not be seen until three or more years after infection. Vein yellowing or light green to yellow rings or blotches may form on the plant leaves. Some leaves, such as those of peaches, may exhibit crinkling, curling, or puckering. Leaf symptoms are typically seen more at cooler temperatures in the spring and fall seasons.

Some larger flowers may exhibit color breaking, such as those on peach trees. The fruit of infected plants may have pigmented rings or patterns (seen in peaches), or look misshapen or deformed and turn brown (Apricots) or get rings or spots as well as discolored reddish flesh (Plums). In most cases, fruit yield and quality will decrease significantly.

Prevention

Careful regulation and control of plant material is important so that only pathogen-free material is used commercially. If you are a grower or a nursery make sure you are buying certified plant materials that have been virus tested. Also, extensive surveys, removal, and destruction of infected trees may help to prevent the disease from spreading further.

The PPV Lab at the New York State Agricultural Experiment Station in Geneva, NY works with the New York State Department of Agriculture and Markets and USDA-APHIS to screen Prunus trees for the plum pox virus in New York State.

For more information visit: http://web.pppmb.cals.cornell.edu/fuchs/ppv/ppv_detection.html
Watch a video about the process: http://web.pppmb.cals.cornell.edu/fuchs/ppv/detectionvideo.html

Control

Early detection of plum pox virus is important because there is no cure once it gets established in an orchard.  Once infected, trees with the virus, and those in a 50-meter radius, need to be removed and destroyed to eradicate PPV. This is important because PPV does not kill trees. If the trees are left to stand, the tree will remain as a reservoir for the virus (Cambra et al. 2006). Chemical control of aphids using insecticides has been found to be ineffective at stopping the spread of PPV. Currently, one of the prospects being looked into as a control and prevention method is developing plant resistance to PPV through the use of genetic engineering. If you have questions about the virus or control methods, contact your local extension office.

Occurrences

PPV spread across most of Europe by the 1970s. In the late 1990s, PPV had spread to many other countries in the eastern hemisphere and then was first detected in Chile in 1992. The first documentation of the disease in the United States was in Pennsylvania in 1999. By 2006, there were reports of the disease in New York and Michigan.  The D strain was originally isolated in France.

 

Introduction | Biology and Identification | Control and Prevention | New York’s Story

Introduction

Oak wilt (Ceratocystis fagacearum) is a systemic, lethal disease caused by a fungus. The fungus grows in the xylem (sapwood) of the infected oak eventually resulting in the vessels clogging with gums and tyloses and death of vascular cells which then prevents the uptake and movement of water.

In areas where oak wilt is established, the disease causes up to an 11% loss of annual growth in oak. (1)

Currently, there are few known infestations of Oak Wilt in New York State. These locations include Islip, Riverhead and Southhold in Suffolk County; Brooklyn in Kings County and Canandaigua in Ontario County. Oakwilt is also found in Glenville, Schenectady County. A small infestation was discovered and treated in 2008 but was found again in 2013. See below for more details on that outbreak. If you think your oak tree is infected with Oak Wilt, please contact your local Cornell Cooperative Extension or NYS Department of Environmental Conservation Lands and Forests office immediately. [Information updated as of 2018]

Hosts

Red oak is most severely affected and white oak is moderately affected. An infested tree begins to show symptoms in early summer. Red oaks typically perish within two month whereas white oaks can survive for many years with the disease.

Biology and Identification

Ceratocystis fagacearum, the oak wilt fungus, is spread to an oak tree via root grafts or beetles feeding on sap (nitidulids) at open wounds or on the leaves of healthy trees (oak bark beetles). Once inside the tree, the oak wilt fungus begins to replicate within the xylem of the tree.

Symptoms first appear near the top of the canopy. The outside of the leaves turn bronze, brown, or dull green, usually starting at the top of the leaf, while the base of the leaf remains green. Some leaves curl, droop and wilt. Leaves begin to drop soon after symptoms first develop.

In some species of oak, brown streaks develop in the outer sapwood of infected branches when leaf symptoms appear. This can be seen when an infected branch is cut diagonally. Eventually the tree loses all its leaves to the wilt.

The year following the defoliation, fungus or spore mats may form on the trunk under the bark and on the opposing wood. Oval mats are gray or tan and turn black with age. The mats develop pressure pads that push out and crack the bark, exposing the fungus mat. The mat has a fruity odor which attracts then contaminates sap feeding beetles. Those contaminated beetles then carry the fungus to open wounds on other oak trees. Mats are primarily formed on red oaks.

Spread

Oak wilt is primarily spread by beetles which feed on the fungus mats under the bark then carry spores to open wounds on nearby oak trees as well as through underground root grafts between oak trees. Infected trees form infection centers and mortality of oak occurs in rings from the initial infestation as the fungus moves through naturally occurring root grafts.

Root grafted oak trees usually die 1-6 years after the first oak is infected, and disease centers can move up to 50 feet per year.

Oak wilt can also be spread long distances through the movement of infested firewood.

Control and Prevention

If an oak tree in a known oak wilt infested area needs to be pruned, do not prune in the spring or summer, especially April, May and June when the fungal mats and the sap beetles are present. If it is necessary to prune, the use of wound paint will prevent contaminated beetles from spreading the fungus to the open wound. (Note: This is one of the few times wound dressing is recommended; normally the pruning wound should be allowed to heal exposed to the air.) Clean pruning equipment between cuts and trees. Do not use climbing irons/spikes on living oak trees.

Vibratory plows or backhoes can be used to break root grafts by creating a trench around individual or groups of trees. This severs roots which prevents the spread through the grafts.

Individual oak trees can also be treated with systemic fungicides. (Only if disease becomes more prevalant in NY. Until then, the tree should be removed.)

If you think you have an infected tree contact your local Cornell Cooperative Extension or DEC Lands and Forest office immediately. Trees found to be infected in New York should be cut, chipped, and burned.

Don’t Move Firewood. Oak wilt can be spread through firewood movement.

NYSDEC Firewood Regulation

 

History of Oak Wilt in NY

In 2008, a small infestation (76 trees) in Glenville, NY (Schenectady County) was found by an observant homeowner. He called his local Cornell Cooperative Extension horticulture educator who recognized it as oak wilt. Once the disease was confirmed by the experts at the USDA Forest Service, the NYS Department of Environmental Conservation –Forest Health Unit was able to quickly mobilize to survey and respond. All infected trees were removed and root zones were trenched (to sever root grafts). Monitoring has continued for three years and no additional oak wilt has been found. If no oak wilt is found in 2012 it will be deemed a successful eradication.

This case is a superb example of interagency cooperation between NYS DEC, NYS Agriculture and Markets, APHIS, Cornell University and Cooperative Extension, and local officials.

Prevention     Impacts     Federal Response    New York State Response

Viral hemorrhagic septicemia or VHS (Novirhabdovirus sp.) is a serious disease of fresh and saltwater fish, both in the wild and those raised for commercial aquaculture. VHS is caused by an aquatic rhabdovirus. The VHS virus is native to eastern and Western Europe (where it has affected cultured rainbow trout), the Pacific coast from California to Alaska (in Pacific herring and cod), and the Atlantic coast of North America (in Atlantic herring and Greenland halibut). The actual vector for the virus’s introduction into the Great Lakes is unknown. It is suspected that it may have been transported in ballast water or by migratory fishes from the Atlantic coast. It is possible that baitfish harvesting and movement, recreational boating and angling, as well as aquaculture activities are responsible for the spread of the virus since it arrived in the Great Lakes. Waterfowl may also play a role.

The virus is believed to have been present in Great Lakes muskellunge in Lake St. Clair since 2003. In 2005, several hundred tons of freshwater drum, muskellunge and round gobies died of VHS in Lake Ontario. Since that time, VHS-related fish kills of black crappie, bluegill, burbot, freshwater drum, gizzard shad, lake whitefish, muskellunge, northern pike, redhorse sucker, rock bass, round goby, smallmouth bass, white bass, yellow perch, and walleye have been confirmed in Lakes Erie, Huron, Michigan and Ontario, and the Niagara and St. Lawrence Rivers. Inland sightings of the virus in New York include Conesus and Skaneateles Lakes, the Seneca-Cayuga Canal, and a private pond in Ransomville (Niagara County).

Impacts

In its most acute form, VHS can cause hemorrhaging in the eyes, skin, gills, fin bases, skeletal muscle and internal organs, leading to high mortality rates. Infected fish may become hyperactive and display such symptoms as swimming in circles or in a corkscrew pattern, sometimes accompanied by a twisting of their bodies. In its chronic form, the disease results in similar symptoms except that fluid accumulation in the organs replaces hemorrhaging and mortality rates are lower. There is no cure. Fish that survive infection with the VHS virus can carry the virus for the rest of their lives, often with no symptoms, spreading the disease and infecting additional fish. Not all infected fish show symptoms but may be carriers of the disease. VHS does not pose a threat to human health.

Almost 50 species of fish are known to be susceptible to VHS, including such commercially and recreationally important species as brook trout, Chinook salmon, lake trout, rainbow trout, walleye, smallmouth bass, northern pike, yellow perch, and muskellunge. The virus has also been found in bluntnose minnows, Chinook salmon and emerald shiners but has not resulted in die offs of those species. The ultimate potential impact of VHS on North American fisheries is still unknown, but there is the potential for significant fishery, angling, tourism, and economic consequences.

VHS can be spread from one waterbody to the next through a variety of means, not all of which are known at this time. One known vector is moving fish from one waterbody to another by importation, stocking, or bait fish transport. Other potential transmittal vectors are natural fish movements, recreational boating/angling, waterfowl, ballast water discharge, and lake resource sampling activities.

 

Prevention

Anglers and boaters can reduce the likelihood of their spreading VHS from waterbody to waterbody by adhering to the following guidelines:

• Do not transport fish of any type from one body of water to another. [Such transport is illegal without a DEC fish stocking permit]
• Do not dispose of dead fish or fish parts in any body of water
• Do not release any baitfish into any waterbody other than the one from which the bait was harvested. Commercially purchased bait should not be released into any waterbody
• Remove all mud, aquatic plants and animals (such as snails, zebra mussels, etc.) from all fishing gear, boats, motors and trailers before leaving a waterbody
• Drain live wells, bait tanks and bilge areas before leaving any waterbody. If the waterbody you are leaving is known to be infected with VHS you should disinfect live wells and bait wells with a 10% chlorine/water solution followed by a thorough rinse to remove any residual chlorine

 

Federal Response to VHS

In order to prevent or delay the spread of VHS to other states, APHIS (the Animal and Plant Health Inspection Service) prohibits the importation of certain species of live fish from the Canadian provinces of Ontario and Quebec and interstate movement of the same species from Illinois, Indiana, Michigan, Minnesota, New York, Ohio, Pennsylvania, and Wisconsin. (The Federal Order was issued on October 24, 2006.)

The species included in the federal prohibition are: black crappie, bluegill, bluntnose minnow, brown bullhead, brown trout, burbot, channel catfish, chinook salmon, emerald shiner, freshwater drum, gizzard shad, lake whitefish, largemouth bass, muskellunge, northern pike, pumpkinseed, rainbow trout, rock bass, round goby, silver redhorse, smallmouth bass, trout perch, walleye, white bass, white perch, and yellow perch. Additional information on the Federal Order can be found on the APHIS website at:

http://www.aphis.usda.gov/animal_health/animal_dis_spec/aquaculture/downloads/vhs_fed_order_amended.pdf

New York State Response to VHS

The New York State Department of Environmental Conservation finalized fish health regulations to prevent the spread of VHS in the inland waters of the state. These regulations include such actions as prohibiting the transport of fish from one body of water to another and restricting the use of baitfish to the waterbody from which they were harvested unless certified as VHS free. These regulations, dated June 6, 2007, can be found at:

http://www.dec.ny.gov/outdoor/33072.html.

Photo and Graphic Credits

2005-2007 Mortality Events Map – Coastwatch, Michigan State University Sea Grant, 2009

Fish kill – US Fish & Wildlife Service

Muskellunge – Dr. Paul Bowser, Dept. Of Veterinary Medicine, Cornell University